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Results for “Coronary collateral circulation”

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PubMed1999

[Effect of puerarin on coronary collateral circulation in dogs with experimental acute myocardial infarction].

OBJECTIVE: To evaluate the effect and mechanism of puerarin on coronary collateral circulation in dogs with experimental acute myocardial infarction. METHOD: Twelve dogs were randomly divided into puerarin (Gegen su, G) group and control(C) group, the acute myocardial infarction model was built in all dogs. Puerarin or saline was administered for 21 days. Coronary angiography was performed before and after ligating coronary artery. The capillaries and distribution vessel density in tissue sections of myocardium were assessed. RESULT: Angiography on hour 2 and day 22 after ligating coronary artery revealed significant augmentation of collateral vessels in G group versus controls. Capillaries and distribution vessel density in ischemic and infarctive zone on day 22 revealed statistically significant augmentation in G group versus controls (P < 0.05 and P < 0.01). CONCLUSION: Puerarin might improve the opening and forming of coronary collateral circulation to ischemic myocardium in dogs and protect ischemic myocardium.

Animals↗
PubMed1982

Effect of physical training on coronary collateral circulation of the rat.

The influence of physical training on coronary collateral circulation following acute ligation of the left coronary artery was determined in pentobarbital-anesthetized rats. Coronary blood flows were determined with 15-microns microspheres during a wide range of perfusion pressures and during adenosine infusion. The demarcation between normal and ischemic tissue was achieved using nitroblue tetrazolium strain and thioflavin S fluorescence. Contractile performance was not altered by training, with the exception of a lower left ventricular end-diastolic pressure when afterload was elevated. Blood flow to and the size of the central ischemic zone were not influenced by training. However, in border zones, where collateral dependent flow is expected to be most pronounced, blood flow as a percent of normal was increased (16%, P less than 0.02) in trained animals. This increased was abolished by coronary vasodilation with adenosine. These results indicate that training caused a limited increase in collateral blood flow to the border zone. Further, tissue reactivity to adenosine following short periods of ischemia is normal in trained rats but decreased in border (11%) and ischemic (21%, P less than 0.05) zones in sedentary rats. Whether his small increase in blood flow to the border tissue, along with a retained capacity for dilatation, could lead to an improved salvage of tissue remains to be evaluated.

Adenosine↗
PubMed1991

The coronary collateral circulation in normal goats.

This study was undertaken to evaluate the coronary collateral circulation of the goat. Year old, castrated male goats were anesthetized with sodium pentobarbital. A branch of the left circumflex coronary artery was dissected and a snare placed around it. Regional myocardial blood flow was measured by injecting colored microspheres into the left atrium before and during 3 hr of occlusion of this coronary artery. The Area At Risk for infarction, as defined by a left atrial injection of Brilliant Green dye, was divided into a central Ischemic zone and a peripheral Ischemic Border zone. The degree of overlap in the blood flow distributions between the risk and the nonrisk areas was quantitatively assessed by injecting microspheres directly into the artery to the Area At Risk. Baseline blood flow to the normally perfused goat myocardium was 1.13 +/- 0.18 ml/min/g (mean +/- SE). Following occlusion, the flow to the Ischemic zone was 0.07 +/- 0.03 ml/min/g and to the Ischemic Border zone was 0.31 +/- 0.18 ml/min/g. Flow to either zone did not increase during the 3-hr observation period. Overlap at the perimeter of the risk and nonrisk areas was approximately 22%. We conclude that flow to the Ischemic zone is low because the goat has few native collateral blood vessels, and that flow to the Ischemic Border zone is significantly affected by overlap with normal myocardium.

Animals↗
PubMed2005

Ultrasound imaging versus morphopathology in cardiovascular diseases. Coronary collateral circulation and atherosclerotic plaque.

This review article is aimed at comparing the results of histopathological and clinical imaging studies to assess coronary collateral circulation in humans. The role of collaterals, as emerging from morphological studies in both normal and atherosclerotic coronary vessels, is described; in addition, present role and future perpectives of echocardiographic techniques in assessing collateral circulation are briefly summarized.

Cardiovascular Diseases↗
PubMed1985

Effect of halothane on coronary collateral circulation.

The authors studied the effect of halothane in a canine model of coronary collateral circulation secondary to chronic occlusion of a coronary artery. Two sets of experiments were performed. In the first experiments, Ameroid constrictors were placed around the left anterior descending coronary artery to produce complete occlusion in three weeks. An inflatable occluder was placed around the circumflex coronary artery in order to apply a mild stenosis to the artery supplying the collateral vessels to produce vasodilation distal to the stenosis. Regional myocardial blood flows were measured using radioactive microspheres. Blood flows to normal and collateralized myocardium were decreased significantly during halothane anesthesia, but perfusion of the subendocardium in both regions was maintained even in the presence of mild stenosis of the circumflex coronary artery supplying the collateral vessels, as indicated by unchanged endocardial/epicardial blood flow ratios. In the second experiments, chronic occlusions of both circumflex and right coronary arteries were produced using Ameroid constrictors. In these animals, sedated using xylazine, pacing-induced tachycardia produced a marked but reversible decrease in blood flow to the collateralized subendocardium. During halothane anesthesia at normal heart rate, blood flow to the collateralized subendocardium was well maintained, but tachycardia produced marked decrease in blood flow to the collateralized subendocardium, leading to the demise of four of seven dogs. The authors conclude that in this chronic canine model, in which control measurements were made during sedation using xylazine, coronary collateral blood flow is well maintained during halothane anesthesia at normal heart rate, but tachycardia during halothane anesthesia severely limits blood flow to the collateralized subendocardium.

