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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of coronary artery reperfusion 3 hr after coronary occlusion on contractile function and the development of myocardial damage at 24 hr was studied experimentally. In 14 control and 6 reperfused dogs, relationships between epicardial ST segment elevation 15 min after coronary occlusion and myocardial creatine phosphokinase activity (CPK) and histologic appearance 24 hr later were examined. The electrocardiograms were recorded from 10 to 15 sites on the left ventricular epicardium and transmural samples for CPK and histology were obtained from the same sites where epicardial electrocardiograms had been recorded. An inverse relation existed between ST segment elevation (mv) 15 min after occlusion and log CPK activity (IU/ mg of protein) 24 hr later, log CPK = - 0.06ST + 1.26. In dogs subjected to coronary artery reperfusion, there was significantly less CPK depression (log CPK = - 0.01ST + 1.31, [P < 0.01]) than that expected from the control group. In the control group 97% of specimens showing ST segment elevations over 2 mv at 15 min showed abnormal histology 24 hr later. In contrast, in the reperfused group 43% of sites exhibiting elevated ST segment at 15 min showed abnormal histology 24 hr later. In six additional dogs it was shown that the paradoxical movement of the left ventricular wall could be reversed within 1 hr of perfusion. Therefore, by enzymatic and histologic criteria, as well as by functional assessment, coronary artery reperfusion 3 hr after occlusion resulted in salvage of myocardial tissue.
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PMID:Coronary artery reperfusion. I. Early effects on local myocardial function and the extent of myocardial necrosis. 505 63

The response of left ventricular function, coronary blood flow, and myocardial lactate metabolism during percutaneous transluminal coronary angioplasty (PTCA) was studied in a series of patients undergoing the procedure. From four to six balloon inflation procedures per patient were performed with an average duration per occlusion of 51 +/- 12 sec (mean +/- SD) and a total occlusion time of 252 +/- 140 sec. Analysis of left ventricular hemodynamics in 19 patients showed that the relaxation parameters, peak negative rate of change in pressure, and early time constants of relaxation, responded earliest to short-term coronary occlusion (peak effect at 17 +/- 7 sec) while other parameters, such as peak pressure, left ventricular end-diastolic pressure, and peak positive rate of change in pressure, responded more gradually, suggesting a progressive depression of myocardial mechanics throughout the procedure. Left ventricular angiograms, available for 14 patients, indicated an early onset of asynchronous relaxation concurrent with the early response in peak negative dP/dt and the time constant of early relaxation. All hemodynamic functions fully recovered within minutes after the end of PTCA. Mean blood flow in the great cardiac vein and proximal coronary sinus and the hyperemic response were measured in 20 patients. Before PTCA mean flow in the great cardiac vein was 69 +/- 17 ml/min and in the coronary sinus it was 129 +/- 34 ml/min. Reactive hyperemia (great cardiac vein) was 55% after the first PTCA and 91% after the third. A more pronounced reaction was observed when the residual functional coronary stenosis was reduced in subsequent dilatations. Arteriovenous lactate difference appeared constant during the first two occlusions (control +0.11 mmol/liter, first PTCA -0.87 mmol/liter, and second PTCA -0.82 mmol/liter) and did not increase during subsequent occlusions. Within minutes after the procedure lactate balance was again positive, demonstrating the reversibility of the metabolic disturbances after repeated ischemia. The results of this study indicate that there is no permanent dysfunction of global or regional myocardial mechanics, myocardial blood flow, or lactate metabolism after PTCA with four to six coronary occlusions of 40 to 60 sec.
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PMID:Left ventricular performance, regional blood flow, wall motion, and lactate metabolism during transluminal angioplasty. 623 47

