Constrictive pericarditis presenting as unexplained recurrent pleural effusion: a case report.

Constrictive pericarditis may exceptionally present as pleural effusion of unknown origin and this form of presentation may cause diagnostic problems. We report a case of subacute constrictive pericarditis in which there were recurrent pleural effusion with no other signs of the disease and the initial echocardiographic study was nondiagnostic. For this reason the patient was initially considered to have primary pulmonary or pleural disease. On the basis of the subsequent development of signs of systemic congestion and the results of computed tomography, Doppler echocardiography and cardiac catheterization, which were consistent with constriction, it was concluded that the patient had constrictive pericarditis. A complete resolution of pleural effusion and signs of systemic congestion was observed following pericardiectomy.

Doppler echocardiographic evaluation of left ventricular end-diastolic pressure in patients with coronary artery disease.

Pulmonary venous flow velocity recordings have been found to be useful in complementing the information obtained from the mitral flow velocity and improving the assessment of left ventricular diastolic pressures. This study was undertaken to evaluate the accuracy of mitral flow and pulmonary venous flow variables, recorded by transthoracic Doppler echocardiography, in estimating left ventricular end-diastolic pressure (LVEDP) in 101 consecutive patients with coronary artery disease undergoing diagnostic left-sided heart catheterization. Patients were assigned to three groups according to the values of LVEDP (group 1, < or = 12 mm Hg; group 2, between 13 and 19 mm Hg; and group 3, > or = 20 mm Hg). LVEDP correlated most strongly with systolic fraction of pulmonary venous flow (r = -0.76), isovolumic relaxation time (r = -0.76), E/A ratio (r = 0.74), deceleration time of early mitral flow (r = -0.74), and mitral A wave duration/pulmonary venous A wave duration (AD/PVAD) ratio (r = -0.70) (p < 0.01 for each correlation). Discriminant analysis demonstrated that deceleration time, AD/PVAD ratio, and isovolumic relaxation time were major determinants of LVEDP, with 87.1% of patients correctly assigned to study groups; 97% of patients of group 1 and 95% of patients of group 3 were identified, whereas the accuracy in identifying the patients of group 2 was lower (41%). Deceleration times of 140 msec or less and AD/PVAD ratios of 0.9 or less were the best cutoff points in predicting an LVEDP of 20 mm Hg or greater. Multiple linear regression analysis demonstrated that the combination of mitral flow and pulmonary venous flow velocity variables provided a better estimation of LVEDP compared with that obtained from mitral flow velocity recordings alone (r = 0.88 versus 0.79; F test, 20.6). We conclude that combined analysis of mitral flow and pulmonary venous flow velocity provides, in patients with coronary artery disease, a noninvasive estimation of LVEDP with an accurate prediction of pressures of 12 mm Hg or less and 20 mm Hg or greater and less accurate prediction of intermediate values.

The diisobutyryl ester of N-methyldopamine, ibopamine: evaluation of electrophysiological properties and arrhythmogenicity studies.

The electrophysiological properties of ibopamine (SB-7505), the 3,4-diisobutyryl ester N-methyldopamine, was evaluated in 8 patients with syncopes of unknown etiology or with suspected disease of the sinus node or due to I-II degree AV block. A complete electrophysiological examination, including atrial and ventricular stimulation, was performed both in baseline conditions and within 1 h after oral administration of ibopamine 200 mg in a single dose. The study showed a slight reduction in effective refractory periods in the right atrium (-4.26%), the atrio-ventricular node (-6.45%) and the right ventricle (-6.79%) after ibopamine. Ibopamine was not found to facilitate the occurrence of atrial and/or ventricular arrhythmias. A 24-h dynamic Holter ECG performed in baseline conditions and during administration of ibopamine 200 mg t.i.d. showed no changes in baseline heart rate, nor was any increase in the number of atrial or ventricular extrasystoles detectable. It may therefore be concluded that ibopamine, when administered at the above dosages to the patients studied, does not modify heart rate or sinus function parameters to a statistically significant extent. It also reduces effective refractory periods in the right atrium, in the atrioventricular node and in the right ventricle without inducing or facilitating the occurrence of atrial or ventricular arrhythmias.