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Biomedical subjects

M V Cohen

Publications and source records attributed to M V Cohen.

At least 145 records · Page 8Linked to original sources
PubMed1979

Constrictive pericarditis: early and late complication of cardiac surgery.

Constrictive pericarditis is not considered a complication of cardiac surgery. However, three cases are presented in which equalization of diastolic pressures and the ventricular pressure pattern of early diastolic dip-late diastolic plateau, characteristic of restrictive disease, appeared after cardiac surgery. In one patients cardiac constriction developed less than 2 weeks after surgery, and loculated clotted and unclotted viscous blood was removed from the pericardial space. In the other two patients the pericardial space was obliterated by dense adhesions. Thus constrictive pericarditis should be considered in postoperative patients who either do not recuperate satisfactorily after surgery or whose condition deteriorates after initial recovery.

Aged↗
PubMed1979

Myocardial performance and collateral flow after transient coronary occlusion in exercising dogs.

Fourteen dogs with prior constriction of the left circumflex (LCf) coronary artery were studied at rest and during treadmill running. Hemodynamics were measured before and after a 1-min LCf occlusion. Coronary and collateral flows were quantitated during occlusion both at rest and during exercise. Group I consisted of 4 dogs with resting collateral flow exceeding one-half (average 78%) of normal flow, and group II consisted of 10 dogs with collateral flows less than one-half (average 30%) of normal. At rest LCf occlusion caused no hemodynamic changes in group I, but stroke volume fell significantly in group II. During running, collateral flow after LCf occlusion doubled in group I, and there was only a small rise in left atrial pressure to 18 mmHg. In group II, collateral flow increased by 50% during running and actually decreased in 4 dogs. Significant cardiac failure developed as stroke volume halved, and left atrial pressure rose to an average 30 mmHg. Therefore exercise-induced depression of left ventricular function in the ischemic heart can be correlated to the amount of coronary collateral flow.

Animals↗
PubMed1979

Mitral valve closure in atrial flutter.

12 patients who had atrial flutter without clinical, echocardiographic or angiographic evidence of aortic insufficiency were studied with simultaneous echo- and phonocardiograms. In patients with high-grade atrioventricular (AV) block, the mitral valve opened and closed with each flutter wave. Of seven patients, two had persistent and five had intermittent early mitral valve closure before QRS inscription. In five patients (three with 2:1 AV block) the mitral valve closed on time. In one patient with a mitral valve prosthesis, echocardiography and cinefluorography demonstrated closure during mid-diastole, with reopening in late diastole after a flutter wave. Final valve closure occurred before the onset of the QRS, and each closure was associated with a click. Simultaneous phonocardiographic analysis in these patients demonstrated that the first heart sound intensity was inversely related to the degree of mitral valve preclosure. This relationship was independent of the length of the RR interval. Thus, atrial flutter independent of any other cause of abnormal hemodynamics may produce early mitral valve closure. The echocardiographic finding of premature mitral arrhythmias, may not have the same diagnostic or prognostic significance previously described in patients with sinus rhythm and normal AV conduction.

Adult↗
PubMed1979

Echocardiographic assessment of left ventricular function in patients with chronic uremia.

Cardiac function was determined non-invasively in 7 patients (average age 24 years) with chronic uremia. Each was on maintenance hemodialysis. Echocardiograms and carotid pulse tracings were recorded 30 minutes prior to dialysis, and again 30 minutes, 24 and 48 hours following hemodialysis. End-diastolic and end-systolic diameters averaged 5.4 +/- 0.2 and 3.4 +/- 0.1 cm, respectively before and 5.0 +/- 0.2 and 3.2 +/- 0.1 cm immediately after hemodialysis (P less than 0.05 for both). Calculated stroke volume fell from 92.1 +/- 8.8 to 76.7 +/- 10.5 ml (P less than 0.025). Heart rate increased minimally, and average cardiac output was not significantly increased. Following dialysis, body weight and systolic and diastolic blood pressures fell significantly. Thus preload as well as afterload declined. Because of the fall in both stroke volume and end-diastolic volume, a shift along the ventricular function curve downwards and to the left occurred implying diminished cardiac pumping function. Nonetheless the indices of myocardial contractility were normal and showed no change from pre-dialysis value. During the 48 hour interval following hemodialysis all measured and calculated values returned to pre-dialysis levels. Thus organic heart disease as evaluated by non-invasive techniques does not appear to be a necessary sequel to kidney failure, at least in young patients in a hemodialysis program. Gross abnormalities of myocardial function may be absent for at least seven years after the onset of chronic uremia.

