The Nadir Oxygen-Specific Heart Rate Response in Sleep Apnea Links With the Occurrence of Acute Myocardial Infarction

Zhihua Huang; Yanpeng Wu; Kaizhuang Huang; Pingyan Chen; Jiyan Chen; Ling Wang

doi:10.3389/fcvm.2022.807436

The Nadir Oxygen-Specific Heart Rate Response in Sleep Apnea Links With the Occurrence of Acute Myocardial Infarction

Front Cardiovasc Med. 2022 Apr 26:9:807436. doi: 10.3389/fcvm.2022.807436. eCollection 2022.

Authors

Zhihua Huang^{1

2}, Yanpeng Wu³, Kaizhuang Huang^{1

4}, Pingyan Chen³, Jiyan Chen¹, Ling Wang¹

Affiliations

¹ Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
² Department of Cardiology, Fuwai Hospital, National Clinical Research Center for Cardiovascular Diseases, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
³ Department of Biostatistics, School of Public Health, Southern Medical University, Guangzhou, China.
⁴ Department of Intensive Care Unit, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.

Abstract

Background: Little is known regarding the quantification of sleep apnea- and hypoxemia-elicited heart rate (HR) response and its prognostic significance of the cardiovascular risk. We sought to explore the impact of HR response and variability specific to obstructive sleep apnea (OSA) on the occurrence of a common cardiovascular event - acute myocardial infarction (AMI).

Methods: Consecutive patients with suspected OSA were enrolled and underwent nocturnal respiratory study and electrocardiography monitoring. The minimal oxygen saturation (minSpO₂) was determined from the oxygen saturation curve under a subject-specific search window. Primary HR metrics such as maximal HR in response to minSpO₂ and respiratory event-specific HR variability were computed from the synchronized recordings. Multivariate regression analyses were conducted to analyze the associations between individualized HR metrics and the occurrence of AMI.

Results: Of 2,748 patients recruited, 39% (n = 1,071) had moderate-to-severe OSA (respiratory event index, REI ≥ 15), and 11.4% (n = 313) patients had AMI. Patients with AMI experienced severe OSA, severe minSpO₂, and greater HR reactions. Patients with minSpO₂ <90% had an adjusted odds ratio (OR) of 1.48 [95% confidence interval (CI): 1.09-2.00, p = 0.012) for AMI. Notably, minSpO₂-induced elevated mean HR response (HR_mean > 73 bpm) was significantly associated with AMI (OR 1.72, 95% CI: 1.32-2.23, p < 0.001). Patients with both severe minSpO₂ (<90%) and elevated HR_mean carried an additive OR of 2.65 (95% CI: 1.74-4.05, p < 0.001) for the risk of AMI after adjustment for potential confounders. A large total power spectrum specific to respiratory events was correlated with an adjusted OR of 0.61 for AMI risk.

Conclusion: Patients with substantial HR reactions to OSA-induced oxygen nadir and restricted cardiac cycle shifting to respiratory events were likely at increased risk of developing AMI. Detection of nocturnal HR response to hypoxemia may help improve cardiovascular risk stratification.

Keywords: cardiovascular risk; heart rate; myocardial infarction; oxygen saturation; sleep apnea.