No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Change in depression as a precursor of cardiovascular events. SHEP Cooperative Research Group (Systoloc Hypertension in the elderly)
Abstract
To determine the relationship between increasing depressive symptoms and cardiovascular events or mortality.
Cohort analytic study of data from randomized placebo-controlled double-blind clinical trial of antihypertensive therapy. Depressive symptoms were assessed semi-annually with the Center for Epidemiological Studies-Depression (CES-D) scale during an average follow-up of 4.5 years.
Ambulatory patients in 16 clinical centers of the Systolic Hypertension in the Elderly Program.
Generally healthy men and women aged 60 years or older randomized to active antihypertensive drug therapy or placebo who were 70% white and 53% women and had follow-up CES-D scores and no outcome events during the first 6 months (N=4367).
All-cause mortality, fatal or nonfatal stroke, or myocardial infarction.
Baseline depressive symptoms were not related to subsequent events; however, an increase in depression was prognostic. Cox proportional hazards regression analyses with the CES-D scale as a time-dependent variable, controlling for multiple covariates, indicated a 25% increased risk of death per 5-unit increase in the CES-D score (relative risk [RR], 1.25;95% confidence interval [CI], 1.15 to 1.36). The RR for stroke or myocardial infarction was 1.18(95%CI,1.08 to 1.30). Increase in CES-D score was an independent predictor in both placebo and active drug groups, and it was strongest as a risk factor for stroke among women (RR,1.29;95%CI,1.07 to 1.34).
Among elderly persons, a significant and substantial excess risk of death and stroke or myocardial infarction was associated with an increase in depressive symptoms over time, which may be a marker for subsequent major disease events and warrants the attention of physicians to such mood changes. However, further studies of casual pathways are needed before wide-spread screening for depression in clinical practice is to be recommended.
... For four studies included in the review, 31-34 the first author was contacted in order to get missing information; in all but one case, 31 the information could be obtained (see Table 1 for details). If a study did not report an age-adjusted RR but provided information on number of cases and total subjects at risk, or provided number of cases, non-cases, and person-years, 35,36 I calculated by hand crude RRs and confidence intervals (CIs), in accordance to the formulas that can be found in standard epidemiologic textbooks (e.g., Hennekens and Buring 37 ). ...
... Of these 83 articles, 11 met the final inclusion criteria (Step 3). [31][32][33][34][35][36][41][42][43][44][45] Studies were excluded at Step 3 because they reported endpoints other than myocardial infarction and coronary/cardiac death (nϭ13), 46 -58 did not report enough information to calculate RRs (nϭ6), 59 -64 or did not use a validated depression scale (nϭ1). 65 Fifty-two studies were excluded because they were focused exclusively on patients with established CHD at baseline. ...
... [32][33][34][35][41][42][43][44] The three other studies included both subjects with and without CHD but had controlled for baseline disease status in multivariate or stratified analyses. 31,36,45 The number of subjects ranged from 730 to 7894 and the number of cases from 50 to 463, with a mean time of follow-up from 3 to 37 years. The percentage of subjects lost to follow-up was reported in six studies and ranged from 0.1% to 7.0%. ...
... 3,6,9,10 Depression has recently emerged as a notable risk factor for both CHD 11,12 and stroke. [13][14][15] Depressive disorders are twice as likely in women as in men, 16 and are the leading causes of disease burden for women worldwide. 17 In the United States, depression is more prevalent among females aged 40 to 59 years than any other age or sex group. ...
... 27 One methodological limitation of studies of SSRI effects in people is the inability to control for treatment indication, often depression, which is a known risk factor for cardiovascular disease. [11][12][13][14][15] Consequently, there is a need for longitudinal, controlled, randomized studies to determine effects of SSRIs on carotid artery atherosclerosis progression independent of depression; however, long-term randomized trials evaluating SSRI effects are not ethical in healthy human populations. The aim of this study was to determine the effects of chronic SSRI treatment and depression on atherosclerosis in several carotid artery anatomical sites using a translational nonhuman primate model of depression. ...
Objective:
Atherosclerosis developed during premenopausal years predicts postmenopausal atherosclerosis burden. Selective serotonin reuptake inhibitor (SSRI) antidepressants, recently approved for hot flushes, have been associated with increased ischemic stroke risk in several observational studies; however, effects on carotid artery atherosclerosis, a strong predictor of future vascular events, are unknown.
Methods:
The effects of chronic administration of a commonly prescribed SSRI, sertraline HCl, on atherosclerosis in the carotid artery was assessed in a placebo-controlled, longitudinal, randomized study of premeonopausal depressed and nondepressed cynomolgus monkeys (Macaca fascicularis; n = 42). Physiologic and behavioral phenotypes were evaluated at baseline and after 18 months of oral sertraline (20 mg/kg, n = 21) or placebo (n = 21). Carotid artery atherosclerosis was measured post mortem via histomorphometry.
Results:
Atherosclerosis extent in the right common carotid artery, on average, was 60% greater in sertraline-treated depressed monkeys compared with all other groups (P = 0.028). The results of linear regression analyses suggested that sertraline and depression effects on atherosclerosis were not mediated by their effects on behavioral and physiological risk factors.
Conclusions:
These findings suggest that chronic SSRI treatment is associated with the progression of carotid artery atherosclerosis, which may increase the risk for future vascular events, particularly in depressed women. The underlying mechanism remains to be determined, but does not appear to be related to SSRI effects on traditional cardiovascular risk factors.
... 16 These results are consistent with an earlier 6-month study analysis of the same (SHEP) cohort. 17 In a retrospective analysis of 17,337 adult health plan members from 1995 to 1997, a dose-response relationship was found between adverse childhood experiences (ACE) and IHD, which was mediated more strongly by individual psychological risk factors, such as depressed affect and anger, than by traditional risk factors, such as smoking, physical inactivity, obesity, diabetes, and hypertension. These findings provide further insights into the potential pathways by which stressful childhood experiences, such as abuse, neglect, and household dysfunction, may increase the risk of IHD in adulthood. ...
... 15 Moreover, depression is clearly associated with nonadherence to risk-reducing behavioral recommendations. 23 A study of 817 patients who underwent coronary artery bypass surgery (CABG) revealed that, during the mean follow-up of 5.2 years, there were 122 deaths (15%), 38% of the patients had mild depression (CES-D score, [16][17][18][19][20][21][22][23][24][25][26], and 12% had moderate to severe depression (CES-D score ࣙ 27). A survival analysis, which controlled for age, gender, number of grafts, diabetes, smoking, LVEF, and previous MI, showed that patients with moderate to severe depression at baseline (adjusted HR = 2.4; P = 0.001) and patients with mild, moderate, or severe depression persisting from baseline for 6 months (HR = 2.2; P = 0.015), had higher rates of death than those who had no depression. ...
Patients with major depression are at an increased risk for developing cardiovascular disease, respond more poorly to treatment, and exhibit worse outcomes, including increased morbidity and mortality. This article reviews the relationship between depression and heart disease, with an emphasis on epidemiology, biological substrates that likely underlie this relationship, and implications for treatment.
© 2015 New York Academy of Sciences.
... Our previous experience in reading this article revealed four instances where relative risk (RR) values were extracted instead of adjusted hazard ratios (HR), as stated by the authors. These articles include "Kawamura et al.," 2 "Simons et al." 3 and "Wassertheil-Smoller et al." 4 Also, the authors may extracted the wrong number from "Liebetrau et al.," 5 which should be "HR = 2.7; 95% CI: 1.5-4.7." Combining two different effect sizes for data analysis is deemed inappropriate. ...
... Given that most strokes occur after the age of 65, many previous studies investigated the association between pre-existing depression and stroke in older adult populations and found that depression was a strong predictor of future stroke in older patients. [26][27][28] Some studies have examined the association of depression and stroke in a younger population of adults. In young to middle-aged adults aged 18 to 45, those with depression had a higher risk of developing stroke later in life. ...
Background: Stroke during pregnancy is rare but contributes to severe maternal morbidity and mortality. Further, studies have linked depression and cardiovascular risk factors. The objective of the current study was to determine if an association between perinatal depression and stroke occurrence existed.
... [4][5][6][7] Depression symptoms that increase or worsen over time may signal HF disease progression in HFrEF patients 8 and heightened hazard of adverse outcomes in cardiac patients. [9][10][11][12] In addition to being an important diagnostic test for HF disease, several studies have demonstrated that B-type natriuretic peptide (BNP) predicts clinical outcomes, including mortality and hospitalizations for patients with HF at all stages of disease. 13,14 HFrEF disease severity, as indicated by BNP, can show marked fluctuations over days or weeks. ...
BACKGROUND Prior studies have demonstrated an association of depression with adverse clinical outcomes in patients with HFrEF, but the possible mechanisms responsible for the association are not unserstood.
METHODS 142 men and women with HFrEF were enrolled through HF clinics and followed over time. At baseline and 6-months, depression was assessed by the Beck Depression Inventory (BDI-II) and disease activity by B-type natriuretic peptide (BNP). Proportional Hazards Regression Models assessed the contribution of depressive symptoms and HFrEF disease biomarkers on death or cardiovascular hospitalization.
RESULTS Over a median follow-up period of 4 years, 42 patients (30%) died, and 84 (60%) had cardiovascular hospitalizations. A 10-point higher baseline BDI-II score was associated with a 35% higher hazard of death or cardiovascular hospitalization. Greater baseline BDI-II scores were associated with poorer HF self-care maintenance (R=-0.30, p<0.001) and fewer daily steps (R=-0.19, p=0.04), suggesting that depression may adversely affect important health behaviors. Increases in plasma BNP over 6 months were associated with worse outcomes. Changes in BDI-II score and plasma BNP over 6 months were positively correlated (R=0.25, p=0.004).
CONCLUSIONS This study underscores the importance of elevated depression symptoms and their association with an increased likelihood of adverse clinical outcomes in patients with HFrEF. Health behaviors may play a greater role than direct biobehavioral pathways in the adverse effects of depression on the HF disease trajectory and resultant clinical outcomes.
... There appears to be evidence of dose-response effects, because greater burden of depression symptoms was associated with increased risk of CVD and CVD events. 106,[108][109][110][111][112][113][114][115][116] A metaanalysis of 11 studies showed elevated relative risk of depression in predicting new-onset coronary artery disease in adults was 1.64 (95% CI, 1.29-2.08). 117 From a familialgenetic perspective, there is evidence from general population and twin studies that depression and CVD are familial, beyond what can be explained by environmental factors such as socioeconomic status and CVRFs such as smoking and obesity. ...
