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2016 APR 30 (NewsRx) -- By a News Reporter-Staff News Editor at Obesity, Fitness & Wellness Week -- Current study results on Cardiology have been published. According to news reporting [...]

Although significant progress in risk assessment for sudden arrhythmic death in patients after myocardial infarction has been made in the last decade, identification of the individual patient at risk for sudden cardiac death has been difficult. Despite several methodologies employed in published studies and results that are often conflicting, left ventricular ejection fraction remains the best predictor of individual risk for sudden death postinfarction, but a low sensitivity and positive predictive value limit even this factor.

The risk of sudden death may be higher for patients with high blood pressure treated with non-potassium-sparing diuretics. Non-potassium-sparing diuretics are a group of drugs that reduce blood pressure by increasing urine output but do not regulate potassium output. Researchers evaluated diuretics, beta-blocking medications, and health characteristics as sudden death risk factors in 257 patients with high blood pressure who died a sudden death (case-patients). They compared these factors in 257 living patients with similar characteristics who were also taking drugs for high blood pressure (controls). Risk for sudden death was higher in case-patients taking non-potassium-sparing diuretics with or without the addition of beta-blocking medication as compared to case-patients taking potassium-sparing diuretics. Risk for sudden death was lower in case-patients taking both non-potassium-sparing diuretics and beta-blocking medication as compared to case-patients taking only non-potassium-sparing diuretics. More case-patients had a history of heart disease, took more combination medications for high blood pressure, and were more likely to smoke cigarettes than the controls.

Objectives: To review the current literature pertaining to the cardiovascular adaptations to exercise and the impact on the physical examination, the electrocardiogram, and the echocardiogram, and to distinguish those physiologic changes from pathologic conditions associated with sudden cardiac death in athletes. Data Synthesis: Specific cardiovascular adaptations occur in response to regular physical exercise. The extent of these changes depend on the type and duration of exercise as well as the gender of the athlete. These cardiac adaptations are morphologically different from those conditions associated with sudden cardiac death. In the athlete younger than 35 years, hypertrophic cardiomyopathy is the most common cardiac condition associated with sudden death. Right ventricular dysplasia, idiopathic left ventricular hypertrophy, coronary anomalies, premature atherosclerosis, and Marfan syndrome compose the majority of the remaining causes of sudden cardiac death in athletes. In the athlete older than 35 years, coronary atherosclerosis is the leading cause of sudden death followed by those conditions responsible for sudden death in the younger athlete. Despite this, regular exercise before or following a myocardial infarction provides a protective effect with respect to overall mortality, cardiovascular mortality, and fatal reinfarction rates. Conclusions: Cardiovascular adaptation to regular physical exercise leads to morphologic changes in the myocardium that influence the cardiac examination, the electrocardiogram, and the echocardiogram. Knowledge and recognition of those changes can allow the clinician to distinguish normal physiologic changes from cardiac abnormality. Proper detection of athletes at high risk for sudden cardiac death and abstention from vigorous physical activity in these athletes may prevent sudden death. (Arch Intern Med. 1995;155:1473-1480)

Cyclic antidepressant overdose involves a risk of generalized seizures and cardiovascular disturbances. We have conducted a retrospective study to test the hypothesis of a relationship between generalized seizures and the onset of arrhythmia, hypotension or cardiac arrest during cyclic antidepressant intoxication. Patients who had seizures after ingestion of toxic amounts of tri- or tetracyclic antidepressants were included. Limb-lead QRS complex duration and systolic blood pressure were recorded before and after seizure. Twenty-four of the 388 patients (6.2%) who were admitted to our ICU over a four-year period had seizures (2.3 [+ or -] 2 seizures/patient). Cardiac repercussions of cyclic-induced seizure were frequent and severe. In the postictal period, broadening of the QRS duration or hypotension occurred or were exacerbated in at least 41% and 29% of cases, respectively. In three patients (12.5%), the seizure-induced cardiovascular state was life-threatening and required massive alkalinization therapy and vasopressors, and two of the three required cardiac massage or cardioversion. Prior to seizure, these three patients had severe intoxications characterized by QRS duration [greater than or equal to] 120 ms and systolic blood pressure [less than or equal to] 80 mm Hg. The results of this work confirm the potential risk of cardiovascular deterioration after cyclic antidepressant-induced seizure and raise the question of a prophylactic approach especially towards the subgroup with unstable hemodynamic status., (Key Words: antidepressant tricyclic; intoxication, seizure; hypotension; QRS interval; acidosis; sodium bicarbonate; sodium lactate.) INTRODUCTION Cyclic antidepressant (CA) overdose involves a risk of cardiac arrhythmia and generalized seizure. Several authors [...]

