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)

The natural history of patients with acute myocardial infarction treated with thrombolytic therapy includes two distinct phases: the initial or acute phase is characterized pathologically by atheromatous plaque rupture and thrombotic coronary arterial occlusion, and clinically by the abrupt onset of symptoms. Prompt restoration of coronary blood flow and myocardial reperfusion during this phase, achieved in a majority of patients given thrombolytic therapy, limits myocardial necrosis, preserves ventricular function, and lowers mortality. Although the thrombus can be pharmacologically removed, an unstable anatomic substrate persists. Therefore following thrombolytic therapy, a subacute phase occurs, during which patients are at risk for recurrent ischemic events. More than a theoretical concept, experience has shown that recurrent ischemia and reinfarction develop in 20% to 30% and 5% of patients, respectively. Morbidity and mortality are elevated considerably in these patients, dictating an aggressive diagnostic and treatment approach.
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PMID:Recurrent myocardial ischemia following thrombolytic therapy: guidelines for practicing clinicians. 161 4

Six hundred ninety-nine patients have required emergency coronary artery bypass after failed elective percutaneous coronary angioplasty during the decade September 1980 through December 1990. This represents 4% of 9860 patients having 12,146 elective percutaneous coronary angioplasty procedures during this interval. Emergency coronary artery bypass was required for acute refractory myocardial ischemia in 82%. Hospital mortality rate for all patients was 3.1%; 3.7% in patients with refractory myocardial ischemia but 0.8% in patients without refractory myocardial ischemia, p = 0.08. Postprocedural Q-wave myocardial infarctions were observed in 21% versus 2.4%, p less than 0.0001, and intra-aortic balloon pumping was required in 19% with versus 0.8% without refractory myocardial ischemia, p less than 0.0001. Multivessel disease, p = 0.004, age older than 65 years, p = 0.005, and refractory myocardial ischemia, p = 0.08, interacted to produce the highest risk of in-hospital death. Follow-up shows that there have been 28 additional late deaths, including 23 of cardiac causes for a 91% survival at 5 years. Freedom from both late death and Q-wave myocardial infarction at 5 years was 61%. In the group going to emergency coronary artery bypass with refractory myocardial ischemia, the late cardiac survival was 90%, and in those without ischemia, 92% at 5 years, p = not significant. The MI--free survival in the group with refractory ischemia, however, was 56% versus 83% in the group without ischemia, p less than 0.0001. Multivariate analysis showed the highest late event rates for patients with Q-wave myocardial infarction at the initial emergency coronary artery bypass, age older than 65 years, angina class III or IV, and prior coronary bypass surgery. In spite of a continuing high incidence of early acute myocardial infarction and an increasing operative mortality rate (7%) in the latest 3 years cohort of patients, excellent late survival and low subsequent cardiac event rates demonstrate the lasting effectiveness of prompt, successful emergency coronary bypass surgery for failed percutaneous coronary angioplasty.
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PMID:Emergency coronary artery bypass surgery for failed percutaneous coronary angioplasty. A 10-year experience. 161 79

Clinical data on 10,451 high-dose (up to 0.84 mg/kg over 10 minutes) dipyridamole-echocardiography tests (DET) performed in 9,122 patients were prospectively collected from 33 echocardiographic laboratories, each contributing greater than 100 tests. All patients were studied for documented or suspected coronary artery disease (1,117 early [less than 18 days] after acute myocardial infarction and 293 had unstable angina). Significant side effects including major adverse reactions and minor but limiting side effects occurred in 113 patients (1.2%). Major adverse reactions occurred in 7 cases (0.07%). In 6 of these cases, adverse reactions were associated with echocardiographically assessed ischemia and included 1 prolonged cardiac asystole (complicated by acute myocardial infarction and coma, with death after 23 days), 1 short-lasting cardiac asystole, 2 myocardial infarctions, 1 pulmonary edema and 1 sustained ventricular tachycardia. In all 6 cases, the cardiologist-echocardiographer performing the study had a limited experience (less than 100 tests) with DET, and at off-line reading in 5 cases, the obvious echo-positivity preceded the onset of complications by 1 to 5 minutes. The only ischemia-independent major side effect was a short-lasting cardiac asystole that was reversed by aminophylline and atropine. Significant side effects associated with echocardiographically assessed ischemia occurred in 89 additional cases (21 with and 68 without concomitant echocardiographically assessed myocardial ischemia). The most frequent of these side effects was hypotension or bradycardia, or both, which occurred in 40 patients with negative and 6 with positive DET. In all cases, side effects promptly subsided after aminophylline. In 1,857 cases, the high dose was not given for echo-positivity before the eighth minute.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety of intravenous high-dose dipyridamole echocardiography. The Echo-Persantine International Cooperative Study Group. 162 16

