Sleep-disordered breathing in heart failure.

Sleep-disordered breathing-comprising obstructive sleep apnoea (OSA), central sleep apnoea (CSA), or a combination of the two-is found in over half of heart failure (HF) patients and may have harmful effects on cardiac function, with swings in intrathoracic pressure (and therefore preload and afterload), blood pressure, sympathetic activity, and repetitive hypoxaemia. It is associated with reduced health-related quality of life, higher healthcare utilization, and a poor prognosis. Whilst continuous positive airway pressure (CPAP) is the treatment of choice for patients with daytime sleepiness due to OSA, the optimal management of CSA remains uncertain. There is much circumstantial evidence that the treatment of OSA in HF patients with CPAP can improve symptoms, cardiac function, biomarkers of cardiovascular disease, and quality of life, but the quality of evidence for an improvement in mortality is weak. For systolic HF patients with CSA, the CANPAP trial did not demonstrate an overall survival or hospitalization advantage for CPAP. A minute ventilation-targeted positive airway therapy, adaptive servoventilation (ASV), can control CSA and improves several surrogate markers of cardiovascular outcome, but in the recently published SERVE-HF randomized trial, ASV was associated with significantly increased mortality and no improvement in HF hospitalization or quality of life. Further research is needed to clarify the therapeutic rationale for the treatment of CSA in HF. Cardiologists should have a high index of suspicion for sleep-disordered breathing in those with HF, and work closely with sleep physicians to optimize patient management.

Sleep-disordered Breathing in Heart Failure.

Sleep-disordered breathing affects over half of patients with heart failure (HF) and is associated with a poor prognosis. It is an under-diagnosed condition and may be a missed therapeutic target. Obstructive sleep apnoea is caused by collapse of the pharynx, exacerbated by rostral fluid shift during sleep. The consequent negative intrathoracic pressure, hypoxaemia, sympathetic nervous system activation and arousals have deleterious cardiovascular effects. Treatment with continuous positive airway pressure may confer symptomatic and prognostic benefit in this group. In central sleep apnoea, the abnormality is with regulation of breathing in the brainstem, often causing a waxing-waning Cheyne Stokes respiration pattern. Non-invasive ventilation has not been shown to improve prognosis in these patients and the recently published SERVE-HF trial found increased mortality in those treated with adaptive servoventilation. The management of sleep-disordered breathing in patients with HF is evolving rapidly with significant implications for clinicians involved in their care.

Breathless after bypass.

A 65-year-old normotensive, non-athletic man presented to the cardiology clinic with exertional dyspnoea and chest discomfort. Echocardiography revealed mild left ventricular hypertrophy with good systolic function but with regional wall motion abnormalities suggesting ischaemia. Coronary angiography showed significant three-vessel disease. He underwent coronary artery bypass surgery, which was complicated by recurrent pericardial and pleural effusions, requiring a pericardial window procedure. Over the following year he became increasingly oedematous and breathless. On ECG the complexes were low voltage with impaired R wave progression and atrial fibrillation. Echocardiography revealed progression of the left ventricular hypertrophy (LVH) with a bright myocardium and restrictive filling pattern. MRI scanning confirmed the diagnosis of cardiac amyloidosis. He was referred for transplant but was considered unsuitable due to extensive mediastinal scarring. This case demonstrates the importance of a high index of suspicion for amyloidosis, especially in patients with unexplained LVH. Cardiac MRI or biopsy may expedite the diagnosis.