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 hypothesis of this study was that inadequate right ventricular hypothermia contributes to the right ventricular dysfunction occasionally observed after cardiac operations. Dogs were placed on cardiopulmonary bypass, and 60 minute periods of hypothermic myocardial ischemia were imposed. Left ventricular temperature was always maintained at 15 degrees C and right ventricular temperatures were maintained at 15 degrees C (Group I, n = 8), 25 degrees C (Group II, n = 8), and 35 degrees C (Group III, n = 8). These temperatures were produced by infusion of hypothermic crystalloid cardioplegic solution and appropriate topical cooling and heating of the left and right ventricles, respectively. Multiple indices of ventricular function were obtained 15, 30, 45, and 60 minutes after bypass and compared to prebypass control values. In all Group I animals (left ventricular temperature = 15 degrees C, right ventricular temperature = 15 degrees C), postischemic indices of right ventricular function were not different from control values (p = NS). In Group II (left ventricular temperature = 15 degrees C, right ventricular temperature = 25 degrees C), two animals died 30 and 45 minutes after bypass, respectively, of right ventricular failure. In the other six animals in Group II, all indices of right ventricular function were significantly reduced (p less than 0.05) except for right ventricular systolic pressure. In Group III (left ventricular temperature = 15 degrees C, right ventricular temperature = 35 degrees C), two animals could not be weaned from cardiopulmonary bypass because of right ventricular akinesia. Six animals were weaned from bypass, but two died 15 minutes, one died 30 minutes, and one 45 minutes after bypass. Two animals lived 60 minutes, but all indices of right ventricular function were decreased. Failure to maintain right ventricular temperatures below 25 degrees C during 1 hour of cardiac ischemia in the dog can result in fatal right ventricular failure.
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PMID:Acute right ventricular failure is caused by inadequate right ventricular hypothermia. 397 74

Nonsustained ventricular tachycardia, although usually asymptomatic, is associated with a high risk of sudden cardiac death in patients with depressed left ventricular function. To test the vulnerability of such patients to symptomatic and potentially life-threatening arrhythmias, complete electrophysiologic studies were performed in 58 patients with clinically documented nonsustained ventricular tachycardia (greater than or equal to three complexes but less than 15 seconds of self-terminating ventricular tachycardia by 24 hour ambulatory electrocardiographic [Holter] or telemetric monitoring) and abnormal left ventricular function (ejection fraction less than 50% by radionuclide angiography). All patients had nonsustained ventricular tachycardia in the absence of antiarrhythmic drugs, acute ischemia, long QT syndrome, recent infarction or electrolyte abnormalities. The stimulation protocol for each patient included the introduction of single, double and triple ventricular extrastimuli at three cycle lengths (sinus, 600 and 450 ms) and two right ventricular sites (apex and outflow tract). A sustained ventricular tachyarrhythmia was induced in 23 patients (40%) and a nonsustained ventricular tachycardia in 14 patients (24%). Induction of sustained tachycardia correlated with the presence of akinesia or aneurysm, or both, by radionuclide angiography, but not with ejection fraction or presence or absence of coronary artery disease. These results indicate that: 1) patients with clinical nonsustained ventricular tachycardia and chronic left ventricular dysfunction have a high incidence of inducible sustained ventricular tachycardia or ventricular fibrillation; and 2) electrophysiologic testing may allow further substratification of risk of sudden cardiac death in high risk patients with nonsustained ventricular tachycardia.
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PMID:Electrophysiologic testing in patients at high risk for sudden cardiac death. I. Nonsustained ventricular tachycardia and abnormal ventricular function. 400 86

The purpose of this study was to investigate the relation between abnormalities of left ventricular (LV) wall thickening during systole in ischemic regions and the interaction of LV pressure and regional intramyocardial pressure. Wall thickness was measured in 10 open-chest dogs with ultrasonic dimension gauges. LV pressure, aortic pressure, and intramyocardial pressure in the subendocardium were measured with catheter-tip micromanometers. Regional ischemia was produced by occlusion of the left anterior descending coronary artery. During the control period, peak subendocardial pressure exceeded LV pressure by 44 +/- 6 mm Hg. With hypokinesia, defined as a 50% to 89% reduction of systolic wall thickening, peak subendocardial pressure exceeded peak LV pressure but to a lesser extent (15 +/- 1 mm Hg). During akinesia, defined as a 90% to 100% reduction of systolic wall thickening, there was less than 1 mm Hg difference between peak subendocardial pressure and peak LV pressure. During dyskinesia, defined as systolic thinning of the ischemic wall, peak LV pressure exceeded peak subendocardial pressure by 29 +/- 6 mm Hg. These observations indicate that regional changes of LV wall thickness characterized by hypokinesia, akinesia, and dyskinesia are associated with pressure gradients between the LV cavity and the LV wall that are compatible with the abnormalities of wall motion.
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PMID:Relation of intramyocardial and intracavitary pressure to regional myocardial asynergy in the canine left ventricle. 621 65

