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Incident depression increases medical utilization in Medicaid patients with hypertension
Abstract
Unlabelled:
Hypertension is an important risk factor for cardiovascular disease and occurs disproportionately among patients with depression. Few studies have rigorously examined outcomes specifically among hypertensive patients with newly diagnosed comorbid depression.
Aim:
We hypothesized that incident depression would exacerbate hypertensive disease and that this would be evident through greater utilization of medical services than would otherwise occur in the absence of depression.
Methods:
Claims data for hypertensive patients enrolled in Maryland Medicaid (2005-2010) were used to estimate the change in annualized utilization following incident depression, compared to a matched cohort of hypertensive patients never diagnosed with depression. Multivariate regression was used to adjust for changes in antihypertensive medications, adherence and comorbidity that followed depression onset.
Results:
While medical utilization increased after incident depression, additional encounters tended to be for nonacute medical care and there was no significant increase in encounters specifically for cardiovascular or hypertension-related conditions.
Discussion:
The results contribute to the discussion on the relationship between depression and cardiovascular disease and will inform future studies that aim to look at longer term outcomes in patients with hypertension.
... We read with interest the Original Research article by Breunig et al. [1] and as investigators experienced in using Medicaid datasets for clinical research, we would like to comment on the methodology used by the authors. We are primarily concerned about the difference-in-difference (DID) analytic methods employed in this study and about some of the conclusions drawn. ...
Aim: We explored the role of histone modification in the association of depression-hypertension by comparing norepinephrine transporter (NET) gene levels in different depression-hypertensive patients. Then, we analyzed the expression of NET correlation with inflammatory cytokines to provide a new direction for detecting the association mechanism between depression and hypertension.
Methods: NE expression levels in serum of diverse groups were detected by enzyme-linked immunosorbent assay. Then histone acetyltransferase (HAT), histone deacetylase (HDAC), H3K27ac, NET, TNF-α, and interleukin-6 (IL-6) were detected by western blot in nine female subjects in different depression and hypertension groups, and Chromatin immunoprecipitation-polymerase chain reaction (Chip-PCR) were used to confirm the degree of acetylation affecting on the transcription level of NET gene. Meanwhile, correlation between NET with TNF/IL-6 was analyzed by SPSS19.0 software program. Finally, Quantitative real-time polymerase chain reaction (qPCR) and western blot were used to detect TNF-α and IL-6 expression levels after NET overexpression or interference treatment in human umbilical vein endothelial cells and Neuro-2a cells.
Results: The expression of HAT and H3K27ac had lower levels in D-H and nonD-H group than nonD-nonH group. The results showed that higher acetylation could promote expression of NET genes. Meanwhile, the expression of NET had a significant negative correlation with IL-6 (R = −0.933, p < 0.01) and tumor necrosis factor (TNF) (R = −0.817, p < 0.01) in subjects. In addition, the results confirmed that TNF-α and IL-6 mRNA and protein partial expressions could be inhibited by NET in both HUVECs and Neuronal cells (p < 0.01).
Conclusion: In conclusion, differential expression of NET gene might function as an important factor in interaction between depression and hypertension by partially targeting TNF-α and IL-6.
In explaining the association between depression and immune system pro-inflammatory cytokines have come to the fore and there appears to be an increase in particular at the cellular immune response. Neopterin measurements enable monitoring of the cellular immune response although its specific function is still not fully described. Similarly, haptoglobin (Hp), a positive acute phase protein, has been mentioned as well. In this study, we aimed to investigate the effects of depressive episodes on serum levels of neopterin and Hp by comparing serum haptoglobin and neopterin levels of the depressive patients in their first attack with those of depression patients suffering from recurrent attacks, and with the healthy control group. Method: Eighty patients who admitted to the outpatient psychiatry clinic of Ankara Gulhane Military Medical Academy (GMMF) were included in the study. Fourty-four individuals were being followed up with a diagnosis of first episode depression. There were 36 patients in the recurrent major depression (MD) group. The control group consisted of 41 healthy individuals. Of recurrent MD patients, 22 patients were in their second episode, 16 patients were in their third attack and 6 patients had four episodes or more. Severity of depression was evaluated with 17-item Hamilton Depression Rating Scale (HAM-D). Peripheral venous blood samples were collected from participants to determine complete blood count, routine biochemistry, serum neopterin, and haptoglobin measurements. The levels of serum neopterin and haptoglobin were measured by using the samples that were collected between the hours of 8:00 am and 11:00 am after 12 hour fasting during the previous night. Results: There was no significant difference between the three groups in terms of gender, age, educational level, and smoking. There was also not significant difference between the first episode MD and recurrent MD groups for HAM-D scores. No significance was detected between the first episode MD and control groups in terms of serum Hp and neopterin levels. In the recurrent MD group serum Hp and neopterin levels were higher than those of the first episode MD patients and the control subjects. HAM-D scores of MD patients (both first-episode MD and recurrent MD group) were correlated with serum levels of Hp, but there was no correlation between serum neopterin levels and HAM-D scores. Conclusion: The independent factor affecting the neopterin and Hp levels in patients with MD was found as the number of episodes of depression. Recurrent episodes have resulted with increased levels of both markers. We believe that this finding is important. Our findings support the hypothesis that major depressive disorder is generally associated with widespread inflammatory reaction and severity of depressive symptoms are positively correlated with the increase in inflammatory markers. Serum levels of Hp were associated with depression severity in patients who had a single episode as well as patients with multiple episodes. The same relationship was not found for neopterin. Further studies are needed to determine the importance of this difference observed between the two markers and also etiological significance of them.
Depression and cardiovascular diseases (CVD) are both common illnesses. Several studies demonstrated that depressed individuals have higher mortality compared to age- and gender-matched population, with an excess of cardiovascular deaths. There is a bidirectional association between depression and CVD. Several factors can interact and influence this relationship: poverty and social inequality, reduced accessibility to health care, biological alterations (as reduced heart rate variability, endothelial dysfunction, increased inflammation and platelet function, and hyperactivity of hypothalamic-pituitary-adrenal axis), side effects of psychiatric medication, lower adherence to medical treatments, and higher frequency of cardiovascular risk factors (higher tobacco use, physical inactivity, obesity, diabetes mellitus). This article aims to update the current evidence of the possible mechanisms involved in the association between depression and CVD.
In patients with cardiovascular disease (CVD), depression is common, persistent, and associated with worse health-related quality of life, recurrent cardiac events, and mortality. Both physiological and behavioral factors-including endothelial dysfunction, platelet abnormalities, inflammation, autonomic nervous system dysfunction, and reduced engagement in health-promoting activities-may link depression with adverse cardiac outcomes. Because of the potential impact of depression on quality of life and cardiac outcomes, the American Heart Association has recommended routine depression screening of all cardiac patients with the 2- and 9-item Patient Health Questionnaires. However, despite the availability of these easy-to-use screening tools and effective treatments, depression is underrecognized and undertreated in patients with CVD. In this paper, we review the literature on epidemiology, phenomenology, comorbid conditions, and risk factors for depression in cardiac disease. We outline the associations between depression and cardiac outcomes, as well as the mechanisms that may mediate these links. Finally, we discuss the evidence for and against routine depression screening in patients with CVD and make specific recommendations for when and how to assess for depression in this high-risk population.
Modifiable risk factors for cardiovascular disease (CVD) account for much of the variability in CVD outcomes and are also related to psychosocial variables. There is evidence that depression can undermine the treatment and advance the progression of CVD risk factors, suggesting that CVD risk factor relationships with CVD events may differ among those with depression.
This study tracked CVD events and mortality over a median of 5.9 years among a prospective cohort of 620 women (mean age 59.6 years [11.6]) completing a diagnostic protocol including coronary angiography and CVD risk factor assessment. Depressive symptoms were assessed using the Beck Depression Inventory (BDI). The study outcome was combined cardiovascular mortality and events.
Over the follow-up interval, 16.1% of the sample experienced one or more of the cardiovascular outcomes. In separate Cox regression models adjusting for age, education history, ethnicity, and coronary angiogram scores, we observed statistically significant CVD risk factor × BDI score interactions for diabetes, smoking, and waist-hip ratio factors. Simple effect analyses indicated that diabetes and smoking status were more strongly associated with cardiovascular outcomes among participants with lower BDI scores, whereas waist-hip ratio values predicted outcomes only among those with higher BDI scores.
