Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of heart rate on the amount and distribution of collateral blood flow was determine in open-chested dogs 1 h after coronary artery ligation. Flows to ischemic and nonischemic regions of left ventricle were measured with 7- to 10- mum diam radioactive microspheres during base-line conditions (118 +/- 6 beats/min) and again during atrial pacing at rates 20 and 40% above control (141 +/- 7 and 165 +/- 9 beats/min). During pacing aortic and left atrial pressures and cardiac output did not change significantly, whereas ST segment elevation in epicardial electrograms increased markedly. In nonischemic myocardium, mean flow increased approximately in proportion to the increase in rate, but subepicardial (EPI) flow increased somewhat more than subendocardial (ENDO) flow. In ischemic myocardium, overall flow did not change significantly, but a redistribution from ENDO to EPO was seen. At the faster rate ENDO flow fell 25% (P less than 0.02), EPI flow increased slightly, and ENDO/EPI fell in 8/9 animals (mean 0.54-0.43, P less than 0.01). The ENDO/EPI maldistribution present in ischemic muscle is thus accentuated by tachycardia; this may account for part of the harmful effect of tachycardia in acute myocardial infarction and may help explain the disproportionate ENDO ischemia seen in angina pectoris.
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PMID:Effect of tachycardia on left ventricular blood flow distribution during coronary occlusion. 126 2

In summary, although exercise is, as is every other procedure, imperfect with regard to sensitivity and specificity, it provides an invalualbe adjunct in the evaluation of patients with coronary disease. The test is simple, inexpensive, safe and rapidly performed and is an invaluable aid in screening patients with possible coronary disease. It is used in an asymptomatic population for industrial purposes, is useful in assessing the etiology of otherwise undiagnosed chest pain, helpful in evaluating the overall severity of ischemia [and therefore in culling-out those patients that might benefit from coronary angiography], is useful in following the course of patients with proven coronary disease [including those with acute myocardial infarction], and has found a place in the follow-up evaluation of individuals having aortocoronary bypass surgery. As a screening procedure, the treadmill test aids in seeking out that group of patients with coronary disease with potentially malignant lesions, i.e. main left coronary lesions, triple-vessel disease and [to a lesser extent] severe proximal left anterior descending coronary disease. Hence, the finding of marked depth of ST depression, prolonged duration of ischemia associated with deep ST segments, serious exercise-induced ventricular arrhythmias and hypotension produced during mild-to-moderate exercise might each be an indication of extensive coronary angiography. In many cases exercise testing is superior to coronary angiography, being a simpler, safer screening procedure, and a more functional test in documenting the presence or absence of coronary insufficiency.
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PMID:Interpretation and limitations in stress testing. 127 86

The antianginal activity of Cardil, 240-360 mg/day, and Cordafen, 30-60 mg/day, was evaluated in 74 patients with non-Q wave acute myocardial infarction. Repeated 24-hour ECG monitoring was used as an objective tool for the evaluation of their therapeutical efficiency in two randomized groups. Unlike Cordafen, Cardil significantly reduced the average heart rate from 4.7 to 1.5 and the average duration from 20.5 to 11.5 min and the average total duration of myocardial ischemic episodes from 95.1 min/day to 16.7 min/day. Both Cardil and Cordafen considerably reduced the total duration of painful ischemic attacks, but only did Cardil reduce silent episodes (p < 0.001). Both Cardil and Cordafen substantially reduced resting ischemia, but Cardil also decreased the rate of exercise-induced ischemic episodes (p < 0.05).
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PMID:[Antianginal activity of cardil and cordafen in patients with non-Q wave myocardial infarction]. 129 76

