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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of brief reversible ischemia on coronary vascular function remains controversial. Studies using a 15-min coronary occlusion have reported an impairment of vasodilator reserve, whereas studies using shorter occlusions have not. To elucidate the relation between postischemic vascular abnormalities and duration of ischemic insult, we evaluated coronary reserve after a 10-min coronary occlusion in the same model previously used for a 15-min occlusion. Open-chest dogs (n = 12) underwent a 10-min left anterior descending coronary artery occlusion followed by reflow. Four hours after reperfusion, coronary resistance was higher in the postischemic "stunned" myocardium than in the nonischemic myocardium, both at rest and during adenosine-induced maximal vasodilation; in addition, all indexes of reactive hyperemia after a 40-s coronary occlusion were significantly lower than at baseline. There was no appreciable correlation between systolic wall thickening in the stunned myocardium and 1) the resting myocardial perfusion, 2) the hyperemia attained during adenosine, and 3) the hyperemic response to a 40-s coronary occlusion. The loss of coronary reserve was less than that previously observed after a 15-min occlusion, suggesting that the magnitude of the postischemic vascular abnormalities increases with the duration of the ischemic insult. In control dogs (n = 8), there was no change in coronary reserve. We conclude that a brief ischemic insult lasting only 10 min is sufficient to cause a prolonged increase in resting vascular resistance and a prolonged impairment in vasodilator responsiveness, both of which persist for at least 4 h, indicating the presence of a postischemic microvascular dysfunction. The severity of these vascular derangements is not related to the severity of the contractile depression, suggesting that they may represent a relatively independent phenomenon. The differences among previous studies may be due, in part, to the fact that the abnormalities observed after a 10-min occlusion are relatively subtle.
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PMID:Decreased flow reserve in "stunned" myocardium after a 10-min coronary occlusion. 188 25

Effects of coenzyme Q9 (25 mg/kg), N6-cyclohexyl adenosine (CHA, 100 micrograms/kg) and their combination were compared in rats with short-term or permanent ligation of the left coronary artery. The following parameters were evaluated in three series of experiments: 1) incidence and duration of ventricular fibrillation and tachycardia during coronary occlusion (10 min) and consecutive reperfusion (5 min); 2) contractility and electrical stability of the heart (ventricular fibrillation threshold) in animals with 2-day myocardial infarction; 3) ischemic myocardial mass after coronary occlusion (5 min) and necrotic tissue mass in 2-day myocardial infarction. The rats were given oral drugs 5 days and 2 hours before the study. All the experiments were performed in open-chest anesthetized (nembutal, 50 mg/kg) rats exposed to ventilation at room air. Both the coenzyme Q9 and CHA significantly reduced the incidence and duration of coronary occlusion and reperfusion arrhythmias, prevented cardiac contractile depression (heart rate.developed pressure) and increased ventricular fibrillation threshold). The effect of coenzyme Q9 was more marked than that of CHA. Coenzyme Q9 substantially reduced necrotic tissue mass while CHA diminished ischemic tissue mass. At the same time the total cardioprotective action of the Q9 + CHA combination was more pronounced than that of them used alone.
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PMID:[Cardioprotective effect of combined use of coenzyme Q9 and cyclohexyladenosine in ischemia, reperfusion and acute myocardial infarction]. 192 Nov 36

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.
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PMID:Dipyridamole-induced decrement of functional recovery of postischemic reperfused myocardium in conscious dogs with well-developed coronary collateral circulation. 201 68

