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

To evaluate the impact of infarct size on morbidity and mortality, blood samples were drawn for CPK-MB determination in 144 consecutive patients with first acute myocardial infarction. Enzymatically estimated infarct size was significantly higher in patients who developed in-hospital arrhythmias, congestive heart failure or mechanical complications, or died. After hospital discharge, infarct size was correlated with the extension score of resting thallium-201 perfusion defects. However, infarct size did not predict the occurrence of long-term complications. Thus, infarct size affects the short-term prognosis. The long-term follow-up is determined by the complex interaction of left ventricular dysfunction, residual ischemia, and arrhythmogenic potential.
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PMID:The role of infarct size in early and late mortality. 248 28

Nitrates are beneficial in post-myocardial infarction patients with stable, unstable, and Prinzmetal's variant angina and as adjunctive therapy in congestive heart failure. They are available in multiple formulations that differ in chemical structure, pharmacokinetics, onset and duration of activity, and peak effect; all of these variables may condition the choice of nitrate preparation and routes of administration. Other conditions, such as different types of angina, intensity of symptomatology, psychological attitude, patient's compliance, and cost of treatment, have to be taken into account. The potential problem of nitrate tolerance requires further evaluation and can be prevented or reversed with intermittent-dosing regimens. Up-to-date nitrates continue to be a mainstay in the treatment of patients with myocardial infarction, especially if complicated by painful or silent ischemia.
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PMID:Chronic treatment after acute myocardial infarction: which drug for which patient? Nitrates. 248 40

Biochemical, pharmacological, and molecular biological data provide evidence for the presence of a cardiac renin-angiotensin system. Tissue angiotensins were demonstrated in all regions of the mammalian heart. Reduction of cardiac angiotensin II formation after oral administration of converting enzyme (CE) inhibitors in nephrectomized animals points to local generation of these peptides. Functional studies in isolated working rat hearts subjected to transient regional ischemia and reperfusion showed that there is aggravation of arrhythmias as well as exhaustion of energy status by angiotensins. This was prevented by CE inhibition and/or perfusion with bradykinin (BK), which in turn could be competitively antagonized with a BK antagonist. Intracoronary infusion of low-dose bradykinin attenuated ischemia-reperfusion injuries and reduced enzyme and lactate release in anesthetized dogs. Oral pretreatment with the CE inhibitor ramipril in rats, in doses that did not affect the elevation of blood pressure caused by aortic constriction, could prevent induction of as well as cause regression of established cardiac hypertrophy. In contrast, pure vasodilation was without effect on cardiac enlargement despite lowering blood pressure, pointing to a possible trophic influence of angiotensin II. Thus, apart from afterload reduction and euvolumia produced by CE inhibition, the outstanding efficacy of this therapeutic approach in congestive heart failure and cardiac hypertrophy and its potential usefulness in myocardial ischemia may also be explained by intracardiac suppression of angiotensin II generation and bradykinin degradation.
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PMID:Pharmacological interference with the cardiac renin-angiotensin system. 248 22

Despite advances in the treatment of congestive heart failure (CHF), the mortality rate continues to be high. A large number of the deaths are sudden, presumably due to ventricular arrhythmias. Complex ventricular arrhythmias are recorded in as many as 80% of patients with CHF, with nonsustained ventricular tachycardia occurring in 40%. The latter appears to be an independent predictor of mortality. Chronic structural abnormalities responsible for CHF may be the basis for the capability of a ventricle to support life-threatening arrhythmias, which are triggered by premature ventricular contractions. The pathogenesis of arrhythmias is multifactorial. Electrolyte abnormalities, ischemia, catecholamines, inotropic and antiarrhythmic drugs may worsen arrhythmias and increase susceptibility of a ventricle to sustained arrhythmias. Beta-adrenergic blockers and angiotensin-converting enzyme inhibitors have a beneficial effect. The role of various drugs in the pathogenesis and treatment of ventricular arrhythmias is discussed. The efficacy of antiarrhythmic therapy targeted to asymptomatic nonsustained ventricular tachycardia, in order to prevent sudden death, is controversial. Pharmacotherapy guided by electrophysiologic testing is the treatment of choice for patients who have manifest sustained ventricular tachycardia, but patients resuscitated from ventricular fibrillation may require automatic implantable cardioverter defibrillator.
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PMID:Ventricular arrhythmias in congestive heart failure. 257 40