Previous studies have shown degradation of cardiac structural proteins and disruption of the sarcolemma as a result of acute myocardial infarction. However, there is no evidence to date on changes in sarcolemmal membrane proteins induced by experimental subacute myocardial infarction. We studied subepicardial layers overlying myocardial infarct 4 days following ligation of the left anterior descending coronary artery in 12 dog hearts. We first demonstrated that this layer provides the anatomic-electrophysiologic substrate for reentrant arrhythmias using activation mapping techniques and histologic correlations. The makeup of membrane proteins was studied using SDS polyacrylamide gel electrophoresis, peptide mapping, and laser densitometry. Sarcolemmal membrane proteins were isolated by ultracentrifugation through a sucrose gradient. We found that a sarcolemmal polypeptide (MW 126,000; n = 12) in the normal tissues has a different mobility than the corresponding protein (MW 124,000; n = 12) of the ischemic tissues although their peptide analysis appeared similar, suggesting that the protein undergoes a post-translational modification. In addition, two proteins (MW 75,000; n = 12 and MW 88,000; n = 12) were present in greater amount in the ischemic than in the control tissues suggesting either acceleration in protein synthesis or slow down of degradation turnover. These results demonstrate that specific changes occur in membrane proteins subjected to ischemic insults which might be responsible for membrane alterations following ischemia and may contribute to the abnormal electrophysiologic properties and arrhythmia seen in vivo at this stage.
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PMID:Changes in sarcolemmal proteins in subacute myocardial infarction in the dog. 130 6

A 9-lead Holter monitor using the lead-switching technique (9-lead DCG) and conventional 12-lead electrocardiograph (12-lead ECG) were simultaneously used for recording during treadmill exercise testing (Td-test) in 140 patients with coronary artery disease. Coronary arteriography was performed in 118 of the 140 patients, and the correlation between coronary stenosis and anterior or inferior projection of ST depressions occurring during the Td-test was investigated. Additionally, 10 patients with acute myocardial infarction (AMI) were studied to test ST elevation detection by the 9-lead DCG. The CM5 lead demonstrated ST depressions in 92 of the 109 patients showing ST depressions in one or more leads. High lateral (HL) and/or low lateral leads detected all ST depressions occurring in the I and aVL leads of the 12-lead ECG. Leads CM1, CM2 and CM3 exhibited low sensitivity (0-32%) and high specificity (56-100%), while leads CM4, CM5, and CM6 provided greater sensitivity (66-95%), but less specificity (3-32%) in detecting diseases of the left anterior descending artery, left circumflex artery and/or right coronary artery (RCA). In contrast, the low back (LB) lead demonstrated high sensitivity (88%) and high specificity (86%) in detecting RCA disease. Lead CM3 detected ST elevations in all 6 patients with anterior AMI, while the LB lead did so in all 4 patients with inferior AMI. With a Holter monitor, 4 leads are needed: CM5 like, CM3 like, lateral (such as HL) and inferior (such as LB). The LB lead is useful in detecting inferior ischemia.
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PMID:Correlation of coronary artery stenosis site with anterior or inferior projection of ST changes induced by treadmill exercise using a newly devised 9-lead Holter method. 130 17

Recent animal studies have suggested that there exists an activated subpopulation of circulating granulocytes which plays an important part in microvascular sequestration and tissue injury during shock and ischemia. In this respect, spontaneous granulocyte activation in form of pseudopod formation, a manifestation of actin polymerization, is a high risk for microvascular entrapment. The present investigation was carried out to determine if there is a significant difference in pseudopod formation in vitro between granulocytes obtained from healthy volunteers without symptoms and patients with acute cardiovascular illnesses. Blood samples from 25 healthy volunteers, 12 patients with acute myocardial infarction (AMI) and 12 patients with acute cerebral infarction (ACI) to determine spontaneous pseudopod formation in granulocytes with a high resolution light microscope over a period of several hours. The results revealed that the mean percentage of cells with pseudopod formation in the control group was below 10% in the first 3 hours, and increased to about 50% at 12 hours. In AMI patients, the level of activation within the first hour was not significantly different from the controls, but it rose rapidly to 90% in 4 to 5 hours. Patients with cerebral infarction, however, showed no significant difference from the control group. When the granulocytes of healthy subjects were incubated in plasma of AMI, the cells were activated similar to AMI granulocytes in their own plasma. When AMI plasma was serially diluted with Ringer's solution, the activation curve fell successively. These results indicate that AMI patients' blood contains plasma factor(s) which can activate granulocytes at a more rapid rate than controls.
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PMID:Spontaneous activation of circulating granulocytes in patients with acute myocardial and cerebral diseases. 130 82

