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Biomedical subjects

E Braunwald

Publications and source records attributed to E Braunwald.

At least 397 records · Page 22Linked to original sources
PubMed1978

Value of the QRS complex in assessing left ventricular ejection fraction.

The relation between electrocardiographic findings and the angiographic left ventricular ejection fraction and the augmented ejection fraction after a premature ventricular contraction was investigated in 73 patients with documented chronic coronary artery disease. The patients were separated into four groups according to the presence or absence of abnormal Q waves. Twenty-four patients had diaphragmatic myocardial infarction, 21 had anterior myocardial infarction, 15 had both and 13 had no myocardial infarction. There was no statistically significant differences in cardiac index, left ventricular end-diastolic pressure or number of coronary vessels showing critical narrowing in the four groups. The sum of R waves (in mv) in leads aVL, aVF and V1 to V6 (sigmaR) was correlated with the ejection fraction (EF) and the augmented ejection fraction (EFa). EF in percent = 6.6 sigmaR mv + 9.4 (no. =73, r = 0.61); and EFa in percent = 8.6 sigmaR mv + 11.0 (no. = 73, r = 0.77). Among patients with sigmaR of less than 4.0 mv, augmented ejection fraction was less than 0.45 in 73 percent; among patients with sigmaR of 4.0 mv or more the augmented ejection fraction was greater than 0.45 in 93 percent (P less than 0.001). Thus, the sigmaR, calculated from six precordial and two augmented leads in patients with chronic coronary artery disease, correlated with both ejection fraction and augmented ejection fraction. The electrocardiogram in patients with coronary artery disease may prove useful as a simple, readily available and noninvasive guide in the assessment of left ventricular function in patients with coronary artery disease.

Blood Pressure↗
PubMed1978

A method for demonstrating the efficacy of interventions designed to limit infarct size following coronary occlusion: beneficial effect of hyaluronidase.

In order to measure the protective effect of interventions following coronary artery occlusions in dogs, the creatine kinase activity of myocardial tissue was assayed after 24 h and related to the myocardial blood flow of that tissue measured with 85Sr labelled microspheres injected 15 min after occlusion. This assay showed normal levels when flow exceeded 50 cm3.min-1.100 g-1. In myocardium with flow reduced to 0 to 15 cm3. min-1.100g-1, creatine kinase activity was 7.6 +/- 0.6 IU.mg-1 protein in control dogs and 13.1 +/- 1.8 IU.mg-1 protein (P less than 0.01) in dogs given 500 NF units.kg-1 of hyaluronidase 20 min after occlusion. Where myocardial blood flow was reduced to 16 to 50 cm3. min-1. 100g-1, creatine kinase activity was increased from 14.1 +/- 1.1 to 20.5 +/- 1.4 IU.mg-1 protein by hyaluronidase. This method therefore assesses ischaemic damage independent of electrophysiological measurements and confirms myocardial preservation by hyaluronidase.

Animals↗
PubMed1978

Extent of utilization of the Frank-Starling mechanism in conscious dogs.

The extent to which an increase in preload increases left ventricular (LV) end-diastolic (ED) diameter (D) was studied in seven conscious dogs instrumented with ultrasonic D transducers and miniature LV pressure (P) gauges. Preload was elevated by three techniques: 1) volume loading with saline infusion, 2) induction of global myocardial ischemia by constricting the left main coronary artery, and 3) infusion of methoxamine. These three interventions increased LVEDP to over 30 mmHg from a control of 10 +/- 1 mmHg. With volume loading, LVEDD rose by only 1.55 +/- 0.39 mm from a control of 44.08 +/- 1.08 mm; with ischemia LVEDD rose by only .96 +/- .29 mm from a control of 42.55 +/- 2.18 mm, while with methoxamine LVEDD rose by only 1.34 +/- 0.38 mm from a control of 43.89 +/- 2.07 mm. In contrast, in the open-chest, anesthetized dog, LVEDD was greatly reduced and volume expansion resulted in a profound increase in LVEDD. Thus, the Frank-Starling mechanism is not an important controlling mechanism in the normal, reclining, conscious animal, since LVEDD appears to be near maximal at rest and does not increase substantially despite striking increases in LVEDP.

Animals↗
PubMed1978

Hemodynamic effects of intravenous sodium nitroprusside in the conscious dog.

