Predictive Value of Sleep Apnea-specific PTT Response for Incident Subclinical Abnormalities in LV Structure and Function in Cohort of moderate-to Severe OSA

This observational study aims to provide evidence for identifying those who mostly suffer from LV injury and will help construct an optimal strategy for clinical practice. The main question it aims to answer is:

Could acute PTT response surrounding obstructive respiratory events predict the incidence of subclinical abnormalities in LV structure and function in moderate-to-severe OSA patients? Participants who had undergone standard polysomnography and were diagnosed with moderate-to-severe OSA 5 years ago were required to complete the cardiac remodeling and function evaluation.

Obstructive sleep apnea (OSA) is a widely prevalent medical condition characterized by recurrent upper airway obstruction with intermittent hypoxia, sleep disruption, and increased ventilation. Serial studies have shown that OSA promotes oxidative stress, sympathetic activity, and intrathoracic pressure fluctuation, resulting in adverse cardiac structures and function. The cumulative data from observational studies have linked the apnea-hypopnea index (AHI), an indicator of OSA severity, with increased LV injury. As OSA is a highly heterogeneous disorder, with diverse pathways to disease, expression of disease, susceptibility to co-morbidities, and response to therapy. Hence, OSA is ideally suited to precision medicine approaches. While the current assessment relies on the AHI, this traditional metric poorly reflects the complex pathophysiological of OSA on cardiac injury.

Asymptotic cardiac dysfunction is not easily identified, and many sufferers remain undiagnosed in clinical practice. Focusing on recognition and treatment of subclinical cardiac injury early is a potentially powerful strategy to prevent progression to clinical or symptomatic heart failure. In OSA patients, the BP and heart rate (HR) changes occurring with obstructive events involve an initial decrease early in the event, a gradual increase during the terminal portion of the event, and an immediate surgeon resumption of ventilation. These acute hemodynamic and autonomic changes may be closely associated with the development and progression of cardiovascular disease. Whether this OSA-specific cardiovascular reactivity pattern is the potentially early warning indicator of cardiac injury is unknown.

A physiologic parameter termed pulse transit time (PTT) has been studied intensively as an indirect marker for variations in cardiovascular-related reactivity. It can be generally referred to as the time difference for a pulse wave to travel between two arterial sites. The speed at which this arterial pressure wave travels was used to assess nocturnal blood pressure variation, arterial stiffness changes, autonomic nervous response, and inspiratory effort. More experimentally focused investigations with PTT as a key measure in cardiovascular-related studies are being reported.

In the present study, the investigators examined acute PTT changes surrounding obstructive events, for PTT can be easily measured in standard polysomnography (PSG). The investigators hypothesized that the specific respiratory events PTT response would predict incident subclinical abnormalities in LV structure and function in a cohort of moderate-to-severe OSA without other confounded morbidities. The results of this study provide evidence for identifying those who mostly suffer from LV injury and will help construct an optimal strategy for clinical practice.

Eligibility Criteria:
Inclusion Criteria:

1. ≥18 years old;
2. Moderate to severe OSA(AHI≥15 times/hour).

Exclusion Criteria:

1. baseline hypoxia;
2. other sleep disorders;
3. received regular CPAP treatment(on average of ≥ 4 hours for CPAP use per night during the retrospective period);
4. the prevalent diseases at baseline might have influenced the results of echocardiographic results: hypertension chronic atrial fibrillation, atrioventricular block, bundle branch blocks, a permanent pacemaker, heart failure, valvular heart disease, pulmonary emboli, abnormal thyroid function, cardiomyopathies, pulmonary hypertension, use of digitalis, use of antiarrhythmic agents, use of beta-blockers, or use of calcium agonists affecting heart rate (HR), including verapamil and diltiazem.