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)

Circadian periodicity was examined in 68 patients with chronic stable angina and in 9 patients with Prinzmetal angina. The frequency and duration of transient ischemic episodes were determined from analysis of 1 or more 24-hour Holter recordings by the compact analog technique. Ninety percent of the episodes in both syndromes were silent; 80% of the episodes of Prinzmetal angina were associated with ST-segment elevation and all episodes of chronic stable angina had ST-segment depression. Ischemic episodes were shorter (3 +/- 2 vs 18 +/- 23 minutes, p less than 0.0005) but more frequent (21 +/- 18 vs 6 +/- 4 per 24 hours, p less than 0.0001) in patients with Prinzmetal angina than in those with chronic stable angina. In patients with chronic stable angina, both silent and painful episodes had a peak occurrence in the morning and early afternoon hours (between 8 AM and 3 PM); the fewest episodes were between 1 AM and 5 AM. This distribution was not random by chi-square test (p less than 0.001). Cosinor analysis of ischemic episodes periodicity showed the acrophase at 1 PM, which was not different from that (3 PM) of the circadian rhythmicity for heart rate. In case of Prinzmetal angina, the acrophase of heart rate changes was at 5 PM, but a clear periodicity in the distribution of the ischemic episodes was not found. These differences in the circadian periodicity may reflect differences in the mechanism of ischemia in chronic stable angina and in Prinzmetal angina and are likely to be of therapeutic significance.
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PMID:Circadian variation in occurrence of transient overt and silent myocardial ischemia in chronic stable angina and comparison with Prinzmetal angina in men. 363 Sep 31

It is hypothesized that myocardium subjected to a 5 minute period of coronary occlusion and a 30 minute period of reperfusion has latent abnormalities that become overt when the reperfused myocardium is "challenged" by a subsequent coronary occlusion. This hypothesis is clinically relevant because reperfused myocardium is frequently subjected to recurrent ischemia, as in patients with unstable angina, vasospastic angina or recurrent thrombosis after initial coronary occlusion and thrombolysis. In 19 open chest dogs, the response of regional myocardial function to brief coronary occlusions was studied. Systolic wall thickening and diastolic thinning were measured using a specially developed miniature 5 MHz echocardiographic transducer fixed to the epicardium by suction. All 19 dogs underwent an initial "challenge" coronary occlusion (30 seconds). Thereafter, the control group (n = 8) underwent no intervention for 30 minutes, while the intervention group (n = 11) underwent 5 minutes of coronary occlusion followed by 30 minutes of reperfusion. All dogs were then subjected to a second "challenge" coronary occlusion (30 seconds). In the control group, responses to the second challenge occlusion were the same as to the first occlusion. In the intervention group, regional and global systolic function and myocardial perfusion after the 5 minute coronary occlusion intervention returned to baseline levels, but the response to the second challenge coronary occlusion was significantly different in the intervention group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Altered response of reperfused myocardium to repeated coronary occlusion in dogs. 365 54

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

During Ergonovine-test a patient with Prinzmetal angina presented (in I, aVL, V3-V6) ST downsloping which, after a temporary phase of alternative normalization (AST) beat to beat in V5, progressed to ST upsloping with typical angina. The M-mode echo-study first discovered, before than ecg, septal impairment (hypokinesia which increased to akinesia in the AST phase) and also asynergy of posterior wall of left ventricle. After intravenous nitrate echo-alterations reversed more rapidly than ecg one (transitional phase of ST decrease). The authors relate the AST to temporary alternative pseudonormalization caused by a phase of electrical instability during progressive vasospastic ischemia involving first the endocardial layers and after the epicardium of a single myocardiocoronary district. Probably also other partially opposite ischaemic districts, as suggested from echo data of posterior wall asynergy took a part in these events. This rare ST-alternans type as new pseudonormalization phenomenon and the usefulness of echo-study during ischaemic attacks are stressed.
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PMID:[Clinical, electrocardiographic and echocardiographic findings in a case of vasospastic angina with alternating pseudonormalization of the ST segment]. 383 2

