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

In summary, although exercise is, as is every other procedure, imperfect with regard to sensitivity and specificity, it provides an invalualbe adjunct in the evaluation of patients with coronary disease. The test is simple, inexpensive, safe and rapidly performed and is an invaluable aid in screening patients with possible coronary disease. It is used in an asymptomatic population for industrial purposes, is useful in assessing the etiology of otherwise undiagnosed chest pain, helpful in evaluating the overall severity of ischemia [and therefore in culling-out those patients that might benefit from coronary angiography], is useful in following the course of patients with proven coronary disease [including those with acute myocardial infarction], and has found a place in the follow-up evaluation of individuals having aortocoronary bypass surgery. As a screening procedure, the treadmill test aids in seeking out that group of patients with coronary disease with potentially malignant lesions, i.e. main left coronary lesions, triple-vessel disease and [to a lesser extent] severe proximal left anterior descending coronary disease. Hence, the finding of marked depth of ST depression, prolonged duration of ischemia associated with deep ST segments, serious exercise-induced ventricular arrhythmias and hypotension produced during mild-to-moderate exercise might each be an indication of extensive coronary angiography. In many cases exercise testing is superior to coronary angiography, being a simpler, safer screening procedure, and a more functional test in documenting the presence or absence of coronary insufficiency.
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PMID:Interpretation and limitations in stress testing. 127 86

Pulmonary vasodilator therapy during increased right ventricular (RV) afterload and insufficient RV myocardial perfusion might further impair RV performance by lowering systemic and, thus, coronary perfusion pressure. This hypothesis was tested by initially inducing pulmonary hypertension (80% increase in resting pulmonary artery pressure by injection of autologous muscle) and subsequent right coronary artery stenosis (40% decrease in flow by external cuff occlusion) in eight open-chest dogs. Then the effects of nitroglycerin (5 micrograms.kg-1.min-1), prostaglandin E1 (0.2 microgram.kg-1.min-1), and hydralazine (mean 0.14 mg/kg) on global and regional (ultrasonic dimension technique) RV performance and coronary hemodynamics (electromagnetic flow probes) were determined. Following all three drugs, right coronary artery flow decreased by 40-65% (mean values) accompanied by severe regional myocardial dysfunction suggestive of ischemia (akinesis, systolic lengthening, and postsystolic shortening). Heart rates increased by 20-40%; aortic pressure decreased by 15-25%; and RV end-diastolic pressure remained unchanged. Despite similarly adverse effects on regional RV performance and comparable effects on heart rate, perfusion and filling pressures with all three drugs, RV systolic pressure, RV dP/dt, and pulmonary artery pressure during nitroglycerin and prostaglandin E1 remained unchanged, and stroke volume and pulmonary artery flow decreased, but they all increased or were maintained (stroke volume) during hydralazine. Gas exchange was not affected by any of the vasodilators. Thus, in this model of combined acute pulmonary hypertension and right coronary artery insufficiency, nitroglycerin, prostaglandin E1, and hydralazine elicited severe regional dysfunction suggestive of ischemia, probably related to concomitant increases in heart rate and decreases in coronary perfusion pressure. Despite such evidence of severe regional RV ischemia, hydralazine maintained global RV pump function. These results indicate 1) that in the presence of increased RV afterload and coronary insufficiency, reduction in coronary perfusion pressure during pulmonary vasodilator therapy may be deleterious, and 2) that even severe regional myocardial ischemia may not necessarily be accompanied by respective changes in global hemodynamics and thus may go undetected.
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PMID:Myocardial ischemia during vasodilator therapy in a canine model of pulmonary hypertension and coronary insufficiency. 157 47

The authors studied the clinical and angiographic findings in two patients who had a myocardial bridge (MB) in the right anterior descending coronary artery and did not have any arteriosclerotic lesions in the coronary arteries. The two patients were men, 57 and 58 years old. Both had a history of arterial hypertension (for 19 years and 6 months, respectively) and angina pectoris (for 7 years and 6 months, respectively). The resting EKG showed subepicardial ischemia in one and was normal in the other. The stress test was positive in both. Coronary artery angiography showed an MB in the right anterior descending coronary artery which caused a systolic constriction of 90% and 80%, 3 and 2 cm. long. Both patients had left ventricular hypertrophy. The authors conclude that MB is a frequent cause of coronary insufficiency and that the appearance of symptoms and their severity depends on the degree of systolic constriction, greater than 75%, and on the presence of left ventricular hypertrophy. The majority of patients are controlled with medical treatment and only a small number require surgical therapy.
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PMID:[Myocardial bridging as a cause of coronary insufficiency]. 160 85

The aim of this study was to determine the significance of the "coronary factor" in patients with essential hypertension (EH). Electrocardiogram Holter monitoring was performed in 61 patients with EH stage II (according to the World Health Organization criteria). Silent, ie, painless ST-segment depression, was found in 34 patients on whom echocardiography, a treadmill test, and transesophageal pacing were performed. In 21 patients with EH and silent ischemia, the examination included 201Tl stress scintigraphy, coronary angiography, and a platelet aggregation test. In 15 patients, catecholamines and beta-endorphins were obtained in blood samples during silent ischemia. 201Tl scintigraphy showed transient defects of perfusion without clearance abnormalities (group I) and with clearance abnormalities (group II). The patients in group I had more severe left ventricular hypertrophy (LVH) and a significantly higher platelet aggregation response to 0.5 mumol/L adenosine diphosphate; one patient in this group had coronary atherosclerosis. LVH and the platelet aggregation response was less pronounced in the patients in group II, but atherosclerotic lesions of a coronary artery were observed in four patients. In both groups, norepinephrine and beta-endorphin levels were increased during silent episodes of ischemia. The results suggest that there are different pathogenetic mechanisms of coronary insufficiency in patients with EH, a hypertensive heart, and silent ischemia.
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PMID:Silent myocardial ischemia in patients with essential hypertension. 163 37

