Biomedical subjects
Publications and source records attributed to M Rubenfire.
Patients with mitral valve disease and extreme enlargement of the left atrium usually exhibit significant decrease in chamber size following corrective mitral valve surgery. We describe a patient in whom extreme right and left atrial enlargement developed, and progressed following mitral valve replacement, with no evidence of prosthetic valve malfunction or tricuspid valve disease.
To assess metabolic cost of extremely slow walking, nine patients with coronary heart disease (means age, 56.1 yr) underwent multistage treadmill testing using standard open circuit calorimetry techniques. Heart rate, blood pressure, minute ventilation, and oxygen uptake in METS (1MET = 3.5 ml/kg/min) were determined at rest and at six submaximal work loads: 0.8, 1.0, 1.5, 2.0, 3.0 and 3.5mph, 0% grade. The oxygen uptake versus walking speed (0.8 to 3.5mph) relationship was y = 0.2064 (x)2 + 0.0180 (x) + 1.7260 (y = METS and x = speed in mph), r = 0.99. Results indicate that low-level exercise test protocols employing work loads between 0.8 and 2.0 mph impose similar metabolic and cardiac demands. Extremely slow walking approximates 2METS and may impose metabolic loads sufficient for exercise training in select patients with coronary heart disease.
A multicenter randomized double-blind withdrawal study was conducted to compare the efficacy of nifedipine to that of placebo in vasospastic angina. Following a 2-week single-blind nifedipine baseline period, during which nifedipine was maintained at prestudy levels, 38 patients, 19 taking placebo and 19 continuing nifedipine therapy, either completed a 4-week randomized phase or were prematurely withdrawn because of therapeutic failure. During the randomized phase, an increase in median anginal frequency (2.8 attacks/wk, p less than 0.003) and nitroglycerin usage (0.5 tablets/wk, p less than 0.03) occurred only in the placebo group. The randomized phase was prematurely terminated because of anginal exacerbation in 7 of 19 placebo patients (37%) (only 1 patient receiving nifedipine [p = 0.02] experienced anginal exacerbation). Double-blind therapy was judged effective in 16 patients (84%) receiving nifedipine and in 3 patients (16%) receiving placebo (p less than 0.001). Nifedipine was well tolerated. This study establishes the efficacy of nifedipine in the treatment of variant and validates previous clinical experience.
Thirty patients with variant angina pectoris (VAP) were analyzed for electrocardiographic features during episodes of VAP. Twenty-nine of these patients had cardiac catheterization, and an autopsy study was performed in one. The patients showed predominantly concave upright T-waves during pain. An increase of R wave amplitude (expressed as delta R) of more than 10% was seen in 17/30 patients (57%). The primary ST-T changes produced by the VAP episodes were conspicuous in two patients with pre-existent complete left and right bundle branch block. Serious dysrhythmias, including ventricular fibrillation (VF), ventricular tachycardia (VT), ventricular premature beats (VPBs) (more than five/min, multifocal and R on T phenomenon), and 2 degrees atrioventricular block were found in thirteen patients (43%). The development of dysrhythmias was related to the duration of VAP episodes. The average time to onset of dysrhythmias was 3.54 min. The dysrhythmias were not contingent upon pre-existing coronary artery anatomy (defined by Friesinger's coronary score), left ventricular ejection fraction or left ventricular segmental abnormalities. The location of the ST-segment elevation and the presence of dysrhythmias during the episodes of VAP (A-V blocks, ventricular tachycardia and fibrillation) were not predictive factors of the coronary anatomy. Eight patients (27%) developed myocardial infarction (MI). Five of them had nontransmural MIs and three developed transmural MIs. The development of MI was not related to the severity of the VAP attacks (appreciated by the magnitude of ST-segment elevation and R wave changes) but showed a relation to the development of an unstable pattern which preceded the infarction. Sixteen patients underwent exercise testing. In eight of them, the coronary arteriograms were normal (Group I); in the remaining eight, significant proximal coronary artery obstructive disease was found (Group II). Group I patients displayed a normal ST-segment response and functional aerobic capacity (FAI = 4.4 +/- 14) as well as normal heart rate (HR) and double product (SBP X HR) responses (HR = 154 +/- 21; SBP X 21; SBP X HR = 290 +/- 71). During exercise, a normal delta R was observed. With one exception, Group II patients showed an abnormal ST-segment response with an overall low exercise capacity (FAI = 57 +/- 17) and decreased hemodynamic response (HR = 27; SBP X HR = 130 +/- 40). FAI, HR, SBP X HR Group I vs. Group II = P less than .005/less than .02/less than .005. The abnormal ST-segment response included elevation in four patients and depression in three. During exercise, Group I with ST-elevation displayed a normal (negative) delta R response; while Group II with ST-depression displayed an abnormal delta R response (positive or no change). There was no difference in the coronary score between Group II patients with ST-segment elevation or depression.
