James A. Ronan

Effects of nadolol on the spontaneous and exercise-provoked heart rate of patients with chronic atrial fibrillation receiving stable dosages of digoxin

Nadolol, a long-acting beta-adrenergic-blocking agent, was evaluated in 20 patients with chronic atrial fibrillation by means of a randomized, double-blind, crossover study. Patients were required either to demonstrate resting heart rates in excess of 80 bpm or to show a rate of 120 bpm or an increment of greater than 50 bpm during mild treadmill exercise provocation (3 minutes, 1.75 mph, 10% grade). With placebo the group averaged a heart rate of 92 +/- 19 bpm, determined by 24 hours of ambulatory ECG recordings; this rate was significantly reduced to 73 +/- 16 bpm (p less than 0.001) with nadolol (mean dosage, 87 +/- 43 mg/day). During standardized exercise testing, heart rates increased to 153 +/- 26 bpm with placebo and to 111 +/- 24 bpm with nadolol (p less than 0.001), representing 65% and 52% increments, respectively. Digoxin blood levels averaged 0.8 +/- 0.5 ng/ml with placebo and were similar with nadolol (0.9 +/- 0.4; p = NS). Total exercise time on a modified Bruce treadmill protocol was 466 +/- 143 seconds with placebo and was significantly decreased by nadolol (380 +/- 143; p less than 0.01). During initial dose titration with nadolol, one patient was dropped from study for intolerable fatigue and one for worsened claudication. No patients were dropped from the double-blind treatment periods, although two patients receiving nadolol and one patient receiving placebo complained of moderate fatigue. We conclude that nadolol is a safe and effective agent for the control of spontaneous and exercise-provoked heart rates in patients with chronic atrial fibrillation who were already receiving digoxin treatment.

Systolic clicks and the late systolic murmur: Intracardiac phonocardiographic evidence of their mitral valve origin☆

Abstract The use of intracardiac phonocardiography has been employed as a method of documenting the origin of systolic clicks associated with an isolated late systolic murmur in a patient with hemodynamic evidence of mitral incompetence. Registration of both of these acoustical events within the left atrial chamber has not been hitherto described. Response of the clicks and murmur to the infusion of pressor amine and to the inhalation of amyl nitrite adds further weight to the concept of their origin at the mitral orifice. These observations confirm and extend previous information relating the late systolic murmur to organic mitral incompetence even if the murmur is accompanied by systolic clicks.

The clinical diagnosis of acute severe mitral insufficiency

Abstract The clinical and hemodynamic data of 8 patients with acute severe mitral insufficiency are presented. The natural history, physical signs, electrocardiogram, X-ray films and findings at cardiac catheterization present a characteristic picture which is distinct from the chronic form of the disease. The murmur is loud, apical and holosystolic with a late systolic decrease. It frequently radiates towards the base, mimicking aortic stenosis, and it is accompanied by an atrial sound and a third heart sound. Physical findings of pulmonary hypertension are present. Left atrial enlargement and atrial fibrillation are conspicuous by their absence. The basic pathology lies in the suspensory apparatus of the valve rather than in the leaflets. Four patients had ruptured chordae tendineae. If careful attention is paid to all of the clinical features, an accurate diagnosis can usually be made on clinical grounds alone.

Bedside diagnosis of arrhythmias

Summary It is obvious that in a treatise of this type not all bedside clues in the diagnosis of arrhythmias can be discussed in detail. It is apparent that the electrocardiogram is necessary for accurate diagnosis and subsequent treatment of arrhythmias, and that a thorough understanding of the electrocardiographic findings is mandatory. Complementing and supporting the electrocardiogram are these bedside clues. They continue to be of great importance not only in better diagnosis and treatment, but also in providing a source of genuine satisfaction to the physician who trains himself to make use of them.

Pseudoischemic “false positive” S-T segment changes induced by hyperventilation in patients with mitral valve prolapse

Hyperventilation-induced S-T segment changes that simulate myocardial ischemia have previously been noted, but the origin of this electrocardiographic finding has never been defined. To investigate further the basis for this response, the records were reviewed of 1,678 consecutive patients who underwent forced hyperventilation for 90 seconds and treadmill exercise testing. Twenty-eight patients (1.7 percent) were identified in whom hyperventilation resulted in ischemic-appearing S-T segment changes, and follow-up was possible in 21 (17 women, 4 men). Of the 21 patients, 16 (76 percent), including 15 (88 percent) of the 17 women, had evidence of mitral valve prolapse, 6 on auscultation alone, 2 on echocardiography alone and 6 with a combination of studies. Ten of the 21 patients had a negative exercise test; of the 11 patients who had a positive exercise test, only 1 had angiographic evidence of coronary arterial narrowing. The finding of ischemic-appearing S-T segment changes in response to forced hyperventilation has a high predictive value for the presence of mitral valve prolapse, particularly in women. The possible association of autonomic factors and mitral valve prolapse in the pathogenesis of an abnormal response to hyperventilation is discussed.