Fifty-five ischemic attacks at rest with ST segment elevation were recorded by two-dimensional echocardiography (2DE) in 20 patients with Prinzmetal angina. Eighteen ischemic attacks were recorded starting from intravenous injection of ergonovine maleate while 37 spontaneous ischemic attacks were recorded from onset of either anginal pain or ECG changes or from the basal state. In each ischemic attack at least one of the following transient alterations was observed by 2DE during ST elevation: (1) Regional hypokinesia, akinesia, or dyskinesia; (2) "step sign," that is, a sharp demarcation between an akinetic or dyskinetic area and an adjacent normal or hypercontracting region; and (3) geometric changes in left ventricular shape, that is, globular appearance in diastole and hourglass silhouette in systole. Regional myocardial asynergy was detected earlier than onset of pain (which was not present in 21 [38%] ischemic episodes) or ST segment elevation on ECG, as documented in 40 ischemic episodes (16 induced and 24 spontaneous) in which echocardiographic monitoring was performed from basal state and carried on up to the appearance of ischemia. All described mechanical changes were fully reversible after pain subsided and ST segment was back to isoelectric, either spontaneously or with nitrates; furthermore, a contractile "rebound phenomenon" of the previously ischemic wall was observed in some episodes. In conclusion, these results outline a role for 2DE in detecting cardiac mechanical impairment due to transient myocardial ischemia with ST segment elevation in humans.
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PMID:Transient changes in left ventricular mechanics during attacks of Prinzmetal angina: a two-dimensional echocardiographic study. 623 83

Experimental animal investigations have shown that already after a few seconds of occlusion of a coronary artery a reduction in the systolic myocardial shortening and wall thickening takes place in the corresponding supply area. Following 1-2 minutes of ischemia systolic expansion occurs. Wall-thickness increase and myocardial shortening then take place during the isovolumetric relaxation phase. When at least 25% of the myocardium of the left ventricle becomes acutely ischemic the end-diastolic pressure and end-diastolic volume increase. As a rule an augmentation of myocardial contraction appears in the non-ischemic section of myocardium, which in part takes place through the Frank-Starling mechanism. With a gradual reduction of the coronary inflow, and a decline in the wall thickening of c. 50% of the control value, a significant reduction in blood flow took place only in the innermost quarter of the ventricular wall. With akinesia of the ischemic area, no reduction of the blood flow could be determined in the subepicardial region. Only with the occurrence of dyskinetic wall motion was a transmural reduction of blood flow effected. The ischemic contraction disturbances are fully reversible if coronary occlusion last only a few minutes. With a 15 minute occlusion the recovery time of the myocardial function can require several days (postischemic "stunned myocardium"). The first myocardial necroses occur after 20 minutes of ischemia, and after 3-6 hours of ischemia the infarction is complete.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamics in ischemia. Systolic phase]. 633 23

Thallium-201 scintigraphy was performed in 20 normals and 60 patients (pts) with angiographically proven coronary artery disease (CAD) at rest after maximal exercise for evaluation of severity and location of CAD. The Tl-scintigrams were quantified by a Tl-score. The results of the Tl-score were compared with invasive and non-invasive parameters. Sensitivity asnd specificity of the Tl-score in evaluation of CAD was 90%. In normals, there were no significant differences from rest to exercise (Tl-score less than or equal to 1.2). Twenty-six of the pts with CAD, who had no evidence of myocardial infarction, showed a significant increase of Tl-score from 5.0 +/- 1.7 to 8.7 +/- 2.6 after exercise (p < 0.001). In 34 pts with CAD and a history of MI, Tl-score increased from 24.9 +/- 3.1 to 33.3 +/- 3.8 (p < 0.001). Exercised-induced ischemia was assessed by exercise electrocardiography in 48%, by Tl-score in 62% and by angina pectoris in 77%. In 37 pts, the Tl-score was compared with the coronary score, ejection fraction (EF) and local wall motion derived from biplane cineventriculograms. There was a significant correlation between the Tl-score and the EF: y = 79.13 - 1.11 x, n = 74, r = 0.688 (p < 0.001). No correlation was found between the coronary score and the Tl-score. Hypokinetic wall motion disturbances were assessed by Tl-score in 34% only, whereas akinesia and dyskinesia were detected in 86% (p < 0.001). The data suggest that Tl-scintigraphy even with a quantitative Tl-score is not sufficient for exact assessment of extent and severity of CAD.
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PMID:[Quantitative Tl-201 scintigraphy in diagnosis of severity and location of coronary artery disease. Comparison of a Tl-score to invasive and non-invasive parameters (author's transl)]. 744 54

