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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report 11 in a group of 21 asymptomatic patients with heterozygous familial hypercholesterolemia (FH) and progressive coronary artery disease to evaluate the role of compensatory mechanism(s), especially coronary collaterals, in providing adequate blood supply to the myocardium, following complete occlusion of one or more major coronary arteries. Diet-colestipol-nicotinic acid treatment decreased their plasma total cholesterol and low density lipoprotein cholesterol (mg/dl, mean +/- SEM) from 442.9 +/- 25.8 and 363.0 +/-24.1, respectively, to 231.2 +/- 11.8 and 185.3 +/- 14.2, respectively, for 6 to 9 years. The initially stenotic lesions of these 11 patients slowly progressed to complete occlusion, while the patients remained free of myocardial ischemia or infarction and exhibited no abnormality on 24-hour ambulatory ECG monitoring, exercise stress, and thallium 201 stress tests. We conclude that coronary occlusion can be retarded in FH patients by strenuous hypocholesterolemic therapy to allow the development of compensatory mechanism including coronary collaterals. Apparently, the angiographically visualizable collaterals combined with subendocardial anastomosis can give adequate myocardial blood supply to this series of FH patients following occlusion of one or more of their major coronary arteries.
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PMID:Protection of myocardium by the compensatory mechanism of coronary collaterals after total occlusion of major coronary arteries shown in patients with familial hypercholesterolemia. 709 Sep 84

The effects of carbocromene, 4 mg/kg intravenously, prior to coronary artery occlusion plus 40 microgram/kg/min during coronary artery occlusion and reperfusion on ventricular fibrillation threshold (VFT) were studied in pentobarbital-anesthetized open-chest dogs and compared to controls receiving saline. Coronary artery occlusion decreased VFT by 46 +/- 4% (mean +/- SEM, p less than 0.02) in controls and by 22+/-3% in drug-treated animals. Reperfusion of the occluded artery decreased VFT by 83+/-7% (p less than 0.01) in controls and by 47+/-5% in carbocromene-treated hearts (p less than 0.02). Hemodynamics did not change in the drug group during coronary artery occlusion. In controls, blood pressure and dP/dtmax decreased while heart rate, end-diastolic pressure and ST-T segments increased significantly during both coronary artery occlusion and reperfusion. The underperfused, ischemic region was assessed by staining with Evans blue and involved 34+/-3% of the left ventricular mass in controls but only 27+/-3% in carbocromene-treated hearts (p less than 0.05). These results indicate protective effects of carbocromene on ventricular vulnerability in canine hearts during coronary artery occlusion and subsequent reperfusion.
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PMID:Effects of carbocromene on ventricular fibrillation during acute myocardial ischemia in anesthetized dogs. 713 63

There is a growing recognition of discrepancies in myocardial temperatures during cold chemical cardioplegia. This study was designed to determine the extent to which coronary arterial stenosis just sufficient to abolish vasodilatory reserve in the working heart, but still compatible with myocardial viability ("critical stenosis"), limits heat transfer from the heart during cardioplegic infusion compared to complete coronary occlusion and no stenosis (control). In nine dogs, temperatures were measured from the subepicardium, midwall, and subendocardium of the left ventricle in the distributions of the circumflex (CCA) and left anterior descending (LAD) coronary arteries plus the aortic root, septum, mediastinum, and ventricular cavities. Cardiopulmonary bypass was instituted with core cooling to 28 degrees C. Three infusions of cold (4 degrees C), radioactive microsphere-labeled, potassium chloride arresting solution were periods of reperfusion. The data (mean +/- SEM) indicate that myocardial cooling was transmurally uniform under all conditions, but was significantly impaired (p less than 0.01) in the CCA region by both critical stenosis (17.4 degrees +/- 1.2 degrees C) and occlusion (23.6 degrees +/- 0.4 degrees C) compared to control (8.3 degrees +/- 0.5 degrees C), because of reduced perfusate flow to regional tissues (4 = 0.62, p less than 0.001). These findings show that coronary artery lesions, including those compatible with myocardial viability, impose a severe constraint on myocardial heat transfer and point to a need for improved cardioplegic technique.
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PMID:Regional and transmural myocardial temperature distribution in cold chemical cardioplegia: significance of critical coronary arterial stenosis. 723 Aug 55

