¹Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Division of Nephrology, Mount Sinai Hospital and University Health Network, and Department of Medicine, University of Toronto, Toronto, Ontario, Canada

Correspondence: Alexander G. Logan, (alogan@mtsinai.on.ca)

Received 21 December 2008; First Decision 26 January 2009; Accepted 9 February 2009; Published online 5 March 2009.

Abstract

This review addresses the cardiovascular, cerebrovascular, and metabolic consequences that accompany obstructive sleep apnea–hypopnea (OSAH) in conjunction with the mechanistic pathways implicated in mediating these effects. Particular emphasis is placed on the association with hypertension (HTN). Varying levels of evidence support a role of OSAH in perpetuating sustained HTN, nocturnal HTN, and difficult to control HTN as well as in contributing to the occurrences of nondipping of blood pressure (BP) and increased BP variability. In this context, the emergence of matched designs, adjusted analyses, meta-analyses as well as longitudinal and interventional studies strengthens causal inferences drawn from older observational studies, which suffered from such limitations as confounding.

American Journal of Hypertension 2009; doi:10.1038/ajh.2009.43