"Painless" or silent myocardial ischemia is common and may be associated with all types of coronary insufficiency. Repeated ischemia impairs the functional and anatomical status of the ventricle and the aim of the treatment of coronary insufficiency must be to reduce not only pain, when present, but also ischemia. A distinction must be drawn between: 1) Painless ischemia after myocardial infarction occurring in a high risk group. This requires investigation of the patient, medical treatment and, according to results, angioplasty or surgery. 2) Painless ischemia associated with stable or unstable angina. It is known that in stable angina 50 per cent of ischemia attacks are painless and that complete treatment must seek to reduce the duration of ischemia. Treatment is adjusted on the basis of the results of investigations and the severity of ischemia. 3) Silent ischemia alone which requires precise diagnostic evaluation and assessment of risk based upon the patient's condition.
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PMID:[Silent ischemia. Therapeutic strategy]. 178 31

The paper presents the results of the study into the diagnostic potentialities of 24-hour ECG monitoring in young patients. The monitoring is a sensitive and informative technique for the diagnosis of coronary heart disease in young patients, allowing the signs of coronary insufficiency to be revealed in 91.4% of the patients with verified coronary heart disease. The young patients were demonstrated to have ischemia accompanied by ST-segment elevation, presumably of vasospastic genesis.
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PMID:[24-hour ECG monitoring in young patients with ischemic heart disease]. 180 59

Experiments on isolated hearts from adult and old rats have proved an age-dependent decrease in the resistance of contractile function and cardiac rhythm to ischemia and reperfusion. The restriction of coronary flow by 70% produced significant changes in various links of the Ca2+ transport system (an increase in sarcolemmal permeability for Ca2+ and a decrease in Ca(2+)-accumulating capacity of sarcoplasmic reticulum included). These changes, more marked in old animals, seemed to play an important role in the mechanisms of disturbances in cardiac function following coronary insufficiency.
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PMID:Age-dependent effects of ischemia and reperfusion on cardiac function and Ca2+ transport in myocardium. 195 76

Drug-induced cardioprotection, that is, protection of the heart from injuries of all kinds, is of particular importance in coronary heart disease, especially in fresh myocardial infarction including unstable angina pectoris, within the framework of secondary prevention after infarction, and in chronic coronary insufficiency (stable angina pectoris, silent ischemia). In the case of fresh infarctions, functional myocardium can be protected or salvaged in particular by early thrombolysis, early administration of calcium antagonists or beta blockers (in particular the combination of calcium antagonists with beta blockers). In the area of secondary prevention, beta blockers predominate. In chronic coronary insufficiency, calcium antagonists, nitrates and beta blockers are the first-choice cardioprotective agents.
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PMID:[Cardioprotection with drugs. 1: Coronary heart disease]. 196 78

Unstable angina is a clinical syndrome characterized by increased rate and severity of angina pectoris attacks and, sometimes but not always, accompanied by ECG changes similar to those seen in coronary insufficiency. According to the present conception of the pathogenesis, ruptures at points of high-grade stenosis in the epicardial coronary arteries with simultaneous apposition of thrombi and vasoconstriction cause critical narrowing of the vascular lumen, which means that with the same level of oxygen consumption, coronary blood flow might be inadequate even at rest. In this way the development of severe ischemia, sudden cardiac death or myocardial infarction is programmed. Therapy must accordingly aim at avoiding or eliminating the progression of thrombosis and at increasing the reduced coronary blood flow. The prognosis is unequivocally improved by aspirin. In addition, heparin, 400 units/kg body weight, should be given. Thrombolysis may be possible after mechanical recanalization, depending on the individual results of coronary angiography. Providing the adverse reactions are monitored, nitroglycerin given intravenously is the basic drug therapy, although comparative studies against other drugs are not available and some data show the development of tolerance during prolonged use. Therefore, an early change to sustained-release nitrates or mononitrates can be justified. beta-receptor blockers reduce the frequency of silent ischemia and of myocardial infarction. By these means, in 80% of the patients affected, unstable angina will be converted to the stable form of the disease. If symptoms persist coronary angiography is urgently indicated, to allow the selection of PTCA or aortocoronary bypass surgery according to the findings.
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PMID:Unstable angina: pathophysiology and drug therapy. 197 60

To demonstrate the importance of age in the prognosis of acute lower limb ischemia, a prospective study was performed in 137 patients over 24 months. Group I contained 75 patients aged under 80 years and group II 62 patients aged over 80 years. Risk factors and previous history were equally distributed in the two groups. The level of arterial blockage and the treatment were comparable in the two groups. Mortality was higher in group II than in group I (p less than 0.01). In both groups deaths were principally due to cardiac causes and a revascularisation syndrome. Amputation at thigh level was more common in group II (p less than 0.01). Mortality was higher in group II for combined thigh level amputation and cardiac or coronary insufficiency (p less than 0.05). This study demonstrated that, in terms of prognosis of acute lower limb ischemia, the critical threshold is 80 years.
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PMID:[Prognosis of acute ischemia of the lower limbs in patients over 80 years of age. A prospective study]. 209 41


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