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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Passive intracoronary perfusion of therapeutic agents has been used in the clinical setting to attenuate the effects of brief episodes of myocardial ischemia. The objective of this study was to assess the effects of low-flow coronary infusion with or without Mg2+ on tissue necrosis and cardiac hemodynamics after prolonged regional ischemia. In 33 anesthetized dogs (5 excluded during study), the left anterior descending coronary artery was occluded for 6 h. Dogs were assigned to three groups: the first group (n = 8) was subjected to 6 h coronary occlusion without low-flow perfusion (controls), the second group (n = 10) received a low-flow coronary infusion of Ringer's lactate (Mg(2+)-free), and the third group (n = 10) received a low-flow coronary infusion of Ringer's lactate plus Mg2+ sulfate (15 mM). Tissue necrosis was evaluated using tetrazolium staining and was normalized to the principal baseline predictors of infarct size including anatomic risk zone (microsphere autoradiography) and coronary collateral flow. In control hearts, infarct size comprised 51.1 +/- 4.1% of the risk zone (40.8 +/- 5.1% left ventricular cross-sectional area (LV)). In the Mg(2+)-free and Mg2+ groups, risk zone size was 17.3 +/- 2.2 and 16.8 +/- 1.8% LV (p < 0.05 vs. controls), while infarct size was 23.1 +/- 3.1 and 24.9 +/- 8.1% (p < 0.05 vs. controls), respectively. Coronary collateral flow in the endocardium was similar for all of the experimental groups; however, hearts subjected to ischemia with low-flow perfusion of Ringer's lactate demonstrated significantly higher epicardial coronary collateral flow levels compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of low-flow infusion and magnesium on tissue necrosis during regional ischemia in the canine myocardium. 145 Oct 22

Myocardial reperfusion is the single most useful therapeutic approach in patients with acute myocardial infarction. The thousands of lives saved each year by this treatment are the result of scientific progress in very different areas, including the biopathology of myocardial ischemia and reperfusion, the mechanisms of coronary occlusion, the pharmacology of the fibrinolytic system, and clinical research. The 30% reduction in mortality achieved by fibrinolytic treatment in patients with acute myocardial infarction does not fit, apparently, with the short time-window during which restoration of blood flow results in significant myocardial salvage in animal models with few collaterals. This discrepancy could be due to the protective effect of intermittent coronary occlusions immediately preceding stable occlusive thrombosis (ischemic preconditioning), or to other possible beneficial effects of reperfusion independent of myocardial salvage, as limitation of ventricular remodelling or reduction of the risk of cardiac rupture or severe arrhythmias. Clearly, the best approach to increase the beneficial effects of reperfusion therapy is to perform it as early as possible; the cost-effectiveness of pre-hospital treatment strategies is now under investigation. In the other hand, current reperfusion therapy cannot be considered optimal. Thrombolytic agents fail to achieve recanalization of the infarct related vessel in 20-30% of patients, and 10-15% of the successfully opened arteries present early reocclusion. In certain subgroups of patients, such in those with cardiogenic shock, failure rate is higher. Mechanical recanalization by "direct" angioplasty represent an alternative reperfusion method, which utility has been established in certain circumstances only. So, well in the "reperfusion era", many questions remain open.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The era of myocardial reperfusion]. 147 4

