Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The comparative sensitivities of exercise (supine ergometer), isoproterenol (ISP) infusion and cold pressor test (CPT) for detecting myocardial ischemia in patients with effort angina (45 cases) and vasospastic angina (16 cases) were investigated. Twenty-three patients with atypical chest pain served as normal controls. Left ventricular function was evaluated by computerized quantitative analysis using the following three graphic methods: 1) radionuclide angiography during exercise (EX-RI) and ISP infusion (ISP-RI), 2) two-dimensional echocardiography during ISP infusion (ISP-2DE) and CPT (CP-2DE) and 3) digital subtraction angiography during CPT (CP-DSA). The incidence of regional wall motion abnormalities (WMA) induced by these three stress tests in patients with effort angina were as follows: 83% in EX-RI, 80% in ISP-2DE, 80% in ISP-RI, 75% in CP-2DE and 86% in CP-DSA. In patients with vasospatic angina, the WMA were as follows: 40% in EX-RI, 0% in ISP-RI and 71% in CP-DSA. In patients with atypical chest pain, the WMA were 0% in EX-RI, 0% in ISP-RI, 8% in ISP-2DE, 13% in CP-2DE and 13% in CP-DSA. The left ventricular ejection fraction (EF) was unchanged during ISP (from 65 +/- 11% to 68 +/- 12%) and it decreased both during exercise (from 64 +/- 10% to 58 +/- 9%, p less than 0.05) and during CPT (from 69 +/- 10% to 65 +/- 9%, p less than 0.05) in patients with effort angina. In patients with vasospastic angina, the EF was unchanged both during exercise (from 70 +/- 7% to 68 +/- 13%) and during the CPT (from 76 +/- 5% to 75 +/- 4%), while it increased during ISP infusion (from 63 +/- 8% to 79 +/- 7%, p less than 0.01). In patients with atypical chest pain, the EF was increased both during exercise (from 72 +/- 7% to 79 +/- 5%, p less than 0.01) and during ISP infusion (from 67 +/- 5% to 78 +/- 7%, p less than 0.01), while it was unchanged during CPT (from 77 +/- 7% to 76 +/- 8%). In exercise and in ISP infusion tests, WMA were provoked concomitantly with ST segment deviations in nearly all patients. However, during CPT, WMA were produced without the occurrence of ST segment deviations. Myocardial ischemia due to organic coronary artery stenosis was difficult to distinguish from coronary artery spasm by exercise test. However, the susceptibility to ISP infusion and CPT differed in producing WMA in patients with vasospastic angina.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Comparative sensitivities of exercise, isoproterenol infusion and cold pressor tests for detecting myocardial ischemia]. 332 25

The antithrombogenic effect of magnesium sulfate in vivo is shown at the site of endothelial damage induced by partial coronary and carotid artery constriction. The left anterior descending coronary artery of dogs and the right common carotid artery of rabbits were subjected to partial constriction with suture thread (40-60% reduction in transluminal diameter). Distal blood flow, as measured by electromagnetic flow probe, was not reduced. Scanning electron-microscopic examination of vessels fixed by glutaraledhyde perfusion and dried by the critical-point technique showed endothelial damage at the site of partial constriction ranging from crater- and balloon-like vesicular defects to cellular desquamation. Marked platelet deposition on exposed subendothelium and microthrombi could be seen with the maximum degree of luminal protrusion reaching 30% of the luminal diameter. Animals pretreated with magnesium sulfate (50 mg/kg, i.v.) showed platelet deposition restricted to a maximum of 1 or 2 discontinuous layers of platelets with most vessels showing only isolated platelets on exposed subendothelium. Microthrombi were not seen in any of the magnesium-treated animals. It is suggested that the therapeutic implications of magnesium in ischemic heart disease might be extended from its use in certain tachyarrhythmias and in arterial spasm associated with Prinzmetal's angina to the more classic episodes of ischemic heart disease where thrombus formation plays an unequivocally major role.
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PMID:Effect of magnesium sulfate on thrombus formation following partial arterial constriction: implications for coronary vasospasm. 344 Nov 41