These results suggest that the relationship between modifiable CVD risk factors and CVD outcomes may vary with depression status in clinical samples of women. This evidence augments prior research by demonstrating that depression may influence CVD risk jointly with or independent of CVD risk factors. It also provides further support for the inclusion of depression assessment in cardiovascular clinic settings.
To conduct a meta-analysis of the association between depression and medication adherence among patients with chronic diseases. Poor medication adherence may result in worse outcomes and higher costs than if patients fully adhere to their medication regimens.
We searched the PubMed and PsycINFO databases, conducted forward searches for articles that cited major review articles, and examined the reference lists of relevant articles. STUDY ELIGIBILITY CRITERIA, PARTICIPANTS, AND INTERVENTIONS: We included studies on adults in the United States that reported bivariate relationships between depression and medication adherence. We excluded studies on special populations (e.g., substance abusers) that were not representative of the general adult population with chronic diseases, studies on certain diseases (e.g., HIV) that required special adherence protocols, and studies on interventions for medication adherence.
Data abstracted included the study population, the protocol, measures of depression and adherence, and the quantitative association between depression and medication adherence. Synthesis of the data followed established statistical procedures for meta-analysis.
The estimated odds of a depressed patient being non-adherent are 1.76 times the odds of a non-depressed patient, across 31 studies and 18,245 participants. The association was similar across disease types but was not as strong among studies that used pharmacy records compared to self-report and electronic cap measures.
The meta-analysis results are correlations limiting causal inferences, and there is some heterogeneity among the studies in participant characteristics, diseases studied, and methods used.
This analysis provides evidence that depression is associated with poor adherence to medication across a range of chronic diseases, and we find a new potential effect of adherence measurement type on this relationship. Although this study cannot assess causality, it supports the importance that must be placed on depression in studies that assess adherence and attempt to improve it.
Purpose. Depression and antidepressant use may independently increase the risk of acute myocardial infarction and mortality in adults. However, no studies have looked at the effect of depression on a broader thrombotic event outcome, assessed antidepressant use, or evaluated elderly adults. Methods. A cohort of 7,051 community-dwelling elderly beneficiaries who experienced a thrombotic cardiovascular event (TCE) were pooled from the 1997 to 2002 Medicare Current Beneficiary Survey and followed for 12 months. Baseline characteristics, antidepressant utilization, and death were ascertained from the survey, while indexed TCE, recurrent TCE, and depression (within 6 months of indexed TCE) were taken from ICD-9 codes on Medicare claims. Time to death and first recurrent TCE were assessed using descriptive and multivariate statistics. Results. Of the elders with a depression claim, 71.6% had a recurrent TCE and 4.7% died within 12 months of their indexed TCE, compared to 67.6% and 3.9% of those elders without a depression claim. Of the antidepressant users, 72.6% experienced a recurrent TCE and 3.9% died, compared to 73.7% and 4.6% in the subset of selective serotonin reuptake inhibitor (SSRI) users. Depression was associated with a shorter time to death (P = .008) in the unadjusted analysis. However, all adjusted comparisons revealed no effect by depression, antidepressant use, or SSRI use. Conclusions. Depression was not associated with time to death or recurrent TCEs in this study. Antidepressant use, including measures of any antidepressant use and SSRI use, was not associated with shorter time to death or recurrent TCE.
Several practice guidelines recommend that depression be evaluated and treated in patients with cardiovascular disease, but the potential benefits of this are unclear.
To evaluate the potential benefits of depression screening in patients with cardiovascular disease by assessing (1) the accuracy of depression screening instruments; (2) the effect of depression treatment on depression and cardiac outcomes; and (3) the effect of screening on depression and cardiac outcomes in patients in cardiovascular care settings.
MEDLINE, PsycINFO, CINAHL, EMBASE, ISI, SCOPUS, and Cochrane databases from inception to May 1, 2008; manual journal searches; reference list reviews; and citation tracking of included articles.
We included articles in any language about patients in cardiovascular care settings that (1) compared a screening instrument to a valid major depressive disorder criterion standard; (2) compared depression treatment with placebo or usual care in a randomized controlled trial; or (3) assessed the effect of screening on depression identification and treatment rates, depression, or cardiac outcomes.
Methodological characteristics and outcomes were extracted by 2 investigators.
We identified 11 studies about screening accuracy, 6 depression treatment trials, but no studies that evaluated the effects of screening on depression or cardiovascular outcomes. In studies that tested depression screening instruments using a priori-defined cutoff scores, sensitivity ranged from 39% to 100% (median, 84%) and specificity ranged from 58% to 94% (median, 79%). Depression treatment with medication or cognitive behavioral therapy resulted in modest reductions in depressive symptoms (effect size, 0.20-0.38; r(2), 1%-4%). There was no evidence that depression treatment improved cardiac outcomes. Among patients with depression and history of myocardial infarction in the ENRICHD trial, there was no difference in event-free survival between participants treated with cognitive behavioral therapy supplemented by an antidepressant vs usual care (75.5% vs 74.7%, respectively).
Depression treatment with medication or cognitive behavioral therapy in patients with cardiovascular disease is associated with modest improvement in depressive symptoms but no improvement in cardiac outcomes. No clinical trials have assessed whether screening for depression improves depressive symptoms or cardiac outcomes in patients with cardiovascular disease.
Addressing the epidemic of poor compliance with antihypertensive medications will require identifying factors associated with poor adherence, including modifiable psychosocial and behavioral characteristics of patients.
Cross-sectional study, comparing measured utilization of antihypertensive prescriptions with patients' responses to a structured interview.
Four hundred ninety-six treated hypertensive patients drawn from a large HMO and a VA medical center.
We developed a survey instrument to assess patients' psychosocial and behavioral characteristics, including health beliefs, knowledge, and social support regarding blood pressure medications, satisfaction with health care, depression symptom severity, alcohol consumption, tobacco use, and internal versus external locus of control. Other information collected included demographic and clinical characteristics and features of antihypertensive medication regimens. All prescriptions filled for antihypertensive medications were used to calculate actual adherence to prescribed regimens in a 365-day study period. MAIN OUTCOME OF INTEREST: Adjusted odds ratios (ORs) of antihypertensive compliance, based on ordinal logistic regression models.
After adjusting for the potential confounding effects of demographic, clinical, and other psychosocial variables, we found that depression was significantly associated with noncompliance (adjusted OR per each point increase on a 14-point scale, 0.93; 95% confidence interval [95% CI], 0.87 to 0.99); in unadjusted analyses, the relationship did not reach statistical significance. There was also a trend toward improved compliance for patients perceiving that their health is controlled by external factors (adjusted OR per point increase, 1.14; 95% CI, 0.99 to 1.33). There was no association between compliance and knowledge of hypertension, health beliefs and behaviors, social supports, or satisfaction with care.
Depressive symptoms may be an underrecognized but modifiable risk factor for poor compliance with antihypertensive medications. Surprisingly, patient knowledge of hypertension, health beliefs, satisfaction with care, and other psychosocial variables did not appear to consistently affect adherence to prescribed regimens.
Relationships between depression, alcohol and illicit drug use, adherence behaviors, and blood pressure (BP) were examined in 190 urban hypertensive Black men enrolled in an ongoing hypertension control clinical trial. More than one fourth (27.4%) of the sample scored greater than 16 on the Center for Epidemiological Studies-Depression Scale (CES-D), indicating a high risk of clinical depression. Depression was significantly associated with an increased likelihood of meeting Diagnostic and Statistical Manual of Mental Disorders (4th ed.) criteria for alcohol abuse or dependence (odds ratio = 5.2; 95% confidence interval = 1.897-14.214). The level of depression was significantly correlated with poor medication (r =.301) and poor dietary compliance (r =.164). Both alcohol intake and illicit drug use were significantly correlated with poor dietary compliance (r =.195 and.185, respectively) and smoking (r =.190 and.269, respectively). Although no direct relationship between depression and the level of BP was substantiated by multivariate analysis, findings of descriptive analyses revealed statistically significant associations among depression, substance use, poor adherence, and poor BP outcomes. Given the harsh environment in which a large number of young urban Black men live, the high prevalence of substance abuse might be an attempt to fight off depression. Further in-depth investigation is needed to identify the role of depression and BP control in urban young Blacks in order to construct effective interventions that address their unique needs.
