Value of the Bruce protocol to determine peak exercise oxygen consumption in patients evaluated for cardiac transplantation.

BACKGROUND: Peak exercise oxygen consumption (peak VO2) is an important discriminator of survival in patients with systolic heart failure and is used to select ambulatory patients for transplantation. The major trials assessing the relationship between peak VO2 and survival have used a variety of low-level exercise protocols. It is unknown how peak VO2 measured in this patient population by the more vigorous Bruce treadmill protocol compares with that obtained on less intense protocols. METHODS: We studied 15 patients (50 +/- 12 years old) with severe heart failure (left ventricular ejection fraction 23.5% +/- 8.6%). Patients randomly performed 3 exercise tests with the Bruce treadmill, modified Naughton treadmill, and modified bicycle protocols within 14 days. To determine the ability of this patient population to perform the Bruce protocol, we also retrospectively analyzed the ability of 84 patients to perform this test on their initial evaluations at our center. RESULTS: All patients reached the anaerobic threshold (AT) on all 3 protocols. The Bruce and modified Naughton treadmill protocols resulted in similar peak VO2 percent predicted peak VO2, and VO2 at AT values (17.7 +/- 3.8 mL/kg/min, 57.2% +/- 21.1% and 15.4 +/- 4.1 mL/kg/min vs 18.0 +/- 4.7 mL/kg/min, 58.1% +/- 22.5% and 15.6 +/- 4.4 mL/kg/min, respectively). Peak VO2 and VO2 at AT on both treadmill protocols were higher than those obtained with bicycle testing (15.3 +/- 3.1 and 11.8 +/- 3.0 mL/kg/min, P <.05). Exercise duration was shorter with the Bruce and bicycle protocols (6.2 +/- 2.2 and 6.7 +/- 2.4 minutes, respectively) compared with the modified Naughton protocol (9.7 +/- 4.3 minutes, both P <.005). In addition, 79 of the 84 patients (94%) evaluated were able to complete the Bruce protocol and reach AT. CONCLUSIONS: The Bruce protocol was more time efficient than the modified Naughton protocol and yielded similar peak VO2, percent predicted peak VO2, and VO2 at AT values. Bicycle exercise may underestimate peak VO2 values. The form of exercise should be considered when assessing peak VO2 criteria for transplant listing.

Accuracy of estimating exercise prescription intensity in patients with left ventricular systolic dysfunction.

PURPOSE: Exercise prescription in patients with left ventricular systolic dysfunction (LVSD) is difficult. Exercising beyond ventilatory threshold (VT) can have negative physiologic effects; therefore, exercise prescribed above VT may be detrimental. A majority of cardiac rehabilitation programs use the Karvonen/heart rate reserve (HRR) method, rating of perceived exertion (RPE), and/or a percentage of oxygen consumption to prescribe exercise intensity. The purpose of this study was to determine if these methods correlate with an exercise intensity below VT in LVSD patients. METHODS: The authors studied 52 patients (37 males, 15 females; age 52 +/- 13 years; left ventricular ejection fraction 27% +/- 8%) who underwent a symptom-limited cardiopulmonary exercise test and reached VT to determine functional capacity and exercise prescription. RESULTS: Peak heart rate (HR) as well as HRR derived minimum (60%), midpoint (70%), and maximum (80%) HR were highly correlated (P < 0.001) with HR at VT. Using these three different HR cutoff formulas from HRR, 15% to 62% of patients were prescribed exercise outside the range of VT-HR +/- 10%. The midpoint (70% HRR) best predicted exercise HR in the VT-HR +/- 10% range (73% of patients). Mean oxygen consumption at VT was 83 +/- 9% of peak oxygen consumption. There was no correlation (P < 0.16) between RPE and VT. CONCLUSIONS: The Karvonen/HRR method failed to estimate HR-VT +/- 10% in a large percentage of patients with LVSD. There was no correlation between RPE and VT. Based on these data, exercise training intensity should ideally be prescribed based on the HR identified at VT using cardiopulmonary exercise testing in patients with LVSD.

Effects of intravenous milrinone followed by titration of high-dose oral vasodilator therapy on clinical outcome and rehospitalization rates in patients with severe heart failure.

This study evaluated the efficacy of intravenous milrinone in improving hemodynamics and facilitating the titration of high-dose oral vasodilator therapy to improve clinical status. Fourteen patients (mean age 52 +/- 12 years) with severe heart failure and a left ventricular ejection fraction of 18 +/- 6% underwent right-side heart catheterization and an intravenous milrinone infusion followed by titration of oral vasodilator and diuretic therapy. Milrinone significantly (p <0.05) improved right atrial pressure (12 +/- 5 to 8 +/- 5 mm Hg), pulmonary capillary wedge pressure (23 +/- 7 to 15 +/- 7 mm Hg), cardiac index (1.9 +/- 0.4 to 3.4 +/- 0.5 L/min/m2), systemic vascular resistance (1,809 +/- 526 to 891 +/- 144 dynes/s/cm(-5)), and pulmonary vascular resistance (285 +/- 151 to 163 +/- 68 dynes/s/cm(-5)), which was maintained in 10 patients with titration of high-dose oral vasodilator therapy. Oral angiotensin-converting enzyme inhibitor and diuretic doses were increased 318% and 89%, respectively. Four patients also received hydralazine to optimize hemodynamics. New York Heart Association functional class improved from 3.8 +/- 0.4 to 2.6 +/- 0.6 following therapy. Ten patients who responded to therapy had fewer hospitalized days during the subsequent year compared with the year before treatment (4 +/- 17 vs 17 +/- 15), and no patient died. In contrast, the 3 patients who responded poorly to therapy tended to have more hospitalized days at 12 months compared with pretreatment (31 +/- 11 vs 20 +/- 18; NS); 1 patient died. We conclude that intravenous milrinone followed by optimization of oral medical therapy may be used as a therapeutic trial to identify patients in need of cardiac transplantation.

Cardiac allograft vasculopathy.

As the survival rates for cardiac transplant patients improve, the long-term complications of the procedure are becoming apparent. One such complication is a rapidly progressing form of coronary artery disease known as cardiac allograft vasculopathy (CAV). CAV is a major limiting factor in long-term graft survival. It is thought to develop immediately after transplantation, although initially it may be unrecognized because of a lack of sensitive screening techniques. It is estimated that 12% of cardiac transplant recipients will develop CAV each year after transplantation. Most researchers agree that CAV is primarily an immune-related response to transplantation. However, other factors such as hyperlipidemia and obesity have also been implicated as predictors of CAV. This article explores the pathophysiology, risk factors, detection, and treatment of CAV in the cardiac transplant population.