Sudden cardiac death in well-trained athletes is most often superimposed on the presence of structural heart disease. However, some athletes die suddenly in the absence of overt heart disease. To improve identification of athletes at high risk for ventricular tachycardia (VT), ventricular repolarization, the signal-averaged electro-cardiogram (ECG), and the echocardiogram from 13 male athletes with symptomatic VT and without evidence of manifest cardiac disease were compared with data obtained in 3 matched control groups (15 apparently healthy professional road cyclists, 10 professional basketball players, and 15 normal control subjects without any sports activity). All patients had apparently normal QRS duration on the routine ECG, and none were taking antiarrhythmic drugs. Echocardiography and signal-averaged electrocardiography were useful in distinguishing the group of athletes with tachyarrhythmias from the group of normal nonsporting controls, but not from both groups of normal athletes. The QT interval ([V.sup.4]) and the QT interval corrected with the cubic root were shorter for the nonsporting controls. Three parameters for QT dispersion showed significant differences (p (Am J Cardiol 1994; 74:1124--1128)

The hypothesis that non-right-handedness is associated with sudden cardiac death was tested based on evidence that sympathetic imbalance may contribute to ventricular arrhythmogenesis and evidence that left-handers may have a shorter lifespan than right-handers. The study included 26 patients with coronary artery disease (CAD), a history of ventricular tachycardia-ventricular fibrillation (VT-VF), and implanted defibrillators, and 26 patients with CAD and no history of serious arrlhythmias who were match for age, sex, and New York Heart Association functional class. Patients with any history of neurololoc disorders were excluded. Left-handers either wrote with the left hand or were convert from left- to right-handedness in childhood. Non-right-handers used the left hand for writing, drawing, or throwing. Handedness rates in patients with VT-VF and case-control subjects were compared with published norms in the general population to take expected rates into account. The rates of left-handedness (6 of 26 or 23.1%) and non-right-handedness (9 of 26 or 34.6%) in patients with VT-VF were significantly higher (p

Ventricular premature complexes (VPCs) after acute myocardial infarction (AMI) remain important determinants of survival in the post-thrombolytic era. The role of thrombolysis, left ventricular function, and Holter ST-segment depression in modulating VPC frequency is unclear. In a placebo-controlled, randomized study of tissue-type plasminogen activator (t-PA) in 103 patients with AMI (Tissue Plasminogen Activator: Toronto study), VPC frequency and ST depression on Holter monitoring (day 7), ejection fraction by radionuclide scan (day 9), and infarct artery patency and cross-sectional area on day 1 (n 42) were assessed. After administering t-PA, VPC frequency was 10 [+ or -] 58/hour (mean [+ or -] SD), similar to that after placebo (23.5 [+ or -] 91.7, p = NS). However, patients with ST depression had greater VPC frequency (56 [+ or -] 140/hour) than those without it (1.3 2.6/hour, p = 0.05). Ejection fraction was negatively correlated with VPC frequency (r = -0.33, p