Despite the high prevalence of depression and hypertension, the relationship between the two diseases has received little attention. This paper reviews the epidemiological, pathophysiological, and prognostic aspects of this association, as well as its implications for treatment. A Medline search was conducted using the following key words: depression, blood pressure, blood pressure variability, physical morbidity, hypertension, mood, stress, hypertension, antidepressive agents, and genetics, from 1980 to 2004. We found descriptions of increased prevalence of hypertension in depressed patients, increased prevalence of depression in hypertensive patients, association between depressive symptomatology and hypotension, and alteration of the circadian variation of blood pressure in depressed patients. There is considerable evidence suggesting that hyperreactivity of the sympathetic nervous system and genetic influences are the underlying mechanisms in the relationship between depression and hypertension. Depression can negatively affect the course of hypertensive illness. Additionally, the use of antidepressive agents can interfere with blood pressure control of patients with hypertension by inducing changes in blood pressure and orthostatic hypotension.
Adherence measures the extent to which patients take medications as prescribed by their health care provider. The control of hypertension is dependent on medication adherence and may vary on the basis of antihypertensive medication class and other factors.
The Department of Veterans Affairs' automated pharmacy database captures pharmacy medication use; International Classification of Diseases, 9th Revision, diagnostic codes; and laboratory and patient demographic data on a monthly basis. Hypertensive patients who used thiazide diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, calcium channel antagonists, and alpha-blockers from July 2002 to December 2003 were studied. The first date of prescription filling for each patient within the date range was the index date from which fill and refill dates were collected for up to 18 months to calculate medication possession ratios and days out of medication ratios. Patients were categorized as adherent if the medication possession ratio was 80% or greater. Logistic regression was used to study the association of medication class, age, gender, ethnicity, Veterans Affairs facility, and co-diagnosis with diabetes, schizophrenia/psychosis, depression, and dementia with medication adherence.
We studied 40,492 hypertensive patients taking at least one antihypertensive drug class. The average age per class ranged from 67.4 to 72.9 years; 96% were male; and 51% were white, 8% were African-American, 4% were Asian-American, and 3% were Hispanic. Unadjusted adherence rates based on the medication possession ratio ranged from 78.3% for thiazide diuretics to 83.6% for angiotensin receptor blockers (P<.001). The number of medications (either total or antihypertensive) and age were independent predictors of better adherence. Black ethnicity and depression were associated with worse adherence.
Adherence rates with all antihypertensive medications were high. Although there were statistical differences by drug class, these differences were small. Ethnicity and depression identified groups that might benefit from programs to improve adherence.
Although universal health care aims for equity in service delivery, socioeconomic status still affects death rates from ischemic heart disease and stroke as well as access to revascularization procedures. We investigated whether psychiatric status is associated with a similar pattern of increased mortality but reduced access to procedures. We measured the associations between mental illness, death, hospital admissions and specialized or revascularization procedures for circulatory disease (including ischemic heart disease and stroke) for all patients in contact with psychiatric services and primary care across Nova Scotia.
We carried out a population-based record-linkage analysis of related data from 1995 through 2001 using an inception cohort to calculate rate ratios compared with the general public for each outcome (n = 215,889). Data came from Nova Scotia's Mental Health Outpatient Information System, physician billings, hospital discharge abstracts and vital statistics. We estimated patients' income levels from the median incomes of their residential neighbourhoods, as determined in Canada's 1996 census.
The rate ratio for death of psychiatric patients was significantly increased (1.34), even after adjusting for potential confounders, including income and comorbidity (95% confidence interval [CI] 1.29-1.40), which was reflected in the adjusted rate ratio for first admissions (1.70, 95% CI 1.67-1.72). Their chances of receiving a procedure, however, did not match this increased risk. In some cases, psychiatric patients were significantly less likely to undergo specialized or revascularization procedures, especially those who had ever been psychiatric inpatients. In the latter case, adjusted rate ratios for cardiac catheterization, percutaneous transluminal coronary angioplasty and coronary artery bypass grafts were 0.41, 0.22 and 0.34, respectively, in spite of psychiatric inpatients' increased risk of death.
Psychiatric status affects survival with and access to some procedures for circulatory disease, even in a universal health care system that is free at the point of delivery. Understanding how these disparities come about and how to reduce them should be a priority for future research.
Poor adherence is one of the biggest obstacles in therapeutic control of high blood pressure. The objectives of this study were (i) to measure adherence to antihypertensive therapy in a representative sample of the hypertensive Pakistani population and (ii) to investigate the factors associated with adherence in the studied population.
A cross-sectional study was conducted on a simple random sample of 460 patients at the Aga Khan University Hospital (AKUH) and National Institute of Cardiovascular Diseases, Karachi, from September 2005-May 2006. Adherence was assessed using the Morisky Medication Adherence Scale (MMAS), with scores ranging from 0 (non-adherent) to 4 (adherent). In addition to MMAS, patient self-reports about the number of pills taken over a prescribed period were used to estimate adherence as a percentage. AKU Anxiety and Depression Scale (AKU-ADS) was incorporated to find any association between depression and adherence. At a cut-off value of 80%, 77% of the cases were adherent. Upon univariate analyses, increasing age, better awareness and increasing number of pills prescribed significantly improved adherence, while depression showed no association. Significant associations, upon multivariate analyses, included number of drugs that a patient was taking (P<0.02) and whether he/she was taking medication regularly or only for symptomatic relief (P<0.00001).
Similar to what has been reported worldwide, younger age, poor awareness, and symptomatic treatment adversely affected adherence to antihypertensive medication in our population. In contrast, monotherapy reduced adherence, whereas psychosocial factors such as depression showed no association. These findings may be used to identify the subset of population at risk of low adherence who should be targeted for interventions to achieve better blood pressure control and hence prevent complications.
The use of nonsteroidal antiinflammatory drugs (NSAIDs) has been associated with increased blood pressure and hypertension. However, less is known about how the risk of hypertension is associated with cyclooxygenase 2 selective inhibitors (coxibs), especially celecoxib, the only coxib remaining on the market.
To compare the risk of incident hypertension associated with the use of celecoxib and nonselective (NS) NSAIDs.
A cohort study was conducted using secondary data from the GE Centricity Electronic Medical Record database, which contains millions of patient records seen by thousands of physicians across the US. The index date was defined as the date of the first NSNSAID or celecoxib prescription between January 1, 1999, and June 30, 2004. Patients were included if they were aged 18 years or older and were enrolled for at least 365 days prior to the index date. Excluded were patients who had any prior diagnosis of hypertension or pregnancy-related hypertension during the pre- or postindex date period. Also excluded were patients who had any prior prescription for antihypertensive drugs, coxibs, or NSNSAIDs. After applying inclusion/exclusion criteria, each celecoxib user was matched to 2 NSNSAID users by sex, age (+/-5 y), propensity score (within 0.2 SD), and number of unique drugs (+/-20%). Descriptive and survival analyses were conducted.
The final sample consisted of 51,444 patients, of whom 17,148 were on celecoxib and 34,296 were on NSNSAIDs. Relative to NSNSAID users, patients on celecoxib had a similar rate of postexposure hypertension incidence (HR 1.013; 95% CI 0.862 to 1.190).
Results from a population-based cohort analysis of electronic medical records did not show any difference in the hazard rates of incident hypertension between celecoxib and NSNSAID users.
