Emergence of electronic home monitoring in chronic heart failure: rationale, feasibility, and early results with the HomMed Sentry-Observer system.

Electronic home monitoring for chronic heart failure is emerging as an available option to add to our armamentarium as a vital part of the multidisciplinary care process. This investigation describes the early clinical results of a multicenter study that suggests that important trends in medical resource utilization may be attained by the use of this modality. (c)2000 by CHF, Inc.

Longitudinal analysis of fibroblast growth factor expression after transplantation and association with severity of cardiac allograft vasculopathy.

BACKGROUND: Vascular smooth muscle cell growth factors are postulated to contribute to cardiac allograft vasculopathy (CAV). Few data quantitatively address the timing, location, or stimuli for growth factor expression and relationship to CAV. METHODS AND RESULTS: Acidic fibroblast growth factor (aFGF) mRNA expression was determined in serial endomyocardial biopsies during the first year after transplantation. Patients with high levels of aFGF mRNA and elevations after the early posttransplant period had significantly more severe CAV than patients with low aFGF and no late elevations. CONCLUSIONS: Parenchymal aFGF expression varies between patients and in the same patient over time and correlates with development of CAV.

Pulmonary hypertension and exercise intolerance in patients with heart failure.

OBJECTIVES: This study was undertaken to investigate the relationship between pulmonary hypertension and exercise performance in patients with heart failure. BACKGROUND: The exercise capacity of patients with heart failure is frequently reduced. Pulmonary hypertension may contribute to this exercise intolerance by impairing blood flow through the pulmonary circulation. METHOD: Three hundred twenty patients with heart failure underwent upright treadmill exercise testing with hemodynamic monitoring. The incidence of pulmonary hypertension and the relationship between pulmonary vascular resistance (PVR) and exercise cardiac output and minute oxygen consumption (VO2) were examined. RESULTS: Pulmonary vascular resistance was normal (<1.5 Wood Units; Group 1) in 28% of the patients, mildly elevated (1.5 to 2.49 Wood Units; Group 2) in 36%, moderately elevated (2.5 to 3.49 Wood Units; Group 3) in 17% and severely elevated (>3.5 Wood Units; Group 4) in 19%. Increasing PVR was associated with significantly lower peak exercise VO2 (Group 1: 13.9+/-3.7; 2:13.7+/-3.4; 3: 11.8+/-2.4; 4: 11.5+/-2.6 L/min, p<0.01 Groups 3 and 4 vs. 1) and lower peak exercise cardiac output (Group 1: 10.0+/-2.8, 2:9.0+/-3.0; 3: 7.4+/-2.1; 4: 6.3+/-2.0 L/min, p<0.05, Groups 2, 3 and 4 vs. 1). The pulmonary wedge pressure decreased during exercise, consistent with impaired left ventricular filling, in 36% of patients with severe pulmonary hypertension (Group 4) versus only 13% of patients with normal PVR (p<0.01). CONCLUSIONS: Pulmonary vascular resistance is frequently increased in heart failure and is associated with a reduced cardiac output response to exercise, suggesting that pulmonary hypertension impairs exercise performance in heart failure.

Relationship between exertional symptoms and functional capacity in patients with heart failure.

OBJECTIVES: The present study was undertaken to investigate the relationship over time between exertional symptoms in heart failure and functional capacity. BACKGROUND: Most clinicians rely on exertional symptoms rather than on exercise testing to assess functional capacity in heart failure. However, it remains uncertain whether the subjective symptoms reported by patients provide a reliable index of functional capacity. METHODS: Fifty patients with heart failure underwent serial cardiopulmonary exercise testing and evaluation of exertional fatigue and dyspnea over a period of one to four years. Exercise testing was performed using the Naughton treadmill protocol and a MedGraphics metabolic cart. Fatigue and dyspnea were each scored from 0 to 3 (p = none, 1 = mild, 2 = moderate, 3 = severe). A composite symptom score was determined by adding together the fatigue and dyspnea scores. RESULTS: Patients underwent a total of 185 tests at an average interval of 4.3 months (average tests/patient = 3.7). Composite symptom scores noted at the time of exercise testing correlated significantly with peak exercise minute oxygen consumption (VO2) (r = 0.47, p < 0.01). In addition, the change in symptoms scores and change in peak VO2 noted between the baseline and final exercise test correlated significantly (r = 0.50, p < 0.01). However, patients reported few or no symptoms (symptom score < or =2) 45% of the time when peak VO2 was <14 ml/min/kg, consistent with a severe functional disability, and 72% of the time when peak VO2 was 14 to 18 ml/min/kg, consistent with moderate functional disability. CONCLUSIONS: Exertional symptoms reported by patients with heart failure generally correlate with maximal exercise capacity. However, exertional symptoms frequently underestimate the severity of functional disability. Cardiopulmonary exercise testing rather than symptoms should be used to assess functional capacity in heart failure.

The utility of exercise testing after cardiac transplantation in older patients.

