Ahmad Munir

Hypoalbuminemia and Lymphocytopenia in Patients With Decompensated Biventricular Failure

Background:In patients hospitalized with decompensated biventricular failure having hypoalbuminemia and lymphocytopenia without underlying hepatic or renal disease, we addressed the presence of a protein-losing enteropathy (PLE). Methods:We studied 78 patients having a dilated cardiomyopathy, who were hospitalized with congestive heart failure (CHF) and hypoalbuminemia of uncertain origin. In the first 19 patients, we investigated the presence of PLE using Tc-Dex70 scintigraphy together with serum albumin 2 to 4 weeks later when compensation had been restored. In the next 59 patients, presenting with reduced serum albumin and relative lymphocyte count at admission, these parameters were again monitored (2–4 weeks) later when symptoms and signs of CHF had resolved. Results:PLE, documented by Tc-Dex70 scintigraphy, was found in 10 of 19 patients and whose hypoalbuminemia (2.7 ± 0.1 g/dL, mean ± standard error of mean) were corrected (3.3 ± 0.1 g/dL; P < 0.05) with the resolution of CHF, whereas in the 9 patients without a PLE, reduced baseline serum albumin (2.6 ± 0.1 g/dL) failed to improve on follow-up (2.6 ± 0.2 g/dL) in keeping with malnutrition. Relative lymphocyte count was reduced (14.6 ± 1.5%) in patients with PLE but was normal (21.4 ± 3.3%; P < 0.05) in those without PLE. Serum albumin and relative lymphocyte count were each reduced at admission (2.8 ± 0.1 g/dL and 14.4 ± 1.0%, respectively) in 59 patients and increased (P < 0.05) to normal values (3.5 ± 0.1 g/dL and 24.9 ± 1.0%) 2 to 4 weeks after they were compensated. Conclusions:Enteral losses of albumin and lymphocytes account for the reversible hypoalbuminemia and lymphocytopenia found in patients hospitalized with CHF having splanchnic congestion.

Toward a broader understanding of aldosterone in congestive heart failure

Discovered some 50 years ago, aldosterone (ALDO) has come to be recognised as a mineralocorticoid hormone with well-known endocrine properties in epithelial cells that contribute to the pathophysiology of congestive heart failure. This includes Na + resorption at the expense of K+ excretion in classic target tissues: kidneys, colon, sweat and salivary glands. Though less well known, Mg2+ excretion is likewise enhanced by ALDO, while adrenal ALDO secretion is regulated by extracellular Mg2+ ([Mg2+ ]o). An emerging body of information has and continues to identify other endocrine actions of ALDO receptor-ligand binding. They include: promoting an efflux of cytosolic free Mg2+, or [Mg2+]i, in exchange for Na+ in such non-epithelial cells as peripheral blood mononuclear cells; its influence on endothelial cell function; and its central actions that involve regulation of cerebrospinal fluid composition produced by epithelial cells of the choroid plexus, activity of the hypothalamic paraventricular nucleus involved in Na+ appetite, Na+ and H2O excretion and sympathetic nerve activity, and the regulation of TNF-α production from central and/or peripheral sources. Extra-adrenal steroidogenesi and auto/paracrine properties of ALDO generated de novo in the cardiovasculature are now under investigation and preliminary findings suggest they contribute to tissue repair. The past decade has witnessed a revival of interest in this steroid molecule. In years to come, an even broader understanding of ALDOs contribution to the pathophysiology of congestive heart failure will undoubtedly emerge.

Very Large Pericardial Effusion Attributable to Minoxidil: Resolution Without Drainage of Fluid

A 52‐year‐old man with a history of chronic hypertension presented with worsening dyspnea and leg edema. He had been on minoxidil for 10 years. The cardiac silhouette was markedly enlarged. Echocardiography and computed tomography showed a large pericardial effusion. His cardiac status was stable and he was in no cardiorespiratory distress. No attempt was made to drain the fluid. Minoxidil was discontinued, and a month later, the effusion had virtually disappeared. Cessation of minoxidil administration and conservative management may suffice, even though the pericardial effusion is large.