Substantial gains have been made toward clarifying the mechanisms of arrhythmia in ischemia in animal models. After coronary occlusion in the dog, ischemic myocardial cells have reduced resting potential and slowed and diminished upstrokes of action potentials due to depression of fast channels. As a result, conduction is slow and irregular, especially at shorter cycle lengths, because refractoriness is altered by a delay in recovery of the fast channels beyond the completion of repolarization. These abnormalities occur during the acute phase of arrhythmia in the first half hour after occlusion and persist in surviving the subepicardial layers of myocardial cells for days to weeks. Reentry has been mapped in these surviving layers. Reentrant circuits form around regions of functional block formed by interfaces between responding and refractory myocardium. Standard antiarrhythmic agents generally are fast-channel blockers that further depress conduction and prolong refractoriness in ischemic tissue, causing block in slow conducting segments of the reentry circuits. However, antiarrhythmic agents may cause or accentuate reentrant arrhythmias by virtue of the same depressant actions. The greater likelihood of antiarrhythmic agents suppressing rather than producing reentrant arrhythmias may be due to enhanced depressant effects of antiarrhythmic agents on very slowly conducting tissues that are involved in reentry circuits. After the acute phase, arrhythmias occurring 1 to 4 days after coronary occlusion are probably largely automatic, although the potential for reentry remains if the cycle length is shortened. Abnormally enhanced automaticity and triggered activity are demonstrable in the surviving Purkinje network in regions of infarction, but the role of these phenomena in vivo has not been clarified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiologic basis for arrhythmias in ischemic heart disease. 636 66

Successive ischemic episodes are commonly seen in clinical and experimental cardiology. Although prolonged abnormalities of the canine myocardium have been described following a single ischemic episode, it is not known whether myocardial injury is cumulative following multiple ischemic episodes. Dogs were subjected to three 15-min left anterior descending coronary artery occlusions, each followed by 30 min of reperfusion. In vivo biopsies were obtained for biochemical analysis before and during the first occlusion and 30 min into each reperfusion period. ATP and creatine phosphate (CP) fell in the endocardium during occlusion by 24% and by 69% respectively (both p less than .0001). While CP recovered during each reperfusion period, ATP remained significantly depressed. Loss of membrane-permeable purine nucleotide synthesis precursors occurred with the first reperfusion period but not with the second and third reperfusion periods. Therefore, reperfusion following one 15-min coronary occlusion is associated with severe depression of myocardial high energy phosphates; however, two additional occlusions do not cause a further decrease of these substances when intermittent reperfusion is allowed for 30 min.
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PMID:Effects of recurrent ischemia on myocardial high energy phosphate content in canine hearts. 648 40

Intramyocardial pressure and segment length were measured during control conditions, during 30 sec coronary artery occlusion, and during reperfusion in the subendocardial (ENDO) and in the subepicardial (EPI) layers of the left ventricular wall, in 9 open-chest dogs. Under control conditions systolic subendocardial pressure, 179 +/- 11 mmHg, exceeded subepicardial pressure, 97 +/- 9 mmHg (P less than .001); the maximal rate of change of pressure in the subendocardium, 2231 +/- 170 mmHg/sec, was greater than in the subepicardium, 960 +/- 125 mmHg/sec, (P less than .001). Subendocardial systolic shortening, 23 +/- 2% was greater than subepicardial systolic shortening 16 +/- 1% (P less than .001). The maximal rate of systolic shortening in the subendocardium, 32 +/- 5 mm/sec, was also higher than in the subepicardial, 14 +/- 1 mm/sec (P less than .001). When the left anterior descending coronary artery was closed, subendocardial and subepicardial systolic pressures decreased immediately; conversely, appreciable changes in segment length were delayed 10-12 heart beats. After 30 sec of coronary occlusion a 35% reduction was observed in subendocardial and subepicardial systolic pressures, and systolic lengthening occurred. During reperfusion systolic shortening showed a brief overshooting and was back to control after 10 +/- 2 sec in subepicardium and 13 +/- 2 sec in subendocardium. Systolic intramyocardial pressure recovered in 14 +/- 3 sec in EPI and 18 +/- 2 sec in ENDO and subsequently rose above control level. Peak rebound occurred after 50-75 sec of reperfusion and was 27% higher than control in subendocardium and 20% in subepicardium. In 5 dogs the effects of coronary occlusions lasting 5, 15, 30, 45 and 60 sec were investigated. A progressive increase in ischemic depression and reperfusion rebound in subendocardial and subepicardial pressures was observed. These data show that subendocardial and subepicardial are both functionally depressed by coronary occlusion and that subendocardial and subepicardial both contribute to reperfusion hyperkinesis. Systolic intramyocardial pressures persist when shortening is abolished. Ischemic depression and reperfusion rebound of systolic intramyocardial pressures are affected by duration of coronary occlusion.
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PMID:Regional myocardial systolic function. Effects of coronary occlusion and reperfusion. 653 84

