Richard G. Sheahan

Primary Prevention of Sudden Cardiac Death in Heart Failure: Will the Solution Be Shocking?

Sudden cardiac death (SCD) may occur in as many as 40% of all patients who suffer from heart failure. This review describes the scope of the problem, risk factors for SCD, the effect of medications used in heart failure on SCD and the potential effect of the implantable cardioverter-defibrillator in primary prevention.

Morphological Patterns of Death by Myocytes in Arrhythmogenic Right Ventricular Dysplasia

There are two forms of nuclear loss from eukaryotic cells: biochemical DNA degradation in apoptosis and nuclear extrusion from the cell body as seen in mammalian erythroblasts. In biopsies of right ventricular myocardium from 8 patients with arrhythmogenic right ventricular dysplasia (ARVD), we found not only a terminal deoxynucleotidyl transferase-mediated digoxigenin-deoxyuridine triphosphate nick-end labeling (TUNEL)-positive nucleus in mononuclear myocytes, but also 1 or 2 TUNEL-positive nuclei in multinuclear myocytes. With electron microscopy, we found a nuclear dislocation to the cell periphery, followed by its extrusion into the extracellular space. Both the migration and extrusion of the nuclei of myocytes resemble the morphogenesis of human erythroblasts. Nuclear extrusion from myocytes may be another form of programmed cell death. In support of this possibility, we also found evidence of cytoplasmic degradation in right ventricular myocytes from our ARVD cases, a process similar to one often seen in developmental programmed cell death and differing from typical nuclear apoptosis. In our ARVD cases, we thus found several different patterns of cell death, all associated with initial preservation of the plasmalemma and avoidance of local inflammation. All these features may be different responses to common signals for selective non-necrotic (apoptotic) death of right ventricular myocytes.

Part I: Use of echocardiography in the evaluation of patients with suspected cardioembolic stroke

One-sixth of all ischemic strokes are a result of embolization from the heart. Echocardiography serves as the cornerstone in evaluating patients who may have had a cardioembolic stroke. This article is the first of a two-part review series focusing on the role of echocardiography in the diagnosis and treatment of cardioembolic stroke. Specifically, this section will focus on nonrheumatic atrial fibrillation as well as cardiovascular masses as potential embolic sources.

The Use of Implantable Cardioverter Defibrillators for the Prevention of Sudden Cardiac Death: A Review of the Evidence and Implications

Sudden cardiac death (SCD) claims approximately 460,000 lives per year in the United States, and half of these deaths occur in people with a history of coronary artery disease. Patients with left ventricular dysfunction and a history of myocardial infarction are at especially high risk. There is now strong evidence from multiple well-designed randomized controlled trials that implantable cardioverter defibrillators (ICDs) save lives when used for both primary and secondary prevention. As indications for ICD implantation have broadened, considerable debate has taken place because of the substantial cost involved in widespread ICD utilization. This article summarizes the epidemiology of SCD, reviews the evidence supporting the use of ICDs in patients with ischemic cardiomyopathy, and explores some of the controversy surrounding ICD utilization that has arisen in the wake of recent trials that have utilized ICDs for the primary prevention of SCD.

The Current Status of Immune Modulating Therapy for Myocarditis: A Case of Acute Parvovirus Myocarditis Treated with Intravenous Immunoglobulin

We present a case of a patient who presented with a febrile illness without obvious source initially, who developed profound cardiac decompensation and left ventricular dysfunction. Viral titers obtained during the course of illness confirmed parvovirus infection. Intravenous aggressive immunoglobulins and medical therapy for heart failure resulted in stabilization and, ultimately, a complete recovery. Recent data from clinical trials are discussed regarding the utility of immunoglobulins in the treatment of myocarditis and heart failure.

Deep venous thrombosis: A review of the pathophysiology, clinical features, and diagnostic modalities

