Use of cardiopulmonary exercise testing with hemodynamic monitoring in the prognostic assessment of ambulatory patients with chronic heart failure.

OBJECTIVES: We studied whether direct assessment of the hemodynamic response to exercise could improve the prognostic evaluation of patients with heart failure (HF) and identify those in whom the main cause of the reduced functional capacity is related to extracardiac factors. BACKGROUND: Peak exercise oxygen consumption (VO2) is one of the main prognostic variables in patients with HF, but it is influenced also by many extracardiac factors. METHODS: Bicycle cardiopulmonary exercise testing with hemodynamic monitoring was performed, in addition to clinical evaluation and radionuclide ventriculography, in 219 consecutive patients with chronic HF (left ventricular ejection fraction, 22 +/- 7%; peak VO2, 14.2 +/- 4.4 ml/kg/min). RESULTS: During a follow-up of 19 +/- 25 months, 32 patients died and 6 underwent urgent transplantation with a 71% cumulative major event-free 2-year survival. Peak exercise stroke work index (SWI) was the most powerful prognostic variable selected by Cox multivariate analysis, followed by serum sodium and left ventricular ejection fraction, for one-year survival, and peak VO2 and serum sodium for two-year survival. Two-year survival was 54% in the patients with peak exercise SWI < or = 30 g x m/m2 versus 91% in those with a SWI >30 g x m/m2 (p < 0.0001). A significant percentage of patients (41%) had a normal cardiac output response to exercise with an excellent two-year survival (87% vs. 58% in the others) despite a relatively low peak VO2 (15.1 +/- 4.7 ml/kg/min). CONCLUSIONS: Direct assessment of exercise hemodynamics in patients with HF provides additive independent prognostic information, compared to traditional noninvasive data.

Hemodynamic profile of submaximal constant workload exercise in patients with heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

Constant workload exercise on an upright bicycle at submaximal levels of exercise intensity is frequently used in physical training programs. Nevertheless, only a few data are currently available on the hemodynamic changes induced by constant workload exercise in patients with heart failure. The aim of this study was to assess the hemodynamic response during submaximal constant-workload exercise at 2 different work rates in patients with heart failure. The hemodynamic profile was assessed by means of right-sided cardiac catheterization in 21 men with moderate heart failure during submaximal-constant workload exercise performed on an upright bicycle for 15 minutes. The intensity of constant work rate exercise was selected during a previous symptom-limited or maximal test. The first submaximal test was performed at the level of the anaerobic threshold workload, corresponding to 64% of peak work rate, and the other test at 70% of anaerobic threshold workload (42% of peak work rate). During both submaximal tests, a marked increase in right heart pressure was observed as compared with baseline. The increase in systolic pulmonary artery pressure was statistically not different between the 2 tests (from 40 +/- 18 to 66 +/- 20 mm Hg during exercise at the anaerobic threshold workload, and from 39 +/- 16 to 63 +/- 21 mm Hg during exercise under anaerobic threshold). The increase in pulmonary arterial wedge pressure was similar (from 20 +/- 10 to 35 +/- 13 mm Hg during exercise at the anaerobic threshold, and from 19 +/- 9 to 32 +/- 12 mm Hg during the other test). Cardiac output and heart rate were significantly higher during submaximal exercise at a higher workload, paralleling the behavior of oxygen uptake. Finally, the hemodynamic profile during submaximal exercise at the anaerobic threshold workload was quite similar to that observed during symptom-limited exercise. Thus, in patients with heart failure, submaximal exercise performed at a constant workload, even at low exercise intensity, may determine relevant pressure changes in pulmonary circulation.

Mechanisms and immediate outcome of in-hospital cardiac arrest in patients with advanced heart failure secondary to ischemic or idiopathic dilated cardiomyopathy.

To differentiate patients with congestive heart failure who are more prone to develop malignant ventricular tachyarrhythmias or severe bradyarrhythmias as the terminal event, we retrospectively evaluated a group of 48 patients with advanced heart failure who experienced a monitored cardiac arrest during hospital stay. We found no significant differences with respect to several variables, apart from clinical status, which was worse in patients whose cardiac arrest was precipitated by severe bradycardia or electromechanical dissociation.

Contribution of left atrial pressure and dimension to signal-averaged P-wave duration in patients with chronic congestive heart failure.

In a group of patients with chronic heart failure, a longer P-wave duration on signal-averaged electrocardiogram was found in those patients with higher pulmonary capillary wedge pressure, whereas the left atrium end-systolic diameter was not significantly different. Furthermore, an acute reduction in pulmonary capillary wedge pressure induced by sodium nitroprusside infusion was associated with a reduction in P-wave duration.

