The concept that inflammation participates pivotally in the pathogenesis of atherosclerosis and its complications has gained considerable attention, but has not yet entered clinical practice. Experimental work has elucidated molecular and cellular pathways of inflammation that promote atherosclerosis. The recognition of atherogenesis as an active process rather than a cholesterol storage disease or a repository of calcium has highlighted some key inflammatory mechanisms. For example, mononuclear phagocytes contribute to all stages of this disease, illustrating the link between inflammation and atherosclerosis. From a clinical perspective, harnessing inflammation may now help target therapeutics, change guidelines, and enter daily practice. Multiple lines of incontrovertible evidence have proven a causal role for low-density lipoprotein (LDL) cholesterol in atherosclerosis, and we have highly effective tools for lowering LDL, consequently reducing events. Yet, even with intense LDL reduction, events still occur. Inflammation can explain some of this residual risk. An anti-inflammatory intervention has now proven capable of improving outcomes in individuals well treated with LDL-lowering agents. A suite of trials are now pursuing anti-inflammatory therapies in this context. Assessment and treatment of residual inflammatory risk are poised to provide new inroads into preventive cardiology. This brief review aims to explore the potential mechanisms underlying the association of inflammation and atherogenesis, and their clinical consequences.

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In a multiethnic cohort, we found increased levels of cardiovascular risk factors in association with OSA, including elevated neutrophil counts, a marker of inflammation. Furthermore, several associations were stronger in men, younger individuals, and African American individuals, highlighting pathways for CVD risk that may explain heterogeneity in the associations between CVD and OSA across population groups.

Background: Heart rate variability (HRV) is a noninvasive method for assessing autonomic function. Age, sex, and chronic conditions influence HRV. Objectives: Our aim was to evaluate HRV measures exploring differences by age, sex, and race in a sample from a rural area. Methods: Analytical sample (n = 1,287) included participants from the 2010 to 2016 evaluation period of the Baependi Heart Study, a family-based cohort in Brazil. Participants underwent 24-hour Holter-ECG (Holter) monitoring. To derive population reference values, we restricted our analysis to a ