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

Although Q wave and non-Q wave MI are often referred to as "transmural" and "nontransmural," there is no anatomic evidence to justify this distinction. Nevertheless, a distinction is important, because the two entities have a different prognosis. At the present time, between 25% and 35% of MIs are non-Q wave. They are frequently observed in patients with previous coronary events. They occur in a relatively older population and involve a slightly higher proportion of women than do Q wave MIs. The degree of cardiac damage is less, reflected by a smaller rise in enzyme level and less impairment of left ventricular ejection fraction; early reperfusion may occur, after spontaneous thrombolysis or resolution of coronary spasm. The immediate mortality rate is half that of Q wave MI but identical in the long term. Reinfarction and angina are more frequent because of a peri-infarction zone of ischemia maintained by a high-grade coronary stenosis and inadequate collateral circulation. Early characterization of those MIs likely to progress is important. Diltiazem seems effective in this context if given between 24 and 72 hours of the onset of the event. Other therapeutic approaches need further assessment.
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PMID:"Non-Q wave," alias "nontransmural," myocardial infarction: a specific entity. 264 80

Hundreds of authors world-wide are responsible for the development of the present state of microvascular free-tissue transplantation. The applied technique represents a true developmental landmark in the field of surgery, now applicable to the broad spectrum of surgical subspecialties. In hand surgery, the revolutionary use of free-tissue transplantation has saved innumerable limbs, and improved the quality of life for tens of thousands of patients. In spite of our comfort level using these techniques and incorporating them into our armamentarium of patient care, we stand only on the threshold of microsurgical clinical applicability. The field has expanded substantially during the last 15 years. First, as a substitute for more conventional solutions to wound coverage problems, substituting for often cumbersome attached random or axial pattern pedicle flaps; then, incorporating neurosurgical techniques to provide sensibility to viable but otherwise anesthetic flaps, and kinetic function to transplanted muscle; and subsequently, with the incorporation of muscle, bone, and total joints. An ever-increasing knowledge of the metabolic consequences of ischemia and hypoxia on different types of tissue has allowed us to be even more aggressive in assessing indications for composite tissue transplantation. In the future we should anticipate continued advances in optics and magnification in the surgical microscope, with particular emphasis on three-dimensional perspective and enhanced video capabilities. Technologic development of instruments and suture material should continue helping to raise the capability of what is presently the most limiting factor--the surgeon--to a higher level of potential for his or her patients. Even with improved links to video equipment, stereoscopic imaging, or even more sophisticated visual images, the lowest common denominator is the skill of the microsurgeon; more rigorous technical development will be necessary during the surgeon's training period. Besides a fundamental knowledge of vascular clotting mechanisms and the effects of anticoagulation, we have only an elementary understanding of chemically induced vasospasm, and a developing appreciation of the physiologic impact of microsurgical trauma on small blood vessels, even with the most sophisticated and delicate techniques. As the field enlarges, our ability to deal with irreversible vessel spasm, inexplicable arterial or venous clotting, or the enormity of other complications associated with microvascular free-tissue transplantation, will only grow. A richer understanding of tissue biology will not only improve our technical capabilities, but will promote consideration of a
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PMID:Microvascular free-tissue transfers to the hand and upper extremity. 267 Sep 69

Calcium plays an essential role in ischemic events observed during cardiac surgery. Many experiments have studied the effects of calcium channel blockers on intracellular calcium overload during the periods of cardiac ischemia and reperfusion. Calcium channel blockers are no longer used before and during cardiac surgery because hypothermia inhibits their pharmacological action. However, during the post-operative period, calcium channel blockers are the drugs of choice to control coronary spasm, and arterial hypertension which is secondary to peripheral vasoconstriction.
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PMID:[Role of calcium blockers in protecting the myocardium in cardiac surgery]. 267 78

In the case we have reported, there is a combination of factors that can be attributed to SLE and its associated complications, which may explain the transient hypodensities seen on cranial CT scan. Vasculitis and uncontrolled hypertension lead to arterial spasm, ischemia, and increased vascular permeability, all of which eventually cause cerebral edema. This edema may manifest itself clinically as profound but transient neurologic deficits.
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PMID:Reversible profound neurologic deficits associated with transient cranial CT abnormalities and systemic lupus erythematosus. 271 92