Aortic insufficiency secondary to spontaneous rupture of a fenestrated leaflet

Abstract Spontaneous rupture of a fenestrated valve leaflet is one of the unusual causes of severe aortic insufficiency. A case is presented of an elderly woman with severe aortic insufficiency who was shown at autopsy to have rupture of a fenestrated valve leaflet. A review of the English literature revealed 4 other cases of spontaneous rupture of a fenestrated aortic valve leaflet. In these cases, as in ours, the patient had either hypertension or syphilitic aortitis in addition to the valvular fenestrations. It would appear that the weakened fenestrated valve in conjunction with the additional stress imposed on the aortic valve by systemic hypertension or syphilitic aortitis are factors which predispose to spontaneous rupture.

Noninvasive techniques in acute myocardial infarction

Abstract It would be ideal if sophisticated assessment of cardiocirculatory performance could be achieved in a safe, uncomplicated, simple, and reproducible manner. Interest in noninvasive techniques has received considerable impetus from this hope. Such methods are especially desirable in patients with acute myocardial infarction, since margins of safety are reduced and diagnostic interventions that would ordinarily be done with impunity are applied with trepidation. The purpose of this essay has been to review the current status of noninvasive techniques chiefly as they apply in acute myocardial infarction. In so doing, the following topics were covered: the time intervals of the cardiac cycle, phonocardiography, electrocardiography, recordings of precordial movements, the external phlebogram, echocardiography, radioactive scanning, electrical impedance cardiography, ballistocardiography, and magnetocardiography.

The angiotensin infusion test as a method of evaluating left ventricular function

Fifteen patients had left ventricular function measured by the angiotensin infusion method. Seven patients had no evidence of heart disease, and eight patients had angina pectoris and coronary arteriographic evidence of coronary disease without congestive heart failure. During angiotensin infusion, those patients without heart disease had a decrease in cardiac index (average, 0.63 L. per minute per square meter) and a decrease in heart rate (average, 12 beats per minute.) The ventricular function curve had a poor SWI response in four of the seven subjects. The patients with coronary artery disease also had a reduction in cardiac index during angiotensin (average, 0.44 L. per minute per square meter) and the heart rate was unchanged in four subjects, increased in two subjects, and decreased in two subjects. Six of the subjects had flat or descending slopes on the function curve, and in one subject there was only a very gradual ascending slope. Many of the curves of both groups looked similar so that the function curves did not differentiate between those patients with or without heart disease. The mechanism for production of bradycardia, reduction of cardiac output, and depressed function curves with angiotensin is multifactorial, but is probably due to the baroreceptor reflex response, the increase in coronary artery resistance, and possible to the direct effect of increased left ventricular afterload itself. The ventricular response to angiotensin is so variable that the angiotensin infusion method of evaluating ventricular function is not reliable.

Left-to-right shunt at atrial level after rupture of papillary muscle from acute myocardial infarction

Abstract Clinical and necropsy observations are described in a patient who developed a large left-to-right shunt at atrial level after rupture of a papillary muscle during acute myocardial infarction. Attention is called to the importance of differentiating this combination from rupture of the ventricular septum and from mitral regurgitation resulting from papillary muscle necrosis with or without rupture.

Congenital stenosis of the pulmonic and tricuspid valves: Clinical, hemodynamic and angiographic observations in a 20 year old woman

Abstract Patients with congenital stenosis of the tricuspid and pulmonic valves are rare, indeed, and are expected to have underdeveloped right ventricles. The three obstructions in series, namely, tricuspid orifice, right ventricular inflow and right ventricular outflow typically result in symptomatic, cyanotic infants or young children with right to left shunts at atrial level. We present unique clinical, hemodynamic and angiographic information on a 20 year old acynotic, virtually asymptomatic woman with normally formed right ventricle and congenital stenosis of the tricuspid and pulmonic valves.