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Biomedical subjects

C M Pratt

Publications and source records attributed to C M Pratt.

At least 19 recordsLinked to original sources
PubMed2001

Hemodynamic effects of tezosentan, an intravenous dual endothelin receptor antagonist, in patients with class III to IV congestive heart failure.

BACKGROUND: Endothelin-1, a powerful mediator of vasoconstriction, is increased in patients with congestive heart failure and appears to be a prognostic marker that strongly is correlated with the severity of disease. However, little is known about the potential immediate beneficial effects of acute blockade of the endothelin system in patients with symptomatic left ventricular dysfunction. We assessed the hemodynamic effects and safety of tezosentan, an intravenous dual endothelin receptor antagonist, in patients with moderate to severe heart failure. METHODS AND RESULTS: This randomized placebo-controlled study evaluated the hemodynamic effects of 6-hour infusions of tezosentan at 5, 20, 50, and 100 mg/h compared with placebo in 61 patients with New York Heart Association class III to IV heart failure. Plasma endothelin-1 and tezosentan concentrations were also determined. Treatment with tezosentan caused a dose-dependent increase in cardiac index ranging from 24.4% to 49.9% versus 3.0% with placebo. Tezosentan also dose-dependently reduced pulmonary capillary wedge pressure and pulmonary and systemic vascular resistances, with no change in heart rate. No episodes of ventricular tachycardia or hypotension requiring drug termination were observed during tezosentan infusion. Tezosentan administration resulted in dose-related increased plasma endothelin-1 concentrations. CONCLUSIONS: The present study demonstrated that tezosentan can be safely administered to patients with moderate to severe heart failure and that by virtue of its ability to antagonize the effects of endothelin-1, it induced vasodilatory responses leading to a significant improvement in cardiac index. Further studies are under way to determine the clinical effects of tezosentan in the setting of acute heart failure.

Blood Pressure↗
PubMed2000

Severity of coronary artery calcification by electron beam computed tomography predicts silent myocardial ischemia.

BACKGROUND: Detection of subclinical coronary artery disease (CAD) before the development of life-threatening cardiac complications has great potential clinical relevance. Electron beam computed tomography (EBCT) is currently the only noninvasive test that can detect CAD in all stages of its development and thus has the potential to be an excellent screening technique for identifying asymptomatic subjects with underlying myocardial ischemia. METHODS AND RESULTS: Over 2.5 years, we prospectively studied 3895 generally asymptomatic subjects with EBCT, 411 of whom had stress myocardial perfusion tomography (SPECT) within a close (median, 17 days) time period. SPECT and exercise treadmill results were compared with the coronary artery calcium score (CACS) as assessed by EBCT. The total CACS identified a population at high risk for having myocardial ischemia by SPECT although only a minority of subjects (22%) with an abnormal EBCT had an abnormal SPECT. No subject with CACS <10 had an abnormal SPECT compared with 2.6% of those with scores from 11 to 100, 11.3% of those with scores from 101 to 399, and 46% of those with scores >/=400 (P<0.0001). CACS predicted an abnormal SPECT regardless of subject age or sex. CONCLUSIONS: CACS identifies a high-risk group of asymptomatic subjects who have clinically important silent myocardial ischemia. Our results support the role of EBCT as the initial screening tool for identifying individuals at various stages of CAD development for whom therapeutic decision making may differ considerably.

Adult↗
PubMed1999

Cost estimates for treatment of cardiac ischemia (from the Asymptomatic Cardiac Ischemia Pilot [ACIP] study).

