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)

We reviewed the literature related to the effects of high-dose zinc in arteriosclerosis-induced angina pectoris. Lipid peroxidation and LDL oxidation are believed to be critical for arteriosclerosis, and consequently angina pectoris. Administration of biologically available zinc was a beneficial treatment in a significant percentage of patients with severely symptomatic, inoperable atherosclerotic disease. In these patients, there was no difference in zinc concentration between patients with and without atherosclerosis in whole blood, erythocytes or hair, but there was a major difference between normal aorta and diseased aortas (40.6 ppm zinc in normal aorta vs. 23.2 ppm zinc in atherosclerotic aorta, 40.6 ppm zinc in normal aorta vs. 19.4 ppm zinc in atherosclerotic aneurysm aorta, and no difference between normal and aneurysm aorta), although copper was low in aneurysm aorta. Medication with high-dose zinc sulfate to raise zinc serum concentrations from 95 to 177 microg/dl resulted in objective improvement in 12 of 16 of these patients, including a patient that also had Raynaud's disease. Long term environmental exposure to zinc resulted in a 40% reduction in the incidence of angina of effort compared to people not exposed to environmental zinc (P<0.01) and a 40% reduction in the incidence of probable ischemia in exercise (P<0.001). Lead had no effect while cadmium exposure resulted in more than tripling the incidence of angina of effort (P<0.001). The antioxidative action of zinc prevents oxidation of LDL cholesterol and consequently stops the main mechanism of atherogenesis. Zinc blocks calcium and its several actions on atherogenesis. Increased amounts of cytotoxic cytokines such as TNF-alpha, IL-beta and IL-8, often produced in the elderly, are blocked by high-dose zinc. We hypothesize that higher serum concentrations of LDL cholesterol resulting from administration of 300 mg of zinc per day is caused by a release of low density cholesterol from cardiovascular tissues, beneficially flushing it into the serum where it is readily observed, thus decreasing arteriosclerosis, increasing circulation, terminating angina pectoris and restoring more youthful cardiac function. Although prevention of cholesterol-induced arteriosclerosis by zinc is predicted from findings related to oxidative stress and lipid peroxidation, removal of LDL might be attributable to action of ionic zinc on ICAM inhibition. In stark contrast to current practice, high-dose zinc should be considered as basic in the strategy of prophylaxis and therapy of the atherosclerosis process to terminate angina pectoris and restore youthful cardiac function.
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PMID:High-dose zinc to terminate angina pectoris: a review and hypothesis for action by ICAM inhibition. 1608 66

This study assessed the incidence, clinical correlates, and prognostic significance of angina during dobutamine stress echocardiography (DSE) in patients who did not have inducible wall motion abnormalities. We studied 2,117 patients (61 +/- 13 years of age; 1,149 men) who underwent large-dose DSE and had no new or worsening wall motion abnormalities during DSE. Follow-up events were hard cardiac events (cardiac death or nonfatal myocardial infarction) and myocardial revascularization. Angina was induced in 217 patients (10%) during stress. DSE was normal in 1,198 patients (57%), whereas 919 patients (43%) had fixed wall motion abnormalities. During a mean follow-up of 5.5 +/- 3.7 years, 143 patients (7%) died of cardiac causes and 78 (4%) had nonfatal myocardial infarction. Patients who developed angina during DSE were more likely to have a history of exertional angina (64% vs 16%, p <0.001) and had a higher wall motion score index at rest (1.29 +/- 0.5 vs 1.17 +/- 0.4, p = 0.01) compared with patients who did not have angina. Annual hard cardiac event rates were 2.2% in patients who had dobutamine-induced angina (DIA) and 2.1% in patients who did not (p = NS). Myocardial revascularization was performed more frequently in patients who had DIA than in those who did not (39% vs 14%, p <0.0001). In Cox's regression model, independent predictors of hard events were age (RR 1.03, 95% confidence interval [CI] 1.02 to 1.04), male gender (RR 1.6, 95% CI 1.1 to 2.2), smoking (RR 1.5, 95% CI 1.1 to 2.9), and wall motion score index at rest (RR 2.6, 95% CI 1.8 to 3.8). In conclusion, in patients who do not have ischemia by echocardiographic criteria during DSE, inducible angina pectoris is associated with a high incidence of revascularization during follow-up. However, the hard cardiac event rate does not differ in patients who develop DIA from those who do not.
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PMID:Clinical and prognostic implications of angina pectoris developing during dobutamine stress echocardiography in the absence of inducible wall motion abnormalities. 1616 62

