Severity of hypoxia modulates effect of CPAP on myocardial stress as measured by highly sensitive troponin T

Excerpt

Obstructive sleep apnea (OSA) is associated with increased risk for cardio- and cerebrovascular diseases [1, 2]. Animal studies propose intermittent hypoxia and the resulting inappropriate activation of sympathetic nervous system [3, 4] as the major link between OSA and cardio- and cerebrovascular comorbidities. However, the OSA severity level at which continuous positive airway pressure (CPAP) therapy offers cardio- and cerebrovascular benefit (reduction in indices of myocardial stress/injury) is a matter of debate. Sub-clinical injury to the myocardium is considered to be a precursor for the development of incident cardiovascular disease including heart failure [5]. Troponin T measured with a high sensitivity assay (Hs-TnT) has been shown to predict incident heart failure and cardiovascular death [6]. Further, increase or decrease in Hs-TnT over time predicted increased or decreased incidence of heart failure and cardiovascular death [7, 8]. Hs-TnT has also shown to be increased with presence and severity of OSA [9]. Stronger correlations were reported with nadir SpO2 [10]. Roca and colleagues, in a cohort of 1645 subjects free of coronary artery disease and heart failure with a median follow up of 12.4 years, reported that hs-TnT was associated with risk of death or incident heart failure across various categories of OSA after adjusting for 17 potential confounders [11]. Surprisingly, a recent study showed increased Hs-TnT after 12 months of CPAP therapy in patients with OSA. However, the utilization of CPAP was not reported [12]. We report changes in Hs-TnT level as a marker of myocardial stress/injury in a cohort of CPAP compliant patients with OSA. …