Sixteen patients undergoing PTCA of a significant lesion of the left anterior descending coronary artery received either 0.3 mg nisoldipine or placebo intravenously. Immediately before and during balloon inflation the following parameters were measured: aortic pressure, post-stenotic pressure, coronary occlusion pressure, diastolic pulmonary artery pressure, coronary sinus flow (thermodilution), and intracoronary ECG. After placebo there were no statistically significant changes. Nisoldipine led to a decrease in aortic pressure from 109 +/- 12 to 93 +/- 11 mm Hg (p less than 0.05) before, and from 103 +/- 14 to 92 +/- 8 mm Hg (NS) during balloon inflation. In contrast, coronary occlusion pressure remained unchanged. Heart rate increased from 80 +/- 13 to 96 +/- 16/min before (p less than 0.05), and from 87 +/- 18 to 97 +/- 17/min during balloon inflation (NS). Coronary sinus flow was increased from 95 +/- 16 to 116 +/- 13 ml/min before balloon inflation (p less than 0.01), and from 70 +/- 25 to 86 +/- 26 ml/min during balloon inflation (NS). ST-segment depression or elevation, severity of angina pectoris, and the diastolic pulmonary artery pressure remained unchanged. Thus, 0.3 mg nisoldipine led to a peripheral vasodilatation. While the aortic pressure decreased, coronary occlusion pressure remained unaffected. This could be explained by a marked dilatation of collateral vessels due to nisoldipine. However, myocardial ischemia remained unaffected as a result of the constant coronary occlusion pressure.
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PMID:[Effect of the calcium antagonist nisoldipine on coronary circulation and myocardial ischemia in temporary coronary occlusion]. 208 55

We presented two cases of acute coronary occlusion after successful percutaneous transluminal coronary angioplasty (PTCA) associated with a treadmill stress testing. Case 1: A 54-year-old man with effort angina was referred to our hospital for cardiac catheterization. At the time of cardiac catheterization, the proximal RCA had a 99% diameter narrowing, and the proximal LCX had a 90% diameter narrowing. PTCA was performed and both lesions were successfully dilated. Eight days after PTCA, he had a symptom-limited treadmill stress testing, using the Bruce protocol. The exercise was terminated at a peak heart rate of 173/min (103% of aged-predicted maximal heart rate), and at a maximal systolic blood pressure of 140 mmHg. A few minutes after the end of exercise, he developed a severe chest pain and ECG changes, which showed ST elevation in leads II, III, aVF and ST depression in leads V4-V6. Emergency coronary angiography disclosed an acute coronary occlusion of RCA at the site of PTCA. Emergency PTCA was performed and the lesion was successfully re-dilated. Case 2: A 68-year-old man was referred to our hospital for cardiac catheterization a month after subendocardial anterior myocardial infarction. At the time of cardiac catheterization, the proximal LAD have a 99% diameter narrowing. PTCA was performed and the lesion was successfully dilated. 18 days after PTCA, he had a symptom-limited treadmill stress testing, using the Bruce protocol. The exercise was terminated at a peak heart rate of 158/min (102% of aged-predicted maximal heart rate), and at a maximal systolic blood pressure of 218 mmHg. Ten minutes after the one of 218 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of acute coronary occlusion after successful coronary angioplasty associated with a treadmill stress testing]. 221 90

Prolonged depression of segmental systolic thickening after brief coronary artery occlusion may result principally from events during reperfusion rather than during the ischemic interval. Thus, cellular calcium overload at reperfusion may be a mediator of contractile dysfunction after brief ischemia, and reduction of calcium entry by diltiazem, a calcium channel antagonist, may enhance recovery of systolic thickening after brief periods of ischemia. Thirteen awake unsedated dogs instrumented with hemodynamic catheters, left anterior descending coronary artery occluders and five to six pairs of intramyocardial sonomicrometers underwent two 15 min coronary artery occlusions with 24 h reperfusion. The order of infusion of diltiazem (15 micrograms/kg per min) or saline solution was alternated. Systolic thickening, hemodynamic variables and regional myocardial blood flow were measured serially over 24 h. Despite equally severe ischemic dysfunction during coronary occlusion, diltiazem-treated segments with systolic thinning during ischemia recovered control segmental thickening significantly earlier than saline solution-treated segments (at 30 versus 180 min of reperfusion). Blood pressure was mildly decreased during diltiazem treatment; therefore, a second group of 10 dogs underwent a similar occlusion and reflow period during infusion of nitroprusside to lower mean arterial pressure equivalently. Decreases in blood pressure in this group resulted in some improvement in segmental systolic function; however, this did not reach statistical significance at any time. Regional myocardial blood flows were similar in the saline solution- and diltiazem-treated groups during ischemia and reflow. Thus, it is concluded that 1) diltiazem infusion significantly enhanced recovery of segmental systolic thickening after 15 min of ischemia and 24 h of reperfusion; 2) the enhancement in segmental systolic function could not entirely be attributed to decreased mean arterial pressure; 3) improvement in postischemic segmental ventricular function was seen only in those segments with systolic thinning during ischemia; thus, segments with the most severe ischemic dysfunction benefited most; and 4) there were no important differences in regional myocardial blood flow during ischemia and reperfusion between saline- and diltiazem-treated animals.
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PMID:Differential enhancement of postischemic segmental systolic thickening by diltiazem. 230 44