Dipyridamole test, isoproterenol test, and treadmill exercise test were performed in two groups of patients with vasospastic angina (Group 1: 10 patients with 70% or greater coronary narrowings, Group 2: 8 patients with narrowings less than 70%. The results were correlated with coronary anatomy. In Group 1, vasodilation of resistance vessels by dipyridamole elicited ischemic episodes in 9 patients and an increase in myocardial oxygen consumption by isoproterenol caused anginal attacks in 7 patients. None of patients of Group 2 showed positive responses to either drug. All patients of Group 1, and 3 patients of Group 2 gave positive responses to treadmill test. These observations show that several different mechanisms are involved in the pathogenesis of myocardial ischemia in patients with vasospastic angina. Pharmacological interventions have higher specificity than exercise tests in predicting coronary anatomy and are useful for the choice of therapy in the patients.
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PMID:Noninvasive demonstration of underlying severe coronary disease in patients with vasospastic angina. 359 56

Standard echocardiography was employed to study the clinical model of myocardial ischemia with ST-segment elevation, well known as Prinzmetal's angina. Ultrasonic monitoring was performed during the appearance of ST-segment elevation, from onset of pain, during an ergonovine maleate test, hemodynamic monitoring, radioisotopic studies and, occasionally, during routine examinations, when spontaneous episodes occurred. Reliability of findings was supported by two important conditions: each patient acted as his own control, since recording was carried out from basal state to basal state, throughout ischemia, or from ischemia to basal state; behaviour of ischemic walls was compared with that of non-ischemic ones. Echocardiographic findings in acute myocardial ischemia were similar both in spontaneous and in induced episodes and were mainly characterized by: decrease in contractility indices of the ischemic segment, such as wall motion and percent systolic thickening; increase in left ventricular end-systolic and end-diastolic diameter, with a decrease in percent fractional shortening; distorted shape of ventricular cavity, transiently deformed as in a "functional" aneurysm; a sharp demarcation between ischemic and non-ischemic adjacent segment, "step sign", was present only in severe cases. Taking ST-segment elevation as a reference the time sequence of events was studied, correlating mechanical, electric and clinical markers of ischemia. At least three different echocardiographic phases were identified in the evolution of ischemic attacks: Pre-electrocardiographic phase, when mechanical impairment is detected by ultrasounds in the absence of both ST-segment changes and pain; Electrocardiographic phase, when echocardiographic signs of ischemia co-exist with obvious electrocardiographic signs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Echocardiography in the study of myocardial ischemia in man: the clinical model of Prinzmetal's angina. 375 79

Myocardial ischemia, particularly when transmural as in variant angina pectoris, may be associated with ventricular tachycardia, ventricular fibrillation and paroxysmal atrioventricular block (15%). Syncope (7%) and sudden death (3%) due to these malignant arrhythmias are sometimes a unique marker of myocardial ischemia. Two-hundred fifty-four patients (220 males and 34 females), aged 5 +/- 9 years with transmural myocardial ischemia related to coronary artery spasm, were studied. Particular attention was paid to the role of syncopal attacks as unique clinical manifestation of silent ischemia. Patients examined were divided into 3 Groups. Group 1 includes 5/254 (2%) patients with atrial fibrillation during acute ischemia. Group 2 was divided into four subgroups: subgroup A includes 17/254 (7%) patients with syncopal attacks due to malignant arrhythmias (ventricular tachycardia and advanced A-V block); subgroup B, 15/254 (6%) patients with documented malignant arrhythmias, without syncopal attacks; subgroup C, 7/254 (3%) with ventricular fibrillation during acute ischemia and subgroup D, 18/254 (7%) patients with history of syncopal attacks without documented arrhythmias during hospital observation. Group 3 includes 17/254 (7%) patients with left anterior hemiblock in basal condition, 7/254 (3%) patients with left anterior hemiblock and one left posterior hemiblock during acute ischemia and one patient with right bundle branch block during acute ischemia. Syncopal symptoms are present in many of these cases of angina pectoris; paroxysmal A-V block is documented in nearly half of the cases with syncope (65%); ventricular tachycardia is frequently demonstrated during ischemia but leads to syncope in only a few cases; patients with syncope do not present specific clinical features.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:When are arrhythmias and conduction disturbances markers of myocardial ischemia at rest? 375

