Daniel T. Anbe

Performance of the failing and nonfailing right ventricle of patients with pulmonary hypertension.

Hemodynamic performance of the right ventricle was measured in 34 patients: 17 with pulmonary hypertension, 9 with pulmonary hypertension and right ventricular failure and 8 control subjects. Among the patients with pulmonary hypertension who did not have right ventricular failure, right ventricular maximal isovolumic rate of development of ventricular pressure (dP/dt) was significantly elevated (P less than 0.001), whereas maximal 1/P dP/dt and maximal velocity of contractile element shortening (Vmax) were comparable with values observed in control subjects. The patients with pulmonary hypertension who had right ventricular failure also showed an augmented right ventricular maximal dP/dt (P less than 0.001) and normal 1/P dP/dt and Vmax. These observations indicate that in pulmonary hypertensive heart disease, even when the right ventricle failed in a clinical sense, the contractile effort was normal. Consequently, right ventricular failure may develop in patients with pulmonary hypertensive heart disease even though the cardiac muscle performs normally as a contractile tissue.

Negative intraventricular diastolic pressure in patients with mitral stenosis: Evidence of left ventricular diastolic suction

Left ventricular diastolic pressure was evaluated in 15 patients with mitral stenosis and 16 patients with no significant heart disease to determine if a stenotic mitral valve can cause the left ventricle to produce a negative diastolic pressure, indicative of ventricular diastolic suction. The minimal level of diastolic pressure in patients with mitral stenosis ranged between 6 and -7 mm Hg; in normal subjects it did not fall below 0. The average value of minimal diastolic pressure in patients with mitral stenosis (-2 +/- 1 mm Hg [mean +/- standard error of the mean]) was significantly lower than in patients without significant heart disease (5 +/- 1 mm Hg) (p less than 0.001). These observations indicate that the human left ventricle, in the presence of mitral stenosis, can generate a negative diastolic pressure. The presence of a negative diastolic pressure in patients with mitral stenosis suggests that the dynamics of the ventricle during diastole may contribute to the filling process.

Radiographic Demonstration of Myocardial Penetration by Permanent Endocardial Pacemakers

Abstract The epicardial fat defines the limit of the myocardium. It can be regularly visualized using image intensification and recorded on spot-films obtained by a special technique. The relationship between the electrode of the transvenous pacemaker and the epicardial fat indicates the relationship between the electrode and the myocardium. If the separation is less than 3 mm, penetration has occurred. Of 33 patients examined, 11 demonstrated some degree of penetration.

Conversion of atrial flutter to atrial fibrillation with carotid sinus pressure

Summary A case of atrial flutter converted to atrial fibrillation with carotid sinus pressure in the postoperative period of a patient with an aortic valve prosthesis is reported. A review of the literature revealed 23 other cases of the apparent excitatory effects of carotid sinus pressure manifested by either an increase of the atrial flutter rate or by conversion of the atrial flutter to atrial fibrillation. The possible mechanism of action is discussed.

Intracardiac sound as a diagnostic adjunct in subaortic stenosis.

The purpose of this investigation is to demonstrate the potential diagnostic value of intracardiac sound recordings in patients with subaortic stenosis. Intra cardiac pressure and sound were measured in 10 patients with various types of subaortic obstructions using a catheter-tip micromanometer. Seven patients had idiopathic hypertrophic subaortic stenosis (IHSS), 2 had a subvalvular membrane, and 1 had a subvalvular tunnel. Within the left ventricular cavity, at the site of maximal systolic left ven tricular pressure, either there was no systolic murmur, or the murmur was of low intensity. However, within the outflow tract of the left ventricle, distal to the site of intraventricular obstruction, a prominent systolic murmur was de tected in all patients. This murmur was of higher intensity than the one mea sured distal to the aortic valve. In one patient, in whom no subvalvular obstruction was present, but in whom entrapment of the tip of the catheter occurred, no murmur was detected in the left ventricle even though a subvalvular pressure gradient was observed. Therefore it appears that a systolic murmur recorded with maximal intensity in the outflow tract of the left ventricle may be of substantial help in distinguish ing between an artifactual intraventricular pressure gradient, and one that re sults from intraventricular obstruction.