Costs for management of myocardial ischemia are enormous, yet comparison cost and outcome data for various ischemia treatment strategies from randomized trials are lacking and will require cost and resource utilization data from a large prospective trial. The Asymptomatic Cardiac Ischemia Pilot provided feasibility data for planning such a trial and an opportunity to estimate the long-term costs of different treatment strategies. Economic implications for ischemia management were compared in 558 patients with stable coronary artery disease and myocardial ischemia during both stress testing and daily life. Participants were randomized to 3 different initial treatment strategies and followed for 2 years. Based on cost trends over follow-up, costs for subsequent care were estimated. As expected, due to initial procedural costs, at 3 months, estimated costs for revascularization were approximately 10 times greater than costs for a medical care strategy. Extrapolated costs for anticipated resource consumption for care beyond 2 years, however, were approximately 2 times greater for an initial medical care strategy than for initial revascularization. This was due to increased need for drugs and hospitalizations for both late revascularizations and other ischemia-related events. Estimated costs for anticipated care in the medical strategies reached the anticipated cost of the revascularization strategy within 10 years. Because this cost-equal time period is well within the median life expectancy for such a patient population, these findings could have important public health implications and require testing in a full-scale prognosis trial. We anticipate that over the patients' life expectancy, early revascularization is likely to become either cost-neutral or cost-effective.

Angioplasty, Balloon, Coronary↗
PubMed1999

Cardiovascular safety of fexofenadine HCl.

Fexofenadine HCl is the acid metabolite of terfenadine (Seldane). The effect of this recently approved nonsedating antihistamine on the corrected QT interval (QTc) was evaluated in dose-tolerance, safety, and drug-interaction studies with healthy volunteers, and in clinical studies in patients with seasonal allergic rhinitis (SAR). Twelve-lead electrocardiographic data were collected once before and after dosing or serially throughout these studies. Outliers were defined as QTc > 440 ms with a > or = 10 ms increase from baseline. The recommended fexofenadine HCl dose is 60 mg twice daily. Fexofenadine HCl doses up to 800 mg once daily or 690 mg twice daily for 28 days resulted in no dose-related increases in QTc. Longer term studies indicated no statistically significant QTc increases compared with placebo in patients receiving fexofenadine HCl 80 mg twice daily for 3 months, 60 mg twice daily for 6 months, or 240 mg once daily for 12 months. Interaction studies showed no significant increases in QTc when fexofenadine HCl 120 mg twice daily was administered in combination with erythromycin (500 mg 3 times daily) or ketoconazole (400 mg once daily) after dosing to steady state (6.5 days). Clinical trials in patients with SAR (n = 1,160) treated with 40, 60, 120, or 240 mg twice-daily fexofenadine HCl or placebo indicated no dose-related increases in QTc and no statistically significant increases in mean QTc compared with placebo. In controlled trials with approximately 6,000 persons, no case of fexofenadine-associated torsades de pointes was observed. The frequency and magnitude of QTc outliers were similar between fexofenadine HCl and placebo in all studies. Based on a large clinical database, we conclude that fexofenadine HCl has no significant effect on QTc, even at doses > 10-fold higher than that is efficacious for SAR.

Double-Blind Method↗
PubMed1999

Evaluation of antiarrhythmic drug efficacy in patients with an ICD. Unlimited potential or replete with complexity and problems?

A report from a Study group, proposed by A. J. Camm, London, of the Working Groups on Arrhythmias and Cardiac Pacing of the European Society of Cardiology; co-sponsored by the North American Society of Pacing and Electrophysiology. The Study Group was convened on 29 August 1997 at Saltsjöbaden, near Stockholm. The meeting was chaired by A. J. Camm, London, and C. M. Pratt, Houston. Based on the presentation and discussions, a first draft of the documents was prepared by C. Pratt and J. Camm which was then circulated to all members three times for their review. All members of the Study Group approved the final manuscript. This report represents the opinion of the members of this Study Group and does not necessarily reflect the official position of either society.The meeting of the Study Group was made possible by unrestricted educational grants from Medtronic, Guidant, Proctor & Gamble, Berlex and Sanofi.Also, presented, in part, at the Cardio-Renal Drugs Advisory Board meeting of the Food and Drug Administration, Bethesda, Maryland, on 30 April 1999.

