Content area
Full Text
VIEWPOINT
http://www.nature.com/clinicalpractice/cardio
Web End =www.nature.com/clinicalpractice/cardio
Despite extraordinary advances in understanding hypertrophic obstructive cardiomyopathy (HOCM) at the molecular and genetic level, the overall clinical management of patients with HOCM remains suboptimum.1 We propose that the presence of obstructive sleep apnea (OSA) in patients with HOCM could be an important contributor to drug-refractory symptoms and worsening left ventricular outflow tract (LVOT) obstruction, as a result of heightened sympathetic activity.
Currently, septal reduction is recommended for patients with HOCM whose septal thickness is 16 mm or more, whose symptoms interfere with lifestyle despite optimum medical therapy, and in whom the LVOT gradient is 30 mmHg or more at rest or 50 mmHg or more on provocation. OSA occurs when inspiratory airflow is either partly (hypopnea) or completely (apnea) occluded during sleep. Approximately 20% of adults in North America and Europe have mild OSA, and another 7% have moderate to severe OSA.2 Although OSA occurs predominantly at night, the combination of sleep-disordered breathing and daytime sleepiness is referred to as OSA syndrome. The hypoxemia and carbon dioxide retention that result from apnea primarily excite peripheral and central chemoreceptors, which increases sympathetic vasoconstrictor activity.3 Furthermore, the repetitive nocturnal stress of hypoxemia, combined with strenuous inspiratory effort because of the occluded upper airway and arousal from sleep, elicit a breadth of neural, humoral, vascular, inflammatory, and metabolic responses that are evident even when the individual is awake. Home-based treatment currently centers on continuous positive airway pressure (CPAP) therapy.
OSA is frequently associated with cardiovascular diseases.4 Although OSA and HOCM are two widely prevalent conditions, the clinical effects of concomitant disease remain uncharacterized. Exertional dyspnea and limited exercise capacity are known clinical features associated with both OSA and HOCM. If our hypothesis is correct, the
Hypertrophic obstructive cardiomyopathy and sleep-disordered breathing: an unfavorable combination
Partho P Sengupta, Dan Sorajja, Mackram F Eleid, Virend K Somers, Steve R Ommen, James M Parish, Bijoy Khandheria and A Jamil Tajik*
PP Sengupta and
D Sorajja are Clinical Fellows, MF Eleidis a Resident in Internal Medicine,B Khandheria is a Consultant and Chair of the Cardiovascular Division, AJ Tajikis a Consultantin the Division of Cardiovascular Diseases, and
JM Parisch is a Consultant in the Division of Pulmonary Medicine, all atthe Mayo Clinic, Scottsdale, AZ.
VK Somers...