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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of intravenous nicardipine in the prevention of vasospasm after subarachnoid hemorrhage has been investigated in a dose escalation study in 67 patients admitted within 1 week of subarachnoid hemorrhage. Favorable outcomes were noted in 52 patients (78%). Vasospasm was found by arteriography in 31 patients (46%). A dose-related trend was noted. At the lower dose levels, angiographic spasm was observed in 68% and symptomatic vasospasm in 27% of 34 patients. Only eight of 33 patients (24%) treated at the highest dose level (approximately 10 mg/hr) developed arteriographic evidence of vasospasm. Symptomatic vasospasm was diagnosed in only two of 33 patients (6%) treated with this dose. No deaths from vasospasm occurred. Verification of changes in tissue calcium has been obtained from the rat middle cerebral artery occlusion model, and we concluded that nicardipine administered after permanent occlusion may offer protection against cerebral ischemia in this animal model. Nicardipine uptake was greater at the infarct site than in surrounding tissue, with the highest concentration in the area of maximal ischemia. Nicardipine appears to affect changes in Ca2+ more than other ions: it significantly reduced Ca2+ accumulation in the territory of the middle cerebral artery by 60% at 6 hours, and significantly reduced Na+ and K+ shifts in the same territory by 40% and 50%, respectively, at 6 hours. Although much research remains to be done, a wide role for the dihydropyridines in a number of cerebrovascular conditions is emerging.
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PMID:The potential use of nicardipine in cerebrovascular disease. 291 83

Persistent intercoronary and intracoronary communications were observed on cineangiograms in four patients having vasospastic angina without significant coronary narrowings. On provocation of coronary spasm using ergonovine maleate, these communications seemed to protect myocardium from ischemia, at least partially.
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PMID:Intercoronary and intracoronary communications in four cases of vasospastic angina. 291 14

Chronic heart failure results from two processes, i.e., myocardial and congestive failure. Myocardial failure is clinically silent, most often progresses slowly, and is documented by a depressed left ventricular ejection fraction. Multiple etiologic factors include systolic and diastolic overloads, myocardial necrosis and/or ischemia, and, perhaps, microvascular spasm. Myocardial failure ultimately leads to exaggerated neurohumoral compensatory mechanisms and derangements of the peripheral circulation, which are the hallmarks of congestive heart failure. At that stage of the syndrome, patients have symptoms, initially, with exercise and, later, at rest. Objective assessment of severity is afforded by determination of maximal oxygen uptake during maximal exercise testing. When congestive heart failure supervenes, the prognosis is poor. Current medical therapy is aimed at improving the derangements of the peripheral circulation, which relieves the symptoms but leaves the primary myocardial process unaffected. The goal of future therapy is to intervene at an earlier stage of the syndrome to halt or even partially reverse the myocardial failure.
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PMID:Central and peripheral components of cardiac failure. 293 38

In 17 anginal patients with critical narrowing of the left anterior descending artery, we studied the effects of acute ischemia, either induced by atrial pacing or by ergonovine, on transmyocardial platelet behavior. Six other patients with atypical chest pain and normal coronary arteries served as controls. Simultaneous arterial and great cardiac vein samples were drawn during control and ischemia to measure the levels of platelet factor four (PF4) and beta-thromboglobulin (BTG). During pacing-induced ischemia the great cardiac vein-arterial differences of PF4 and BTG decreased significantly, indicating a reduced platelet aggregability; no significant changes were observed in the control patients. By contrast, when ischemia resulted from ergonovine-induced spasm of the left anterior descending artery (five patients), the great cardiac vein-arterial differences increased, indicating enhanced platelet aggregability. Again no differences were observed in the patients with a negative ergonovine test. The results of our study suggest that the transcardiac platelet behavior may vary during different ischemic conditions. When ischemia is due to increased myocardial demands and flow is normal or increased, myocardial metabolites released from the ischemic area may oppose platelet aggregation. By contrast, spasm and the stagnant flow resulting from it may enhance platelet aggregation.
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PMID:Differential transmyocardial platelet behavior in response to pacing and ergonovine-induced myocardial ischemia. 294 47

