Vincent M. Figueredo

Infective endocarditis epidemiology over five decades: a systematic review.

Aims To Assess changes in infective endocarditis (IE) epidemiology over the last 5 decades. Methods and Results We searched the published literature using PubMed, MEDLINE, and EMBASE from inception until December 2011. Data From Einstein Medical Center, Philadelphia, PA were also included. Criteria for inclusion in this systematic review included studies with reported IE microbiology, IE definition, description of population studied, and time frame. Two authors independently extracted data and assessed manuscript quality. One hundred sixty studies (27,083 patients) met inclusion criteria. Among hospital-based studies (n=142; 23,606 patients) staphylococcal IE percentage increased over time, with coagulase-negative staphylococcus (CNS) increasing over each of the last 5 decades (p<0.001) and Staphylococcus aureus (SA) in the last decade (21% to 30%; p<0.05). Streptococcus viridans (SV) and culture negative (CN) IE frequency decreased over time (p<0.001), while enterococcal IE increased in the last decade (p<0.01). Patient age and male predominance increased over time as well. In subgroup analysis, SA frequency increased in North America, but not the rest of the world. This was due, in part, to an increase in intravenous drug abuse IE in North America (p<0.001). Among population-based studies (n=18; 3,477 patients) no significant changes were found. Conclusion Important changes occurred in IE epidemiology over the last half-century, especially in the last decade. Staphylococcal and enterococcal IE percentage increased while SV and CN IE decreased. Moreover, mean age at diagnosis increased together with male:female ratio. These changes should be considered at the time of decision-making in treatment of and prophylaxis for IE.

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

The Time Has Come for Physicians to Take Notice: The Impact of Psychosocial Stressors on the Heart

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. Copyright

Alcoholic cardiomyopathy: a review.

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.

Chemical Cardiomyopathies: The Negative Effects of Medications and Nonprescribed Drugs on the Heart

Alcohol abuse can cause cardiomyopathy indistinguishable from other types of dilated nonischemic cardiomyopathy. Most heavy drinkers remain asymptomatic in the earlier stages of disease progression, and many never develop the familiar clinical manifestations that typify heart failure. We review the current thinking on the pathophysiology, clinical characteristics, and treatments available for alcoholic cardiomyopathy. The relationship of alcohol to heart disease is complicated by the fact that in moderation, alcohol has been shown to afford a certain degree of protection against cardiovascular disease.

Primary cardiac tumors.

The heart is a target of injury for many chemical compounds, both medically prescribed and not medically prescribed. Pathophysiologic mechanisms underlying the development of chemical-induced cardiomyopathies vary depending on the inciting agent, including direct toxic effects, neurohormonal activation, altered calcium homeostasis, and oxidative stress. Numerous chemicals and drugs are implicated in cardiomyopathy. This article discusses examples of medication and nonprescribed drug-induced cardiomyopathies and reviews their pathophysiologic mechanisms.

Tachycardia mediated cardiomyopathy: Pathophysiology, mechanisms, clinical features and management

Primary cardiac tumors are a rare entity compared to tumors that metastasize to the heart. Patients with such tumors may be asymptomatic. Many cases are found incidentally during evaluation of an unrelated medical condition. It is important for the clinician to have a high index of suspicion when evaluating a patient presenting with signs and systemic symptoms concerning possible malignancy, plus cardiac specific symptoms or complications. These can include new onset dyspnea, congestive heart failure, arrhythmias or murmurs varying with body positions. Imaging, particularly the use of echocardiography, remains the cornerstone of diagnosis, and may be combined with new imaging modalities of cardiac CT and MRI. The aim of this paper is to describe the epidemiology and pathophysiology of the various benign and malignant primary cardiac tumors.

Alcohol consumption reduces ischemia-reperfusion injury by species-specific signaling in guinea pigs and rats.