Neurocardiology emphasizes the role of the higher cerebral mechanisms in cardiovascular disorders. Several large clinical trials (BHAT, MIAMI, and ISIS) have consistently shown that treatment with a beta-receptor blocker (propranolol, metoprolol, or atenolol) will produce a 26% to 29% reduction in mortality in high-risk survivors of acute myocardial infarction. Because all beta-blockers cross the blood-brain barrier, it is not clear whether the salutary action is on the central or peripheral receptors. Therefore the effects of intracerebral versus intravenous propranolol were observed in 30 conscious pigs following complete occlusion of the left anterior descending coronary artery. Controls showed the propranolol to remain confined throughout the experiment to the central or peripheral compartment into which it was injected. To assure the occurrence of ventricular fibrillation (VF), each pig was psychologically stressed by being unconditioned to the laboratory. Intracerebral propranolol (0.05 mg/kg) prevented VF within a 20 min period of reversible ischemia in 6 of 9 pigs, whereas VF was prevented in 0 of 11 controls injected intravenously with either dextro-propranolol (2 pigs) or vehicle (9 pigs) (P less than .0006, binomial probability ratio). In some pigs in which VF was not manifested by 20 min, the ischemia was reversed and additional control observations were achieved; a total of 10 counter-balanced within-subjects experiments confirmed the between-subjects result (P less than .01, paired-t test). In contrast intravenous propranolol (0.2 to 2.0 mg/kg) in 7 pigs had no effect on VF latency compared to 7 vehicle controls. It is concluded that beta-receptor antagonists prevent VF in the ischemic myocardium by their effect on the brain and not the heart.
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PMID:Neurocardiology shows that the central, not peripheral, action of propranolol reduces mortality following acute coronary artery occlusion in the conscious pig. 165 74

The potential protective effects of serotonin receptor antagonism during the process of acute myocardial infarction were studied in anesthetized male dogs, which were subjected to a 90-min left circumflex coronary artery occlusion followed by 5 h of reperfusion. Either vehicle (0.9% NaCl) or the serotonin (5HT2) receptor antagonist LY53857 was infused i.v. at a dose of 0.5 mg/kg, followed by a constant infusion of 2 mg/kg/min beginning 5 min before left circumflex coronary artery occlusion and continuing throughout the duration of the ischemia and subsequent reperfusion. Verification of functional 5HT2 receptor antagonism in the circulating blood of the LY53857-treated dogs was monitored throughout the experiments by periodic assessment of ex vivo platelet reactivity to exogenous serotonin. After 5 h of reperfusion, the hearts were excised and analyzed utilizing histochemical staining with triphenyltetrazolium, which demarcates myocardial infarct size and anatomical area of myocardium at risk of infarction. There was not a significant reduction of infarct size with LY53857 treatment: control infarct/area at risk = 38.6 +/- 4.7%, n = 9 LY53857 infarct/area at risk = 33.4 +/- 3.8%, n = 6. Similarly, when myocardial infarct size was analyzed as a function of myocardial collateral blood flow, there were no significant effects of drug treatment on the relationship between collateral blood flow and infarct size. The effects of 5HT on neutrophil activation were determined by measuring the potential ability of 5HT to enhance the chemotactic peptide-induced production of superoxide. 5HT did not activate human neutrophils in vitro and LY53857 had no effect on neutrophil superoxide production.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of serotonin (5HT2) receptor blockade in myocardial reperfusion injury: effects of LY53857 in a canine model of myocardial infarction. 165 47

Esmolol is a new cardioselective beta blocker with unique pharmacokinetic properties resulting in a half-life of only 9 minutes. The present multicenter, randomized, placebo-controlled study examined the hemodynamic and antiischemic effects of this compound given as an adjunctive to conventional medical therapy in 113 patients with unstable angina. Fifty-nine patients received esmolol and 54 received matching placebo infusions. Esmolol was titrated in a step-wise manner at dosages of 2 to 24 mg/min until a 25% reduction in the double product was achieved; thereafter, esmolol was continuously infused for up to 72 hours. Esmolol caused a significant and persistent decline in heart rate and blood pressure throughout the entire study period. Clinical events, such as development of acute myocardial infarction or the need for urgent revascularization, occurred in 3 esmolol compared with 9 placebo patients (p = 0.06). There was also a trend toward reduction of silent ischemia as judged by Holter monitoring (mean [+/- standard deviation] duration/patient/24 hours, 21 +/- 81 minutes in the esmolol and 35 +/- 128 minutes in the placebo groups). Esmolol-related adverse effects were mostly cardiovascular in origin and could be managed promptly by downward dose titration or cessation of drug infusion. Thus, esmolol appears to be a safe and effective drug for patients with unstable angina because it permits a large degree of flexibility in adapting the desired level of beta blockade to the patient's changing clinical presentation.
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PMID:Usefulness of esmolol in unstable angina pectoris. European Esmolol Study Group. 167 36