This narrative review, emphasizing children and adolescents, addresses the link between five psychiatric disorders and cardiovascular risk: attention deficit hyperactivity disorder (ADHD), autism spectrum disorders, anxiety disorders, depression, and bipolar disorders. The evidence regarding cardiovascular risk factors, non-invasive measures of early atherosclerosis, and cardiovascular disease prevalence and/or mortality is summarized. Whereas multiple studies have examined stimulant treatment of ADHD in relation to cardiovascular death, and autonomic-vagal function in autism spectrum disorders, little is known regarding atherosclerotic cardiovascular disease in these conditions. For anxiety disorders, there is a gap in knowledge regarding cardiovascular risk in clinical samples of youth. In contrast to the adult literature, there are few studies regarding depression diagnoses, as opposed to self-reported symptoms, in relation to cardiovascular risk in youth. For bipolar disorder, youth studies focusing on epidemiologic samples and various mood-stabilizing medications are warranted. General recommendations for future research include: larger samples, prospective repeated-measures studies, and the integration of clinical and biological mediators with non-invasive measures of early atherosclerosis. Overall, the potential implications of cardiovascular risk factors are multiplied in youth with psychiatric conditions, as these risk factors are relevant not only to cardiovascular disease but to mental health and cognitive function. A shift in thinking regarding treatment paradigms for youth with psychiatric disorders is warranted. Pending changes in clinical practice guidelines and care delivery models, patients, families, clinicians, and policy makers can act on currently available information to reduce cardiovascular risk among children and adolescents with psychiatric disorders.
... factor for stroke among older adults with hypertension (Simonsick et al., 1995). Increased depressive symptoms over time are associated with increased risk for stroke and myocardial infarction (WassertheilSmoller et al., 1996). Given that psychological health has substantial implications for the wellbeing of hypertensive individuals, we address this gap by examining a pathway to psychological health among this sample. ...
Hypertensive individuals represent a “vulnerable” population regarding psychological health. While African Americans are disproportionally burdened with hypertension, pathways predicting their psychological health remain understudied. We examine if discrimination is associated with psychological health, through an indirect effect of perceived control within a sample of African American individuals with prevalent hypertension ( n = 990). Discrimination was significantly associated with an increase psychological distress and a decrease in psychological well-being through a reduction in perceived control, supporting Minority Stress Theory. Cardiovascular disease risk factor management implications are discussed.
... Patients with depression have a high rate of coronary ischemia and development of a recurrent MI [14], depression representing a predictor of the high mortality risk compared with non-depressive patients. The most frequent cardiovascular symptoms associated with depression, prior to MI, are high blood pressure (HBP) mainly systolic, associated or not with angina pectoris episodes [15]. ...
Epidemiological data confirm the rising incidence of depression associated with suicidal ideation and cardiovascular comorbidities of coronary type. In contradiction with the large number of antidepressant drugs, the therapeutic results are not satisfactory, with numerous existing incomplete remissions characterized by maintained cellular dysfunctionalities that amplify the cognitive deterioration and the risk of several somatic comorbidities. The surprising fact is the relatively high number of deaths in this type of patients due to acute coronary disease (myocardial infarction - MI). The vulnerability of hippocampal and frontal cortex cerebral structures is presented as obtained on animal model consecutive to hypothalamic-pituitary-adrenal (HPA) axis hyperactivity and on theoretical model where the hypothalamic disconnectivity determines the activation in the sympathetic autonomic nervous system, leading to heart disorders: high blood pressure, left ventricular hypertrophy and coronary illness. Identifying the association of psychological risk factors, patients fitting in a model of psychosomatic dominant personality traits, where the main risk factors are represented by inflexibility, guilt and self-accusation feelings, associated with increase of biological indicators (proinflammatory factors, endothelial dysfunction and cytokine aggressiveness) and neuroimaging indicators (frontal, temporal, hippocampal atrophy, ventriculomegaly, cerebellum atrophy). Changes identified post-mortem in the arterioles from the frontal cortex were found also in the coronary vessels, suggesting a symmetric evolution The highlighted personality factors are responsible for the decrease of adherence and compliance both in the psychiatric and the cardiologic treatment, the patient being exposed to behavioral risks regarding life style and nutrition, factors that increase the risk for acute coronary accident. The psycho-neurobiological inspired theoretical models argument the importance of a differentiated and customized approach of the patients with depressive disorder and suicidal ideation, and they can be the base for initiating strategies for prevention of unfavorable evolution and risk of death by MI.
... Kawachi, Spiro, Weiss, Vokonas, & Sparrow, 1997;Wassertheil-Smoller, Applegate, Berge, Chang, Davis, Grimm et al. ...
Das Modell beruflicher Gratifikationskrisen (engl. effort-reward-imbalance, ERI model) gilt in der Stressforschung als ein viel versprechendes Modell zur Vorhersage des Erkrankungsrisikos insbesondere kardiovaskulärer Erkrankungen. Kernpunkt des Modells ist die Annahme, dass ein Ungleichgewicht zwischen beruflicher Verausgabung und Belohnung mit Gesundheitsrisiken verbunden ist. In dieser Arbeit wird die prädiktive Validität des Modells unter Einbezug von Indikatoren allostatischer Last sowie psychologischer Aussenkriterien (gesundheitsbezogene Lebensqualität, depressive Verstimmung, vitale Erschöpfung, Schlafqualität) untersucht. Weiterhin wurde die zugrunde liegende Faktorenstruktur des ERI-Modells durch Strukturgleichungsmodellierung getestet. Die Studienpopulation umfasste mehrere hundert Mitarbeiter in der Fertigung eines europäischen Flugzeugherstellers. Die Ergebnisse bestätigen die prädiktive Validität des Modells im Hinblick auf gesundheitsbezogene Lebensqualität, vitale Erschöpfung, depressive Verstimmung und Schlafstörungen, sowie im Hinblick auf Indikatoren biologischer Verschleissprozesse (Allostatic Load). Konfirmatorische Faktorenanalysen bestätigten die faktorielle Validität des ERI Modells mit der Annahme von "effort" und "reward" und "overcommitment" als eigenständige Subskalen. Die Befunde unterstreichen die Bedeutung der subjektiv wahrgenommenen Austauschgerechtigkeit für die psychische und biologische Gesundheit der Mitarbeitenden. The effort-reward-imbalance model has received considerable attention in occupational health research. This model defines stressful experiences at work as an imbalance between high effort and low reward - a combination that can be aggravated by a particular individual coping style (overcommitment). General aim of this thesis was to evaluate the predictive and internal validity of this model in terms of a wide range of biological indicators of allostatic load and several indices of self-reported health and well-being (health-related quality of life, depressed mood, vital exhaustion, and sleep quality). Further, it was aimed to evaluate the underlying factorial structure of the current ERI model, using the structural equation approach. The studies of this thesis are based on a stratified random sample of employees from two European aircraft manufacturing plants. In general, the studies demonstrate that the effort-reward- imbalance model provides important measures for the evaluation of an adverse working environment. Its predictive validity is high for various psychological health outcomes, such as vital exhaustion, self-reported quality of life, depressed mood, and indicators of allostatic load. The model has high reliability and factorial validity. The findings underline the significance of effort-reward-imbalance as a critical psychological factor for employees' health.
... Several studies have shown that a higher depression score is associated with a poor prognosis in patients after myocardial infarction [2][3][4]. A higher depression score has also been associated with mortality and cardiovascular events in hypertensive patients [5,6] and patients with diabetes [7][8][9]. Therefore, the identification of depression can help predict cardiovascular events in individuals with cardiovascular disease or cardiovascular risk factors. ...
Depression is associated with mortality in patients with cardiovascular risk factors. The frequency and severity of depression and the association between depression and cardiovascular events have sex-specific and ethnic differences. We conducted this study to evaluate the sex-specific difference in the association between depression and cardiovascular prognosis in patients with cardiovascular risk factors. We enrolled 4025 patients (64.7 ± 10.9 years, 53% women, 47% men) with cardiovascular risk factors in the Japan Morning Surge-Home Blood Pressure study. Depressive symptoms were assessed using the Beck Depression Inventory (BDI). The follow-up period was 47 ± 24 months. The primary end points were all-cause mortality and nonfatal cardiovascular events. The BDI scores and the prevalence of depression were significantly higher in women than in men. When a BDI score of 16 was the cutoff, the primary end points in the depression group (n = 217) were significantly higher than those in the nondepression group (n = 1677) among men (adjusted hazard ratio 1.76, 95% confidence interval: 1.17, 2.64; P = 0.007). In women, the primary end points in the depression and nondepression groups were similar when BDI scores of 16, 14, and 10 were the cutoffs. In conclusion, depression defined by a BDI score ≥16 was associated with cardiovascular events in men with cardiovascular risk factors.
... Poststroke Depression-Consistent with prior studies, (11,(17)(18)(19) we defined depression using two data sources. The first was using the Center for Epidemiologic Studies Depression Scale (CES-D), a 20-item screening tool capturing levels of depressive symptoms. ...
To better identify stroke survivors at risk for depression who may benefit from early prevention through targeted strategies in the acute-subacute poststroke period, we examined 118 Framingham Heart Study stroke survivors with longitudinal prestroke depression assessments. Among those who developed poststroke depression, most lacked a history of depressive symptoms 5 years prior to their stroke. Sex (female), advanced age, and prestroke factors (smoking and functional dependence) were associated with new-onset depression poststroke. These findings suggest fully characterizing and accounting for prestroke factors, including psychosocial and behavioral determinants, may inform the predictive modeling needed to determine whether targeted preventive trials early in stroke recovery will improve stroke outcomes.
... This has been done in middle-aged population in post Myocardial infarction patients 23 and in elderly adults from the community. 24 This approach was hardly exportable here as a substantial numbers of incident CVD and noncardiovascular deaths occurred between study visits. To limit survival bias and maximize the follow-up information at hand, we used time dependent Cox proportional hazard models. ...
Backround:
Baseline depressive symptoms have been consistently associated with the onset of cardiovascular disease (CVD).
Objectives:
Since depressive symptoms vary over time in elderly persons, and to help clarify whether or not depression is an etiological factor for CVD, we quantified the association between the course of depressive symptoms and occurrence of first coronary heart disease (CHD) and stroke events in older adults.
Design:
A population-based prospective observational study.
Setting:
Participants were randomly selected from the electoral rolls of three large French cities.
Participants:
A total of 9,294 participants were examined at baseline between 1999 and 2001, and thereafter at repeated study visits over 10 years.
Measurements:
High levels of depressive symptoms (HLDS) were defined as a score≥16 on the 20-item Center for Epidemiologic Studies Depression Scale. The number of study visits with HLDS was used as a time dependent variable in Cox proportional hazard models.