* Purpose: To integrate information from the various disciplines that contribute to the understanding of the cause and prevention of sudden cardiac death: identification of new approaches from applied clinical epidemiology; identification and control of transient risk factors; and evaluation of the results of interventions. * Data Sources: A broad range of research reports and interpretations of data from English-language journal articLes and reviews, published primarily between 1970 and 1993. The fields of study included epidemiology, experimental electrophysiology, clinical observations, and interventions. * Study Selection: Continuous literature surveys, done in relation to ongoing clinical and experimental research on sudden cardiac death since 1972. * Data Extraction: Included on the basis of relevance to the topics discussed and with confirmation of data and concepts by more than one investigator when available. * Data Synthesis: Information from several disciplines was integrated by the authors to synthesize new ways to view the problem of sudden cardiac death. Quantitative information was used primarily to derive qualitative statements about new perspectives on sudden cardiac death. * Conclusions: Progress in the prevention of sudden death will require development of new approaches, including epidemiologic techniques to address risk characteristics specific to the problem; characterization of triggering events and identification of specific persons at risk for responding adversely to these events; and methods of evaluating outcomes appropriate to the nature of sudden cardiac death., The risk of sudden cardiac death and possible treatment interventions can only be determined by considering interactions between risk characteristics, specific triggering events and outcome measurements. Although more than 300,000 sudden cardiac deaths occur in the US per year, they are only a fraction of the deaths in the adult population. Risk factors for sudden cardiac death include chronic rapid heart rate and abnormal heart muscle contraction, decreased blood supply, structural heart abnormalities, chemical imbalances and changes in heart function after heart attack. These wide-ranging causes make the task of identifying and treating at-risk people difficult. Therapeutic interventions that apply to the total population must balance the benefit to the at-risk population with the possible adverse effects on the healthy population. Outcome measures must include analysis of intermediate points in care, not just mortality or survival rates.

This study was undertaken to examine whether clinical factors predict reinfarction within 1 year of a first acute myocardial infarction (AMI) and to quantity the subsequent influence of reinfarction on long-term mortality. Data from 3,695 patients with a first AMI included in the Secondary Prevention Reinfarction Israeli Nifedipine Trial Registry were analyzed. The 1-year reinfarction incidence was 6.0% (220 of 3,695) and in-hospital mortality during reinfarction was 31%. Patients with reinfarction were older (63.0 vs 60.8 years) at entry. The independent clinical prodictors for 1-year reinfarction were (adjusted relative odds): peripheral vascular disease (2.12), anterior location of the first AMI (1.62), angina before the first AMI (1.53), congestive heart failure on admission (1.34), diabetes (1.33), systemic hypertension (1.28) and age increment (1.13). One-year reinfarction rate increased from 4.0% in patients with 0 or 1 risk factor to 23.3% in patients with 5 to 6 risk factors (p

One hundred twenty-two patients treated chronically with amiodarone for sustained ventricular tachyrardia or ventricular fibrillation after failing conventional antiarrythmic therapy were analyzed to determine which factors were predictive of sudden cardiac death during follow-up. The mean left ventricular ejection fraction in the study group was 0.32, and 87% of the patients had coronary artery disease with a prior myocardial infarction. During a median follow-up of 19.5 months, 30 patients died suddenly. The only variable that was predictive of sudden death was left ventricular ejection fraction. Twenty-nine of the 84 patients with ejection fractions (Am J Cardiol 1993;71:823-826)

Programmed stimulation n patients with nonsustained ventricular tachycardia (VT) and coronary artery disease (CAD) induces sustained VT in 30 to 50% of patients at high risk for sudden death. This study sought to determine whether patients with nonsustained VT who have inducible, sustained VT would have differences of left ventricular endocardial activation and conduction compared with those of patients without inducible, sustained VT would have differences of left ventricular endocardial activation and conduction compared with those of patients without inducible sustained VT. Thirty-six patients with CAD referred for evaluation of nonsustained VT underwent programmed ventricular endocardial activation. Using previously validated methods, electrograms were classified as normal abnormal or fractionated based on measurement of local eletrogram duration and amplituted. Programmed stimulation induced sustatined, uniform VT in 16 of 36 patients (44%). Patients with inducible, sustained, uniform RV had significantly more sites with abnormal (48%) and fractionated (5.5%) electrograms than did those without inducible VT (35T abnormal and 0.4% fractionated; p = 0.05 and 0.01, respectively). Patients with inducible VT had a mean of 15% of mapped sites displaying late electrograms versus only 3% in those without inducible VT (p

Thallium 201 myocardial imaging is a powerful, noninvasive prognostic tool for evaluating a wide spectrum of coronary artery disease. Although patients with refractory angina require coronary revascularization, patients responding to medical therapy may undergo effective risk stratification by stress thallium 201 imaging.