The hemodynamic effects of 7 min i.v. sodium nitroprusside (NP) were studied in conscious dogs previously instrumented for measurement of arterial pressure, cardiac output, regional blood flow distribution, left ventricular (LV) pressure, and internal dimensions. Nitroprusside, 25 microgram/kg/min, reduced mean arterial pressure by 23 +/- 3%. Cardiac output increased initially by 39 +/- 7% and returned toward control by the end of the infusion. Regional blood flows increased initially; the relative rise was greatest in the coronary (+ 225 +/- 39%), intermediate in the mesenteric (+ 98 +/- 23%) and iliac (+ 38 +/- 6%), and least in the renal (+ 10 +/- 3%) bed. By the end of the infusion period the vasodilation was unchanged in the iliac bed, less intense in the coronary and mesenteric, while in the iliac bed, blood flow was reduced and resistance was actually increased by 33 +/- 11% above control. A generalized vasonconstriction ensued after cessation of infusion. In contrast, when the drug was administered intra-arterially to the iliac bed, arterial pressure did not fall and only iliac vasodilation was observed. Peak cardiac effects were characterized by increases in heart rate and LV dP/dt, along with marked reduction in LV end-systolic diameter (- 13 +/- 2%), and in end-diastolic diameter (-17 +/- 2%) and pressure. LV end-diastolic diameter fell even heart rate was maintained at a constant rate by pacing. Thus, in the conscious dog, NP reduced LV dimensions substantially, while inducing changes in peripheral beds. The differences in these effects depend on interactions between the direct effects of NP and the opposing effects of reflex adjustments which appear sufficiently powerful to result in net constriction of the iliac bed late during the infusion.

Animals↗
PubMed1978

Mummification of the infarcted myocardium by high dose corticosteroids.

There is evidence that glucocorticoids reduce infarct size but their use in myocardial infarction remains controversial because of their potential adverse effects on healing of the infarct. To investigate the healing process, rats received either four parenteral doses of 50 mg/kg of methylprednisolone (MP) or saline 5 min, 3,6 and 24 hr after coronary occlusion and their hearts were examined by light and electron microscopy 48 hr and seven days after occlusion. At 48 hr, in five untreated rats, only 12 +/- 7% of injured myocytes showed the persistence of striations and a relatively intact sarcolemma despite loss of nuclei and hence appeared "mummified" whereas in six MP-treated rats 72 +/- 8% of myocytes exhibited this appearance (P less than 0.001). In treated rats there were fewer phagocytes than in controls. At seven days, in seven MP-rats, mummified cells were still more prominent than in five untreated rats and there were fewer phagocytes and less collagen. In conclusion, high dose of MP delays the inflammatory process and retards the disintegration of necrotic myocytes, resulting in impaired healing.

Animals↗
PubMed1978

The prognostic implications of acute myocardial infarct scintigraphy with 99mTc-pyrophosphate.

The predictive value of the myocardial scintigraphy with 99mTc-pyrophosphate was studied in 100 patients admitted to the coronary care unit with suspected acute myocardial infarction. None of the 21 patients with normal scintigrams had acute myocardial infraction by other criteria. Fifty-five percent of patients with diffuse uptake (pattern B), 73% of patients with focal uptake (pattern C) and all patients with intense focal uptake (pattern D) and massive uptake (pattern E) had acute infarction. The complication rate in the hospital and after discharge (mean followup: 6.1 months) for patients with pattern E was 88% compared to 42% for D, 30% for C, 36% for B and 10% for patients with normal scintigrams (A). For patients with acute infarction with patterns C, D and E, the complication rate rose with increasing size of the myocardial uptake of 99mTc-pyrophosphate. In addition to its diagnostic potential, scintigraphy provides prognostic information which is useful for patient triage and for therapeutic decisions early in the evolution of the infarct.

Angina Pectoris↗
PubMed1978

Long-term preservation of ischemic myocardium in the dog by hyaluronidase.

The administration of hyaluronidase is a promising intervention to protect the ischemic myocardium in man, but evidence of the extent to which it may reduce the ultimate size of an infarct is not well-defined. Hence, open chest, anesthetized dogs were randomized into 10 control dogs which received saline and eight treated dogs which received three doses of hyaluronidase (500 NF units/kg I.V.) at 15 minutes, 2 hours and 24 hours after occlusion of the left anterior descending coronary artery (CAO). Regional myocardial blood flow (RMBF) assessed by the microsphere technique was measured 12 minutes after CAO. The chest was then closed and the dogs were allowed to recover. Twenty-one days after CAO, the hearts were excised, divided into 1 cm thick slices and incubated in triphenyl tetrazolium chloride. Infarct size was then determined by planimetry. The left ventricular myocardium was divided into multiple samples for RMBF analysis. In control dogs 23.2 +/- 2% of the left ventricle was infarcted, compared to only 9 +/- 2.8% (P less than 0.001) in hyaluronidase-treated dogs. RMBF in noninfarcted myocardium directly adjacent to the infarct was similar to that in the normal zone remote from the infarct in the control dogs; however, in the hyaluronidase-treated dogs, blood flow in the myocardium adjacent to the infarct was significantly reduced to 68% of normal (P less than 0.01) in the outer myocardial wall and to 86% of normal (P less than 0.02) in the inner myocardial wall, which indicates that this tissue, at least in some part, was in jeopardy, but was salvaged by hyaluronidase. Epicardial electrocardiographic data showed that three weeks after CAO, Q waves were less frequent and smaller in hyaluronidase compared to untreated dogs. Preservation of the frequency and magnitude of R waves was greater in the hyaluronidase-treated group at three weeks. We conclude that hyaluronidase resulted in long-term preservation of the ischemic myocardium.