We present a patient with a history of coronary artery disease and exertional angina after an acute anterior myocardial infarction. Angiography and ventriculography revealed multivessel coronary artery disease and a large apical aneurysm. Echocardiography and gated SPECT studies were performed for further evaluation of ischemia and assessment of left ventricular function. Gated SPECT and echocardiography failed to detect a large apical aneurysm due to a hyperdynamic left ventricular wall at the neck of the aneurysm. This case demonstrates the importance of using multiple imaging modalities in the evaluation of ventricular function in the setting of coronary artery disease.
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PMID:Failure of gated SPECT and echocardiography to detect large apical aneurysm secondary to hyperdynamic left ventricular wall at the aneurysm neck. 1717 75

The coronary slow flow phenomenon is an angiographic finding characterized by delayed distal vessel opacification in the absence of epicardial coronary artery disease. We reported that a 33-year-old male patient with a history of exertional angina (Canadian Class II). Electrocardiographic and transthoracic echocardiographic examination were found to be completely normal. Myocardial perfusion scintigraphy revealed reversible ischemia on the anteroseptal wall of the left ventricle. Coronary angiography revealed slow flow in the left anterior descending coronary artery without any other coronary pathology.
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PMID:Does coronary slow flow phenomenon lead to myocardial ischemia? 1793 24

Based on retrospective analysis of 2446 in-patient cards, autopsy protocols, outpatient medical documentation, prevalence and features of clinical manifestation of cardiorespiratory pathology (CRP): coronary heart disease (CHD) combined with chronic obstructive pulmonary disease (COPD)--1 stage of study, and also (after randomization and forming of main and control groups), efficiency of myocardial cytoprotector trimetazidin (TMZ) at its long-term use (1 year) in combined therapy (2 stage of study): 135 CHD patients (stable exertional angina functional class II-III: 92 and 43 persons respectively) with COPD of medium severe (111 persons) and severe course (24 persons), were studied. It is shown that CRP is prevailed in elder age groups (after 45 years) and noticed in 56.7% CHD patients. More sevenre course with great risk of myocardial infarction with Q wave (twice, p < 0.001), prolongation of painless ischemia (62.4+/-11.5 min/day vs. 22.8+/-11.1 min/day), inclination to complicated rhythm disturbances (38 vs. 21.9, p < 0.05) and earlier clinical manifestations of heart failure (4.3+/-0.6 years earlier, p < 0.001) is typical for CHD with COPD vs. patients without pulmonary pathology. In one year after beginning of treatment with TMZ (35 mg) number of weekly pain attacks was decreased in patients of 1st group vs. 2nd group (at the average -50.8% -29.3% vs. +12.5% +16.6% respectively); significant (p < 0.05) decrease in duration of painless myocardial ischemia was registered. Decrease in number of supraventricular and ventricular extrasystoles (42.7+/-1.48 vs. 20.5+/-1.07 cases in a day, a < 0.0001), significant (p < 0.05) increase in ejection fraction and decrease in left ventricle end-diastolic volume (12.2+/-0.4% E 12.2+/-0.3% respectively), in dimensions of left (10.9+/-0.03%) and right (8.8+/-0.9%) atrium, in risk of development of acute coronary syndrome were noticed in the patients of main group received TMZ. Thus, long-term (not less then 1 year) use of TMZ (35 mg) in combined treatment assists to normalization of cardiovascular indices, decreases cardiovascular complication occurrence, improves disease prognosis and do not has negative side-effects.
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PMID:[Clinicopathogenetic features of coronary heart disease combined with chronic obstructive pulmonary diseases and efficiency of therapy with trimetazidin]. 1872 Jul 10