Anti-Arrhythmia Agents↗
PubMed1999

Evaluation of antiarrhythmic drug efficacy in patients with an ICD: unlimited potential or replete with complexity and problems?

There are a number of novel ways in which implantable cardioverter defibrillator (ICD) endpoints can be used in clinical trials to evaluate antiarrhythmic drugs. The advances in ICD technology (storage, retrieval, and accurate interpretation of ICD electrograms) expand the potential to include the use of an ICD endpoint as a clinical surrogate for sudden death. The ICD also provides the necessary safety net to test new drugs. The frequent need for antiarrhythmic drugs in patients already fitted with an ICD (e.g., for atrial fibrillation) necessitates knowledge of the drugs' effect on defibrillator threshold. There are interpretative problems and challenges associated with all types of ICD trials. A particular difficult issue is the degree to which the results of data on antiarrhythmic drug efficacy and safety acquired in the context of an ICD endpoint trial might be extrapolated to patient populations in which the device is not used. These and other challenging issues are discussed, with the goal of enhancing the design and interpretation of clinical trials featuring ICD endpoints.

Anti-Arrhythmia Agents↗
PubMed1999

Predicting antiarrhythmic performance.

Antiarrhythmic therapy in the past was guided by observational studies. However, optimum patient care now demands evidence derived from large clinical trials. Unfortunately, because large-scale mortality trials are expensive and time consuming, surrogate markers were used in many clinical studies. However, the use of surrogate markers for antiarrhythmic drug efficacy was called into question after the publication of studies such as the Cardiac Arrhythmia Suppression Trial (CAST) and the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial. Currently, in order to predict antiarrhythmic performance, clinicians must rely on mortality trials for guidance in treating atrial and ventricular arrhythmias. Although the practicing physician has a large number of studies to draw from, the study design and patient population are critical variables that must be understood before trial results can be applied to patient care. This review focuses on the results of the major clinical antiarrhythmic drug trials published in the last 10 years. Patient variables (e.g., the presence or absence of structural heart disease) and problems in study design that may have affected outcome are emphasized as an aid to interpreting results of current and future clinical trials.

Anti-Arrhythmia Agents↗
PubMed1998

Intensive medical therapy versus coronary angioplasty for suppression of myocardial ischemia in survivors of acute myocardial infarction: a prospective, randomized pilot study.

BACKGROUND: Patients who have inducible ischemia after acute myocardial infarction (AMI) generally undergo coronary angiography with the intent to revascularize. Whether this approach is superior to intensive treatment with anti-ischemic medications is unknown. METHODS AND RESULTS: We performed a prospective, randomized pilot study comparing intensive medical therapy with coronary angioplasty (PTCA) for suppression of myocardial ischemia in 44 stable survivors of AMI. Myocardial ischemia was quantified with adenosine 201Tl tomography (SPECT) performed 4.5+/-2.9 days after AMI. All patients at baseline had a large total (>/=20%) and ischemic (>/=10%) left ventricular perfusion defect size (PDS). SPECT was repeated at 43+/-26 days after therapy was optimized. The total stress-induced PDS was comparably reduced with medical therapy (from 38+/-13% to 26+/-16%; P<0.0001) and PTCA (from 35+/-12% to 20+/-16%; P<0.0001). The reduction in ischemic PDS was also similar (P=NS) in both groups. Cardiac events occurred in 7 of 44 patients over 12+/-5 months. Patients who remained clinically stable had a greater reduction in ischemic PDS (-13+/-9%) than those who had a recurrent cardiac event (-5+/-7%; P<0.02). Event-free survival was superior in the 24 patients who had a significant (>/=9%) reduction in PDS (96%) compared with those who did not (65%; P=0.009). CONCLUSIONS: In this small pilot study, intensive medical therapy and PTCA were comparable at suppressing ischemia in stable patients after AMI. Sequential imaging with adenosine SPECT can track changes in PDS after anti-ischemic therapies and thereby predict subsequent outcome. Corroboration of these preliminary findings in a larger cardiac-event trial is warranted.