A long-term follow-up of healthy subjects documented a significant association of QT-interval prolongation with risk of cardiovascular and coronary heart disease death. These results suggest that QT-interval length may prove to be a useful addition to the cardiovascular risk profile.

2015 JUN 20 (NewsRx) -- By a News Reporter-Staff News Editor at Obesity, Fitness & Wellness Week -- Investigators publish new report on Cardiology. According to news reporting originating from [...]

Patients with COPD are a third more likely to suffer sudden cardiac death, with their risk rising in proportion to the severity of the disease, a study suggests. The findings [...]

Reduced heart rate (HR) variability is associated with increased risk of cardiac arrest in patients with coronary artery disease. In this study, the power spectral components of HR variability and their circadian pattern in 22 survivors of out-of-hospital cardiac arrest not associated with acute myocardial infarction were compared with those of 22 control patients matched with respect to age, sex, previous myocardial infarction, ejection fraction and number of diseased coronary arteries. Survivors of cardiac arrest had significantly lower 24-hour average standard deviation of RR intervals than control patients (29 [+ or -] 10 vs 51 [+ or -] 15 ms, p

Investigation of a cohort of post-myocardial infarction patients suggests that inducible ventricular tachycardia (VT) on electrophysiologic testing may be the best predictor of spontaneous VT and sudden cardiac death in this setting. Patients with inducible VT were more than 15 times as likely to suffer electrical events than were patients without inducible VT Low ejection fraction delayed ventricular activation, and high-grade ventricular ectopy were associated with relative risks of 4.8, 4.4, and 3. 1, respectively.

* Purpose: To review the methods used for preoperative cardiac risk stratification of patients having peripheral vascular surgery. * Data Sources: Relevant studies published before August 1991 were identified using a MEDLINE search of the English-language literature, followed by a manual search of the references of all identified articles. * Study Selection: All clinical studies evaluating methods used for preoperative cardiac risk stratification of patients having peripheral vascular surgery. * Data Extraction: The key data extracted from each article included the inclusion and exclusion criteria of the study patients, the techniques used for testing and the corresponding definitions of positive test results, and the clinical outcomes of the tested patients. Data were analyzed using a Bayesian conceptual framework, and pretest probabilities were converted to post-test probabilities using calculation of likelihood ratios. * Results: Patients with high scores on clinical cardiac risk indexes (Goldman index > 12 or Detsky index > 15), or more than three of the criteria identified by Eagle (age > 70 years, diabetes, angina, Q waves on electrocardiogram, or ventricular arrhythmias) are likely to be at higher risk for cardiac death and myocardial infarction after vascular surgery. Those with both low scores and none of Eagle's criteria may be at lower risk, but this result has not been reproduced by independent studies. Neither group of patients would benefit from further investigation for cardiac risk stratification. Patients with one or two of these criteria may be at intermediate risk and would benefit most from further testing for the purposes of risk stratification. Most of the published evidence shows that the absence of redistribution on dipyridamole-thallium scanning identifies a low risk for postoperative cardiac complications, whereas the presence of redistribution predicts a high risk. Preliminary reports suggest that preoperative monitoring for silent myocardial ischemia may also be useful in identifying a high-risk subset of patients. * Conclusions: Patients identified clinically to be at either very low or high risk for cardiac complications after peripheral vascular surgery are unlikely to benefit from further risk stratification. Dipyridamole-thallium scanning is the test of choice for further evaluation of patients at intermediate clinical risk because studies have shown that it is sensitive enough to rule out a high-risk status for patients who do not have redistribution.