The long-term course of angina and the electrocardiographic signs of ischemia were assessed in 13 patients (10 women and 3 men, mean age 49 +/- 6 years) with typical angina pectoris, positive exercise tests, no evidence of coronary spasm and angiographically normal coronary arteries (syndrome X). Clinical and electrocardiographic parameters as well as results of exercise testing and 24-hour electrocardiographic monitoring were assessed at presentation and after a mean follow-up of 6.3 years (range 3 to 9). Mean number of anginal episodes and nitroglycerin consumption per week were similar at presentation and at the last follow-up. Furthermore, no significant difference was noted in heart rate-systolic blood pressure product at 0.1 mV of ST-segment depression (20,363 +/- 5,747 vs 21,649 +/- 5,687 beats/min x mm Hg), at angina (19,223 +/- 5,680 vs 20,126 +/- 6,023 beats/min x mm Hg) and at peak exercise (22,057 +/- 5,669 vs 22,868 +/- 6,122 beats/min x mm Hg). Time to 0.1 mV of ST-segment depression, to angina and to peak exercise was also similar (595 +/- 163 vs 631 +/- 184 s, 524 +/- 156 vs 571 +/- 168 s and 671 +/- 168 vs 718 +/- 186 s, respectively). The number of episodes of ST-segment depression greater than or equal to 0.1 mV during electrocardiographic monitoring was similar at presentation and follow-up (31 vs 25) as was the proportion of painful episodes (39 vs 36%). None of the patients developed major coronary events or cardiomyopathy during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term variability of angina pectoris and electrocardiographic signs of ischemia in syndrome X. 274 23

Thirteen patients, seven with acute myocardial infarction and six survivors of sudden death after sport, underwent coronary angiography within a mean of 104 min after the onset of symptoms. The admission electrocardiogram showed transmural myocardial ischemia in all patients. The ischemia-related vessel was occluded in all cases of sudden death and in three cases of acute myocardial infarction. Reperfusion was achieved in eight vessels: after intracoronary streptokinase in three, after intracoronary nitroglycerin in three, and mechanically in two. Coronary spasm was demonstrated in three vessels, and coronary thrombi, in four. The coronary lesion was described as either concentric in two or eccentric with irregular borders in eight. There was a high incidence of eccentric lesions consistent with ruptured plaques. The acute coronary angiographic findings of acute myocardial infarction and sudden death after sport are similar. Physical exercise can provoke myocardial infarction and sudden death probably by inducing plaque rupture that can evoke coronary spasm, thrombosis, or both.
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PMID:Myocardial infarction and sudden death after sport: acute coronary angiographic findings. 276 51

The G. A. Ilizarov's method was used for the treatment of 46 patients with occlusion of the arteries of the lower extremities at stages III and IV of ischemia. The treatment has proved to be ineffective in 10 patients. The use of a method in active aggravation of the inflammatory-necrotic process, postoperative arterial spasm and thrombosis, excess in the permissible rate of the bone split distraction, wrong choice of the level of osteotomy were the main causes of unsatisfactory outcomes.
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PMID:[Causes of unsatisfactory results of the treatment of chronic ischemia of the lower limbs using G. A. Ilizarov's method]. 279 70

