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Results for “Coronary collateral circulation”

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At least 109 records · Page 6Linked to original sources
PubMed1985

The effect of cardiac hypertrophy on the coronary collateral circulation.

We have previously shown that dogs with renal hypertension and left ventricular hypertrophy have larger infarcts (per risk area size) than do control animals. A potential explanation for this is that collateral resistance is higher in these dogs. Paradoxically, previous postmortem studies in human hearts with left ventricular hypertrophy have suggested that coronary collaterals are actually increased in this condition. To test the hypothesis that left ventricular hypertrophy is associated with alterations in coronary collateral resistance, studies were performed in dogs with renal hypertension and left ventricular hypertrophy and in patients with aortic valvular disease at the time of cardiac surgery. With an isolated, adenosine-vasodilated, blood-perfused cardiac preparation, collateral and normal zone pressure-flow relationships were established by means of radioactive microspheres in nine dogs with renal hypertension and left ventricular hypertrophy and in 17 controls. Collateral resistance calculated from these pressure-flow relationships were similar in both groups (4.0 +/- 0.7 in dogs with renal hypertension and left ventricular hypertrophy and 3.9 +/- 0.4 mm Hg/ml/min/100 g in controls). In addition, normal zone resistance was not different between groups (transmural resistances 0.17 +/- 0.01 in controls and 0.18 +/- 0.02 in dogs with renal hypertension and left ventricular hypertrophy. In five patients with aortic valve disease, left ventricular hypertrophy, and normal coronary arteries and in six patients without left ventricular hypertrophy who had normal left anterior descending coronary arteries, a 7 MHz suction-mounted echo transducer was used to monitor systolic wall thickening during transient occlusions of the left anterior descending artery at the time of cardiac surgery. Because noncollateralized myocardium ceases to contract promptly after coronary occlusion, this approach provides an indirect index of collateral perfusion. Twenty seconds after the onset of coronary occlusion, systolic thickening had markedly decreased in both groups (15 +/- 10% of control values in nonhypertrophied hearts and 10 +/- 10% in hearts with left ventricular hypertrophy; p = NS between groups). Thus the severity of contraction abnormality induced during transient coronary occlusion in these two groups of patients was similar, suggesting that the degree of severity of ischemia was comparable between the two groups. We conclude that collateral resistance is not altered by hypertension and left ventricular hypertrophy and that left ventricular hypertrophy in patients is not associated with functional evidence of an enhanced collateral circulation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

[Effect of nonachlazine on systemic hemodynamics and the collateral coronary circulation in acute myocardial ischemia].

Systemic hemodynamics (thermodilution), retrograde coronary blood flow, oxygen tension and bioelectric activity of the myocardium were examined in dog experiments to show that nonachlazin produces an intensive and long-lasting increase in the collateral blood flow to the zone of acute myocardial ischemia and in the pressure in the ligated venous artery. Concurrently it elevates oxygen tension in the affected part of the heart. The cardiostimulant effect of the drug was associated with augmentation of the heart volume on account of an elevated stroke output in the presence of diminished general peripheral vascular resistance.

Acute Disease↗
PubMed1996

Angiographically assessed coronary collateral circulation increases vulnerability to myocardial ischemia during vasodilator stress testing.

In patients with a major coronary vessel occluded, the presence of good coronary collateral circulation increases vulnerability to myocardial ischemia induced by pharmacologic coronary vasodilation. The presence of good collaterals results in a greater frequency, severity, and extent of dipyridamole-induced regional left ventricular dysfunction, consistent with the hypothesis of angiographically assessed collaterals facilitating "steal phenomena" during dipyridamole-induced coronary vasodilation.

Aged↗
PubMedDate not supplied

[Role of the collateral coronary circulation in the mechanism of action of verapamil and diltiazem on the ischemic myocardium].

In experiments on anesthetized cats and dogs it was shown that the anti-ischemic action of verapamil and diltiazem injected intravenously in acute permanent occlusion of the coronary artery is not related to their effect on the collateral blood supply to the myocardial ischemic focus. The protective effect of the drugs in this case is due to other mechanisms one of which is a decrease of oxygen consumption by the heart.

Animals↗
PubMed1991

Dipyridamole-induced decrement of functional recovery of postischemic reperfused myocardium in conscious dogs with well-developed coronary collateral circulation.

The effects of dipyridamole (20 and 40 micrograms/kg/min intravenously) on the time course of functional recovery of myocardium after five 5-minute coronary artery occlusions and four 5-minute reperfusions and a subsequent 5-hour reperfusion period were studied in chronically instrumented, conscious dogs with well-developed coronary collateral circulation. In comparison with vehicle-treated control dogs, those given dipyridamole (20 and 40 micrograms/kg/min, respectively) 15 minutes before and during coronary occlusion had a greater depression of regional segment shortening (38 +/- 7% and 19 +/- 4%, respectively, vs control levels of 69 +/- 10% of preocclusion values) during acute coronary artery occlusion. After a 5-hour reperfusion period, segment shortening returned to preocclusion values in the control group but remained decreased in the dipyridamole groups (87 +/- 4% and 75%, respectively). These results suggest that dipyridamole in a dose-dependent manner exacerbates recovery of contractility of postischemic reperfused myocardium in dogs with well-developed coronary collateral circulation.