Coronary vasodilators known to be effective in effort and vasospastic angina were studied in 93 patients undergoing catheterization for evaluation of chest pain. The ischemia-provoking stresses were isometric handgrip (25% of maximum for 4 to 5 minutes) or ergonovine maleate (0.2 mg intravenously). Hemodynamic changes and changes in angiographic diameter of epicardial coronary arteries were measured during these stresses, with and without drug administration. Drugs included intravenous diltiazem (0.25 mg/kg load + 0.003 mg/kg/min), intravenous verapamil (0.14 mg/kg load + 0.0075 mg/kg/min) and intracoronary (0.012 mg/min X 4 minutes) and sublingual (0.4 mg) nitroglycerin. From these studies, the following statistically valid conclusions were reached. First, nitroglycerin is a potent dilator of epicardial coronary arteries, increasing normal luminal area an average of 28% and luminal area in significantly stenotic segments by 29%. Second, verapamil and diltiazem are nonsignificant epicardial coronary dilators (9% and 4% luminal area increase, respectively). Similarly, diltiazem does not dilate significant coronary stenoses. Third, sustained isometric handgrip increases systemic blood pressure and heart rate by reflex activation of the sympathetic nervous system. By this means, handgrip also constricts luminal area in normal and diseased coronary segments by 20% and 22%, respectively. One result of these changes is a handgrip-induced, ischemic 56% rise in pulmonary wedge pressure in patients with significant stenosis. Fourth, intracoronary nitroglycerin, in very small doses, does not block the systemic hemodynamic response to handgrip, but prevents handgrip-induced coronary constriction and the associated ischemic left ventricular dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of normal and diseased epicardial coronary arteries to vasoactive drugs: quantitative arteriographic studies. 390 24

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

In a study of 93 patients who met criteria for Prinzmetal's angina, alternans of the ST segment was observed in 28 of 93 patients (30%). In 8 of these 28 patients, a hitherto undescribed variant of alternans, namely alternation (larger than or equal to 1 mm shift in 2:1 pattern) in the amplitude of the baseline or TQ segment (TQ Alt) was observed. In all eight patients serious ventricular arrhythmias were noted, namely, ventricular fibrillation in two, ventricular tachycardia in four, and multiform or advanced ventricular ectopic activity in eight. The TQ Alt developed only after ST segment alternans occurred. It is postulated that the alternations of the ST and TQ segments are due to differences in current flows due to inhomogeneity of depolarization and repolarization of the action potential caused by ischemia. Furthermore, the associated arrhythmias observed are related to the inhomogeneous state initiated by the ischemia.
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PMID:TQ segment (baseline) alternans during Prinzmetal's variant angina. 616 55

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

The strategy of treatment in vasospastic angina is mainly based on the results of coronary angiography. In a series of 165 patients with coronary spasm documented by angiography, 51 patients (31 per cent) had angiographically normal arteries and 69 per cent had organic atherosclerotic lesions. Patients with fixed atherosclerotic lesions were divided in two subgroups depending on whether the lesions were operable. The first subgroup (47 cases) comprised patients with operable lesions and coronary spasm. They underwent aorto-coronary bypass associated with a procedure to prevent spasm (plexectomy) (40 cases). Depending on the site of the lesions, some patients with operable lesions may benefit from coronary angioplasty followed by treatment with calcium antagonist drugs. Patients in the second subgroup (67 cases) with inoperable fixed atherosclerotic lesions were treated with calcium antagonists. Betablockers, which may be considered in organic coronary artery disease, are theoretically contra-indicated because of the vasospastic factor. The remaining patients with "angiographically normal" vessels (51 cases) were treated with nitrate derivatives and calcium antagonists. Treatment should be directed to the suppression of the clinical symptoms and, above all, of ECG signs of ischemia as proved by repeated Holter monitoring. The clinical course may also be assessed by repeated provocation tests. Results may depend on the doses and their timing during the 24 hour period. Duration of treatment in patients with angiographically normal vessels has not yet been established. Isolated cardiac denervation may be indicated in these patients who fail to respond to medical treatment (8 cases).
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PMID:[Strategy of the treatment of vasospastic angina pectoris]. 640 40


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