The efficacy of the adenosine receptor blocker aminophylline on exercise capacity in patients with effort ischemia and documented coronary artery disease has been previously documented. In this study the effect of aminophylline on effort electrocardiographic (ECG) alterations and chest pain was tested in eight patients with syndrome X (anginal chest pain on effort, ischemic ECG changes during exercise, positive dipyridamole test, normal epicardial coronary arteries on angiography and absence of coronary spasm after ergonovine). After double-blind, randomized intravenous infusion of aminophylline (6 mg/kg body weight over 15 min) or placebo (20 ml of saline solution over 15 min), the eight patients with syndrome X underwent an upright bicycle exercise stress test on 2 consecutive days. After aminophylline, there was an increase in effort tolerance (aminophylline 7.7 +/- 1.2 min of exercise versus placebo 5.6 +/- 0.9, p less than 0.01) paralleled by an increase of the rate-pressure product (mm Hg x beats/min x 1/100) at 0.1 mV of ST segment depression or at peak exercise (aminophylline 278 +/- 55 versus placebo 230 +/- 24, p less than 0.05). Aminophylline provoked the abolition of ECG signs of ischemia in all eight patients. Thus, at a dosage that should effectively inhibit adenosine receptors, aminophylline infusion exerts a beneficial effect on exercise-induced chest pain and ischemia-like ECG changes in syndrome X. This effect occurs possibly through the prevention of myocardial flow maldistribution elicited by inappropriate adenosine release during effort in the presence of increased coronary resistance at the level of small intramural coronary arteries. This study, however, does not document the ischemic nature of effort-induced pain and ECG alterations in syndrome X.
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PMID:Improved exercise capacity with acute aminophylline administration in patients with syndrome X. 280 3

Assuming one knows that myocardial ischemia is present, rational management will first require a careful history to assess the severity of symptoms, such as angina, the lifestyle of the patient, his/her age, and the availability of resources. When a patient is greater than or equal to 70 years, has little angina, even the demonstration of ischemia will not require early arteriography; pharmacological therapy on a trial basis is the preferred approach. Judging the response to oral nitroglycerine, isosorbide dinitrate, beta blockers and calcium antagonists, (often combined and in modest doses) is good rational management. If symptoms persist despite therapy or when the patient is younger and has symptoms which cannot be alleviated by changes in lifestyle and/or workload, the established ischemia assumes much greater significance and nearly always requires a coronary arteriogram for proper management. Once the coronary arteriogram has been analyzed in terms of severity of flow impairment, correlation with the tests showing the extent of myocardial ischemia must be made, best during exercise. If single vessel disease is found with a local dyskinetic (echo, scintigraphy, or angio) segment, which corresponds to a stenosis of greater than or equal to 70%, particularly when found in the anterior descending artery, balloon dilatation (PTCA) or bypass surgery (CABG) should follow. When tests, such as the ECG, are obtained during an attack of angina, the Chahine classification may be used first. In Class IIa with pure ST-segment elevation significant atherosclerotic lesions are absent in most patients, while local spasm can be shown upon provocation. Here rational management can be limited to calcium antagonists sometimes combined with beta blockers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rational management following diagnosis of myocardial ischemia. 287 74

If myocardial ischemia always results from an imbalance between the needs and supplies in oxygen of the myocardium cells, the physiopathology of this process seems today infinitely more complex than the mere diminution or interruption of the output in a coronary artery. The extension of atheromatous lesions, the platelets aggregation, thrombosis, the coronary spasm, the release of products from the arachidonic cascade, the reactivity of the vascular endothelium, the profibrinolytic activity of the tissues are many of the intricate factors inducing myocardial ischemia. Cellular alterations, of which some are triggered by the release of oxygenated free radicals, lead then to an irreversible necrosis. The medications used until now in the treatment of angina are oxygen scavengers and research goes on in this direction with vaso-dilators beta-blockers, prolonged action nitro-compounds (nicorandil) or nitro-compounds with an action reinforced by N-acetyl-cysteine, bradycardiac derivates of alinidine and the new calcium antagonists dihydropyridine. However, the new physiopathological concepts of ischemia have opened new directions for the research: products which modify the arachidonic cascade by increase of synthesis or release of PGI2 (nafazatrom, defibrotide), by inhibition of TXA2 synthesis or blocking of TXA2 receptors, and similar products of PGI2 (iloprost); thrombolytic agents more specific of thrombin (PTA) or fibrinolysis activators (defibrotide), and anticoagulants with extended action; chelating agents of oxygenated free radicals (peroxide dismutase, catalase, peroxidase) or xanthine oxidase inhibitors; platelets anti-aggregates like ticlopidine which blocks the platelets receptors to fibrinogen, or inhibitors of the synthesis of pro-aggregating agents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Current therapeutic concepts in the treatment of myocardial ischemia. Current and future drugs]. 287 4


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