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Heparin-induced thrombocytopenia (HIT) remains under-recognized despite its potentially devastating outcomes. It begins when heparin exposure stimulates the formation of heparin-platelet factor 4 antibodies, which in turn triggers the release of procoagulant platelet particles. Thrombosis and thrombocytopenia that follow comprise the 2 hallmark traits of HIT, with the former largely responsible for significant vascular complications. The prevalence of HIT varies among several subgroups, with greater incidence in surgical as compared with medical populations. HIT must be acknowledged for its intense predilection for thrombosis and suspected whenever thrombosis occurs after heparin exposure. Early recognition that incorporates the clinical and serologic clues is paramount to timely institution of treatment, as its delay may result in catastrophic outcomes. The treatment of HIT mandates an immediate cessation of all heparin exposure and the institution of an antithrombotic therapy, most commonly using a direct thrombin inhibitor. Current "diagnostic" tests, which primarily include functional and antigenic assays, have more of a confirmatory than diagnostic role in the management of HIT. Special attention must be paid to cardiac patients who are often exposed to heparin multiple times during their course of treatment. Direct thrombin inhibitors are appropriate, evidence-based alternatives to heparin in patients with a history of HIT, who need to undergo percutaneous coronary intervention. As heparin remains one of the most frequently used medications today with potential for HIT with every heparin exposure, a close vigilance of platelet counts must be practiced whenever heparin is initiated. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases are a major cause of morbidity and mortality in patients after orthotopic liver transplantation (OLT). This review includes major original articles published in the English-language literature of patients who underwent dobutamine stress echocardiography (DSE) before OLT for cardiac risk stratification. Of a total of 10 original articles (total 1699 patients undergoing DSE), 6 studies used DSE to predict major adverse cardiac events (MACE) in patients undergoing OLT and 4 reported the role of DSE in coronary artery disease (CAD) prediction in patients with end-stage liver disease. The composite incidence of MACE was 11.4%. In predicting postoperative MACE, DSE had a composite sensitivity of 0.12 (95% CI, 0.07-0.19), a specificity of 0.96 (95% CI, 0.94-0.97), a positive predictive value (PPV) of 0.26 (95% CI, 0.16-0.38), and a negative predictive value (NPV) of 0.89 (95% CI, 0.88-0.91). The presence of known CAD in a patient was shown to increase the risk of cardiac events after OLT significantly in three of six studies. The average prevalence of CAD was 14.4%. In predicting CAD, DSE had a composite sensitivity of 0.47 (95% CI, 0.32-0.62), specificity of 0.74 (95% CI, 0.68- 0.79), PPV of 0.23 (95% CI, 0.15-0.33), and NPV of 0.89 (95% CI, 0.84-0.93). This review emphasizes the need for standardizing cardiac risk stratification protocol to screen and prevent cardiac morbidity after OLT, standardizing MACE definition to allow more uniform reporting, and the need for safer and efficacious alternatives to DSE in the evaluation of OLT candidates.

Cardiomyopathies are practically classified as either ischemic or nonischemic based on the presence or absence of coronary artery disease. Although conventional twodimensional echocardiography can assess left ventricular ejection fraction, wall motion, and diastolic function, it does not fully capture myocardial mechanics or tissue characterization, and does not accurately identify patients with nonischemic cardiomyopathy (NICMP) at risk for sudden cardiac death. This article discusses advanced imaging modalities for assessment of NICMP, namely, three-dimensional echocardiography, strain imaging, cardiac magnetic resonance, cardiac computed tomography, and sympathetic innervation imaging.

Phosphodiesterase-5 (PDE5) inhibitors have been approved by the US Food and Drug Administration for the treatment of erectile dysfunction and more recently for pulmonary arterial hypertension (World Health Organization functional class I). PDE5 inhibitors can induce vasodilation; in addition, through a complex pathway involving nitric oxide, cyclic guanosine monophosphate, and protein kinase G, it can reduce apoptosis and suppress cell proliferation. The presence of PDE5 inhibitors in various tissues and systemic vasculature make them potential targets in a variety of cardiovascular diseases. In many in vitro and in vivo studies, PDE5 inhibitors have been shown to have positive effects in systolic and diastolic congestive heart failure, ischemic heart disease, doxorubicin cardiomyopathy, and pulmonary arterial hypertension. They also improved vasoconstriction in Raynaud phenomenon, peripheral artery disease, and hypoxic brain conditions. This article reviews the therapeutic potentials of PDE5 inhibitors in different cardiovascular diseases.