Adolescent↗
PubMed1978

Quantitation of collateral and ischemic flows with microspheres and diffusible indicator.

Flow to myocardium following coronary occlusion may not originate solely from collateral channels. Some flow might be derived from overlapping coronary arteries which also perfuse tissue within the territory of the obstructed vessel prior to occlusion. Left atrial microsphere injection during perfusion of the left anterior descending (LAD) artery from a special reservoir containing microsphere-free blood and again after LAD occlusion permitted measurement of noncollateral overlap and total ischemic LAD (TIF) flows, respectively, and mathematical derivation of true collateral flow (TCF). Whereas TIF averaged 0.25 +/- 0.03 ml/min per g, TCF was 0.14 +/- 0.03 ml/min per g, only 50.6% of TIF. The remainder of the TIF represented either inadvertant inclusion of normally perfused tissue with the ischemic LAD myocardium or actual overlap of LAD and left circumflex circulations. 86RbCl was injected simultaneously with the microspheres following coronary occlusion. 86Rb and microsphere densities in the whole heart and ischemic area were closely correlated, although microsphere distribution tended to be more heterogeneous. No segment of ischemic myocardium containing 86Rb was free of microspheres. Therefore, the geometry of undeveloped collateral channels is adequate to permit passage of 15-micron particles. Absolute 86Rb flows were consistently less than microsphere flows.

Animals↗
PubMed1978

Effect of exercise on collateral development in dogs with normal coronary arteries.

To determine the effects of chronic exercise on the coronary collateral circulation of dogs with normal coronary arteries, 1-yr-old purebred beagles were divided into sedentary control and exercising groups. The latter were trained to run on a treadmill. A lower maximal heart rate during a standardized exercise test protocol after a 10- to 12-week training period and a higher gastrocnemius cytochrome oxidase activity in the runners attested to the presence of cardiovascular and skeletal muscle training effects. However, left ventricular weights, left ventricle/body weight ratios, myocardial myofibrillar and myosin ATPases, and hemodynamics were similar in sedentary and exercising dogs except for a significantly higher resting cardiac output in the runners. After occlusion of the left anterior descending coronary artery, both collateral conductance (retrograde flow/aortic pressure) and collateral flow measured with microspheres tended to be lower in the trained dogs, but differences were not significant. The endocardial/epicardial flow ratio in the ischemic area after coronary occlusion did not distinguish between exercisers and controls. Thus treadmill running in the dog with normal coronary arteries produced a training effect, but had no effect on coronary collateral vessels.

Adenosine Triphosphatases↗
PubMed1976

Comparative effects of nitroglycerin and isosorbide dinitrate on coronary collateral vessels and ischemic myocardium in dogs.

To determine the effect of isosorbide dinitrate or ischemic myocardium, this agent was administered to dogs with well developed coronary collateral vessels 8 to 14 weeks after embolization and subsequent occlusion of the left anterior descending coronary artery. After thoracotomy the left coronary artery was cannulated and perfused with blood from the femoral artery. The distal left anterior descending artery was cannulated to monitor peripheral coronary pressure. Regional contractile force in the normal left circumflex and potentially ischemic left anterior descending regions was measured with isometric strain gauge arches sewn to the epicardium. Moderate decreases in coronary perfusion pressure averaging 27 mm Hg produced selective ischemia in the myocardium beyond the site of occlusion of the left anterior descending artery. Under these conditions the average increase in peripheral coronary pressure produced by intracoronary injection of isosorbide dinitrate was 9.0 mm Hg, whereas contractile force in the ischemic region increased by 30 percent. The contractile force was unchanged in the normal regions. Therefore, isosorbide dinitrate can dilate coronary collateral vessels and improve contractile force in ischemic areas. Intracoronary injection of nitroglycerin had similar effects. The durations of responses to isosorbide dinitrate and nitroglycerin were remarkably similar: 6.4 and 6.7 minutes, respectively. Although isosorbide dinitrate can directly dilate coronary collateral vessels, its effects are not longer lasting than those of nitroglycerin.

Animals↗
PubMed1976

Coronary steal: its role in detrimental effect of isoproterenol after acute coronary occlusion in dogs.

