Journal of the American College of Cardiology
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J. Am. Coll. Cardiol. · Dec 1987
Comparative StudyComparison of the ventricular response during atrial fibrillation in patients with enhanced atrioventricular node conduction and Wolff-Parkinson-White syndrome.
Although ventricular fibrillation is a well known sequel to atrial fibrillation in the Wolff-Parkinson-White syndrome, ventricular fibrillation is not generally associated with supraventricular tachycardia in the presence of enhanced atrioventricular (AV) node conduction without pre-excitation. It was hypothesized that the ventricular response during atrial fibrillation may be less in patients with enhanced AV node conduction than in their counterparts with Wolff-Parkinson-White syndrome matched for anterograde effective refractory period. Slower ventricular rates during atrial fibrillation would suggest an increased propensity for concealed conduction in the enhanced AV node conduction group than in the group with an accessory pathway. ⋯ Patients with enhanced AV node conduction and Wolff-Parkinson-White syndrome were well matched for anterograde effective refractory period (245 +/- 22 versus 258 +/- 25 ms) and minimal cycle length, maintaining 1:1 anterograde conduction (261 +/- 21 versus 260 +/- 40). There was no difference in intervals during atrial fibrillation (average RR interval = 372 +/- 37 versus 346 +/- 66) or shortest RR interval (266 +/- 27 versus 243 +/- 51). Thus, patients with Wolff-Parkinson-White syndrome and those with enhanced AV node conduction matched for anterograde refractory period exhibit similar ventricular rates during atrial fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)
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J. Am. Coll. Cardiol. · Dec 1987
Quantitative two-dimensional echocardiography in massive pulmonary embolism: emphasis on ventricular interdependence and leftward septal displacement.
In 14 patients requiring aggressive therapy for circulatory failure resulting from massive pulmonary embolism, hemodynamic and two-dimensional echocardiographic data were obtained at bedside (acute phase) and again after circulatory improvement (intermediate phase) and during recovery. The acute stage was characterized by a low cardiac output state despite inotropic support (cardiac index 1.9 +/- 0.6 liters/min per m2) associated with increased right atrial pressure (12.4 +/- 4.2 mm Hg), increased right ventricular end-systolic and end-diastolic area (12.4 +/- 3.4 and 15.4 +/- 4.1 cm2/m2, respectively) and reduced right ventricular fractional area contraction (20.1 +/- 8.6%). Two-dimensional echocardiography also revealed interventricular septal flattening at both end-systole and end-diastole and markedly decreased left ventricular end-diastolic dimensions. ⋯ Hemodynamic improvement occurred during the intermediate phase as shown by restoration of cardiac index (3.3 +/- 0.6 liters/min per m2), decrease in right atrial pressure (8.3 +/- 4.8 mm Hg), reduction in right ventricular end-systolic area (9.0 +/- 3.6 cm2/m2 at the intermediate stage and 6.1 +/- 1.8 cm2/m2 at recovery) and end-diastolic area (10.5 +/- 3.6 cm2/m2 at the intermediate stage and 8.9 +/- 2.9 cm2/m2 at recovery) and improvement in right ventricular fractional area contraction (31.5 +/- 16.4%). The interventricular septum progressively returned to a more normal configuration at both end-systole and end-diastole, and left ventricular diastolic dimension steadily increased. It is concluded that circulatory failure secondary to massive pulmonary embolism was mediated through a profound decrease in left ventricular preload, resulting from both pulmonary outflow obstruction and reduced left ventricular diastolic compliance.(ABSTRACT TRUNCATED AT 250 WORDS)