BACKGROUND: The criteria for cardiac transplantation recipient selection, including the appropriate recipient upper age limit, continue to expand with an increasing number of recipients greater than 60 years of age. While others have reported their transplant experience in older recipients in terms of quality of life assessment, we have examined the role of exercise cardiopulmonary testing post-transplantation in older cardiac transplant recipients. METHODS: We reviewed inpatient and outpatient charts of 28 patients 60 years of age or older who underwent orthotopic heart transplantation at Vanderbilt University Medical Center. RESULTS: In this population, perioperative mortality of 7.1% and Kaplan-Meier survival at 1 and 5 years of 89 and 77%, respectively, were similar to the institutional 1-year (89%) and 5-year (75%) survival among younger adult transplant recipients. Exercise cardiopulmonary testing results were available in 22/25 patients surviving greater than 1 year. Both peak oxygen consumption and percentage of maximum VO2 were significantly greater among patients reporting NYHA Class 1 or 2 functional status, in comparison with those NYHA Class 3 or greater. CONCLUSION: Following cardiac transplantation, survival of patients greater than 60 years of age is equivalent to that of younger patients at our institution. Exercise testing provides an objective measure of performance and correlates with subjective status following heart transplantation. Most patients demonstrate good functional status, with minimal symptoms and good exercise capacity. These results, although retrospective, suggest that cardiac transplantation remains a reasonable therapeutic option for patients greater than 60 years of age with end-stage cardiomyopathy.

Treatment of subclinical fluid retention in patients with symptomatic heart failure: effect on exercise performance.

BACKGROUND: Patients with heart failure frequently have elevated intracardiac diastolic pressures but no clinical evidence of excess fluid retention. We speculated that such pressure elevations may indicate subclinical fluid retention and that removal of this fluid could improve exercise intolerance. METHODS: To test this hypothesis, we studied 10 patients with right atrial pressure > or = 8 mm Hg but without rales, edema, or apparent jugular venous distension. Right-sided heart catheterization was performed, after which patients underwent maximal treadmill cardiopulmonary testing. Patients were then hospitalized and underwent maximal diuresis, after which exercise was repeated. RESULTS: Before diuresis, right atrial pressure averaged 16 +/- 5 mm Hg (+/-standard deviation), pulmonary capillary wedge pressure 30 +/- 6 mm Hg, and peak exercise Vo2 11.2 +/- 2.3 ml/min/ kg. Patients underwent diuresis of 4.5 +/- 2.2 kg over 4 +/- 2 days to a resting right atrial pressure of 6 +/- 4 and wedge pressure of 19 +/- 7 mm Hg. After diuresis, all patients reported overall symptomatic improvement. Maximal exercise duration increased significantly from 9.2 +/- 4.2 to 12.5 +/- 4.7 minutes. At matched peak workloads, significant improvements were also seen in minute ventilation (45 +/- 12 to 35 +/- 9 L/min), lactate levels (42 +/- 16 to 29 +/- 9 mg/dl), and Borg dyspnea scores (15 +/- 3 to 12 +/- 4) (all p < 0.05). CONCLUSIONS: Invasive hemodynamic monitoring allows the identification of excess fluid retention in patients with heart failure when there are no clinical signs of fluid overload. Removal of this subclinical excess fluid improves exercise performance and exertional dyspnea.

Effect of sympathoinhibition on exercise performance in patients with heart failure.

BACKGROUND: In patients with heart failure, excessive sympathetic activation during exercise could interfere with exercise performance by impairing arteriolar dilation in working muscle and by adversely altering skeletal muscle metabolic behavior. To test this hypothesis, we examined the effect of sympathoinhibition with clonidine, a central sympatholytic agent, on skeletal muscle blood flow and metabolism in patients with heart failure. METHODS AND RESULTS: Swan-Ganz and femoral venous catheters were inserted in 20 patients with chronic heart failure and exercise intolerance (peak exercise VO2 = 9.3 +/- 1.4 [SEM] mL.min-1.kg-1). Central hemodynamic measurements, leg blood flow determined by thermodilution, and systemic and leg metabolic parameters were measured during maximal treadmill exercise before and 2 hours after clonidine 2 micrograms/kg IV (n = 15) or 0.9% normal saline (n = 5). During-control exercise before the administration of clonidine, leg blood flow increased from 0.3 +/- 0.1 to 1.8 +/- 0.2 L/min and plasma norepinephrine increased from 485 +/- 61 to 2155 +/- 186 pg/mL (both P < .01). Treatment with clonidine markedly suppressed norepinephrine levels during exercise (matched peak exercise workload: control, 2137 +/- 187 versus clonidine, 1430 +/- 161 pg/mL), increased leg blood flow (control, 1.8 +/- 0.2 versus clonidine, 2.3 +/- 0.4 L/min), reduced systemic oxygen consumption (control, 1002 +/- 70 versus clonidine, 966 +/- 68 mL/min), reduced pulmonary artery lactate concentration (control, 3.2 +/- 0.3 versus clonidine, 2.6 +/- 0.2 mEq/L), and decreased minute ventilation (control, 39.7 +/- 2.1 versus clonidine, 34.9 +/- 2.4 L/min) (all P < .05). CONCLUSIONS: These findings suggest that sympathetic activation during exercise reduces leg blood flow, increases muscle glycolysis, and decreases muscle efficiency in patients with heart failure.