Results:
There were 7,313 participants (36.6% males) aged 73.8±5.4 years with no history of CHD, stroke or dementia at baseline. After a median follow-up of 8.4 years (SD 2.3 years), 629 first CHD or stroke events occurred. After adjustment for sociodemographic characteristics and vascular risk factors, the risk of CHD and stroke combined increased 1.15-fold (95% CI: 1.06 to 1.25) per each additional study visit with HLDS. The results remained unchanged when accounting for the presence of disability and antidepressant intake at baseline and during follow-up.
Conclusion:
Elderly persons exposed to HLDS at several occasions over 10 years showed substantial increased risk of coronary heart disease and stroke events.
... Depression is increasingly recognized as an important risk factor for adverse cardiovascular events. Investigators from the Framingham Heart Study reported a 4-fold increase in risk of stroke or transient ischemic attack among cohort participants aged ≤65 years with depressive symptoms (CES-D≥16). 1 However, results from other studies have been less conclusive, 21,22 and the majority of work to date has been conducted in white populations. Evidence from the Chicago Health and Aging Project suggests that unadjusted stroke incidence rates were higher among older blacks (mean age, 77 years; n=2649) reporting psychological distress (a composite measure of depressive symptoms, perceived stress, neuroticism, and life dissatisfaction) than those who reported no distress. ...
Background:
Most studies of depression and cardiovascular risk have been conducted in white populations. We investigated this association in a community-based cohort of blacks.
Methods and results:
We used data from the Jackson Heart Study to investigate associations of baseline depressive symptoms between 2000 and 2004 with incident stroke and coronary heart disease (CHD) during 10 years. We used Kaplan-Meier estimates and Cox proportional hazards models to assess cardiovascular event risk using 3 exposure variables: any depressive symptoms (Center for Epidemiological Studies Depression score ≥16); none (score <16), minor (score 16 to <21), and major depression (score≥21); and Center for Epidemiological Studies Depression score per 1-SD increase. Models were adjusted for a stroke or CHD risk score and behavioral risk factors. Of 3309 participants with no stroke history, 738 (22.3%) had baseline depressive symptoms. A similar proportion with no previous CHD had baseline depressive symptoms (21.8%). The unadjusted 10-year risk of stroke was similar among participants with any compared with no depressive symptoms (3.7% versus 2.6%; P=0.12). Unadjusted CHD rates were higher among participants with depressive symptoms (5.6% versus 3.6%; P=0.03), and differences persisted after adjustment for clinical and behavioral risk factors but not after adjustment for coping strategies. In adjusted models comparing major versus no depressive symptoms, patients with major depressive symptoms had a 2-fold greater hazard of stroke (hazard ratio, 1.95; 95% confidence interval, 1.02-3.71; P=0.04). In continuous models, a 1-SD increase in Center for Epidemiological Studies Depression score was associated with a 30% increase in adjusted incident stroke risk (P=0.04). Similar associations were observed for incident CHD in models adjusted for clinical and behavioral risk factors, but associations were not significant after adjustment for coping strategies.
Conclusions:
In a community-based cohort of blacks, major depressive symptoms were associated with greater risks of incident stroke and CHD after adjustment for clinical and behavioral risk factors.
... (12) The results of these studies indicate a high significant prevalence of major depression in the patients with CAD, compared with healthy populations, in whom the prevalence of depression is only of 6.6%. (13) A review of studies that have followed the incidence and prevalence of depression in primary care reported numerous design differences between studies regarding the characteristics of participants and the methods used to diagnose depression. The same differences were seen in the studies that have sought to determine the prevalence of depression in the patients with various forms of heart disease. ...
During the last 15 years, numerous studies were conducted for detecting the prevalence of depression in the patients with coronary artery disease. The reported rate of depression vary a lot from study to study because of the differences between patients' demographic characteristics, such as gender, age or the type of coronary artery disease, as well as because of the method used to assess depression. Also, the patients with silent ischemia, heart failure, ischemic cardiomiopathy or arrhythmias because of coronary artery disease were not included in the analysis, as well as the patients from the control group (formed usually by healthy subjects), who were not screened for silent ischemia. Aim: the aim of the study was to determine the prevalence and the severity of depression in the patients with ischemic heart disease and to check if there are some differences of the depression rate between the forms of ischemic cardiopathy. Method: the study was conducted on 231 patients with ischemic heart disease recently diagnosed. Depression was screened using the PHQ questionnaire with 2 items. This questionnaire was applied at the inclusion into the study and at intervals of 1 month. The presence of depression was confirmed by the psychiatrist. A comparison between the prevalence of depression was done by the forms of ischemic cardiopathy and by gender. Results: at the end of the study, depression was diagnosed in 33,8% of the patients (n=81). This was more frequently encountered in the patients with myocardial infarction (43,1%) and in the patients with ischemic cardiomiopathy (42,9%) and less in the patients with silent ischemia (21,7%) and stable angina (27,1%). Depression was more frequent in women but this appeared earlier in men (8,09± 5,65 month vs 5,59±4,87 month, p=0,03), who also presented more severe depression in comparison with women. Cuvinte cheie: depresie, boală coronariană ishemică Rezumat: Pe parcursul ultimilor 15 ani, numeroase studii au fost efectuate pentru a detecta prevalența depresiei la pacienții cu boală coronariană. Rata de raportare a depresiei variază foarte mult de la studiu la studiu, din cauza diferențelor dintre caracteristicile demografice, cum ar fi: sexul, vârsta sau tipul de boală coronariană, precum metodele folosite pentru evaluarea depresiei. De asemenea pacienții cu cardiopatie ischemică din insuficiența cardiacă, cardiomiopatia ischemică sau aritmii din cauza unei boli coronariene nu au fost incluşi în analize, precum și pacienții din grupul de control (subiecți sănătoși) care nu au fost diagnosticaţi cu ischemie silențioasă. Scopul: Scopul studiului a fost de a determina prevalența și severitatea depresiei la pacienții cu boală cardiacă ischemică și pentru a verifica dacă există unele diferențe între rata depresiei în formele de cardiopatie ischemică. Metoda: Studiul a fost efectuat pe 231 de pacienți cu boală cardiacă ischemică diagnosticaţi recent. Screeningul pentru depresie s-a efectuat utilizând chestionarul PHQ-2 cu 2 itemi. Acest chestionar a fost aplicat la includerea în studiu și la intervale de 1 lună. Prezența depresiei a fost confirmată de medicul psihiatru. A fost făcută o comparație între prevalența depresiei, în formele de cardiopatie ischemică și sex. Rezultate: La sfârșitul studiului depresiei a fost diagnosticată la 33,8% dintre pacienți (n = 81). Acest lucru a fost mai frecvent la pacienții cu infarct miocardic (43,1%) și la pacienții cu cardiomiopatie ischemică (42,9 %) și mai puțin la pacienții cu ischemie silențioasă (21,7%) şi angină pectorală stabilă (27,1%). Depresia a fost mai frecventă la femei, dar aceasta a apărut mai devreme la bărbați (8,09 ± 5,65 vs 5,59 ± luni 4,87 luni, p = 0,03), care au prezentat de asemenea depresie mai severă în comparație cu femeile.
... Zale¿noae zgonów przewlek³ych oraz niezakoñczonych zgonem zawa³ów serca nie osi¹gnê³a natomiast istotnoci statystycznej [46]. W opublikowanym z kolei w 1996 r. badaniu Systolic Hypertension in the Elderly (SHEP) dowiedziono, ¿e obecnoae objawów depresyjnych istotnie wp³ywa na ryzyko zapadalnoci na zawa³ serca, udar mózgu oraz liczbê zgonów [47]. W badaniu tym obserwowano 4367 pacjentów w wieku powy¿ej 60 lat rednio przez 4,5 roku. ...
Objectives. To review the research literature concerning: (1) the effect of depression on the development and course of ischemic heart disease (IHD), (2) probable pathophysiological mechanisms underlying the association between IHD and depression, and (3) most recent studies on the impact of antidepressants on the course of IHD and comorbid depression (including SADHART, CREATE, ENRICHD, CAST, CASH, MIND-IT). Review. The hitherto conducted retrospective and prospective clinical studies, as well as meta-analyses clearly indicate a high correlation between the presence of depression and the risk for developing IHD in currently healthy persons, and between the incidence and severity of depressive symptoms on one hand and coronary symptoms severity in persons diagnosed with IHD, on the other hand. Among numerous data suggesting probable mechanisms of the association between depression and IHD, the following seem to be most important: hyperreactivity of the hypothalamic-pituitary-adrenal (HPA) axis with the associated catecholaminergic system activation, platelet dysfunction with the coagulation system activation, the immune system pathological hyperactivity of an inflammatory character, vascular endothelium dysfunction, and increased homocysteine concentrations. The most recent evaluative studies show that appropriate pharmacotherapy and psychotherapy of depression significantly improve the course and prognosis of IHD, among others, by reducing the risk of heart stroke and death. The SSRI medications turned out to be the safest. Conclusions. (1) Depression increases the risk for IHD development, is frequently comorbid with IHD, and has a significant effect on its course and prognosis . thus, there is a need for early diagnosis and effective treatment of depression. (2) Appropriate pharmacological treatment and psychotherapy may improve the course of IHD and its prognosis.
... 1,2 Several epidemiological studies 3,4 have suggested that high depression scores may predispose an individual to an increased risk of developing cardiovascular disease (CVD). Although most, [3][4][5][6][7][8][9][10][11] but not all [12][13][14] prospective studies of middle-aged populations addressing this issue have reported positive associations, data regarding the relationship between depressive symptoms and cardiovascular risk in the elderly are sparse. ...
Background—Several epidemiological studies have associated depressive symptoms with cardiovascular disease. We investigated whether depressive symptoms constituted a risk for coronary heart disease (CHD) and total mortality among an apparently healthy elderly cohort.
Methods and Results—In a prospective cohort of 5888 elderly Americans (≥65 years) who were enrolled in the Cardiovascular Health Study, 4493 participants who were free of cardiovascular disease at baseline provided annual information on their depressive status, which was assessed using the Depression Scale of the Center for Epidemiological Studies. These 4493 subjects were followed for 6 years for the development of CHD and mortality. The cumulative mean depression score was assessed for each participant up to the time of event (maximum 6-year follow-up). Using time-dependent, proportional-hazards models, the unadjusted hazard ratio associated with every 5-unit increase in mean depression score for the development of CHD was 1.15 (P=0.006); the ratio for all-cause mortality was 1.29 (P<0.0001). In multivariate analyses adjusted for age, race, sex, education, diabetes, hypertension, cigarette smoking, total cholesterol, triglyceride level, congestive heart failure, and physical inactivity, the hazard ratio for CHD was 1.15 (P=0.006) and that for all-cause mortality was 1.16 (P=0.006). Among participants with the highest cumulative mean depression scores, the risk of CHD increased by 40% and risk of death by 60% compared with those who had the lowest mean scores.
