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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The definition, pathogenesis, incidence and characteristics, detection, treatment, and prognosis of silent myocardial ischemia (SMI) are reviewed. SMI is the occurrence of myocardial ischemia for which there is objective evidence (electrophysiological, hemodynamic, and metabolic changes) but no angina. Patients with SMI are classified as type 1 (completely asymptomatic), type 2 (SMI after myocardial infarction), and type 3 (both symptomatic and silent ischemia). Episodes of SMI are true ischemic events. The absence of pain may be due to defects in pain perception, an altered physiological response to ischemia, or a lesser degree of ischemia. The incidence of SMI is 2-5% in totally asymptomatic patients, 20-30% in patients who have suffered myocardial infarction, and 44-84% in patients who have symptomatic ischemia. SMI can be detected by exercise testing, portable electrocardiographic monitoring, or imaging techniques. Patients with SMI have more frequent adverse cardiac events (except death) than patients without SMI. The frequency of adverse cardiac events is similar in patients with angina and patients with SMI. SMI has been treated with nitrates, calcium-channel blockers, and beta blockers. Beta blockers appear to be the most consistent in reducing the number and duration of episodes. Combination therapy with beta blockers and nifedipine may be more effective than therapy with either agent alone. Because of the limited number of studies and the possible contribution to the results of spontaneous variability in the occurrence of SMI, no definite conclusions can be drawn about drug efficacy. There is no evidence that the prognosis of patients with SMI is altered by drug therapy; routine treatment with anti-ischemic drugs cannot be recommended. Patients must be evaluated individually, with aggressive management being reserved for those at high risk for myocardial infarction or other serious cardiac events.
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PMID:Current concepts of silent myocardial ischemia. 197 45

For purposes of clinical management, ventricular arrhythmias have been divided into risk categories of benign, prognostically important (potentially malignant) and malignant. Benign arrhythmias occur in the setting of structurally normal hearts and do not require therapy unless associated with debilitating symptoms. Malignant arrhythmias such as sustained ventricular tachycardia or fibrillation deserve aggressive therapy to prevent recurrence. Arrhythmias occurring in the presence of organic heart disease (often ischemic disease) are frequently asymptomatic but prognostically important as a risk factor for sudden death or cardiac arrest. The common empiric practice to treat such arrhythmias (by about 40 to 50% of cardiologists in the United States) needs to be reassessed in the face of the Cardiac Arrhythmia Suppression Trial. For malignant arrhythmias, class IA agents (procainamide and quinidine) continue to be the standard of treatment, and class IB agents (e.g., mexiletine) may be used as alternative or additive therapy. Class IC agents are used as second-line therapy, especially in the setting of ischemic heart disease. Class III therapy with amiodarone is reserved for refractory patients because of potential toxicity. Sotalol, a new class II-III agent, may become a first-line drug. For prognostically important arrhythmias, beta blockers remain the agents of choice, class IC agents are contraindicated, and class IA or IB drugs, or both, should be used conservatively (i.e., only for symptomatic arrhythmias). For symptomatic but benign arrhythmias requiring treatment, beta blockers are safe although not always effective. Class IA, IB and IC agents may then be considered. In these patients, the proarrhythmic potential of quinidine and class IC agents remains a concern.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical implications of new studies in the treatment of benign, potentially malignant and malignant ventricular arrhythmias. 210 50

Left ventricular hypertrophy is a problem in itself in patients with hypertension. Hypertensives with left ventricular hypertrophy have a higher incidence of ventricular arrhythmias and sudden death. This article reviews the epidemiological evidence in favour of this association. Although the mechanism of ventricular arrhythmias in patients with left ventricular hypertrophy in unclear, several hypotheses have been suggested including cellular electrophysiological changes, alterations of the myocardial tissue and silent myocardial ischemia. The management of ventricular arrhythmias in hypertensive patients implies an effort to prevent left ventricular hypertrophy by early and aggressive treatment and a judicious choice of antihypertensive agents capable of reducing left ventricular hypertrophy. It is also important to avoid hypokalemia and other electrolytic disorders. Antiarrhythmic drugs should be reserved for symptomatic patients who do not respond to other preventive measures.
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PMID:[Ventricular arrhythmia in patients with hypertension and left ventricular hypertrophy]. 215 Apr 75

In conclusion, the PIA patient is at high risk, with higher early as well as late mortality. The pathophysiology of PIA is complex and may vary from patient to patient. The concepts of ischemia at a distance and ischemia in the infarct zone have led to a better understanding of early PIA. Coronary spasm may play an important role in most PIA patients as in the general population of patients with angina pectoris. Medical therapy is efficacious in many, although it may on rare occasion aggravate myocardial ischemia. Urgent coronary arteriography is generally safe and should be performed as soon as possible for medically refractory PIA. CABG appears to be safe in experienced hands, but its timing must be individualized. The IABP should be reserved for more unstable patients for fear of vascular complications. Randomized controlled trials such as the BARI Trial will further compare PTCA with CABG.
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PMID:Postinfarction angina. 288 57