The effect of hyperbaric oxygen (HBO) on infarct size associated with myocardial infarction remains uncertain. Accordingly, the present study was performed in 46 conscious dogs with experimental infarction to determine the effect of HBO on enzymatic estimates of infarct size. Since HBO may affect plasma creatine kinase (CK) release or disappearance, parameters used to calculate enzymatic estimates of infarct size from plasma CK, we assessed infarct size by directly measuring myocardial CK depletion. Twenty-three animals were given HBO (2 atm of pressure) for 3 h immediately after coronary occlusion and results of infarct size compared to those in 23 dogs with occlusion who remained in room air. In 10 other animals CK release was measured after coronary occlusion in 5 controls and compared to 5 treated. In 5 normal animals the CK disappearance rate of purified canine CK was determined before and after HBO. Infarct size was determined 24 h after coronary occlusion and in the treated animals averaged 25.4 +/- 1.3% of LV (mean +/- SEM), and being similar to controls (26.7 +/- 1.4, P greater than 0.25). The plasma CK disappearance rate before and after HBO was the same being 0.0072 +/- 0.0022 (min-1) and 0.0073 +/- 0.0021, respectively. Total CK released into the plasma was also the same in treated and controls (2232 +/- 210 IU and 2011 +/- 232), as was the ratio of CK released to that depleted from the myocardium (0.15 +/- 2% vs 0.15 +/- 3%). Our results indicate: (1) HBO does not reduce infarct size produced experimentally in the conscious dog; (2) HBO does not affect CK release or disappearance; and (3) estimates of infarct size by plasma CK remain valid despite administration of HBO.
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PMID:The effect of hyperbaric oxygen on infarct size in the conscious animal. 728 17

The effect of vagal stimulation on the myocardial ischaemia produced by acute coronary occlusion during beta-receptor blockade has been examined. Epicardial ST-segment elevation, myocardial surface temperature and regional blood flow were determined 10 min after coronary occlusion in the dog. Coronary occlusion after beta-receptor blockade alone raised the average ST-segment from 0.5 +/- 0.3 to 3.1 +/- 0.5 mV (SEM) (p less than 0.001). Subsequent vagal stimulation with beta-receptor blockade, which reduced heart rate from 129 to 50 beats/min, mean arterial pressure from 123 to 78 mmHg, but increased cardiac output from 1164 to 1855 ml/min, resulted in marked reduction in ST-segment elevation to 0.3 +/- 0.2 mV which was not different from the control before occlusion. Epicardial temperature was markedly decreased in the ischaemic area following coronary occlusion. The temperature difference between central ischaemic and surrounding areas became smaller after beta-receptor blockade, and vanished during vagal stimulation. Vagal stimulation caused a 55% decrease of blood flow in all non-ischaemic regions. A smaller reduction took place in the border zone where flow values close to those of the non-ischaemic myocardium were obtained. In the central ischaemic area blood flow remained unchanged despite the reduction in arterial pressure. Thus, vagal stimulation resulted in decreased collateral resistance in the ischaemic area and a marked reduction of myocardial oxygen requirement of both non-ischaemic and border zone myocardium, additional to that obtained with beta receptor blockade. The provision of energy to the ischaemic myocardium is therefore very favourably balanced with its actual demand during vagal stimulation.
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PMID:Beneficial effects of vagal stimulation on the ischaemic myocardium during beta-receptor blockade. 731 22

Hemodilution is used frequently for patients undergoing elective coronary bypass surgery but relatively little is known about the effects of hemodilution on acute myocardial infarction. Left ventricular infarctions were planimetered after acute coronary occlusion in dogs treated with and without hemodilution. The control group was maintained at a normal hematocrit (40-45) while the intervention group was hemodiluted with 6% dextran in saline 30 min after left anterior descending coronary artery occlusion to a hematocrit less than 50% of control (20). Systemic arterial and left atrial pressure were maintained at control levels as were arterial pO2 and pH. Mean infarct size in the control group was 20.72 +/- 1.38% (SEM) of the left ventricle while the hemodiluted group had a mean infarct size of 18.80 +/- 2.11% of the left ventricle. Reduction of red cell mass to less than 50% of normal does not increase the size of myocardial infarction after acute coronary artery occlusion suggesting that oxygen supply to ischemic areas is maintained if systemic hypoxia is prevented.
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PMID:The effect of hemodilution on experimental myocardial infarct size. 738 66

A major diagonal branch of the left anterior descending coronary artery (LAD) was acutely occluded in 17 baboons. Complete left ventricular (LV) decompression was achieved with a left heart bypass (LHB) system in six baboons while 11 baboons served as untreated controls. In the treated group, LHB was initiated after 30 minutes of coronary occlusion. For a period of 6 hours after occlusion, aortic pressure, LV pressure, left atrial pressure, and cardiac output were monitored. During the same monitoring period, electrograms were recorded from a high resolution matrix of fixed epicardial electrodes. Regional myocardial blood flow was determined prior to and at intervals following the initiation of LHB with radioactive microspheres. Infarct size was assessed histologically from serial cross sections of the left ventricle. The degree of salvage achieved by LHB was assessed by comparing the epicardial area of infarction 6 hours after occlusion (AI) to the area of epicardial St-segment elevation (STE) 30 minutes after occlusion (maxAST). In the LHB-treated group, 40.0% +/- 8.1% (SEM) of maxAST showed subsequent infarction; in the control group, 79.8% +/- 2.7% of maxAST showed eventual infarction (p less than 0.01). STE overlying the region of ischemia in the LHB-treated group did not undergo the spontaneous decline observed in the control group, which is normally associated with the progression of necrosis. Regional myocardial blood flow did not change significantly in the ischemic region during the period of occlusion following LHB. LHB. The results suggest that LHB is capable of substantial salvage of acutely ischemic myocardium by reducing myocardial work and thus reducing myocardial oxygen requirements.
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PMID:Effect of left ventricular--to--aortic bypass on infarct size and infarct microcirculation in baboons. 746 4

