Transmural distribution of myocardial blood flow and of coronary reserve in canine left ventricular hypertrophy

Holtz, J.; Restorff, W. v.; Bard, Philip; Bassenge, E.

doi:10.1007/978-3-642-85299-2_31

Cited by 14 publications

(37 citation statements)

References 11 publications

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“…Moreover, in contrast to the results ofthe present study, coronary vascular adjustments to exercise of the hypertrophied left ventricle appear to be largely normal (21,22,(26)(27)(28). Although slight degrees of relative endocardial underperfusion during exercise have been reported (21,22,28), similar changes were observed in the non-hypertrophied control group (22,28). One possible explanation for the divergent results between these studies and the present study is the difference in the ventricle being subjected to the chronic pressure overload.…”

Section: Influence Of Perfusion Pressure On Coronary Vascular Responscontrasting

confidence: 99%

“…Whereas RV hypertrophy is characterized by a marked increase in blood flow per gram of ventricle at rest (1), blood flow to the hypertrophied left ventricle has been shown to be either modestly reduced (16)(17)(18)(19), unchanged (20)(21)(22)(23)(24), or only slightly increased (25). Moreover, in contrast to the results ofthe present study, coronary vascular adjustments to exercise of the hypertrophied left ventricle appear to be largely normal (21,22,(26)(27)(28).…”

Section: Influence Of Perfusion Pressure On Coronary Vascular Responscontrasting

confidence: 94%

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Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Murray¹,

Vatner²

1981

J. Clin. Invest.

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A B S T R A C T Measurements of right coronary artery blood flow, aortic and right ventricular (RV) pressures and heart rate were radiotelemetered during strenuous, spontaneous exercise in normal dogs and dogs with severe RV hypertrophy induced by chronic (5-6 mo) pulmonary artery stenosis. With fixed pulmonic stenosis, dogs with RV hypertrophy exhibited a decrease (P < 0.01) in arterial pressure during exercise. Under these conditions, exercise increased right coronary artery blood flow and decreased right coronary vascular resistance less (P < 0.05) in dogs with RV hypertrophy compared with normal. This attenuated response of right coronary artery blood flow of dogs with RV hypertrophy was not observed when arterial pressures remained at preexercise values during exercise. However, regardless of changes in arterial pressures during exercise, all dogs with RV hypertrophy demonstrated a striking postexercise coronary hyperemia (P < 0.01), suggesting a perfusion deficit of the hypertrophied right ventricle during exercise. These results imply a fundamental defect in the ability of the coronary circulation of the severely hypertrophied right ventricle to provide sufficient nutrient supply in the face of elevated metabolic demands of exercise.

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Section: Influence Of Perfusion Pressure On Coronary Vascular Responscontrasting

confidence: 99%

Section: Influence Of Perfusion Pressure On Coronary Vascular Responscontrasting

confidence: 94%

Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Murray¹,

Vatner²

1981

J. Clin. Invest.

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“…6 If minimal vascular resistance is increased by hypertrophy to a similar degree in different layers of the left ventricle, as in our studies, then maximal vasodilation at a given myocardial load would not only occur sooner than normal in all layers but would still take place first in the subendocardial muscle. Recently, Holtz et al 23 banded the ascending aorta in puppies aged 6 weeks and studied them in the conscious state at 1 year of age when the left ventricles were 87% heavier than in controls. They found that subendocardial diastolic coronary resistance during maximal vasodilation was 53% higher in the dogs with hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

Coronary blood flow in experimental canine left ventricular hypertrophy.