* Silent myocardial ischemia has been shown to occur far more frequently than anginal episodes in patients with coronary artery disease. Both an increase in myocardial oxygen demand and abnormalities of coronary vasomotor tone appear to play a significant role in the genesis of silent ischemia. Recent data show that in excess of 40% of patients with stable angina have frequent episodes of silent ischemia. The presence of silent ischemia predicts an increased risk of coronary events and cardiac death. Based on these data, it has been proposed that anti-ischemic therapy should be directed toward control of total ischemic burden. Although several recent studies have demonstrated efficacy of various antianginal drugs in reducing the number and duration of silent ischemic episodes, none has demonstrated beneficial effect on the associated adverse prognosis. (Arch Intern Med. 1991;151:2373-2382

This randomized study evaluates survivors of out-of-hospital ventricular fibrillation (VF) not associated with a Q-wave acute myocardial infarction who are deemed to be at a high risk of recurrence of VF. it compares the outcome of treatment with empirically administered amiodarone with the outcome of treatment with other antiarrhythmic agents guided by electrophysiologic testing or Holter recording, or both. The goal of therapy guided by electrophysiologic testing is to suppress inducible ventricular tachycardia (VT) or VF. Holter recording is used as the primary means of adjusting therapy only if patients are noninducible at the baseline electrophysiologic study. Patients are stratified according to cardiac diagnosis, ejection fraction, and whether they had previously received an antiarrhythmic agent that failed to suppress their arrhythmias. The primary end point of the study is total cardiac mortality. The first patient was enrolled in a pilot study on April 26, 1984. By October 1988, 142 patients had been enrolled in the full study and, as of May 1990, 199 patients have been enrolled. Compliance with therapy has been good, with no patients lost to follow-up and 8% of patients, equal in both drug groups, crossing over to alternate therapy. Baseline clinical characteristics remain similar in amiodarone and conventional drug groups. Pulmonary toxicity with amiodarone is 7% at 1 year, with no patients dying of pulmonary toxicity. in the first 142 patients, the overall 1-year cardiac mortality was 19%, with a 17% arrhythmic mortality (either VF or presumed arrhythmic death). Because of this relatively high mortality, even with aggressive evaluation, treatment and follow-up, the investigators concluded that all patients who were participants in the study should also have an automatic defibrillator implanted when possible. Enrollment will continue until March 31, 1991, with follow-up for an additional year thereafter. This study should provide data about the relative efficacy of empirically administered amiodarone compared with other antiarrhythmic agents guided by electrophysiologic study and Holter monitoring. (Am J Cardiol 1991;67:578-584), Under normal circumstances, the heart muscle has synchronized, rhythmic contractions while pumping blood to the body. Under a variety of conditions, this contractile pattern is disrupted; the resulting cessation of pumping is known as cardiac arrest, and is fatal if not reversed immediately. Patients who recover from an out-of-hospital episode of cardiac arrest are at high risk for recurrence of this condition. Frequently the episode of cardiac arrest results from an occurrence of ventricular fibrillation (VF; desynchronized, ineffectual contraction of individual heart muscle fibers), and recurrence of VF is common as well. It is assumed, but not proven, that administration of antiarrhythmic drugs will prevent another episode of VF. Because antiarrhythmic medication is almost universally administered to patients following VF, it has not been possible to compare drug therapy with placebo control. Amiodarone is a commonly prescribed, long-acting antiarrhythmic; the high rate of side effects makes it desirable to know if amiodarone is superior to other drugs of this class. To evaluate its usefulness, 199 patients have enrolled to date in the Cardiac Arrest in Seattle: Conventional Versus Amiodarone Drug Evaluation (CASCADE) study after suffering an episode of out-of-hospital VF. The goal of this ongoing study is to assess the outcome of treatment with amiodarone and the outcome of treatment with other antiarrhythmic drugs (conventional therapy). Drug dosages are titrated to prevent either physician-inducible bouts of VF, or in cases where VF can not be experimentally induced, spontaneous bouts of arrythmia as determined by ambulatory electrocardiographic monitoring. Thus far, baseline clinical data remain similar in amiodarone and conventional therapy groups. Pulmonary toxicity has occurred in about seven percent of the amiodarone patients; no patients have died of this complication. In the first 142 patients, overall one-year cardiac mortality was 19 percent, with 17 percent dying from VF or presumed arrythmia. Because of the high mortality rate even with closely monitored drug therapy, the investigators recommend that all participants in the study have an automatic defibrillator implanted when possible. (Consumer Summary produced by Reliance Medical Information, Inc.)