Calcium channel blockers suppress early ischemic arrhythmias, possibly by diminishing intracellular calcium overload and its effect on the ventricular action potential. To explore this, we compared the effects of diltiazem on ischemic "injury" potentials and ventricular fibrillation during serial coronary artery occlusions in dogs. Injury potentials and ventricular fibrillation were elicited every 15-25 minutes by simultaneous occlusion of the left anterior descending and circumflex arteries during rapid atrial pacing. DC epicardial electrograms were recorded differentially between the ischemic region and a small nonischemic region supplied by a proximal branch of the left anterior descending artery. Injury potentials developed with a uniform time course during five control occlusions, but were reduced by diltiazem infusion (0.5 mg/kg over 25 minutes) in each of eight dogs. The mean diastolic injury potential (T-Q depression) at 150 seconds of ischemia was 9.1 +/- 2.7 mV before diltiazem and 6.1 +/- 1.6 mV afterward (P less than 0.001). Diltiazem increased the mean time between coronary occlusion and ventricular fibrillation from 186 to 366 seconds (P less than 10(-5), but did not change the magnitude of the diastolic injury potential at onset of ventricular fibrillation. Diltiazem also delayed ischemia-induced conduction impairment to the same extent that it delayed injury potential development. In five dogs, the effect of diltiazem on regional blood flow near the epicardial electrodes was measured by infusion of radionuclide-labeled microspheres. Coronary occlusion reduced flow to the ischemic zone from 0.86 to 0.05 ml/min per g (P = 0.001). Diltiazem increased preocclusion flow by 11% (P = 0.03), but did not significantly alter flow during occlusion. Hemodynamic measurements show that diltiazem did not diminish cardiac work. Diltiazem therefore produced a flow-independent reduction of cellular depolarization during ischemia, which may be due to relief of calcium overload, and which may explain the antifibrillatory effect.
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PMID:Reduction of ischemic depolarization by the calcium channel blocker diltiazem. Correlation with improvement of ventricular conduction and early arrhythmias in the dog. 669 97

The effects of tachycardia on the QRS complex in the absence and in the presence of coronary arterial constriction are of possible clinical significance. To study the spatial and temporal distributions of these effects, a canine model simulating progressive coronary occlusion was studied. Tachycardia was induced by atrial pacing, coronary narrowing was produced by implantation of an ameroid constrictor about the left circumflex coronary artery and electrocardiographic effects were studied by isopotential mapping techniques at rates of up to 250 beats per minute, one to three weeks after constrictor implant. In five dogs. pacing without coronary constriction demonstrated the spatial and temporal dependence of QRS changes; tachycardia-induced changes varied from one torso site to another at any instant, and from one moment to another at any one torso location. Patterns in ten dogs with constrictors were dependent upon time after ameroid placement. Resting QRS and S-T segment distributions remained unchanged. One week after surgery, QRS and S-T segment patterns during pacing were as in controls. Two weeks after surgery, QRS patterns were as in controls but flat S-T segment depression resulted at high rates. After three weeks, QRS patterns during pacing were abnormal and S-T segment depression was observed. At each of the later times, the QRS response was similar at rates which did and which did not cause S-T depression. Thus, the effects of tachycardia on excitation and recovery forces in the presence of restricted coronary flow are independent of one another. This suggests that the two responses to ischemia may be due to different basic mechanisms and, hence, that their detection may reflect different myocardial abnormalities.
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PMID:Electrocardiographic effects of myocardial ischemia induced by atrial pacing in dogs with coronary stenosis. II. Comparison of S-T segment and QRS changes in dogs with left circumflex arterial narrowing. 669 23

