Myocardial blood flow and capillary density in chronic pressure overload of the feline left ventricle

Breisch, Eric; Houser, Steven R.; Carey, Roberta B.; Spann, James F.; Bové, Alfred A.

doi:10.1093/cvr/14.8.469

Cited by 116 publications

(47 citation statements)

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“…9 ' "• 37 The maintenance of total coronary resistance suggests that the functional cross-sectional area of the coronary circulation does not grow in parallel with ventricular mass. 38 In accordance with Wicker and Tarazi, 37 the level of maximal coronary blood flow was closely correlated with the value of the MAP/LVW ratio. In our experiment, maintenance of this ratio could explain the unchanged maximal coronary blood flow.…”

Section: Coronary Hemodynamicssupporting

confidence: 77%

Diltiazem and left ventricular hypertrophy in renovascular hypertensive rats.

1988

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SUMMARY The effects of diltiazem treatment (40-50 mg/kg/day orally for 8 weeks) of left ventricular hypertrophy on systemic and coronary hemodynamics and mechanical cardiac performance were investigated in renovascular hypertensive rats (Goldblatt, two-kidney, one clip). Systemic and coronary hemodynamics were determined by using radioactive microspheres in conscious, unrestrained rats. Mechanical performance was measured on isolated papillary muscle from the same animal. Nine treated hypertensive rats were compared with control groups: 12 untreated hypertensive and nine sham-operated rats. Diltiazem treatment led to an effective but incomplete control of blood pressure (from 208 ± 5 mm Hg in the untreated hypertensive group to 155 ± 3 mm Hg in the treated hypertensive group; p < 0.01) associated with a significant but incomplete decrease of the left ventricular mass (from 3.10 ± 0.19 mg/g in untreated hypertensive rats to 2.35 ± 0.04 mg/g in treated hypertensive rats; p < 0.01). A close correlation was found between left ventricular mass and systolic blood pressure in untreated, treated, and pooled groups (r = 0.84, p < 0.001, n = 30). The left ventricular weight to systolic blood pressure ratio was equivalent in all three groups, so that the reduction of left ventricular mass in diltiazem-treated rats was commensurate with the reduction of blood pressure. At rest, treated hypertensive rats showed a rise in cardiac output (426 ± 12 vs 298 ± 22 ml/min/kg in sham-operated rats; p < 0.001) and in coronary blood flow (598 ± 17 vs 453 ± 19 ml/min/100 g; p < 0.05) related to the decrease in total peripheral resistance and in total left ventricular coronary resistance. A reversal of impaired myocardial mechanical parameters toward control values was observed except for time to half-maximal relaxation (92 ± 2 msec in the treated group vs 79 ± 5 msec in sham-operated rats) and time to peak force. Our results demonstrate that even incomplete control of blood pressure with diltiazem is associated with significant but partial reduction of left ventricular mass and improvement of mechanical function. (Hypertension 11: 495-501, 1988) 6 " 8 However, these drugs exhibit substantial differences in their antihypertensive potency, site of action, and degree of sympathetic stimulation. The 1,4-dihydropyridines are very potent antihypertensive drugs, with a proven ability to lower blood pressure

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Section: Coronary Hemodynamicssupporting

confidence: 77%

Diltiazem and left ventricular hypertrophy in renovascular hypertensive rats.

1988

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“…Whether myocardial blood flow rates during maximum coronary vasodilation are normal or decreased may be related to the different models used and the degree of hypertrophy. In dogs in which the ascending aorta was banded in adulthood, the increase in myocardial blood flow during maximum coronary vasodilation with adenosine or dipyridamole tended to be less in hypertrophied than in normal hearts, although this difference did not achieve statistical significance (O'Keefe et al, 1978;Breisch et al, 1980). In dogs with left ventricular hypertrophy secondary to renovascular hypertension, Mueller et al (1978) found that adenosine Results are expressed as mean ± SE.…”

Section: 55±014tmentioning

confidence: 99%

Alterations of myocardial blood flow associated with experimental canine left ventricular hypertrophy secondary to valvular aortic stenosis.

