Mustafa Hassan

Coronary artery disease and depression : Patients with more depressive symptoms have lower cardiovascular reactivity during laboratory-induced mental stress

Objective: To investigate the relationship between symptoms of depression and cardiovascular reactivity during mental stress in patients with coronary artery disease (CAD). Depressive symptoms are common in patients with CAD and are related to an increased risk of cardiac events and death. Some researchers have proposed that negative outcomes in depressed patients with CAD may be related to exaggerated cardiovascular reactivity and psychological stress. However, the data are unclear. Methods: Patients with CAD (n = 128; mean age = 64 years) were recruited for this study. Participants underwent psychological stress testing and 2-day (stress/rest) radionuclide imaging. The Beck Depression Inventory (BDI) results were collected at baseline. Cardiac function data were also gathered and stress data were compared with baseline findings. Results: The change in systolic blood pressure (SBP) from rest to stress was 47 ± 18 (mean ± standard deviation) mm Hg, diastolic blood pressure (DBP) = 30 ± 11 mm Hg, double product difference (DP) = 5887 ± 3095, and heart rate (HR) = 20 ± 13 beats/minute (p < .001 for all). The BDI score was 8.7 ± 5.6. The BDI score was negatively correlated with all hemodynamic variables, although only significant with stress SBP and DP, and HR and DP changes. BDI scores also predicted changes in HR and DP. HR remained significant in regression analyses controlling for other sample characteristics. Conclusions: This study showed a negative relationship between depressive symptoms and cardiovascular reactivity to mental stress. In contrast to the mechanism proposed by earlier researchers, this study suggests that decreased cardiovascular reactivity occurs with increased depressive symptomology. The mechanism by which this effect occurs and its clinical significance are still unknown. BDI = Beck Depression Inventory; SBP = systolic blood pressure; DBP = diastolic blood pressure; DP = double product difference; HR = heart rate.

Variability of myocardial ischemic responses to mental versus exercise or adenosine stress in patients with coronary artery disease.

Background. Mental stress precipitates myocardial ischemia in a significant percentage of coronary artery disease (CAD) patients. Exercise or adenosine stresses produce different physiologic responses and cause myocardial ischemia via different mechanisms. Little is known about the comparative severity and location of myocardial ischemia provoked by these different stressors. In this study we sought to compare the within-individual ischemic responses to mental versus exercise or adenosine stress in a cohort of CAD patients.Methods and Results. All patients underwent mental stress and either exercise or adenosine testing within a 1-week period. Mental stress was induced via a public speaking task. Rest-stress myocardial perfusion imaging was used with all testing protocols. Participants were 187 patients (65 women [35%]) with a documented history of CAD and a mean age of 64 ± 9 years. Mental stress-induced myocardial ischemia (MSIMI) was less prevalent and frequently of less magnitude than exercise- or adenosine-induced ischemia. Ischemia induced by exercise or adenosine testing did not accurately predict the development or the location of MSIMI. The overall concordance between these stressors for provoking ischemia was weak (percent agreement, 71%; κ [± SE], 0.26 ± 0.07). In a minority of patients (11%) mental stress provoked ischemia in the absence of exercise- or adenosine-induced ischemia. Moreover, in patients who had myocardial ischemia during both stressors, there were significant within-individual differences in the coronary artery distribution of the ischemic regions. MSIMI was more likely to occur in a single-vessel distribution (86%) compared with exercise- or adenosine-induced ischemia (54%). The stressors had moderate agreement if the ischemic region was in the right coronary artery territory (percent agreement, 76%; κ, 0.52 ± 0.19) or the left anterior descending coronary artery (percent agreement, 76%; κ, 0.51 ± 0.19) and significantly lower agreement in the left circumflex territory (percent agreement, 62%; κ, 0.22 ± 0.18).Conclusions. Our findings indicate that mental and exercise or adenosine stresses provoke different myocardial ischemic responses. These observations suggest that exercise or adenosine testing may not adequately assess the likelihood of occurrence or severity of MSIMI and that different mechanisms are operative in each condition.