Animals↗
PubMed2004

[Effect of different angiotensin converting enzyme inhibitors on coronary collateral circulation].

OBJECTIVE: To observe the effects of different angiotensin converting enzyme inhibitors (ACEI) on coronary collateral circulation. METHODS: Twenty-four healthy dogs underwent measurement of distolic aortic pressure (DAP) and ligation of the left anterior descending coronary artery. The distolic coronary pressure (DCP) and retrograde blood flow (Qret) were measured. Five days after the operation the dogs were randomly divided into three groups of 8 dogs: benazepril group (benazepril 10 mg qd); captopril group (captopril 12.5 mg bid) and control group (starch tablet was given). Thirty days after the operation a reflux catheter was inserted to measure the DCP and Qret again. Then the dogs were killed and their hearts were taken out to examine the pathologic changes. The angiotensin converting enzyme (ACE) activity levels in plasma and myocardium were examined by FAPGG spectrophotometry. RESULTS: (1) In the captopril group the plasma ACE activity was (24.1 +/- 0.6) U/L 10 days after medication, and 24.3 +/- 0.6 U/L twenty-five days after medication, both significantly lower than that before medication [(57.6 +/- 0.8) U/L, both P < 0.01]; in benazepril group the plasma ACE activity was (24.4 +/- 0.4) U/L ten days after medication, and (24.0 +/- 0.5) U/L 25 days after medication, both significantly lower than that before medication [(59.5 +/- 1.3) U/L, both P < 0.01]. The plasma ACE activity levels of captopril and benazepril groups, especially of the benazepril group, after medication were significantly lower than that of the control group. The tissue ACE activity levels of the captopril and benazepril groups were lower than that of the control group. (2) The values of DCP in the control and captopril group were higher after medication than before medication. A tendency of decrease of DCP was shown in the benazepril group, however, without statistical significance. (3) In the control group Qcol was (2.01 +/- 0.31) ml/min 25 days after medication, significantly than that before medication [(0.91 +/- 0.15) ml/min], the corresponding values in captopril group were (2.24 +/- 0.46) ml/min and (0.88 +/- 0.13) ml/min respectively in the captopril group and (3.18 +/- 0.27) ml/min and (0.89 +/- 0.11) ml/min respectively in the benazepril group with the value 25 days after in the benazepril group being the highest. (4) 30 days after operation collateral circulation was established in the ischemic myocardium in all 3 groups. The microvessel density in the ischemic zone of myocardium was higher than that in the nonischemic zone in all 3 groups. The microvessel density in the ischemic zone of myocardium was greater in the benazepril group than in the captopril and control groups. There was no difference in microvessel density between the captopril group and control group. CONCLUSION: Benazepril increases the microvessel density and collateral flow, promotes the creation of collateral circulation in ischemic area, but captopril has not such effects.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

[Role of collateral coronary circulation in the compensation of regional disorders of energy metabolism in the myocardium in experimental myocardial ischemia].

Patterns of glucose, pyruvate and lactate consumption by the ischemized myocardium were studied in dog experiments with reference to the leve of retrograde inflow to the network of the ligated coronary artery. For this purpose, blood samples were taken from distal portion of ligated anterior descending coronary artery and the great cardiac vein accompanying the branches of the former. The increase of the lactate level, "excessive" lactate, the redox potential of the lactate/pyruvate system (E), delta E was shown to be less pronounced in those experiments where collateral coronary flow volumetric rate was above 1.5 ml/min, whereas pH and pO2 values dropped more steeply following coronary ligation in the experiments with small retrograde inflow to the ischemized area. The differences between glucose and pyruvate consumption by the ischemized myocardium were not significant.

Adaptation, Physiological↗
PubMed1989

[Changes in platelet aggregation and coronary collateral circulation during the early phase of myocardial ischemia in dogs].

Experiments were performed on 18 anesthetized open-chest dogs to observe the changes in platelet aggregation and coronary collateral circulation during the early phase of acute myocardial ischemia. An increase in platelet aggregation rates (PAgR) and a decrease in platelet counts (PC) were found in the blood collected from the ischemic myocardium after coronary occlusion. PAgR was increased by 58.7 +/- 5.6% and PC was reduced by 39.5 +/- 23.6% at 50 min after occlusion (P less than 0.01). Under the condition of controlling aortic blood pressure, collateral coronary vascular capacity (CVC) was not changed (P greater than 0.05), but the effective collateral coronary flow to the ischemic zone, calculated by Wyatt et al's equation, was significantly reduced by 23.5 +/- 9.7% at 50 min after occlusion (P less than 0.05). There was a negative correlation between the changes in PAgR and the effective collateral coronary flow ( r = -0.857, P less than 0.01), and between the collateral indices and infarct size (r = -0.847, P less than 0.01). Abnormal changes in parameters of platelet and coronary collateral circulation after myocardial ischemia were nearly abolished by intravenous injection of aspirin before coronary occlusion. The results suggest that the deleterious changes of platelet aggregation during the early phase of the acute myocardial ischemia may decrease the effective collateral coronary flow significantly and thereby enlarge the infarct size.