There exists a growing body of evidence linking depression with cardiovascular events, although the mechanisms responsible remain unknown. We investigated the role of the autonomic nervous system and inflammation in the link between coronary heart disease and major depressive disorder (MDD), and examined the cardiac risk modification following pharmacological treatment of depression. We measured cardiac baroreflex function, heart rate variability, pulse pressure and high sensitivity C-reactive protein (hsCRP), all of which have an impact on cardiac risk, pre- and post-treatment in 25 patients with MDD, with no history of coronary heart disease, and in 15 healthy subjects. Treatment consisted of selective serotonin reuptake inhibitors for approximately 12 weeks. No significant differences were observed between untreated MDD patients and healthy subjects in blood pressure, heart rate, baroreflex sensitivity or heart rate variability. Pulse pressure and hsCRP, however, were significantly elevated in patients with MDD prior to treatment (p=0.023 and p=0.025, respectively). Moreover, while pharmacotherapy was effective in alleviating depression, surprisingly, each of cardiac baroreflex function, heart rate variability, pulse pressure and hsCRP was modified (p<0.05) in a manner likely to increase cardiac risk. In conclusion, this study demonstrated higher pulse pressure and hsCRP plasma levels in patients with MDD, which might contribute to increased cardiac risk. Following treatment vagal activity was reduced, as indicated by reductions in baroreflex sensitivity and heart rate variability, accompanied by increases in pulse pressure and plasma hsCRP levels. Mechanisms potentially responsible for generating cardiac risk in patients treated with selective serotonin reuptake inhibitors may need to be therapeutically targeted to reduce the incidence of coronary heart disease in this population.
Many studies have documented the negative effects of depression on adherence to recommended treatment; however, little is known about the mechanism underlying this relationship. Using the Kenny and Baron analytic framework of mediation, the authors assessed whether self-efficacy mediated the relationship between depression and medication adherence in 167 hypertensive African Americans followed in a primary care practice. Depressive symptoms are associated with poor medication adherence (beta=.013, p=.036) and low self-efficacy (beta=-.008, p=.023). Self-efficacy is negatively associated with medication adherence at follow-up (beta=-.612, p<.001). The relationship between depressive symptoms and medication adherence becomes nonsignificant when controlling for self-efficacy (beta=.010, p=.087). Implications for further examination into the mediating role of self-efficacy and the deleterious effect of depression on medication adherence are discussed.
The objective of this study was to develop a prospectively applicable method for classifying comorbid conditions which might alter the risk of mortality for use in longitudinal studies. A weighted index that takes into account the number and the seriousness of comorbid disease was developed in a cohort of 559 medical patients. The 1-yr mortality rates for the different scores were: "0", 12% (181); "1-2", 26% (225); "3-4", 52% (71); and "greater than or equal to 5", 85% (82). The index was tested for its ability to predict risk of death from comorbid disease in the second cohort of 685 patients during a 10-yr follow-up. The percent of patients who died of comorbid disease for the different scores were: "0", 8% (588); "1", 25% (54); "2", 48% (25); "greater than or equal to 3", 59% (18). With each increased level of the comorbidity index, there were stepwise increases in the cumulative mortality attributable to comorbid disease (log rank chi 2 = 165; p less than 0.0001). In this longer follow-up, age was also a predictor of mortality (p less than 0.001). The new index performed similarly to a previous system devised by Kaplan and Feinstein. The method of classifying comorbidity provides a simple, readily applicable and valid method of estimating risk of death from comorbid disease for use in longitudinal studies. Further work in larger populations is still required to refine the approach because the number of patients with any given condition in this study was relatively small.
Objectives: Implementation of the International Statistical Classification of Disease and Related Health Problems, 10th Revision (ICD-10) coding system presents challenges for using administrative data. Recognizing this, we conducted a multistep process to develop ICD-10 coding algorithms to define Charlson and Elixhauser comorbidities in administrative data and assess the performance of the resulting algorithms. Methods: ICD-10 coding algorithms were developed by "translation" of the ICD-9-CM codes constituting Deyo's (for Charlson comorbidities) and Elixhauser's coding algorithms and by physicians' assessment of the face-validity of selected ICD- 10, codes. The process of carefully developing ICD-10 algorithms also produced modified and enhanced ICD-9-CM coding algorithms for the Charlson and Elixhauser comorbidities. We then used data on in-patients aged 18 years and older in ICD-9-CM and ICD-10 administrative hospital discharge data from a Canadian health region to assess the comorbidity frequencies and mortality prediction achieved by the original ICD-9-CM algorithms, the enhanced ICD-9-CM algorithms, and the new ICD-10 coding algorithms. Results: Among 56,585 patients in the ICD-9-CM data and 58,805 patients in the ICD-10 data, frequencies of the 17 Charlson comorbidities and the 30 Elixhauser comorbidities remained generally similar across algorithms. The new ICD-10 and enhanced ICD9-CM coding algorithms either matched or outperformed the original Deyo and Elixhauser ICD-9-CM coding algorithms in predicting in-hospital mortality. The C-statistic was 0.842 for Deyo's ICD9-CM coding algorithm, 0.860 for the ICD-10 coding algorithm, and 0.859 for the enhanced ICD-9-CM coding algorithm, 0.868 for the original Elixhauser ICD-9-CM coding algorithm, 0.870 for the ICD-10 coding algorithm and 0.878 for the enhanced ICD-9-CM coding algorithm. Conclusions: These newly developed ICD-10 and ICD-9-CM comorbidity coding algorithms produce similar estimates of comorbidity prevalence in administrative data, and may outperform existing ICD-9-CM coding algorithms.
Objectives:
Although a link between depression and poor adherence to antihypertensive medication (AHM) has been found, it is not known whether depression actually leads to poorer adherence or whether poor adherence only is a marker of depression. In this study we aimed to determine the time order between hypertension, depression and changes in adherence to AHM.
Methods:
The analyses were based on data gathered from a longitudinal cohort of Finnish employees (The Finnish Public Sector Study). A total of 852 chronically hypertensive men and women at baseline with a recorded onset of depression during the 9-year observation window and 2359 hypertensive control participants matched for age, sex, socio-economic status, time of study entry, employer and geographic area were included in the study. Individuals with any sign of depression during 4 years before the beginning of the study were excluded. To describe long-term trajectories (4 years before and 4 years after the recorded depression) of AHM adherence in relation to the onset of depression, annual data on reimbursed AHM prescriptions were gathered from the national Drug Prescription Register. Annual nonadherence rates (i.e. number of 'days-not-treated') were based on filled prescriptions.
Results:
Among male cases, the rate of 'days-not-treated' was 1.52 times higher (95% confidence interval 1.08-2.14) in the years after the onset of depression compared to preonset levels. In women and in male controls, no change in adherence to AHM was observed between these time periods.
Conclusion:
In hypertensive men, the onset of recorded depression increases the risk of nonadherence to AHM.
Growing evidence supports a causal relationship between cardiovascular disease and psychosocial factors such as mental health and behavioral disorders, acute and chronic stress, and low socioeconomic status. While this has enriched our understanding of the interaction between cardiovascular risk factors, much less is known about its economic implications. In this review, we evaluate the economic impact of psychosocial factors in persons at risk for or diagnosed with cardiovascular disease. Most studies have focused on depression and almost uniformly conclude that patients with cardiovascular disease and comorbid depression use a greater number of ambulatory and hospital services and incur higher overall costs. Additionally, comorbid depression may also reduce employment productivity in patients with cardiovascular disease, further magnifying its economic impact. Recent randomized trials have demonstrated that innovative care delivery models that target depression may reduce costs or at least be cost neutral while improving quality of life. The growing population burden and overlap of cardiovascular disease, comorbid mental illness, and other psychosocial factors suggest that future research identifying cost-effective or cost-saving treatment models may have significant health and economic implications.
Approximately one out of every five patients with cardiovascular disease (CVD) suffers from major depressive disorder (MDD). Both MDD and depressive symptoms are risk factors for CVD incidence, severity and outcomes. Great progress has been made in understanding potential mediators between MDD and CVD, particularly focusing on health behaviors. Investigators have also made considerable strides in the diagnosis and treatment of depression among patients with CVD. At the same time, many research questions remain. In what settings is depression screening most effective for patients with CVD? What is the optimal screening frequency? Which therapies are safe and effective? How can we better integrate the care of mental health conditions with that of CVD? How do we motivate depressed patients to change health behaviors? What technological tools can we use to improve care for depression? Gaining a more thorough understanding of the links between MDD and heart disease, and how best to diagnose and treat depression among these patients, has the potential to substantially reduce morbidity and mortality from CVD.