Association of 1 -Adrenergic Receptor Genetic Polymorphism With Mental Stress-Induced Myocardial Ischemia in Patients With Coronary Artery Disease

BACKGROUND Mental stress is associated with sympathetic adrenergic stimulation and concomitant increases in blood pressure and heart rate. Heritable individual differences in cardiovascular functional response to mental stress may arise from genetic variations in adrenergic receptors, which might produce excessive hemodynamic response to mental stress or create other conditions favoring the development of myocardial ischemia. METHODS We examined the relationship between hemodynamic response to mental stress and mental stress-induced myocardial ischemia (MSIMI) and 5 common functional polymorphisms of beta1-adrenergic receptors (ADRB1 [OMIM 109630, accession No. 153]) and beta2-adrenergic receptors (ADRB2 [OMIM 109690, accession No. 154]). Participants were 148 patients (45 female [30.4%]) with a documented history of coronary artery disease and a mean (SD) age of 64 (9) years. Patients were enrolled between December 9, 2004, and February 21, 2007. Mental stress was induced via a public-speaking task. Rest and stress myocardial perfusion imaging was performed. Blood samples were collected and genotyped for 5 common functional polymorphisms of ADRB1 (codons 49 and 389) and ADRB2 (codons 16 and 27 and nucleotide 523). The main outcome measures were hemodynamic and myocardial ischemic responses to mental stress. Mental stress-induced myocardial ischemia was defined as new or worsening perfusion defects during mental stress with a summed (stress to rest) difference score of at least 3. RESULTS A statistically significant difference was noted in the prevalences of MSIMI between genotype groups for codon 49 of ADRB1. Mental stress-induced myocardial ischemia occurred 3 times more frequently among patients homozygous for the Ser49 allele (31 of 104 patients [29.8%]) compared with 4 of 39 patients (10.3%) among the Gly49 allele carriers (P=.02). The adjusted odds ratio for the effect of genotype (Ser/Ser vs Gly carriers) on MSIMI was 3.9 (95% confidence interval, 1.2-12.5) (P=.02). CONCLUSIONS Our findings indicate an association between a common genetic variation in ADRB1 and myocardial ischemic response to mental stress in patients with coronary artery disease. This polymorphic genetic marker may help identify patients at increased risk for mental stress-induced adverse outcomes.

Usefulness of Peripheral Arterial Tonometry in the Detection of Mental Stress‐Induced Myocardial Ischemia

Mental stress‐induced myocardial ischemia (MSIMI) identifies a subset of coronary arterial disease (CAD) patients at increased risk for adverse cardiovascular events. Peripheral arterial vasoconstriction has been consistently reported as an underlying mechanism for ischemia development in this setting and as such affords a unique opportunity for the noninvasive detection of this phenomenon.

Comparison of Peripheral Arterial Response to Mental Stress in Men versus Women with Coronary Artery Disease

There are profound gender-related differences in the incidence, presentation, and outcomes of coronary artery disease (CAD). These differences are not entirely explained by traditional cardiovascular risk factors. Nontraditional risk factors, such as psychological traits, have increasingly been recognized as important contributors to the genesis and outcomes of CAD. Mental stress induces significant peripheral arterial vasoconstriction, with consequent increases in heart rate and blood pressure. These changes are thought to underlie the development of myocardial ischemia and other mental stress-induced adverse cardiac events in patients with CAD. This study examined for gender-related differences in peripheral arterial response to mental stress in a cohort of patients with CAD using a novel peripheral arterial tonometric (PAT) technique. There were 211 patients (77 women; 37%) with a documented history of CAD and a mean age of 64 +/- 9 years. Patients were enrolled from August 18, 2004, to February 21, 2007. Mental stress was induced using a public speaking task. Hemodynamic and PAT measurements were recorded during rest and mental stress. The PAT response was calculated as a ratio of pulse wave amplitude during stress to at rest. PAT responses were compared between men and women. The PAT ratio (during stress to at rest) was significantly higher in women compared with men. Mean PAT ratio was 0.80 +/- 0.72 in women compared with 0.59 +/- 0.48 in men (p = 0.032). This finding remained significant after controlling for possible confounding factors (p = 0.037). In conclusion, peripheral vasoconstrictive response to mental stress was more pronounced in men compared with women. This finding may suggest that men have higher susceptibility to mental stress-related adverse effects. Additional studies are needed to determine the significance of this finding.

Do men and women differ on measures of mental stress-induced ischemia?

