Cheyne-Stokes in hypertrophic cardiomyopathy Pedrosa et al. CLINICS 2010;65(9):927-929 Figure 1 - Polysomnographic recording (5 minutes tracing) of an HCM patient with normal left ejection fraction presenting a Cheyne- Stokes respiration during sleep. The patient was on stage 2 sleep; top channel is related to sleep recordings. rThe following channels, from top to bottom, trac respiration by monitoring motion of the thorax, abdomen, respiratory flow (nasal canulla), ear lobe oxymetry, and derived heart rate. Black arrows show how the circulation time is measured (time from the first breath after a central apnea to the subsequent nadir of SaO2 detected at the ear by an oximeter). hyperventilation are not completely understood. Increased pulmonary capillary vascular pressures may trigger hyper- ventilation through stimulation of pulmonary vagal affer- ent-nerve activity. Left ventricular systolic dysfunction has been suggested as the cause of pulmonary congestion, but diastolic dysfunction could also lead to pulmonary congestion. Diastolic dysfunction has also been associated with increased hypercapnic ventilatory responsiviness.5 Increased chemorreflex could contribute to respiratory instability due to increased loop gain.3 A previous study that evaluated 20 patients with diastolic dysfunction found that 2 patients presented central sleep apnea and CSR pattern of breathing.6 The present case report extends these findings by showing that CSR may also be present in patients with HCM. To the best of our knowledge, this is the first time this association was presented in a patient with hypertrophic cardiomyopathy and normal systolic function. It is important to stress, however, that the presence of atrial fibrillation is a marker for loss of atrial contraction and poor cardiac pumping function and may contribute to the genesis of CSR in the present case.7 Atrial fibrillation is 8 times more common among patients with central sleep apnea than among normal controls.8 Another important finding en- countered in this patients that helps explain the respiratory pattern is that mean pulmonary transit time was prolonged, denoting increased circulation time, a hallmark of CSR, previously described in association with systolic dysfunc- tion. It also has been found that the duration of hyperpnea is directly proportional to the lung to peripheral chemorecep- tor circulation time, and inversely proportional to cardiac output. Patients with heart failure and CSR present with the periodic cycle duration averaging approximately 60 seconds, compared with only 35 seconds in patients with 928 idiopathic central sleep apnea or high-altitude periodic breathing without heart failure.9 Hall et al.10 compared central apnea in patients with normal systolic function versus patients with systolic dysfunction. While the dura- tion of apnea was similar, patients with normal heart function presented a significantly shorter hyperpnea and cycle length time than patients with systolic dysfunction. The investigators concluded that prolonged periodic breath- ing cycle and hyperpnea durations, typical of CSR, are a consequence of left ventricular systolic dysfunction, low cardiac output, and prolonged circulation time. However, the patient described presented values of cycle length, apnea length, and LECT similar to those described in patients with CSR and heart failure due to systolic dysfunction:11 hyperpnea time (42 ¡ 3 vs 35 ¡ 7), apnea time (19 ¡ 3 vs 27¡ 3), cycle length (62 ¡ 5 vs 62 ¡ 10) and LECT (29 ¡ 2 vs 27 ¡ 3). Therefore, we extend the concept proposed by Hall et al.10 by showing that prolonged circulation time can also occur in patients with normal left ventricular systolic function but impaired left ventricular diastolic function. We conclude that patients with normal left ventricular function but with severe diastolic dysfunc- tion and atrial fibrillation may present the typical CSR. REFERENCES 1. Arteaga E, Ianni BM, Fernandes F, Mady C. Benign outcome in a long- term follow-up of patients with hypertrophic cardiomyopathy in Brazil. Am Heart J. 2005;149:1099-105, doi: 10.1016/j.ahj.2004.09.049. 2. Pedrosa RP, Drager LF, Genta PR, Amaro AC, Antunes MO, Matsumoto AY, et al. Obstructive sleep apnea is common and independently associated with atrial fibrillation in patients with hypertrophic cardio- myopathy. Chest. 2010;137:1078-84, doi: 10.1378/chest.09-2335. 3. Lorenzi-Filho G, Genta PR, Figueiredo AC, Inoue D. Cheyne-Stokes respiration in patients with congestive heart failure: causes and consequences. Clinics. 2005;60:333-44.