Retrospective and prospective analyses of chest radiographs of patients following coronary artery bypass surgery were undertaken. Left lower lobe pulmonary infiltrate and/or atelectasis developed in 13 of 40 (32.5%) patients who were operated upon without topical cooling of the heart with ice, and in 77 of 122 (63.1%) patients in one group and 34 of 40 (85.0%) patients in another group who were operated upon with topical cooling of the heart with ice. This difference was highly significant (p less than 0.001). Of the patients in one group in whom left lower lobe abnormality developed, 69.2% had paralysis or paresis of the left hemidiaphragm. It is evident that application of ice to the phrenic nerve can lead to temporary paralysis of the left of the diaphragm, with subsequent development of left lower lobe pulmonary infiltrate and/or atelectasis.
The use of intravenous xenon- 133 for determination of radionuclide first pass right ventricular ejection fraction is described. First pass determinations of right ventricular ejection fraction were made with both xenon- 133 and technetium-99m in 13 subjects (15 right ventricular ejection fraction determinations); results obtained with xenon- 133 show an excellent correlation (r = 0.98, p less than 0.002) with results obtained using technetium-99m. Because of rapid pulmonary elimination of xenon- 133 from the body, the use of this radioisotope allows multiple first pass right ventricular ejection fraction determinations within a short period of time, without significant radiation exposure for the patient.
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We report clinical experience with the coronary vasodilator nifedipine in 127 patients with symptoms of myocardial ischemia associated with electrocardiographic or angiographic evidence, or both, of coronary-artery spasm. In the majority of patients conventional antianginal therapy including nitrates and beta-adrenergic blockers failed, and in one third of the patients at least one episode of ventricular tachycardia developed during an attack of angina. Nifedipine (40 to 160 mg every 24 hours) significantly reduced the mean weekly rate of anginal attacks from 16 to two (P less than 0.001). Similar marked reductions in the nitroglycerin requirement were noted. In 63 per cent of the patients complete control of anginal attacks was achieved, and in 87 per cent the frequency of angina was reduced by at least 50 per cent. Nifedipine was generally well tolerated, with only 5 per cent of the patients requiring termination of the drug because of intolerable side effects. This experience with nifedipine suggests that it is a highly effective drug for the treatment of coronary-artery spasm and variant angina.
Procainamide is probably the most common offending drug responsible for the drug-induced lupus erythematosus syndrome today. Pericarditis has been reported to occur in from 14 to 18 per cent of the cases of procainamide-induced lupus erythematosus, and occasional reports of massive pericardial effusion, pericardial tamponade and constrictive pericarditis have appeared in the literature. We describe a patient who presented with features of procainamide-induced lupus erythematosus without any clinical evidence of pericarditis. He underwent coronary bypass surgery 12 days after administration of the drug was stopped and was found to have a significant pericardial effusion at the time of surgery; histologic examination of pericardial tissue and pericardial fluid confirmed that the pericardial effusion was related to the procainamide-induced lupus syndrome. The incidence of pericarditis in procainamide-induced lupus erythematosus may be higher than presently accepted figures would indicate. Symptoms and signs related to procainamide-induced lupus pericarditis may cause diagnostic confusion with common postoperative bypass complications; the full implications of this disease entity to the patient undergoing coronary bypass are unknown.
The echocardiographic features of patients with parachute mitral valve have revealed the combination of an early systolic movement of the mitral valve and late systolic prolapse. Cross-sectional echocardiographic and angiographic studies showed that the early systolic anterior motion was produced by the presence of a flail scallop of the anterior mitral leaflet in the left ventricular outflow tract.
Two patients who had idiopathic hypertrophic subaortic stenosis (IHSS) and type A ventricular preexcitation were studied and showed variations of the subvalvular flow gradients. The increase in subvalvular gradient, occurring at a time when preexcitation developed, was associated with significant increase of the systolic murmur and the systolic anterior motion of the mitral valve. In patient 1, the significant increase in subvalvular gradient during ventricular preexcitation was also confirmed by catheterization of the left side of the heart. The increase of the gradient with the development of the ventricular preexcitation was apparently due to decreased end-diastolic volume. The importance of ventricular volume considered as a variable affecting outflow tract gradient in idopathic hypertrophic subaortic stenosis is emphasized.