Conclusions—Among elderly Americans, depressive symptoms constitute an independent risk factor for the development of CHD and total mortality.
Aim
The current study aims to investigate the association of serum brain‐derived neurotrophic factor (BDNF) levels with symptoms of depression in adults with and without prevalent cardiovascular disease (CVD), an often burdensome comorbidity.
Methods
This cross‐sectional study included participants from FHS (Framingham Heart Study) who had available serum BDNF levels. Depressive symptoms were assessed using the Center for Epidemiological Studies–Depression Scale (CES‐D) with a score ≥16 indicating mild to moderate and ≥21 severe depression. Participants taking antidepressant medications were excluded from the study.
Results
Altogether 3716 FHS participants were included in the final analysis (mean age, 64.3 ± 11.5 years; 55% women). After adjusting for potential confounders, greater BDNF levels were associated with reduced severe depression risk (odds ratio [OR], 0.78 [95% CI, 0.64–0.96]; P = 0.016). Among participants with CVD, greater BDNF levels were related to lower risk of depressive symptoms (CES‐D ≥ 16 OR, 0.63 [95% CI, 0.45–0.89], P = 0.008; CES‐D ≥ 21 OR, 0.49 [95% CI, 0.31–0.76], P = 0.002). The inverse relationship between BDNF and depressive symptom risk was present in women with CVD (CES‐D ≥ 16 OR, 0.63 [95% CI, 0.40–0.99], P = 0.047; CES‐D ≥ 21 OR, 0.38 [95% CI, 0.21–0.70], P = 0.002) but not in men.
Conclusion
Lower serum BDNF levels are associated with a higher risk of depressive symptoms in CVD, particularly among women. These findings implicate BDNF in the complex biological mechanisms that underlie prior associations observed between CVD and depression. To reduce the burden of depression in the large proportion of midlife and older adults with CVD, a better understanding of how BDNF may modify these pathways is merited.
Introduction
Stroke is a significant global health concern, and numerous studies have established a link between depression and an increased risk of stroke. While many investigations explore this link, some overlook its long-term effects. Depression may elevate stroke risk through physiological pathways involving nervous system changes and inflammation. This systematic review and meta-analysis aimed to assess the association between depression and stroke.
Methodology
We conducted a comprehensive search of electronic databases (PubMed, Embase, Scopus, and PsycINFO) from inception to 9 April 2023, following the Preferred Reporting Items for Systemic Review and Meta-analysis (PRISMA) and Meta-analysis Of Observational Studies in Epidemiology (MOOSE) guidelines. We included all articles assessing the association between different stroke types and depression, excluding post-stroke depression. Two investigators independently extracted data and assessed quality using the Newcastle–Ottawa Scale and Cochrane Risk of Bias tool, utilizing a random-effects model for data synthesis. The primary outcome was the association of depression with stroke, with a secondary focus on the association of antidepressants with stroke.
Results
The initial search yielded 10,091 articles, and 44 studies were included in the meta-analysis. The pooled analysis revealed a significant association between depression and stroke risk, with an overall hazard ratio of 1.41 (95% CI 1.32, 1.50; p < 0.00001), indicating a moderately positive effect size. Subgroup analyses showed consistent associations with ischemic stroke (HR = 1.30, 95% CI 1.13, 1.50; p = 0.007), fatal stroke (HR = 1.39, 95% CI 1.24, 1.55; p < 0.000001), and hemorrhagic stroke (HR = 1.33, 95% CI 1.01, 1.76; p = 0.04). The use of antidepressants was associated with an elevated risk of stroke (HR = 1.28, 95% CI 1.05, 1.55; p = 0.01).
Conclusion and relevance
This meta-analysis indicates that depression moderately raises the risk of stroke. Given the severe consequences of stroke in individuals with depression, early detection and intervention should be prioritized to prevent it.
Systematic review registration
Prospero (CRD42023472136).
Objective
Whether late‐life depression or depressive symptoms are a risk factor of future stroke in elders is important for prevention measures. A systematic review and meta‐analysis were used to investigate the association between depression or depressive symptoms and risk of stroke in elders.
Methods
Embase, MEDLINE, PsychINFO, and Web of Science were searched for studies published from inception to January 6, 2023. Prospective cohort studies reporting quantitative estimates of the association between depression or depressive symptoms and stroke morbidity in participants aged over 60 years were included. Reviews, meta‐analyses, case reports, retrospective, cross‐sectional, and theoretical studies were excluded. Study screening and data extraction were conducted by two researchers independently. Random‐effects meta‐analysis was used to estimate pooled adjusted hazard ratios (HRs). Publication bias was evaluated via the symmetry of funnel plots and Egger tests. The Newcastle Ottawa Scale was used to assess the risk of bias. The quality of evidence of synthesis was assessed by the Grading of Recommendations Assessment, Development and Evaluation (GRADE). The primary outcome was any stroke, including non‐fatal, fatal, ischemic and hemorrhagic sub‐types.
Results
Seventeen studies of 57,761 patients in total were included in the meta‐analysis. A positive association was found between depressive disorder or symptoms and stroke risk (HR: 1.39; 95% CI: 1.22–1.58; p < 0.001).
Conclusions
Late‐life depression or depressive symptoms are a significant risk factor for stroke in older people. Regular assessment and more effective management of associated comorbidities are recommended to reduce stroke risk.
Background:
High sensitivity C-reactive protein (hsCRP) is a marker of systemic inflammation that has been associated with persistent depressive symptoms. Depression and anxiety are frequently associated with a chronic inflammatory state, yet the nature of this relationship has not been rigorously examined in diverse Hispanic/Latino populations. We aimed to study the association of anxiety and depressive symptoms as well as comorbid presentations, with circulating high sensitivity C-reactive protein (hsCRP) levels in a large Latino cohort of diverse heritages. We hypothesized a significant positive associations of both anxiety and depressive symptoms and hsCRP levels and potential variations among the heritage groups.
Methods:
Depressive symptoms and anxiety were measured by the Center for Epidemiological Studies Depression Scale (CES-D) and State-Trait Anxiety Inventory (STAI), respectively. Serum hsCRP (hsCRP) levels of 15,448 participants (age 18 to 75 years; 52.3% women) from the Hispanic Community Health Study/Study of Latinos (HCHS/SOL) were measured and categorized based on the established cardiovascular disease (CVD) risk reference values (< 1mg/L, low; 1-<3 mg/L, intermediate; ≥ 3mg/L, high).
Results:
Mean CES-D, STAI scores, and hsCRP levels were 7.0 (SD = 5.9), 17.0 (SD = 5.7), and 3.84 (SD = 7.85), respectively. Generalized linear modeling, adjusted for sociodemographic characteristics revealed significant associations between depression (exp(β) = 1.12; p<0.01) and anxiety symptoms (exp(β) = 1.10; p<0.05) with continuous hsCRP levels. For categorical values of hsCRP, one SD increase in CES-D and STAI scores was associated with a 10% and 8% increase in the RRRs of high vs. low hsCRP, respectively. However, these relationships between CES-D or STAI and hsCRP were no longer statistically significant after adjustment for CVD risk factors and medications.
Conclusion:
We found modest associations between anxiety and depressive symptoms and systemic inflammation measured by hsCRP among diverse Hispanics/Latinos that did not appreciably differ between heritage groups.
Introduction:
Stroke is a significant cause of death, and the leading cause of severe long-term disability for individuals over 80 (the very old), yet few studies of such risk factors for ischemic stroke, or the known mitigation techniques, in this population, and the evidence base regarding risk modification strategies in this susceptible population can be inconsistent and incomplete. This article examines current guidelines and evidence regarding medical management, lifestyle changes, and psychosocial interactions that can contribute to the primary and secondary prevention of ischemic stroke in the very old.
Areas covered:
The authors conducted a literature search for ischemic stroke prevention and risk assessment in the elderly via PubMed. Furthermore, they describe current strategies for monitoring risk and preventing ischemic stroke in the elderly population.
Expert opinion:
Ischemic stroke poses a significant health risk to the elderly, with prevention relying on managing modifiable risk factors such as hypertension, atrial fibrillation, diabetes, and high cholesterol, as well as promoting healthy lifestyle choices like quitting smoking, regular physical activity and a heart-healthy diet. Healthcare providers must adopt a multifaceted approach, addressing individual and population-level factors while remaining vigilant in monitoring and managing risk factors to reduce the incidence and impact of stroke in older adults.
Objectives:
The objective was to determine odds of frailty syndrome with coexistence of hypertension and depression among oldest-old adults.
Methods:
We analysed secondary data from 167 community-dwelling hypertensive participants aged 80 years and older from a cross-sectional study of frailty conducted in India. Data included sociodemographic, medical history, physical performance, functional limitations, mobility-disability, cognition, depression, sleep, frailty syndrome and chronic diseases. Odds of frailty syndrome was compared among individuals having only hypertension, and individuals having hypertension and depression. Chi-square test, t-test and logistic regression were performed to determine odds of frailty.
Results:
Frailty was significantly higher (OR: 4.93;95% CI: 1.89-12.84) among individuals having hypertension and coexisting depression, compared to individuals having only hypertension. Men (OR: 5.07;95% CI: 1.02-25.17) and women (OR: 4.58;95% CI: 1.36-15.40) with hypertension and depression showed a higher risk of frailty, compared with hypertension alone. Logistic regression models were adjusted for age, sex, cognitive impairment, chronic obstructive pulmonary disease, cardiovascular diseases, anaemia, diabetes, obesity, physical performance, activities of daily living and 4-meter walking speed.
Conclusion:
Coexistence of hypertension and depression increased risk of frailty syndrome among men and women above 80 years of age by almost 5 folds. Treating depression in hypertensive older individuals may reduce the risk of frailty among them.
Aim:
To explore the cross-sectional and longitudinal associations between social frailty (SF) and incident depressive symptoms in a Chinese population.
Methods:
SF was measured with 6 questions (6 points maximum; 0-1 = non-SF, 2-3 = pre-SF, 4-6 = SF). Depressive symptoms were defined as a score of ≥6 on the Geriatric Depression Scale. Compared to baseline, participants with a ≥2-point increase in the Geriatric Depression Scale score were considered to have worsening depressive symptoms.
