Effect of clinical factors on length of stay after coronary artery bypass surgery: results of the cooperative cardiovascular project.

BACKGROUND: Rising health care costs have prompted careful review of comparative hospital resource use. Length of stay after bypass surgery has received particular attention. However, many providers assert that these variations are caused by differences in the clinical mix of patients treated. Our goals were to identify the major clinical predictors of postoperative length of stay (PLOS) after coronary artery bypass graft surgery (CABG), document variations in PLOS among 28 hospitals, and assess the degree to which patient characteristics account for hospital variations in PLOS. METHODS: Detailed clinical data on 3605 Medicare patients undergoing CABG in 28 Alabama and Iowa hospitals were analyzed by stepwise linear regression to identify significant clinical predictors of PLOS. Analysis of variance was used to compare hospitals' PLOS while controlling for significant patient risk factors. RESULTS: The mean age was 72.1 years, 34.7% were female, and the in-hospital mortality rate was 5.6%. The median and mean PLOS were 8 and 11.1 days, respectively. Significant predictors of longer PLOS included increasing age, female sex, history of chronic obstructive pulmonary disease, cerebrovascular disease, or mitral valve disease, elevated admission blood urea nitrogen, and preoperative placement of an intraaortic balloon pump. Hospitals varied significantly (P =.0001) in their unadjusted PLOS. These hospital-level variations persisted despite adjustment for both preoperative patient characteristics (P =.0001) and postoperative complications and death (P =.0001). CONCLUSIONS: This study found significant between-hospital variations in PLOS that were not explained by patient factors. This finding suggests the potential for increased efficiency in the care of patients undergoing CABG at many institutions. Further research is needed to determine the practice patterns contributing to variations in length of stay after bypass surgery.

Unexpected instant death following successful coronary artery bypass graft surgery (and other clinical settings): atrial fibrillation, quinidine, procainamide, et cetera, and instant death.

Primum non nocere. Atrial fibrillation (AF) occurs commonly following coronary artery bypass graft surgery, although new onset atrial fibrillation in this setting is usually transient. When AF reverts or is converted to sinus rhythm it is unlikely to recur, whether or not the patient takes preventive medication. As no benefit (and sometimes increased risk) associated with reduced mortality or morbidity in this setting has been reported for antiarrhythmic agents, standard treatment should consist of observation or control of ventricular response with an appropriate agent until AF relapses to sinus rhythm. If an antiarrhythmic agent, especially a class I agent, is used because of persistent or recurrent AF in the early postoperative period, heart rhythm should be monitored as long as the class I agent is administered and treatment initiated if an undersirable rhythm develops. Atrial fibrillation in other clinical settings in patients with structural heart disease presents a more difficult management problem. Class I agents are reported to be associated with an increased risk of death, despite an efficacious effect of maintaining sinus rhythm. Amiodarone is reported to be well tolerated with respect to the cardiovascular system, but unacceptable noncardiac effects are reported. A safe amiodarone-like agent is greatly needed. Atrial fibrillation in patients with no structural heart disease is not discussed in this presentation.

Risk factors and noncontraceptive estrogen use in women with and without coronary disease.

To evaluate the risk factors for coronary disease, 345 women, aged 35 to 59 years, who had undergone coronary arteriography for suspected coronary disease completed a mail questionnaire, telephone interview, or both. Two hundred eight women with angiographically normal coronary arteries constituted the control group, and 137 with a 70% or more occlusion of one or more coronary vessels were classified as having severe coronary occlusive disease. Age-adjusted odds of severe coronary disease based on the logistic regression model for the risk factors evaluated were as follows: smoking, 5.73 (p less than 0.001); diabetes, 5.09 (p less than 0.001); cholesterol level greater than 240 mg/dl, 2.35 (p less than 0.05); a parental history of death from heart disease before age 60 years, 2.03 (p less than 0.05); and estrogen use for 6 months or longer, 0.50 (p less than 0.01). There were no differences with regard to the presence of obesity and a history of hypertension in women with and without coronary disease. These data support the hypothesis that use of noncontraceptive estrogen significantly reduces the risk of severe coronary disease, whereas smoking, an elevated cholesterol level, and a parental history of heart disease all increase the risk of ischemic heart disease in women.

Prognostic cardiac catheterization variables in survivors of acute myocardial infarction: a five year prospective study.