The purpose of this study was to determine whether streptokinase exacerbates intramyocardial hemorrhage during coronary reperfusion, has any intrinsic effect on myocardial infarct size other than its ability to lyse proximal thrombi in coronary arteries, and can abolish the no-reflow phenomenon. Anesthetized open-chest dogs underwent coronary occlusion for 3 hr followed by 3 hr of reperfusion. Area of infarct was assessed by tetrazolium staining, anatomic zone of no-reflow by injection of the fluorescent dye thioflavin S at the end of the reperfusion period, regional blood flow during occlusion and reperfusion by the radioactive microsphere technique, and extent of gross hemorrhage by assessment of photographic enlargements of the heart slices. Area of infarction of the left ventricle was similar in control (13.4 +/- 3.6%) and streptokinase-treated dogs (13.0 +/- 2.9%; p = NS). Seven of eight dogs in the untreated group had anatomic perfusion defects as assessed by thioflavin S at the end of the reperfusion phase; seven of eight dogs in the streptokinase group had anatomic perfusion defects. There was no difference in the extent of gross hemorrhage between the two groups (6.5 +/- 2.1% of left ventricle in controls and 5.7 +/- 2.3% in streptokinase-treated dogs). Severe depression of regional blood flow during reperfusion was present within the infarcted tissue and was associated with an anatomic perfusion defect as defined by thioflavin S; there was moderate depression of flow within the noninfarcted, salvaged subepicardium. In a separate series of experiments, infarcts were assessed for hemoglobin content. Intramyocardial hemoglobin levels were not higher after fibrinolytic therapy plus reperfusion compared with reperfusion alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of streptokinase on intramyocardial hemorrhage, infarct size, and the no-reflow phenomenon during coronary reperfusion. 674 55

We quantitated hemorrhage associated with reperfusion after varying periods of myocardial ischemia and examined the flow characteristics that accompany reperfusion hemorrhage. Anesthetized dogs were reperfused after 2, 6 or 24 hours of circumflex occlusion. A control group underwent coronary occlusion without reperfusion. Radioactive microspheres were injected before and 5 minutes and 24 hours after reperfusion. The papillary muscles were analyzed for hemoglobin content, flow during myocardial ischemia and flow early and 24 hours after reperfusion. Myocardial creatine kinase activity was assayed to determine the severity of myocardial necrosis in the papillary muscles. Hemorrhage into the posterior papillary muscle was dependent upon the duration of coronary artery occlusion. Posterior papillary hemoglobin averaged 14 mg/g in the 2-hour group, 28 mg/g in the 6-hour group and 36 mg/g in the group reperfused 24 hours after occlusion, compared with 8.7 mg/g in the control group. Myocardial hemorrhage was associated with severe depression in myocardial CK and marked depression in flow to the ischemic area (i.e., collateral flow) during the occlusion. Early reflow averaged 112 ml/min/100 g in the 2-hour group, 61 ml/min/100 g in the 6-hour group and only 5.8 ml/min/100 g in the 24-hour group. Therefore, myocardial hemorrhage induced by reperfusion of the acutely ischemic myocardium is associated with severe ischemia during occlusion and severe myocardial necrosis, but does not depend upon the magnitude of early reflow. Myocardial hemorrhage may occur even though initial reflow values are markedly decreased.
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PMID:The time course and characterization of myocardial hemorrhage after coronary reperfusion in the anesthetized dog. 683 66

The effect of intracoronary nifedipine on regional and global left ventricular performance, coronary vasomotility, and myocardial oxygen consumption is reported. Left ventricular pressures and volume indices of contractility and relaxation were simultaneously recorded in five patients without coronary artery disease. In these patients, nifedipine in the left main coronary artery not only delayed (+115 ms) anterior wall contraction but also slowed (3.5 vs 1.9 cm/s) and depressed it (-26%), resulting in a depression of global left ventricular ejection. This asynchrony and depression of regional contraction is considered to be responsible for the slowed isovolumic contraction and relaxation of the whole ventricle. In 10 other patients with coronary artery disease, coronary sinus blood flow and myocardial oxygen consumption were measured before and after intracoronary nifedipine. The observed decrease in myocardial oxygen consumption (-28%) depended primarily on a decrease in contractility and left ventricular performance. In a third study group of 12 patients with coronary artery disease, the effects of intracoronary nifedipine on the coronary vasomotility of 40 coronary segments (normal, prestenotic, stenotic, poststenotic) were quantitatively determined. Left ventricular haemodynamics and coronary sinus saturation were monitored while the cineangiograms were recorded before and after nifedipine. Nifedipine provoked vasodilatation of the normal (+10.3%), prestenotic, stenotic (+4 to 30%), and poststenotic (+16.4%) coronary segments, which persisted after the disappearance of its direct effects on the myocardium. This transient regional "cardioplegic" effect of nifedipine, associated with an increase in coronary blood flow, a reduction in myocardial oxygen consumption, and a vasodilatation of the epicardial vessels is likely to be beneficial during temporary coronary occlusion such as occurs in spasm or transluminal angioplasty.
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PMID:Influence of intracoronary nifedipine on left ventricular function, coronary vasomotility, and myocardial oxygen consumption. 683 31


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