Results:
At baseline, among 1764 participants, 9.9% (n = 175) had depressive symptoms, 3.6% (n = 61) were SF, and 38.2% (n = 650) were pre-SF. The percentage of depressive symptoms increased with SF status from 5.1% (non-SF) to 12.9% (pre-SF), to 41.0% (SF). In cross-sectional analysis, after adjustments for multiple covariates, depressive symptoms were significantly associated with both pre-SF (odds ratio (OR) = 2.94, 95% confidence interval (CI) 2.01-4.32) and SF (OR = 16.70, 95% CI 8.80-31.71). During the 3-year follow-up period, 10.0% (n = 117) of the participants developed depressive symptoms. In longitudinal analyses, after multiple adjustments, SF and pre-SF were associated with a 2.31-fold (95% CI 1.10-4.88) and 1.58-fold (95% CI 1.05-2.38) increased risk of incidence of depressive symptoms, respectively. Among participants without depressive symptoms at baseline, 23.2% had worsening depressive symptoms, and SF was associated with increased risk of worsening depressive symptoms (OR = 2.07, 95% CI 1.18-3.65).
Conclusions:
Our findings suggested that SF may be a predictor of depression among Chinese community-dwelling older adults. In addition, in elders with no depressive symptoms at baseline, those with SF had greater odds of worsening depressive symptoms 3 years later.
Background:
This is the second substantive update of this review. It was originally published in 1998 and was previously updated in 2009. Elevated blood pressure (known as 'hypertension') increases with age - most rapidly over age 60. Systolic hypertension is more strongly associated with cardiovascular disease than is diastolic hypertension, and it occurs more commonly in older people. It is important to know the benefits and harms of antihypertensive treatment for hypertension in this age group, as well as separately for people 60 to 79 years old and people 80 years or older.
Objectives:
Primary objective• To quantify the effects of antihypertensive drug treatment as compared with placebo or no treatment on all-cause mortality in people 60 years and older with mild to moderate systolic or diastolic hypertensionSecondary objectives• To quantify the effects of antihypertensive drug treatment as compared with placebo or no treatment on cardiovascular-specific morbidity and mortality in people 60 years and older with mild to moderate systolic or diastolic hypertension• To quantify the rate of withdrawal due to adverse effects of antihypertensive drug treatment as compared with placebo or no treatment in people 60 years and older with mild to moderate systolic or diastolic hypertension SEARCH METHODS: The Cochrane Hypertension Information Specialist searched the following databases for randomised controlled trials up to 24 November 2017: the Cochrane Hypertension Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE Ovid (from 1946), Embase (from 1974), the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. We contacted authors of relevant papers regarding further published and unpublished work.
Selection criteria:
Randomised controlled trials of at least one year's duration comparing antihypertensive drug therapy versus placebo or no treatment and providing morbidity and mortality data for adult patients (≥ 60 years old) with hypertension defined as blood pressure greater than 140/90 mmHg.
Data collection and analysis:
Outcomes assessed were all-cause mortality; cardiovascular morbidity and mortality; cerebrovascular morbidity and mortality; coronary heart disease morbidity and mortality; and withdrawal due to adverse effects. We modified the definition of cardiovascular mortality and morbidity to exclude transient ischaemic attacks when possible.
Main results:
This update includes one additional trial (MRC-TMH 1985). Sixteen trials (N = 26,795) in healthy ambulatory adults 60 years or older (mean age 73.4 years) from western industrialised countries with moderate to severe systolic and/or diastolic hypertension (average 182/95 mmHg) met the inclusion criteria. Most of these trials evaluated first-line thiazide diuretic therapy for a mean treatment duration of 3.8 years.Antihypertensive drug treatment reduced all-cause mortality (high-certainty evidence; 11% with control vs 10.0% with treatment; risk ratio (RR) 0.91, 95% confidence interval (CI) 0.85 to 0.97; cardiovascular morbidity and mortality (moderate-certainty evidence; 13.6% with control vs 9.8% with treatment; RR 0.72, 95% CI 0.68 to 0.77; cerebrovascular mortality and morbidity (moderate-certainty evidence; 5.2% with control vs 3.4% with treatment; RR 0.66, 95% CI 0.59 to 0.74; and coronary heart disease mortality and morbidity (moderate-certainty evidence; 4.8% with control vs 3.7% with treatment; RR 0.78, 95% CI 0.69 to 0.88. Withdrawals due to adverse effects were increased with treatment (low-certainty evidence; 5.4% with control vs 15.7% with treatment; RR 2.91, 95% CI 2.56 to 3.30. In the three trials restricted to persons with isolated systolic hypertension, reported benefits were similar.This comprehensive systematic review provides additional evidence that the reduction in mortality observed was due mostly to reduction in the 60- to 79-year-old patient subgroup (high-certainty evidence; RR 0.86, 95% CI 0.79 to 0.95). Although cardiovascular mortality and morbidity was significantly reduced in both subgroups 60 to 79 years old (moderate-certainty evidence; RR 0.71, 95% CI 0.65 to 0.77) and 80 years or older (moderate-certainty evidence; RR 0.75, 95% CI 0.65 to 0.87), the magnitude of absolute risk reduction was probably higher among 60- to 79-year-old patients (3.8% vs 2.9%). The reduction in cardiovascular mortality and morbidity was primarily due to a reduction in cerebrovascular mortality and morbidity.
Authors' conclusions:
Treating healthy adults 60 years or older with moderate to severe systolic and/or diastolic hypertension with antihypertensive drug therapy reduced all-cause mortality, cardiovascular mortality and morbidity, cerebrovascular mortality and morbidity, and coronary heart disease mortality and morbidity. Most evidence of benefit pertains to a primary prevention population using a thiazide as first-line treatment.
Background:
This is the first update of a review published in 2009. Sustained moderate to severe elevations in resting blood pressure leads to a critically important clinical question: What class of drug to use first-line? This review attempted to answer that question.
Objectives:
To quantify the mortality and morbidity effects from different first-line antihypertensive drug classes: thiazides (low-dose and high-dose), beta-blockers, calcium channel blockers, ACE inhibitors, angiotensin II receptor blockers (ARB), and alpha-blockers, compared to placebo or no treatment.Secondary objectives: when different antihypertensive drug classes are used as the first-line drug, to quantify the blood pressure lowering effect and the rate of withdrawal due to adverse drug effects, compared to placebo or no treatment.
Search methods:
The Cochrane Hypertension Information Specialist searched the following databases for randomized controlled trials up to November 2017: the Cochrane Hypertension Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (from 1946), Embase (from 1974), the World Health Organization International Clinical Trials Registry Platform, and ClinicalTrials.gov. We contacted authors of relevant papers regarding further published and unpublished work.
Selection criteria:
Randomized trials (RCT) of at least one year duration, comparing one of six major drug classes with a placebo or no treatment, in adult patients with blood pressure over 140/90 mmHg at baseline. The majority (over 70%) of the patients in the treatment group were taking the drug class of interest after one year. We included trials with both hypertensive and normotensive patients in this review if the majority (over 70%) of patients had elevated blood pressure, or the trial separately reported outcome data on patients with elevated blood pressure.
Data collection and analysis:
The outcomes assessed were mortality, stroke, coronary heart disease (CHD), total cardiovascular events (CVS), decrease in systolic and diastolic blood pressure, and withdrawals due to adverse drug effects. We used a fixed-effect model to to combine dichotomous outcomes across trials and calculate risk ratio (RR) with 95% confidence interval (CI). We presented blood pressure data as mean difference (MD) with 99% CI.
Main results:
The 2017 updated search failed to identify any new trials. The original review identified 24 trials with 28 active treatment arms, including 58,040 patients. We found no RCTs for ARBs or alpha-blockers. These results are mostly applicable to adult patients with moderate to severe primary hypertension. The mean age of participants was 56 years, and mean duration of follow-up was three to five years.High-quality evidence showed that first-line low-dose thiazides reduced mortality (11.0% with control versus 9.8% with treatment; RR 0.89, 95% CI 0.82 to 0.97); total CVS (12.9% with control versus 9.0% with treatment; RR 0.70, 95% CI 0.64 to 0.76), stroke (6.2% with control versus 4.2% with treatment; RR 0.68, 95% CI 0.60 to 0.77), and coronary heart disease (3.9% with control versus 2.8% with treatment; RR 0.72, 95% CI 0.61 to 0.84).Low- to moderate-quality evidence showed that first-line high-dose thiazides reduced stroke (1.9% with control versus 0.9% with treatment; RR 0.47, 95% CI 0.37 to 0.61) and total CVS (5.1% with control versus 3.7% with treatment; RR 0.72, 95% CI 0.63 to 0.82), but did not reduce mortality (3.1% with control versus 2.8% with treatment; RR 0.90, 95% CI 0.76 to 1.05), or coronary heart disease (2.7% with control versus 2.7% with treatment; RR 1.01, 95% CI 0.85 to 1.20).Low- to moderate-quality evidence showed that first-line beta-blockers did not reduce mortality (6.2% with control versus 6.0% with treatment; RR 0.96, 95% CI 0.86 to 1.07) or coronary heart disease (4.4% with control versus 3.9% with treatment; RR 0.90, 95% CI 0.78 to 1.03), but reduced stroke (3.4% with control versus 2.8% with treatment; RR 0.83, 95% CI 0.72 to 0.97) and total CVS (7.6% with control versus 6.8% with treatment; RR 0.89, 95% CI 0.81 to 0.98).Low- to moderate-quality evidence showed that first-line ACE inhibitors reduced mortality (13.6% with control versus 11.3% with treatment; RR 0.83, 95% CI 0.72 to 0.95), stroke (6.0% with control versus 3.9% with treatment; RR 0.65, 95% CI 0.52 to 0.82), coronary heart disease (13.5% with control versus 11.0% with treatment; RR 0.81, 95% CI 0.70 to 0.94), and total CVS (20.1% with control versus 15.3% with treatment; RR 0.76, 95% CI 0.67 to 0.85).Low-quality evidence showed that first-line calcium channel blockers reduced stroke (3.4% with control versus 1.9% with treatment; RR 0.58, 95% CI 0.41 to 0.84) and total CVS (8.0% with control versus 5.7% with treatment; RR 0.71, 95% CI 0.57 to 0.87), but not coronary heart disease (3.1% with control versus 2.4% with treatment; RR 0.77, 95% CI 0.55 to 1.09), or mortality (6.0% with control versus 5.1% with treatment; RR 0.86, 95% CI 0.68 to 1.09).There was low-quality evidence that withdrawals due to adverse effects were increased with first-line low-dose thiazides (5.0% with control versus 11.3% with treatment; RR 2.38, 95% CI 2.06 to 2.75), high-dose thiazides (2.2% with control versus 9.8% with treatment; RR 4.48, 95% CI 3.83 to 5.24), and beta-blockers (3.1% with control versus 14.4% with treatment; RR 4.59, 95% CI 4.11 to 5.13). No data for these outcomes were available for first-line ACE inhibitors or calcium channel blockers. The blood pressure data were not used to assess the effect of the different classes of drugs as the data were heterogeneous, and the number of drugs used in the trials differed.
