Abe Walston

Comparison of pulmonary wedge and left atrial pressure in man

Abstract Values of mean pulmonary wedge and mean left atrial pressure were compared in 700 patients including normals and patients with a variety of heart diseases. An over-all correlation coefficient r = 0.93 was found between mean wedge and mean left atrial pressure and this correlation was unrelated to the etiology of the heart disease. No significant difference between the average value of wedge and left atrial pressure was found until the wedge pressure exceeded 25 mm. Hg. In patients with mean wedge pressures of 10 mm. Hg or less, left atrial pressure could be predicted with an accuracy of ± 2 mm. Hg (95 per cent confidence limits). However, at higher wedge pressures the prediction of mean left atrial pressure was subject to considerable error. Thus, caution should be employed in using mean wedge pressure as an accurate index of mean left atrial pressure unless the wedge pressure is within the low normal range.

The Electrocardiographic Manifestations of Spontaneous Left Pneumothorax

Abstract The electrocardiograms (ECG) of seven patients with spontaneous left pneumothorax showed these changes resulting from left pneumothorax: a rightward shift of frontal QRS axis, diminution o...

Clinical implications of pulmonary hypertension in mitral stenosis

The relation of mean pulmonary arterial and mean left atrial pressure was examined in 200 patients with pure mitral stenosis and compared with that in a heterogenous group of 313 patients, including 27 with normal hemodynamic and angiographic findings, 40 with coronary artery disease, 106 with aortic stenosis, 73 with aortic insufficiency and 67 with mitral insufficiency. Linear regression analysis of mean pulmonary and left atrial pressures of the patients without mitral stenosis revealed nine patients with increased pulmonary pressure greater than 2 standard errors from the regression line. Three of these nine had acute pulmonary emboli, three had severe obstructive lung disease and one had severe congestive heart failure. Mean pulmonary and left atrial pressures were compared in the patients with mitral stenosis using the values for the regression line and standard error obtained from the patients without mitral stenosis. Thirty-seven of the 200 patients with mitral stenosis had increased pulmonary pressure greater than 2 standard errors from the regression line. Fifteen of these 37 patients (41 percent) demonstrated pulmonary emboli or severe obstructive lung disease as compared with 9 patients (4 percent) of the 164 patients with mitral stenosis within 2 standard errors. From these data we conclude that pulmonary arterial pressure markedly in excess of left atrial pressure is common in mitral stenosis and carries an implication of pulmonary thromboembolism or severe lung disease.

Acute coronary occlusion and the “power failure” syndrome

Abstract Thirty-seven patients with acute myocardial infarction were studied post mortem. Twenty-five had acute coronary artery occlusion (thrombosis and/or intramural hemorrhage); 22 of these patients showed the clinical “power failure” syndrome (88 per cent). In contrast, only 2 out of 12 patients (17 per cent) who had no demonstrable acute coronary artery occlusion had evidence of “power failure”.

Spectrum of coronary artery disease in idiopathic hypertrophic subaortic stenosis.

The spectrum of coronary arterial involvement is described in 42 patients with hemodynamically proved idiopathic hypertrophic subaortic stenosis. Of nine patients with significant coronary arterial involvement, six had atheromatous disease and three had coronary arterial anomalies. The hemodynamic and clinical features of patients with coronary arterial involvement did not differ significantly from those of patients with normal coronary arteries. Neither the severity nor the character of the chest pain distinguished those patients with coronary disease. The diagnostic electrocardiographic features of myocardial infarction classically seen in patients with idiopathic hypertrophic subaortic stenosis were not present in the 9 patients with coronary arterial involvement but were found in 8 of the 33 patients with normal coronary arteries. The data demonstrate a significant incidence of coronary arterial involvement in patients with idiopathic hypertrophic subaortic stenosis after age 45 years.

Some Problems Concerning Coronary Artery Occlusion and Acute Myocardial Infarction

IT HAS BECOME APPARENT that the concept of a simple cause-and-effect relationship between coronary artery thrombosis and myocardial infarction is no longer tenable. Each of these events involves several factors that may or may not be interrelated. For example, understanding of acute coronary occlusion entails knowledge of events that occur in the origin and evolution of the atherosclerotic plaque, as well as the factors leading to an acute occlusive episode. Furthermore, recent studies have pointed to more complicated metabolic, hormonal, and hemodynamic interactions than have traditionally been considered relevant to the myocardial necrosis process.1 This report will review some of our experiences in studying coronary artery disease from a clinicopathological point of view. We will address ourselves to the following questions: 1. How can one explain the variable incidences of acute coro-nary occlusion that are reported in patients with acute myocardial infarction? 2. Are there clinical clues to the presence or absence of acute coronary occlusion in patients with acute myocardial infarction?