Vascular elastic properties in vivo (dynamic incremental elastic modulus [Ep(dyn)]) of large coronary arteries were assessed from the pressure-diameter relationships of the large coronary arteries in 46 patients with suspected ischemic heart disease. Ep(dyn) represents the vascular stiffness primarily determined by the organic sclerotic changes of the vascular wall and the vascular smooth muscle tone. Coronary arterial diameter was obtained from the magnified cine coronary arteriograms by using a computerized caliber measurement technique. The mean Ep(dyn) of the left main coronary artery and the proximal portions of the left anterior descending and circumflex coronary arteries with apparently normal angiograms were significantly (P less than 0.01) increased as the number of involved coronary vessels was increased. Mean Ep(dyn) values in multi-vessel disease were comparable with those of dilated segment by the percutaneous transluminal coronary angioplasty, indicating that the vascular sclerotic changes are not localized to the narrowed segments but diffusely distributed to the angiographically normal vascular wall. In 4 patients who had successful percutaneous transluminal coronary angioplasty, Ep(dyn) of the dilated coronary segment showed markedly higher values (0.21-0.30 X 10(6) Nm-2) than the normal values (0.16 +/- 0.06 X 10(6) Nm-2 in left anterior descending coronary artery). In contrast, there was no significant difference in Ep(dyn) values of the angiographically normal left main coronary trunk, proximal portions of left anterior descending and circumflex arteries between patients with and without vasospastic angina. During myocardial ischemia induced by ergonovine maleate, vasospastic response of the non-diseased segment was comparable with that in patients who did not have an anginal attack during the ergonovine test. Thus, in contrast to the sclerotic change, abnormal vasoconstrictive property of the coronary artery may be localized to the diseased segment.
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PMID:Clinical assessment of elastic properties of large coronary arteries: pressure-diameter relationship and dynamic incremental elastic modulus. 377 Oct

Effect of 48-72 hour infusion of prostaglandin E1 (PGE1) was studied in 17 patients with angina refractory to conventional medical treatment (combination of propranolol, 160 mg/day nifedipin, 30 mg/day and nitrates) by the double blind test. PGE1 was infused to 11, placebo to 6 patients. There was no difference between PGE1 and placebo groups in the number of ischemic episodes and duration of myocardial ischemia as evidenced by Holter ECG monitoring. But in 2 patients with vasospastic angina attacks of ischemia were almost completely abolished by PGE1.
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PMID:[Infusion of prostaglandin E1 in resting angina resistant to conventional therapy]. 390 82

Elevated electrical alternans of the elevated ST segment (STEA) was documented in a patient with non-Prinzmetal's or classical angina and severe atherosclerotic coronary artery disease. STEA was precipitated during graded exercise testing. The disappearance of this phenomenon after aortocoronary bypass surgery suggests that the coronary obstructions were the etiologic factors. These findings emphasize that the STEA may occur in myocardial ischemia caused by conditions other than Prinzmetal's angina.
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PMID:Electrical alternans of the ST segment in non-Prinzmetal's angina. 616 57

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

Coronary spasm was first demonstrated by Gensini in 1962, and the diagnostic value of spontaneous spasm during coronary angiography is now generally accepted. In its absence, provocation tests with ergonovine or its derivatives form part of routine hemodynamic investigation for confirming the spastic nature of atypical chest pain or pain suggestive of Prinzmetal angina. The coronary spasm so induced gives rise to reduced coronary flow, an increase in coronary resistance and myocardial ischemia as shown by an increased lactate extraction in coronary sinus blood; therefore, once it is documented, it must be treated in order to avoid myocardial necrosis or ventricular arrhythmias. Three groups of drugs of drugs are used to counteract spontaneous or provoked spasm: alpha-blockers, especially phentolamine, nitrate derivatives, trinitroglycerine or isosorbide dinitrate, and calcium inhibitors nifedipine or diltiazem, which have a direct antispastic effect. The hemodynamic and pharmacological actions of these three groups of drugs depend on whether they are given orally, intravenously or by intracoronary injection. Twenty six coronary spasms were observed in 23 patients out of a total of 780 coronary angiographies (3,3 per cent) performed between June 1980 and June 1981: 12 spasms were spontaneous (1,5 per cent), 6 provoked by the catheter (0,8 per cent) and 8 by methylergometrine. There were no complications. Five coronary spasms were also observed during 70 coronary angioplasties (7,1 per cent). The spasm was relieved in all cases by intravenous injection of 1,5 to 3 mg of trinitrin (Lenitral). Calcium inhibitors, especially nifedipine, have been used successfully by Hugenholtz and Bertrand who consider that nifedipine has a slower action and the coronary dilatation obtained is never as great with the nitrate derivatives. Trinitrin remains the treatment of choice for the rapid relief of provoked spasm.
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PMID:[Treatment of coronary artery vasospasm during coronary arteriography]. 640 34


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