Authors' conclusions:
First-line low-dose thiazides reduced all morbidity and mortality outcomes in adult patients with moderate to severe primary hypertension. First-line ACE inhibitors and calcium channel blockers may be similarly effective, but the evidence was of lower quality. First-line high-dose thiazides and first-line beta-blockers were inferior to first-line low-dose thiazides.
Both literature and folklore have long acknowledged a relationship between depression and mortality. Even our language refers to the relationship between grief and the heart — in speech, poem, and song we describe people dying of a broken heart. However, in spite of this widespread common recognition, scientific evidence supporting these relationships has come only recently.
Selective serotonin reuptake inhibitor (SSRI) use is ubiquitous because they are widely prescribed for a number of disorders in addition to depression. Depression increases the risk of coronary heart disease (CHD). Hence, treating depression with SSRIs could reduce CHD risk. However, the effects of long term antidepressant treatment on CHD risk, as well as other aspects of health, remain poorly understood. Thus, we undertook an investigation of multisystem effects of SSRI treatment with a physiologically relevant dose in middle-aged adult female cynomolgus monkeys, a primate species shown to be a useful model of both depression and coronary and carotid artery atherosclerosis. Sertraline had no effect on depressive behavior, reduced anxious behavior, increased affiliation, reduced aggression, changed serotonin neurotransmission and volumes of neural areas critical to mood disorders, and exacerbated coronary and carotid atherosclerosis. These data suggest that a conservative approach to prescribing SSRIs for cardiovascular or other disorders for long periods may be warranted, and that further study is critical given the widespread use of these medications.
White et al [1][1] examined the relationship between the duration of depressive symptoms and mortality in adults aged 50 or older in a follow-up study. The authors assessed depressive symptom duration as the sum of screen-positive number by an eight-item Center for Epidemiologic Studies Depression
Marmot u. Winkelstein (1975) stellten fest, dass sich lediglich 50% der Varianz der koronaren Ereignisse durch die Standardrisikofaktoren erklären lässt, und sie leiteten aus diesem Befund die Hypothese ab, dass psychosoziale Bedingungen an Entstehung, Manifestation und Verlauf der koronaren Herzerkrankung wesentlich mitbeteiligt sind. Die entsprechende „Multiple-risk“-Theorie besagt, dass das koronare Risiko bei Präsenz eines oder mehrer psychosozialer Merkmale erhöht ist; und dass ein aufgrund von Standardrisikofaktoren bereits bestehendes Risiko durch psychosoziale Risikofaktoren deutlich erhöht werden kann und dass bei Vorliegen von psychosozialen Risikofaktoren und Standardrisikofaktoren synergetische Interaktionen zu erwarten sind.
Ein psychosoziales Merkmal qualifiziert sich als koronarer Risikofaktor vorrangig aufgrund prospektiver Studien mit anfänglich Gesunden oder Patienten, retrospektiver Längsschnittsstudien mit oder ohne Kontrollgruppendesign sowie retrospektiver Querschnittsstudien mit oder ohne Kontrollgruppendesign (Rudolf u. Eich 1999).
Das Herz hat nicht nur aus medizinischer Sicht, sondern auch in der Wahrnehmung des Menschen zentrale Bedeutung für die Funktionsfähigkeit des Körpers. Auch wird das Herz psychisch als Sitz von Emotionen verstanden. Gebräuchliche Redensarten wie „das geht mir zu Herzen“ oder „das bricht mir das Herz“ verdeutlichen diese Empfindung. Forschungsergebnisse, insbesondere der letzten 10 Jahre, haben empirisch belegt, dass Interaktionen zwischen Körper und Psyche in Bezug auf Herzerkrankungen eine erhebliche Bedeutung zukommt. Herzerkrankungen verursachen emotionale Belastungen: Die existenzielle Bedrohung durch eine Herzerkrankung mit der Möglichkeit abnehmender Leistungsfähigkeit, Invalidität oder Herztod kann persistierende Ängste und Beeinträchtigungen von Stimmung und Antrieb bis hin zur manifesten psychiatrischen Erkrankung verursachen. Umgekehrt sind auch psychiatrische Erkrankungen wie Depression, Panikstörung und andere Angsterkrankungen heute als unabhängige Risikofaktoren für die Entstehung von koronaren Herzerkrankungen anzusehen. Schließlich können die gleichen Symptome entweder auf eine primär kardiologische oder eine primär psychiatrische Erkrankung hinweisen, was in der klinischen Praxis häufig zu differenzialdiagnostischen Schwierigkeiten führt. So kann sich bekanntermaßen eine Panikstörung in Form von Thoraxschmerzen präsentieren oder eine kardiale Ischämie kann als akute Angsterkrankung fehlgedeutet werden. Die vielfältigen Problemkonstellationen an der Schnittstelle zwischen Psyche und Herzerkrankung sind eine besondere Herausforderung für den psychiatrischen bzw. psychosomatischen Konsiliarius.
Recenti studi dimostrano che i fattori psicologici contribuiscono in modo rilevante allo sviluppo e al decorso delle patologie cardiache. Mediante l’utilizzo delle nuove tecnologie e degli studi sperimentali condotti su animali, le ricerche hanno prodotto risultati che hanno contribuito a spiegare le basi patofisiologiche del legame tra fattori psicologici e patologia cardiaca (Compare, Gondoni e Molinari, 2006; Compare, Proietti et al. 2011; Compare, Germani et al. 2011a, 2011b).
Objective Symptoms of anxiety and depression often co-exist with cardiovascular disease (CVD), yet little is known about the association with left ventricular (LV) subclinical dysfunction. We aimed to study the cross-sectional associations of previous, current and repeated depression or anxiety symptoms, with sensitive indices of LV systolic and diastolic function, based on tissue Doppler (TD) and speckle tracking (ST) imaging methods.
Methods A random selection of 1296 individuals free from known CVD, hypertension and diabetes were examined with echocardiography at baseline of the third Nord-Trøndelag Health Study, (HUNT3, 2006–2008). The primary outcomes were LV diastolic function (e′) and LV systolic function (longitudinal global strain). The primary exposures were self-report on the Hospital Anxiety and Depression Scale (HADS). Associations between outcomes and baseline exposures were available for 1034 (80%), and with previous and repeated exposures for 700 participants who also participated in HUNT2 (1995–1997).
Results Previous and repeated depression symptoms, but not current depression, were linearly associated with a reduction in e′. The average sum of two repeated HADS-D scores 10 years apart had the strongest effect on e′ (−8.3%; 95% CI −13.9% to −2.7%) per 5 units. We observed a sex difference between depression symptoms and longitudinal global strain (p for interaction 0.019), where women had a marginal negative effect. Anxiety symptoms, neither previous, current nor repeated were associated with subclinical LV dysfunction.
Conclusions In a healthy sample, confirmed free of CVD, past and repeated depression symptoms were associated with subclinical LV dysfunction. Thus, depression symptoms might represent a modifiable risk factor for future CVD.
The first two editions of Stroke Syndromes were widely welcomed as authoritative reference works in the assessment and diagnosis of stroke. This revised and updated third edition remains the definitive guide to patterns and syndromes in stroke. A comprehensive survey of all types of neurological, neurophysiological and other clinical dysfunction due to stroke. The book contains descriptions of clinical problems encountered in stroke patients and their differential diagnosis, enhancing pattern recognition and enabling clinicians to differentiate between possible locations on the basis of symptoms and signs. The companion volume Uncommon Causes of Stroke completes this highly authoritative reference work which clinicians in neurology will find essential to the understanding and diagnosis of stroke.
Objectives The aim of this study was to investigate whether depressive symptoms are related to the risk factors for sudden death in patients with hypertrophic cardiomyopathy (HCM).
Design 121 patients diagnosed as having HCM were assessed for depressive symptomatology using the Beck Depression Inventory and the Center for Epidemiological Studies Depression Scale (CES-D) and followed up for a period of 2 years. For the interview, the authors used the Structured Clinical Interview for DSM-III/DSM-III-R. A multidimensional longitudinal study was carried out with both somatic and psychological symptoms and signs taken into consideration. SPSS was used for the statistical analysis.
Results (1) Patients with HCM are more depressed than the general population. (2) There is no positive correlation between the occurrence of depressive symptoms and the risk factors for sudden death in patients with HCM. (3) Patients at high risk for sudden death are not more depressed than the others. (4) Time from diagnosis of the cardiac disease is not related to the presence and severity of depressive symptoms.
Conclusions Patients with HCM are more depressed than the general population. The authors suggest that depressive symptoms and risk factors for sudden death in these patients are not related. It is important to screen for mood disorders in this patient population in order to provide an early diagnosis and treatment of the psychiatric disease.
In a nation of almost 300 million people, ischemic heart disease (IHD) and depression remain two of the nation's most pressing public health issues. Cardiovascular disease remains the leading cause of death and hospitalization in the USA, and according to the American Heart Association, IHD alone demonstrated a total prevalence of 13 million individuals (6.9% of the US population) and was responsible for 2,125,000 hospital discharges, 656,000 deaths, and $142 billion in health care spending in 2002 [1]. As a growing proportion of patients survive myocardial infarction (MI), the number of patients with chronic, often nonrevascularizable IHD continues to increase. According to the National Institute of Mental Health (NIMH), 5% of the American population suffers from major depressive disorder (MDD) in any given 1-year period [2], and depression has been identified by the World Health Organization (WHO) as the leading cause of disability worldwide [3].