The prognostic variables from predischarge coronary angiography and left ventriculography in survivors of acute myocardial infarction during the years 1974 to 1978 were evaluated in 143 patients (less than or equal to 66 years of age) with documented myocardial infarction who were then followed up prospectively for 5 years. One half of the study population had triple vessel coronary disease (greater than or equal to 50% stenosis). However, only 7% of patients had severely depressed left ventricular function with an ejection fraction less than or equal to 29%. Evaluation of the contribution of many clinical and angiographic variables to a first cardiac event (death, nonfatal reinfarction or coronary artery bypass surgery) was considered with Kaplan-Meier actuarial curves and multivariate Cox's hazard function analysis. A risk segment was defined as an area of contracting myocardium supplied by a coronary artery with a greater than 50% stenosis. Multivariate analysis demonstrated that right plus left anterior descending coronary artery stenoses (p less than 0.01), ejection fraction (p less than 0.01) and the presence of risk segments (p less than 0.05) were significant predictors of outcome. Furthermore, on separate multivariate analyses, the angiographic variables added significantly to the clinical variables to predict cardiac events over 5 years of follow-up. Therefore, in survivors of acute myocardial infarction who undergo cardiac catheterization, additive prognostic information is obtained that can be used to stratify risk over 5 years.

Pharmacokinetics of moricizine HCl.

Moricizine HCl is a phenothiazine derivative with antiarrhythmic properties. It was developed in the USSR and is now undergoing clinical evaluation. Although preliminary work has shown moricizine HCl to be effective in treating both atrial and ventricular arrhythmias, little is known of its pharmacokinetics. There is a 4-fold variability in range for its elimination half-life and in volumes of distribution and clearance. There is a linear relation for peak plasma levels and area under the plasma concentration/time curve with regard to single-dose administration of moricizine HCl. The bioavailability of moricizine HCl connotes extensive first-pass effect, or presystemic metabolism. Very little of moricizine is excreted unchanged; it is extensively metabolized to certain compounds that are present in plasma for extended periods. Moricizine is extensively (92% to 95%) bound to plasma protein. Its coadministration with cimetidine leads to additive systemic effects; however, there is no evidence of alterations in steady-state levels when moricizine HCl is coadministered with digoxin. Because moricizine is a drug with active metabolites, its concentration/effect profile is complex; this poses a challenge for accurate dose titration. This may, however, be a helpful challenge in that the metabolites may one day prove useful in therapy. This surmise warrants further study.

Prophylactic antiarrhythmic therapy of high-risk survivors of myocardial infarction: lower mortality at 1 month but not at 1 year.

To determine whether prophylactic antiarrhythmic therapy influences mortality in high-risk patients after acute myocardial infarction, 143 such patients were randomized in a double-blind individually dose-adjusted, placebo-controlled trial an average of 14 +/- 7 days after myocardial infarction and followed for 1 year. Patients were judged to be at high risk on the basis of (1) ejection fraction less than 40% (n = 60), (2) arrhythmias of Lown class 3 or higher (n = 26), or (3) both (n = 57). Aprindine was chosen because of its long half-life, few side effects, and antiarrhythmic efficacy. Baseline characteristics in the treatment arms did not differ. Holter-detected arrhythmias were reduced in aprindine-treated patients at 3 months (p less than .001) and at 1 year (p less than .001). One patient was lost to follow-up; in the remaining patients 1 year mortality was 20% (28/142; 12 aprindine and 16 placebo). There was no significant difference between the two study arms in overall mortality and sudden death. However, among those who died, median duration of survival was longer in aprindine-treated patients (86 vs 21.5 days) (p = .04). Although antiarrhythmic treatment with aprindine of high-risk patients after myocardial infarction does not affect 1 year survival, mortality appears to be delayed; thus there may be a role for short-term treatment before more definitive therapy such as surgery.

Myocardial infarction in sickle cell anemia.

A review of the electrocardiograms (ECG) of 108 patients with sickle cell anemia found only 3 with patterns consistent with myocardial infarction. Two of the 3 patients with ECG infarct patterns had postmortem examination confirmation of the infarction. These two patients had no significant coronary atherosclerosis nor did the other six autopsied patients in the present series. Literature reports of postmortem examinations on patients with sickle cell anemia confirm the scarcity of coronary atherosclerosis and myocardial infarction in these patients. Forty of the 108 ECGs showed signs of left ventricular hypertrophy and 20 others had nondiagnostic ST and T wave abnormalities. Nine showed first degree AV block and four right bundle branch block.

Acute myocardial infarction: pharmacologic treatment in the coronary care unit.

It is reasonable to consider treating the patient with an uncomplicated infarction with as many as 10 drugs: a benzodiazepine, a sedative, oxygen, morphine, lidocaine, a nitrate, an anticoagulant, a thrombolytic agent, a beta blocker, and possibly a calcium-channel antagonist. Obviously, experienced judgment must be used in selecting the appropriate agents for each patient. A properly staffed and equipped coronary care unit continues to be the most important preventative for unnecessary deaths during the acute phase of myocardial infarction.