Coronary artery spasm unresponsive to intracoronary nitroglycerin was observed in eight patients undergoing percutaneous transluminal coronary angioplasty for unstable ischemic symptoms (unstable angina or recent nontransmural infarction, or both). All patients manifested eccentric lesions angiographically with the right coronary artery involved in four, circumflex artery in two and left anterior descending in two. Severe coronary spasm was documented angiographically in all patients after angioplasty and resulted in symptomatic and electrocardiographic evidence of ischemia. Multiple sites of spasm were present in the dilated vessel in three patients. Coronary artery spasm persisted despite the infusion of large doses of intracoronary nitroglycerin (200 to 2,000 micrograms, mean 850 micrograms) over 10 min. Administration of intracoronary verapamil (1 to 1.5 mg over 10 min) resulted in complete relief of spasm with restoration of brisk anterograde flow in all patients. These findings suggest that intracoronary verapamil may be a useful agent for the relief of coronary spasm occurring in the setting of coronary angioplasty.
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PMID:Intracoronary verapamil for reversal of refractory coronary vasospasm during percutaneous transluminal coronary angioplasty. 297 6

Cardiac failure remains a life-threatening complication for certain patients undergoing intracardiac repair. Despite improvements in surgical techniques, methods of myocardial protection, and postoperative care, patients are frequently at risk to develop postoperative low output syndrome. Approximately 1% of cardiac surgical patients cannot be weaned from extracorporeal circulation in spite of adequate volume loading, the use of inotropic support, and initiation of intraaortic balloon pumping. In these cases, ventricular assist devices (VAD) can mechanically aid the failing heart and reverse the low output state. The concept of mechanical support for the failing left ventricle was first proposed by Clauss et al. in 1961. By 1968, Kantrowitz and associates had developed and refined the first intraaortic balloon pump (IABP). Through the efforts of Moulopolous and others, this device evolved into the present-day intraaortic balloon pump (IABP). Clinical evidence for the efficacy of left ventricular assist devices (LVAD) remained questionable until 1980, when the National Heart, Blood and Lung Institute evaluated short-term LVADs by comparing various types of mechanical aids. This report focused attention primarily on the failing left ventricle (LV). As the use of inotropic support, intraaortic balloon pumping, and LVADs improved, a small group of patients emerged who could not be separated from extracorporeal circulation due to a failing right ventricle. The failing right ventricle emerged as a unique clinical entity similar to postcardiotomy left ventricular failure that also benefited from mechanical cardiac assistance. Current therapy at major centers incorporating mechanical assist devices is based on the premise that the low output state will allow the failing heart to recover from a reversible injury. The frequent occurrence of postcardiotomy ischemia may be due to several factors such as poor myocardial protection, overdistension of the LV, emboli, coronary spasm or technical problems. Whatever the etiology, the end product of cardiac failure is a demand for oxygen consumption that cannot be met, thus leading to cardiac demise.
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PMID:Mechanical support for postcardiotomy heart failure. 298 17

A 54-year-old man was admitted to our hospital complaining of back pain and right hypochondrial pain. Ultrasonography and celiac angiography revealed a large tumor sized 9.4 X 8.1 cm. The tumor appeared hypervascular on angiogram. During the second angiography, an attempt at superselective hepatic angiography for the purpose of infusing a combination of Adriamycin and Lipiodol, spasm of the celiac artery occurred. High fever continued for 11 days after the spasm and serum transaminase was elevated. At the third angiography, the nature of the tumor was seen to have changed remarkably to one of hypovascularity. Percutaneous transhepatic tumor biopsy was done. Pathological diagnosis was necrosis of hepatocellular carcinoma. Due to heart disorders, ligation of the right hepatic artery was performed instead of hepatic resection. Postoperatively, the size of the tumor decreased further. It is thought that this patient had a tendency to suffer from vasospasm and that the tumor had a relatively low resistance to ischemia.
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PMID:[A case of necrosis of a hepatocellular carcinoma, caused by spasm of the celiac artery]. 303 94

