The time has come for physicians to take notice: the impact of psychosocial stressors on the heart.

A rapidly growing body of evidence supports a relationship between psychosocial factors and cardiovascular disease. In this article, a review of the epidemiologic and clinical research investigating this relationship concludes that psychosocial stressors can be both a cause and a consequence of cardiovascular disease events. Furthermore, recent data have shown that stress management might reduce future cardiac events in patients with cardiovascular disease. Unfortunately, the influence of psychosocial risk factors on cardiovascular disease remains underrecognized compared with traditional cardiac risk factors. Physicians and their associates should screen for psychosocial stressors and recognize potential symptoms. Consideration should be given to developing improved liaison relationships with psychologic or behavioral specialists to facilitate more specialized interventions when appropriate. A variety of interventions conducted by appropriately trained mental health professionals have successfully improved stress in patients with cardiovascular disease and other chronic diseases. The time has come for physicians to recognize the impact of psychosocial stressors on cardiovascular disease

Low-density lipoprotein cholesterol lowering therapies: what is on the horizon?

Elevated low-density lipoprotein cholesterol (LDL-C) levels are associated with an increased risk for cardiovascular disease (CVD). Statins have been the cornerstone of lipid therapy to lower LDL-C for the past two decades, but despite significant clinical efficacy in a majority of patients, a large residual risk remains for the development of initial or recurrent atherosclerotic CVD. In addition, owing to the side-effects, a significant percentage of patients cannot tolerate any statin dose or a high enough statin dose. Thus, novel therapeutic agents are currently being developed to lower LDL-C levels further. This review will highlight these novel therapeutic agents including antisense oligonucleotides focused on apolipoprotein B, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, and microsomal triglyceride transfer protein inhibitors. For each therapeutic class, an overview of mechanism of action, pharmacokinetic data, and efficacy/safety evidence will be discussed

Alcohol and arrhythmias: a comprehensive review.

The use of alcohol as a social lubricant has been ubiquitous in human societies since ancient times. It has also long been recognized that alcohol produces undesirable cardiovascular effects, especially when imbibed in excess. Numerous investigators have noted a causal relationship between alcohol and arrhythmias, as well as sudden cardiac death. We have undertaken a comprehensive review of the literature on alcohol as a potential trigger for arrhythmias. We have reviewed the major epidemiological studies undertaken on this subject. We have also explored pathophysiological mechanisms that drive the arrythmogenic effects of alcohol. In conclusion, although there is definite proof in the literature to implicate alcohol as a culprit in arrhythmias, the relationship is complex

Cocaine and the heart.

The use of cocaine may be associated with either acute or chronic toxicity, and approximately 5% to 10% of emergency department visits in the United States are believed to be secondary to cocaine usage. Chest pain is the most common cocaine-related medical problem, leading to the evaluation of approximately 64,000 patients annually for possible myocardial infarction, of which approximately 57% are admitted to the hospital, resulting in an annual cost greater than $83 million. There is a plethora of cocaine-related cardiovascular complications, including acute myocardial ischemia and infarction, arrhythmias, sudden death, myocarditis, cardiomyopathy, hypertension, aortic ruptures, and endocarditis. There is no evidence to suggest that preexisting vascular disease is a prerequisite for the development of a cocaine-related cardiovascular event, although it may be a potentiating factor, as may be nicotine and alcohol

Incidence of, predictors for, and mortality associated with malignant ventricular arrhythmias in non-ST elevation myocardial infarction patients.

BACKGROUND: The incidence of non-ST elevation myocardial infarction (NSTEMI) is increasing. Although life-threatening ventricular arrhythmias have been well-documented in patients with ST elevation MI (STEMI), their incidence and importance in NSTEMI have not been examined in similar detail. We examined the incidence, predictors, and mortality rates of ventricular arrhythmias in a cohort of NSTEMI patients undergoing an early invasive strategy. METHODS: Consecutive patients admitted with NSTEMI who underwent cardiac catheterization within 48 h of admission were identified by chart review. Presence and type of ventricular arrhythmias and 30-day mortality were recorded. Malignant arrhythmias were defined as sustained ventricular tachycardia (VT, \u3e100 beats/min lasting \u3e30 s) or fibrillation (VF). Clinical risk factors, laboratory values, findings on electrocardiogram, echocardiogram, cardiac catheterization, and revascularization procedure data were recorded. RESULTS: VT/VF occurred in 21 (7.6%) of 277 NSTEMI patients. Sixty percent of these events occurred within the first 48 h after hospital admission, with a median occurrence at 72 h. Twelve patients (4.3%) required defibrillation. Troponin levels were higher and left ventricular ejection fraction was lower in the VT/VF group. Multivariable analysis also identified the presence of left bundle branch block and need for urgent coronary artery bypass grafting as significant predictors of malignant ventricular arrhythmias. Thirty-day mortality was significantly higher in NSTEMI patients with malignant ventricular arrhythmias than without (38 vs. 3%, P\u3c0.001). CONCLUSION: Despite an early invasive strategy, malignant ventricular arrhythmias are frequent in NSTEMI patients and are associated with increased 30-day mortality

Cardioprotection by regular ethanol consumption: potential mechanisms and clinical application.

