Search PubMed⌕ Search

Biomedical subjects

W Grossman

Publications and source records attributed to W Grossman.

At least 181 records · Page 10Linked to original sources
PubMed1979

Inappropriate coronary vasoconstriction in patients with coronary artery disease: a role for nifedipine?

Coronary arterial vasoconstriction, well recognized in Prinzmetal's variant angina, may participate in the pathogenesis of classic angina as well. Several recent studies in patients with obstructive coronary artery disease suggest that apparently spontaneous reductions in coronary blood flow can result in myocardial ischemia and even infarction. Evidence supporting the alpha adrenergic nervous system as a cause of such coronary vasoconstriction is reviewed, particularly the results of provocative testing with the cold pressor stimulus. Upon exposure of the skin to cold, patients with coronary artery disease demonstrate an inappropriate coronary vasoconstrictor response, often sufficient to produce angina. Normal patients, by contrast, show no change in coronary vascular resistance. In patients with a diseases coronary circulation, inappropriate vasoconstriction further restricts myocardial perfusion and appears to be little affected by beta adrenergic blocking agents or nitrates in the usual dosages. Nifedipine has proved effective in preventing coronary arterial spasm in patients with Prinzmetal's angina. Studies currently in progress suggest that it is also effective in blocking inappropriate coronary vasoconstriction in patients with typical angina. Nifedipine may thus be a useful addition to the treatment of ischemic heart disease.

Angina Pectoris, Variant↗
PubMed1979

Right ventricular diastolic pressure in coronary artery disease.

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P less than 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P less than 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P less than 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.

Aortic Valve Stenosis↗
PubMed1979

Myocardial contractile function in aortic stenosis as determined from the rate of stress development during isovolumic systole.

To assess myocardial contractile function in the chronically hypertrophied human left ventricle, the rate of stress development (dsigma/dt) as a function of developed stress (sigmaD) during isovolumic systole was examined. Results for eight patients with aortic stenosis were compared with those for seven subjects with normal left ventricular function and with those for five patients with idiopathic congestive cardiomyopathy. The rate of stress development (dsigma/dt) was nearly identical in patients with aortic stenosis and in normal subjects over a wide range of values of sigmaD but was significantly lower in patients with cardiomyopathy (P less than 0.01 versus control subjects and patients with aortic stenosis). Normal values for dsigma/dt held not only for patients with compensated pressure overload, but also for those patients with aortic stenosis with depressed left ventricular ejection fraction and overt congestive failure. Similar findings were obtained when the first derivative of left ventricular pressure (dP/dt) was examined as a function of developed left ventricular pressure in normal subjects and patients with aortic stenosis or cardiomyopathy. These results indicate that contractile function as characterized by the isovolumic rate of stress development is not necessarily impaired in chronic pressure overload hypertrophy.

Adult↗
PubMed1979

Factors contributing to altered left ventricular diastolic properties during angina pectoris.

Mechanisms involved in the altered left ventricular (LV) diastolic properties during angina were studied in 26 patients with coronary artery disease. Angina was induced by rapid atrial pacing and measurements were made at rest and during angina in the immediate post-pacing period. No changes occurred in heart rate (71 +/- 3 to 73 +/- 3 beats/min, NS) or right ventricular (RV) end-diastolic pressure (10 +/- 1 to 11 +/- 1 mm Hg, NS), while significant increases occurred in LV end-diastolic pressure (17 +/- 1 to 30 +/- 1 mm Hg, p less than 0.01), aortic diastolic pressure (74 +/- 3 to 80 +/- 3 mm Hg, p less than 0.01), coronary sinus blood flow (133 +/- 15 to 212 +/- 32 ml/min, p less than 0.01), and the time constant (T) of LV pressure fall in early diastole (43 +/- 2 to 58 +/- 4 msec, p less than 0.01). Despite the rise in arterial pressure, a significant fall was observed in peak negative dP/dt (1961 +/- 106 to 1751 +/- 80 mm Hg/sec, p less than 0.01). Changes in RV end-diastolic pressure do not explain the increased LV end-diastolic pressure during angina. Increased aortic pressure and coronary blood flow may contribute, but the simultaneous fall in peak negative dP/dt and rise in T suggest that impaired ventricular relaxation is an important factor contributing to the previously demonstrated alteration in LV diastolic properties during angina pectoris.

Angina Pectoris↗
PubMed1979

Physiologic determinants of the electrocardiographic diagnosis of left ventricular hypertrophy.