To evaluate, in the absence of lung inflation, the cardiovascular effects of single and repetitive pleural pressure increments induced by thoracic vest inflations and timed to occur during specific portions of the cardiac cycle, seven chronically instrumented dogs were studied. Reflexes and left ventricular (LV) performance were varied by autonomic blockade, circumflex coronary occlusion (with and without beta-blockade), or cardiac arrest. Single late systolic, but not early systolic, vest inflations significantly increased LV stroke volume both before (+12.4%) and after myocardial depression by coronary occlusion+beta-blockade (+18.5%) when performed after a period of apnea to control preload and rate. During vest inflations, LV and aortic pressures increased to a greater degree than esophageal pressure (by 51 vs. 39 mmHg, P = 0.0001). Lung inflations (26 trials in 3 dogs) during early or late systole failed to increase stroke volume, despite peak esophageal pressures of 11-26 mmHg. With autonomic reflexes intact, repetitive vest inflations coupled to early systole, late systole, or diastole induced a large (40%) but unspecific systemic flow increase. In contrast, during autonomic blockade, flow increased slightly (7.5%, P < 0.05) with late systolic compared with diastolic inflations but not relative to baseline. During coronary occlusion (with or without beta-blockade), no cycle-specific differences were seen, whereas matched vest inflations during cardiac arrest generated 20-30% of normal systemic flow. Thus only single late systolic thoracic vest inflations associated with large increments in pleural pressure increased LV emptying, presumably by decreasing LV afterload and/or focal cardiac compression. However, during myocardial ischemia and depression, coupling of vest inflation to specific parts of the cardiac cycle revealed no hemodynamic improvement, suggesting that benefits of this circulatory assist method, if any, are minor and may be restricted to conditions of cardiac arrest.
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PMID:ECG-synchronized thoracic vest inflation during autonomic blockade, myocardial ischemia, or cardiac arrest. 149 Sep 33

During successful and uncomplicated angioplasty (PTCA), we studied the effect of a short lasting myocardial ischemia on plasma creatine kinase, creatine kinase MB-activity, and creatine kinase MM-isoforms (MM1, MM2, MM3) in 23 patients. Eleven patients, in whom diagnostic coronary angiography was performed, served as the control group. Blood was sampled after PTCA and every 2 h for the next 12 h, and after 24 h. CK- and CK-MB activities were determined enzymatically, the MM-isoforms by isoelectric focussing. After PTCA total CK and CK-MM3 increased significantly from 23 +/- 10 to 40 +/- 31 U/I (p less than 0.01) and from 18 +/- 5 to 32 +/- 10% (p less than 0.0005), respectively. The ratio MM3:MM1 also increased significantly from 0.4 +/- 0.1 to 1.2 +/- 0.7 (p less than 0.0005). Enzyme maxima for CK-MM3 and the ratio MM3:MM1 were reached 6 h after PTCA, for total CK 10 h after PTCA. This increase was independent of changes in the ECG, of symptoms during PTCA, as well as of the number and duration of balloon inflations. In the control group no changes in enzyme activity were found. Thus, after uncomplicated PTCA a significant increase of total CK and CK-MM-isoforms can be found, which may be due to the short-lasting myocardial ischemia following coronary occlusion.
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PMID:[Increase in creatine kinase and its MM isoforms after successful and uncomplicated coronary angioplasty]. 149 53

Ventricular arrhythmias are primarily responsible for sudden cardiac death early after the onset of acute myocardial ischemia. We designed an experimental model to simultaneously characterize regional myocardial function, myocardial blood flow, and electrophysiological parameters, and to determine predisposing factors for the development of early ventricular arrhythmias (EVA). The left circumflex coronary artery was occluded in six anesthetized (n = 2 piritramide/N2O, n = 4 chloralose/urethane) mongrel dogs. Systolic wall thickening (%WT) in a control zone and in the central ischemic zone was measured with sonomicrometry and regional myocardial blood flow (RMBF) with colored microspheres. Excitability and relative refractory period at the stimulus electrode and conduction times to all other electrodes were determined with a three-dimensional transmural multi(16)-electrode assay using a computer algorithm. In three of six dogs spontaneous EVA occurred 4 to 6 min after coronary occlusion, degenerating to ventricular fibrillation in two of these dogs. The three dogs developing EVA were not distinguished from those not developing EVA, neither by the kind of anesthesia nor by ischemic % WT (-6.6 +/- 3.8 [SD] vs -7.8 +/- 1.6, ns). Also, dogs with and without EVA did not differ significantly in excitability and relative refractory period. In contrast, dogs with EVA were characterized by a greater mass of severely ischemic myocardium, i.e., exhibiting a RMBF reduction to less than 0.1 ml/(min.g) (18 +/- 3 g vs 7 +/- 4 g, p less than 0.05), and by an increase in subendocardial conduction times of greater than 100% above the respective pre-ischemic values (120 +/- 18% vs 66 +/- 9%, p less than 0.05). Dogs with and without EVA were not as clearly distinguished by the increases in subepicardial (81 +/- 22% vs 46 +/- 15%, ns) and transmural (98 +/- 31% vs 67 +/- 14%, ns) conduction times. The development of EVA is associated with a greater mass of severely ischemic myocardium and a greater increase in subendocardial conduction times.
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PMID:Three-dimensional analysis of regional mechanical function, blood flow and electrophysiological parameters during early myocardial ischemia in dogs. 152 Feb 47