Dipyridamole-echocardiography may be considered, at this time, an useful test not only in post-infarction risk stratification, but also in diagnosis and functional evaluation of coronary artery disease, having a satisfying sensibility (67%) and a very high specificity (96%). We report a particular case of "false positive" with a review of the literature. The patient, male, aged 45, without important risk factors for coronary artery disease, experimented recurrent events of spontaneous chest pain, typical per angina pectoris. Physical examination, chest roentgenogram and blood samples were normal. Slight signs of subendocardial ischemia, lateral, were present at ECG. Forced hyperpnea resulted in onset of chest pain, with increase of ECgraphic signs of ischemia; resolution of both was obtained with sublingual nitrate administration. A stress test with myocardial flow scintigraphic assessment using sestaMIBI, was performed: ECG showed significant ST downsloping at low workload (1-11 steps of Bruce protocol) and radionuclide tomography showed reversible hypoperfusion in anterior and septal regions. High dose dipyridamole-echocardiography test (a first bolus of 0.56 mg/kg in 4', followed after 4' by a second bolus of 0.28 mg/kg) gave these results: basal echocardiogram was normal; after first bolus of dipyridamole apical hypokinesia appeared; after second bolus complete akinesia was observed. ECG showed subendocardial injury wave and the patient experimented typical anginal pain. Clinical, electrocardiographic and echocardiographic changes were immediately reversed after intravenous bolus of aminophylline, 240 mgs. Coronary arteriography was performed: coronary arteries were angiographically normal, without even any marginal irregularity: left ventricle was normal in volume, wall kinesis and ejection fraction. Dipyridamole is a powerful ischemic stressor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Problem of false positives in dipyridamole-echocardiography test. Description of a case and review of the literature]. 770 May 41

Toxic manifestations of digitalis are one of the most prevalent adverse drug reactions encountered in clinical practice. The estimated incidence is about 20% in hospitalized patients in the USA. The authors describe a rare case of myocardial "catecholamine necrosis" (anteroseptal myocardial infarction) during accidental digitalis intoxication. A male patient, 75 years old, suffering from cirrhosis and ascites, take on by mistake a tablet of digoxin 0.25 mg. four times at day for eleven days. He hadn't heart disease in the past. At the eleventh day the patient showed a deep tiredness and so he was submitted to a clinical examination and electrocardiogram. The ECG demonstrated an anteroseptal myocardial infarction in the second-third electrical stage. The patient was hospitalized. The successive examination revealed: very high plasma digitalis concentrations; an increase of the serum levels of CPK and LDH; a significant increase of plasmatic and urinary catecholamine levels which return to normal values after fifteen days; apical akinesia at the echocardiographic examination; no signs of residual myocardial ischemia to the echo-dypiridamole stress test; normal coronary artery to the coronary arteriography and absence of coronary artery spasm to the ergonovine test. Furthermore the abdominal echography and the abdominal computerized tomography didn't reveal surrenal disease but showed an important liver disease. The patient was free from other cardiac events in the follow-up. Generally, during the digitalis intoxication we observe various rhythm and conduction disturbances. Instead in this case no serious arrhythmias were registered and the main expression of the drug toxicity was an anteroseptal myocardial infarction with undamaged coronary artery. Also the usual extracardiac symptoms and signs of the digitalis intoxication were absent in this case. All these observations can be explained with the pathological increase of the cathecholamine levels, indirectly induced by digitalis; with the direct toxic effect of the drug at the myocardic level; with the contemporary absence of ionic disturbances; with the concomitant liver disease. The direct toxic effect of the digitalis produced an increase in calcium ions availability for the electromechanical coupling and an increase of the intramyocardial pressure; the increase of the adrenergic activity determined contemporary an increase in the oxygen consumption of the myocardial cells, a rise of vascular tone and coronary artery tone and a reduction of the duration of the diastole. All these factors provoked a "primary and secondary" ischemia which evolved toward a real "cathecholamine necrosis" and produced a myocardial infarction. This hypothesis explains the myocardial infarction in absence of injury at the coronary arteriography and without coronary spasm at the ergonovine test; moreover it explains the transient increase in cathecholamine plasma levels observed in the acute phases an normalized after fifteen days. The "cathecholamine necrosis" is an anatomical definition, nevertheless in our opinion it gives account of the rare clinical situation observed.
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PMID:[An unusual case of "catecholamine necrosis" caused by accidental digitalis poisoning]. 855 67