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

A 73-year-old Japanese man with a history of partial gastrectomy due to gastric cancer 4 years previously was admitted because of intermittent fever. The patient developed abdominal pain, erythema, and myalgia in addition to the fever during the final clinical course, and died of acute heart failure. Autopsy disclosed atrophy of the left lobe of the liver and acute myocardial infarction. Neither metastasis nor recurrence of the cancer was observed. Small- and medium-sized arteries of the visceral organs showed various stages of necrotizing vasculitis with narrowing of the lumina. The vasculitis was most prominent in the left lobe of the liver and in the heart. Narrowing of the portal vein due to portal tract inflammation in addition to vasculitis of the hepatic arteries may have induced ischemia and infarction, which had resulted in atrophy of the left hepatic lobe.
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PMID:Polyarteritis nodosa with atrophy of the left hepatic lobe. 136 33

This study examined whether the adenosine potentiator, 5-aminoimidazole-4-carboxamide riboside (AICAr), could limit tissue necrosis during acute myocardial infarction in rabbit hearts with minimal coronary collateral flow. Forty-four rabbits underwent 45 min of ischemia with or without coronary reperfusion for 180 min. Five groups were studied. Saline or AICAr (20 mg/kg, i.v.) was administered as a bolus either 10 min before coronary occlusion or 10 min before the onset of coronary reperfusion. The anatomic risk zone size was assessed by radiolabeled microsphere autoradiography and the area of tissue necrosis was defined using the tetrazolium staining method. Coronary collateral flow in the central ischemic zone was assessed using the radiolabeled microsphere technique. No differences were observed for tissue necrosis (normalized to risk zone size) for saline- and AICAr-treated rabbits (66.2 +/- 10.9% vs. 70.8 +/- 19.9%, p = NS) subjected to 45 min of coronary occlusion without reperfusion. Similarly, tissue necrosis in rabbit hearts with 45 min of coronary occlusion followed by 180 min of reperfusion was not significantly reduced when AICAr was administered either 10 min before ischemia or 10 min before reperfusion (79.8 +/- 17.5 and 76.4 +/- 8.1%, respectively) compared to saline-treated controls (68.1 +/- 22.7%). Coronary collateral flow in these hearts was almost nonexistent. The risk zone size and cardiac hemodynamics were similar between the treatment groups. These results demonstrate that AICAr was unable to limit myocyte necrosis when administered either before ischemia or before coronary reperfusion in this experimental preparation of acute myocardial infarction.
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PMID:Failure of AICA riboside to limit infarct size during acute myocardial infarction in rabbits. 137 90

Carvedilol is a multiple-action cardiovascular agent that is both a beta-adrenoceptor antagonist and a vasodilator and has recently been made available for the treatment of mild-to-moderate hypertension. Clinical trials are ongoing to establish the efficacy of carvedilol in angina and congestive heart failure. beta-Adrenoceptor antagonists are known to reduce myocardial work secondary to reductions in heart rate and contractility; accordingly, they have been shown to be cardioprotective in animals and in humans. Because carvedilol has beta-adrenoceptor antagonist activity, it also should provide significant cardioprotection. The additional vasodilating activity of carvedilol, which will further reduce myocardial work by decreasing afterload and myocardial wall tension, should provide more salvage of ischemic myocardium than that afforded by a pure beta-adrenoceptor antagonist, such as propranolol. We investigated the ability of carvedilol and propranolol to reduce infarct size in experimental models of acute myocardial infarction in the rat, pig, and dog. The left anterior descending coronary artery was occluded for 30 (rat) or 45 min (pig) and then reperfused for 24 h (rat) or 4 h (pig). In the dog, the left circumflex coronary artery was occluded for 60 min and reperfused for 24 h. Vehicle, carvedilol, or propranolol was administered intravenously 15 min before ischemia (and, in the rat only, repeated 4 h after ischemia). An additional group of dogs was subjected to permanent left anterior descending coronary artery occlusion for 6 h, and carvedilol or propranolol was given 15 min after occlusion. Infarct size was examined on stained tissue sections using quantitative image analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial protection with carvedilol. 137 42


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