Brian O'Kelly

Prognostic Importance of Postbypass Regional Wall-Motion Abnormalities in Patients Undergoing Coronary Artery Bypass Graft Surgery

Regional wall motion abnormalities (RWMA) detected by intraoperative transesophageal echocardiography (TEE) are thought to be sensitive markers of myocardial ischemia. To assess the prognostic significance of RWMA as compared with other less costly technologies such as electrocardiography (ECG) and hemodynamic measurements [blood pressure (BP) and pulmonary artery (PA) pressure], 50 patients were prospectively studied who were undergoing elective coronary artery bypass graft (CABG) surgery using continuous TEE, ECG (Holter), and hemodynamic measurements during the prebypass, postbypass, and early postoperative intensive care unit (ICU) periods (first 4 h). Echocardiographic and ECG evidence of ischemia was characterized during each of these three periods and related to adverse clinical outcomes (postoperative myocardial infarction, ventricular failure, and cardiac death). Clinicians were blinded to the TEE and ECG information. The prevalence of myocardial ischemia during the perioperative periods was as follows: prebypass, 20% (TEE) versus 7% (ECG); postbypass, 36% (TEE) versus 25% (ECG); ICU 25% (TEE) versus 16% (ECG). Neither prebypass TEE ischemia nor ECG ischemia occurring in any of the three periods predicted adverse outcome. In contrast, postbypass TEE ischemia was predictive of outcome: six of 18 patients with postbypass TEE ischemia had adverse outcomes versus 0 of 32 without TEE ischemia (P = 0.001). Seventy-three percent of the echocardiographic ischemic episodes occurred without acute change (+/- 20% of control) in heart rate, BP, or PA pressure. The authors conclude that: 1) prebypass myocardial ischemia was relatively uncommon, 2) the incidence of ECG and TEE ischemia was highest in the postbypass period, and 3) postbypass RWMA were related to adverse clinical outcome.

RELATIONSHIP OF REGIONAL WALL MOTION ABNORMALITIES TO HEMODYNAMIC INDICES OF MYOCARDIAL OXYGEN SUPPLY AND DEMAND IN PATIENTS UNDERGOING CABG SURGERY

To investigate the hemodynamic correlates of perioperative regional wall motion abnormalities (RWMA), we measured wall motion continuously via transesophageal echocardiography (TEE), and related RWMA to continuously measured hemodynamic indices of myocardial oxygen supply and demand (heart rate [HR] and systemic and pulmonary arterial blood pressures). Fifty patients undergoing coronary artery bypass graft (CABG) surgery were studied throughout the prebypass postbypass, and intensive care unit (ICU) periods. Only 28% of TEE episodes (RWMA suggestive of ischemia) were preceded by acute changes in any hemodynamic parameter. Specifically, 7% of TEE episodes were preceded by increases in HR (20% deviation from control), 14% by increases in systolic blood pressure (SBP), 13% by decreases in diastolic blood pressure (DBP), and 9% by increases in pulmonary artery diastolic pressure (PAD). Twelve per cent of TEE episodes were associated with increases in rate-pressure product (RPP) to greater than 12,000, and 27% were associated with decreases in mean arterial pressure (MAP)/HR to less than 1 at the onset of TEE episodes. Comparison among periods revealed that postbypass TEE episodes were more frequently associated with either increases in demand or decreases in supply than were prebypass episodes (53% vs. 25%, P less than 0.05). ECG ischemic episodes also were infrequently (30%) associated with acute changes in HR, SBP, DBP, or PAD. We conclude that perioperative TEE episodes are infrequently triggered by changes in hemodynamics, suggesting that a primary decrease in myocardial oxygen supply may be an important mechanism for most perioperative RWMA. In addition, neither pulmonary artery catheter pressure measurements nor specialized indices (RPP and MAP/HR) appear to be useful in predicting TEE episodes.

What is the role of silent coronary artery disease and left ventricular hypertrophy in the genesis of ventricular arrhythmias in men with essential hypertension