Neomammalian and paleomammalian (limbic) brain structures control different behaviors and the autonomic support specific to each. Both neural systems are involved in cardiovascular disorders. Our previous studies showed that bilateral cryoblockade of a neomammalian structure (the frontal lobes) reduces blood pressure elevations in experimental hypertension and prevents lethal arrhythmogenesis in experimental myocardial infarction. Other studies showed that bilateral lesions in a paleomammalian structure (amygdala) also reduce the blood pressure elevations. Thus, we hypothesized that cryoblockade of the amygdala would prevent lethal arrhythmogenesis. We found that cooling of cryoprobes implanted bilaterally in the amygdala prevented ventricular fibrillation in five of eight pigs during a 20-minute period of reversible myocardial ischemia, whereas cryoblockade in structures surrounding the amygdala (five pigs), unilateral cryoblockade in the amygdala (two pigs), or sham operations (three pigs) did not prevent ventricular fibrillation (p less than 0.003). In two of the five pigs with amygdaloid blockade, the cooling was reversed at 20 minutes while the coronary occlusion continued (24 hours), and still ventricular fibrillation did not occur. In all other cases, ischemia was reversed at 20 minutes so that the heart could recover; this enabled histochemical documentation that the heart was normal at the time(s) ischemia was induced, and it allowed within-subject control experiments. Amygdaloid cryoblockade produced a small but significant increase in heart rate (10 beats per minute) without a change in blood pressure. We conclude that the paleomammalian brain, like its neomammalian counterpart, mediates brain effects on fatal arrhythmogenesis.
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PMID:Cryoblockade in limbic brain (amygdala) prevents or delays ventricular fibrillation after coronary artery occlusion in psychologically stressed pigs. 153 95

Calcium antagonists may have a valuable role in ameliorating the extent and duration of myocardial ischemia following infarction. The precise cellular effects of these agents are being revealed through studies using the model of transient coronary occlusion induced by coronary angioplasty. The class of calcium antagonists is not uniform, and these diverse agents may have a favorable effect on ischemia through one or more of the following mechanisms: direct cardioprotective effects, prevention of calcium accumulation in the mitochondria in ischemic cells, reduction in oxygen consumption or in coronary artery vasoconstriction or coronary spasm, prevention of ischemia-induced arrhythmias, and increased coronary blood flow to ischemic tissue directly or through enhancement of collateral flow. Recent studies of diltiazem, nifedipine, nicardipine, nisoldipine, and amlodipine, as representative agents, are reviewed.
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PMID:Perspective: the cellular influences of calcium antagonists on systemic and coronary hemodynamics. 154 39

