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)

Three women with well-documented migraine associated with intracerebral hemorrhage are described. In each case, migraine headaches began during adulthood. Unusually severe and protracted headache heralded the onset of fixed neurological deficits associated with lobar intracerebral hemorrhage. Striking carotid artery tenderness was characteristic. Except for a history of migraine, no cause for intracerebral hemorrhage could be established. In each case arteriography showed extensive spasm of the appropriate extracranial or intracranial artery. Surgical pathology following evacuation of two hematomata demonstrated signs of vessel wall necrosis associated with subacute inflammatory changes. Vasospasm associated with severe migraine attacks may result in ischemia of intracranial vessel walls, leading to necrosis and subsequent vessel rupture when perfusion pressure is restored.
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PMID:Migraine with vasospasm and delayed intracerebral hemorrhage. 198 18

Anesthesia-induced coronary vasospasm has been reported only rarely. We report a case, without previous cardiac history, in which immediately after anesthesia induction a marked ST elevation was noted on the EKG monitor. Premature ventricular contractions as well as non-sustained ventricular tachycardia were noted. These changes resolved immediately after nitroglycerin infusion and 75 mg of lidocaine were given. A coronary angiogram revealed normal coronary arteries and left ventriculogram. Ergonovine stimulation was not performed. The patient was discharged home on calcium entry blockers and nitrates. Exercise stress test two weeks after discharge was negative for ischemia. Induction of anesthesia triggering coronary spasm has been reported rarely, and to our knowledge never in the presence of angiographically normal coronary anatomy. Coronary vasospasm with typical EKG changes--namely, ST elevation and ventricular arrhythmias--has to be included as a possible complication of general anesthesia. Recognition of this syndrome allows prompt treatment and prevention of future episodes.
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PMID:Coronary artery spasm induced by anesthesia: a case report and review of the literature. 229 59

To analyze the usefulness of a single exercise test to predict the presence of fixed obstructive coronary artery disease in patients with active coronary spasm, 91 consecutive patients with angiographically proven symptomatic coronary artery spasm who had performed a symptom-limited exercise test within the week before diagnostic coronary angiography were studied. Coronary angiography revealed significant coronary obstructions in 61 patients (67%). According to the type of angina, the prevalence of significant coronary stenosis was 53% for patients with angina at rest, 68% for those with effort angina, and 92% for those with mixed angina. Exercise-induced ST segment elevation was present in eight patients (9%), ST segment depression was seen in 37 patients (41%), and no ST abnormalities in 46 (50%). There was not a significant relationship between the ST segment response to exercise and the clinical variables assessed except for coronary anatomy. Abnormal exercise test results were significantly more frequent in patients with significant coronary obstructions than in those without significant coronary occlusions (62% versus 23%; p less than 0.01). ST elevation was not useful to predict the presence of fixed coronary lesions. However, ST depression strongly suggested the presence of underlying coronary lesions with a sensitivity of 54%, a specificity of 87%, and a positive predictive value of 89%. Using this criterion, 65% of the patients were correctly classified. The results indicate that despite the functional component of ischemia in patients with coronary spasm, ST segment depression with exercise is still a highly specific sign with a high positive predictive value for the presence of significant coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The value of exercise testing in patients with coronary artery spasm. 203 10

The peak incidence of ventricular fibrillation in acute myocardial infarction usually occurs during the first hours after the onset. Electrophysiological changes immediately after the onset have been studied in animal models, but are still incompletely understood in humans. For clarification of the characteristic features of ventricular arrhythmias during acute myocardial ischemia, ventricular arrhythmias were studied in 81 patients with vasospastic angina pectoris induced by ergonovine. Ventricular arrhythmias occurred in 45 of these patients, including ventricular tachycardia in 15, and ventricular fibrillation requiring repeated DC defibrillation in two patients. Most ventricular extrasystoles occurred before the ST segment reached maximum elevation, while reperfusion arrhythmias were less common. In many patients the coupling intervals varied, and the configuration was multiform. It is concluded that ventricular arrhythmias occurring during ergonovine-induced coronary spasm show different characteristics from those occurring during chronic ischemia. As the arrhythmias in this study seem, in some ways, to resemble arrhythmias occurring at the onset of myocardial infarction, the results might provide useful information on ventricular arrhythmias in myocardial ischemia in humans.
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PMID:The nature of ventricular arrhythmias during ergonovine-induced vasospastic angina pectoris. 244 15

In the hamster cheek pouch, microvascular effects of iloprost at a nonhypotensive dose include vasodilatation at the level of arterioles and venules without changes in microvascular permeability, increased number of perfused capillaries/cm2, prevention of microvascular spasm and capillary ischemia as caused by LTD4, and inhibition of histamine- and 5-HT-induced venular leakage of FITC-dextrane. As regards the effects on basal vessel tone, capillary density, and prevention of LTD4 effects, PGE1 had similar effects as also shown by others in the human cutaneous microcirculation. However, PGE1 did not prevent the microvascular leakage caused by histamine. The Ca2+-antagonist nifedipine, apart from arteriolar vasodilatation, neither increased venular diameter and capillary perfusion nor prevented the effects of LTD4 and histamine. The microvascular actions of iloprost by improvement of tissue perfusion and prevention of mediator-induced tissue edema and vasospasm could contribute to the beneficial effects observed in ischemic diseases.
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PMID:Microvascular effects of iloprost in the hamster cheek pouch. 244 80