The prognosis for patients with non-Q-wave myocardial infarction (MI) remains controversial, although a number of studies have shown a less favorable outlook after hospital discharge for patients with non-Q-wave than for those with Q-wave infarction. Numerous management strategies are available to the clinician, many of which involve an interventional strategy (myocardial revascularization with coronary bypass surgery or angioplasty) or a more conservative approach which emphasizes secondary prevention with medical therapy. This review summarizes the role of identifying risk variables in patients with non-Q-wave MI and their importance to clinical decision making. Based on data obtained from the Diltiazem Reinfarction Study (DRS), it has been shown that 20% of patients experience one or more episodes of spontaneous postinfarction angina which is associated with a significant increased (33%) 2-week mortality and an appreciable fivefold increased incidence of early reinfarction compared to patients without early recurrent ischemia. Similar findings have been observed in this same cohort of patients who were followed for one year, in that there was twofold higher incidence of death and late reinfarction at one year of follow-up. Other risk factors also appear to be important determinants of adverse long-term outcome after non-Q-wave MI and include persistent ST segment depression on serial electrocardiograms, congestive heart failure, and left ventricular hypertrophy. Medical therapy employed for secondary prophylaxis after non-Q-wave MI has failed to show a convincing therapeutic rationale for beta blocker administration. In contrast, diltiazem has been shown to influence the early and late outcome following non-Q-wave MI favorably.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Strategies for managing the patient with acute non-Q-wave myocardial infarction. 257 20

After more than two centuries of administration of digitalis glycosides to patients with cardiac disease, empirical observation and tradition remain the basis for much of the clinical application of these drugs. Many questions remain, and the role of digitalis in the management of congestive heart failure and cardiac rhythm disturbances is changing with improvement in our understanding of the pathophysiology of these conditions and the availability of newer effective agents that may have less potential to cause life-threatening toxicity. Nevertheless, digitalis glycoside therapy is a familiar therapeutic intervention for the majority of physicians and remains appropriate in carefully selected patients. The development of digoxin-specific Fab fragments has led to improvement in treatment of advanced and refractory digitalis toxicity and opens up the possibility of improvement in diagnosis of less clinically obvious cases of digitalis intoxication. The role of digitalis glycosides in the management of supraventricular tachyarrhythmias and congestive heart failure in the presence of sinus rhythm should now be revised. In each of these clinical circumstances, alternative drugs or other modes of therapy have been developed that reduce the dependence of clinicians on digitalis as the sole or primary approach to management. In the immediate management of paroxysmal reentrant supraventricular tachyarrhythmias, verapamil has largely replaced digoxin as the drug of choice, although digoxin has an ancillary role, especially in patients with impaired ventricular function. In the management of patients with atrial fibrillation or atrial flutter with a rapid ventricular response, verapamil or diltiazem and beta-adrenergic-blocking drugs will effectively slow the ventricular response, thus reducing the likelihood of approaching the threshold of digitalis toxicity to achieve adequate rate control. In the treatment of patients with congestive heart failure and normal sinus rhythm, one must now recognize a subset of patients with diastolic rather than systolic dysfunction who are best treated by correcting underlying causes of left ventricular hypertrophy or ischemia rather than inotropic support with cardiac glycosides. Symptomatic patients with dilated ventricles and impaired contractile function should undergo correction of abnormalities of preload with vasodilators acting on the venous bed as well as diuretics, and reduction of elevated afterload with vasodilators that reduce arteriolar resistance and thus improve ventricular emptying.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Current concepts in the use of digitalis. 264 67