Hemoptysis is an unusual complication of flow-directed (Swan-Ganz) catheters. Over-inflation of the balloon with a shearing-induced rupture of a small pulmonary artery, and the spear effect of the catheter tip appear to be the mechanisms in the two cases presented. Diligent care to avoid overinflation of the balloon in the pulmonary capillary wedge position by observation of the pressure waveform is critical. The spear effect that is frequently seen during insertion may be eliminated by deflating the balloon at the first appearance of the pulmonary artery waveform and gradual advancement of the catheter five to eight cm, when the balloon is then reinflated to obtain the wedge.
Long electrocardiographic strips were analyzed from an aged patient whose heart rhythm had periods of unifocal ventricular extrasystoles with fixed coupling intervals. Periods of gradual prolongation of the coupling interval finally led to omission of a ventricular premature beat. This sequence was repetitive and is considered to be the results of reentrant extrasystoles with a 3:2 Wenckebach type of conduction delay within the reentry loop. The mechanism of concealed conduction due to overlong propagation within the reentry loop is discussed.
Intravenous injection of phentolamine potentially offers a better provocative test for aortic left ventricular outflow tract obstruction than do Valsalva's maneuver, inhalation of isoproterenol, or of amyl nitrite. In hemodynamic studies, phentolamine enhanced myocardial contractility, and decreased afterload with only induction of slight tachycardia. Phentolamine (5 mg.) was administered intravenously to five patients who had idiopathic hypertrophic subaortic stenosis, and 35 patients who had valvular dysfunctions, after which echocardiographic and phonocardiographic recordings were performed. Recordings were of high quality despite changing hemodynamics. Systolic pressures fell an average of 20 mm. Hg; no pressure fell below 90 mm. Hg; there was no notable increase in heart rate. In the five patients with typical idiopathic hypertrophic subaortic stenosis, the amyl nitrite increased the obstructive index from 39.6 +/- 12 to 51 +/- 18.9 (P less than 0.05); whereas, phentolamine increased the obstructive index to 69.8 +/- 25.6 (P less than 0.015). After a 2 week course of oral administration of 80 mg. of propranolol daily, and then either inhalation of amyl nitrite or injection of phentolamine, there was no change from the mean resting obstructive index. Phentolamine appears to be a safe, simple and specific diagnostic agent, and more potent than amyl nitrite in eliciting dynamic obstruction in IHSS; phentolamine and amyl nitrite do not affect the obstructive index in patients with beta blockade.
A mobile instrumentation and noninvasive method developed recently for external His bundle recording and employing the signal averaging technique was applied for intra-atrial recording of the pre-P (sino-atrial node region) activity. Recordings were obtained in ten anesthetized dogs and five patients at the time of right heart catheterization. A bipolar intra-atrial lead was used for triggering of the averaging process and a unipolar intra-atrial lead was used for signal recording. Direct bipolar epicardial recordings were obtained for comparison from the sino-atrial (S-A) node area in experimental animals. In animals studies, the averaged intra-atrial recording showed 30 muV amplitude deflections beginning 40-45 ms prior to the onset of P wave and were preceded by a slow rise and lower frequency and amplitude deflections arising 60-70 ms earlier. There was good correlation between the pre-P activity recorded intra-atrially and from the epicardium. Deflections of similar configuration but smaller amplitude (1 muV) were recorded in human studies. They preceded the onset of large atrial activity deflections (P wave) in the reference electrocardiogram by 40-80 ms. The exact source of these pre-P activity potentials has not been definitely established, but they appear to originate from the S-A node region, based on their similarity to the direct epicardial recordings and time relationship to the preceding T and following P wave.
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A study of single-plane right anterior oblique left ventricular angiography was undertaken to determine the importance of obtaining correct positioning of a magnification grid and to develop a simple but accurate technique to minimize magnification errors. Theoretical and experimental volume determinations demonstrated 3% to 28% volume errors for grid placement errors ranging from 1 centimeter to 5 centimeters. An experiment was designed whereby cross table lateral radiographs of the chest were taken during contrast injections of the left ventricle. The relative position of the left ventricular center was found at a point 66% of the distance from the anterior to the posterior margin of the heart. Finding this point on noncontrast lateral films of the chest for positioning of a square centimeter grid should yield a more accurate determination of the magnification factor than other current emperic methods.
Patterns indicative of concealed atrial extrasystoles were observed in two patients with frequent premature atrial depolarizations. In the first patient, the predominant pattern was such that most of the numbers (S) of sinus P waves between atrial extrasystoles satisfied the equation S = 3n-1, where n is any positive integer. This pattern is characteristic of concealed trigeminy. Over a sequence of 49 interectopic intervals, this patient vacillated between concealed atrial trigeminy and bigeminy. A second patient displayed a pattern characteristic of the "even number" variant of concealed bigeminy. The numbers of sinus P waves in consecutive interectopic intervals were predominantly even. These various patterns of concealed atrial extrasystoles closely resemble previously reported patterns of concealed ventricular extrasystoles.