The relative importance of left ventricular (LV) geometry, wall thickness, and mass on the inscription of left ventricular hypertrophy (LVH) on the ECG was examined in 93 patients; 36 had no LVH on the ECG, 10 had borderline voltage for LVH, and 47 had LVH on the ECG. LV cineangiograms in the right anterior oblique projection were analyzed for LV end-diastolic volume, free wall thickness (h), semiminor radius (R), LV mass index (LVMI), and the geometric relations described by h/R, mass/volume, and h . R. Although mean LVMI was greater in patients whose ECG voltage was either borderline or diagnostic of LVH, increased LVMI also occurred without LVH on the ECG. None of the variables (h, R, h/R or mass/volume) reliably indicated when LVH would be inscribed on the ECG. The product of h . R, however, defined three electrocardiographic groups; all patients with LVH on their ECG had h . R greater than 2.6 cm2. Wall thickening sufficient to result in an increased LV mass did not result in LVH on the ECG unless sufficient concurrent chamber dilatation was present. Thus, a critical geometric relationship resulting from the interplay of wall thickness and chamber dilatation is necessary for LVH to appear on the ECG. This finding is consistent with the solid-angle theory of electrocardiography as it relates to ventricular hypertrophy.

Action Potentials↗
PubMed1979

Low-pressure cardiac tamponade.

An elderly man developed cardiac tamponade from a tuberculous pericardial effusion but without such typical manifestations as pulsus paradoxus and jugular-vein distension. This case illustrates the difficulties in clinical recognition of low-pressure cardiac tamponade, which can develop in the presence of dehydration and hypovolemia. The hemodynamic factors that account for this phenomenon are discussed.

Aged↗
PubMed1978

Hemodynamic assessment of amrinone. A new inotropic agent.

Amrinone, a new bipyridine derivative, exerts a positive inotropic action in experimental preparations and is effective when administered orally to dogs. To assess its immediate effects in man, we studied by cardiac catheterization the hemodynamic responses to amrinone (1.85 to 3.5 mg per kilogram given intravenously) in eight patients with congestive heart failure already receiving full doses of digitalis. the following statistically significant (P less than 0.01) effects were noted: cardiac index increased from a mean +/- 1 S.D. of 1.8 +/- 0.3 to 2.6 +/- 0.3 liters per minute per square meter; peak rate of left ventricular pressure rise rose from 849 +/- 233 to 1206 +/- 456 mm Hg per second; left ventricular end-diastolic pressure fell from 25 +/- 9 to 14 +/- 7 mm Hg; pulmonary-capillary pressure fell from 28 +/- 8 to 15 +/- 4 mm Hg; and right atrial pressure fell from 12 +/- 6 to 7 +/- 5 mm Hg. Mean heart rate was unchanged, and aortic mean pressure declined slightly (86 +/- 10 to 80 +/- 7 mm Hg, P less than 0.025). No toxicity was observed. Amrinone, whose mechanism of action has not yet ben defined, warrants further study as a possible treatment for heart failure.

Drug Evaluation↗
PubMed1978

Extrinsic compression of the heart by tumor masquerading as cardiac tamponade.

A patient with known intrathoracic tumor presented with findings suggestive of cardiac tamponade. At cardiac catheterization, the entire heart was displaced superiorly and anteriorly by the tumor mass, and this accounted for the observed cardiac hemodynamics, in the absence of discernible pericardial effusion.

Cardiac Tamponade↗
PubMed1978

Effusive-constrictive hemodynamic pattern due to neoplastic involvement of the pericardium.

Eight patients with metastatic malignancy of the pericardium who demonstrated the hemodynamics of subacute effusive-constrictive pericarditis were studied. All patients had clinical evidence of cardiac tamponade due to malignant pericardial effusion and were referred for therapeutic pericardiocentesis. In six in whom pericardiocentesis was successfully performed, right atrial pressure remained elevated after pericardiocentesis and return of the intrapericardial pressure to zero; in these patients, hemodynamic data were initially compatible with tamponade but suggested constriction after removal of the pericardial fluid. In the remaining two patients, echocardiography revealed pericardial fluid, but attempted pericardiocentesis was unsuccessful. In these two patients, the hemodynamic data suggested pericardial constriction; subsequent pathologic examination revealed neoplastic involvement of the visceral pericardium. Thus, subacute effusive-constrictive pericarditis, previously recognized as a complication of tuberculosis or mediastinal radiation, may also be due to metastatic malignancy. The syndrome can readily be demonstrated when right heart catheterization is performed in conjunction with pericardiocentesis.

Cardiac Tamponade↗