Rezumat: Pe parcursul ultimilor 15 ani, numeroase studii au fost efectuate pentru a detecta prevalența depresiei la pacienții cu boală coronariană. Rata de raportare a depresiei variază foarte mult de la studiu la studiu, din cauza diferențelor dintre caracteristicile demografice, cum ar fi: sexul, vârsta sau tipul de boală coronariană, precum metodele folosite pentru evaluarea depresiei. De asemenea pacienții cu cardiopatie ischemică din insuficiența cardiacă, cardiomiopatia ischemică sau aritmii din cauza unei boli coronariene nu au fost incluşi în analize, precum și pacienții din grupul de control (subiecți sănătoși) care nu au fost diagnosticaţi cu ischemie silențioasă. Scopul: Scopul studiului a fost de a determina prevalența și severitatea depresiei la pacienții cu boală cardiacă ischemică și pentru a verifica dacă există unele diferențe între rata depresiei în formele de cardiopatie ischemică. Metoda: Studiul a fost efectuat pe 231 de pacienți cu boală cardiacă ischemică diagnosticaţi recent. Screeningul pentru depresie s-a efectuat utilizând chestionarul PHQ-2 cu 2 itemi. Acest chestionar a fost aplicat la includerea în studiu și la intervale de 1 lună. Prezența depresiei a fost confirmată de medicul psihiatru. A fost făcută o comparație între prevalența depresiei, în formele de cardiopatie ischemică și sex. Rezultate: La sfârșitul studiului depresiei a fost diagnosticată la 33,8% dintre pacienți (n = 81). Acest lucru a fost mai frecvent la pacienții cu infarct miocardic (43,1%) și la pacienții cu cardiomiopatie ischemică (42,9 %) și mai puțin la pacienții cu ischemie silențioasă (21,7%) şi angină pectorală stabilă (27,1%). Depresia a fost mai frecventă la femei, dar aceasta a apărut mai devreme la bărbați (8,09 ± 5,65 vs 5,59 ± luni 4,87 luni, p = 0,03), care au prezentat de asemenea depresie mai severă în comparație cu femeile. Abstract: During the last 15 years, numerous studies were conducted for detecting the prevalence of depression in the patients with coronary artery disease. The reported rate of depression vary a lot from study to study because of the differences between patients' demographic characteristics, such as gender, age or the type of coronary artery disease, as well as because of the method used to assess depression. Also, the patients with silent ischemia, heart failure, ischemic cardiomiopathy or arrhythmias because of coronary artery disease were not included in the analysis, as well as the patients from the control group (formed usually by healthy subjects), who were not screened for silent ischemia. Aim: the aim of the study was to determine the prevalence and the severity of depression in the patients with ischemic heart disease and to check if there are some differences of the depression rate between the forms of ischemic cardiopathy. Method: the study was conducted on 231 patients with ischemic heart disease recently diagnosed. Depression was screened using the PHQ questionnaire with 2 items. This questionnaire was applied at the inclusion into the study and at intervals of 1 month. The presence of depression was confirmed by the psychiatrist. A comparison between the prevalence of depression was done by the forms of ischemic cardiopathy and by gender. Results: at the end of the study, depression was diagnosed in 33,8% of the patients (n=81). This was more frequently encountered in the patients with myocardial infarction (43,1%) and in the patients with ischemic cardiomiopathy (42,9%) and less in the patients with silent ischemia (21,7%) and stable angina (27,1%). Depression was more frequent in women but this appeared earlier in men (8,09± 5,65 month vs 5,59±4,87 month, p=0,03), who also presented more severe depression in comparison with women.
Depression is commonly present in patients with coronary heart disease (CHD) and is independently associated with increased cardiovascular morbidity and mortality. Screening tests for depressive symptoms should be applied to identify patients who may require further assessment and treatment. This multispecialty consensus document reviews the evidence linking depression with CHD and provides recommendations for healthcare providers for the assessment, referral, and treatment of depression.
Aim:
To study the prevalence of depressive and anxiety disorders in postmenopausal disorders and their relationship with the manifestations of climacteric syndrome.
Subjects and methods:
The study enrolled 203 women, including 142 patients with surgical menopause and 61 with natural menopause. Psychometric testing using the Hamilton depression rating scale and the Spielberger test anxiety inventory, and 24-hour blood pressure (BP) monitoring with assessment of the 24-hour BP profile were performed.
Results:
Depressive disorders (DD) were found in 82.5% of the postmenopausal women; all the patients had higher levels of situational and personality anxiety. The women with natural menopause developed moderate and severe DD and those who had undergone ovariectomy had mild DD. The prevalence of DD was higher in patients with essential hypertension (EH) than in those with normal BP (88.6 and 78.3%, respectively; p < 0.01); DD was more marked in these patients. The severity of DD also depended on the type of diurnal BP variations; the highest level of depression was recorded in patients without nocturnal BP reduction. The same group was found to have the highest level of personality and situational anxiety.
Conclusion:
The magnitude of DD depends on the type of menopause, the presence of EH, and the specific features of diurnal BP variations. The findings necessitate a detail examination of postmenopausal women for identification of affective disorders and their further correction.
Hypertension Research, official publication of the Japanese Society of Hypertension, publishes papers reporting original clinical and experimental research in the field of hypertension and related cardiovascular diseases.
Depression is the main emotional variable being investigated with respect to coronary heart disease (CHD). This chapter focuses on the negative emotion (depression) as a risk factor for CHD in women. Two meta-analyses, including major prospective studies of CHD, evaluated association of personality variables and negative emotions with CHD outcomes. Negative emotions were indeed related to CHD outcomes in both studies. Although these early attempts to link negative emotions to CHD are promising, most of the data included in the meta-analyses came from men; when women were included, results were not reported by gender. Not surprisingly, depressive symptoms among patients with heart disease are significantly more common than among people in the general population. It should be noted, however, that some prospective studies do not support a link between negative emotions and heart disease. One study among elderly hypertensive patients found no relationship between depression measured at baseline and subsequent cardiovascular outcomes but did find that heart disease increased both in men and in women as their levels of depression increased over the follow-up period.
Objective-To study the prevalence of depression at least 6 months after various coronary heart disease (CHD) events (bypass grafting, coronary angioplasty, myocardial infarction, myocardial ischaemia without infarction) and the associations between depression and clinical variables. Design-In the course of the study 414 (284 males, 130 females) patients younger than 71 years (mean age for men 60.9 years and for women 63.6 years) were interviewed and examined. Smoking habits, body mass index, lipid levels and diabetic status were recorded. The New York Heart Association (NYHA) class was assessed. Depression was screened using a self-rated depression scale. Results-In the four diagnostic categories, one-sixth of the patients (14-19%) suffered from depression. Depression was associated with smoking (OR 1.7,95% CI 1.2; 2.4) and poor NYHA class (OR 1.9, 95% CI 1.4; 2.6). Conclusion-Depression is common after CHD events, and is associated with smoking and poor NYHA class. The identification and treatment of depression should be one of the elements in the rehabilitation of cardiac patients.
Recent evidence suggests that psychiatric and/or psychological factors could be independent risk factors for stroke. Some of these factors may act as stroke triggers producing short-term physiological changes that may directly lead to stroke onset. Most data is related to four distinct domains: (1) depression and/or anxiety and related syndromes, (2) personality and character traits, (3) psychological stress, and (4) psychotropic medication. Some factors (e.g., depression) are closely related to stroke risk, and there is some evidence that psychological stress could be an important risk factor. However, many studies have methodological limitations (small sample size, lack of adjustment for stroke risk factors, or residual confounding) and lack of standardized definition and/or measurement. Data about stroke triggers is scarce but epidemiological studies suggest a triggering effect of acute or subacute life stress exposure. The potential pathophysiological ways by which psychiatric and/or psychological factors may promote stroke include a higher frequency of unhealthy behaviors and direct biological effects on the cardiovascular system, notably through activation of the sympathetic nervous system. More research is still needed to improve measurement and to better investigate the impact of psychiatric and/or psychological factors. The clarification of pathophysiological mechanisms could help to consider preventive strategies.
Concomitant disorders at the time of surgery in addition to psychological and socioeconomic patient characteristics may influence treatment outcomes in hip arthroplasty.
To describe the impact of these factors on perioperative complications and postoperative results in terms of function, quality of life, and patient satisfaction .
Review of relevant clinical studies, meta-analyses, and presentation of our own results .
Comorbidities in general, especially in combination, increase the perioperative risk profile. Socioeconomic factors (education, professional qualifications, social deprivation) in addition to psychological variables (depression, distressed personality) can have a major impact on postoperative functional outcomes and patient satisfaction.
It is of crucial importance to avoid inequalities in the provision of joint replacement for patients with hip osteoarthritis and co-existing risk factors. Preventive strategies should be implemented to reduce the negative impact of comorbidities on treatment outcome. Personalized communication and education may be helpful in avoiding unrealistic patient expectations before hip replacement.
Age differences on the 20-item Center for Epidemiological Studies Depression Scale (CES-D) were examined for 4 age-cohort groups: 20-39 years (n = 548), 40-54 years (n = 218), 55-69 years (n = 352), and 70-98 years (n = 212). On total CES-D, there was a significant age effect and quadratic trend, with means for the middle aged least and those for the oldest most elevated. On 4 CES-D subscales--Depressed Mood, Psychomotor Retardation, Lack of Well-being (i.e., reverse-scored items), and Interpersonal Difficulties--the oldest group scored highest only on lack of well-being. Somatic symptoms of depression were not elevated. Young adults scored highest on depressed mood. Adults who are now old were not generally characterized by elevated self-reports of depressive symptoms; however, on items asking whether the respondent has a hopeful outlook, those aged 70 and older were more likely to endorse a lack of such positive feelings.
The relation between psychiatric disorders, defined by the Diagnostic Interview Schedule (DIS), and mortality over 15 months is compared in 3007 adults age 55 and over in the New Haven Epidemiologic Catchment Area (ECA) project. Our results indicate that the odds of dying are more than four times greater for individuals with affective disorders than for others in the sample, controlling for age, sex, and physical health. Cause of death is also examined. There were no suicides or deaths from external causes.
: Correlations between serum cholesterol levels and self-reported intensities of various moods and feelings--namely, motivation, arousal, happiness, depression, anger, fear and lethargy--were investigated in 20 subjects over a 2-month period. Consistent and occasionally significant negative correlations were seen between subjects' serum cholesterol levels and their moods and feelings of motivation, arousal and happiness. Consistent and more frequently significant positive correlations were evidenced between subjects' serum cholesterol concentrations and their moods and feelings of depression, anger, fear and lethargy. Copyright (C) 1971 by American Psychosomatic Society
The CES-D scale is a short self-report scale designed to measure depressive symptomatology in the general population. The items of the scale are symptoms associated with depression which have been used in previously validated longer scales. The new scale was tested in household interview surveys and in psychiatric settings. It was found to have very high internal consistency and adequate test- retest repeatability. Validity was established by pat terns of correlations with other self-report measures, by correlations with clinical ratings of depression, and by relationships with other variables which support its construct validity. Reliability, validity, and factor structure were similar across a wide variety of demographic characteristics in the general population samples tested. The scale should be a useful tool for epidemiologic studies of de pression.
Many authors have observed a decrease in glucose-tolerance (G.T.) in melancholia (sec reviews by McFarland and Goldstein, 1939; Altschule, 1953). Using an intravenous test, the present author confirmed that G.T., and also body weight, were significantly lower in a group of depressions than in a matched control group (Pryce, 1958a), but that within the depressions G.T. was not related to body weight. In a subsequent study also (Pryce, 1958b) change in G.T. after treatment was not related to change in body weight nor to three measures of change in emotional state. These studies, therefore, failed to support the views that the decreased G.T. in depressions is related either to nutritional or to emotional factors.