Animals↗
PubMed1994

Importance of the coronary collateral circulation for the distribution of anterograde and retrograde delivered cardioplegic solution in aortocoronary bypass surgery: a haemodynamic study.

The importance of coronary collateral circulation for homogeneous distribution of anterograde and retrograde delivery of cardioplegia was evaluated in 36 patients undergoing myocardial revascularization. All patients had three-vessel coronary artery disease, with a stenosis of the right coronary artery of at least 80%. The patients were randomized into two groups: group A (n = 19) received anterograde delivered cardioplegic solution and group B (n = 17) received retrograde. Both groups were further subdivided depending on the pathology of the right coronary artery, as evaluated on preoperative coronary angiography. In group A1 (n = 8) and group B1 (n = 7) there was no visualization of collateral circulation from the left to the right coronary artery system, whereas in group A2 (n = 11) and group B2 (n = 10) there was retrograde filling of the right coronary artery by collateral circulation. Right atrial pressure increased significantly (P < 0.05) in group A1 and was elevated in group A2, but not significantly (P = 0.07). By contrast, right arterial pressure decreased in groups B1 and B2. Analysis of the individual differences in the right atrial filling pressure showed a statistical significance between the two subgroups (group B1-1.0(0.5) versus group B2-1.8(1.1), P < 0.05), although the individual decrease of the right ventricular stroke work index was not significant. It is concluded that collateral circulation is important for an adequate distribution of anterogradely delivered cardioplegia and is also beneficial in cases of retrograde delivery.

Adult↗
PubMed1976

Coronary collateral circulation during stress and the effects of aorta-coronary bypass grafts.

The ability of coronary collateral vessels to supply an adequate volume of blood to the subendocardium during the resting state and during periods of stress was studied. Regional myocardial blood flow was determined by the radioactive microsphere technique. Ameroid constricting devices were placed around the left circumflex coronary artery in 22 adult mongrel dogs. Three months later, regional myocardial blood flow was measured in a normal area of the left ventricle as well as in the area supplied entirely by coronary collateral vessels. Collateral blood flow was sufficient in the resting state to prevent myocardial ischemia distal to a gradually occluded coronary artery. However, in 10 animals (Group I) without aorta-coronary bypass grafts (ACBG), a selective underperfusion of the collateralized subendocardium occurred during periods of stress. In 12 animals (Group II), this selective underperfusion of the collateralized subendocardium with stress was abolished by placing ACBG's distal to the site of the coronary artery occlusion.

Animals↗
PubMed2006

Serum level of lipoprotein (a) is inversely associated with the development of coronary collateral circulation.

BACKGROUND: This study sought to determine the relationship between serum lipoprotein (a) levels and angiographically visible coronary collateral circulation and to evaluate whether lipoprotein (a) exerts any effect on vascular endothelial cell growth factor. METHODS: The study population included 60 patients (39 men, mean age 59+/-13 years) with angiographically documented total occlusion in one of the major coronary arteries. Development of collaterals was classified by Rentrop's method. Patients were defined as having poorly developed collaterals for grades 0 and 1 (group 1), or well-developed collaterals for grades 2 and 3 (group 2). Serum lipoprotein (a) and vascular endothelial cell growth factor levels were determined by enzyme-linked immunosorbent assay. RESULTS: In group 1, lipoprotein (a) levels were significantly higher and vascular endothelial cell growth factor levels were significantly lower than in group 2 (34+/-19 vs. 20+/-12 mg/dl, P<0.001, and 2.5+/-0.7 vs. 3.4+/-0.8 ng/dl, P<0.001, respectively). Poorly developed collaterals were significantly more frequent in patients with lipoprotein (a) levels >or=30 mg/dl than in patients with levels <30 mg/dl (72 vs. 37%, P=0.008). A strong negative correlation was observed between lipoprotein (a) and vascular endothelial cell growth, factor (r=-0.708, P<0.0001). Multivariate analysis revealed that a high level of lipoprotein (a) negatively affected the development of collaterals, whereas the duration of angina had a positive effect. CONCLUSION: This study demonstrated for the first time that the high level of lipoprotein (a) negatively affects the formation of coronary collateral vessels in human beings. Reduced production or bioactivity of vascular endothelial cell growth factor caused by high levels of lipoprotein (a) may be the possible responsible mechanisms of hyperlipoprotein (a)-related poor collateral formation.

Adult↗