Disease of the coronary arteries, the major blood vessels supplying the heart, frequently results in sudden death. Ventricular arrhythmias, or abnormal heart rhythms arising in the ventricles, are a common cause of sudden death, and may be the only symptom of coronary artery disease. Exposure to carbon monoxide, a common environmental pollutant, may cause ventricular arrhythmias and, thereby, contribute to the occurrence of sudden death in patients with coronary artery disease. Exposure to carbon monoxide leads to elevated blood levels of carboxyhemoglobin, the product of the interaction between carbon monoxide and hemoglobin, the oxygen-carrying pigment of the blood. Whether or not carbon monoxide-induced elevations in carboxyhemoglobin cause ventricular arrhythmias was assessed in 41 patients with coronary artery disease. Patients were exposed to room air, and to carbon monoxide levels which produced four and six percent carboxyhemoglobin. They were then required to perform exercise on a bicycle. The heart ventricles were X-rayed during exercise, and the electrical activity of the heart was recorded throughout the procedure to detect the occurrence of ventricular arrhythmias. During the exercise period, the frequency of single or multiple ventricular arrhythmias was greater after the patients were exposed to carbon monoxide producing six percent carboxyhemoglobin. This result did not occur at levels of four percent carboxyhemoglobin. The results also revealed that the patients who developed more frequent ventricular arrhythmias were older. In addition, patients who developed multiple or complex ventricular arrhythmias exercised longer and under greater workloads. These findings demonstrate that, during exercise, the number and complexity of ventricular arrhythmias increase in patients with coronary artery disease who achieve six percent carboxyhemoglobin after carbon monoxide exposure. (Consumer Summary produced by Reliance Medical Information, Inc.)

A prospective study correlated the effect of quinidine or procainamide versus no antiarrhythmic drug on sudden cardiac death, total cardiac death and total death in 406 elderly patients with heart disease and asymptomatic complex ventricular arrhythmias detected by 24-hour ambulatory electrocardiograms. Of 397 patients treated with quinidine, 184 (46%) developed adverse effects during the first 2 weeks of therapy and were given no further antiarrhythmic therapy. Of 9 patients treated with procainamide, 2 (22%) developed adverse effects during the first 2 weeks of therapy and were given no further antiarrhythmic therapy. Adverse effects developed during long-term therapy in 6 patients 2%) receiving quinidine and in 3 patients (33%) receiving procainamide. Mean follow-up was 24 [+ or -] 15 months in both groups. Sudden cardiac death, total cardiac death and total death occurred in 21, 43 and 65% of patients receiving quinidine or procainamide, respectively, and in 23, 44 and 63% of patients receiving no antiarrhythmic drug, respectively (difference not significant). Survival by Kaplan-Meier analysis showed no significant difference between the 2 groups for sudden cardiac death, total cardiac death or total death through 4 years. Patients with abnormal left ventricular ejection fraction had a 3.4 times higher incidence of sudden cardiac death, a 2.4 times higher incidence of total cardiac death and a 1.4 times higher incidence of total death than patients with normal left ventricular election fraction. These data showed no significant difference in sudden cardiac death, total cardiac death or total death between patients treated with quinidine or procainamide or with no antiarrhythmic therapy. The presence or absence of antiarrhythmic therapy did not affect the event risk regardless of left ventricular ejection fraction [is greater than or equal to] 50% versus (Am J Cardiol 1990;66:423-428), The effects of the cardiovascular drugs quinidine and procainamide on sudden cardiac death, total cardiac death, and total death were assessed in 406 elderly patients with heart disease and ventricular arrhythmias (abnormal heart rhythms). Within the first two weeks of treatment, 184 of 397 patients treated with quinidine and 2 of 9 patients treated with procainamide developed adverse reactions and discontinued drug therapy. During long-term therapy, toxic effects developed in six patients treated with quinidine and three patients treated with procainamide. Patients were assessed over a 24-month period. The incidence of sudden cardiac death, total cardiac death, and total death was 21, 43, and 65 percent, respectively, in patients treated with antiarrhythmic agents and 23, 44, and 65 percent, respectively, in patients not receiving these agents. At four years there was no difference in survival between the two groups of patients. However, abnormal left ventricular ejection fraction (the proportion of blood emptied from the left heart ventricle at the end of a contraction) was associated with higher incidences of sudden cardiac death, total cardiac death, or total death through four years. The incidences of sudden cardiac death, total cardiac death, or total death were similar among patients who were and were not treated with these antiarrhythmic agents. These findings confirm that treatment with quinidine or procainamide did not alter the risks of sudden and total cardiac death and total death. In addition, the lack of effect of these antiarrhythmic agents on the risks of cardiac and total death was not influenced by abnormal left ventricular ejection fraction, ventricular arrhythmias, or ischemic heart disease. (Consumer Summary produced by Reliance Medical Information, Inc.)

