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| CT images of intracranial artery calcification. According to Babiarz's method, calcifications were graded as follows: (A) Calcifications in the right internal carotid artery (green), 3 for extent and 2 for thickness; left internal carotid artery (white), 4 for extent and 3 for thickness. (B) Calcifications in the right vertebral artery (yellow), 3 for extent and 3 for thickness; left vertebral artery (blue), 2 for extent and 2 for thickness. According to Woodcock scoring, calcifications were graded as follows: (C) Calcifications in the basilar artery, severe (thick, continuous). (D) Calcifications in the middle cerebral artery calcification, moderate (thick, discontinuous). (A,B) Were from Wu et al. (2016).
Source publication
Stroke is a leading cause of death worldwide. Vascular calcification (VC), defined as deposition of calcium-phosphate complexes in the vessels, is considered as the characteristic of vascular aging. Calcifications at different vessel layers have different implications. Intimal calcification is closely related to atherosclerosis and affects plaque s...
Context in source publication
Context 1
... number of studies have looked into the association between IAC and risk of stroke in a variety of populations. According to a cohort study of 276 patients with transient ischemic attack (TIA) or acute ischemic stroke (AIS), intracranial internal carotid artery (IICA) is the most commonly affected site of calcification (incidence rate 64.8%), followed by vertebral artery (30.2%), basilar artery (19.5%), and middle cerebral artery (MCA) (6.3%) (CT images are shown in Figure 2) (Chen et al., 2019). Other studies also reported similar results ( Koton et al., 2012;Quiney et al., 2017;Strobl et al., 2018). ...
Citations
... [68,69] The high prevalence of shared risk factors, such as traditional vascular risk factors, intracranial artery calcifications, cervicocephalic artery stenosis, and atherosclerosis, may explain the frequent co-occurrence of cardiovascular and cerebrovascular disease, suggesting a reciprocal relationship between the two. [49,[70][71][72] The incidence of significant cardiac arrhythmias surges within the first day of care for 501 acute neurovascular patients. [35,73,74] Autonomic dysfunction, [30,75] myocardial infarction, [59,76] cardiac arrhythmias, [77] takotsubo syndrome (TTS) [15,78] and higher BPV, [79][80][81] are prevalent clinical features signifying dysregulation of brain-heart axis. ...
The emergence of acute ischemic stroke (AIS) induced cardiovascular dysfunctions as a bidirectional interaction has gained paramount importance in understanding the intricate relationship between the brain and heart. Post AIS, the ensuing cardiovascular dysfunctions encompass a spectrum of complications, including heart attack, congestive heart failure, systolic or diastolic dysfunction, arrhythmias, electrocardiographic anomalies, hemodynamic instability, cardiac arrest, among others, all of which are correlated with adverse outcomes and mortality. Mounting evidence underscores the intimate crosstalk between the heart and the brain, facilitated by intricate physiological and neurohumoral complex networks. The primary pathophysiological mechanisms contributing to these severe cardiac complications involve the hypothalamic‐pituitary‐adrenal (HPA) axis, sympathetic and parasympathetic hyperactivity, immune and inflammatory responses, and gut dysbiosis, collectively shaping the stroke‐related brain–heart axis. Ongoing research endeavors are concentrated on devising strategies to prevent AIS‐induced cardiovascular dysfunctions. Notably, labetalol, nicardipine, and nitroprusside are recommended for hypertension control, while β‐blockers are employed to avert chronic remodeling and address arrhythmias. However, despite these therapeutic interventions, therapeutic targets remain elusive, necessitating further investigations into this complex challenge. This review aims to delineate the state‐of‐the‐art pathophysiological mechanisms in AIS through preclinical and clinical research, unraveling their intricate interplay within the brain–heart axis, and offering pragmatic suggestions for managing AIS‐induced cardiovascular dysfunctions.
... The intertwined relation between microvascular dysfunction and endothelial inflammation is seen most vividly in arterial wall calcification. Calcium deposition takes place in vessels affected by chronic endothelial inflammation leading to loss of elasticity with stiff, non-compliant arteries [160][161][162][163][164][165][166][167][168]. Arterial wall calcification can occur anywhere in the body. ...
