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Left ventricular hypertrophy, history of hypertension, diabetes mellitus, coronary artery disease, and digoxin use predicted postoperative myocardial ischemia

ACP J Club. 1992 Nov-Dec;117:89. doi:10.7326/ACPJC-1992-117-3-089

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Source Citation

Hollenberg M, Mangano DT, Browner WS, et al. Predictors of postoperative myocardial ischemia in patients undergoing noncardiac surgery. JAMA. 1992 Jul 8;268:205-9.



To determine the risk factors for postoperative myocardial ischemia in men having major noncardiac surgery.


Cohort study of hospitalized patients.


Department of Veterans Affairs tertiary care hospital.


407 men (mean age, 68 y) at high risk for or with definite coronary artery disease and with interpretable Holter recordings who were scheduled for elective noncardiac surgery requiring general anesthesia. Patients with pacemakers or conduction defects were excluded.

Assessment of risk factors

Demographic and clinical data, including cardiac history and risk factors and medication use, were collected preoperatively by chart review and clinical evaluation.

Main outcome measures

An ischemic episode, defined as a horizontal or down-sloping ST-segment depression from baseline of ≥ 1 mm lasting ≥ 1 minute or elevation of the ST segment from baseline of ≥ 2 mm measured at the J-point. All ambulatory electrocardiographic (ECG) recordings were obtained continuously for up to 48 hours preoperatively, intraoperatively, and for 48 hours postoperatively.

Main results

167 patients (41%) developed ≥ 1episode of myocardial ischemia postoperatively. When the presence of Holter-detected preoperative ischemia (odds ratio [OR] 7.7, 95% CI 4.0 to 15.0) and intraoperative ischemia (OR 5.5, CI 3.3 to 9.0) were excluded in a multivariate logistic analysis, 5 independent preoperative clinical predictors of postoperative myocardial ischemia were identified: left ventricular hypertrophy by ECG (OR 3.2, CI 1.6 to 6.7); history of hypertension (OR 1.7, CI 1.1 to 2.7); diabetes mellitus treated with medications (OR 1.9, CI 1.2 to 3.2); definite coronary artery disease (OR 1.6, CI 1.0 to 2.4); and preoperative use of digoxin (OR 2.1, CI 1.1 to 4.2). The likelihood of a patient experiencing episodes of postoperative ischemia increased progressively with the number of preoperative predictors present (P < 0.001): in 22% with no predictors, in 31% with 1 predictor, in 46% with 2 predictors, in 70% with 3 predictors, and in 77% with 4 predictors (only 1 patient had all 5 predictors).


Left ventricular hypertrophy by electrocardiogram, history of hypertension, diabetes mellitus treated with drugs, definite coronary artery disease, and use of digoxin preoperatively predicted postoperative myocardial ischemia in men who had major noncardiac surgery. The risk for postoperative myocardial ischemia increased progressively with the number of risk factors present.

Source of funding: National Institutes of Health.

For article reprint: Dr. M. Hollenberg, Veterans Affairs Medical Center, 4150 Clement Street (111C3), San Francisco, CA 94121, USA.


These 2 of a series of important Veterans Affairs studies examined predictive factors for postoperative ischemia and mortality after noncardiac surgery. The study by Hollenberg and colleagues found a high (41%) overall rate of postoperative myocardial ischemia. The strongest predictors were Holter-detected preoperative and intraoperative ischemia followed by 5 clinical predictors. 3 of the 5 (left ventricular hypertrophy on ECG, hypertension, and digoxin use) may be associated with ST-segment depression not necessarily caused by ischemia. Further, only one of these clinical markers, hypertension, predicted postoperative in-hospital mortality in the study by Browner and colleagues.

The possibility of confounding by various cardiac medications exists, although the authors tried to address this issue by stratifying patients into groups based on medication use. Other intraoperative factors that may be important in the development of postoperative ischemia and subsequent cardiac events are not mentioned, such as anesthetic agent, amount of blood loss or fluid shift, pain control, and other intraoperative events.

The study by Browner and colleagues showed an overall 5% (26 of 474 patients) in-hospital mortality, but only 6 deaths had a cardiac cause. They suggest that preoperative evaluation should pay particular attention to patients with hypertension, low creatinine clearance, or severe limitation in physical activity.

Previous studies have shown varying proportions of postoperative mortality due to cardiac causes. Goldman and colleagues (1) found that of the 59 of 1001 patients having noncardiac surgery who died, 19 died of cardiac causes. In contrast, Detsky and colleagues (2) found that 11 of 16 deaths were cardiac in nature in a sample of 524 patients. These mortality rates and causes of death probably differ because of differences in the sample characteristics.

Although many patients in the Browner sample had major surgery associated with a high rate of subsequent cardiac events (e.g., vascular and orthopedic surgery), their cardiac mortality rate was only 1%, perhaps reflecting improved patient selection and perioperative monitoring in recent years. This study also found that late mortality (up to 2 years after surgery) was predicted by cancer, decreased renal function, congestive heart failure, or bronchodilator use.

The results of both studies should be interpreted with caution. Patients were uniformly male, veterans, and had a definite or high likelihood of cardiac disease. All these factors affect the generalizability of the results.

Early postoperative ST changes appear to be quite important in predicting subsequent ischemic events. These patients may benefit from intensified medical management and consideration of further cardiac evaluation. Major questions remain, however, about the identification of these patients. Who should be monitored; how should they be monitored; and what is the cost-effectiveness of routine preoperative ST-segment monitoring? Further, the value of predicting noncardiac death will remain unclear until additional studies confirm these results and define the implications of attempting to modify risk factors.

Sumita D. Paul, MD, MPH
Nicholas I. Kondo, MD
Kim A. Eagle, MD
Massachusetts General HospitalBoston, Massachusetts, USA

Sumita D. Paul, MD, MPH
Massachusetts General Hospital
Boston, Massachusetts, USA

Nicholas I. Kondo, MD
Massachusetts General Hospital
Boston, Massachusetts, USA

Kim A. Eagle, MD
Massachusetts General Hospital
Boston, Massachusetts, USA


1. Goldman L, Caldera DL, Nussbaum SR, et al. N Engl J Med. 1977;297:845-50.

2. Detsky AS, Abrams HB, McLaughlan JR, et al. J Gen Intern Med. 1986;1:211-9.