Reflex sympathetic dystrophy (RSD) usually occurs in an individual who has been experiencing significant personal stress, a state associated with increased discharge of norepinephrine (NE) from perivascular postganglionic sympathetic neurons. RSD is often precipitated by this sequence: traumatic arterial spasm, regional ischemia, neurogenic inflammation, and ischemic/edematous damage to membranes of preterminal perivascular nociceptive neurons. In the natural repair of these membranes, it is suggested that adrenoceptors appear and are ordinarily transitory; but in RSD, they are retained by the increased adjacent NE. This process delays further healing, produces pain, and releases inflammatory substances, resulting in interacting pathophysiologic vicious cycles.
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PMID:Norepinephrine in reflex sympathetic dystrophy: an hypothesis. 252 Apr 21

A case of Isaacs' syndrome with Trousseau's phenomenon is reported. Myokymia, pseudomyotonia (difficulty relaxing after forceful contraction), and ischemia-induced carpal spasm (Trousseau's phenomenon) were not abolished by nerve block distal to the cuff or by intravenous infusion of calcium. Inhalation of oxygen suppressed the pseudomyotonia and Trousseau's phenomenon, but myokymia persisted. Phenytoin abolished all types of abnormal discharges. The morphological abnormality in biopsied short peroneal muscle consisted of intraterminal and ultraterminal sprouting. We postulate that the trigger zone for abnormal discharge in our case is in the distal segment of the intramuscular nerve axon, including the nerve terminal. Hypoxia-sensitive hyperexcitability of the axon membrane might be responsible for the generation of pseudomyotonia and Trousseau's phenomenon, although the mechanism underlying myokymia remains unknown.
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PMID:Hypoxia-sensitive hyperexcitability of the intramuscular nerve axons in Isaacs' syndrome. 253 95

Non-Q-wave myocardial infarction (MI) differs from Q-wave MI in three important respects: (1) smaller infarct size possibly due to early reperfusion as a result of spontaneous thrombolysis, relief of spasm, or both; (2) more frequent patency of the infarct-related artery; and (3) a larger residual mass of viable but jeopardized myocardium within the perfusion zone of the infarct-related vessel. Left ventricular function, unless impaired by previous MI, is generally better. The prognosis is worse after the acute phase, when residual ischemia is present, and reinfarction rates during hospitalization and in the subsequent year of follow-up are higher. Obviously, since myocardial ischemia is potentially reversible, its presence should be energetically sought in all patients with recognized non-Q-wave MI. Based on our current understanding and available data, the following guidelines for the management of non-Q-wave MI patients can be recommended: (1) antiplatelet therapy along with diltiazem should be administered to patients as soon as the diagnosis is established, unless contraindications exist; (2) patients who develop early recurrent ischemia on therapy, that is, angina with associated ST-T-wave changes, should undergo prompt cardiac catheterization and myocardial revascularization; (3) patients with entirely uncomplicated hospital courses who are asymptomatic should undergo exercise stress testing, preferably in conjunction with thallium-201 imaging, before hospital discharge. Only those with evidence of significant residual ischemia need cardiac catheterization and myocardial revascularization.
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PMID:Management of acute non-Q-wave myocardial infarction: role of prophylactic pharmacotherapy and indications for predischarge coronary arteriography. 257 19

Current research suggests that ischemia induces a massive shift of calcium from the extracellular fluid to the intracellular space. This is associated with a precipitous decrease in the concentration of adenosine triphosphate, the energy source required to drive the ion pumps of the calcium channels that maintain intracellular calcium homeostasis. The result is a further increase in free intracellular calcium, leading to calcium overload and thus to cell catabolism and cell necrosis. Treatment with calcium-channel blockers may therefore offer a new approach to arresting and, possibly, preventing destruction of cerebral tissue in stroke victims. Animal studies using nimodipine, a calcium antagonist with marked vasodilator effects, have shown that this agent prevents both spasm of the isolated rabbit basilar artery, produced either by depolarization or by receptor stimulation, and postischemic impairment of cerebral blood flow (CBF), which may be a major contributor to neuronal damage. In patients with acute ischemic stroke, intravenous nimodipine therapy caused a dose-dependent increase in hemispheric CBF. These data prompted us to conduct a prospective, single-blind, randomized trial of 60 patients to determine whether nimodipine treatment would reduce neurologic deficits in patients with acute ischemic stroke. The 29 treated patients were given standard dextran therapy supplemented with daily 120 mg doses of nimodipine, and the 31 control subjects received dextran therapy alone. Mathew scale neurologic scores indicated decreased consciousness and impaired cerebral function in both treated and control groups; however, cerebral deficits were significantly smaller in patients who received nimodipine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium-channel blockers: effects on cerebral blood flow and potential uses for acute stroke. 257 24

It is widely known that other causes than recent coronary thrombosis may precipitate acute myocardial infarction in the presence of coronary atherosclerosis. A 48 year old male patient was admitted due to acute coronary insufficiency. The ECG showed anterolateral necrosis and lateral ischemia. Despite medication angina persisted and he died immediately after coronary angiography. At autopsy, established coagulation necrosis was observed in the internal half and the subendocardium of the lateral and posterior walls, of the left ventricle. Early coagulation necrosis occupied the inner half of the anterior, posterior and septal walls. Severe atherosclerotic coronary lesions were found in all major coronary trunks. An extensive panarteritis, involving extra and intramyocardial branches, consisting of mononuclear cells and prominent edema, was observed. A mixed mechanism may be invoked to explain the extensive myocardial necrosis: panarteritic infiltrates and extensive edema and humoral-induced coronary spasm.
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PMID:Panarteritis precipitating extensive circumferential acute myocardial infarction. A case report. 260 69


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