In this paper we examine HF and CKD through the lens of a new causal paradigm: as a conjoined energy deficiency syndrome whose progression is governed by impaired energy generation by the cardiovascular system leading to subsequent deterioration of blood energy dynamics. Due to the immense complexity of this topic our intention is not to go into unnecessary and laborious detail on specific cellular and molecular aspects of the syndromes but, instead, to use illustrative examples to establish overarching principles and to highlight the connection between the deteriorating energy field and all resultant aberrations. Indeed, once the energy dynamics are recognized cellular and molecular descriptions become superfluous. Our use of the term 'causal' is meant to imply that future breakthroughs in the treatment (and potential reversal) of these complex disease states necessarily entails recognition and correction of underlying energy deficits.
... Intracranial artery calcification (IAC) is a noninvasive imaging marker that is incidentally detected on brain computed tomography (CT), especially in advanced age [9][10][11] . The author supposes that arterial calcification (AC) is caused by the accumulation of calcium-phosphate complexes in the vessels. ...
... Some studies claim that AC is a part of the active process of atherosclerosis and may be affected by aging, diabetes mellitus, and chronic kidney disease 9,[11][12][13][14] . AC may occur in up to 90% of atherosclerotic lesions in vessels 13 . ...
... An unenhanced CT is thought to be the best tool for detecting calcifications 13 . A density ≥130 HU on CT imaging is generally accepted as a diagnostic criterion for calcification 9,10 . ...
Objective:
This study aimed to investigate the correlation between dizziness and intracranial artery calcification.
Methods:
A total of 107 consecutive patients were recruited for this study. These patients were categorized into first (case) and second (control) groups. The first and second groups had complaints of dizziness and headache, respectively. All the patients had noncontrast cranial computed tomography images. Bilateral internal carotid arteries, bilateral vertebral arteries, and basilar arteries were evaluated for detecting burden of intracranial artery calcification. Finally, demographic characteristics, stroke risk factors, and burden of intracranial artery calcification of these two groups were compared. The Mann-Whitney U test, chi-square test, and Spearman's correlation were performed to analyze the study.
Results:
It was found that the first and second groups included 39 and 68 patients, respectively. The mean age of the first group was significantly higher than that of the second group. The mean burden of intracranial artery calcification of the posterior circulation in the first and second groups were not statistically different from each other (p=0.555). The mean burden of intracranial artery calcification of the anterior circulation in the first group was found to be significantly higher than the second group (p=0.005). However, no significant difference was found between the two groups in terms of burden of intracranial artery calcification of anterior or posterior circulation, when the age variable was synchronized in both groups.
Conclusion:
Although this study found a limited correlation between dizziness and intracranial artery calcification, this situation was basically related to aging.
... [76] Stable, calcified plaques are more often associated with transient ischemic attacks (TIAs) whereas unstable, non-calcified plaques are more often associated with stroke. [90] Most patients with carotid stenosis are asymptomatic until the artery severely narrows or a clot forms. This results in a decrease or even block of blood flow to the brain, so the patient will have symptoms of a transient ischemic attack. ...
Carotid artery stenosis (CAS) is one of the leading causes of cerebral ischemia and stroke.7 When plaque builds up in the internal carotid artery, it blocks blood flow to the brain. Oftentimes, this condition only comes to light after a patient experiences a stroke or stroke-like symptoms. When this occurs, cholesterol-lowering medications and blood thinners can help to increase blood flow to the brain. However, if the plaque is so large that it severely narrows the lumen of the artery, surgery may be required to restore blood flow to the brain. Patients with severe stenosis can undergo procedures such as carotid endarterectomies (CEA), stenting, and transcarotid artery revascularization (TCAR) for this purpose. In this review, we discuss these procedures and which patients warrant which type of intervention. We look at the pathophysiology of internal carotid artery stenosis and current treatment options, while highlighting emerging treatment options. This review aims to increase understanding of the management of symptomatic carotid artery stenosis as well as provide a groundwork for more innovative treatments.
