To the Editors:
A 58-yr-old male was referred for participation in a cardiac rehabilitation programme. He had a long-term history of hypertensive cardiomyopathy and systolic dysfunction and was clinically stable, being treated with β-blocker carvedilol, losartan, digitalis, diuretics and spironolactone, with no changes in medication in the previous 16 weeks. An echocardiogram showed a 17% left ventricular ejection fraction and the patient was in New York Heart Association Functional Class III.
Before starting the exercise training programme, the patient was submitted to a maximal progressive cardiopulmonary exercise test, on an electromagnetically braked cycle ergometer (Medifit 400L; Medical Fitness Equipment, Maarn, The Netherlands), with work rate increments of 5 W every 1 min at 60 rpm until exhaustion. Oxygen uptake (V′O2) and carbon dioxide production were determined by means of gas exchange on a breath-by-breath basis in a computerised system (Vmax 229 model; SensorMedics, BuenaVista, CA, USA). Peak V′O2 was defined as the maximum attained V′O2 at the end of the exercise period in which the patient could no longer maintain the cycle rate. During this test, the patient showed a very low exercise capacity, with a peak V′O2 of 9.3 mL·kg−1·min−1 and 35 W of peak power load. Evaluation of ventilation during exercise revealed the presence of periodic breathing (fig. 1⇓), as identified by the criteria proposed by Leite et al. 1 and others 2.
The patient underwent 4 months of exercise training, which consisted of 60-min exercise sessions 3 times·week−1 under medical supervision at the Heart Institute (affiliation) 3. Each exercise session consisted of 5 min stretching exercises, 25 min cycling on an cycle ergometer in the first month and up to 40 min in the next 3 months, 10 min local strengthening exercises (sit-ups, push-ups and pull-ups) and 5 min of cool down with stretching exercises. The exercise intensity was established by heart-rate levels that corresponded to anaerobic threshold up to 10% below the respiratory compensation point obtained in the cardiopulmonary exercise test. When a training effect was observed, as indicated by the patient using a Borg perceived exertion scale, the cycle workload was slightly increased. Heart-rate reduction was rarely used to adjust the bicycle workload, since the patient was under β-blocker treatment. Aerobic exercise training duration increased progressively so that the patient could perform 40 min of bicycle exercise at the established intensity. Throughout the training period, medication was kept the same and no major clinical event occurred.
After 4 months of exercise training, left ventricular ejection fraction remained the same (17%), New York Heart Association Functional Class improved to II, and the patient was submitted to another cardiopulmonary exercise test, following the same exercise increment protocol and the same equipment used in the first evaluation. Peak results of both tests are presented in table 1⇓. As noted in figure 1⇑, maximal exercise time increased. Although the ventilation pattern in the second test still presented some oscillation, it was much closer to the expected physiological linear increase and thus, did not comply with the criteria for exercise periodic breathing 2.
Ribeiro et al. 4 have shown reversal of periodic breathing with pharmacological intervention, more specifically, with milrinone or cardiac transplantation. To our knowledge, this is the first report of reversal of periodic breathing related to exercise training in a patient with chronic heart failure.
Periodic breathing seems to be related to mechanisms within central nervous system, more specifically with nuclei involved in respiratory control 5. In addition, Yajima et al. 6 found that periodic breathing was consequent to fluctuations in pulmonary blood flow during exercise in heart failure patients. Although periodic breathing independently predicts cardiac mortality in heart failure patients 1, it is not a phenomenon directly correlated to low left-ventricular ejection fraction, as it could be suspected. For example, the occurrence of periodic breathing could predict cardiac mortality in patients who were waiting for cardiac transplantation, independent of ejection fraction. Indeed, in the present case report, left-ventricular ejection fraction and peak oxygen pulse (which is directly correlated to maximum cardiac output) remained the same, despite the improvements in peak V′O2 and New York Heart Association Functional Class. Although the mechanisms involved in the development of periodic breathing are not completely understood, its role as a marker of worse prognosis in heart failure is well established. Thus, the reversal of periodic breathing after exercise training may have practical implications.
One could hypothesise that the non-occurrence of periodic breathing after exercise training could have happened by chance. Although a single case is not a strong enough evidence to exclude this possibility, it is important to notice that medication and clinical status were stable throughout exercise training period. In addition, Corra et al. 7 have shown that occurrence of exercise periodic breathing is a reproducible phenomenon; thus, it is very unlikely that the reversal of periodic breathing was not consequent to exercise training. Whether the reversal of periodic breathing after exercise training will occur in larger series of heart failure patients and if this reversal is related to prognosis improvement desires further investigation.
Support statement
This study was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP # 2005/59740-7), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq #474621/2004-9), Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ #E-26/100.461/2007) and, in part, Fundação Zerbini. L.M. Ueno was supported by FAPESP as post-doctoral fellow (#03/10881-2). C.E. Negrão, M.U.P.B. Rondon, L.M. Antunes-Correa and A.C.L. Nóbrega were supported by CNPq #302146/2007-5, #303518/2008-1, 142366/2009-9 and #301168/2006-7, respectively.
Statement of interest
None declared.
- Received November 8, 2009.
- Accepted December 8, 2009.
- © ERS