Animals↗
PubMed1978

Initial myocardial adjustments to brief periods of ischemia and reperfusion in the conscious dog.

The changes in left ventricular (LV) dynamics induced by brief periods of ischemia (100 seconds) and subsequent reperfusion were analyzed in conscious dogs. Global LV ischemia, induced by partially occluding the left main coronary artery, reduced LV flow homogeneously and impaired LV function as reflected by decreases in LV stroke "work" (89 +/- 4% M +/- SE), systolic shortening (72 +/- 4%), velocity of shortening (56 +/- 6%), LV systolic pressure (34 +/- 5%), and dP/dt (59 +/- 6%). Regional LV ischemia, induced by occluding either the left circumflex or anterior descending coronary artery completely, reduced flow to the ischemic segment (82 +/- 3%) while decreasing segment work (96 +/- 5%), shortening (82 +/- 3%), and velocity of shortening (70 +/- 5%), with minimal depression of overall LV function. In both groups the extent of shortening was reduced more rapidly and greater (P less than 0.01) than shortening velocity. Moreover, with localized ischemia, segment work was reduced more (P less than 0.01) than shortening. With reperfusion, a transient overshoot in function above preischemic control levels was observed in both groups (global work increased by 60 +/- 12% and regional work by 28 +/- 4% above control). This overshoot was not dependent on adrenergic mechanisms, but was prevented by inhibiting reactive hyperemia. Thus myocardial ischemia induces a dissociation between extent and rate of myocardial shortening. A further dissociation between shortening and work is apparent with regional ischemia. After reperfusion there is a transient overshoot in function which appears to be dependent upon the associated reactive hyperemia.

Animals↗
PubMed1978

Long-term preservation of ischemic myocardium after experimental coronary artery occlusion.

The results of experiments with indirect methods have suggested that various interventions reduce infarct size after coronary artery occlusion. To determine and quantify directly both the short- and long-term effects of several interventions on myocardial salvage without relying on indirect methods, the left coronary artery was occluded in 880 rats; they were then given either no treatment or one of the following interventions: (a) hyaluronidase, an enzyme that hydrolyzes interstitial glycoproteins, 1,500 National Formulary (NF) U/kg i.v. 5 min and 24 h after occlusion; (b) cobra venom factor, a protein that depletes the third component of complement, 20 U/kg i.v. 5 min after occlusion; (c) a glucocorticoid: hydrocortisone, 50 mg/kg i.v. 5 min after occlusion; or the five-fold more potent methylprednisolone (MP): (i) 50 mg/kg i.v. 5 min after occlusion or (ii) 50 mg/kg i.v. 5 min after occlusion followed by 50 mg/kg i.m. 3, 6, and 24 h after occlusion; or (d) reserpine, an agent that depletes the heart of catecholamines, 0.5 mg/kg i.m. once on each of the 3 days before occlusion. The animals were sacrificed either 2 days after occlusion, i.e., at the time of peak necrosis, or after 3 wk, i.e., after the infarct was completely healed. The amount of preserved myocardium was then assessed by two independent techniques: planimetric measurement of serial histologic sections and creatine kinase activity of the whole left ventricle. The amount of normal myocardium preserved at 21 days postocclusion was significantly increased, by 22.3+/-7.8% (P < 0.025) after the administration of hyaluronidase, by 25.3+/-5.8% (P < 0.005) after cobra venom factor, by 14.5+/-6.9% (P < 0.05) after hydrocortisone, by 20.8+/-8.2% (P < 0.025) after the single dose of MP, by 20.9+/-3.9% (P < 0.001) after the four doses of MP, and by 10.2+/-3.7% (P < 0.05) as a result of pretreatment with reserpine. The four doses of MP significantly thinned the infarct-by 25.6+/-2.9% (P < 0.001)-and although ventricular rupture did not occur, the intervention caused distension of the left ventricle as a result of stretching of the infarcted tissue during scar formation. Thus, myocardium acutely jeopardized by ischemia can be preserved on a long-term basis.

Animals↗