The effect of basic fibroblast growth factor (bFGF) administration on regional myocardial function and blood flow in chronically ischemic hearts was studied in 26 pigs instrumented with proximal circumflex coronary artery (LCX) ameroid constrictors. In 13 animals bFGF was administered extraluminally to the proximal left anterior descending (LAD) and LCX arteries with heparin-alginate beads and 13 other animal served as controls. bFGF-treated pigs showed a fourfold reduction in left ventricular infarct size compared to untreated controls (infarct size: 1.2 +/- 0.4% vs. 5.1 +/- 1.3% of LV mass, mean +/- SEM, P < 0.05). Percent fractional shortening (% FS) in the LCX area at rest was reduced compared with the LAD region in both bFGF and control pigs. However, there was better recovery in the LCX area after rapid pacing in bFGF-treated pigs (% FSLCX/% FSLAD, 22.9 +/- 7.3%-->30.5 +/- 8.5%, P < 0.05 vs. prepacing) than in controls (16.0 +/- 7.8%-->14.3 +/- 7.0%, P = NS). Furthermore, LV end-diastolic pressure rise with rapid pacing was less in bFGF-treated than control pigs (pre-pacing; pacing; post-pacing, 10 +/- 1; 17 +/- 3; 11 +/- 1* mmHg vs 10 +/- 1; 24 +/- 4; 15 +/- 1 mmHg, *P < 0.05 vs. control). Coronary blood flow in the LCX territory (normalized for LAD flow) was also better during pacing in bFGF-treated pigs than in controls. Thus, periadventitial administration of bFGF in a gradual coronary occlusion model in pigs results in improvement of coronary flow and reduction in infarct size in the compromised territory as well as in prevention of pacing-induced hemodynamic deterioration.
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PMID:Basic fibroblast growth factor improves myocardial function in chronically ischemic porcine hearts. 751 40

The effects of pre-existing collaterals (PC) and the perfusion size (PS) on the ischemia-induced collateral development were studied in a canine model. Under aseptic conditions, the dogs were instrumented with pairs of ultrasonic crystals to measure regional wall motion in the territory of the left circumflex (LCX) and left anterior descending coronary artery. A micromanometer was used to measure left ventricular (LV) pressure. Two to 3 weeks after surgery, 2 min coronary occlusion (CO) of LCX was repeated every 32 min consecutively day and night using a remote control, motor-driven hydraulic cuff occluder. Regional wall motion and LV pressure were monitored via a telemetry system in 23 dogs. The functional state of PC was estimated by the level of % reduction of regional wall motion at the end of the first 2 min CO, which ranged from -11 to -141%. PS of LCX area at risk determined by the post mortem angiograms ranged from 35 to 54% (mean +/- SEM; 44 +/- 1%) of LV. Number of CO needed for collateral development ranged from 8 to 628, and was exponentially related to the functional state of PC (r = -0.77, n = 23, p < 0.01), but not to PS (r = 0.43, n = 19, p = 0.07). These results suggest that the functional maturity of pre-existing collaterals is one of the major determinants of collateral development related to ischemic stimuli.
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PMID:Collateral development induced by repetitive brief coronary occlusion relates to the functional state of pre-existing collaterals. 751 87

It is hypothesized that because of its potential to increase coronary flow and simultaneously decrease myocardial performance and O2 consumption, midazolam would minimize regional metabolic impairment during myocardial ischemia. Therefore, the hemodynamic and regional metabolic effects of systemic midazolam administration were compared during moderate and severe constrictions of the left anterior descending artery (LADa) to nontreated but ischemic animals in a canine model of acute coronary occlusion. In 16 anesthetized, ventilated, surgically prepared, and catheterized dogs, resting flow in the LADa was decreased by 50% and 75% for 15 minutes with 1 hour of normal flow in between. By arbitrary assignment, 7 dogs received midazolam (0.3 mg/kg and then 0.05 mg/kg/min) before thoracotomy. In all dogs, heart rate, electrocardiogram, LADa flow, left ventricular (LV) first time-derivative, and aortic, pulmonary artery, LADa, and LV pressures were measured continuously. Before and during constrictions, cardiac output by thermodilution and regional myocardial blood flow by microspheres were measured and blood was sampled for analysis. Data (mean +/- SEM) were compared within and between groups using ANOVA. Before placement of the LADa ligature, midazolam decreased heart rate and mean aortic pressure. Before ischemia, heart rate and LADa pressure were lower with midazolam than without it, but baseline metabolic variables were similar between the two groups (except for O2 consumption in the ischemic zone, which was lower with midazolam than without it). During 75% constriction with midazolam, LV end-diastolic pressure, coronary resistance, and ischemic zone O2 consumption were lower than without midazolam. Ischemic zone O2 delivery/consumption ratio was higher.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Midazolam's effects on myocardial load and coronary perfusion: reduced regional O2 consumption and lactate production during ischemia in dogs. 806 Dec 64


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