Reduced Relative Lymphocyte Count in African-Americans With Decompensated Heart Failure

Background:A reduction in relative lymphocyte count (%L) has been reported in whites with heart failure that inversely correlated with jugular venous pressure thereby implicating systemic venous hypertension with splanchnic congestion. Objectives:To study whether a reduced %L (<20%) occurs in African-Americans (AA) with heart failure and to address pathophysiologic mechanisms having the potential to influence lymphocyte biology and survival, we monitored patients with or without systemic venous hypertension, hypoalbuminemia, hypovitaminosis D, and secondary hyperparathyroidism. Methods:In 131 AA (90 men; 53 ± 12 years): 113 were hospitalized, 50 with decompensated biventricular failure (DecompHF), 24 with acute left heart failure, and 39 with heart disease, but no heart failure (HDNHF); and 18 were outpatients with compensated heart failure. At the time of admission or outpatient visit, we monitored: white blood cell count and %L; and serum albumin, 25(OH)D, and parathyroid hormone (PTH). Results:White blood cell count did not differ among the groups, whereas %L was reduced only in those with DecompHF (15 ± 1%; P < 0.05) versus 25 ± 2% with left heart failure, 29 ± 1% in HDNHF, and 28 ± 3% in compensated heart failure. Serum albumin was reduced in DecompHF (2.8 ± 0.1; P < 0.05), but not in any of the other groups. Reduced 25(OH)D (<30 ng/mL), in keeping with hypovitaminosis D, was found in all AA, whereas elevated serum PTH (>65 pg/mL) was found only in those with DecompHF (123 ± 22 pg/mL). Conclusions:A relative lymphocytopenia, together with hypoalbuminemia and elevated PTH, were found only in hospitalized AA with DecompHF. These findings implicate splanchnic congestion and the enteric loss of lymphocytes and albumin with an associated secondary hyperparathyroidism.

Hypovitaminosis D and Valvular Calcification in Patients With Dilated Cardiomyopathy

Background:In patients with dilated (idiopathic) cardiomyopathy (DCM), little is known about the presence of valvular calcification and its association with hypovitaminosis D, which may predispose affected tissues to calcification. Our objectives were 2-fold: to conduct a retrospective assessment of echocardiographic evidence of valvular calcification in patients with DCM who were known to have hypovitaminosis D (25(OH)D <30 ng/mL) and to conduct a prospective assessment of serum 25(OH)D in patients with DCM, who had demonstrated echocardiographic evidence of valvular calcification. Methods:The retrospective study consisted of 48 African American patients (34 men, 14 women; 52.3 ± 1.5 years) having DCM and ejection fraction <35% with serum creatinine <2.0 mg/dL and 25(OH)D <30 ng/mL; and 20 white patients in the prospective study (20 men; 71.0 ± 3.0 years) having DCM and ejection fraction <35% with serum creatinine <2.0 mg/dL and echocardiographic evidence of valvular calcification. In the retrospective study, a transthoracic echocardiogram was obtained to address mitral valvular and annular calcification, aortic valvular calcification, and sinotubular calcification; whereas in the prospective study, serum 25(OH)D level was monitored in patients with known valvular calcification. Serum parathyroid hormone (PTH) was monitored in both studies. Results:In the retrospective study, hypovitaminosis D was found in 19 patients (31%) with valvular calcification and in whom serum PTH was increased (83 ± 8 pg/mL). In the prospective study, 15 of 20 elderly patients (80%) with known DCM and valvular calcification were found to have hypovitaminosis D (25(OH)D <30 ng/mL), whereas serum PTH was normal (43 ± 4 pg/mL). Conclusions:In patients with DCM without marked renal dysfunction, valvular calcification was seen more frequently and associated with hypovitaminosis D, whereas in elderly patients with valvular calcification, hypovitaminosis D is common, suggesting that the duration of vitamin D deficiency may determine the extent of valvular calcification. The role of hypovitaminosis D in the appearance of valvular calcification deserves further study.