Objective: To consider the effects of gender on ischemia in a larger sample, with broadly defined coronary artery disease (CAD). Mental stress has been shown to cause transient myocardial ischemia in a significant percentage of people with CAD. However, little is known about the effects of mental stress on ischemic processes in women. Most studies to date either had few women or required a positive exercise stress test. Methods: Participants (61 women, 93 men; average age = 63 years) had documented CAD (positive stress test, abnormal catheterization even with minimal disease, or previous myocardial infarction). They underwent mental stress testing and radionuclide perfusion imaging (stress/ rest). Cardiac function data were collected and stress was compared with baseline. The data were then submitted to a series of analyses of variance. Results: A total of 50 (32%) participants exhibited reversible ischemia post psychological stress. This reflects a relative rate of 33% (n = 31of 93) for men and 31% (n = 19 of 61) for women. No difference between men and women were observed on any measure of hemodynamic functioning (blood pressure, heart rate, or cardiac perfusion). Conclusions: Results of this study showed no significant differences between men and women on measures of hemodynamic functioning or cardiac perfusion. ACE = angiotensin-converting enzyme; BMI = body mass index; CABG = coronary artery bypass graft; CAD = coronary artery disease; DBP = diastolic blood pressure; &Dgr; DBP = change in diastolic blood pressure; LVEF = left ventricular ejection fraction; HR = heart rate; &Dgr; HR = change in heart rate; MI = myocardial infarction; SBP = systolic blood pressure; &Dgr; SBP = change in systolic blood pressure; SDS = summed difference score; VAMS = Visual Analogue Mood Scale.

Left internal mammary artery graft decompression by covered stent treatment of an adjacent saphenous vein graft pseudoaneurysm.

A 75-year-old man with a history of coronary artery bypass grafting and recent pacemaker site infection was transferred to our institution for treatment of a descending aortic pseudoaneurysm. A computed tomography scan performed upon arrival also revealed a suspected mycotic aneurysm of the

The Effect of Acute Psychological Stress on QT Dispersion in Patients with Coronary Artery Disease

Background: An acute psychological stress can precipitate ventricular arrhythmias and sudden cardiac death in patients with coronary artery disease (CAD). However, the physiologic mechanisms by which these effects occur are not entirely clear. Mental stress‐induced myocardial ischemia occurs in a significant percentage of the CAD population. It is unknown if the proarrhythmic effects of psychological stress are mediated through the development of myocardial ischemia.

Vitamin D deficiency and risk of cardiovascular diseases: a narrative review

Vitamin D, a fat-soluble prohormone, has wide-ranging roles in the regulation of many physiological processes through their interactions with the vitamin D receptors (VDR). It plays a major role in bones and calcium metabolism. Vitamin D deficiency is not uncommon and it has been associated with many health-related issues, including skeletal and non-skeletal complications. The association of low vitamin D and cardiovascular diseases and risk factors has been explored in both animal and human studies. However, studies and trials on the effect of vitamin D supplementation on cardiovascular risk factors and hypertension are conflicting with inconsistent results. Therefore, large, well-powered randomized controlled trials are warranted. If successful, supplementation with easy and low-cost vitamin D can impact our health positively. Here, we summarized the evidence for the association of vitamin D, cardiovascular diseases and risk factors, including coronary artery diseases, stroke, and hypertension, and mortality, with special consideration to resistant hypertension.

Meta-Analysis of Genotype-Guided Versus Standard Dosing of Vitamin K Antagonists

Vitamin K antagonist (VKA) is a commonly prescribed anticoagulant with a narrow therapeutic window. Genetic polymorphisms account for high VKA dosage variability. Hence, we performed an updated meta-analysis of all randomized clinical trials (RCTs) comparing genotype-guided VKA versus standard dosing algorithms. We conducted a systematic search of electronic databases from inception to October 2017 for all RCTs. The primary outcome was the percentage of time in therapeutic range (TTR). Secondary outcomes were international normalized ratio >4, major and all bleeding events, thromboembolism, adverse and serious adverse events, and all-cause mortality. We calculated the weighted mean difference for the primary outcome and risk ratio (RR) for secondary outcomes using a random-effect model. We included 20 RCTs and analyzed a total of 5,980 adult patients. Our pooled analysis showed greater improvement in TTR for the genotype-guided group in comparison with the standard group (mean difference 3.41%, 95% confidence interval [CI] 0.71 to 6.10, p = 0.01). In addition, there were significant reductions in major and all bleeding events ((RR 0.35, 95% CI 0.20 to 0.63, p = 0.0004) and (RR 0.79, 95% CI 0.66 to 0.95, p = 0.01), respectively). However, there were no significant differences between the groups for international normalized ratio >4 (RR 0.89, 95% CI 0.80 to 1.00, p = 0.06), thromboembolism (RR 0.81, 95% CI 0.56 to 1.17, p = 0.25), serious adverse events (RR 0.79, 95% CI 0.61 to 1.03, p = 0.08), any adverse events (RR 0.94, 95% CI 0.88 to 1.01, p = 0.07), or all-cause mortality (RR 0.73, 95% CI 0.32 to 1.66, p = 0.46). In conclusion, genotype-guided VKA dosing can improve the TTR and reduce the risk for bleeding episodes, in comparison with standard dosing algorithms.