Relationship between ventricular depolarization and QRS in right and left bundle branch block

Summary QRS prolongation in experimental BBB was reated to the increased time required for unidirecional spread of activation across the septum and into and through the blocked ventricle. There was no focal or diffuse slowing of propagation velocity in the septum, it averaged 0.4M/sec. There was an abnormal pattern of excitation of the blocked free wall indicating that the Purkinje network was not operating to distribute the impulse normally. LBBB was associated with a longer period of ventricular activation (QRS) than RBBB, and the mechanism of this difference was explained from the data. The mechanism of the altered QRS potentials in right and left BBB was studied by correlating ECGs and VCGs with the activation data. The spread of excitation in the septum was an important factor in the increased magnitude of QRS in BBB. Also several of the characteristic features of QRS, such as the midpoint slowing of velocity and plateau in LBBB, were explained from the activation data. The sequence and pattern of spread of activation indicates why QRS changes due to myocardial infarction may be more apparent in RBBB than LBBB.

Effect of different epicardial ventricular pacing sites on left ventricular function in awake dogs.

Left ventricular performance was assessed during both atrial and sequential and nonsequential ventricular pacing from multiple epicardial sites in 12 awake dogs. All animals had an electromagnetic flow probe chronically implanted on the ascending aorta and pressure catheters implanted in the aorta and left ventricle. The mean pacing rate was 106 beats/min. Compared to results obtained with right atrial pacing alone, sequential ventricular pacing resulted in a 14 percent decrease in left ventricular stroke volume. This decrease is most likely due to the ventricular asynchrony from ectopic depolarization. No significant differences in the hemodynamic variables measured (stroke volume, left ventricular end-diastolic pressure, aortic pressure) or computed (stroke work, peak power) could be detected among any of the right or left ventricular pacing sites during either sequential or nonsequential pacing. From these data we conclude that no optimal site for epicardial ventricular pacing exists.

Pressure-flow studies in man: effect of atrial systole on ventricular function in mitral stenosis

The effect of atrial contraction on left ventricular function in six patients with varying degrees of mitral stenosis was determined by utilizing the pressure gradient technique to measure instantaneous aortic blood flow and pressure. Aortic flow was measured as ventricular rate was controlled by right ventricular pacing to create A-V (atrioventricular) dissociation at varying rates (90-150 beats/min). At each heart rate, beats with preceding P waves, effective atrial systole, were grouped according to the duration of the P-R interval. Beats without P waves served as controls. There was always a significant increase in stroke volume, created by effective atrial systole, but the P-R interval at which it took place was different for each patient. There was no difference in the stroke volume for beats preceded by P waves having a P-R interval within the range of 0.05-0.20 sec. These beats were grouped for each patient, subjected to regression analysis, and compared to control beats. The absolute and percent change created by effective atrial systole was inversely proportional to the severity of the disease as determined by mitral valve orifice size. Effective atrial systole plays less of a role in augmenting left ventricular function in patients with mitral stenosis than in patients with normal valves.

Electrocardiographic and hemodynamic correlations in patients with idiopathic hypertrophic subaortic stenosis.

The ECG and Frank VCG were compared to the hemodynamic findings in 33 patients with idiopathic hypertrophic subaortic stenosis in whom cardiac catheterization had excluded concomitant valvular heart disease, congenital heart disease, or occlusive coronary artery disease. The patients were divided into two groups according to the absence (Group I) or presence (Group II) of left ventricular hypertrophy on the ECG and/or VCG. The 11 patients in Group I were found to have neither mitral insufficiency nor a resting left intraventricular gradient, and only six patients in whom mitral valve movement was visualized demonstrated systolic anterior movement of the anterior leaflet. The papillary muscles and left ventricular wall were either normal or only mildly hypertrophied in 10 of 11 Group I patients. Group II (22 patients) demonstrated either a resting left intraventricular gradient and/or mitral insufficiency in 18 patients. Twenty-one of the 22 patients showed systolic anterior movement of the anterior leaflet of the mitral valve on a cineangiogram and the papillary muscles and left ventricular wall were moderately to severely hypertrophied in 18 patients. These data suggest that specific hemodynamic and anatomic characteristics of hypertrophic subaortic stenosis may be predicted with reasonable accuracy from the ECG and VCG.