Epidemiological studies demonstrate that excessive drinking is associated with hypertension, cerebral bleeding and loss of cardiac contractility. Conversely, studies have shown that mortality rates for people who regularly drink ethanol in moderation are lower than in abstainers, primarily due to decreased fatal ischemic heart disease. Further, moderate ethanol consumers have lower rates of myocardial infarction compared with abstainers. These beneficial cardiac effects may be due to pleiotropic effects of ethanol on lipids, platelets, and fibrinolytic activity. During the past decade, studies conducted in several animal models have revealed that light to moderate regular ethanol consumption renders hearts more tolerant to myocardial ischemia-reperfusion injury; to a degree similar to cardiac ischemic preconditioning (brief episodes of ischemia dramatically limit infarct size following prolonged ischemia). Recent clinical evidence suggests that light to moderate ethanol consumption in the year prior to myocardial infarction is associated with reduced mortality following myocardial infarction. These findings suggest that light to moderate ethanol consumption not only prevents myocardial infarction but also improves survival after myocardial infarction. Proposed mechanisms of cardioprotection by regular ethanol consumption include activation of adenosine A1 receptors, alpha(1)-adrenoceptors, protein kinase C-delta and epsilon, adenosine triphosphate-dependent potassium (K(ATP)) channels, nitric oxide synthase and reduced leukocyte-endothelial cell adhesive interactions. In this review, we focus on the recent progress in elucidating the endogenous myocyte signaling mediating cardioprotection by light to moderate ethanol consumption

Update on ranolazine in the management of angina.

Mortality rates attributable to coronary heart disease have declined in recent years, possibly related to changes in clinical presentation patterns and use of proven secondary prevention strategies. Chronic stable angina (CSA) remains prevalent, and the goal of treatment is control of symptoms and reduction in cardiovascular events. Ranolazine is a selective inhibitor of the late sodium current in myocytes with anti-ischemic and metabolic properties. It was approved by the US Food and Drug Administration in 2006 for use in patients with CSA. Multiple, randomized, placebo-controlled trials have shown that ranolazine improves functional capacity and decreases anginal episodes in CSA patients, despite a lack of a significant hemodynamic effect. Ranolazine did not improve cardiovascular mortality or affect incidence of myocardial infarction in the MERLIN (Metabolic Efficiency with Ranolazine for Less Ischemia in Non-ST-Elevation Acute Coronary Syndrome)-TIMI (Thrombolysis In Myocardial Infarction) 36 trial, but significantly decreased the incidence of recurrent angina. More recently, ranolazine has been shown to have beneficial and potent antiarrhythmic effects, both on supraventricular and ventricular tachyarrhythmias, largely due to its inhibition of the late sodium current. Randomized controlled trials testing these effects are underway. Lastly, ranolazine appears to be cost-effective due to its ability to decrease angina-related hospitalizations and improve quality of life

Wandering acute myocardial infarction.

Incorrect electrode placement or cable connection during electrocardiographic (ECG) recording can significantly alter the ECG morphology. We report a case of ST-segment elevation myocardial infarction causing a diagnostic dilemma due to cable interchange

Meditation: should a cardiologist care?

Meditation refers to a family of practices that may share many similarities, but can have differences in underlying methods and goals. Religious and spiritual associations are common but are not requisite for meditation practice and it should be recognized that the basis of many if not all practices is the training of the brain and body, a process that appears to have profound effects on both structure and function. In recent decades there has been interest regarding the effects of these ancient practices on the cardiovascular system, as meditation has intuitive appeal for benefit in this area. Though there is a relative shortage of quality data, available evidence suggests that meditation may exert beneficial effects on autonomic tone, autonomic reflexes, and decrease blood pressure acutely and after long term practice. In addition, meditation has the potential to positively influence the cardiovascular system through the mind-heart connection and the anti-inflammatory reflex. There is limited but promising data to suggest that meditation based interventions can have beneficial effects on patients with established cardiovascular disease. More high quality and unbiased studies of meditation practices on relevant endpoints in cardiovascular disease are needed, including the effects of such practices on inflammation, baseline heart rate variability, arrhythmias, myocardial infarction, and cardiovascular mortality

Utility of the QT interval in predicting outcomes in patients presenting to the emergency department with chest pain.

OBJECTIVES: The aim of this study was to investigate whether prolongation of the heart rate-corrected QT interval (QTc) is an independent risk factor for predicting future acute coronary syndrome (ACS) occurrence or mortality in patients with at least one cardiac risk factor presenting with chest pain to the emergency department (ED). METHODS: This is a single-center, retrospective study of patients presenting with chest pain to the ED of Einstein Medical Center, Philadelphia, between 2011 and 2012. Proportional hazards models were used to calculate hazard ratios (HRs) for occurrence of ACS or death within 1 year. Kaplan-Meier curves were used to determine the time to event for QTc low (\u3c460 \u3ems) versus QTc high (≥460 ms) groups. RESULTS: A total of 595 patients met the inclusion criteria. Older age, hypertension, diabetes mellitus, and hyperlipidemia were more common in the QTc high group. Patients in the QTc high group were more likely to experience subsequent ACS or death (HR 8.12, 95% confidence interval 4.00-16.72), even after adjusting for traditional cardiac risk factors (HR 7.68, 95% confidence interval 3.57-16.61). CONCLUSION: QTc prolongation at ED presentation with chest pain and at least one cardiac risk factor predicts subsequent ACS and death