Causes and Consequences of Systemic Venous Hypertension

The causes of systemic venous hypertension (SVHT) include cardiac- and circulatory-related factors, whereas its consequences include the congestion of hepatic, splanchnic, and peripheral circulations, which contribute significantly to the clinical congestive heart failure syndrome. Based on a disequilibrium in hydrostatic and oncotic pressures, the increased filtration and formation of interstitial fluid at these sites with an accompanying increase in lymph flow mandates an increment in lymphatic drainage to protect against such congestion and the appearance of edema and ascites. However, lymph flow via the thoracic duct into systemic veins is opposed by elevations in central venous pressure. Various management strategies have the potential to prevent and/or correct SVHT. The case of a 54-year-old man with a dilated cardiomyopathy who presented with decompensated biventricular failure, expressed as anasarca and ascites, is used to illustrate the importance of SVHT.

Compression of intrapericardial structures in tamponade, including "new" echocardiographic manifestations.

Right atrial and right ventricular collapses are well-known echocardiographic manifestations of large circumcardiac pericardiac effusions with tamponade. Left atrial collapse has been described in tamponade but is less widely known. Compression of the pulmonary trunk (main pulmonary artery) has not yet been reported except as an abstract by one of us (IAD).1 Compression of the thoracic inferior vena cava has never been reported yet.

Fatal spontaneous left main coronary artery thrombosis as a rare complication of noncardiac surgery

A 72-year-old man with a history of anterior wall myocardial infarction, who had stenting to his left anterior descending artery, developed an acute episode of dyspnea, hypoxemia and anginal chest pain three days after above-the-knee amputation for dry gangrene of the left leg. A physical examination revealed bilateral lung rales and a soft ejection systolic murmur at the left sternal border. Transient new lateral ST segment elevation associated with reciprocal inferior ST segment depression and prior anterior-septal infarct were evident on his electrocardiogram. Cardiac catheterization showed a filling defect in the middle segment of the left main coronary artery (Figure 1). During the procedure, the patient became more dyspneic and developed fatal cardiopulmonary arrest; he did not respond to resuscitative measures (1). Figure 1) Coronary angiogram showing a filling defect (arrow) in the middle segment of the left main coronary artery, representing a thrombus. Also noted was severe in-stent stenosis of the proximal left anterior descending artery

Cardiac Tamponade With Fibrin Strands Leading to the Diagnosis of Systemic Lupus Erythematosus

A 59-year-old male with an unremarkable past medical history presented with worsening dyspnea and a history of chest tightness for 2 weeks. He had arthritis of multiple hand and foot joints bilaterally. Muffled heart sounds and pulsus paradoxus of 15 mm Hg were noted on examination. Laboratory findings were remarkable for anemia, with a hemoglobin level …

Mediastinal hematoma causing compression of the right ventricular outflow tract – the role of transthoracic echocardiography in diagnosis

A 57-year-old man presented with acute coronary syndrome for which he was initially treated medically with a regimen that included acetylsalicylic acid, clopidogrel and heparin. Later, he was found to have two-vessel coronary artery disease requiring coronary artery bypass grafting. His postoperative period was complicated by hypotension and excessive bleeding, requiring multiple transfusions of blood products. His continued hemodynamic instability led to the suspicion of a mechanical complication. A transthoracic left parasternal short-axis view at the mitral valve level showed an anterior mediastinal hematoma compressing the right ventricular outflow tract (Figure 1). Figure 1) Transthoracic left parasternal short-axis view showing an anterior mediastinal hematoma (MH) compressing the right ventricular outflow tract. LV Left ventricle; RV Right ventricle The hematoma was also compressing the main pulmonary artery with its bifurcation, as well as the aorta, as shown by the transthoracic high right parasternal short-axis view (Figure 2). Figure 2) Transthoracic high right parasternal short-axis view showing the mediastinal hematoma (MH) compressing the aorta (Ao), as well as the main pulmonary artery with its bifurcation. LMPA Left main pulmonary artery The patient was taken back to the operating room, where the hematoma was evacuated. He did very well after that and left the hospital five days later (1).