Acute coronary insufficiency: Pathological and physiological aspects

Horn, Henry; Field, Leonard E.; Dack, Simon; Mastér, Arthur M.

doi:10.1016/0002-8703(50)90150-5

Cited by 89 publications

(17 citation statements)

References 17 publications

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“…• Patchy necrosis and fibrosis of left ventricular subendocardial muscle occur in patients whose coronary arteries are normal or narrowed by atheroma (1)(2)(3)(4)(5). These changes could be due to a discrepancy between myocardial oxygen demand and available blood supply in subendocardial muscle, but this hypothesis has not yet been tested in 68 BUCKBERG, FIXLER, ARCHIE, HOFFMAN no obstruction, and diastolic intramyocardial pressure is probably similar to intracavitary pressure (12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Experimental Subendocardial Ischemia in Dogs with Normal Coronary Arteries

Buckberg

Fixler

Archie

et al. 1972

Circulation Research

809

403

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Subendocardial ischemia without anatomic coronary artery obstruction may result from a discrepancy between metabolic needs and available blood supply. We studied this in open-chest anesthetized dogs and measured pressures in aorta and left ventricle (LV), phasic left coronary arterial blood flow (CBF) by electromagnetic flowmeter, total CBF and LV subendocardial (endo) and subepicardial (epi) flow with radioactive microspheres 8-10fi in diameter. Since LV subendocardial flow is mainly or entirely diastolic, it should depend on coronary driving pressure and duration of diastole (i.e., the area between aortic and left ventricular diastolic pressures). This diastolic pressure time index (DPTI) was varied by opening arteriovenous fistulas to lower aortic diastolic pressure, constricting the ascending aorta to raise LV diastolic pressure and pacing to shorten diastole. Myocardial oxygen needs were estimated from the tension time index (TTI). Normal endo-epi flow ratios per gram (1:1) fell to 0.1:1 with these procedures and paralleled a fall in diastolic flow fraction (often nearly zero) and postischemic coronary reactive hyperemic responses. These changes occurred despite normal or raised mean CBF and 300-500% increase in systolic CBF. The altered flow ratios were best predicted by relating them to the ratio of DPTI (supply) to TTI (demand). KEY WORDSregional coronary blood flow arteriovenous fistula subepicardial flow aortic constriction radioactive microspheres ventricular pacing reactive hyperemia tension time index phasic coronary blood flow diastolic pressure time index• Patchy necrosis and fibrosis of left ventricular subendocardial muscle occur in patients whose coronary arteries are normal or narrowed by atheroma (1-5). These changes could be due to a discrepancy between myocardial oxygen demand and available blood supply in subendocardial muscle, but this hypothesis has not yet been tested in

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Section: Introductionmentioning

confidence: 99%

Experimental Subendocardial Ischemia in Dogs with Normal Coronary Arteries

Buckberg

Fixler

Archie

et al. 1972

Circulation Research

809

403

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“…Such a redistribution of myocardial blood flow possibly is the result of a transmural gradient of intramyocardial pressure during systole. Therefore, the increased vulnerability of the subendocardium to ischemic coronary artery disease results from reduced blood flow to this tissue during part of the cardiac cycle (3)(4)(5).…”

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confidence: 99%

Distribution of the Coronary Blood Flow across the Canine Heart Wall during Systole

Downey

Kirk

1974

Circulation Research

140

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The transmural distribution of left coronary blood flow during systole was studied by measuring the myocardial uptake of a bolus of M Rb introduced into the coronary circulation when the perfusion was limited to the periods of systole. The measurement revealed a transmural gradient of systolic blood flow with a flow rate in the outer fourth of the left ventricle about twice that in the inner fourth. A gradient of flow encompassing all depths of myocardial tissue revealed that intramyocardial pressure during systole was not sufficient to completely collapse the vessels and, therefore, did not exceed intraventricular pressure. The results of this experiment indicate that intramyocardial pressure limits coronary blood flow through a vascular sluice mechanism. • Contraction of the heart inhibits coronary blood flow (l). An earlier study (2) has demonstrated that systole reduces blood flow in the myocardial layers near the endocardium more than it reduces blood flow in the layers near the epicardium. Such a redistribution of myocardial blood flow possibly is the result of a transmural gradient of intramyocardial pressure during systole. Therefore, the increased vulnerability of the subendocardium to ischemic coronary artery disease results from reduced blood flow to this tissue during part of the cardiac cycle (3-5).To date the redistribution of coronary blood flow during systole has not been adequately described quantitatively. No direct measurements of this redistribution have been reported. Furthermore, it has not been possible to calculate the magnitude of the redistribution during systole, because (1) the physical process whereby intramyocardial pressure influences coronary blood flow has not been postulated and (2) the reported values of intramyocardial pressure disagree considerably (6-10).In the present study a technique has been developed to determine the transmural distribution of Since ventricular pressure falls to near zero during diastole, forward flow and thus the delivery of the tracer was confined to the periods of systole. In light of this technique, a theoretical model that quantitatively describes the relationship between intramyocardial pressure and coronary blood flow is presented in this paper. MethodsFive mongrel dogs of either sex (13-16.5 kg) were anesthetized with sodium pentobarbital (30 mg/kg, iv); additional anesthesia was administered as needed. The hearts were exposed by a left thoracotomy in the fourth intercostal space, and electrocautery was used to promote hemostasis. The dogs were ventilated with a positive-pressure respirator while their chests were open. Heparin (10,000 units, iv) was administered to prevent clotting in the perfusion tubing.Aortic blood pressure was obtained from a stiff vinyl catheter passed through a femoral artery into the thoracic aorta, and perfusion pressure was recorded from a branch of the perfusion circuit near the coronary cannula. Ventricular pressure was measured by another vinyl catheter passed through the left carotid artery into the left ve...

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“…• Histological evidence indicates that the subendocardial layers of the left ventricle are vulnerable to ischemia: areas of necrosis in the subendocardium are greater than they are in the epicardium in transmural infarction (1) and in coronary insufficiency (2), suggesting that antegrade coronary blood flow in the subendocardial layers is less than that in the epicardium because of the proximity of the former to intracavitary left ventricular pressure (3). Initial studies showed a gradient in tissue pressure with systolic pressure in the subendocardium exceeding that in the left ventricular cavity and suggested that systolic extravascular compression could be a significant feature in the transmural distribution of coronary blood flow (3).…”

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confidence: 99%