Cardiovascular health disparities continue to pose a major public health problem. The authors evaluated the effect of education administered within social networks on the improvement of hypertension in 248 African Americans compared with historical controls. Patients formed clusters with peers and attended monthly hypertension education sessions. The authors assessed the likelihood of reaching goal below predefined systolic blood pressure (SBP) and diastolic blood pressure (DBP) thresholds as well as the absolute reduction in SBP and DBP, controlling for diabetes, smoking, baseline hypertension, and demographics. The intervention group was more likely to have ever reached treatment goal at 12-month follow-up (odds ratio, 1.72; P=.11). At 18-month follow-up, the Maryland Cardiovascular Disease Promotion Program group had a statistically significant larger drop in SBP (-4.82 mm Hg, P<.0001) and DBP (-3.37 mm Hg, P=.01) than the control group. The clustering of patients in social networks around hypertension education has a positive impact on the management of hypertension in minority populations and may help address cardiovascular health disparities.
Chronic obstructive pulmonary disease (COPD) imposes a significant and growing economic burden on the US health care system. A brief exploration of reviews on the therapeutic management of COPD reveals a range of pharmacologic and nonpharmacologic options for reducing deleterious and costly exacerbations. Consensus is that both forms of therapy provide the greatest benefit to all patients. However, prescribing physicians must account for availability of resources and patients' ability to pay, as well as patient response and their likely persistence or adherence to recommended therapies. The ongoing challenge is to overcome barriers to comprehensive, real-world economic evaluations in order to establish the most cost-effective mix of therapies for every patient in the heterogeneous COPD population. Only then can evidence-based guidelines be translated into the most cost-effective delivery of care.
Aims:
Many people with depression may be undiagnosed and thus untreated. We sought to assess the prevalence and correlates of undiagnosed depression among adults with diabetes.
Methods:
Data of U.S. adults from the Behavioral Risk Factor Surveillance System in 2006 were analyzed. Cox proportional hazard regression analysis was used to estimate prevalence ratios (PRs) and 95% confidence intervals (CIs) of correlates for undiagnosed depression.
Results:
The unadjusted and age-adjusted prevalences of undiagnosed depression were 8.7% and 9.2%. About 45% of diabetes patients with depression were undiagnosed. After adjustments for all correlates, female gender (PR, 1.4; 95% CI: 1.1-1.8), poor or fair health (PR, 2.8; 95% CI: 2.1-3.6), lack of social and emotional support (PR, 2.5; 95% CI: 1.8-3.3), life dissatisfaction (PR, 3.5; 95% CI: 2.2-5.5), use of special equipment (PR, 1.4; 95% CI: 1.1-1.8), no leisure-time physical activity (PR, 1.5; 95% CI: 1.2-1.9), and comorbid cardiovascular disease (PR, 1.5; 95% CI: 1.2-1.9) were associated with undiagnosed depression.
Conclusions:
Undiagnosed depression among people with diabetes was common. Because depression is associated with increased risk of diabetes-related complications, early detection of depression is needed in clinical settings.
Depression is characterized by inflammation and cell-mediated immune (CMI) activation and autoimmune reactions directed against a multitude of self-epitopes. There is evidence that the inflammatory response in depression causes dysfunctions in the metabolism of 5-HT, e.g. lowering the 5-HT precursor tryptophan, and upregulating 5-HT receptor mRNA. This study has been undertaken to examine autoimmune activity directed against 5-HT in relation to CMI activation and inflammation.
5-HT antibodies were examined in major depressed patients (n=109) versus normal controls (n=35) in relation to serum neopterin and lysozyme, and plasma pro-inflammatory cytokines (PIC), i.e. interleukin-1 (IL-1) and tumor necrosis factor-α (TNFα). Severity of depression was assessed with the Hamilton Depression Rating Scale (HDRS) and severity of fatigue and somatic symptoms with the Fibromyalgia and Chronic Fatigue Syndrome (FF) Rating Scale.
The incidence of anti-5-HT antibody activity was significantly higher in depressed patients (54.1%), and in particular in those with melancholia (82.9%), than in controls (5.7%). Patients with positive 5-HT antibodies showed increased serum neopterin and lysozyme, and plasma TNFα and IL-1; higher scores on the HDRS and FF scales, and more somatic symptoms, including malaise and neurocognitive dysfunctions. There was a significant association between autoimmune activity to 5-HT and the number of previous depressive episodes.
The autoimmune reactions directed against 5-HT might play a role in the pathophysiology of depression and the onset of severe depression. The strong association between autoimmune activity against 5-HT and inflammation/CMI activation is explained by multiple, reciprocal pathways between these factors. Exposure to previous depressive episodes increases the incidence of autoimmune activity directed against 5-HT, which in turn may increase the likelihood to develop new depressive episodes. These findings suggest that sensitization (kindling) and staging of depression are in part based on progressive autoimmune responses.
J Clin Hypertens (Greenwich). 2011;13:563–570. ©2011 Wiley Periodicals, Inc.
Hypertension is a major risk factor for developing cardiovascular disease and is more prevalent in African Americans compared with Caucasians. African Americans are often underrepresented in clinical trials. This study was composed of a largely urban African American cohort of hypertensive patients. This was a prospective, 4-arm, randomized controlled trial designed to evaluate the comparative effectiveness of both physician and patient education (PPE), patient education only (PAE), and physician education only (PHE) vs usual care (UC). Hypertension specialists gave a series of didactic lectures to the physicians, while a nurse educator performed the patient education. The mean adjusted difference in systolic blood pressure (SBP) from baseline in the PPE group was an average reduction of 12 mm Hg (95% confidence interval [CI], −4.5 to −19.4) at 6-months, followed by average reductions of 4.6 mm Hg (6.9 to −16.12) in the PAE group, 4.1 mm Hg (3.4 to −11.7) in the PHE group, and 2.6 mm Hg (3 to −8.2) in the UC group. The PPE group achieved a significantly better reduction in SBP compared with the UC group. Additional research should be conducted to evaluate whether the use of certified hypertension educators in collaboration with physicians will result in a similar blood pressure reduction.
Patients who left against medical advice (AMA) may be at higher risk for a hospital readmission if the unauthorized discharge was premature. The objective of this study is to examine the relationship between discharges AMA from nonfederal acute care hospitals and cardiovascular disease (CVD) hospital readmissions while addressing bias due to potential confounding, selection, and hospital-level clustering.
This cross-sectional study used hospital discharge data covering the period between 2000 and 2005. The outcome variables captured readmissions for a CVD-related condition following an index CVD-related discharge. The covariate of interest was an indicator for a discharge AMA in the index hospitalization. The relationship between discharges AMA and 7-day, 31-day, and 180-day readmissions was examined using multivariate models with adjustment for clustering and selection bias.
The sample included 348,572 patients, of which 7001 (2%), 19,779 (6%), and 48,855 (14%) were readmitted within 7, 31, and 180 days, respectively. The percentage of patients who were readmitted (7 days; 31 days; 180 days) was higher among the AMA group versus the non-AMA group (2.2% vs. 1%, P < 0.002; 1.3% vs. 1%, P < 0.001; 1.2% vs. 1%, P = 0.02). The adjusted odds of a CVD-related readmission to the same hospital within 7 days, 31 days, and 180 days were 154% (P < 0.001), 51% (P < 0.001), and 19% (P = 0.004) higher, respectively, for patients who left AMA. Results were robust in examining readmissions to any hospital as well as corrections for observable selection bias through propensity score analysis.
A discharge AMA among patients with a discharge diagnosis for CVD during the index hospitalization was predictive of CVD-related readmissions. The strength of the association between a discharge AMA and readmission was greatest within the first week after discharge.