Studies on animal models demonstrate that platelet products contribute to vascular spasm in ischemic syndromes and that this is reversible with administration of ketanserin and thromboxane synthesis inhibitors. Laboratory animals (dogs, rabbits, and rats) that had femoral artery ligations exhibited supersensitivity to serotonin within days in their collateral blood vessels. This supersensitivity lasted at least 6 months. The response to serotonin was reversed by ketanserin, but not by 5HT-1 antagonists. Supersensitivity does not extend to norepinephrine, and alpha blockers do not influence the response to serotonin. It appears that platelet activation by endothelial injury contributes to ischemia through blood vessel occlusion and vascular spasm. When platelet activation occurs in vivo, blood vessel occlusion and vascular spasm are reversible in part by using ketanserin or agents that block thromboxane synthesis or its action. Combining both classes of agents reverses spasm completely. These findings support existing evidence that platelet products contribute to vascular disease, and provide an approach to improved management with currently available pharmacologic agents.
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PMID:Serotonin, atherosclerosis, and collateral vessel spasm. 304 34

It is a well-known fact that systemic hypertension is one of the major risk factors for myocardial infarction (MI). Extensive studies on hypertensive rats revealed that calcium is excessively elevated in the myocytes, as well as in the coronary artery wall of these animals, which results in a higher resting tension and a stronger contractile response of those muscle strips. Over many years coronary spasm has been claimed by various authors to be greatly involved in the pathophysiology of early phase of acute MI (AMI). It can be shown that thrombocytes that aggregate at the injured vessel wall next to atherosclerotic plaques release vasoconstrictive factors that induce series of severe spasms at the sites with defective endothelium that end up in myocardial infarction; the pathophysiologic pathway is called the thrombo-ischemic reentry mechanism. This local contractile response may be enhanced in the presence of systemic hypertension since intracellular calcium is elevated in the coronary smooth muscle. On the other hand, it has been shown that heart muscle fibers undergo severe alterations finally resulting in necrotization, as soon as free calcium ions penetrate excessively through the sarcolemma membrane into the myoplasm so that the capacities of the calcium binding or extrusion processes become overpowered; this is especially the case during ischemia. Since free intracellular calcium is already ten times elevated in the myocytes in systemic hypertension, the myocardium may be more vulnerable to further calcium overload owing to the ischemia and necrotization is augmented. The elevation of intracellular Ca of the myocytes of the cardiovascular system in systemic hypertension enhances the pathologic response of the coronary arteries and the myocardium. This work gives a complete overview of the pathophysiologic principles involved in AMI occurring with systemic hypertension.
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PMID:The interdependence of hypertension, calcium overload, and coronary spasm in the development of myocardial infarction. 304 54

The incidence of spontaneous electrical activity during ischemia was studied in normal and spasmophilic subjects with a Bronk electrode inserted in the first dorsal interosseous muscle. Subjects were of both sexes, aged 16 to 65 years. The diagnosis of spasmophilia was established electromyographically by a variant of the Alajouanine test. Ischemia induced in many cases an electrical activity consisting of discharge potentials that have the amplitude, duration and morphology of motor unit potentials. The number of discharging motor units varied, sometimes leading to an electrical Trousseau associated to a carpal spasm. The discharge of individual motor units was irregular and practically uninfluenced by passive manipulations on the muscle or voluntary contraction. The activity started usually 30 sec to 1 min after the onset of ischemia, reached a maximal intensity (as to the number of motor units and frequency of discharge) in about 1 min and declined gradually in the following minutes. This activity was encountered in 55.06% of 770 cases of spasmophilia and only in 11.66% of 283 normal subjects, with a tendency to more intense discharge in spasmophilia. Its incidence in the spasmophilic group was closely related to the intensity of spontaneous repetitive discharges appearing electromyographically after the activation test, reaching 78.63% in most severe cases. The behaviour was interpreted as indicating a higher susceptibility in spasmophilia of axons to depolarization induced by hypoxia. This higher susceptibility appears as an important component of the excitability alterations leading to the complex neuromuscular disorders occurring in spasmophilia.
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PMID:Electrical activity induced by ischemia in the skeletal muscle of patients with spasmophilia. 313 73


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