Reperfusion after brief, reversible myocardial ischemia is associated with prolonged depression of contractile function (myocardial "stunning"); however, the effect on coronary vascular function has not been defined. Thus, open-chest dogs (n = 14) underwent a 15-minute left anterior descending coronary artery (LAD) occlusion followed by reflow. Four hours after reperfusion, regional myocardial blood flow (microspheres) was significantly (p less than 0.01) lower and coronary vascular resistance significantly (p less than 0.01) higher in the postischemic as compared with the nonischemic endocardium. Furthermore, during maximal vasodilation elicited by intravenous adenosine (n = 6), myocardial blood flow was lower (p less than 0.05) and coronary vascular resistance higher (p less than 0.05) in the postischemic as compared with the nonischemic myocardium, both in the endocardial and in the epicardial layers. Similarly, during maximal dilation elicited by intravenous papaverine (n = 8), myocardial blood flow was lower (p less than 0.05) and vascular resistance higher (p less than 0.05) in the postischemic as compared with the nonischemic endocardium; a directionally similar trend was observed in the epicardium. Four hours after reperfusion, all indexes of reactive hyperemia after a 40-second coronary occlusion were significantly lower in the LAD than in the control circumflex coronary artery (n = 8). There was no appreciable correlation between systolic wall thickening in the stunned myocardium and 1) the resting myocardial perfusion, 2) the hyperemia attained during adenosine or papaverine, and 3) the hyperemic response to a 40-second coronary occlusion. In control dogs that did not undergo a 15-minute LAD occlusion (n = 15), there were no differences in myocardial blood flow or vascular resistance between the LAD-dependent and the circumflex-dependent bed, either before or during adenosine (n = 7) or papaverine (n = 8). Furthermore, reactive hyperemia after a 40-second occlusion did not differ between the LAD and the circumflex artery (n = 8). In conclusion, a brief (15 minute), reversible ischemic insult causes a prolonged increase in resting vascular resistance and a prolonged impairment in vasodilator responsiveness, both of which persist for at least 4 hours. The severity of these vascular derangements is not related to the severity of contractile depression, suggesting that they may represent a relatively independent phenomenon. It is proposed that, in addition to myocardial "stunning," reversible ischemia also causes a microvascular "stunning."
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PMID:Prolonged impairment of coronary vasodilation after reversible ischemia. Evidence for microvascular "stunning". 237 75

