Circulation
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Hemodynamic studies were performed before and after pericardiocentesis in 19 patients with pericardial effusion. Right atrial pressure decreases significantly, from 16 +/- 4 mm Hg (mean +/- SD) to 7 +/- 5 mm Hg in 14 patients with cardiac tamponade. This change was accompanied by significant increases in cardiac output (3.87 +/- 1.77 to 7 +/- 2.2 l/min) and inspiratory systemic arterial pulse pressure (45 +/- 29 to 81 +/- 23 mm Hg). ⋯ This results in pulsus paradoxus. However, if pulmonary arterial wedge pressure is markedly elevated before the onset of tamponade, as in patients with chronic renal failure, then pericardial compliance may only determine right ventricular filling pressure. In such cases, pulsus paradoxus may be absent.
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Both heterologous IgG and Fab fragments of appropriate affinity and specificity have been shown capable of reversing advanced cardiac glycoside toxicity. Fab fragments are more rapidly excreted and theoretically have a smaller risk of unwanted immunologic effects, but relative rates of toxicity reversal have not been established. Rates of reversal of advanced digoxin toxicity by digoxin-specific IgG and Fab fragments were therefore compared in a dog model of advanced digoxin intoxication. ⋯ In contrast, six of six dogs given an equivalent dose of specific Fab fragments returned to sinus rhythm in a significantly shorter mean time of 36 minutes (P less than 0.01). Variability of time to arrhythmia reversion was less in Fab-treated dogs. These data demonstrate a decisive advantage of specific Fab fragments over intact IgG for potential clinical use in advanced, life-threatening digoxin intoxication.
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Randomized Controlled Trial Clinical Trial
Unexplained in-hospital fever following cardiac surgery. Natural history, relationship to postpericardiotomy syndrome, and a prospective study of therapy with indomethacin versus placebo.
In Part I of this study, the in-hospital course of 219 patients who had undergone a cardiac operation is analyzed. Fever (greater than or equal to 37.8 degrees C, rectal) was present after postoperative day 6 in 159 patients (73%) and was of unexplained cause in 118. Fever decay in the population of unexplained fever patients was exponential. ⋯ Indomethacin resulted in a shorter duration of fever (2.4 vs 3.5 days, P is less than 0.01) and in a shorter duration of chest pain, malaise, and myalgias compared to placebo. Sixty-seven percent of the patients in Part I and all of the patients in Part II were contacted 2-8 months following hospital discharge. Five percent had experienced an illness that we considered to be acute pericarditis, but its occurrence was unrelated to whether the patient had had in-hospital unexplained postoperative fever, in-hospital rub or chest pain, or in-hospital administration of indomethacin.
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Patients with hypertrophic cardiomyopathy (i.e., asymmetric septal hypertrophy) may show obstruction to left ventricular outflow under basal conditions or with provocative maneuvers. The presence of dynamic left ventricular outflow tract obstruction in patients with concentric ventricular wall thickening (but without abnormalities of the aortic valve) has been less well appreciated. Clinical and morphologic features of five patients with nondilated left ventricles and with left ventricular outflow obstruction are presented. ⋯ Each patient had echocardiographically documented systolic anterior motion of the anterior mitral leaflet, which was apparently responsible for the outflow obstruction, and concentric left ventricular wall thickening (septal-free wall thickness ratio of less than 1.3). Two of the five patients had evidence of genetically transmitted hypertrophic cardiomyopathy, as evidenced by disorganized muscle cells in the ventricular septum or asymmetric septal hypertrophy in first degree relatives. Hence, left ventricular outflow tract obstruction associated with systolic anterior motion of the anterior mitral leaflet may occur in some patients with concentric left ventricular hypertrophy who do not have typical hypertrophic cardiomyopathy.
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Echocardiographic or necropsy studies were performed in 151 patients with coronary artery disease. Prevalence of disproportionate septal thickening (septal to free wall ratio greater than or equal to 1.3) was 11%. An abnormally increased septal-free wall ratio in these patients had two principal etiologies. ⋯ This latter conclusion was suggested by negative echocardiographic studies in some families of patients with both coronary artery disease and disproportionate septal thickening. In addition, numerous disorganized cardiac muscle cells, characteristically present in patients with genetically transmitted hypertrophic cardiomyopathy, were absent from the septum of all patients with disproportionate septal thickening studied at necropsy. Although the mechanism responsible for this secondary type of disproportionate septal thickening is unknown, our results indicate that the presence of disproportionate septal thickening in a patient with coronary artery disease does not, per se, indicate the coexistence of genetically transmitted hypertrophic cardiomyopathy.