Dobutamine-induced changes in pulmonary artery pressure in patients with congestive heart failure and their relation to abnormalities of lung diffusing capacity.

Short-term infusion of dobutamine may determine a mild, statistically significant increase in pulmonary artery pressure from baseline in 30% of patients with moderate to severe heart failure despite systemic effects (changes in cardiac index and systemic vascular resistance) similar to those observed in patients showing a large reduction in right heart pressures. The increase in pulmonary artery pressure observed seems to be associated with a lower pulmonary diffusing capacity, probably reflecting a reduction in recruitment and distension capacity of pulmonary circulation.

Effects of maximally tolerated oral therapy on the six-minute walking test in patients with chronic congestive heart failure secondary to either ischemic or idiopathic dilated cardiomyopathy.

In patients with heart failure, therapy with "maximally tolerated" oral doses of diuretics, vasodilators, and digitalis results in a significant increase in the distance walked during the 6-minute walking test, compared with conventional therapy at "standard" doses, indicating an improvement in exercise tolerance. The 6-minute walk test is a simple, inexpensive, and well-tolerated test to measure changes in exercise tolerance induced by pharmacologic interventions, even on a short-term basis.

Prevalence of isolated left ventricular diastolic dysfunction in hypertension as assessed by combined transmitral and pulmonary vein flow Doppler study.

In a relatively large population of patients with treated systemic hypertension and normal left ventricular systolic function, prevalence of abnormalities of left ventricular diastolic function, as assessed by Doppler echocardiographic study of mitral and pulmonary vein flow, was high, with 51% of patients showing indirect signs of increased left ventricular end-diastolic pressure. Furthermore, our data documented that a "normal" mitral flow profile does not exclude the presence of an abnormality of left ventricular filling, which could be otherwise identified by combined analysis of a pulmonary vein flow profile.

Relative contribution of resting haemodynamic profile and lung function to exercise tolerance in male patients with chronic heart failure.

OBJECTIVE: To clarify the relative contribution of resting haemodynamic profile and pulmonary function to exercise capacity in patients with heart failure. SETTING: Cardiology department and cardiac rehabilitation unit in a tertiary centre. DESIGN: 161 male patients (mean (SD) age 59 (9) years) with heart failure (New York Heart Association class II-IV, left ventricular ejection fraction 23 (7)%) underwent spirometry, alveolar capillary diffusing capacity (DLCO), and mouth inspiratory and expiratory pressures (MIP, MEP, respectively, in 100 patients). Right heart catheterisation and a symptom limited cardiopulmonary exercise test were performed in 137 patients within 3-4 days. RESULTS: Mean peak exercise oxygen consumption (VO(2)) was 13 (3.9) ml/kg/min. Among resting haemodynamic variables only cardiac index showed a significant correlation with peak VO(2). There were no differences in haemodynamic variables between patients with peak VO(2) 14 ml/kg/min. There was a moderate correlation (p < 0.05) between several pulmonary function variables and peak VO(2). Forced vital capacity (3.5 (0.9) v 3.2 (0.8) l, p < 0.05) and DLCO (21.6 (6.9) v 17.7 (5.5) ml/mm Hg/min, p < 0.05) were higher in patients with peak VO(2) > 14 ml/kg/min than in those with peak VO(2)

Doppler echocardiographic assessment of hemodynamic progression of valvular aortic stenosis over time: comparison between aortic valve resistance and valve area.

BACKGROUND: Doppler-derived aortic valve resistance (AVR), i.e. the ratio between pressure gradient and flow rate, has been proposed as an alternative parameter to valve area (AVA) for assessing the hemodynamic severity of aortic stenosis (AS). There are no data on the evaluation of hemodynamic progression of AS using AVR. METHODS: Forty-five adult patients (24 women and 21 men, mean age 72 +/- 10 years) with AS were followed up for 18 months (range 6 to 45 months) with serial Doppler-derived AVR (Isaaz, JACC 1991; 18: 1661) and AVA (continuity equation). Rates of change of AVR and AVA over time were indexed for year of follow-up; furthermore, variations of these parameters during follow-up were expressed as percent change from baseline. RESULTS: During the follow-up period, AVA decreased from 0.74 +/- 0.28 to 0.6 +/- 0.17 cm2 (p < 0.05), with a rate of change of -0.1 +/- 0.13 cm2/year; AVR increased from 349 +/- 187 to 462 +/- 180 dyne/s/cm-5 (p < 0.05), with a rate of change of 79 +/- 69 dyne/s/cm-5/year. Variations observed in AVR, expressed as percent change from baseline, were larger than those observed in AVA (51 +/- 62% versus -16.5 +/- 15%). AVR percent change from baseline significantly correlated with AVA percent change from baseline (r = 0.83, p < 0.05). During follow-up, 6 patients showed no change in AVA: AVR was unchanged in 3 and increased in the remaining 3 patients (6, 11 and 58%, respectively), indicating a progression of AS severity that could not be appreciated from AVA alone. CONCLUSIONS: Serial changes in AVR, as assessed by Doppler echocardiography, significantly correlate with changes in AVA. Thus, the noninvasive assessment of AVR may be utilized in the evaluation of hemodynamic progression of AS and, in conjunction with AVA, may also provide complementary information for the management of these patients.

