Biomedical subjects

R Lazzara

Publications and source records attributed to R Lazzara.

At least 199 records · Page 11Linked to original sources

PubMed1975

Mitral valve prolapse and coronary artery disease. Clinical, hemodynamic, and angiographic correlations.

Among 95 patients with angina pectoris and angiographically documented coronary artery disease (CAD), prolapse of the scallops of the posterior leaflet of the mitral valve (PLMV) was noted in 30 patients. Left ventriculograms in the right anterior oblique (RAO) projection revealed isolated prolapse of the posteromedial commissural scallop (PMCS) in 12 patients and the anterolateral commissural scallop (ALCS) in two patients. Seven patients had prolapse of both PMCS and ALCS, three had prolapse of the PMCS and middle scallop (MS), and six had prolapse of all three scallops of the PLMV. Left ventricular dilatation with increase trabeculations was observed in 19 patients. Contractility determined in a quantitative fashion by segmental motion analysis was markedly impaired in 29 patients. None of the patients had angiographic evidence of mitral insufficiency. Left ventricular dysfunction was documented in 28 patients by either elevated left ventricular end-diastolic pressure (LVEDP), low cardiac index (CI) or decreased ejection fraction (EF). In two patients in whom left ventricular contractility improved after aortocoronary by pass, previously prolapsed scallops could not be identified in the postoperative ventriculogram. Prolapsed PLMV is a frequent angiographic finding in patients with angiographically observed CAD. Impaired contractility of the ventricular myocardium and papillary muscles, left ventricular dilatation, and hypertrophy appear to play a significant role in the pathogenesis of this abnormality through distortion of the directional axis of the papillary muscles, asynergic contraction of the related free wall of the left ventricle, and changes in the normal spatial alignment necessary for mitral valve closure. The syndrome of papillary muscle dysfunction in patients with coronary artery disease represents a wider clinical spectrom than previously described.

Adult↗

PubMed1975

Disorders of cellular electrophysiology produced by ischemia of the canine His bundle.

In the first 4 hours after occlusion of the anterior septal coronary artery, 18 dogs developed bundle branch block, heart block, or both. The hearts were then excised, and preparations were dissected to expose the His bundle and the bundle branches, which were superfused with modified Tyrode's solution at 37 degrees C. In the His bundle and the most proximal bundle branches, resting potentials were reduced and diminutive action potentials had slow upstrokes, often with notches or steps. Action potentials were generated by fibers that had resting potentials between--40 and --50 mv. Conduction was impaired; conduction velocities less than 0.01 m/sec were sometimes observed. In more severely affected cells, refractoriness outlasted repolarization. Encroachment on the prolonged refractory period resulted in further diminution of action potentials and continuous rather than intermittent block. More commonly, the response to rapid rate took the form of intermittent block with progressive conduction delay in the series of conducted beats, culminating in a blocked beat (Wenckebach sequence). There was a fatigue factor that accumulated at short cycle lengths and depressed the action potential. Automaticity was not enhanced, but pacemaker function was abnormal. The threshold potential shifted erratically, and pacemaker potentials sometimes were intermittently diminished, resulting in intermittent failure to propagate. During prolonged superfusion, there was a tendency to recover with a drift of the maximum diastolic potentials toward more negative levels. None of these changes were found in ten hearts excised from dogs in which the coronary artery had not been ligated.

Action Potentials↗

PubMed1975