In the current pathophysiological model of chronic ischemic heart disease (IHD), myocardial ischemia and exertional angina are caused by obstructive atherosclerotic plaque, and the clinical management of IHD is centered on the identification and removal of the stenosis. Although this approach has been in place for years, several lines of evidence, including poor prognostic impact, suggest that this direct relationship may present an oversimplified view of IHD. Indeed, a large number of studies have found that IHD can occur in the presence or absence of obstructive coronary artery disease and that atherosclerosis is just 1 element in a complex multifactorial pathophysiological process that includes inflammation, microvascular coronary dysfunction, endothelial dysfunction, thrombosis, and angiogenesis. Furthermore, the high recurrence rates underscore the fact that removing stenosis in patients with stable IHD does not address the underlying pathological mechanisms that lead to the progression of nonculprit lesions. The model proposed herein shifts the focus away from obstructive epicardial coronary atherosclerosis and centers it on the microvasculature and myocardial cell where the ischemia is taking place. If the myocardial cell is placed at the center of the model, all the potential pathological inputs can be considered, and strategies that protect the cardiomyocytes from ischemic damage, regardless of the causative mechanism, can be developed.
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PMID:Obstructive coronary atherosclerosis and ischemic heart disease: an elusive link! 2332 16

Contrast-enhanced magnetic resonance tomography (1.5 Tl) was used to examine 101 patients with coronary heart disease. It was shown that angina of effort was associated with disturbed myocardial perfusion manifest during the first passage of the contrast agent at sites with a hypointense signal. Patients with acute myocardial infarction exhibited, besides defective perfusion, hyperintense edematous regions on T2-weighted images as well as hyperintense sites of delayed contrast enhancement. The main symptoms of post-infarction cardiosclerosis in hyperintense zones of delayed contrast enhancement related to cicatrical lesions in myocardium. Disturbances of local contractility depending on the severity of ischemia and cicatrical lesions resulted in the impairment of overall left ventricular contractility.
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PMID:[Magnetic resonance tomography in diagnostics of coronary heart disease]. 2415 93

Coronary artery anomalies are congenital changes in their origin, course, and/or structure. They are the second most frequent cause of sudden death in young athletes. Dual LAD artery is a rare coronary anomaly. We present the case of a 44-year-old man with recent onset exertional angina and documented ischemia whose coronary angiogram and computed tomography (CT) showed type 4 dual LAD artery, the rarest and most interesting variant.
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PMID:Type 4 dual left anterior descending artery: a very rare coronary anomaly circulation. 2594 31

Coronary subclavian steal syndrome (CSSS) is a relatively uncommon entity, and its clinical spectrum is characterized by stable exertional angina and rarely as acute coronary syndrome. The diagnosis can be established easily by angiography. We report a case series of three patients with CSSS and acute coronary syndrome and we review the literature in the attempt to understand the nature of symptomatology and the mechanisms of ischemia in this condition. Our study raised some questions about the correct definition of this entity, the pathophysiology of coronary steal and the mechanisms of ischemia, in the setting of unstable angina and acute myocardial infarction.
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PMID:Coronary-Subclavian Steal: Case Series and Review of the Literature. 2652 53

Coronary artery fistula is a rare anomaly; large fistulae may result in myocardial ischemia from coronary steal. We present the case of a 73-year-old male who presented with exertional angina; imaging demonstrated severe coronary artery disease and a large coronary artery fistula. Ligation of the fistula resulted in severe right ventricular failure and cardiogenic shock. After reestablishing flow to the fistula, the patient recovered. We speculate that the ischemia-induced angiogenesis from the congenitally present fistula made what may have otherwise been an innocent fistula into an important nutritive supply, which remained important despite distal revascularization. To our knowledge, this is the first report describing the critical nutritive value of a coronary fistula.
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PMID:Coronary Fistula and Myocardial Ischemia: What is the Relationship? 2780 62


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