Adrenergic beta-Antagonists↗
PubMed1998

Transdermal nitroglycerin patch therapy improves left ventricular function and prevents remodeling after acute myocardial infarction: results of a multicenter prospective randomized, double-blind, placebo-controlled trial.

BACKGROUND: Nitrates are widely used in the treatment of angina in patients with acute myocardial infarction (AMI). Short-term administration prevents left ventricular (LV) dilation and infarct expansion. However, little information is available regarding their long-term effects on LV remodeling in patients surviving Q-wave AMI. METHODS AND RESULTS: This was a randomized, double-blind, placebo-controlled trial designed to investigate the long-term (6-month) efficacy of intermittent transdermal nitroglycerin (NTG) patches on LV remodeling in 291 survivors of AMI. Patients meeting entry criteria had baseline gated radionuclide angiography (RNA) followed by randomization to placebo or active NTG patches delivering 0.4-, 0.8-, or 1.6-mg/h. RNA was repeated at 6 months and 6.5 days after withdrawal of double-blind medication. The primary study end point was the change in end-systolic volume index (ESVI). Both ESVI and end-diastolic volume index (EDVI) were significantly reduced with 0.4-mg/h NTG patches (-11.4 and -11.6 mL/m2, respectively, P<.03). This beneficial effect was observed primarily in patients with a baseline LV ejection fraction < or =40% (deltaESVI, -31 mL/m2; deltaEDVI, -33 mL/m2; both P<.05) and only at the 0.4-mg/h dose. After NTG patch withdrawal, ESVI significantly increased but did not reach pretreatment values. CONCLUSIONS: Transdermal NTG patches prevent LV dilation in patients surviving AMI. The beneficial effects are limited to patients with depressed LV function and only at the lowest (0.4-mg/h) dose. Continued administration is necessary to maintain efficacy. Whether these remodeling effects confer a clinical or survival advantage will need to be addressed in an adequately powered cardiac event trial.

Administration, Cutaneous↗
PubMed1998

Mortality in the Survival With ORal D-sotalol (SWORD) trial: why did patients die?

The Survival With ORal D-sotalol (SWORD) trial tested the hypothesis that the prophylactic administration of oral d-sotalol would reduce total mortality in patients surviving myocardial infarction (MI) with a left ventricular ejection fraction (LVEF) of < or = 40%. Two index MI groups were included: recent (6 to 42 days) and remote (> 42 days) with clinical heart failure (n = 915 and 2,206, respectively). The trial was discontinued when the statistical boundary for harm was crossed (RR = 1.65; p = 0.006). All baseline variables known to be associated with mortality risk (e.g., LVEF, heart failure class, age) as well as variables related to torsades de pointes (e.g., time from beginning of therapy, QTc, gender, potassium, renal function, dose of d-sotalol) were assessed for interaction of each variable with treatment assignment, computing RR and 95% confidence interval (CI) from Cox regression models. The d-sotalol-associated mortality was greatest in the group with remote MI and LVEFs of 31% to 40% (RR = 7.9; 95% CI 2.4 to 26.2). Most variables known to be associated with torsades de pointes were not differentially predictive of d-sotalol-associated risk, except female gender (RR = 4.7; 95% CI 1.4 to 16.5). These findings suggest that (1) most of the d-sotalol-associated risk was in patients remote from MI with a LVEF of 31% to 40%; comparable placebo patients had a very low mortality (0.5%); and (2) very little objective data supports torsades de pointes or any specific proarrhythmic mechanism as an explanation for d-sotalol-associated mortality risk.

Administration, Oral↗
PubMed1998

Can antiarrhythmic drugs survive survival trials?

