Inadequate Myocardial Perfusion Research Articles

Subendocardial infarction in two young boys

Two cases of subendocardial infarction noted at autopsy in young boys are reported. Both patients were resuscitated and maintained on ventilation following significant periods of cardiac arrest. Presumably the infarct occurred at the time of arrest, secondary to inadequate myocardial perfusion, and became visible at autopsy because both children were maintained on assisted ventilation long enough for the gross and microscopical changes to develop. The significance of this phenomenon for survivors of successful post cardiac arrest resuscitation is discussed.

Dynamic myocardial scintigraphy with 123I-labeled free fatty acids in patients with myocardial infarction.

We have already shown that myocardial imaging properties of radio-iodinated long-chain free fatty acids (123I-FFA) and thallium 201 (201TI) are comparable in detecting areas of inadequate myocardial perfusion (van der Wall et al. 1980). Besides confirming our earlier observations, the present study tests the potential of 123I-FFA, hexadecenoic acid (123I-16-ha), and heptadecanoic acid (123I-17-H degree A), in assessing regional myocardial metabolism in 30 patients within a week of proven myocardial infarction. The clearance rates (t1/2) of FFA were estimated from mono-exponential time-activity curves, obtained by external detection over infarcted and normally perfused areas during a 30-min period after IV administration of 3-5 mCi 123I-16-HA or 123I-17-H degree A. Six normal subjects served as controls. The t1/2 values in the infarcted areas were found to be significantly lower (18.5 +/- 2.1 min; mean +/- SD, with 123I-16-HA and 16.8 +/- 3.5 min with 123I-17-H degree A) than in non-infarcted areas (34.0 +/- 8.4 min with 123I-16-HA and 34.8 +/- 7.7 with 123I-17-H degree A). The t1/2 values in the control group (27.5 +/- 3.0 min with 123I-17-H degree A) were not significantly different from values found in non-infacted areas in the patient group. Our findings of faster FFA turn-over rates in infarcted tissue are in contrast to previous studies, which have shown prolonged turn-over rates in reversibly ischaemic myocardiu. We conclude that the study of turn-over rates of FFA provides a means to distinguish normally perfused, reversibly ischaemic and irreversibly ischaemic myocardium.

Effect of renal hypertension and left ventricular hypertrophy on the coronary circulation in dogs.

SUMMARY The purpose of this study was to investigate the effects of pressure-induced left ventricular hypertrophy on the coronary circulation. Hypertrophy was induced by single-kidney renal vascular hypertension in 12 dogs. Ventricular mass in the dogs with hypertrophy was about 50% greater than in 11 controls. A third group of six dogs, with a similar amount of left ventricular hypertrophy but normal blood pressure after repair of the renal artery stenosis, also was studied. Total and regional myocardial blood flow was measured with radioactive microspheres at rest, during pacing at a rate of 200 (in the control and hypertensive dogs), and during maximal vasodilation induced with adenosine (4.7 juM/kg x min). Results were as follows. (1) Regional distribution of coronary flow was normal at rest in dogs with hypertension and left ventricular hypertrophy and in dogs with hypertrophy alone. (2) Pacing caused at 16% decrease in the endocardial-epicardial perfusion ratio only in the hypertrophied ventricles of the hypertensive dogs. (3) During maximal coronary vasodilation, the coronary vascular resistance of the entire left ventricle was no different among the three groups: the controls, the hypertensive dogs with left ventricular hypertrophy, and the normotensive dogs with left ventricular hypertrophy (0.14 ± 0.02 SEM, 0.16 ± 0.02, and 0.14 ± 0.02 mm Hg/ml x min, respectively). The use of the minimal coronary vascular resistance measured during maximal vasodilation as an index of the functional cross-sectional area of the coronary bed suggests that the cross-sectional area does not increase with hypertrophy. This failure of the cross-sectional area of the coronary bed to increase commensurate with the degree of hypertrophy is due to an anatomical or architectural alteration of the relationship between the coronary bed and the cardiac muscle and is not due to a functional alteration caused by hypertension alone. Thus, the hypertrophied ventricle may be at greater risk of ischemic injury. CLINICAL SUSPICION of inadequate myocardial perfusion due to pressure-induced hypertrophy of the left ventricle has existed for many years.'" 4 Although several investigators have found that blood flow per unit mass of the myocardium of hypertrophied ventricles is normal, 5 " 8 the decreases in capillary density described in hypertrophied myocardium 9 ''" and preliminary reports suggesting relative endocardial hypoperfusion"' 12 imply that the regional distribution of coronary flow may be abnormal in hypertrophied ventricles and that such ventricles might be at increased risk for ischemic injury. To study possible physiological limitations of the coronary circulation in pressure-induced hypertrophy, we produced single-kidney renal vascular hypertension in mongrel dogs. After left ventricular hypertrophy developed, we assessed regional myocardial perfusion at rest, during pacing, and during maximal vasodilation produced by an iv adenosine infusion. We also studied another group of dogs at rest and during adenosine infusion which had ventricular hypertrophy induced in the same manner but were rendered normotensive by repair of the renal artery stenosis. In this manner we were able to isolate the effects of hypertrophy

Angina with "normal coronary arteries". A misnomer.

Angina with "normal coronary arteries" might best be thought of as "angina with coronary dysfunction". It seems likely that this syndrome is due to inadequate regional myocardial perfusion with manifestations similar to those seen when ischemia results from occlusive coronary artery disease. The prognosis of the disorder is favorable, but occasional catastrophic events occur. It appears likely that maldistribution of perfusion results from dynamic changes affecting proximal, and perhaps distal coronary vessels, potentially mediated by vasoactive substances released from platelets precipitating or exacerbating coronary arterial spasm. Clarification of the pathogenesis of the syndrome should permit implementation of more effective therapy and prevention of the rare malignant sequelae of this disorder.