Apical hypertrophic cardiomyopathy or left ventricular non-compaction? A difficult differential diagnosis

[No abstract available

Management of hypertrophic cardiomyopathy

[No abstract available

Distinguishing hypertension from hypertrophic cardiomyopathy as a cause of left ventricular hypertrophy

Distinguishing Hypertension From Hypertrophic Cardiomyopathy as aCause of Left Ventricular HypertrophyIn most hypertensive patients, left ventricular (LV) wallthickness is normal or only mildly increased (≤13 m

Multiplane transesophageal echocardiography and stroke

Transesophageal echocardiography (TEE) is considered a basic tool in the diagnostic and follow-up evaluation of stroke patients, since vp to 40% of cerebral ischemic events are presumed to have a cardiac origin. TEE offers a superior resolution of the posterior cardiac structures, such as left atrium and appendage and atrial septum, as well as of the aorta. By means of TEE, evidence has accumulated that some cardiovascular abnormalities (left-sided thrombi, tumors and vegetative lesions, complicated plaques of the aortic arch) are associated with ischemic stroke. Nevertheless, some issues remain unresolved. Will exclusion of atrial thrombus by multiplane TEE preclude embolism after cardioversion of atrial fibrillation? If anticoagulation before and after cardioversion is needed to provide adequate protection against embolism, will TEE be indicated in all patients? Moreover, can the detection of spontaneous echo contrast or enlarged and hypokinetic left atrial appendage in atrial fibrillation modify the therapeutic strategy? Is atrial septal aneurysm (ASA) a real embolic source, particularly when a right-to-left shunt is not associated? Considering the high prevalence of patent foramen ovale (PFO) in normal subjects, how can we identify patients at higher risk of embolism? Furthermore, methodologic points have to be taken into account when we analyze data from the literature. First, most studies are retrospective; a sole prospective study demonstrated that atherosclerotic plaques >4 mm thick in the aortic arch are significant predictors of recurrent brain infarction and other cardiovascular events in patients greater than or equal to 60 years of age. Second, the association between the aforementioned cardiac abnormalities (mainly ASA and PFO) and cardiogenic embolism is biased by the patient-enrollment criteria used in those studies so that their pathogenetic role has not yet been established. prospective studies with the enrollment of appropriate control groups will be necessary to define what can be considered a marker of embolic risk; the diagnosis "cardiogenic embolism" will not be a definitive diagnosis in most cases. (C) 1998 by Excerpta Medica, Inc

Old and new therapeutic solutions in the treatment of hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is a genetic disease of the myocardium that is relatively common in the general population, with an autosomal dominant inheritance as a genetic basis. Clinical and natural history pathways can be very different among patients with HCM. Treatment strategies have made very important advances in the last two decades, especially reducing cases of sudden death through effective risk stratification and the use of implantable defibrillators. Heart failure has become the predominant cause of morbidity and mortality in patients with HCM, being responsible for as many as 60% of disease-related deaths. HCM is most often characterized by the presence of left ventricular outflow tract (LVOT) obstruction, and this obstruction is the most frequent cause of impaired exercise tolerance in HCM and a strong independent predictor of heart failure progression and mortality. The different treatment strategies of LVOT obstruction in HCM are discussed below: surgical, invasive, and the more recent pharmacological

Natriuretic Peptides. It Is Time for Guided Therapeutic Strategies Based on Their Molecular Mechanisms

Natriuretic peptides (NPs) are the principal expression products of the endocrine function of the heart. They exert several beneficial effects, mostly mediated through guanylate cyclase-A coupled receptors, including natriuresis, diuresis, vasorelaxation, blood volume and blood pressure reduction, and regulation of electrolyte homeostasis. As a result of their biological functions, NPs counterbalance neurohormonal dysregulation in heart failure and other cardiovascular diseases. NPs have been also validated as diagnostic and prognostic biomarkers in cardiovascular diseases such as atrial fibrillation, coronary artery disease, and valvular heart disease, as well as in the presence of left ventricular hypertrophy and severe cardiac remodeling. Serial measurements of their levels may be used to contribute to more accurate risk stratification by identifying patients who are more likely to experience death from cardiovascular causes, heart failure, and cardiac hospitalizations and to guide tailored pharmacological and non-pharmacological strategies with the aim to improve clinical outcomes. On these premises, multiple therapeutic strategies based on the biological properties of NPs have been attempted to develop new targeted cardiovascular therapies. Apart from the introduction of the class of angiotensin receptor/neprilysin inhibitors to the current management of heart failure, novel promising molecules including M-atrial natriuretic peptide (a novel atrial NP-based compound) have been tested for the treatment of human hypertension with promising results. Moreover, different therapeutic strategies based on the molecular mechanisms involved in NP regulation and function are under development for the management of heart failure, hypertension, and other cardiovascular conditions

Metabolic disorders and cardiovascular risk in HIV-infected patients treated with antiretroviral agents.

The clinical management of HIV-infected individuals is based on highly active antiretroviral combination therapy, which provides significant clinical benefit in most patients, but causes in a high proportion of them a metabolic syndrome that includes body fat redistribution, hypercholesterolemia, hypertriglyceridemia, and insulin resistance. These effects are particularly evident in patients treated with protease inhibitors. It is likely that the metabolic disorders related to anti-HIV treatment will eventually translate into an increased cardiovascular risk in patients submitted to such regimens

Erythropoietin and the heart: facts and perspectives.

EPO (erythropoietin) has long been identified as a primary regulator of erythropoiesis. Subsequently, EPO has been recognized as playing a role in a broad variety of processes in cardiovascular pathophysiology. In particular, the tight interactions of EPO with the nitric oxide pathway, apoptosis, ischaemia, cell proliferation and platelet activation appear of great interest. Although enhanced EPO synthesis is viewed as an appropriate compensatory mechanism in the cardio-renal syndrome, which features CHF (congestive heart failure) and CRF (chronic renal failure), maladaptative excessive EPO synthesis in the advanced stages of these diseases appears to be predictive of higher mortality. Clinical trials based on the use of EPO in both heart and renal failure have so far produced contradictory results, whereas treatment targeted to restore low Hb levels appears rational and is supported by regulatory authorities. New areas for therapeutic use of EPO, such as acute coronary syndromes, are under investigation, and they are discussed in the present review together with other clinical applications in cardiovascular diseases. The revisited concept of a potential use of endogenous EPO levels as a predictor of CHF severity, as well as in the monitoring of responses to treatment, deserves appropriate investigation, as this may identify EPO as a useful biomarker in the clinical management of cardiovascular diseases. © The Authors Journal compilation © 2011 Biochemical Society