This paper reviews the body of evidence that not only tryptophan and consequent 5-HT depletion, but also induction of indoleamine 2,3-dioxygenase (IDO) and the detrimental effects of tryptophan catabolites (TRYCATs) play a role in the pathophysiology of depression. IDO is induced by interferon (IFN)γ, interleukin-6 and tumor necrosis factor-α, lipopolysaccharides and oxidative stress, factors that play a role in the pathophysiology of depression. TRYCATs, like kynurenine and quinolinic acid, are depressogenic and anxiogenic; activate oxidative pathways; cause mitochondrial dysfunctions; and have neuroexcitatory and neurotoxic effects that may lead to neurodegeneration. The TRYCAT pathway is also activated following induction of tryptophan 2,3-dioxygenase (TDO) by glucocorticoids, which are elevated in depression. There is evidence that activation of IDO reduces plasma tryptophan and increases TRYCAT synthesis in depressive states and that TDO activation may play a role as well. The development of depressive symptoms during IFNα-based immunotherapy is strongly associated with IDO activation, increased production of detrimental TRYCATs and lowered levels of tryptophan. Women show greater IDO activation and TRYCAT production following immune challenge than men. In the early puerperium, IDO activation and TRYCAT production are associated with the development of affective symptoms. Clinical depression is accompanied by lowered levels of neuroprotective TRYCATs or increased levels or neurotoxic TRYCATs, and lowered plasma tryptophan, which is associated with indices of immune activation and glucocorticoid hypersecretion. Lowered tryptophan and increased TRYCATs induce T cell unresponsiveness and therefore may exert a negative feedback on the primary inflammatory response in depression. It is concluded that activation of the TRYCAT pathway by IDO and TDO may be associated with the development of depressive symptoms through tryptophan depletion and the detrimental effects of TRYCATs. Therefore, the TRYCAT pathway should be a new drug target in depression. Direct inhibitors of IDO are less likely to be useful drugs than agents, such as kynurenine hydroxylase inhibitors; drugs which block the primary immune response; compounds that increase the protective effects of kynurenic acid; and specific antioxidants that target IDO activation, the immune and oxidative pathways, and 5-HT as well.
J Clin Hypertens (Greenwich). 2010;12:826‐832. © 2010 Wiley Periodicals, Inc.
This study explored trends over time in diabetes prevalence, glycemic control, and antidiabetic therapy choices among adults (18–64 years) and older adults (≥65 years). Factors that predict diabetes outcomes were explored. The study was cross‐sectional, with data from the 1999 to 2004 National Health and Nutrition Examination Survey. The study group consisted of 1211 persons with self‐reported diabetes. Other information obtained from the study included self‐reported medication for diabetes, hypertension, stroke, heart failure, and health status. The survey also provided examination or laboratory tests of obesity, nephropathy, and glycosylated hemoglobin level. Descriptive and logistic regression analyses were used in the study. The study showed that the proportion of diabetics with good glycemic control increased during the period from 1999 to 2004. However, nearly half of the adults and one third of older adults with diabetes did not reach glycemic control in 2003–2004. Overall, 59% of adults and 46% of older adults were obese. There was a high prevalence of hypertension, heart failure, stroke, and nephropathy among patients with diabetes, especially in older adults. The results indicate a high percentage of poor glycemic control among persons with diabetes. There were also a substantial number of comorbid conditions associated with diabetes.
Poor adherence to antihypertensive medications remains a significant challenge in the management of patients with hypertension1–4. Physicians and other healthcare providers are well aware that the benefits of prescribed medications are only available to those patients who take them; yet, medication adherence is seldom adequately addressed in the outpatient clinical setting. In fact, clinicians often do not ask patients about their medication-taking behavior; and this may be for a variety of reasons 5;6.
For years, there has been discussion regarding adherence to the therapeutic alliance as a key factor in the management of hypertension. Initially termed “compliance,”7 the problem was unfairly placed on the patient’s subservience to the dictates of the provider. Harriet Dustan and one of the authors (EDF) brought this issue to the attention of the National High Blood Pressure Education Program suggesting that a more reasonable term might be a mutual “adherence” to the doctor-patient relationship. A special adherence program followed. Nevertheless, the terms ‘adherence’ and ‘compliance’ are often used interchangeably, although the term ‘adherence’ seems to more accurately recognize the mutual responsibility of patients and caregivers to their joint involvement in medical care1;8.
Regardless of the term, the fact remains that many adults with hypertension do not take their medications as prescribed, and poor adherence results in up to 50% of treatment failures9. Even for patients who partially adhere to prescribed therapies and may intermittently achieve blood pressure control, there is growing evidence that partial adherence may not provide adequate protection from target organ damage10. The multi-factorial nature of poor adherence to prescribed antihypertensive medications has been well documented1;2. These include factors which may be ascribed to the patient, the patients’ medical condition(s) and prognosis, the healthcare provider, the healthcare system, the prescribed treatment, socio-economic variables and, clearly, other intangible factors (Table 1).
Table 1
Summary of Barriers to Antihypertensive Medication Adherence 1;2
This discussion relates to one of these factors, the existence of one comorbid condition that complicates the clinical management of hypertension –-endogenous depression. Although the association between depressive symptoms and poor adherence to medications has been recognized by investigators, it is critical that clinicians realize that this association is more than an ‘epidemiological finding’ and that all of us take action in clinical settings to address the heretofore clinically under-recognized issue. We suggest herein that the ability for patients to cope with their problem of depressive symptoms and the need for the clinician to recognize that this comorbid condition is a barrier to hypertension management, if not in the management of the patient’s depression, should be addressed. These are important challenges that confront both parties of the doctor-patient relationship and contribute to the issue of therapeutic adherence.
Excess mortality from heart disease is observed in patients with severe mental disorder. This excess mortality may be rooted in adverse effects of pharmacological or psychotropic treatment, lifestyle factors, or inadequate somatic care.
To examine whether persons with severe mental disorder, defined as persons admitted to a psychiatric hospital with bipolar affective disorder, schizoaffective disorder, or schizophrenia, are in contact with hospitals and undergoing invasive procedures for heart disease to the same degree as the nonpsychiatric general population, and to determine whether they have higher mortality rates of heart disease.
A population-based cohort of 4.6 million persons born in Denmark was followed up from 1994 to 2007. Rates of mortality, somatic contacts, and invasive procedures were estimated by survival analysis.
Incidence rate ratios of heart disease admissions and heart disease mortality as well as probability of invasive cardiac procedures.
The incidence rate ratio of heart disease contacts in persons with severe mental disorder compared with the rate for the nonpsychiatric general population was only slightly increased, at 1.11 (95% confidence interval, 1.08-1.14). In contrast, their excess mortality rate ratio from heart disease was 2.90 (95% confidence interval, 2.71-3.10). Five years after the first contact for somatic heart disease, the risk of dying of heart disease was 8.26% for persons with severe mental disorder (aged <70 years) but only 2.86% in patients with heart disease who had never been admitted to a psychiatric hospital. The fraction undergoing invasive procedures within 5 years was reduced among patients with severe mental disorder as compared with the nonpsychiatric general population (7.04% vs 12.27%, respectively).
Individuals with severe mental disorder had only negligible excess rates of contact for heart disease. Given their excess mortality from heart disease and lower rates of invasive procedures after first contact, it would seem that the treatment for heart disease offered to these individuals in Denmark is neither sufficiently efficient nor sufficiently intensive. This undertreatment may explain part of their excess mortality.
The present study compared blood pressure levels between subjects with clinical anxiety and depressive disorders with healthy controls. Cross-sectional data were obtained in a large cohort study, the Netherlands Study of Depression and Anxiety (N=2981). Participants were classified as controls (N=590) or currently or remittedly depressed or anxious subjects (N=2028), of which 1384 were not and 644 were using antidepressants. Regression analyses calculated the contributions of anxiety and depressive disorders and antidepressant use to diastolic and systolic blood pressures, after controlling for multiple covariates. Heart rate and heart rate variability measures were subsequently added to test whether effects of anxiety/depression or medication were mediated by vagal control over the heart. Higher mean diastolic blood pressure was found among the current anxious subjects (beta=0.932; P=0.03), although anxiety was not significantly related to hypertension risk. Remitted and current depressed subjects had a lower mean systolic blood pressure (beta=-1.74, P=0.04 and beta=-2.35, P=0.004, respectively) and were significantly less likely to have isolated systolic hypertension than controls. Users of tricyclic antidepressants had higher mean systolic and diastolic blood pressures and were more likely to have hypertension stage 1 (odds ratio: 1.90; 95% CI: 0.94 to 3.84; P=0.07) and stage 2 (odds ratio: 3.19; 95% CI: 1.35 to 7.59; P=0.008). Users of noradrenergic and serotonergic working antidepressants were more likely to have hypertension stage 1. This study shows that depressive disorder is associated with low systolic blood pressure and less hypertension, whereas the use of certain antidepressants is associated with both high diastolic and systolic blood pressures and hypertension.
This study aimed to assess the levels of adherence in a sample of hypertensive patients being cared for in primary care in Northern Ireland and to explore the impact of depressive symptoms and medication beliefs on medication adherence.