Ventricular arrhythmias are not uncommon in patients with hypertension, are often attributed to left ventricular hypertrophy and are thought to be associated with an increased risk of sudden death. However, underlying silent coronary artery disease, another potential cause of ventricular arrhythmias, is often present in the same patient group. Therefore, the prevalence of ventricular arrhythmias was prospectively examined in 183 consecutive asymptomatic men with hypertension with neither clinical nor electrocardiographic (ECG) evidence of coronary artery disease in whom technically adequate echocardiograms could be obtained. After previous therapy had been withdrawn for greater than or equal to 4 days, each patient underwent exercise or dipyridamole thallium-201 scintigraphy, 48-h Holter ambulatory ECG monitoring and echocardiography for measurement of the left ventricular mass index. Forty patients (22%) had frequent ventricular ectopic activity, defined on the basis of greater than 10 premature ventricular complexes/h (38 patients) or ventricular tachycardia (11 patients), or both. A higher proportion of patients with than without a reversible thallium-201 defect had frequent premature ventricular complexes (33% vs. 18%, p less than 0.02) or ventricular tachycardia (14% vs. 4%, p less than 0.02). Similarly, more patients with than without left ventricular hypertrophy (defined as left ventricular mass index greater than or equal to 134 g/m2) had frequent premature ventricular complexes (29% vs. 15%, p less than 0.05) and ventricular tachycardia (12% vs. 2%, p less than 0.01). By stepwise logistic regression analysis, both findings were independent predictors of ventricular arrhythmia, which was present in 53% of patients with both abnormalities, but in only 12% of those with neither abnormality.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertensive heart disease: the critical role of left ventricular hypertrophy.

The presence of left ventricular hypertrophy in hypertensive patients has been linked with increased likelihood for developing congestive heart failure, the potential for myocardial ischemia and the inherent risk for sudden death. In this paper we review current knowledge regarding the role of left ventricular hypertrophy in cardiac morbidity and mortality and emphasize the need for further study to explore the efficacy of pharmaceutical agents in reducing cardiac complications of hypertension in high-risk patients.

Coronary Morbidity and Mortality, Pre-existing Silent Coronary Artery Disease, and Mild Hypertension

Experimental findings in animals and epidemiologic studies in humans provide strong evidence that hypertension promotes the onset and progression of atherosclerosis. However, effective antihypertensive therapy has not consistently reduced the incidence of cardiac events in the major trials of treatment for mild hypertension. In reviewing these trials and the recent data on the pathophysiologic interrelationships among hypertension, atherosclerosis, and myocardial ischemia, two factors stand out: First, the power of these trials to produce a positive result was limited because of their size, entry criteria, duration, and other considerations; second, autopsy and epidemiologic data suggest that some patients in these trials probably had advanced coronary artery disease at the time of entry. Because these patients probably developed symptomatic coronary artery disease by virtue of this pre-existing disease, the failure of antihypertensive therapy alone to prevent cardiac events in trials of relatively short duration should not be construed as evidence against its value as a long-term therapy.

Measurement of left ventricular contractility using transesophageal echocardiography in patients undergoing coronary artery bypass grafting

Optimal assessment of left ventricular function requires the use of load-independent indices of myocardial contractility, which often are difficult to obtain in patients undergoing coronary artery bypass graft (CABG) surgery. We have investigated whether the relation between left ventricular end-systolic stress (ESS) (derived from high-fidelity intraventricular pressure measurements and transesophageal-derived wall thickness) and end-systolic area (ESA) (derived from transesophageal echocardiography [TEE]) could provide a load-independent index of left ventricular function. We studied seven men undergoing coronary revascularization. Multiple data points at varied loading conditions were generated for each patient by infusions of sodium nitroprusside and phenylephrine during the period immediately after induction of general anesthesia and preceding surgical incision. While peak systolic blood pressure was pharmacologically altered between 78 and 204 mm Hg, the correlations between ESS and ESA were excellent for all patients (range r = 0.90 to 0.99). Additionally, the slopes of these relations showed a close correlation to their respective baseline thermodilution cardiac indices (r = 0.85, p = 0.02). Appropriate shifts of the ESS/ESA relationships were documented during postextrasystolic potentiation. The authors conclude that the left ventricular ESS/ESA correlation, derived using TEE and intraventricular pressure measurements, may provide a load-independent index of left ventricular inotropic state in patients undergoing CABG surgery.

Segmental analysis of resting echocardiographic function and stress scintigraphic perfusion: Implications for myocardial viability

In 73 patients with coronary artery disease, we performed segmental analysis of resting two-dimensional echocardiography and stress thallium-201 single photon emission computed tomographic scintigraphy with 24-hour delayed imaging to test the hypotheses that (1) combined analysis of stress thallium-201 scintigraphy (with 24-hour redistribution) and echocardiography provides an evaluation of the viability of most myocardial segments; and (2) the severity of the scintigraphic perfusion abnormality in a given segment is equivalent to the severity of its echocardiographically determined functional impairment. Scintigraphy showed 14% of the 1168 segments analyzed to have fixed severe defects. Echocardiography showed 11% of the 1070 segments analyzed to be akinetic or dyskinetic. However, with combined analysis, only 62 (5%) segments showed no evidence of viability by either imaging technique. We conclude that in this group of patients, 95% of segments have evidence of viability by one of these two conventional imaging techniques.