Sudden cardiac death due to arrhythmic events is the major cause of mortality among early post-myocardial infarction (MI) patients, accounting for > 250,000 deaths annually in the United States alone. Antiarrhythmic drugs can be used in such patients as well as in those who have not had a recent MI but are at high risk for sudden cardiac death (e.g., those with ventricular tachycardia/fibrillation, or who have survived cardiac arrest). Most antiarrhythmic drugs available, however, have limitations arising from their toxic and proarrhythmic potential. Thus, research and development of new agents and treatment modalities are desirable. This article seeks to enumerate the lessons of past clinical trials with these agents and to provide guidelines for future trials. That a variety of antiarrhythmic drugs have been associated with an increased mortality has been a disturbing observation. It is therefore imperative that candidates for antiarrhythmic therapy be selected appropriately. We recommend that future clinical trials use stringent criteria for the identification of patients at "high risk" for arrhythmia or sudden cardiac death, and limit recruitment to such patients. Traditional markers, such as the increased frequency and complexity of ventricular premature beats, and low left ventricular ejection fraction, have not been successful in identifying these high-risk patients. However, decreased heart rate variability and cardiac late potentials recorded on a signal-over-aged electrocardiogram appear to be more specific markers of post-MI arrhythmia or sudden cardiac death and may, in conjunction with the traditional markers, be used to improve selection of trial populations. Since the risk of sudden cardiac death diminishes with time after MI, it is also recommended that the temporal window of treatment with antiarrhythmic agents be limited to 1 year post-MI. It is also important to define clearly the endpoints of efficacy evaluations. A short-term reduction on markers like ventricular ectopic beats, for example, does not translate into a long-term decrease in arrhythmia-related mortality. Therefore, a reduction in overall mortality is the only meaningful endpoint to define the true risk-benefit ratio. To limit exposure to the potentially adverse effects of these agents, target populations for prophylactic antiarrhythmic drugs should be limited to recent post-MI patients at high risk for sudden cardiac death due to arrhythmia. Avoiding exposure of low-risk patients to antiarrhythmic drugs is equally imperative. "Low risk" of all-cause mortality includes the group of post-MI patients with a left ventricular ejection fraction >36%. Risk must be continuously evaluated in the setting of other pharmacologic (angiotensin-converting enzyme [ACE] inhibitors, aspirin, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors ["statins"], and others) and/or nonpharmacologic interventions (coronary artery bypass graft, angioplasty, implantable cardioverter/defibrillator). There is also a need to improve noninvasive techniques for identifying patients in the high-risk category-at present, the presence of ventricular premature beats and a left ventricular ejection fraction <36% is considered somewhat predictive of sudden cardiac death. Thus, patients with a recent MI and moderately low left ventricular ejection fraction (< or = 36% but not <20%) may be considered for antiarrhythmic therapy. A subset analysis of patients with low heart rate variability can provide valuable additional information. It is important to note that although all-cause mortality is a valid endpoint for such trials, stratification by specific cause of mortality is desirable.

Anti-Arrhythmia Agents↗
PubMed1998

The azimilide post-infarct survival evaluation (ALIVE) trial.