A previous article (Part I) described the patient population and operative management of 666 patients who had surgery for nonruptured abdominal aortic aneurysms. This article details the perioperative complications and, by chi-square and logistic regression analysis, identifies the variables that are associated with each complication. In summarizing the results (below) the incidence of each complication is listed, along with the predictive risk factors in parentheses that have significance levels less than 0.05. Vascular morbidity data are as follows: intraoperative bleeding, 4.8%; postoperative bleeding requiring transfusion, 2.3% or repeat operation, 1.4% (large volume of blood transfusion and/or use of an autotransfusion device); intraoperative limb ischemia, 3.5%; graft thrombosis, 0.9% (femoropopliteal disease and/or distal anastomosis at the femoral level); distal thromboembolism, 3.3% (male sex, femoral popliteal disease, and/or intraoperative graft thrombosis); amputation, 1.2%; graft infection, 1 case. General morbidity data are as follows: cerebrovascular event, 0.6%; paraplegia, 1 case; cardiac event, 15.1% (age, previous episode of congestive heart failure, and/or electrocardiogram [ECG] evidence of a previous myocardial infarction); myocardial infarction, 5.2% (advancing age, angina, and/or prolonged aortic cross-clamp time); congestive heart failure, 8.9% (previous history of congestive heart failure, ECG evidence of ischemia, and/or chronic obstructive lung disease); arrhythmia requiring treatment, 10.5% (preoperative ventricular premature beats and/or respiratory failure requiring ventilation for more than 48 hours); new arrhythmia, 8.4% (angina and/or chronic obstructive lung disease); respiratory failure, 8.4% (chronic obstructive lung disease, large volume of blood transfused, and/or occurrence of postoperative bleeding, cerebrovascular accident, congestive heart failure, or myocardial infarction); renal damage with rise in creatinine or blood urea nitrogen, 5.4% and/or renal failure requiring dialysis, 0.6% (elevated preoperative creatinine, suprarenal aortic cross-clamping, and/or renal vein ligation); diarrhea without evidence of ischemia colitis, 7.1% and ischemic colitis, 0.6% (pelvic flow interrupted); prolonged ileus, 11.0% (aortoiliac occlusive disease, deterioration of renal function, prolonged ventilation, and/or preoperative history of angina); superficial wound infection, 1.5% and deep infection, 0.5% (femoral anastomosis and/or female sex); coagulopathy, 1.1% (large volume of blood transfused).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Multicenter prospective study of nonruptured abdominal aortic aneurysm. Part II. Variables predicting morbidity and mortality. 264 60

Cardiovascular complications of surgery--myocardial infarction (MI), chest pain, stroke, heart failure, and rhythm disturbances--are a major cause of post-operative a major cause of post-operative morbidity and mortality. Numerous studies have been conducted on postoperative MI in diverse populations, including patients with previous MI and others with coronary artery disease (CAD) who have or have not undergone coronary artery bypass graft (CABG) surgery. This review presents data from a number of these studies, which attempted to identify predictive tools and contributing factors to postoperative MI and other ischemic events. These potentially predictive methods and factors include previous MI, hemodynamic aberrations and monitoring, drug regimens, presence of CAD, CABG surgery, preoperative and intraoperative ischemia, congestive heart failure, thallium scintigraphy, and anesthesia.
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PMID:Perioperative cardiac problems. 265 71

Exercise tolerance in patients with normal cardiac function can improve with an exercise program. Controversy exists whether this is also true for patients with congestive heart failure (CHF). The limiting symptoms in patients with CHF are shortness of breath and fatigue. Hemodynamic parameters do not correlate well with exercise capacity in patients with CHF. These symptoms may be more related to factors that cause fatigue during exercise than to hemodynamic parameters or even to changes in pulmonary capillary pressure. The factors that cause symptoms include an increased lactate production and metabolic and blood flow abnormalities in the skeletal muscle. Exercise training can improve vasodilation and oxidation capacity, thereby reducing lactate production. Exercise programs may improve exercise capacity in the majority of patients with CHF due to coronary artery disease or idiopathic cardiomyopathy. However, certain patients with ischemia and with anterior infarctions may experience a detrimental effect on their cardiac function. Further studies are needed to better enable recognition of these patients but until this is possible, good clinical judgement must suffice.
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PMID:Cardiac rehabilitation for heart failure patients. 268 76

Acute myocardial infarction can be stratified into electrocardiographic subsets based on the presence or absence of new Q waves. This stratification has important clinical and prognostic utility. Coronary angiography during acute non-Q-wave compared with Q-wave infarction shows much higher infarct-related artery patency rates (about 75 vs. 10%) and increased coronary collateralization. Culprit legion morphology in non-Q-wave infarction commonly is complex. The frequent demonstration of recurrent clinical ischemia, or residual thallium-201 uptake abnormalities, and metabolic activity on persistent emission tomography suggest the presence of viable myocardium in the distribution of the non-Q-wave infarction usually represents 20-25% of acute myocardial infarctions. The University of California San Diego Collaborative Postinfarction Database and other large studies have found non-Q-wave infarctions to be more common in patients with a history of previous infarction and congestive heart failure, although their mortality during acute hospitalization is lower. However, in long-term followup to one year and beyond, non-Q-wave infarct mortality rates equal those of Q-wave infarction. Patients at low early and late risk of mortality include those with a first infarction who are under age 70, whereas patients with evidence of residual ischemia postinfarction are at increased risk of events. It is interesting to speculate that the settings of unstable angina pectoris, non-Q-wave infarction, and perhaps the picture after thrombolysis for acute myocardial infarction, have pathophysiologic similarities which may carry implications for future research and therapy.
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PMID:Non-Q-wave myocardial infarction: incidence, pathophysiology, and clinical course compared with Q-wave infarction. 269 Nov 40


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