Although there is an overall increased risk of cardiac death associated with physical exertion, the risk is small. Yet it warrants consideration by physicians and their adult patients who pursue exercise because, in any individual patient, the risk may be high. To advise patients properly on the risks and benefits of exercise, physicians should have an understanding of the risks of exercise, a strategy for patient evaluation that effectively identifies patients at risk, and a knowledge of appropriate exercise procedures that minimize risk. Patients should also know proper exercise procedures, be aware that there is some degree of risk in exercise, know their exercise tolerance, understand self-monitoring procedures, and be sensitive to prodromal symptoms. The essential feature of prudent exercise is a gradual progression during which an individual remains well within the limits of his/her exercise tolerance. (Am J Cardiol 1990;66:183-188), Physical exertion may be associated with a small, but increased, risk of sudden cardiac death, the irreversible cessation of heart beat. The risk of cardiac death associated with exercise must be taken into consideration by physicians and cardiac patients interested in exercise. To advise patients on the risks and benefits of exercise, physicians must have an understanding of the risks of exercise, a plan for evaluating and identifying patients at risk, and knowledge about the exercise procedures that reduce the risk of sudden cardiac death. Patients should be informed of suitable exercise procedures, the degree of risk associated with exercise, and their ability to tolerate exercise. In addition, patients should understand methods of monitoring themselves and be aware of symptoms that precede and are associated with sudden cardiac death. Essentially, exercise should be performed with gradually increasing intensity and within the limits of a patient's ability to withstand physical exertion. (Consumer Summary produced by Reliance Medical Information, Inc.)

Certain factors increase the risk of death in the year after an acute myocardial infarction (heart attack). These include ventricular premature complexes, which are abnormal heart rhythms arising in the ventricles of the heart, and impaired left ventricular ejection fraction, which is a decreased volume of blood emptied from the left ventricle at the end of a heart contraction. Recent studies have suggested that certain psychosocial factors, such as depression, the interaction between social isolation and life stress, and type A-B behavior, may influence the development of heart disorders. The relation between biobehavioral or psychosocial factors and clinical cardiac events was evaluated, based on results obtained from the Cardiac Arrhythmia Pilot Study (CAPS). The study included 502 patients with 10 or more ventricular complexes per hour, or five or more episodes of nonsustained ventricular tachycardia (an abnormally rapid ventricular rate) which were recorded 6 to 60 days after a heart attack. In 66 percent of the patients psychosocial questionnaires were used to assess anxiety, depression, social desirability and support, and type A-B behavior patterns. Blood pressure and pulse rate were recorded when patients played a video game. Death or cardiac arrest were used as indicators of outcome. The results indicate that a type B behavior patterns, higher levels of depression and lower pulse rates while playing the video game were associated with an increased risk of death and cardiac arrest. (Consumer Summary produced by Reliance Medical Information, Inc.)

EVIDENCE-BASED ANSWER Patients with atypical chest pain and no history of cardiovascular events coronary artery disease, unstable angina, or history of percutaneous transthoracic coronary angioplasty [PTCA]) and a negative stress [...]