Inheritance of the mitral valve prolapse syndrome. Discussion of a three-dimensional penetrance model.

The families of 12 probands with classic mitral valve prolapse were studied for evidence of mitral valve prolapse. Seventy parents, sibs, and progeny were included in the analysis. Forty-seven percent (16 of 34) of progeny were affected compared with 30 percent (3 of 10) of parents. Thirty-eight percent (10 of 26) of sibs were affected. A three-compartmental penetrance model was devised to account for the variation in expression with age. This includes a latent stage (time before onset of signs), an affected stage, and a stage in which the subjects are withdrawn (because of treatment, regression, or death). The implications of this model are discussed.

Complex ventricular arrhythmias after myocardial infarction during convalescence and follow-up: a harbinger of multi-vessel coronary disease, left ventricular dysfunction and sudden death.

Sixty-one medically treated patients had coronary and left ventricular angiography and 24-hour electrocardiographic monitoring 10-24 days after myocardial infarction, and then had serial 24-hour electrocardiographic monitoring during the 13 +/- 11 months after myocardial infarction. Complex ventricular arrhythmias (2 or more sequential ventricular premature depolarizations (VPDs), multiform VPDs, bigeminy) during follow-up were associated with a high mortality rate and occurred most commonly in the setting of three-vessel coronary disease, proximal left anterior descending coronary disease and low left ventricular ejection fraction. By contrast, patients without complex VPDs in either the late hospital or posthospital phase of myocardial infarction had no mortality during the year following myocardial infarction; furthermore, these patients had a higher incidence of single-vessel coronary disease and less left ventricular dysfunction. These results emphasize the adverse prognostic significance of complex ventricular arrhythmias in the year after myocardial infarction and their association with extensive coronary artery disease and left ventricular damage.

Predictors of clinical course, coronary anatomy and left ventricular function after recovery from acute myocardial infarction.

Patients who survive an acute myocardiac infarction (AMI) have significant coronary disease and are at risk for angina pectoris, recurrent myocardiac infarction and sudden death. This study provides data gathered prospectively for 106 patients surviving myocardial infarction who had coronary arteriography, left ventriculography and 24-hour electrocadiographic recordings before hospital discharge and were followed 30 months. Univariate analysis showed that low ejection fraction, proximal left anterior descending coronary disease and significant disease in all three coronary arteries were associated with a high risk of sudden cardial death. The ECG location or type of infarction was not helpful in predicting mortality, reinfarction or continuing angina. Multivariate analysis of 30 clinical and laboratory variables identified previous myocardial infarction and an ejection fraction less than 40% as the best predictors of mortality; all 13 patients who died were identified by these two variables. Three-vessel coronary artery disease, proximal left coronary disease and complicated late hospital-phase ventricular arrhythmias did not provide additional information about mortality once the information provided by the first two variables was considered. Multivariate analysis identified hypertension, three-vessel coronary disease, postinfarction angina pectoris and previous AMI as significant predictors of recurrent AMI during the 30 month follow-up.

Clinical and arteriographic variables predictive of survival in coronary artery disease.

Survival, subsequent myocardial infarction and current anginal status were determined for 90 nearly consecutive patients who underwent coronary arteriography at the Johns Hopkins Hospital between 1960 and 1967. All patients had at least one coronary arterial narrowing equal to or greater than 70 percent; 78 of 90 patients would be candidates for coronary bypass surgery by present criteria. Twenty-nine of the 78 surgically "suitable" patients died of cardiac causes; 7 of 49 survivors sustained an acute myocardial infarction (mean follow-up period 9.9 years). Patients with a 70 percent or greater narrowing proximal to the first septal branch of the left anterior descending coronary artery had a significantly greater mortality compared with patients with equivalent narrowing distal to the first septal branch or with patients without 70 percent or greater narrowing of the left anterior descending artery. The patients with a 70 percent or greater narrowing of the left anterior descending artery who died were those with a significant narrowing in at least one other major coronary artery. Multivariate stepwise discriminate function analysis of all clinical, electrocardiographic (except stress electrocardiographic) and arteriographic variables identified three independent predictors of mortality: (1) the simultaneous occurrence of a narrowing in left anterior descending and right coronary arteries, (2) prior myocardial infarction; and (3) 70 percent or greater narrowing proximal to the first anterior descending septal branch. When stress electrocardiographic findings were included, a "positive" stress electrocardiographic test was also an independent predictor of mortality.