This study examined the effect of treatment with dimethylthiourea (DMTU), a highly cell-permeable scavenger of hydroxyl radicals, on tissue necrosis in rabbit hearts during myocardial ischemia and reperfusion. Sixty-two rabbits underwent 45 minutes of coronary occlusion with, or without, coronary reperfusion for 3 hours. A saline vehicle, or DMTU (500 mg/kg intravenously [iv]) was administered over 45 minutes starting either 10 minutes before or 10 minutes after coronary occlusion, or 10 minutes before coronary reperfusion. Anatomic risk zone size was assessed using microsphere autoradiography, and the area of necrosis was determined using tetrazolium staining. Cardiac hemodynamics and risk zone size were similar for all treatment groups. No differences were observed in the extent of tissue necrosis (normalized to risk zone size) for saline- and DMTU-treated rabbits subjected to 45 minutes (61.2 +/- 23.1% vs. 70.6 +/- 16.5%) or 225 minutes (82.8 +/- 5.4% vs. 78.3 +/- 5.9%) of permanent coronary occlusion without reperfusion. Similarly, tissue necrosis in rabbits with 45 minutes coronary occlusion followed by 3 hours reperfusion was not significantly reduced when DMTU was administered either 10 minutes before coronary occlusion, 10 minutes after coronary occlusion, or 10 minutes before coronary reperfusion (67.0 +/- 9.9%; 57.6 +/- 10.6%; 68.3 +/- 13.3%) compared to saline-treated controls (76.6 +/- 10.5%). These results demonstrate that the hydroxyl radical scavenger DMTU does not appear to influence the progression of myocyte injury in this experimental model of acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inability of dimethylthiourea to limit tissue necrosis during acute myocardial infarction in rabbits. 845 91

The purpose of this study was 1) to clarify whether augmented myocardial contraction after a brief coronary occlusion, i.e. post-ischemic hypercontraction, depends on a transient increase in coronary blood flow or preceding myocardial ischemia, and 2) to identify the role of catecholamines or calcium flux in this phenomenon. Sixteen mongrel dogs were examined in open-chest anesthetized condition. One-minute reperfusion after two-minute total coronary occlusion of the left anterior descending artery resulted in a transient increase in segment shortening. Intracoronary administration of adenosine caused hyperemia without any changes in segment shortening. Two minutes of total coronary occlusion with adenosine caused post-ischemic hypercontraction to the same degree, but without any additional hyperemia. Two minutes of partial occlusion with 75% flow reduction caused less post-ischemic hypercontraction. Post-ischemic hypercontraction did not occur after partial occlusion with 50% flow reduction, irrespective of hyperemia with adenosine during reperfusion. Propranolol or verapamil did not prevent this phenomenon. Thus, post-ischemic hypercontraction is not dependent on the transient increase in coronary blood flow, but is related to the preceding myocardial ischemia. Local release of catecholamines is not likely to be the cause. A calcium antagonist, verapamil, did not modify this phenomenon. The precise mechanism of this phenomenon is still uncertain, although some alterations in cellular hemostasis, such as ionic changes, are likely to be the cause.
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PMID:Mechanisms of transient augmentation of myocardial contraction after a brief coronary occlusion. 157 8

From October 1, 1986 to December 31, 1989 directional coronary atherectomy was performed during 1,020 procedures (1,140 lesions) at 14 clinical centers. Abrupt vessel closure, defined as a total coronary occlusion or subtotal occlusion associated with clinical evidence of myocardial ischemia, occurred in 43 procedures (4.2%). It developed in the catheterization laboratory in 34 patients, but was delayed 1 to 96 h after directional atherectomy in 9 patients. By univariate analysis the incidence of abrupt closure was higher in directional atherectomy of de novo lesions (p less than 0.001), lesions in the right coronary artery (p = 0.001) and diffuse lesions (p = 0.04). The incidence of abrupt closure tended to be lower in directional atherectomy of saphenous vein grafts as opposed to native coronary arteries (1.6% vs. 4.4%; p = 0.08). Clinical findings during abrupt closure included severe angina in 26 patients, myocardial infarction in 17 patients, hypotension in 5 patients and death in 2 patients. Balloon angioplasty was attempted in 32 patients after abrupt vessel closure. In 16 patients balloon angioplasty resulted in initial resolution of the closure episode, although 1 patient died 96 h after the procedure. Fifteen of 16 patients without initial improvement after balloon angioplasty underwent coronary bypass operation; 9 additional patients with abrupt closure were referred directly for bypass operation. It is concluded that abrupt vessel closure develops relatively infrequently after directional coronary atherectomy. In the absence of severe coronary dissection, abrupt closure after directional atherectomy may be effectively managed with balloon angioplasty in some cases, although coronary bypass operation is often required.
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PMID:Abrupt vessel closure after directional coronary atherectomy. The U.S. Directional Atherectomy Investigator Group. 159 28


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