The study was conducted in 97 community pharmacies across Northern Ireland. A questionnaire containing measures of medication adherence, depressive symptoms and beliefs about medicines was completed by 327 patients receiving antihypertensive medications.
Analysis found that 9.3% of participants were non-adherent with their antihypertensive medication (self-report adherence scale) and 37.9% had scores indicative of depressive symptoms as determined by the Center for Epidemiological Studies Depression Scale (CES-D). In the univariate analysis, concerns about medications had negative effects on both adherence and depressive symptomatology. However, logistic regression analysis revealed that patients over the age of 50 were more likely to be adherent with their medication than those younger than 50. Depressive symptomatology and medication beliefs (concerns) were not significantly related to adherence in the regression analysis.
Depressive symptomatology was high in the sample as measured by the CES-D. Age was the only significant predictor of medication adherence in this population.
Health care professionals should consider the beliefs of the patient about their hypertensive medications and counsel younger patients on adherence.
The objective of this study was to develop a prospectively applicable method for classifying comorbid conditions which might alter the risk of mortality for use in longitudinal studies. A weighted index that takes into account the number and the seriousness of comorbid disease was developed in a cohort of 559 medical patients. The 1-yr mortality rates for the different scores were: "0", 12% (181); "1-2", 26% (225); "3-4", 52% (71); and "greater than or equal to 5", 85% (82). The index was tested for its ability to predict risk of death from comorbid disease in the second cohort of 685 patients during a 10-yr follow-up. The percent of patients who died of comorbid disease for the different scores were: "0", 8% (588); "1", 25% (54); "2", 48% (25); "greater than or equal to 3", 59% (18). With each increased level of the comorbidity index, there were stepwise increases in the cumulative mortality attributable to comorbid disease (log rank chi 2 = 165; p less than 0.0001). In this longer follow-up, age was also a predictor of mortality (p less than 0.001). The new index performed similarly to a previous system devised by Kaplan and Feinstein. The method of classifying comorbidity provides a simple, readily applicable and valid method of estimating risk of death from comorbid disease for use in longitudinal studies. Further work in larger populations is still required to refine the approach because the number of patients with any given condition in this study was relatively small.
Depression and anxiety are common in medical patients and are associated with diminished health status and increased health care utilization. This article presents a quantitative review and synthesis of studies correlating medical patients' treatment noncompliance with their anxiety and depression.
Research on patient adherence catalogued on MEDLINE and PsychLit from January 1, 1968, through March 31, 1998, was examined, and studies were included in this review if they measured patient compliance and depression or anxiety (with n>10); involved a medical regimen recommended by a nonpsychiatrist physician to a patient not being treated for anxiety, depression, or a psychiatric illness; and measured the relationship between patient compliance and patient anxiety and/or depression (or provided data to calculate it).
Twelve articles about depression and 13 about anxiety met the inclusion criteria. The associations between anxiety and noncompliance were variable, and their averages were small and nonsignificant. The relationship between depression and noncompliance, however, was substantial and significant, with an odds ratio of 3.03 (95% confidence interval, 1.96-4.89).
Compared with nondepressed patients, the odds are 3 times greater that depressed patients will be noncompliant with medical treatment recommendations. Recommendations for future research include attention to causal inferences and exploration of mechanisms to explain the effects. Evidence of strong covariation of depression and medical noncompliance suggests the importance of recognizing depression as a risk factor for poor outcomes among patients who might not be adhering to medical advice.
Depressive and anxiety disorders are prevalent and cause substantial morbidity. While effective treatments exist, little is known about the quality of care for these disorders nationally. We estimated the rate of appropriate treatment among the US population with these disorders, and the effect of insurance, provider type, and individual characteristics on receipt of appropriate care.
Data are from a cross-sectional telephone survey conducted during 1997 and 1998 with a national sample. Respondents consisted of 1636 adults with a probable 12-month depressive or anxiety disorder as determined by brief diagnostic interview. Appropriate treatment was defined as present if the respondent had used medication or counseling that was consistent with treatment guidelines.
During a 1-year period, 83% of adults with a probable depressive or anxiety disorder saw a health care provider (95% confidence interval [CI], 81%-85%) and 30% received some appropriate treatment (95% CI, 28%-33%). Most visited primary care providers only. Appropriate care was received by 19% in this group (95% CI, 16%-23%) and by 90% of individuals visiting mental health specialists (95% CI, 85%-94%). Appropriate treatment was less likely for men and those who were black, less educated, or younger than 30 or older than 59 years (range, 19-97 years). Insurance and income had no effect on receipt of appropriate care.
It is possible to evaluate mental health care quality on a national basis. Most adults with a probable depressive or anxiety disorder do not receive appropriate care for their disorder. While this holds across diverse groups, appropriate care is less common in certain demographic subgroups.
This study investigated whether differences in quality of medical care might explain a portion of the excess mortality associated with mental disorders in the year after myocardial infarction.
This study examined a national cohort of 88 241 Medicare patients 65 years and older who were hospitalized for clinically confirmed acute myocardial infarction. Proportional hazard models compared the association between mental disorders and mortality before and after adjusting 5 established quality indicators: reperfusion, aspirin, beta-blockers, angiotensin-converting enzyme inhibitors, and smoking cessation counseling. All models adjusted for eligibility for each procedure, demographic characteristics, cardiac risk factors and history, admission characteristics, left ventricular function, hospital characteristics, and regional factors.
After adjusting for the potential confounding factors, presence of any mental disorder was associated with a 19% increase in 1-year risk of mortality (hazard ratios [HR], 1.19; 95% confidence interval [CI], 1.04-1.36). After adding the 5 quality measures to the model, the association was no longer significant (HR, 1.10; 95% CI, 0.96-1.26). Similarly, while schizophrenia (HR, 1.34; 95% CI, 1.01-1.67) and major affective disorders (HR, 1.11; 95% CI, 1.02-1.20) were each initially associated with increased mortality, after adding the quality variables, neither schizophrenia (HR, 1.23; 95% CI, 0.86-1.60) nor major affective disorder (HR, 1.05; 95% CI, 0.87-1.23) remained a significant predictor.
Deficits in quality of medical care seemed to explain a substantial portion of the excess mortality experienced by patients with mental disorders after myocardial infarction. The study suggests the potential importance of improving these patients' medical care as a step toward reducing their excess mortality.
Depression increases the risk of cardiac mortality and morbidity in patients with coronary heart disease (CHD), but the mechanisms that underlie this association remain unclear. This review considers the evidence for several behavioral and physiological mechanisms that might explain how depression increases the risk for incident coronary disease and for subsequent cardiac morbidity and mortality. The candidate mechanisms include: (1). antidepressant cardiotoxicity; (2). association of depression with cardiac risk factors such as cigarette smoking, hypertension, diabetes, and reduced functional capacity; (3). association of depression with greater coronary disease severity; (4). nonadherence to cardiac prevention and treatment regimens; (5). lower heart rate variability (HRV) reflecting altered cardiac autonomic tone; (6). increased platelet aggregation; and (7). inflammatory processes. Despite recent advances in our understanding of these potential mechanisms, further research is needed to determine how depression increases risk for cardiac morbidity and mortality.
Depression has been linked to poor health outcome in a number of studies; however, the mechanism underlying this relationship has received little attention. This paper explores the possibility that adherence mediates the relationship between depression and outcome. Principal findings regarding the relationship between depression, adherence, and outcome are reviewed. The data suggest that depression is related, at least moderately, to poorer adherence to a variety of treatment components. The relationship between adherence and outcome is more difficult to establish. In addition, current data, albeit limited, do not support the hypothesis that adherence mediates the relationship between depression and outcome. An alternative model in which adherence precedes and influences both mood state and health outcome is discussed. Finally, possible explanations for these relationships are explored and suggestions for future research provided.