A 57-year-old man presented to the emergency room complaining of 2 hours of shortness of breath and chest pain. Two weeks before, he had a similar episode associated with swelling and pain of the left lower extremity. He was hospitalized and diagnosed with pulmonary embolism resulting from deep vein thrombosis (DVT) of the left thigh veins. Treatment consisted of intravenous heparin followed by chronic warfarin therapy. A ventilation-perfusion scan revealed new segmental defects consistent with recurrent pulmonary embolism. A Doppler ultrasound of the lower extremities showed a persistent left lower extremity DVT. He was treated with low-molecular-weight heparin and an inferior vena cava (IVC) filter was placed because of recurrent pulmonary embolism despite anticoagulation. Two days after the filter placement, the patient complained of dizziness upon standing. His blood pressure was 126/80 in supine position and decreased to 96/60 on standing. There was no change in hemoglobin and no evidence of bleeding. Intravenous fluids were administered but his orthostatic hypotension persisted. On the third day, swelling of his right lower extremity became evident. A computed tomogram of retroperitoneal region and pelvis showed a large thrombus in the IVC extending to the right iliac vein. A repeat Doppler ultrasound showed right iliofemoral DVT and a persistent thrombus in the left femoral vein. An infusion of tissue plasminogen activator was administered through a catheter placed in the IVC via the popliteal vein. Thrombus resolution was assessed by daily venograms. Four days after initiation of thrombolysis, there was significant resolution of the thrombus in the IVC and right iliofemoral system. The catheter was removed on the fifth day. Low-molecular-weight heparin was continued. His dizziness, orthostatic hypotension and the swelling in the right lower extremity subsided. The patient was subsequently sent to the rehabilitation unit where he made a complete recovery.

Mitral Valve Prolapse: A Review of the Literature

M valve prolapse (MVP) is a common valvular disorder characterized by abnormalities of the mitral valve apparatus that result in “billowing” of 1 or both mitral leaflets into the left atrium during systole, with or without mitral regurgitation (MR).1–3 It is the most frequently diagnosed valve abnormality in the industrial world,4,5 and the most common primary cause for dysfunction requiring mitral valve repair or replacement.6 Clinical classification may have significant overlap and “the pathogenesis of symptoms is not completely understood.”7 The overall incidence (by echocardiography) in the Framingham study was 5%, with a frequency in women approximately twice that of men.8 Table 1 highlights the variability in the prevalence of MVP by different diagnostic methods. MVP is classified as an inheritable connective tissue disorder that is regarded as an autosomal dominant disorder with variable penetrance and is divided into primary and secondary MVP. Primary MVP accounts for the vast majority of the cases and many, but not all, of these are associated with myxomatous degeneration of the mitral valve (MV). Secondary MVP is caused by chordae tendineae rupture and/or abnormal left ventricular (LV) wall motion. Potential causes of secondary MVP include coronary artery disease, rheumatic heart disease, cardiomyopathies, and infective endocarditis.9 Also, MVP may be associated with heritable disorders such as the Marfan syndrome, the Ehlers-Danlos syndrome, and other connective tissue disorders in which myxomatous degeneration of the MV is a prominent feature. Variables that decrease LV size can worsen MVP and similarly, variables that increase LV size can mask MVP. LV size is affected by blood volume, body position (supine, standing, etc.), and maneuvers (eg, Valsalva). A decrease in LV volume is the probable cause of the increased incidence of MVP in atrial septal defect and anorexia nervosa.10–12

Use of Intraluminal Stents in the Treatment of Carotid, Renal, and Peripheral Arterial Disease

Abstract Arterial disease involving renal, carotid, and lower extremity arteries [labeled as peripheral artery disease (PAD) for the purposes ofthis review] is increasing in frequency as the baby boomer generation ages and more patients are successfully treated for and survive longer with atherosclerotic coronary artery disease (CAD). Until the introduction of percutaneous transluminal angioplasty (PTA), surgery was the only option for treating limb ischemia, renal vascular hypertension, and carotid artery stenoses. The advent of catheter-based therapies has revolutionized therapeutic alternatives for patients with PAD. The advantages of percutaneous intervention compared with vascular surgery are reduced morbidity, diminished hospitalization time, rapid return to work, and significant cost-effectiveness. Furthermore, PTA may complement vascular surgery by increasing inflow and/or outflow so that difficult surgical procedures may be performed more successfully.

Prosthetic Valve Thrombosis and Thrombolysis: A Case Report and Review of the Literature

&NA; Prosthetic valve thrombosis is a rare but serious complication of implanted mechanical valves. Thrombolysis has emerged as an alternative to surgical therapy in the management of these patients. The indications for such therapy and appropriate patient selection are evolving. Our report describes management of a patient we encountered with this complication and reviews the current status of thrombolysis in such patients.

Hemodynamic Changes of Aortic Regurgitation

Hemodynamic changes associated with acute AR include a rapid increase in LV pressures during diastole, markedly elevated pressures at end diastole, and premature closure of the mitral valve. Systemic diastolic pressures may be low, but there is a minimal increase in pulse pressure. In very severe cases of acute AR, cardiac output may decrease, leading to hypotension. In chronic AR, the LV remodels to accommodate the regurgitant volume flow, and stroke volume increases to maintain effective forward blood flow. These adaptations lead to a dilated LV, a widened pulse pressure, and a low diastolic blood pressure, which are the classic findings of chronic AR.