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Dive into the research topics where Allan G. Adelman is active.

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Featured researches published by Allan G. Adelman.


American Journal of Cardiology | 1972

Prinzmetal's variant form of angina with arteriographic evidence of coronary arterial spasm☆

Raja W. Dhurandhar; David Watt; Malcolm D. Silver; Alan S. Trimble; Allan G. Adelman

Abstract Spasm of the proximal right coronary artery was arteriographically demonstrated during an episode of chest pain in a patient with Prinzmetals variant form of angina. A right aortocoronary saphenous vein bypass procedure was performed but, despite a patent graft, the angina recurred and the patient died. The only significant finding at autopsy was an eccentric atherosclerotic plaque that narrowed the right coronary artery by 75 percent at the site of the spasm. These findings support Prinzmetals hypothesis that this variant form of angina is produced by spasm of a coronary artery with a seriously compromised lumen.


Circulation | 1971

Role of Echocardiography in Diagnostic and Hemodynamic Assessment of Hypertrophic Subaortic Stenosis

Pravin M. Shah; Raymond Gramiak; Allan G. Adelman; E. Douglas Wigle

An abnormal sharp anterior motion of the anterior mitral leaflet has been previously described as a diagnostic abnormality in hypertrophic subacute stenosis (HSS). The present prospective study explored the diagnostic sensitivity and specificity of this finding in 26 patients studied without knowledge of clinical diagnosis. When the abnormality observed was complete and persistent, a correct diagnosis of HSS was made in every case. In the absence of systolic abnormality at rest and on provocation, the diagnosis of HSS could be excluded. When the abnormality was small and inconstant (nine patients) two thirds of the patients were shown to have a latent or labile form of outflow obstruction whereas the remaining third had no evidence of HSS.In an extended part of the study on 31 patients with known HSS, comparisons of resting pressure gradients across left ventricular outflow tract were made with the echocardiographic findings at rest. Those with persistently abnormal mitral valve movement had an average pressure gradient of 78 mm Hg, those with inconstant abnormality had an average gradient of 24 mm Hg, and those with no resting abnormality had no gradients at rest.


American Journal of Cardiology | 1980

Hypertrophic cardiomyopathy: Subclassification by M mode echocardiography

Brian W. Gilbert; Charles Pollick; Allan G. Adelman; E. Douglas Wigle

Abstract Seventy-four patients with hypertrophic cardiomyopathy, hemodynamically classified into well defined subgroups (left ventricular outflow tract obstruction at rest [27 patients], labile obstruction [4 patients], latent obstruction [28 patients] and no obstruction [15 patients]) were studied with M mode echocardiography. Significant echocardiographic differences were found among these groups. The most important differentiating feature was the degree of systolic anterior motion of the anterior mitral leaflet. Combined with prolonged interventricular septal contact (that is, for more than 30 percent of echocardiographic systole), it occurred in all 27 patients with obstruction at rest but in no patient with latent or no obstruction. Another differentiating feature was aortic valve midsystolic notching, which occurred in all 25 patients with obstruction at rest (in whom adequate aortic valve echograms could be obtained) but in only 3 of 17 patients with latent obstruction and in no patients without obstruction. The third most useful differentiating feature was left atrial enlargement, which occurred in 25 of 27 in the group with obstruction at rest, but in only 4 of 28 in the group with latent obstruction and in 2 of 15 in the group without obstruction. Other M mode echocardiographic findings in patients with hypertrophic cardiomyopathy showed overlap among subgroups and therefore could not be relied on for noninvasive subclassification. These echocardiographic abnormalities included septal and posterior wall thickness, septum to posterior wall thickness ratio, septal and posterior wall systolic thickening, left ventricular internal diameter, left ventricular outflow tract size at the onset of systole, mitral leaflet position and percent diastolic anterior mitral leaflet-interventricular septal contact. It is concluded that a noninvasive classification of patients with hypertrophic cardiomyopathy into hemodynamic subgroups of obstruction at rest, latent obstruction and no obstruction can be made by assessing the degree of systolic anterior motion, the presence of aortic valve mid systolic notching, and left atrial size. This noninvasive M mode echocardiographic subclassification has important clinical implications.