The AzimiLide post-Infarct surVival Evaluation (ALIVE) trial is a new clinical trial using an innovative design to examine the potential of azimilide, a novel type of antiarrhythmic, for improving survival in post myocardial infarction (MI) patients at high risk of sudden cardiac death. Azimilide is the first of a unique class of antiarrhythmic drugs that blocks both slow and rapid components of the delayed rectifier potassium currents in human myocardium. Preclinical studies have shown the drug to be effective in reducing cardiac tachyarrhythmias, even under ischemic conditions. Currently, azimilide is in Phase III trials for the treatment of supraventricular arrhythmias. The ALIVE study design is based on lessons learned from the Cardiac Arrhythmia Suppression Trials (CAST), the Survival With Oral d-Sotalol (SWORD) trial, and the European Myocardial Infarction Amiodarone Trial (EMIAT) and identifies recent post-MI patients at high risk of sudden cardiac death. The hypothesis underlying this trial is that azimilide will improve survival in this patient population. The ALIVE trial is designed as a double-blind, placebo-controlled, multinational trial that will overcome the shortcomings of previous antiarrhythmic trials by using left ventricular ejection fraction and heart rate variability as predictors to target a post-MI patient population at high risk of sudden death. The major inclusion criteria for the study are adult patients of either gender with a left ventricular ejection fraction of 15-35% who have had a recent MI (within 6-21 days). Additional stratification will be based on patients with heart rate variability < or = 20 U (heart rate variability index). Exclusion criteria include factors that may predispose a patient to nonarrhythmia-induced death or to low risk of sudden cardiac death caused by arrhythmia. Sample size is based on the assumption that the all-cause mortality rate (the primary endpoint) for 1 year in placebo patients at high risk for sudden cardiac death (heart rate variability < or = 20 U) is 15% and that azimilide will decrease all-cause mortality by at least 45% in these patients. The trial consists of 3 groups-patients receiving 75 mg azimilide orally each day, patients receiving 100 mg azimilide orally each day, and patients receiving placebo. No dose adjustments for age, gender, renal or hepatic failure, or concomitant use of warfarin or digoxin are thought necessary with azimilide. Enrollment for the trial is expected to continue for 24 months, and treatment is scheduled to be administered for a 1-year follow-up period.

Adult↗
PubMed1998

Design of a randomized, placebo-controlled multicenter trial on the long-term effects of intermittent transdermal nitroglycerin on left ventricular remodeling after acute myocardial infarction. Transdermal Nitroglycerin Investigators Group.

Nitrates are widely used in the treatment of patients with ischemic heart disease and in those with angina following acute myocardial infarction. Short-term studies indicate that the administration of nitrates may prevent left ventricular (LV) dilation and infarct expansion. Animal models suggest that prolonged nitroglycerin use after infarction may limit LV remodeling similar to that observed with angiotensin-converting enzyme inhibitors. However, to date there have been no trials evaluating the effects of nitrates on LV volumes in patients surviving acute myocardial infarction. We therefore performed a randomized double-blind, placebo-controlled trial designed to investigate the long-term (6 month) efficacy of intermittent transdermal nitroglycerin patches on LV remodeling in 291 survivors of acute myocardial infarction. Patients were randomized to receive either placebo or a nitroglycerin patch that delivered 0.4, 0.8, or 1.6 mg/hour. Gated radionuclide angiography was used to assess serial changes in LV ejection and cardiac volumes. The baseline characteristics of the study population were similar in all 4 treatment groups. The study protocol and the main design-related issues are described.

Administration, Cutaneous↗
PubMed1998

Impact of managed care on the treatment of atrial fibrillation.

In the era of managed care, it has been necessary to develop new and innovative treatment strategies for the treatment of cardiovascular disease. This article examines our experience providing cardiovascular services to a large health maintenance organization (HMO). The focus of this article is on our development and implementation of a systematic approach to the management of atrial fibrillation (AFib), encouraging the active participation of the family practice and internal medicine physicians. With > 22 geographically diverse satellite clinics, the standardization of treatment of a common disease such as AFib is both challenging and difficult. The first objective for Baylor Cardiology was to adapt to such a system and provide an efficient and flexible schedule encouraging communication with the primary care doctor. A telephone consultation service was instituted to provide instant cardiology consultation. The HMO organizational structure allowed us to implement standardized procedures and clinical approaches. Guidelines were implemented to address all practical clinical issues in AFib such as: (1) the necessity for hospitalization; (2) baseline noninvasive studies; and (3) standardization of protime and international normalized ratio (INR) measurements between all the satellite clinics. Also, algorithms for the selection of antiarrhythmic drugs for maintenance of sinus rhythm and rate control are presented.