Using epicardial electrograms others have established that infusion of isoproterenol increases myocardial injury after acute coronary occlusion. To define the contribution of alterations in collateral blood flow to this increased ischemia, isoproterenol was administered to 10 dogs. After pretreatment with practolol in doses that successfully block inotropic but not vascular effects of beta adrenergic stimulants, intracoronary isoproterenol continued to enhance the magnitude of S-T segment elevation in ischemic areas. Thus, vasodilation induced by isoproterenol appears to divert flow from the ischemic area. To test this hypothesis, intracoronary adenosine was given to cause coronary vasodilation without enhancing inotropy. S-T segment elevation at ischemic and adjacent sites was significantly increased. Neither agent had systemic effects, but each increased coronary blood flow while concomitantly decreasing collateral flow as evidenced by a reduction in retrograde coronary flow and peripheral coronary pressure. In addition, adenosine significantly diminished the rate of xenon-133 clearance from the ischemic myocardium. Thus, isoproterenol, in addition to its positive inotropic effect, increases myocardial injury by its vascular action. Collateral blood flow to acutely ischemic myocardium is diminished by the production of a coronary steal. Intravenously administered isoproterenol additionally diminishes collateral flow by decreasing coronary perfusion pressure. It is postulated that any agent that causes either a primary or secondary coronary vasodilation may cause a coronary steal and subsequently enhance myocardial injury.

Adenosine↗
PubMed1976

Double mitral leaflet prolapse: echocardiographic-phonocardiographic correlation.

Ten per cent of all patients referred to the echocardiography laboratory for diagnostic evaluation had mitral valve prolapse. Of these 35 patients, 19 (54 per cent) had prolapse of both the anterior and posterior mitral leaflets. Of the 19 patients, 13 had Type A or midsystolic prolapse, whereas six had Type B or pansystolic prolapse of the mitral leaflets. Simultaneous phonocardiographic examination of the patients revealed either midsystolic click and late systolic murmur, pansystolic murmur, or isolated click and short systolic murmur. There was no apparent correlation between the echocardiographic prolapse pattern and the auscultatory events. One patient with Type A prolapse had no auscultatory abnormalities at the time of the examination. It is suggested that the abnormal sounds may be generated by a redundant mitral leaflet rather than chordae tendineae.

Echocardiography↗
PubMed1976

B-scan ultrasonography in idiopathic hypertrophic subaortic stenosis. Study of left ventricular outflow tract and mechanism of obstruction.

Studies were made with standard time motion and B-scan echocardiography on 48 patients including 5 with idiopathic hypertrophic subaortic stenosis (hypertrophic obstructive cardiomyopathy), undergoing diagnostic cardiac catheterization. The dimensions of the left ventricular outflow (O) and inflow (I) tracts were measured on the B-scan images. The outflow tract was significantly narrowed in idiopathic hypertrophic subaortic stenosis at both end-systole (1-1+/-0-1 cm) and end-diastole (1-3+/-0-1 cm) when compared with the average width in other patients (2-6+/-0-1 and 3-0+/-0-1 cm, at end-systole and end-diastole, respectively) (P less than 0-001) or normal subjects (2-4+/-0-3 and 2-9+/-0-2 cm) (P less than 0-01). Furthermore, the O/I ratio differed significantly in idiopathic hypertrophic subaortic stenosis (0-5+/-0-1 at end-systole and 0-6+/-0-1 at end-diastole) from that in all other groups (1-4+/-0-1 at both end-systole and end-diastole) (P less than 0-005). There was no appreciable change in the width of the outflow tract from mid- to end-systole in the two patients in whom this was examined. The data support the contention that the anterior leaflet of the mitral valve assumes an abnormally anterior position in idiopathic hypertrophic subaortic stenosis. Though the systolic anterior movement of the tip of the anterior leaflet of the mitral valve shown by M-mode echocardiography could not readily be confirmed with B-scans, we believe that the narrowed outflow tract found in the present investigation contributes to the obstruction that occurs in this disease. We suggest that this outflow tract narrowing is probably caused by hypertrophy of the ventricular septum which in itself contributes to the narrowing, but which also displaces the papillary muscles and thus produces abnormal traction on the mitral valve and striking anterior displacement of the valve apparatus.

Adult↗
PubMed1975

Echocardiographic analysis of mitral valve motion after acute myocardial infarction.

To examine the effects of acute myocardial infarction on mitral valve diastolic velocity, echocardiograms were performed in 18 patients on admission, daily in the Coronary Care Unit, and at 3-day intervals during the remainder of hospitalization. These patients were divided into three groups based on the time interval between onset of symptoms and initial echocardiogram. Five of six patients admitted within 5 hours of onset of myocardial infarction had a triphasic response of mitral valve diastolic velocity with a transient rise above initial values, followed by a fall to below initial values, and then a slow rise during recovery. Seven of eight patients admitted 1-2 days after onset of myocardial infarction had a biphasic response, i.e., a fall from initial values and then a slow rise. Four patients admitted later in the course of myocardial infarction had a monophasic response, i.e. low initial velocity followed by a slow recovery. We conclude that in patients with myocardial infarction the mitral valve diastolic velocity following myocardial infarction shows a triphasic response which may appear biphasic or monophasic depending on the interval between myocardial infarction and admission. The temporal pattern of mitral valve diastolic velocity changes may reflect the dynamic alterations of myocardial function and compliance that are occurring after acute myocardial infarction and during the recovery period.