American Journal of Cardiology | 1983

Effects of negative pleural pressure on left ventricular hemodynamics

Sheldon A. Magder; Samuel Lichtenstein; Allan G. Adelman

Negative pleural pressure alters left ventricular (LV) function. LV volume changes have been studied in human subjects, but little is known of the hemodynamic effects. The effect of changes of pleural pressure on LV hemodynamics during a Mueller maneuver (inspiration against an obstruction) was studied in 11 subjects and during quiet, unobstructed inspiration in 3. During the Mueller maneuver, there was an initial decrease in pulmonary wedge pressure and aortic systolic pressure, almost as great as the decrease in pleural pressure. Thereafter, these pressures increased despite a sustained reduction in pleural pressure. Toward the end of the Mueller maneuver, pulmonary wedge transmural pressure averaged 31 +/- 12 mm Hg and in 6 patients large v waves developed. The increase in aortic transmural pressure averaged 30 +/- 16 mm Hg. Aortic pulse pressure decreased on the first beat from control levels of 59 +/- 21 to 47 +/- 21 (p less than 0.001) and then returned to control levels. During normal breathing in 3 subjects, studied with intraesophageal balloons, there was a similar increase in both transmural aortic and transmural pulmonary wedge pressures with a decrease in pleural pressure 6 mm Hg during inspiration. Thus, increased negative pleural pressure was associated with a marked increase in pulmonary wedge transmural pressure; the increase was approximately proportionate to the decrease in pleural pressure. It is suggested that this increase was due to increased impedance to LV ejection and to right ventricular expansion interfering with LV diastolic filling.


Circulation | 1972

Echocardiographic Assessment of the Effects of Surgery and Propranolol on the Dynamics of Outflow Obstruction in Hypertrophic Subaortic Stenosis

Pravin M. Shah; Raymond Gramiak; Allan G. Adelman; E. Douglas Wigle

The long-term effects of surgery (ventriculomyotomy) and oral propranolol therapy were assessed by echocardiographic recordings in 51 studies conducted on 37 patients with hypertrophic subaortic stenosis. The incidence and severity of echocardiographic findings in 19 patients treated with propranolol and in 18 not so treated showed no significant differences. Likewise these findings were unaltered by administration of propranolol in 12 patients who were studied both while they were on the drug and while they were not. In contrast, of 14 patients studied after surgery, only one had persistently abnormal mitral valve motion, two had inconstant abnormality, and 11 had no abnormality at rest. The echocardiographic findings correlated well with independent postoperative hemodynamic assessment. The echocardiographic studies provide a noninvasive objective method for longitudinal evaluation of patients with hypertrophic subaortic stenosis (HSS).


American Heart Journal | 1970

Morphology of a prolapsed posterior mitral valve leaflet

J.K. Trent; Allan G. Adelman; E.D. Wigle; M.D. Silver

Abstract A case of prolapsed posterior mitral valve leaflet in a 63-year-old woman is presented. Morphologically, the middle scallop of the leaflet was lengthened and showed myxomatous change. Chordae tendineae to the scallop were thickened. A brief discusston of the possible pathogenesis of this change is included and attention drawn to the possibility of recognizing in cineangiograms whether one or more scallops of the posterior leaflet have prolapsed.


Circulation | 1968

Two Types of Intraventricular Pressure Difference in the Same Patient: Left Ventricular Catheter Entrapment and Right Ventricular Outflow Tract Obstruction

Allan G. Adelman; E. Douglas Wigle

Two types of intraventricular pressure difference were encountered in a single patient who presented with clinical evidence of obstruction to right ventricular outflow and nonobstructive cardiomyopathy of the left ventricle. On the basis of measurements of inflow tract pressure, the pressure difference in the right ventricle was demonstrated to be due to muscular subvalvular obstruction to right ventricular outflow, whereas the pressure difference in the left ventricle resulted from catheter entrapment in the myocardium. This combination of intraventricular pressure differences must be differentiated from the situation in muscular subaortic stenosis, in which biventricular obstruction to outflow occurs.


national computer conference | 1971

The television/computer system: the acquisition and processing of cardiac catheterization data using a small computer

H. Dominic; J. Covvey; Allan G. Adelman; Clarence H. Felderhof; Paul Mendler; E. D. Wigle; Kenneth W. Taylor

One of the prime objectives of cardiovascular research is to assess the functional state of the heart especially the left ventricle, its main pumping chamber. The functional state of the left ventricle is determined by its dimensions, volume, the velocity of wall movement, the intracavity pressure, and the wall tension and stress.


Progress in Cardiovascular Diseases | 1968

Surgery in muscular subaortic stenosis

E. Douglas Wigle; Alan S. Trimble; Allan G. Adelman; Wilfred G. Bigelow


Chest | 1974

Sinus Rhythm with Ineffective Left Atrial Contraction in Severe Mitral Stenosis

Amadeo Betriu; Gines Sanz; Allan G. Adelman; E. Douglas Wigle

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Pravin M. Shah

Toronto General Hospital

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Amadeo Betriu

Toronto General Hospital

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Andrew J. Buda

Toronto General Hospital

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David Watt

Toronto General Hospital

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