Infiltrative diseases targeting the cardiovascular system are a subgroup of restrictive cardiomyopathies. An early diagnosis is critical in initiating therapy to mitigate the deleterious effects of the pathologic process underlying these forms of cardiomyopathies. Infiltrative cardiac disease is rare and therefore often underdiagnosed. This review outlines the prevalence of 3 of the most common forms of restrictive cardiomyopathy: sarcoidosis, hemochromatosis, and amyloidosis. Infiltrative cardiomyopathy can have a variable prognosis depending on its etiology. It is a progressive disorder that, if left untreated, can lead to early mortality. A summary of the pathology, diagnosis, disease course, and therapy is provided, along with the utility of noninvasive testing as a means of diagnosis.

The acute aortic syndromes carry significant morbidity and mortality, especially when detected late. Symptoms may mimic myocardial ischemia, and physical findings may be absent or, if present, can be suggestive of a diverse range of other conditions. Maintaining a high clinical index of suspicion is crucial in establishing the diagnosis. All patients with suspected aortic disease and evidence of acute ischemia on electrocardiogram should undergo diagnostic imaging studies before thrombolytics are administered. The demonstration of an intimal flap separating 2 lumina is the basis for diagnosis. Tear detection and localization are very important because any therapeutic intervention aims to occlude the entry tear. The goals of medical therapy are to reduce the force of left ventricular contractions, decrease the steepness of the rise of the aortic pulse wave, and reduce the systemic arterial pressure to as low a level as possible without compromising perfusion of vital organs. Surgical therapy still remains the gold standard of care for type A aortic dissection, whereas in type B dissection, percutaneous aortic stenting and fenestration techniques have been developed and are sometimes used in conjunction with medical therapy in certain situations.

Although cardiac manifestations such as pericardial, myocardial, and valvular involvement are common in patients with systemic lupus erythematosus (SLE), coronary artery involvement is less frequent. Clinical manifestations of coronary artery disease in SLE can result from accelerated atherosclerosis, arteritis, abnormal coronary flow reserve, spasm, and thrombosis. In SLE, the classic valvular abnormality consists of noninfective, verrucous vegetation. Thickening of the leaflets due to inflammation followed by fibrosis is common, occurring in about 50% of patients, whereas vegetations are present in about 40%. Mitral valve involvement is most common, with valvular regurgitation more frequent than valvular stenosis. The tricuspid valve and the aortic valve may also be affected. Its frequency varies widely: 13% to 74% in the general population. We report a case of a woman with acute myocardial infarction and normal coronary arteries, who was subsequently diagnosed with Libman-Sacks endocarditis and SLE.

Approximately 20% of coronary artery anomalies produce sudden death or life-threatening symptoms, including arrhythmias, syncope, and myocardial infarction. The most common clinical symptom of coronary artery anomaly is angina or exertional syncope. Physical examination is usually unrevealing in the absence of myocardial infarction or symptoms of ongoing ischemia. The rapid advent of cardiac computed tomography (CT) technology has made it an important adjunct to the diagnosis of coronary anomalies by angiography. The authors describe the case of a 54-year-old white man who presented with gangrenous toes. He had severe peripheral vascular disease, a femoral-popliteal bypass graft, residual hemiparesis from an ischemic stroke, hypertension, deep vein thrombosis, and a recent myocardial infarction. He underwent a 64-slice cardiac CT angiogram, which showed an interarterial course of the left main coronary artery between the aorta and the pulmonary trunk.

Constrictive pericarditis and restrictive cardiomyopathy are 2 forms of diastolic dysfunction with similar presentation but different treatment options. Whereas constrictive pericarditis has the potential of being cured with pericardiectomy, restrictive cardiomyopathy is usually incurable. It is therefore crucial to differentiate between the 2 disorders. In the last few years, new diagnostic techniques have become available to differentiate these causes of diastolic dysfunction from each other. This review provides a complete, in-depth comparison of the 2 disorders with regard to their symptoms and clinical features, etiology, pathophysiology, hemodynamics, echocardiographic presentation, and finally the different available management options.