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Acute stressor states are associated with a homeostatic activation of the hypothalamic-pituitary-adrenal axis. A hyperadrenergic state follows and leads to a dyshomeostasis of several intra- and extracellular cations, including K, Mg, and Ca. Prolongation of myocardial repolarization and corrected QT interval (QTc) of the ECG are useful biomarkers of hypokalemia and/or hypomagnesemia and should be monitored to address the adequacy of cation replacement. A dyshomeostasis of several trace elements, including Zn and Se, are also found in critically-ill patients to compromise metalloenzyme-based antioxidant defenses. Collectively, dyshomeostasis of these electrolytes and trace elements have deleterious consequences on the myocardium: atrial and ventricular arrhythmias; induction of oxidative stress with reduced antioxidant defenses; and adverse myocardial remodeling, including cardiomyocytes lost to necrosis and replaced by fibrous tissue. To minimize such consequences during hyperadrenergic states, systematic surveillance of electrolytes and trace elements, together with QTc, are warranted. Plasma K and Mg should be maintained at > or =4.0 mEq/L and > or =2.0 mg/dL, respectively (the 4 and 2 rule).

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-Dex 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-Dex(70) 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.

Background: In nondiabetic patients hospitalized with multiorgan failure, neurohormonal activation can lead to stress-induced hyperglycemia (>140 mg/dL), as could Mg(2+) and Zn(2+) deficiencies. However, it is currently uncertain whether nondiabetic African Americans (AA) hospitalized with either chronic, decompensated biventricular failure (DecompHF) having hepatic and splanchnic congestion, ionized hypomagnesemia and hypozincemia, or acute left heart failure (LHF) would exhibit hyperglycemia at admission., Methods: We retrospectively examined admission serum glucose in 77 AA patients without a history of diabetes, who were hospitalized with heart failure. This examination included 41 patients admitted during a 4-month period with chronic DecompHF and whose clinical presentation included findings of expanded intra- and extravascular volumes, together with echocardiographic evidence of marked tricuspid regurgitation and distended inferior vena cava, without respiratory variation. These patients were compared with 14 nondiabetic patients hospitalized during the same time period with acute LHF. We also studied admission serum glucose in 22 patients who were admitted with DecompHF having documented hypomagnesemia and hypozincemia., Results: Admission serum glucose (mean +/- standard error of mean) in patients with chronic DecompHF was 105.41 +/- 4.08 mg/dL and was modestly elevated (140-160 mg/dL) in 3 patients. In those with acute LHF, glucose was 94.86 +/- 3.96 mg/dL and did not exceed 140 mg/dL in any patient. Glucose (103.2 +/- 4.3 mg/dL) was not elevated in patients having chronic DecompHF and reduced ionized Mg(2+) and serum Zn(2+) (0.44 +/- 0.01 mmol/L and 69.6 +/- 3.2 mug/dL, respectively)., Conclusions: Hyperglycemia at admission was infrequent in nondiabetic AA patients hospitalized with either acute LHF or chronic DecompHF, which may have also included hypomagnesemia and hypozincemia. This calls into question the need for intensive insulin therapy in these patients.

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.

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.

Background: Serum cobalamin (vitamin B12), bound to transcobalamin II, is taken up by the endothelium of the hepatic vasculature via a receptor-mediated membrane transport process. We hypothesized hepatic congestion is associated with elevated serum B12 without hepatocyte necrosis., Methods and Results: Serum B12, aspartate and alanine transaminases, alkaline phosphatase, bilirubin (Bili), and brain natriuretic peptide (BNP) were monitored at the time of admission in 91 hospitalized patients: (a) 38 with decompensated biventricular failure having systemic venous distention, tricuspid regurgitation (TR), and echocardiographic evidence of inferior vena cava dilation and moderate to marked TR; (b) 18 with acute left heart failure having a myocardial infarction, an ischemic cardiomyopathy, or hypertensive heart disease; and (c) 35 without clinical evidence of failure despite myocardial infarction, pericarditis, or atrial arrhythmia. Serum cobalamin (normal 180-600 pg/mL) was elevated with biventricular failure (861.4 +/- 53.0 pg/mL) compared with (P < 0.0001) left heart or no failure, where B12 remained normal. Serum aspartate, alanine, and alkaline phosphatase were normal in each group whereas Bili was increased (1.8 +/- 0.2 mg/dL; P < 0.05) with biventricular failure. Plasma BNP was elevated in each group., Conclusions: Elevated cobalamin and Bili are respective biomarkers of hepatocellular dysfunction and cholestasis in patients having decompensated biventricular failure with systemic venous distention and TR without hepatocyte necrosis vis-à-vis left heart failure or in the absence of clinical failure. Elevated plasma BNP did not distinguish between the presence or absence of systemic venous congestion.

A subset of patients with mitral valve disease has a marked rise in pulmonary vascular resistance (PVR) that is disproportionate to elevations in pulmonary venous pressure. Termed a "hyperactive" pulmonary vasculature, the elevation in PVR falls promptly and dramatically in response to mitral valve replacement. We report a 55-year-old man with progressive, exertional dyspnea of several months' duration who had signs of congestive heart failure (CHF) with moderate mitral valvular regurgitation and aortic stenosis by echocardiographic interrogation. These lesions in combination, together with his CHF and disproportionate elevation in pulmonary artery systolic pressure (90 mm Hg) and PVR (527 dyne x s x cm(-5)), raised the prospect of valvular replacement. There followed a normalization of PVR and marked improvement in his symptoms and signs of CHF in response to pharmacologic management with an ACE inhibitor, loop diuretic, and aldosterone receptor antagonist to negate any further consideration of surgery.

An 18-year-old woman without previously documented medical history delivered a healthy 32-week-old preterm infant. Severe bleeding occurred during week 1 postpartum secondary to ruptured vaginal condylomas. The consequent anemia was accompanied by complaints of exercise intolerance that resolved with blood transfusion. Six weeks later, the patient was brought to the emergency department of the regional medical center, where she was found to be unresponsive, with a left-sided hemiparesis and with hypoxemia that failed to correct with assisted ventilation and 100% oxygen. A cardiology consultation was obtained, which identified the patient as having central cyanosis and heretofore unappreciated marked clubbing of fingers and toes. This suggested a diagnosis of right-to-left shunting, likely at the cardiac level, together with presumptive embolic stroke, which was documented by magnetic resonance imaging and magnetic resonance angiography as a left pontine infarct. Transthoracic and transesophageal echocardiography identified anomalous drainage of the inferior vena cava into the left atrium, which was confirmed by a three-dimensional computed tomographic angiogram. Corrective surgery in the form of atrial septostomy and redirection of the inferior vena cava to the right atrium was performed. The patient was subsequently discharged and is in stable condition 3 months later without effort intolerance and with normal arterial oxygen saturation on room air.