Effects of postextrasystolic potentiation on systolic time intervals.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to N Ranganathan.
Explore the source record for details and available documents.
Transcutaneous bidirectional Doppler jugular venous flow velocity patterns were classified and correlated in 82 patients with right heart hemodynamics. The normal forward flow pattern was biphasic with systolic flow (Sf) greater than the diastolic flow (Df). With rare exceptions, flow patterns of Sf = Df, Sf is less than Df and Df alone indicated abnormal right heart hemodynamics. Abnormal flow patterns (Sf = Df and Sf is less than Df) seen in post cardiac surgery states, and in some rare patients with severe mitral regurgitation despite normal right-sided pressures, were probably secondary to postoperative change in right atrial compliance in the former and to a Bernheim effect in the latter. The most common cause of retrograde systolic flow in the absence of atrioventricular dissociation was tricuspid regurgitation. Persistent retrograde end-diastolic flow with normal forward flow was associated with high right atrial "a" wave pressures, indicating significant decrease in right ventricular compliance with a vigorous atrial contraction. The study clearly established that the jugular venous flow velocity pattern truly reflected derangements in the right heart hemodynamics, irrespective of the underlying etiology. The applicability to bedside evaluation of the jugular venous pulse and the right heart hemodynamics is emphasized.
A patient had a congenital intracardiac band lying across the aortic valve that caused combined aortic and mitral valvular regurgitation. The band was excised, and the damaged aortic valve was replaced with a prosthesis. The case illustrates that not all congenital intracardiac bands are completely asymptomatic and not all bivalvular incompetence is rheumatic in origin.
Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
Angiographic clinical correlations were made in 59 patients with prolapsed mitral leaflet syndrome. Eight had nonejection systolic clicks (group I), 20 had early, mid or late systolic murmurs with or without a systolic click (group II), and 31 had pansystolic murmurs (group III). Isolated prolapse of posterior leaflet (PL) scallops occurred in 42 and 17 had combined leaflet prolapse. The study demonstrated the following: (I) Group II patients usually had isolated PL prolapse with a predominant biscallop involvement while a high incidence of triple scallop prolapse and combined mitral leaflet prolapse occurred in group III. (II) Severe mitral regurgitation and a greater incidence of atrial fibrillation were seen in patients with triscallop prolapse and combined mitral leaflet prolapse. Mitral regurgitation was milder in patients with single and biscallop prolapse and, when severe, was associated with ruptured chordae. (III) ST-T wave abnormalities in the inferior leads were most frequent in patients with isolated PL prolapse. (IV) Systolic and diastolic asynergy occurred in 41 patients, most frequently in group II but also relatively frequently in group III (19 of 31). Segmental anterior dysfunction with normal ejection fraction was found in 18 patients, of whom 13 had early anterior wall relaxation. (V) Patients without asynergy were slightly older than those with it. More in the former group had severe mitral regurgitation and were clinically disabled from it.