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Biomedical subjects

N Ranganathan

Publications and source records attributed to N Ranganathan.

At least 19 recordsLinked to original sources
PubMed1989

Abnormalities in jugular venous flow velocity in pulmonary hypertension.

Doppler recordings of jugular venous flow velocity previously performed in this laboratory in patients with pulmonary hypertension had shown variations from the normal dominant systolic flow (SF) greater than diastolic flow (DF), to SF = DF, SF less than DF or DF alone. The mechanisms underlying these flow alterations were studied in 25 patients and correlated with hemodynamics. The patients with abnormal flow patterns had increased right atrial V-wave pressures. This was associated with an increased right ventricular early diastolic pressure. The incidence of clinical heart failure was higher in patients with SF less than DF or DF alone (8 of 11) compared with 5 of 10 patients with SF = DF. Thus, in patients with pulmonary hypertension, the abnormal jugular venous flow patterns appear to be caused by both an increased DF velocity and a decrease in SF velocity. Because the right atrial V-wave pressures were similar in patients with both SF = DF and SF less than DF or DF alone and the incidence of heart failure was higher in the latter, the decrease in SF must be a later phenomenon. Serial observations confirmed this temporal sequence. The applicability of these observations to bedside evaluation of patients with pulmonary hypertension is emphasized.

Adult↗
PubMed1989

Changes in jugular venous flow velocity after coronary artery bypass grafting.

The factors underlying postoperative jugular venous flow velocity and pulse contour changes were studied in 25 patients undergoing coronary artery bypass grafting. Before operation, all patients had normal right-sided cardiac hemodynamics, normal jugular pulse contours and normal jugular venous flow velocity patterns, i.e., systolic flow (SF) velocity greater than diastolic flow (DF) velocity. After operation, jugular venous flow velocity was abnormal in 24 patients (SF = DF in 14 and SF less than DF in 10). Neither the right-sided cardiac pressures after the operation nor any of the perioperative factors examined had any bearing on these flow alterations. Postoperative right ventricular ejection fraction was normal in all 5 patients with SF greater than DF and SF = DF flow patterns (mean +/- standard error of the mean 48 +/- 3%). It was significantly depressed in all 6 patients with SF less than DF flow pattern (34 +/- 1%, 2p less than 0.001). These findings suggest that the right atrium behaves as a conduit rather than a capacitance chamber. However, the postoperative abnormal flow pattern of SF less than DF as opposed to SF = DF indicates the additional presence of right ventricular dysfunction. The implications of these observations for the clinical assessment of right ventricular function in the postoperative patients are discussed.

Adult↗
PubMed1988

Prophylaxis of post-myocardial infarction dysrhythmias by long-term timolol therapy.

The antiarrhythmic efficacy of timolol maleate was assessed in 94 patients with acute myocardial infarction. No significant differences were noted between early treatment with timolol and placebo in the mean and peak hourly ventricular premature complex rates, ventricular premature complex couplets, or runs. However, compared to the placebo treatment, there was a significant (p less than 0.001) 66% reduction in the relative fraction of early-cycle ventricular premature complexes 7 to 9 days after initiation of timolol therapy and a more prolonged significant (p less than 0.001) 73% reduction in the fraction of early-cycle supraventricular complexes throughout the 28-day timolol and placebo comparison period. The frequency distribution of QRS duration was significantly different between the placebo- and timolol-treated patients, with the mean duration 8 msec longer in the placebo-treated patients (p = 0.008). Adverse effects from early administration of timolol did not differ from those in the placebo-treated patients.

Cardiac Complexes, Premature↗
PubMed1986

Sarcoidosis simulating pulmonary veno-occlusive disease.

We describe a young woman who presented with a 6-month history of progressive pulmonary hypertension. At autopsy she was found to have noncaseating granulomas obliterating pulmonary veins, without granulomatous involvement of pulmonary arteries. Noncaseating granulomas were also present in the liver and hilar lymph nodes, confirming the diagnosis of sarcoidosis. To our knowledge this is the first reported case of pulmonary hypertension caused by sarcoidosis simulating pulmonary veno-occlusive disease.

Adult↗
PubMed1985

The apical impulse in coronary heart disease.

Forty patients (36 with coronary artery disease), who had angiographic assessment of left ventricular function were studied using apexcardiography with a new method of standardization, the objective being to define the parameters of the apical impulse which reflect changes in the left ventricular function and correlate them with clinical assessment of the apical impulse. Based on measurements from patients with normal left ventricular function, abnormalities in apexcardiograms were identified. An increase in amplitude of percent A wave alone (greater than 13.3%) (palpable as an atrial kick in approximately half of these patients) was not associated with significant left ventricular dysfunction. An isolated abnormality in isovolumic slopes, although associated with mild left ventricular dysfunction, could not be detected clinically. Moderate to severe left ventricular dysfunction was always associated with abnormal ejection phase slopes and all had sustained apical impulses. The additional presence of a palpable atrial kick or an increased percent A wave on the apexcardiogram was more indicative of moderate rather than severe dysfunction. Thus this study clearly establishes that left ventricular function does in fact affect the nature of the apical impulse in patients with coronary artery disease and these can be easily defined.

Angiography↗
PubMed1982

Management of a malignant hyperthermia patient during cardiopulmonary bypass.

The anaesthetic management of cardiopulmonary bypass (CPB) for a patient with biopsy-proven malignant hyperthermia is reported. Specific changes in the technique used, such as venting the oxygenator before use, monitoring mixed venous PO2 and PCO2, as well as the safety of cold hyperkalaemic cardioplegia are described. Controversial aspects of malignant hyperthermia management such as the safety of calcium and catechol inotropes are discussed in relationship to the successful use of cardio-pulmonary bypass in our patient. We chose to treat left ventricular dysfunction by aggressive vasodilator (nitroglycerine) therapy. We detected no myocardial or respiratory depression secondary to dantrolene therapy either before or after operation.

Anesthesia↗
PubMed1978

Transcutaneous doppler jugular venous flow velocity recording.

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.

Atrial Fibrillation↗
PubMed1977

Congenital intracardiac band: a rare cause of nonrheumatic combined aortic and mitral regurgitation.

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.

Aortic Valve Insufficiency↗
PubMed1976

Mitral valve prolapse.

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.

Electrocardiography↗
PubMed1976

Idiopathic prolapsed mitral leaflet syndrome. Angiographic-clinical correlations.

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.

Angiography↗