Skeletal muscle mass and exercise performance in stable ambulatory patients with heart failure.

The purpose of this study was to determine whether skeletal muscle atrophy limits the maximal exercise capacity of stable ambulatory patients with heart failure. Body composition and maximal exercise capacity were measured in 100 stable ambulatory patients with heart failure. Body composition was assessed by using dual-energy X-ray absorption. Peak exercise oxygen consumption (VO2peak) and the anaerobic threshold were measured by using a Naughton treadmill protocol and a Medical Graphics CardioO2 System. VO2peak averaged 13.4 +/- 3.3 ml.min-1.kg-1 or 43 +/- 12% of normal. Lean body mass averaged 52.9 +/- 10.5 kg and leg lean mass 16.5 +/- 3.6 kg. Leg lean mass correlated linearly with VO2peak (r = 0.68, P < 0.01), suggesting that exercise performance is influences by skeletal muscle mass. However, lean body mass was comparable to levels noted in 1,584 normal control subjects, suggesting no decrease in muscle mass. Leg muscle mass was comparable to levels noted in 34 normal control subjects, further supporting this conclusion. These findings suggest that exercise intolerance in stable ambulatory patients with heart failure is not due to skeletal muscle atrophy.

Prostaglandin production contributes to exercise-induced vasodilation in heart failure.

Endothelial release of prostaglandins may contribute to exercise-induced skeletal muscle arteriolar vasodilation in patients with heart failure. To test this hypothesis, we examined the effect of indomethacin on leg circulation and metabolism in eight chronic heart failure patients, aged 55 +/- 4 yr. Central hemodynamics and leg blood flow, determined by thermodilution, and leg metabolic parameters were measured during maximum treadmill exercise before and 2 h after oral administration of indomethacin (75 mg). Leg release of 6-ketoprostaglandin F1alpha was also measured. During control exercise, leg blood flow increased from 0.34 +/- 0.03 to 1. 99 +/- 0.19 l/min (P < 0.001), leg O2 consumption from 13.6 +/- 1.8 to 164.5 +/- 16.2 ml/min (P < 0.001), and leg prostanoid release from 54.1 +/- 8.5 to 267.4 +/- 35.8 pg/min (P < 0.001). Indomethacin suppressed release of prostaglandin F1alpha (P < 0.001) throughout exercise and decreased leg blood flow during exercise (P < 0.05). This was associated with a corresponding decrease in leg O2 consumption (P < 0.05) and a higher level of femoral venous lactate at peak exercise (P < 0.01). These data suggest that release of vasodilatory prostaglandins contributes to skeletal muscle arteriolar vasodilation in patients with heart failure.

Hemodynamic exercise testing. A valuable tool in the selection of cardiac transplantation candidates.

BACKGROUND: Peak exercise oxygen consumption (Vo2), a noninvasive index of peak exercise cardiac output (CO), is widely used to select candidates for heart transplantation. However, peak exercise Vo2 can be influenced by noncardiac factors such as deconditioning, motivation, or body composition and may yield misleading prognostic information. Direct measurement of the CO response to exercise may avoid this problem and more accurately predict prognosis. METHODS AND RESULTS: Hemodynamic and ventilatory responses to maximal treadmill exercise were measured in 185 ambulatory patients with chronic heart failure who had been referred for cardiac transplantation (mean left ventricular ejection fraction, 22 +/- 7%; mean peak Vo2, 12.9 +/- 3.0 mL. min-1.kg-1). CO response to exercise was normal in 83 patients and reduced in 102. By univariate analysis, patients with normal CO responses had a better 1-year survival rate (95%) than did those with reduced CO responses (72%) (P < .0001). Survival in patients with peak Vo2 of > 14 mL.min-1.kg-1 (88%) was not different from that of patients with peak Vo2 of < or = 14 mL.min-1.kg-1 (79%) (P = NS). However, survival was worse in patients with peak Vo2 of < or = 10 mL.min-1.kg-1 (52%) versus those with peak Vo2 of > 10 mL.min-1.kg-1 (89%) (P < .0001). By Cox regression analysis, exercise CO response was the strongest independent predictor of survival (risk ratio, 4.3), with peak Vo2 dichotomized at 10 mL. min-1.kg-1 (risk ratio, 3.3) as the only other independent predictor. Patients with reduced CO responses and peak Vo2 of < or = 10 mL.min-1.kg-1 had an extremely poor 1-year survival rate (38%). CONCLUSIONS: Both CO response to exercise and peak exercise Vo2 provide valuable independent prognostic information in ambulatory patients with heart failure. These variables should be used in combination to select potential heart transplantation candidates.