Left Ventricular Structural Adaptations to Obstructive Sleep Apnea in Dilated Cardiomyopathy
Obstructive sleep apnea is common among patients with heart failure and exposes the left ventricle to trophic mechanical and adrenergic stimuli. We hypothesized that in heart failure patients with nonischemic dilated cardiomyopathy (a condition characterized by eccentric hypertrophy), those with obstructive sleep apnea would have a higher prevalence of left ventricular hypertrophy by wall thickness criteria (> or = 12 mm), and greater septal thickness than those without obstructive sleep apnea.
We performed echocardiography and polysomnography in 47 patients with nonischemic dilated cardiomyopathy. Obstructive sleep apnea was present in 45% of these patients. The prevalence of left ventricular hypertrophy was greater in those with than in those without obstructive sleep apnea (47.6 vs. 15.4%, p = 0.016). Interventricular septal thickness (p < 0.001) and relative wall thickness (p = 0.011) were significantly greater in those with than in those without obstructive sleep apnea. However, there was no significant difference in posterior wall thickness between the groups. The frequency of obstructive apneas and hypopneas during sleep was the only significant independent correlate of septal thickness (p = 0.001).
In patients with nonischemic dilated cardiomyopathy, the presence of obstructive sleep apnea is associated with an increased prevalence of left ventricular hypertrophy. The higher relative wall thickness and interventricular septal thickness in patients with obstructive sleep apnea indicate that the left ventricle is relatively less eccentric than in patients without obstructive sleep apnea, and that such remodeling affects mainly the septum. These structural adaptations may reflect unique nocturnal mechanical and adrenergic stimuli associated with obstructive sleep apnea.
Available from: Thibaud Damy
- "Several studies in patients without CHF have already demonstrated that OSA was associated with a concentric LVH (Drager et al., 2007a; Dursunoglu et al., 2005; Hedner et al., 1990). In CHF, Usui et al. (2006) have observed a relative increase in RWT in their patients with CHF with OSA versus those without. However, if the prevalence of concentric LVH was not indicated, the majority of patients with CHF with OSA had an eccentric LVH, as their mean RWT (0.35 ± 0.07) was under the value required to define the concentric LVH. "
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ABSTRACT: Sleep-disordered breathing (SDB) is associated with left ventricle (LV) remodelling in patients with normal LV function. Sleep-disordered breathing is common in chronic heart failure (CHF) with systolic LV dysfunction, and may contribute to LV remodelling and CHF progression. Our aim was to determine the consequence of SDB on LV geometry in patients with CHF. We hypothesised that SDB severity was correlated with the degree of LV hypertrophy (LVH). One-hundred and sixty patients with CHF with a non-ischaemic systolic LV dysfunction were assessed by overnight polygraphy and echocardiography. Patients were classified in four groups according to their apnoea-hypopnoea index (AHI): <5 (no-SDB); 5-14 (mild); 15-29 (moderate); ≥30 (severe). Left ventricular mass index (LVM Ind) was calculated using the usual echocardiographic M-Mode parameters. Their mean age, New York Heart Association and left ventricular ejection fraction were, respectively: 56 ± 13 years, 2.4 ± 0.8 and 30 ± 10%, and 77% were men. Body mass index, interventricular septal and posterior LV wall thicknesses, and LVM Ind were significantly increased in severe SDB versus no-SDB. LVM Ind was correlated to the AHI (R = 0.27, P = 0.0006) and, using logistic regression, AHI was the unique independent factor of LVH in this population. In non-ischaemic CHF, SDB severity is associated with LV remodelling.
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ABSTRACT: ÖZET: Obstrüktif uyku apne sendromu (OUAS) ile kardiyovasküler hastaliklar arasinda bağimsiz bir ilişki olduğunu destekleyen önemli kanitlar bulunmaktadir; bu kanitlar özellikle sistemik arte- riyel hipertansiyon için güçlüdür ve iskemik kalp hastaliği, inme, kalp yetmezliği, atrial fibrilas- yon ve ani kardiyak ölüm için de giderek artmaktadir. OUAS'daki kardiyovasküler hastaliklarin patogenezi tam olarak anlaşilamamiştir ancak olasi- likla çok faktörlüdür ve sempatik sinir sisteminin aşiri aktivitesi, enflamatuar moleküler yollarin selektif aktivasyonu, endotel fonksiyon bozukluğu, anormal koagülasyon ve metabolik düzenin bozulmasi gibi farkli mekanizmalari içerebilir; bu sonuncu mekanizma özellikle insülin direnci ve lipit metabolizmasi bozukluklarini kapsamaktadir. Avrupa Birliğinin OUAS üzerine (COST B26) Bilimsel ve Teknik Araştirmalar konusunda İşbirliği'nden (COST) ortaya çikan bu rapor, bağimsiz bir ilişki için güncel kanitlari gözden geçir- mekte ve yeni tedavi stratejileri belirleme amaciyla, olaya katilan altta yatan mekanizmalarin belirlenebilmesi için araştirma öncelikleri önermektedir. Obstrüktif uyku apne sendromuna sahip, olasi kariştirici faktörler açisindan yeterince kontrol altina alinmiş, dikkatlice belirlenmiş hasta popülasyonlarinda yapilan geniş ölçekli işbirliği çaliş- malarina gerek vardir. Bu tür çalişmalar obstrüktif uyku apne sendromu ve kardiyovasküler has- talikta rol oynayan farkli temel mekanizmalar arasindaki potansiyel etkileşimleri ve obezite, diya- bet ve dislipidemi gibi diğer ilgili hastaliklarla etkileşimleri değerlendirme olasiliğini taşimakta- dirlar. Ayrica, temel mekanizmalari klinik hastaliklarla bütünleştirebilmek için, obstrüktif uyku apne sendromu hastalarina ilişkin çalişmalara bağlanmiş, hücre kültürü ve hayvan modellerini de içeren translasyonel çalişmalar yapilmasi gerekmektedir.
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