O’Keefe¹,

Hoffman²,

Cheitlin³

et al. 1978

Circulation Research

160

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With maximal coronary vasodilation due to adenosine or carbochrome, mean coronary vascular resistance was 84% higher in LVH than in normal hearts; with isoproterenol, resistance was 54% higher in LVH. These changes were similar in right and left ventricles. Minimal coronary resistance at end diastole also was higher in LVH-64% and 94% for the two sets of vasodilators, respectively. There were no significant differences in capillary or large vessel proportional volumes in LVH and control dogs, but arterial capacity could not be estimated. The raised minimal coronary resistance suggests the possibility that, with stress, coronary flow, especially to subendocardial muscle, might be inappropriate and perhaps cause ischemic damage. However, the changes noted might have been due to coronary arterial responses to raised coronary pressures rather than to hypertrophy itself.LEFT ventricular hypertrophy (LVH) may impair cardiac function but the mechanisms for this change are not clear. Hypertrophy alters excitation-contraction coupling, energy utilization, and contractile proteins, 1 but it is not known whether these changes are primary or secondary to other mechanisms. One of those other mechanisms, myocardial ischemia, could occur in two ways: Roberts and Wearn 2 showed that in rabbits with left ventricular Original manuscript received February 28, 1977; accepted for publication March 7, 1978. hypertrophy the capillary-fiber ratio remained at its normal value of 1:1 so that the mean diffusion distance must have increased; these findings have been confirmed in man. 3 ' 4 Then Linzbach 3 and Woods 5 reported that, although the main coronary arteries increased in diameter in people with LVH, this increase in diameter did not match the increased heart weight. They therefore inferred that in hypertrophy there might be a reduced coronary vascular reserve that might impair cardiac function. However, no one has shown that the increased diffusion distance for oxygen does impair cardiac function nor that coronary vascular reserve is reduced in hypertrophy.We wished to test another hypothesis that involves myocardial blood flow, one which also fits in with the known vulnerability of the subendocardial muscle to is-

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“…A variety of possible causes have been suggested: a reduction in coronary reserve, an occlusive disease of small coronary arteries not visualized by coronary arteriography, an inadequate growth of the coronary microvasculature, or an augmentation of the extravascular component of coronary resistance. [5][6][7][8][9][10][11][12][13] To further evaluate hypertensive patients with angina but with normal coronary arteriograms, the following studies were performed in addition to left ventricular and coronary angiography: (1) coronary blood flow (CBF) was measured at rest and during dipyridamoleinduced coronary vasodilation and (2) biopsy specimens were taken from left ventricular myocardium for microscopic evaluation of intramyocardial vessels and of the myocardial cells.…”

mentioning

confidence: 99%

Reduction of coronary reserve: a mechanism for angina pectoris in patients with arterial hypertension and normal coronary arteries.

Opherk¹,

Mall²,

Zebe³

et al. 1984

Circulation

355

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The pathogenesis of angina pectoris in patients with left ventricular hypertrophy secondary to arterial hypertension and with normal coronary arteries remains uncertain. We measured coronary blood flow (argon method) in 12 control subjects and in 16 patients with arterial hypertension at rest and after intravenous administration of dipyridamole (0.5 mg/kg). In the patients with arterial hypertension, coronary blood flow response to dipyridamole was markedly reduced ( the extravascular component of coronary resistance.5-13 To further evaluate hypertensive patients with angina but with normal coronary arteriograms, the following studies were performed in addition to left ventricular and coronary angiography: (1) coronary blood flow (CBF) was measured at rest and during dipyridamoleinduced coronary vasodilation and (2) biopsy specimens were taken from left ventricular myocardium for microscopic evaluation of intramyocardial vessels and of the myocardial cells. Materials and methodsGroup A (control subjects) consisted of 12 patients (seven men, five women; mean age 44.8 years) without detectable heart disease. These patients suffered from recurrent atypical chest pain and they were referred for coronary arteriography to exclude an organic cause of the symptoms. All patients in this group had normal electrocardiograms (ECGs) at rest and during exercise and normal coronary and left ventricular angiograms.Group B comprised 16 patients (11 men, five women; mean age 51.4 years) with arterial hypertension class 1 or 11.14 The history of hypertension varied from 4 to more than 20 years (average 9.5 + 6.2 years). Patients were treated in addition to thiazide-type diuretics with /-adrenergic blocking agents (n = 12) and/or hydralazine (n = 3) or prazosin (n = 3). All patients had typical stress-induced angina pectoris that could be promptly relieved by nitroglycerin. The ECG showed evidence of left

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Transmural distribution of myocardial blood flow and of coronary reserve in canine left ventricular hypertrophy

Cited by 14 publications

References 11 publications

Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Abnormal coronary vascular response to exercise in dogs with severe right ventricular hypertrophy.

Coronary blood flow in experimental canine left ventricular hypertrophy.

Reduction of coronary reserve: a mechanism for angina pectoris in patients with arterial hypertension and normal coronary arteries.

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