Algorithms↗
PubMed1997

Prognostic significance of myocardial ischemia detected by ambulatory electrocardiography, exercise treadmill testing, and electrocardiogram at rest to predict cardiac events by one year (the Asymptomatic Cardiac Ischemia Pilot [ACIP] study)

Myocardial ischemia identified by ambulatory electrocardiography (AECG), exercising treadmill testing, (ETT), or 12-lead electrocardiogram at rest is associated with an adverse prognosis, but the effect of improving these ischemic manifestations by treatment on outcome is unknown. The Asymptomatic Cardiac Ischemia Pilot (ACIP) study was a National Heart, Lung, and Blood Institute funded study to determine the feasibility of conducting a large-scale prognosis study and to assess the effect of 3 treatment strategies (angina-guided strategy, AECG ischemia-guided strategy, and revascularization strategy) in reducing the manifestations of ischemia as indicated by AECG and ETT. The study cohort for this database study consisted of 496 randomized patients who performed the AECG, ETT, and 12-lead electrocardiogram at rest at both the qualifying and week 12 visits. The effect of modifying ischemia by treatment on the incidence of cardiac events (death, myocardial infarction, coronary revascularization procedure, or hospitalization for an ischemic event) at 1 year was examined. In the 2 medical treatment groups (n = 328) there was an association between the number of ambulatory electrocardiographic ischemic episodes at the qualifying visit and combined cardiac events at 1 year (p = 0.003). In the AECG ischemia-guided patients there was a trend associating greater reduction in the number of ambulatory electrocardiographic ischemia episodes with a reduced incidence of combined cardiac events (r = -0.15, p = 0.06). In the revascularization strategy patients this association was absent. In the medical treatment patients the exercise duration on the baseline ETT was inversely associated with an adverse prognosis (p = 0.02). The medical treatment strategies only slightly improved the exercise time and the exercise duration remained of prognostic significance. In the revascularization group strategy patients this association was absent. Thus, myocardial ischemia detected by AECG and an abnormal ETT are each independently associated with an adverse cardiac outcome in patients subsequently treated medically.

Electrocardiography↗
PubMed1997

Anginal status and prediction of cardiac events in patients enrolled in the asymptomatic cardiac ischemia pilot (ACIP) study. ACIP investigators.

We hypothesized that among the patients enrolled in the Asymptomatic Cardiac Ischemia Pilot (ACIP) trial, those who reported angina either within the previous 6 weeks or experienced angina during ambulatory electrocardiographic (ECG) monitoring during activities of daily life or during stress testing would be more likely to experience an adverse cardiac event within a year than those who did not experience angina. Of the 558 patients enrolled in ACIP, 325 (58.2%) reported angina in the previous 6 weeks, 300 (53.8%) had stress-induced angina, and 63 (11.3%) reported angina during activities of daily life associated with ST-segment changes on the 48-hour ambulatory electrocardiogram. Some patients had > 1 of these angina symptoms and thus 8 angina status categories were identified. Adverse cardiac events were defined as death, nonfatal myocardial infarction (MI), or hospitalization for ischemic events, which included revascularization not specified by the ACIP protocol. One hundred and sixty-seven patients (29.9%) were asymptomatic (i.e., they never had angina) by our defined criteria. Three hundred ninety-one patients (70.1%) were symptomatic. Symptomatic patients had a higher incidence of death, MI, or hospitalization for ischemic events (15.3% symptomatic vs 7.8% asymptomatic, p = 0.016). History of angina within 6 weeks before randomization was predictive of death, MI, or hospitalization for ischemic event (p = 0.007). This finding was due to a large difference in the need for hospitalizations which would be expected to be driven by the presence of angina. By contrast, angina during ambulatory electrocardiogram or stress test was not predictive of an adverse cardiac event. The asymptomatic status of coronary disease patients who have objective documentation of ischemia is not uniformly defined and many different categories can be identified. In this population of patients with proven coronary artery disease and myocardial ischemia, a history of angina in the previous 6 weeks was a good predictor of an adverse event occurring in the next year.

Angina Pectoris↗