This article explores the relationship between depression and cardiovascular disease from a mechanistic standpoint. Depression and cardiovascular disease are two of the most prevalent health problems in the United States and are the two leading causes of disability both in the United States and worldwide. Although depression is a known risk factor for the development of cardiovascular disease, as well as an independent predictor of poor prognosis following a cardiac event, the mechanistic relationship between the two remains unclear. Depression is associated with changes in an individual's health status that may influence the development and course of cardiovascular disease, including noncompliance with medical recommendations, as well as the presence of cardiovascular risk factors such as smoking and hypertension. In addition, depression is associated with physiologic changes, including nervous system activation, cardiac rhythm disturbances, systemic and localized inflammation, and hypercoagulability, that negatively influence the cardiovascular system. Further, stress may be an underlying trigger that leads to the development of both depression and cardiovascular disease. This article reviews seven potential mechanisms for the relationship between depression and cardiovascular disease and presents the available evidence surrounding each mechanism. Finally, future directions for research are discussed.
This study assessed the relation of comorbid depressive syndrome with utilization of emergency department services and preventable inpatient hospitalizations among elderly individuals with chronic medical conditions.
A cross-sectional study.
Individuals greater than or equal to 65 years of age living in the United States with Medicare part A and B fee-for-service coverage in 1999.
A 5% random sample of elderly Medicare recipients (N = 1,238,895) of whom 60,382 (4.9%) met criteria for a depressive syndrome.
Medicare beneficiaries were stratified based on the presence of at least 1 of the following medical conditions: coronary artery disease, diabetes mellitus, congestive heart failure, hypertension, prostate cancer, breast cancer, lung cancer, or colon cancer. For each stratum, we compared the odds of emergency department visits, all-cause hospitalization, and hospitalization for ambulatory care sensitive conditions (ACSC), conditions for which timely and effective medical care could decrease risk of hospitalization, for beneficiaries with and without a depressive syndrome.
Compared with those without a depressive syndrome, beneficiaries with a depressive syndrome were more likely to be older, white, and female (P <0.001). For each of the 8 chronic medical conditions, elderly beneficiaries with a depressive syndrome were at least twice as likely to use emergency department services (range of adjusted odds ratios, 2.12-3.16; P <0.001); medical inpatient hospital services (range of adjusted odds ratios, 2.59-3.71; P <0.001); and medical inpatient hospital services associated with an ACSC (range of adjusted odds ratios, 1.72-2.68; P <0.001) as compared with those without a depressive syndrome.
For elderly individuals with at least 1 chronic medical condition, the presence of a depressive syndrome increased the odds of acute medical service use, suggesting that improvements in clinical management, access to mental health services, and coordination of medical and mental health services could reduce utilization.
As the proportion of the US population over the age of 65 continues to rise, it is likely that the number of individuals with concomitant benign prostatic hyperplasia and hypertension will also increase. To reduce morbidity and mortality, it is important to treat patients with hypertension optimally. Evidence from outcome trials suggests that alpha1 blockers should not be used as first-line antihypertensive therapy. Although some clinicians previously recommended alpha1 blocker monotherapy for patients with both hypertension and benign prostatic hyperplasia, the most recent American Urologic Association and Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure guidelines recommend independent treatment with the most appropriate pharmacologic agents for each condition. When treating patients with benign prostatic hyperplasia, clinicians should be aware of the potential impacts that alpha1 blockers may have on blood pressure and potential adverse events in patients who are normotensive as well as in patients with treated hypertension.
Until relatively recently, depression has been considered a purely "mental" disorder and therefore in the natural domain of psychologists and psychiatrists. However, recent epidemiological studies have revealed that aging, physical and psychological stress, chronic pain, several metabolic disorders such as insulin resistance and established diabetes, alcoholism, inflammatory conditions, and vascular disorders such as arterial hypertension all may be associated with depression. The present review examines some of these depression-associated factors and the mechanisms by which they might give rise to vascular disorders such as atherosclerosis, microcirculation endothelial dysfunction, and interstitial disturbances leading to organ damage. A number of disorders involving the circulation can lead progressively and insidiously to large artery rigidity, remodeling of peripheral arteries, and alterations of the microcirculation of large blood vessels. Perturbations in vasa vasorum blood flow may contribute to atherogenesis, in addition to the influence of numerous cellular events involved in inflammation (tumor necrosis factor alpha, interleukin 1 beta, etc). Since Hans Selye first described the neuroendocrine cascade generated by experimentally induced stress half a century ago, phenomena such as the axonal release of neurotransmitters (including serotonin), accumulation of metabolites such as homocysteine, platelet-activating factor, and nitric oxide also have been implicated in the pathogenesis of depression. Moreover, vascular consequences of depression such as heart rate and pulse pressure variations may lead to endothelial dysfunction in critical microcirculation networks (cerebral, myocardial, and renal) and initiate physicochemical alterations in interstitial compartments adjacent to vital organs. The appropriate use of ambulatory monitoring of vascular parameters, such as heart rate and pulse pressure, and eventually, early identification of genetic and metabolic markers may prove helpful in the early detection of events preceding and predicting the clinical manifestations of depression.
Recent studies in primary care settings indicate that African Americans face health disparities in the treatment of major depression. We reviewed the literature to find evidence of specific patient, physician, and practice-setting factors related to such barriers.
We searched for and retrieved articles in Medline (1966-2004) and hand-checked bibliographies to find additional articles that were relevant to the evaluation and treatment of African Americans with depression.
Two investigators (AKD, MO) independently examined the abstracts retrieved from the literature search, and excluded articles that did not match a predefined search strategy. Two other investigators (HLC, MMW) identified potential articles through bibliographic review. In the extracted set articles, we examined cited barriers to diagnosis and effective management.
We found 24 articles that fulfilled our criteria. These studies indicate that African Americans face a number of barriers in the recognition and treatment of major depression including clinical presentation with somatization, stigma about diagnosis, competing clinical demands of comorbid general medical problems, problems with the physician-patient relationship, and lack of comprehensive primary care services.
Research indicates that African Americans who have depression may be frequently under diagnosed and inadequately managed in primary care as a result of patient, physician, and treatment-setting factors. Our systematic review can assist family physicians in understanding how to overcome such barriers to the diagnosis and treatment of depressive disorders in African American patients.
Major depressive disorder is a risk factor for the development of incident coronary heart disease events in healthy patients and for adverse cardiovascular outcomes in patients with established heart disease. Depression is present in 1 of 5 outpatients with coronary heart disease and in 1 of 3 outpatients with congestive heart failure, yet the majority of cases are not recognized or appropriately treated. It is not known whether treating depression improves cardiovascular outcomes, but antidepressant treatment with selective serotonin reuptake inhibitors is generally safe, alleviates depression, and improves quality of life. This article evaluates the importance of major depression in patients with cardiovascular disease, and provides practical guidance for identifying and treating this disorder.
To examine predictors of intentional and unintentional nonadherence to antihypertensive medication regimens and their relationships to blood pressure outcomes.
Although poor adherence to medical regimens is a major concern in the care of patients with high blood pressure (HBP), our understanding of the complex behavior related to adherence is limited. Moreover, few studies have been devoted to understanding adherence issues in ethnic minority groups, such as the interplay between cultural beliefs and HBP medication-taking behaviors.
A cross-sectional analysis was performed to assess the factors affecting nonadherence to antihypertensive medication regimens.
The data used in this analysis came from an ongoing HBP intervention trial involving middle-aged (40-64 years) Korean Americans with HBP. A total of 445 Korean Americans with HBP was enrolled in the trial at baseline. Of these, 208 participants who were on antihypertensive medication were included in the analysis. Using multivariate logistic regression, we examined theoretically selected variables to assess their relationships to intentional and unintentional nonadherence in this sample.
Approximately 53.8% of the subjects endorsed 1 or more types of nonadherent behaviors. After controlling for demographic variables, multivariate analysis revealed that a greater number of side effects from the medication (adjusted odds ratio [OR], 1.19; 95% confidence interval [CI], 1.07 to 1.33) and a lower level of HBP knowledge (adjusted OR, 0.89; 95% CI, 0.79 to 0.99) were significantly associated with intentional nonadherence. Unintentional nonadherence was less strongly associated with the study variables examined in the analysis.
Our findings indicate that intentional nonadherence to antihypertensive medication that stems from incomplete knowledge of HBP treatment is prevalent among middle-aged Korean Americans with HBP. The results highlight the strong need for an intervention that focuses on increasing patient knowledge about HBP, including the benefits and side effects of antihypertensive medication. This type of focused intervention may help reduce intentional nonadherence to antihypertensive medications and ultimately result in achieving adequate BP control in this high-risk group.