This study reports the results of a household survey and search of death certificates that show a relationship between depression, anxiety, and subsequent mortality. It is part of an effort to develop practical epidemiologic techniques for continuous assessment of community mental health. Use is made of the population attributable mortality rate, estimated from a comparison of the prevalence of a given factor in life and at death. The study estimated attributable mortality prospectively by following up participants in a mental health survey of Alachua County, Florida, for up to four years. Of eight mental scales examined, five (mood, depression, somatic symptoms of anxiety, the Health Opinion Survey, and selected psychopathologic symptoms) showed significant association of scores with community mortality. The data suggest linkages of mental factors to mortality of an order of magnitude sufficient to warrant consideration of these factors as leading causes of death.
The author reviews concepts important to understanding the emotional causes of sudden death, which occurs in the psychological setting of hopelessness, powerlessness, and intense emotions. The cardiovascular system responds to stress in a way that makes sudden death more likely. Studies pertinent to the effect of stress on blood pressure and arrhythmia in animals and man indicate that sudden death as a response to stress can occur only when certain factors are present simultaneously. Collaboration between psychiatrists and cardiologists is necessary for further progress in this field.
Prior to undergoing diagnostic coronary angiography, 94 men responded to tests for the coronary-prone behavior pattern, anxiety, depression, and neuroticism. Independently, cardiologists rated cineangiograms by the percent of atheromatous luminal obstruction in four major coronary arteries. The patients with greater atheromatous obstruction scored significantly higher than those with lesser disease on all four scales of the test for the type A coronary-prone behavior pattern. Those with more seriously diseased vessels also scored significantly higher on anxiety and depression scales but significantly lower on a denial scale. Men rated as having more frequent and intense angina pain scored significantly higher on hypochondriasis, depression, and admission of symptoms than men less subject to ischemic pain. Multivariate statistical analyses revealed that the findings regarding extent of atherosclerosis are independent of anginal pain or congestive heart failure.
Both cardiologists and psychiatrists have observed that the onset of myocardial infarction is often preceded by feelings of decreasing energy, general malaise, and minor depression. This paper describes these observations and tries to integrate the findings. It is proposed that the mental state preceding myocardial infarction can be best described as 'vital exhaustion'.
Depression is widely accepted as occurring in response to acute myocardial infarction (AMI), and to be an important determinant of recovery. A review of the literature reveals that three categories of patients with depressive symptomatology may be identifiable. First, many patients show depressive symptoms before admission with AMI; these may intensify during hospitalisation. For these patients, the depressive symptoms may contribute etiologically to the onset of AMI or derive from a common source along with AMI. The second group constitute patients with a history of AMI, and who on readmission with chest pain or suspected AMI are more likely to report depressive symptoms. The third group of patients are non-depressed first time admissions for AMI. These patients appear to show transient depressive reactions, much of which it is argued, occurs as a reaction to hospitalisation and not to AMI per se. This review considers the theoretical context whereby depressive symptoms may arise from the same circumstances that generate the coronary heart disease which underlies AMI, and links this to the generation of helplessness and cardiopathic processes.
Despite considerable progress in the epidemiology of late life depressive disorders, the determinants and course of late life depressive symptoms remain unclear. The apparent reciprocal relationship between depression and disability, a consistent finding in cross-sectional studies further confounds efforts to estimate the importance of depressive symptoms in the elderly. In a longitudinal study of 1457 aged community residents who completed the Center for Epidemiologic Studies Depression scale at baseline and 24 months later, a significant level of depressive symptoms emerged in 163 respondents (11%), while 1080 (74%) remained symptom free. Unlike other studies, we found that the number of medical conditions, social support, life events, and demographic characteristics contributed little to distinguish those with emerging symptoms from those who remained symptom free. However, increasing disability and declining health preceded the emergence of depressive symptoms and accounted for seventy percent of the variance explained by discriminant analysis. These findings have etiologic implications for both the course and determinants of depression in late life.
In order to study the association between vital exhaustion and different manifestations of coronary heart disease, a prospective study was conducted among 3877 males, aged 39-65. This group was studied during a mean period of 4.2 years. Vital exhaustion, a mental state characterized by unusual fatigue, a feeling of being dejected or defeated, and increased irritability, were assessed by means of the Maastricht Questionnaire. Subjects who scored in the upper third were labelled as exhausted and were compared with those who scored in the lower or middle third. The age-adjusted relative risk of angina pectoris at screening that was associated with vital exhaustion was 4.17 (p less than 0.01); that of unstable angina pectoris at screening was 17.21 (p less than 0.001). No association was observed between vital exhaustion and past myocardial infarction, except in the youngest age group (OR = 3.76; p = 0.05). Among the subjects free from coronary heart disease at screening, 54 cases of angina pectoris, 38 cases of non-fatal myocardial infarction, and 21 cases of fatal myocardial infarction were observed during follow-up. The age-adjusted relative risk of angina pectoris at follow-up was found to be 1.86 (p less than 0.03) and that of non-fatal myocardial infarction was found to be 2.28 (p less than 0.001). No association was found between vital exhaustion and fatal events.
Type A behavior and a Vital Exhaustion/Depression cluster seem to be the most crucial elements of the psychological 'coronary risk profile'. The question is, what physiological mechanisms intervene between these characteristics and CHD risk. In the present study the relationship was investigated between type A behavior and Vital Exhaustion on the one hand and the reaction of blood pressure, catecholamines and cholesterol to a real life stressor (Ph.D. thesis defence) on the other. Type A was shown to be related to a stronger response of adrenaline and diastolic blood pressure to the stressor. Vital Exhaustion was also positively correlated with the adrenaline reaction, and moreover, with cholesterol base level, stress induced cholesterol change, and noradrenaline and cholesterol stress levels. It was suggested that the relation between Vital Exhaustion and cholesterol parameters may originate in noradrenaline induced lipolysis. Type A and Vital Exhaustion may exert their influence on coronary risk by way of different physiological mechanisms. Type A via exaggerated hemodynamic reactivity, and Vital Exhaustion via lipid metabolism.
The damaging effect of sympathetic catecholamines on the cardiovascular system is reviewed. The catecholamines in high dose cause diffuse necrotic lesions in the myocardium with accompanying inflammation and subsequent fibrous scarring. This can be readily demonstrated in the experimental animal. The clinical counterpart is seen in patients dying after prolonged treatment with norepinephrine and among patients dying with pheochromocytoma. The various theories suggested to explain this phenomenon are presented, and the recent data that suggests that intravascular platelet aggregation is of etiologic importance is reviewed. The possible relation of these effects of catecholamines to myocardial infarction that occurs during stress is discussed. High doses of catecholamines cause medial necrosis, destruction of the elastic lamellae, and atrophic scarring of the walls of large vessels. The relationship of this lesion and other effects of catecholamines to atherosclerosis is reviewed.
THE frequency of psychiatric difficulties in intensive-care units ranges from 30 to 70 per cent. Confinement in these units is described as an "ordeal,"1 and the patient's expected psychologic response is presented as one of "catastrophic reaction."2 Although the study from which this last term developed was conducted on postcardiotomy patients in the setting of the recovery room, there has been a growing tendency to apply it to all situations of intensive care. This is an unfortunate application because intensive-care settings differ remarkably as do the emotional responses of the patients they house. The question of whether patients in coronary-care . . .
The death rate for persons in Stockholm born in 1905 has been investigated during a 9-year period (1971-1979). In 1971 these persons were invited to participate in a health check-up. Another check-up was carried out 3 years later, during which a psychiatric examination of 589 persons was undertaken. The correlation between depressive disorders and mortality was investigated in two steps. The death rates for those subjects who had responded affirmatively to items in a questionnaire indicating depression were compared with the death rate for the remaining responders. The death rates for those subjects considered to have neurotic disorders or sleeping disturbances in the psychiatric examination were compared with the death rates for the members of a control group considered to be without psychiatric symptoms. Both methods gave fundamentally the same result: there is an excess mortality among persons with depressive symptoms compared to persons without. The death rates were significantly higher in the populations that did not participate in the health check-ups than in those who did. The rates of suicide were also greater in the non-response populations. None of the persons who participated in the 1974 health check-up committed suicide during the next 3 years. The study shows that physically and mentally healthier persons were overrepresented among those who participated in the health check-ups at the ages of 66 and 69.
In 1971–1972 a systematic, representative sample of 70-year-olds living in Gothenburg, Sweden, was studied. The study included a psychiatric examination, during which the subjects were questioned concerning important aspects of their life history, and mental symptoms during the previous month. Any mental signs observed were recorded. Symptoms and signs were rated on rating scales, and summed up in diagnoses. The subjects also filled in three different personality inventories. The examination was performed in 166 men and 226 women. In 1976–1977 we ascertained from parish records which subjects had died before reaching the age of 75. Thirty-two men and 23 women had died. Associations between the psychiatric variables and mortality were studied.
There was a positive association in men between mortality and organic psycho-syndromes. There was a positive, but nonsignificant association with indications of previous alcohol abuse. There was no association with anxiety, depressive and obsessive compulsive neuroses or with personality deviations and few associations with personality dimensions and psychogenic needs. There was a positive association in married men between mortality and early cessation of sexual intercourse. There was also a positive association in men between mortality and loss of parents by death before the age of 16.
Glucose tolerance values and various physical and mental data were obtained from two groups: 19 depressions and 9 controls,.of similar age distribution. An intravenous test which gave a numerical index for glucose tolerance was used.
A highly significant decrease in glucose tolerance and in body weight is found in the depressions compared with the controls. However, within the group of depressions, there is no correlation between glucose tolerance and body weight. Low food intake during the four days before testing (4 cases) is correlated with a low glucose tolerance. The glucose tolerance in 8 patients with involutional melancholia is significantly lower than in 7 patients with manic depressive psychosis. Explanations for these findings are discussed.
In a recent investigation the present author has shown that glucose tolerance (G.T.) was significantly lower in a group of middle-aged mental hospital patients suffering from severe depression, than in a non-psychiatric group of similar age distribution (Pryce, 1958). This observation is similar to many others reported earlier (see review by McFarland and Goldstein, 1939). The cause of this impairment of G.T. is unknown; it cannot be explained by defective absorption of glucose from the alimentary canal since an intravenous G.T. test was employed in the investigation mentioned. Again, defective dietary intake during the days before testing could have contributed to the decreased G.T. in only a few cases; there was also no correlation between G.T. and either general symptomatology or the patients' behaviour during testing. However, it was observed that the group of depressions weighed significantly less than the control group, though again no correlation was found between body weight and G.T. among the depressions themselves. McCowan and Quastel (1931) and others have reported a close parallel between decreased G.T. and “emotional tension”, evidence which favours an emotional cause for the phenomenon, in line with the theories of W. B. Cannon (1911).