An overall low tendency to complain of pain, due to a low perception of pain, has been suggested in the pathogenesis of silent ischemia, independent of the extent of the diseased coronaries and a history of previous acute myocardial infarction. This hypothesis has been tested indirectly in this retrospective study by comparison of the use of analgesics during admission for a first acute myocardial infarction with the occurrence of silent ischemia at exertion tests four weeks after discharge from hospital. The study did not show a lower use of analgesics in patients with silent ischemia, but this may be due to methodologic problems. Suggestions are given for another study design to overcome these problems.
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PMID:Silent ischemia and severity of pain in acute myocardial infarction. 167 76

Electrocardiographic (ECG) monitoring for long periods documents circadian patterns in myocardial ischemic episodes. The rise begins between 6 AM and 8 AM for patients with effort angina, the zenith of ischemic activity occurs at about noon. Similar peaks occur in the frequency of acute myocardial infarction and sudden death. Triggering mechanisms common to all of these events may include rises in catecholamine secretion, sympathetic nervous system activity, blood pressure, heart rate, cortisol secretion, and aggregability of platelets, as well as a trough in fibrinolytic activity. These coincident peaks and troughs would be expected to increase myocardial oxygen demand and decrease oxygen supply after a person arises in the morning. This vulnerable period merits recognition. Tailoring the dosing and choice of medication to prevent or reduce ischemia may be important if potential disease-activity triggering mechanisms are to be attenuated. By modifying triggering mechanisms, we may be able to modify the frequencies of adverse outcomes such as acute myocardial infarction and sudden death.
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PMID:Therapeutic implications of circadian variations in myocardial ischemia and related physiologic functions. 168 Mar 45

Ambulatory electrocardiographic monitoring now makes it possible to document silent ischemic type ST segment changes that are seen in patients who suffer from stable angina and that often occur during periods of modest physical activity and mental arousal. These observations suggest that ischemic episodes occur as a consequence of a relatively complicated interplay of changes in oxygen supply and demand. Furthermore, silent ischemia displays a circadian variation with the greatest frequency in the morning, a pattern similar to that noted for the onset of acute myocardial infarction and the occurrence of sudden death. Ischemic episodes, whether symptomatic or silent, carry a serious prognosis in subsets of patients with coronary artery disease; therefore, prophylactic treatment may be desirable. Ideally this should be based on an understanding of the pathophysiological processes involved and should also be directed at the other coronary artery risk factors of the patients. The effects of beta-blockers, which reduce the duration and frequency of silent ischemic episodes, is well described. The effect is most pronounced in the morning, when the frequency of ischemia is highest, and the mechanism of action seems mainly mediated through a reduction in myocardial oxygen demand. beta-Blockers have shown effectiveness in both effort-induced angina and mixed angina, and increased anti-ischemic potency may be achieved by combination therapy with a calcium antagonist. Abrupt withdrawal of beta-blockers is associated with a rebound increase in ischemic activity, which is mainly silent. Further studies are needed to determine whether improved control of silent ischemia reduces the risk of adverse cardiac outcomes.
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PMID:Silent ischemia and beta-blockade. 168 14

Several therapeutic agents have been tested for secondary prevention after acute myocardial infarction. Each patient presents a clinical challenge and gives the physician an opportunity to use the tests and therapy most likely to benefit the clinical course. The presence of other associated medical conditions, the type of myocardial infarction, the presence or absence of accompanying ischemia, left ventricular dysfunction, intracardiac thrombus, or ventricular arrhythmias dictate the choices that are to be made. It is apparent from this review that no single class of agents can be considered a cure, although beta-adrenergic blocking agents come the closest to this role. Analysis of these drugs helps individualize drug therapy and provides a physiologic probe to understanding the pathophysiologic processes that characterize the period after myocardial infarction. To address the impact of developing technology and drug availability on the practice and cost of medical care, the American College of Cardiology and the American Heart Association have developed guidelines for the management of patients with myocardial infarction. The clinical trial remains the best test for the assessment of therapeutic choices and can also expand our knowledge of the natural history of the disease process. Nevertheless, the issue of appropriate therapy is ever-changing, affected by the explosion of new technology and the continued investigation into the pathophysiology of coronary artery disease.
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PMID:Medical therapy after acute myocardial infarction. 168 44


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