Alyono

Anderson

Parrish

et al. 1986

Circulation Research

108

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SUMMARY. Experimental renovascular hypertension or supravalvular aortic constriction results in left ventricular hypertrophy and impaired minimum coronary vascular resistance. However, these experimental models expose the coronary arteries to increased intra-arterial pressure, so that hypertensive vascular changes might be responsible for the impaired minimum coronary resistance. This study was performed to test the hypothesis that left ventricular hypertrophy in the absence of increased coronary pressure results in abnormalities of myocardial perfusion. Aortic valve stenosis was produced by plication of the noncoronary aortic cusp of 11 dogs at 6-8 weeks of age. Studies were carried out when the animals reached adulthood; mean left ventriculanbody weight ratio was 7.1 ± 0.4 as compared to 4.4 ± 0.3 g/kg in 11 normal dogs (P < 0.01). Under quiet resting conditions, myocardial blood flow measured with microspheres was significantly greater than normal in dogs with aortic stenosis. However, during maximum coronary vasodilation with adenosine, mean left ventricular blood flow in dogs with hypertrophy (3.29 ± 0.39) was substantially less than in normal dogs (6.19 ± 0.54 ml/min per g; P < 0.01), whereas minimum coronary resistance was increased from 14.1 ± 1.7 in normal dogs to 23.7 ± 5.4 mmHgmin-g/ml (P < 0.01). To examine the response of myocardial perfusion to cardiac stress, blood flow was measured during pacing at 200 and 250 beats/min. Compared with normal dogs, animals with hypertrophy had a subnormal increase in myocardial blood flow during tachycardia; this perfusion deficit was most marked in the subendocardium. These data demonstrate that left ventricular hypertrophy alone, without increased coronary artery pressure, is associated with impaired minimum coronary vascular resistance and with abnormalities of myocardial blood flow during pacing stress. (Circ Res 58: 47-57, 1986)

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“…This mechanism must play a role in the angina observed in some patients with LVH who also have normal epicardial coronary anatomy, although most patients with LVH and reduced flow reserve do not develop angina. Explanations for reduced endocardial flow and reduced flow reserve in LVH have centered around reduced capillary density per unit of myocardium 9 and increased resistance to flow. Decreased capillary density in LVH presumably occurs because capillary growth does not match muscle growth.…”

Section: Coronary Blood Flow In Normal Subjects and Those With Lvhmentioning

confidence: 99%

Understanding Coronary Blood Flow

Carabello

2006

Circulation

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Fick's principle states that oxygen consumption of an organ or organism is equal to the product of blood flow and oxygen extraction from the blood. Among all organs, the heart is unique in that oxygen extraction is constantly close to maximal. Thus, the only way that this metabolically demanding organ can increase oxygen consumption is by increasing coronary blood flow. In this aspect of oxygen delivery, the heart also is unique because most flow occurs in diastole instead of in systole. In other organs, blood flows down a pressure gradient from its arterial source through the resistance of the arterioles into the capillary bed and thence venous return. In the heart, the compression of the vasculature by its surrounding muscle during systole impedes flow so that while the pressure head for flow is maximum in systole, flow is maximum in diastole. Thus, a simple "vascular waterfall" model in which flow moves from highest to lowest pressure does not fully explain observed myocardial flow phenomena. Article p 1768In this week's Circulation, Davies et al 1 used computer analysis of recordings of blood flow and pressure to detect and quantify intracoronary waves and to study coronary flow events in normal subjects and those with left ventricular hypertrophy (LVH). Waves were generated from both ends of the coronary tree. Proximal waves moved forward; distal waves moved backward. In this schema, proximal "pushing" waves and distal suction waves accelerate forward blood flow, while proximal suction waves and distal pushing waves do the opposite. Although the authors consistently detected 6 waves, 2 were dominant: a forward-moving pushing wave and a backward-moving suction wave (although this wave moves proximally, it propels blood forward). The forwardmoving pushing wave is generated by systolic pressure. It probably drives blood primarily into the epicardial coronaries where it might be stored until it is released for forward flow when the myocardium relaxes. The second important wave, typically the largest, is a suction wave generated by relaxation of the left ventricle and is probably the main driver in diastolic coronary blood flow. Coronary Blood Flow in Normal Subjects and Those With LVHIn normal subjects, endocardial blood flow exceeds epicardial flow, so the ratio of endocardial to epicardial blood flow is Ϸ1.2:1. 2,3 It is generally held that this distribution matches the nutrient requirements of the endocardium where wall stress higher than that of the epicardium increases endocardial oxygen demand. It has been known for decades that this distribution is reversed in the presence of concentric LVH, predisposing toward endocardial ischemia. 2-5 Indeed, such ischemically mediated endocardial contractile dysfunction has been demonstrated. 6,7 Furthermore, it is known that coronary flow reserve is reduced in LVH. 8 Although normal myocardium can increase its flow 5-to 8-fold under stress, it can be reduced by Ն50% in concentric LVH. This mechanism must play a role in the angina observed in some patients with LVH wh...

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Myocardial blood flow and capillary density in chronic pressure overload of the feline left ventricle

Cited by 116 publications

References 0 publications

Diltiazem and left ventricular hypertrophy in renovascular hypertensive rats.

Diltiazem and left ventricular hypertrophy in renovascular hypertensive rats.

Alterations of myocardial blood flow associated with experimental canine left ventricular hypertrophy secondary to valvular aortic stenosis.

Understanding Coronary Blood Flow

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