Ventricular tachyarrhythmia is the most common terminal event causing sudden cardiac death. Risk stratification using 24-hour Holter monitoring to identify ventricular ectopy and noninvasive techniques to detect abnormal left ventricular function is becoming routine. Many cardiologists treat patients with potentially lethal ventricular arrhythmias even though it is unknown as yet whether sudden cardiac death can be prevented. Patients with lethal ventricular arrhythmias are always treated. A number of new oral antiarrhythmic agents have become available to the clinician. The modified Vaughan-Williams classification system categorizes the drugs according to their electrophysiologic and clinical characteristics. The class IC antiarrhythmic agents are emerging as the potential drugs of first choice for patients with benign or potentially lethal ventricular arrhythmias. The betablockers (class II) are used as antiarrhythmic agents, particularly in the presence of active myocardial ischemia or high catecholamine levels and in the postmyocardial infarction patient. Amiodarone (class III) may cause serious side effects and is reserved for patients with lethal ventricular arrhythmias when all other available agents have failed.
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PMID:Oral antiarrhythmic agents for ventricular arrhythmias. 353 46

The uses of the exercise test continue to grow and diversify. Familiarity with the mechanics, logistics, and interpretation of these tests leads to their optimal use. The application of exercise testing for competitive or recreational sports, cardiovascular fitness exercise training, and cardiac rehabilitation is the focus of this review. Many test protocols are available, but treadmill testing is the most widely used. The inclusion of thallium scintigraphy in the exercise protocol requires additional time and expense and is best reserved for those in whom the exercise electrocardiographic response cannot be adequately interpreted. Exercise testing is a relatively safe procedure, providing that adequate screening of individuals for unstable cardiac or medical conditions has been performed. The test must be administered by experienced personnel in a setting where the necessary emergency resuscitative equipment is available. Adequate interpretation of the exercise test requires knowledge of the individual being tested and of the reason the test is being performed. Complete analysis of the exercise test includes electrocardiographic response (ST segment changes and rhythm disturbances), hemodynamic response (heart rate and blood pressure before, during, and after exercise), and functional capacity (exercise duration, symptoms, conversion to MET's). When exercise tests are employed to establish a diagnosis of coronary artery disease, an assessment of the pretest likelihood (prevalence) of disease is essential in deriving a reasonable assessment of the probability of disease after the test has been performed and reviewed. This information is particularly important when screening asymptomatic subjects for underlying coronary disease before they engage in an exercise program. Exercise testing of individuals with known cardiac disease prior to engaging in competitive or recreational sports can yield much useful information. In addition to a knowledge of the underlying cardiac condition, the type and intensity of the sport being performed must be taken into account when exercise testing is performed for athletic screening. Individuals with congenital or acquired valvular heart disease, coronary artery disease, and rhythm disturbances should undergo an exercise test as part of the pretraining evaluation. Patients with ischemic heart disease, especially those who have had a recent myocardial infarction or have undergone coronary artery bypass surgery, require counseling regarding their ability to perform certain activities of daily living and to return to work. Exercise testing can be a useful tool in establishing activity guidelines for these individuals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Exercise testing for sports and the exercise prescription. 355 96

A retrospective study was conducted of 101 hospitalized patients who had one or more episodes of syncope. The etiology of syncope was established with relative ease in 61% of these patients. History and physical examination revealed the cause in 34%, resting ECG in 11% and 24-h ECG monitoring in 16%. Additional tests (electroencephalograms, Doppler studies of the cervical arteries, computerized tomography of the brain, ultrasonography of the heart and cardiac catheterization) either were noncontributory or did not contribute to confirmed diagnoses already established by other means. Cardiac causes were responsible for the syncope in 34% and noncardiac causes in 27%. Comparison between diagnosed and undiagnosed patients revealed no significant differences with respect to age, number of syncopal episodes or presence of hypertension or diabetes. There were, however, significantly more women, and a lower frequency of ischemic heart disease and other associated diseases in the undiagnosed group. It is concluded that all patients with syncope should undergo ambulatory ECG and 24-h ECG monitoring, and that hospitalization should be reserved for patients whose clinical condition requires admission or when further investigation is necessary.
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PMID:Syncope: a retrospective study of 101 hospitalized patients. 391 52

