Blood pressure profile and nocturnal oxygen desaturation

In this issue of The Journal of Clinical Hypertension, the study by Chen and colleagues provides evidence of the positive association of 24‐hour, daytime, and nighttime systolic and diastolic blood pressure (BP) and BP variability indices with nocturnal oxygen desaturation. The study was conducted among 2342 outpatients referred for ambulatory BP monitoring in a specialized hypertension clinic. The association was stronger for nighttime than daytime BP and was partially mediated by pulse rate, which is a measure of sympathetic activity.

1. SLEEP DISORDERS AND CARDIOVASCULAR HEALTH

These findings confirm and expand the existing body of knowledge whereby sleep can dramatically affect physiological processes and health outcomes. Over the past decades, the growth in sleep medicine and advances in basic and clinical research identified fascinating relationships between sleep disorders and cardiovascular structure and function.1 Obstructive sleep apnea syndrome is the most common sleep‐disordered breathing abnormality, affecting 2% to 7% of the adult population,2, 3 and it represents one of the modifiable risk factors for the development of hypertension and hypertension‐associated end‐stage organ damage, including coronary heart disease, arrhythmia, stroke, and dementia.4, 5

Intermittent hypoxia, intrathoracic pressure changes, arousals, and sleep fragmentation, occurring in association with obstructive sleep apneas, likely contribute to alter systemic BP profile through the synergistic combination of heterogeneous mechanisms.6

Enhanced sympathetic activity is one main pathway. It results both from the activation of carotid body chemoreceptors triggered by episodic hypoxemia and the generalized stress induced by sleep structure disruption, and contributes to catecholamine surge and baroreceptor sensitivity impairment.7 Recurrent intermittent hypoxia and subsequent reoxygenation, which resembles the ischemia‐reperfusion cycle, promote the release of reactive oxygen species, cytokines, and vasoactive mediators that cause endothelial injury and dysfunction.8, 9, 10 Moreover, upregulation of the atrial natriuretic peptide and renin‐angiotensin‐aldosterone systems, which occurs in response to intrapleural pressure swings and increase of renin levels, can determine body fluid redistribution.11, 12 All of these autonomic and neurohumoral derangements result in a disturbance of the overall circadian BP rhythm. Although obstructive sleep apnea syndrome is more extensively responsible for the nocturnal BP surge and failure of the normally observed “dipping” phenomenon,13 it can also increase awake BP levels during daytime and BP variability.14, 15 On this ground, there is overwhelming evidence that other than absolute BP levels, either short‐ or long‐term fluctuations of BP over time are closely related to the development and progression of target organ disease, and confer an increased risk of major cardiac adverse events, cerebral infarcts, neurocognitive dysfunction, and kidney disease16, 17, 18, 19, 20, 21, 22, 23 by promoting microvascular and macrovascular remodeling, hemodynamic instability, and blood flow imbalance, inflammatory response, and oxidative stress.24, 25, 26, 27, 28, 29

2. CLINICAL AND RESEARCH OPPORTUNITIES AND CHALLENGES

Unraveling the pathophysiology of obstructive sleep apnea syndrome and the characteristics of obstructive sleep apnea syndrome–related hypertension is a worthwhile endeavor to achieve perfect BP control over a 24‐hour period. Patients with sleep apneas present with different combinations of abnormalities in airway anatomy, respiratory chemosensitivity, neuromuscular responsiveness, and loop gain, and are profoundly heterogeneous with respect to disease pathogenesis.30 The individual susceptibility to symptoms and systemic sequelae suggests the need to define improved disease measurements that may be useful to better characterize patients’ subgroups and understand the variability in treatment response.1 In the beginning of the era of “individualized precision medicine,” the joined knowledge of patient features, BP patterns, pathophysiological mechanisms causing and maintaining hypertension, tolerability of pharmacological and pressure therapies and their distinctive effects on nocturnal and diurnal BP, and BP variability profiles would be of high value to develop practicable single or combined therapeutic interventions to obtain tangible improvements in hard cardiovascular outcomes.1, 10, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40

These goals may be best gained by strengthening collaboration and creating partnerships and cross‐fertilization between primary care practitioners, cardiologists, neurologists, sleep medicine specialists, internists, and clinical trial communities.1 Such synergies would allow advances in a clinical and research agenda targeted to improve the evidence‐based treatment of sleep‐disordered breathing and to design effective integrated models of care.

CONFLICT OF INTEREST

None.

Lattanzi S, Brigo F, Silvestrini M. Blood pressure profile and nocturnal oxygen desaturation. J Clin Hypertens. 2018;20:656‐658. 10.1111/jch.13259