Adult↗
PubMed1975

Main left coronary artery disease. Clinical experience from 1964-1974.

Obstructive lesions of the main left coronary artery (LCA) were demonstrated angiographically in 73 patients, comprising 4.3% of the total population referred to us for diagnostic evaluation of chest pain. Although there were no specific historical or clinical features which could absolutely distinguish this subgroup from the larger population of coronary artery disease patients, 81% (34/42) of the double Master's exercise tests, in which the patient achieved a heart rate of at least 110 beats/min. demonstrated greater than or equal 2 mm R-ST segmental depression. Of the total group of 73, 32 were evaluated during the six-year period from 1964 to 1971 and a preliminary report made in 1972. The diagnosis in the remaining 41 patients was established in the 1/2 year period from 1971 to 1973. The initial 32 patients were seen before the significance of a main LCA lesion was appreciated. In this subgroup there were five deaths at the time of cardiac catheterization. However, in the more recent group improved recognition of patients with possible main LCA disease prior to catheterization has led to a much lower death rate related to diagnostic catheterization. Only one of the last 41 patients undergoing coronary angiography has died. Nineteen patients were managed medically. Of this group 17 were considered to be under the same risk of death as the surgical candidates. Their mortality rate, as high. The risk of hying was 43.6% after 24 months, 51.1% after 36 months, and 73.6% after 42 months of observation. Although the initial surgical experience, using internal mammary artery implants and saphenous venin bypass grafts, was associated with a high mortality, direct revascularization surgery over the last 2 1/2 years has been accomplished with a perioperative mortality of only 6.2%. All deaths in the group of 40 patients receiving elective revasularization with saphenous vein bypass grafts occurred in the first six months following surgery. The risk of dying was 12.5% after six months of observation and was unchanged for the remainder of the follow-up period. After 21 months the difference in survival between the two groups is statistically significant (P less than 0.05). The one late death among the surgical survivors occurred four months after the operative procedure and was related to noncardiovaxcular surgical complications. The surgical survivors have been followed for an average of 27 months. Thus revascularization surgery has improved the prognosis for patients with main LCA disease. We currently advise prompt evaluation for any patient suspected of having this type of obstruction and urgent idrect revascularization surgery if this lesion is demonstrated angiographically.

Adult↗
PubMed1975

Regional myocardial function in idiopathic hypertrophic subaortic stenosis. An echocardiographic study.

To assess regional contractility in idiopathic hypertrophic subaortic stenosis (IHSS), a primary myopathic disorder with documented hyperdynamic ventricular contractions, systolic wall thickening and velocity of contraction of the septum and left ventricular posterior wall were measured in echocardiograms from 16 patients with IHSS and 16 normal subjects. The average thickening of the normal septum and posterior wall was 75.9+/-8.8% and 84.8+/-6.3%, respectively. The posterior wall in IHSS thickened by 75.1+/-6.8%. None of these values differed significantly. However, the increase in thickness of the IHSS septum averaged 22.5+/-2.4%, significantly less than that of either the IHSS posterior wall or the normal septum. Velocity measurements confirmed the impression of diminished septal function. The mean velocity of normal septal contraction averaged 37.0+/-2.3 mm/sec, normal posterior wall 42.3+/-2.0 mm/sec and IHSS posterior wall 55.7+/-3.5 mm/sec, whereas the septum in IHSS contracted at the rate of 26.0+/-2.5 mm/sec. Thus, the IHSS septum contracted significantly more slowly than the normal septum or IHSS posterior wall. However, the posterior wall velocity in IHSS was significantly more rapid than that measured in normal ventricles--perhaps to compensate for the septum. Normalization of all velocities for left ventricular end-diastolic internal diameter did not alter the sifnificance of the results. Consideration of IHSS as an asymmetric myopathy based on prior observations of predominantly septal hypertrophy and distorted septal cellular architecture is now supported by the above evidence of functional left ventricular asymmetry. Although the total left ventricular function in IHSS may be hyperdynamic, regional function is not uniform. The septum appears to be hypodynamic, while the contractile capacity of the posterior wall is increased.

Adolescent↗