There are no standard criteria for the diagnosis of myocardial ischemia in akinetic segments during dobutamine stress echocardiography (DSE). The aim of the study was to assess the relation between different responses of akinetic segments during DSE and ischemia assessed by thallium-201 single-photon emission computed tomography (SPECT). Dobutamine-atropine stress echocardiography with simultaneous stress-reinjection thallium-201 SPECT was performed in 67 patients with old myocardial infarction significant and coronary artery stenosis. Fourteen myocardial segments were matched for both DSE and SPECT. Ischemia on SPECT was defined as reversible thallium defects. In 257 akinetic segments, 4 patterns during DSE were identified: (1) biphasic response in 41 segments (16%), defined as improvement at low dose (5 to 10 microgram/kg/min) followed by worsening at high dose; (2) persistent akinesia in 155 segments (60%); (3) akinesia becoming dyskinesia in 39 segments (15%); and (4) sustained improvement in 22 segments (9%). Reversible thallium defects were detected in 21 segments (51%) in group 1, in 20 segments (13%) in group 2, none in group 3, and in 2 segments in group 4 (9%). The prevalence of reversible defects in biphasic segments was higher compared with other patterns (p <0.00001 vs groups 2 and 3, p <0.005 vs group 4). The ischemic perfusion defect score was significantly higher in group 1 than group 2. The positive predictive value of biphasic response for reversible thallium defects was similar to that of stress-induced dyssynergia in normal segments at rest (51% vs 58%). It is concluded that of the various responses of akinetic segments to dobutamine infusion, the biphasic response is associated with the highest prevalence and greatest severity of ischemic on thallium SPECT. Observation of contractile response at both low- and high-dose DSE is a valuable approach for the diagnosis of myocardial ischemia in akinetic segments.
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PMID:Relation between contractile response of akinetic segments during dobutamine stress echocardiography and myocardial ischemia assessed by simultaneous thallium-201 single-photon emission computed tomography. 864 45

Emotional disturbances, such as lack of motivation or depression, are common after stroke. The drugs mainly used to treat these syndromes in Japan are the cerebral metabolic enhancers whose biochemical and pharmacological profiles are similar to those of antidepressant drugs. In order to examine the possible therapeutic effect of T-794 [(5R)-3-(6-(cyclopropylmethoxy) 2-naphthalenyl)-5-(methoxymethyl) 2-oxazolidone], a new reversible inhibitor of monoamine oxidase (MAO) type A, on those emotional disturbances, its antidepressant activity was compared with those of major cerebral metabolic enhancers in rodents with or without treatment of cerebral ischemia. Oral administration of T-794 potently prevented reserpine-induced ptosis (ED50 = 4.41 mg/kg), akinesia (ED50 = 3.29 mg/kg), and hypothermia (minimum effective dose = 3 mg/kg) in mice. It was at least 3.7, 13.0, and 3.3 times more potent than cerebral metabolic enhancers tested (indeloxazine, bifemelane, amantadine and idebenone) in antagonism of the ptosis, the akinesia, and the hypothermia, respectively. Effect of T-794 was also examined in the behavioral despair test in rats subjected to forebrain ischemia. The ischemia was induced by a combination of bilateral common carotid artery occlusion (15 min) and systemic hypotension (sodium nitroprusside 5 mg/kg, s.c). From 13 d after the surgery, drugs were orally administered twice daily 7 times, and following the last administration rats were assessed for their behavior. T-794 reduced the duration of immobility in the behavioral despair test at 30 mg/kg without affecting spontaneous motor activity, whereas indeloxazine showed no significant effect. Antidepressant-like activity of T-794 was suggested in rodents with as well as those without cerebral ischemia. The results suggest that T-794 may make an important contribution to the treatment of emotional disturbances following stroke.
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PMID:Possible therapeutic effect of T-794, a novel reversible inhibitor of monoamine oxidase-A, on post-stroke emotional disturbances, assessed in animal models of depression. 914 8


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