... First, measuring calcification manually can affect the objectivity of calcification grading. However, it was defined that there are some disadvantages to both manual and automatic measurement methods in the literature (38). Moreover, a study in the literature comparing semiautomatic and manual measurements reported a good level of concordance between the two methods (39). ...
Aim:Cerebral small vessel disease (CSVD) is a representative cause of stroke, cognitive impairment, and age-related disability, and it is shown to be associated with some traditional atherosclerotic risk factors. This study investigated relationship between the presence and severity of intracranial arterial calcification (ICAS) and the findings of CSVD.Methods:Three hundred eighty-nine patients over the age of 40 who underwent non-enhanced cranial computed tomography (CT) and magnetic resonance imaging between January 01 and December 31, 2018, were included in the retrospective study. ICAS was scored on CT. CSVD findings, enlarged perivascular spaces (BGPVS, CSPVS), white matter hyperintensities [white matter hyperintensity was scored at periventricular (PVWMHI), white matter hyperintensity was scored at subcortical (SCWMHI)], cortical atrophy [global atrophy (GA) score, and medial temporal atrophy (MTA), Koedam score] were scored in MR images. The presence of acute, chronic, and lacunar infarcts was recorded. After controlling for age and gender, the correlation between ICAS and CSVD markers was examined.Results:A positive correlation was found between ICAS score and BGPVS (r: 0.463 p
... Numerous classes of medications are available to treat hypertension, and electrolyte imbalance is one of several important side effects considered in the choice of medication [36]. The protective effects of low serum calcium levels with respect to MACE outcomes that we observe may be related to the direct appearance of Ca 2+ ions in the aterial plaques, promoting both stroke [80] and AMI [38]. ...
High dimensional predictive models of Major Adverse Cardiac Events (MACE), which includes heart attack (AMI), stroke, and death caused by cardiovascular disease (CVD), were built using four longitudinal cohorts of Veterans Administration (VA) patients created from VA medical records. We considered 247 variables / risk factors measured across 7.5 years for millions of patients in order to compare predictions for the first reported MACE event using six distinct modelling methodologies. The best-performing methodology varied across the four cohorts. Model coefficients related to disease pathophysiology and treatment were relatively constant across cohorts, while coefficients dependent upon the confounding variables of age and healthcare utilization varied considerably across cohorts. In particular, models trained on a retrospective case-control (Rcc) cohort (where controls are matched to cases by date of birth cohort and overall level of healthcare utilization) emphasize variables describing pathophysiology and treatment, while predictions based on the cohort of all active patients at the start of 2017 (C-17) rely much more on age and variables reflecting healthcare utilization. In consequence, directly using an Rcc-trained model to evaluate the C-17 cohort resulted in poor performance (C-statistic = 0.65). However, a simple reoptimization of model dependence on age, demographics, and five other variables improved the C-statistic to 0.74, nearly matching the 0.76 obtained on C-17 by a C-17-trained model. Dependence of MACE risk on biomarkers for hypertension, cholesterol, diabetes, body mass index, and renal function in our models was consistent with the literature. At the same time, including medications and procedures provided important indications of both disease severity and the level of treatment. More detailed study designs will be required to disentangle these effects.
... Calcification usually formed in patients with T2DM is characterized by the coexistence of intimal and media calcifications [6]. Moreover, studies have shown that CAC can not only increase the risk of interventional cardiology, but also increase the risk of stroke and ischemic heart disease, but it is also the leading cause of death, cardiac death, and valvular calcification [7,8]. ...
