Daniel J. Lenihan

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

Native Valve Infective Endocarditis: What Is the Optimal Timing for Surgery?

IE remains a dreaded disease masquerading under a myriad of presentations in an evolving epidemiological environment. In our continuing endeavor against this deadly disease, echocardiography has evolved into an indispensable diagnostic tool to define structural complications and guide therapy. Timing of surgical intervention for IE remains a subject of intense debate and depends on the cardiac and systemic complications of the infection, the virulence of the organism, and the responsiveness to medical therapy. A judicious agreement among cardiologist, cardiovascular surgeon, and infectious disease specialist should define whether surgical intervention is warranted and, if so, the optimal timing. Further optimization of guidelines will help in the diagnosis and treatment of endocarditis but will never be a substitute for sound judgment and experience.

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.

Heart Failure With Preserved Left Ventricular Function: Diagnostic and Therapeutic Challenges in Patients With Diastolic Heart Failure

Abstract:Heart failure associated with preserved left ventricular ejection fraction (HFpEF) is a condition of increasing importance, not only due to its rising prevalence but also due to the lack of clinical evidence for pharmacologic therapies that are beneficial. Thus, a recent case encountered at the Vanderbilt University Medical Center illustrates the clinical challenges one may encounter in patients with HFpEF. A careful review of the diagnostic challenges of HFpEF or diastolic heart failure, current recommendations for management and a glimpse of upcoming research are presented.

Sarcoidosis-induced right ventricular hypertrophy and pulmonary hypertension: echocardiographic imaging.

A 40-year-old African American male with a history of sarcoidosis diagnosed by bronchial biopsy on chronic corticosteroids presented with progressive shortness of breath and lower extremity edema. He had marked jugular venous distention with pitting edema up to his knees and a prominent right ventricular impulse without a third heart sound. His chest radiograph showed marked bilateral interstitial pattern, hilar adenopathy, and prominent pulmonary arteries. A transthoracic echocardiogram showed mildly reduced left ventricular (LV) function with marked right ventricular (RV) hypertrophy, particularly in the apical portion (Fig. 1). There was a signix8ecant paradoxical septal wall motion. There was moderate-to-severe tricuspid regurgitation (Fig. 2) and a RV pressure estimate of . 100 mmHg by Doppler interrogation (Fig. 3). Upon review of the biopsy specimen (Fig. 4), the classic noncaseating granuloma (arrow) can be seen. Although a myocardial biopsy might have conx8ermed sarcoidosis involvement of the myocardium, this was not performed due to substantial risk to the patient without clear benex8et regarding therapeutic decision-making. Sarcoidosis is a multisystem, granulomatous disorder whose cause remains elusive. Though not pathognomonic, its main pathologic feature is the noncaseating granuloma, and the most frequent organ involved is the lung. Clinically signix8ecant cardiac symptoms are relatively rare (5%–10%),1 but pathologic involvement of the heart occurs at much higher rates.2 Among the cardiac symptoms, arrhythmias and congestive heart failure are the most frequently encountered.3 The patchy distribution of the granulomas in the myocardium can lead to segmental LV wallmotion abnormalities mimicking coronary artery disease and additionally may render endomyocardial biopsy misleading. The usefulness of biopsy to guide therapy with suggestive evidence of cardiac involvement has been questioned.4 Address for correspondence and reprint requests: Daniel J. Lenihan, M.D., The University of Texas Medical Branch at Galveston, Division of Cardiology, Department of Internal Medicine, 301 University Boulevard, 5.106 John Sealy Annex, Galveston, Texas 77555-0553. Fax : 409-747-1878; E-mail: djleniha@utmb.edu Figure 1. 2-D image demonstrating severe right ventricular hypertrophy. Reprinted with permission from ECHOCARDIOGRAPHY, Volume 18, No. 1, January 2001 Copyright ©2001 by Futura Publishing Company, Inc., Armonk, NY 10504-0418