Assessment of oxygen uptake during the 6-minute walking test in patients with heart failure: preliminary experience with a portable device.

In patients with heart failure, the 6-minute walking test (6-MWT) is considered a useful measure of submaximal exercise capacity. Few data are available on oxygen uptake (VO2) during a standard 6-MWT. The aim of this study was to measure the 6-MWT VO2 by using a recently validated portable instrument in 26 patients (24 men, 2 women; mean age, 56 +/- 11 years) with mild to severe heart failure (New York Heart Association class II, 10 patients; III, 10 patients; IV, 6 patients; left ventricular ejection fraction: 22 +/- 6%). Peak VO2 was measured during a symptom-limited cardiopulmonary exercise test performed in a period of 1 to 3 days (10 watt/m increment). Peak VO2 was 15 +/- 4 ml/kg/m during the symptom-limited test and 12.9 +/- 4.4 ml/kg/m during the 6-MWT (p < 0.05), corresponding to 86% of peak VO2. Seven (27%) of 26 patients showed a 6-MWT VO2 equal to or higher than peak VO2. Anaerobic threshold (AT) was identified in 23 of 26 patients during maximal exercise and in 19 of 26 patients during the 6-MWT; VO2 at AT was similar in the two tests (12.2 +/- 3.5 ml/kg/m vs 11.9 +/- 4.2 ml/kg/m). The distance walked during the 6-MWT (mean, 418 +/- 20 m) significantly correlated with 6-MWT VO2 (r = 0.71) and peak VO2 (r = 0.63); the 6-MWT VO2 also showed a high correlation with peak VO2 (r = 0.86). Thus in patients with failing hearts, VO2 during 6-MWT (considered a classic submaximal exercise) is, on average, only 15% lower than peak VO2 and is largely supported by anaerobic metabolism (work above the anaerobic threshold).

Effects of body position on the carbon monoxide diffusing capacity in patients with chronic heart failure: relation to hemodynamic changes.

OBJECTIVE: Pulmonary diffusion has been found to be reduced in patients with congestive heart failure. The effects of postural changes on the diffusing capacity had been evaluated in healthy subjects, but not in patients with heart failure. The aim of this study was to evaluate the posture-induced changes in diffusing capacity in patients with chronic heart failure and their relation to the hemodynamic profile. METHODS: The pulmonary carbon monoxide diffusing capacity (DLCO) was measured in the supine position, with 20 degrees passive head elevation, and in the sitting position, both postures maintained for 10 min, in a group of 32 male patients with mild to moderate chronic heart failure due to left ventricular systolic dysfunction (ejection fraction <35%). On a separate day, in the absence of any changes in clinical status and therapy, the hemodynamic parameters were measured by right-heart catheterization. The sequence of postures was assigned randomly. RESULTS: The mean values of DLCO were slightly reduced and did not differ in the two positions (20.3 +/- 5.7 vs. 19.4 +/- 5.6 ml/min/mm Hg, 77 +/- 23 vs. 75 +/- 20% of predicted, respectively). The patients were then subdivided according to changes in DLCO from the supine to the sitting position: DLCO increased (+23%) in 9 patients (28%, group 1), decreased (-17.5%) in 17 patients (53%, group 2), and remained within the coefficient of reproducibility ( +/- 5 %) in 6 patients (group 3). As compared with group 2, group 1 patients showed a significant increase in mean pulmonary artery pressure (+7 vs. -15%, p < 0.01) and pulmonary capillary wedge pressure (+8 vs. -22%, p < 0.005) from the supine to the sitting position, while the cardiac index showed a smaller - but not significant - decrease in group 1 (-5 vs. -12%). The percent changes in DLCO significantly correlated with changes in pulmonary capillary wedge (r = 0.54, p < 0.0005) and mean pulmonary artery (r = 0.47, p < 0.005) pressures. CONCLUSIONS: In chronic heart failure postural changes may induce different responses in diffusing capacity. To a greater extent than in healthy subjects, the most common response is a decrease in DLCO in the sitting as compared with the supine position. The DLCO changes correlate with variations in pulmonary circulation pressure, probably due to changes in pulmonary vascular recruitment and pulmonary capillary blood volume.