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Biomedical subjects

A N DeMaria

Publications and source records attributed to A N DeMaria.

At least 199 records · Page 11Linked to original sources
PubMed1979

Left ventricular thrombi identified by cross-sectional echocardiography.

We studied 25 patients with anterior myocardial infarction and two with congestive cardiomyopathy to evaluate two-dimensional echocardiography in the diagnosis of left ventricular thrombi. Five coronary patients had systemic emboli. Four of these patients manifested apical filling defects on cineangiogram, while a levophase cine was equivocal for clot in the fifth patient. Neither echocardiography nor cineangiography visualized ventricular thrombi in the nonembolus coronary patients. Echoes from a distinct apical mass, however, were visualized in all five patients in the embolus group by two-dimensional echocardiography at the cardiac apex. Apical thrombi were confirmed in all four patients in the embolus group undergoing surgery. The irregular configuration of recent thrombi in the coronary patients differed from the circumscribed appearance of chronic thrombi in the cardiomyopathy patients on two-dimensional echocardiogram. Thus, two-dimensional echocardiography can be used to detect and characterize left ventricular thrombi.

Adult↗
PubMed1978

Hemodynamic assessment of the new aortic Carpentier-Edwards bioprosthesis.

Although glutaraldehyde-preserved porcine aortic Hancock heterografts have lower thromboembolism incidence than mechanical aortic valves, Hancock xenografts provide less functional aortic outflow orifices and thereby greater transvalvular gradients than mechanical prostheses. The newly developed aortic Carpentier-Edwards porcine heterografts comprise a thin-walled Elgiloy flexible metal stent covered with Teflon which provides somewhat wider internal orifices than aortic Hancock valves of the same external annulus diameter. Since aortic Carpentier-Edwards xenografts have not been clinically evaluated previously, the present study assessed cardiac function and heterograft performance (1.7 months postoperation) and clinical status (4.2 months postoperation) of 19 patients with severe aortic stenosis and/or regurgitation prior to surgery. Left ventricular end-diastolic pressures decreased (17 to 9 mm Hg), cardiac index remained normal, and clinical symptomatology diminished markedly. Mean peak transxenograft systolic pressure was only 16 mm Hg (valve area 1.73 cm2), without meaningful regurgitation. Thus aortic Carpentier-Edwards bioprostheses provide generally excellent heterograft function which appears more favorable than previous reports of Hancock xenografts.

Adolescent↗
PubMed1978

Hemodynamic evaluation in acute myocardial infarction.

Bedside right heart catheterization in patients with acute myocardial infarction and hemodynamic dysfunction provides a rational basis for therapy aimed at maximizing cardiac performance and limiting infarct size. Readily performed and associated with minimal risk, this diagnostic approach is primarily indicated when myocardial infarction is associated with evidence of hemodynamic dysfunction. It affords precise information on cardiac performance and prognosis, allows identification of specific complications such as ventricular septal defect and acute mitral regurgitation, and is of critical importance in selection of therapy. Hemodynamic monitoring is also essential for safe, effective application of certain forms of treatment such as vasodilator therapy for the failing ventricle.

Acute Disease↗
PubMed1978

Alterations in ventricular mass and performance induced by exercise training in man evaluated by echocardiography.

Few data are available regarding the effects of exercise training upon cardiac structure and performance in man. We evaluated the echograms of 24 normals before (PRE) and after (POST) 11 weeks of endurance exercise training. Conditioning consisted of a walk-jog-run protocol at 70% maximal heart rate for one hour four days per week. Training reduced heart rate and increased maximal duration and estimated oxygen consumption of treadmill exercise. Compared to PRE, the echogram in the POST training period revealed an increased left ventricular (LV) end-diastolic dimension (EdD), a decreased end-systolic dimension (EsD) and thus an increased stroke volume (EdD3-EsD3) and shortening fraction (EdD-EsD)/EdD). Cardiac output (CO) and peripheral vascular resistance (BP/CO X 80) were identical PRE and POST conditioning. Importantly, an increase in mean fiber shortening velocity was observed POST training as were increases in LV wall thickness, ECG voltage of S in V1 + R in V5, and LV mass. Thus endurance training was accompanied by increases in both LV dimension and mass as well as LV shortening fraction and contraction velocity as observed by echocardiogram.

Adult↗
PubMed1978

Vasodilators in myocardial infarction: rationale and current status.

While digitalis and diuretics constitute conventional therapy of congestive heart failure due to acute myocardial infarction, systemic vasodilator drugs offer an innovative approach of decreasing left ventricular systolic wall tension (afterload) by reducing aortic impedance and/or by reducing cardic venous return. Thus, vasodilators increase lowered cardiac output by diminishing peripheral vascular resistance and/or decreasing increased left ventricular end-diastolic pressure (ventricular preload) by reducing venous tone. Concomitantly, there is a reduction of myocardial oxygen demand thereby potentially limiting infarct size and ischaemia. The vasodilators produce disparate modifications of cardiac function depending on their differing alterations of preload versus impedance: nitrates principally cause venodilatation (decrease left ventricular end-diastolic pressure); sodium nitroprusside, phentolamine and prazosin produced relatively balanced arterial and venous dilatation (decrease left ventricular end-diastolic pressure while increasing cardiac output, provided upper limits of normal left ventricular end-diastolic pressure are maintained); and hydrallazine solely effects arteriolar dilatation (increases cardiac output). Combined sodium nitroprusside and dopamine therapy synergistically enhances cardiac output and decreases left ventricular end diastolic pressure. In addition, sodium nitroprusside is aided by mechanical counterpulsation which sustains myocardial perfusion pressure in acute myocardial infarction.

Animals↗