In recent years an enhanced interest among researchers combined with the availability of new technologies has increased our knowledge of the mechanisms that generate arrhythmias in patients with ischemic heart disease. Convincing evidence has been obtained to support the occurrence of reentry in ischemic myocardium. This has been especially apparent in canine studies in the surviving layers overlying infarctions several days after coronary occlusion. In this planar model, the reentry circuit forms a figure-8 configuration around an arc of functional block due to refractoriness; the center of the arc is the site of unidirectional block and reentry. The reentry circuit is sustained by wavefronts of activation encircling segments in which the tissue on either side is alternately receptive and refractory, a variant of the leading circle model of reentry. The relatively prolonged refractoriness in ischemic tissue is due to time-dependent refractoriness, i.e., postrepolarization refractoriness, which is most prominent in more severely depolarized cells. Slow conduction is related in part to primary depression of the fast channels. There is a great variation in refractory periods in ischemic tissue because of variation in action potential duration and in the duration of time-dependent refractoriness. The depolarized resting potentials of cells in acute ischemia are due in part to extracellular accumulation of potassium and intracellular accumulation of calcium. In the latter stages of ischemia it is likely that abnormalities of ion distribution across the sarcolemma play a role. It has also been demonstrated that ischemic Purkinje fibers show abnormal automaticity, i.e., enhanced phase 4 depolarization at depolarized diastolic potentials, and afterdepolarizations with triggered firing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Generation of arrhythmias in myocardial ischemia and infarction. 244 70

To examine whether coronary occlusion causing transmural ischemia was accurately reflected by ST-segment elevation on routine electrocardiograms, intracoronary and surface electrocardiograms were simultaneously recorded during percutaneous transluminal coronary angioplasty (PTCA). The study group consisted of 54 patients who had intracoronary ST-segment elevation during transient coronary occlusion (left anterior descending [LAD]: 25 patients, left circumflex [LC]: 19 patients, right coronary artery: 12 patients). Elevation of the ST segment on the surface electrocardiogram (greater than or equal to 0.1 mV) was recorded in 84% of patients during LAD dilatation, in 32% of patients during LC dilatation (p less than 0.01 vs LAD and right), and in 92% of patients during right coronary dilatation (not significant vs LAD). The magnitude of intracoronary ST elevation was 1.10 +/- 0.8, 1.68 +/- 1.2 and 0.8 +/- 0.6 mV for the LAD, LC and right occlusions, respectively (not significant). Thus, despite the comparable magnitude of intracoronary ST elevation, LC occlusion resulted in ST-segment elevation on the surface electrocardiogram in significantly fewer patients than did LAD or right occlusion. During LC occlusion, 9 patients had no electrocardiographic changes and 4 had only precordial ST depression. Thus, in patients with transmural ischemia during right or LAD occlusions, concordant ST elevation on the surface electrocardiogram is common. In contrast, ST-segment elevation is an insensitive marker of LC occlusion. In patients with ongoing ischemic symptoms and isolated precordial ST depression or no repolarization abnormalities, LC occlusion should be considered in the differential diagnosis.
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PMID:Surface electrocardiogram in the detection of transmural myocardial ischemia during coronary artery occlusion. 252 Nov 94

To evaluate the significance of "reciprocal" ST segment depression resulting from coronary occlusion, 27 patients with single vessel coronary disease were studied with intravenous digital subtraction left ventriculography before and during angioplasty of the left anterior descending coronary artery. During balloon inflation, 13 patients developed inferior lead ST depression in addition to anterior lead ST elevation (Group 1), whereas the remaining 14 patients did not (Group 2). The degree of anterior lead ST elevation in Group 1 (5 mm) was greater than that in Group 2 (1.5 mm, p less than 0.001) as was the reduction in left ventricular ejection fraction (24% versus 13%, respectively; p less than 0.02). Anterior and apical regional shortening decreased in both groups similarly, but an additional decrease in anterobasal shortening was confined to Group 1 (from 38% to 21%; p less than 0.002). Despite the presence of inferior lead ST depression in Group 1, inferior regional shortening did not change and inferobasal contraction was enhanced (from 4% to 29%; p less than 0.01). Inferior lead ST segment depression during anterior descending coronary angioplasty reflects a greater degree of anterior wall ischemia. The concurrent preservation of inferior wall contraction and the augmentation of infero-basal shortening confirm that this electrocardiographic feature is a "reciprocal" phenomenon rather than a manifestation of remote ischemia.
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PMID:Significance of "reciprocal" ST segment depression: left ventriculographic observations during left anterior descending coronary angioplasty. 252 57


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