The beta-blocker trials published so far may be subdivided into three different categories: 1) retrospective, 2) prospective non-conclusive, 3) prospective conclusive studies. The retrospective studies suffer the weaknesses of the retrospective method and may only be used as supportive evidence. There have so far been four prospective studies producing positive results, three with alprenolol and one with practolol. The studies presented support the concept that practolol and alprenolol reduce the long-term mortality due to sudden death from ischemic heart disease after myocardial infarction. All the studies have been criticized on various grounds and a list of unanswered remaining issues may be made. Acute and long-term effects of betablockade need not be the same. Our knowledge about the necessary doses and plasma levels is incomplete. All the studies published so far cover a maximum period of two years. If the study observation periods were prolonged it is likely that at some time the relative benefit becomes less. Ideal treatment should be reserved for those patients likely to derive significant benefit from it. At the present time identification of such patients is not sufficiently precise. Whether or not the beta-blockers have an antiarrhythmic effect, for instance demonstrated on chronic PVC's, this information is of little value in interpreting the proper mechanism of the beta-blockers in acute ischemia and lethal arrhythmias. In order to contribute new knowledge future studies should involve sufficiently large numbers of representative groups of patients, a stratified study design and a beta-blocker with ancillary properties different from alprenolol.
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PMID:Beta blockers after myocardial infarction--aspects on study design based on current knowledge. 611 77

The pharmacokinetics, clinical efficacy, and adverse effects of three calcium-channel blocking agents--verapamil, nifedipine, and diltiazem--are reviewed. Verapamil, nifedipine, and diltiazem are absorbed well after oral dosing, but absolute bioavailability of each is reduced substantially by a first-pass effect. Each drug is metabolized extensively (verapamil and diltiazem to moderately active metabolites) by the liver. A substantial percentage of each drug is bound to plasma proteins, but the binding is of clinical importance only for nifedipine (92--98% protein bound). Intravenous verapamil has become the agent of first choice for treatment of acute paroxysmal supraventricular tachycardia (PSVT); use of chronic oral verapamil therapy for prophylaxis remains controversial. Verapamil and diltiazem have been evaluated with mixed results for atrial flutter and fibrillation. For treatment of myocardial ischemia, calcium-channel blockers may be of some value (possibly in combination with nitrates of B blockers). All three agents have been studied in patients with exertional angina with good results. Calcium-channel blockers appear to be equal with nitrates for treatment of variant angina. Patients with hypertropic cardiomyopathy have been treated with verapamil and nifedipine with promising results. Nifedipine has been effective for treatment of essential hypertension. Adverse effects of calcium-channel blockers have been relatively minor or infrequent. Diltiazem overall has the best side-effect profile, with adverse effects causing discontinuation of therapy in about 2--10% of patients; verapamil in intermediate (8--10%) and nifedipine the worst (17%) in this respect. The most common side effects generally are fatigue, headache, dizziness, skin rash, and peripheral edema. While they generally should be reserved for patients in whom more conventional therapy has failed (except those with PSVT), calcium-channel blockers appear to have a valid role as reserve agents for exertional and variant angina, cardiomyopathy, and hypertension.
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PMID:Update on calcium-channel blocking agents. 635 66

Effort angina is the result of acute myocardial ischemia on exercise due to an imbalance between myocardial oxygen demand and supply. During exercise, ischemia is provoked by an increase in myocardial oxygen needs (tachycardia, increased blood pressure, etc.) which cannot be met by increased coronary blood flow. The commonest cause of insufficient flow is coronary atherosclerosis. Coronary spasm does, however, play a role, whether it occurs during exercise on normal or atheromatous coronary vessels. Classical anti-anginal therapy is directed towards a reduction in the intense adrenergic activity associated with exercise, and to the limitation of myocardial oxygen consumption. Calcium inhibitors which cause peripheral vasodilation, decrease ventricular wall tension and coronary resistance, are usually reserved for unstable or resistant angina. We studied 10 patients with stable effort angina for over 2 years with significant (greater than 70 per cent) atheromatous lesions on coronary angiography unsuitable for surgical treatment. The patients underwent a randomised double blind trial to compare the effects of propranolol, diltiazem and placebo. Exercise ECG was performed after a treatment period of one week, 3 hours after drug administration. The results showed a significant improvement of work capacity with propranolol and diltiazem as compared to placebo. Propranolol (160 mg/day) was more effective than diltiazem (180 mg/day) in 6 patients. In 4 cases, the improvement with diltiazem and propranolol was the same. The association of the two drugs in one open study in 5 patients was even more effective in 3 patients. The small number of patients studied makes it impossible to draw any firm conclusions. Although calcium inhibitors are the treatment of choice in coronary spasm and betablockers in effort angina, diltiazem exerts an anti-anginal effect by reduction of myocardial oxygen consumption without depression of myocardial contractility, as other workers have shown.
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PMID:[Are calcium inhibitors useful in the treatment of effort angina pectoris]. 640 53


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