Coronary artery calcification (CAC) increases the risk of acute coronary syndrome. This study examined the correlation between C1q/TNF-related protein 9 (CTRP9) and CAC and explored CTRP9 as a biomarker for prognosis. We divided 275 patients with coronary heart disease into four groups. In order to balance the baseline confounding factors, propensity score matching (PSM) was performed to match CAC patients with non-CAC patients in a 1:1 ratio. Optical coherence tomography (OCT) calcification scoring was performed in 126 patients with CAC. Moreover, 140 patients who underwent OCT were followed-up for 9 months for analysis of the correlation between CTRP9 levels and clinical prognosis. Based on OCT calcification scores, 126 patients with CAC were divided into the 0–2 and 3–4 groups. Plasma CTRP9 levels were significantly lower in the type 2 diabetes mellitus (T2DM), CAC and CAC with T2DM groups than in the control group. CTRP9 played roles as a protective factor and potential predictor in CAC severity. The AUC of the OCT calcification score 3–4 group predicted by the plasma CTRP9 level was 0.766. During the follow-up period, the cumulative event-free survival rate was significantly lower in the low-level CTRP9 (L-CTRP9) group than in the high-level (H-CTRP9) group, and the incidence of major endpoint events was significantly higher in the L-CTRP9 group than in the H-CTRP9 group. CTRP9 can be a valuable biomarker for CAC occurrence and severity and can predict patients’ clinical prognosis.
Calcification is a process of accumulation of calcium in tissues and deposition of calcium salts by the crystallization of PO43− and ionized calcium (Ca2+). It is a crucial process in the development of bones and teeth. However, pathological calcification can occur in almost any soft tissue of the organism. The better studied is vascular calcification, where calcium salts can accumulate in the intima or medial layer or in aortic valves, and it is associated with higher mortality and cardiovascular events, including myocardial infarction, stroke, aortic and peripheral artery disease (PAD), and diabetes or chronic kidney disease (CKD), among others. The process involves an intricate interplay of different cellular components, endothelial cells (ECs), vascular smooth muscle cells (VSMCs), fibroblasts, and pericytes, concurrent with the activation of several signaling pathways, calcium, Wnt, BMP/Smad, and Notch, and the regulation by different molecular mediators, growth factors (GFs), osteogenic factors and matrix vesicles (MVs). In the present review, we aim to explore the cellular players, molecular pathways, biomarkers, and clinical treatment strategies associated with vascular calcification to provide a current and comprehensive overview of the topic.
Background
Coronary artery disease (CAD) and cognitive impairment (CI) have become significant global disease and medical burdens. There have been several reports documenting the alterations in regional brain function and their correlation with CI in CAD patients. However, there is limited research on the changes in brain network connectivity in CAD patients. To investigate the resting-state connectivity and further understand the effective connectivity strength and directionality in patients with CAD, we utilized degree centrality (DC) and spectral dynamic causal modeling (spDCM) to detect functional hubs in the whole brain network, followed by an analysis of directional connections. Using the aforementioned approaches, it is possible to investigate the hub regions and aberrant connections underlying the altered brain function in CAD patients, providing neuroimaging evidence for the cognitive decline in patients with coronary artery disease.
Materials and Methods
This study was prospectively conducted involving 24 patients diagnosed with CAD and 24 healthy controls (HC) who were matched in terms of age, gender, and education. Functional MRI (fMRI) scans were utilized to investigate brain activity in these individuals. Neuropsychological examinations were performed on all participants. DC analysis and spDCM were employed to investigate abnormal brain networks in patients with CAD. Additionally, the association between effective connectivity strength and cognitive function in patients with CAD was examined based on the aforementioned results.
Results
By assessing cognitive functions, we discovered that patients with CAD exhibited notably lower cognitive function compared to the HC group. By utilizing DC analysis and spDCM, we observed significant reductions in DC values within the left parahippocampal cortex (PHC) and the left medial temporal gyrus (MTG) in CAD patients when compared to the control group. In terms of effective connectivity, we observed the absence of positive connectivity between the right superior frontal gyrus (SFG) and PHC in CAD patients. Moreover, there was an increase in negative connectivity from PHC and MTG to SFG, along with a decrease in the strength of positive connectivity between PHC and MTG. Furthermore, we identified a noteworthy positive correlation (r = 0.491, p = 0.015) between the strength of connectivity between the PHC and the MTG and cognitive function in CAD patients.
Conclusions
These research findings suggest that alterations in the connectivity of the brain networks involving SFG, PHC, and MTG in CAD patients may mediate changes in cognitive function.