Animals↗
PubMed1993

Coronary collateral circulation in the transplanted heart.

BACKGROUND: The concept that coronary collateral (CC) circulation can develop in cardiac transplant recipients (CTR) is controversial. Indeed, a decreased occurrence of CC in CTR has been previously reported. METHODS AND RESULTS: We reviewed 102 coronary angiograms in 73 CTR to evaluate the presence and significance of CC in denervated human hearts. These angiograms were compared with angiograms of 70 nontransplanted patients. Twenty-six CTR who had undergone at least two coronary angiograms, thus allowing comparative evaluations, form the basis for this study. Angiograms were analyzed using a modification of CC classification (Rentrop et al) from grade 0 for complete absence to grade 4 representing mature collateral with clear filling of epicardial vessels. Coronary artery disease was classified according to the scheme reported by Gao et al. For the purpose of this study, all type A lesions were grouped as large vessel disease (LVD), and types B1, B2, and C were collectively grouped as small vessel (epicardial) disease (SVD). The presence of CC circulation in all 73 CTR was grade 0, 7 (10%); grade 1, 41 (56%); grade 2, 33 (45%); grade 3, 30 (41%); and grade 4, 5 (7%). However, in control nontransplanted subjects grades 0, 1, 2, 3, and 4 were found in 47 (67%), 22 (31%), 4 (6%), 11 (15%), and 16 (20%) patients, respectively. The presence of mature collaterals (grade 4) in both groups were associated with type A lesions and was frequent in nontransplanted hearts. In contrast, grade 2 and grade 3 vascular channels probably representing CC with "myocardial blush" was more frequent in CTR and was mostly associated with small vessel coronary arteriopathy. CONCLUSIONS: These results suggest the presence of atypical CC in patients with cardiac allograft arteriopathy. It is speculated that this atypical form of CC with "blush pattern" may represent an angiogenic response to microvascular ischemia due to allograft coronary arteriopathy.

Adult↗
PubMed1989

Coronary collateral circulation: clinical significance and influence on survival in patients with coronary artery occlusion.

In a consecutive series of 96 patients with coronary artery occlusion, 67 had good and 29 had no or poor collateral circulation. Patients with good collaterals had the severest degree of coronary artery disease. Good collaterals are associated with a higher incidence of angina pectoris and normal electrocardiogram and with lower incidence of Q-waves, positive exercise tests, heart failure, previous myocardial infarction, and dyskinesia at ventriculography. Survival rates after 10 years were (1) 51.5% with good and 34.5% with poor collaterals (p less than 0.1), (2) 59.4% with angina pectoris and good collaterals and 41.2% with angina pectoris and poor collaterals (p less than 0.05), (3) 64.8% without and 24.4% with heart failure and good collaterals (p less than 0.001), and (4) 58.3% without and 16.1% with heart failure and poor collaterals (p less than 0.01). Good collaterals protect the myocardium by prevention of acute myocardial infarction and heart failure and thus improve survival.

Angina Pectoris↗
PubMed1989

Vasomotor activity of moderately well-developed canine coronary collateral circulation.

This study examined the ability of moderately well-developed coronary collateral vasculature to undergo vasoconstriction in response to alpha-adrenergic agonists, vasopressin and angiotensin, and vasodilation in response to nitroglycerin. Studies were performed in 20 dogs 4-16 wk after left anterior descending coronary artery occlusion had been produced by an Ameroid constrictor or hollow intravascular plug. Collateral flow was estimated from retrograde flow from the cannulated left anterior descending artery. Tissue flow was measured with microspheres. Agonists were introduced into the left main coronary artery to reach collaterals arising from the left circumflex and septal arteries. Vasopressin and angiotensin II decreased retrograde flow from 22.7 +/- 5.5 to 15.5 +/- 2.7 and from 19.2 +/- 2.8 to 14.3 +/- 1.9 ml/min, respectively (each P less than 0.05). Both agents also significantly decreased tissue flow to normally perfused and collateral dependent myocardium. Neither the selective alpha 1-adrenergic agonist phenylephrine nor the alpha 2-agonist B-HT 933 decreased retrograde flow. Nitroglycerin increased retrograde flow by 63 +/- 27% (P less than 0.01). Thus, although the moderately well-developed coronary collateral circulation is capable of vasoconstriction in response to vasopressin and angiotensin II, these data fail to support a role for alpha-adrenergic mechanisms in modulating collateral flow.

Adrenergic alpha-Agonists↗
PubMed1977

Complete occlusion of the left main coronary artery and the importance of coronary collateral circulation.

Study of four patients who survived complete occlusion of the left main coronary artery forms the basis of conclusions concerning the functional significance of coronary collateral circulation. Each of these patients had prominent collateral circulation from the right coronary artery. Global left ventricular function was maintained to the extent that congestive heart failure did not occur; the biplane ejection fraction was normal in the two patients where measurement was possible. The peak rate of systolic wall thickening by roentgen videometry in anterior left ventricular segments was normal in one patient and mild to moderately depressed in another. Experience with the patients described herein indicates that coronary collateral flow can provide critically needed circulatory support for the patient with coronary artery disease.

Collateral Circulation↗
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↗