Tachycardia mediated cardiomyopathy (TMC) is a reversible form of dilated cardiomyopathy that can occur with most supraventricular and ventricular arrhythmias. Despite the plethora of literature describing this entity in animal models, as well as humans, it remains poorly understood. Over the last decade, new etiologies of TMC, such as frequent premature ventricular complexes in normal hearts, have been identified. Recent advances in catheter-based ablation therapies, particularly for atrial fibrillation and ventricular arrhythmias, have added a new dimension to the treatment of this condition. This review describes the pathophysiology, proposed mechanisms, clinical features and management in various arrhythmic conditions.

Alcohol and arrhythmias: a comprehensive review.

We recently discovered that regular alcohol consumption reduces ischemia-reperfusion injury to the same degree as ischemic preconditioning in guinea pig hearts. Ischemic preconditioning, like this cardioprotective effect of alcohol, is mediated by adenosine signaling in guinea pigs. In rats, ischemic preconditioning may be mediated predominantly by α1-adrenergic signaling. To be certain that this protective effect of alcohol is a general biological response, we searched for alcohols cardioprotection in rat and identified a potential signaling mechanism. Hearts isolated from alcohol-fed guinea pigs and rats were subjected to ischemia-reperfusion. Hearts from alcohol-fed animals showed greater recovery of left ventricular developed pressure than controls (guinea pigs, 46 vs. 29%; rats, 50 vs. 31%) and decreased myocyte necrosis assessed by creatine kinase release (guinea pigs, 204 ± 42 vs. 440 ± 70 U ⋅ ml-1 ⋅ g dry wt-1; rats 158 ± 13 vs. 328 ± 31 U ⋅ ml-1 ⋅ g dry wt-1). Adenosine receptor blockade [8-( p-sulfophenyl)theophylline] abolished alcohols protection in guinea pig but not rat hearts. By contrast, α1-adrenergic blockade (prazosin) abolished alcohols protection in rat but not guinea pig hearts. We conclude that regular alcohol consumption reduces ischemia-reperfusion injury and is mediated by species-specific signaling mechanisms. A major goal of cardiovascular research is to find a pharmacologically induced chronic state of preconditioning. Understanding the mechanisms of alcohols cardioprotection against ischemia-reperfusion injury may aid in reaching this goal.We recently discovered that regular alcohol consumption reduces ischemia-reperfusion injury to the same degree as ischemic preconditioning in guinea pig hearts. Ischemic preconditioning, like this cardioprotective effect of alcohol, is mediated by adenosine signaling in guinea pigs. In rats, ischemic preconditioning may be mediated predominantly by alpha1-adrenergic signaling. To be certain that this protective effect of alcohol is a general biological response, we searched for alcohols cardioprotection in rat and identified a potential signaling mechanism. Hearts isolated from alcohol-fed guinea pigs and rats were subjected to ischemia-reperfusion. Hearts from alcohol-fed animals showed greater recovery of left ventricular developed pressure than controls (guinea pigs, 46 vs. 29%; rats, 50 vs. 31%) and decreased myocyte necrosis assessed by creatine kinase release (guinea pigs, 204 +/- 42 vs. 440 +/- 70 U . ml-1 . g dry wt-1; rats 158 +/- 13 vs. 328 +/- 31 U . ml-1 . g dry wt-1). Adenosine receptor blockade [8-(p-sulfophenyl)theophylline] abolished alcohols protection in guinea pig but not rat hearts. By contrast, alpha1-adrenergic blockade (prazosin) abolished alcohols protection in rat but not guinea pig hearts. We conclude that regular alcohol consumption reduces ischemia-reperfusion injury and is mediated by species-specific signaling mechanisms. A major goal of cardiovascular research is to find a pharmacologically induced chronic state of preconditioning. Understanding the mechanisms of alcohols cardioprotection against ischemia-reperfusion injury may aid in reaching this goal.

Improvement in Left Ventricular Systolic and Diastolic Performance During Ranolazine Treatment in Patients With Stable Angina

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.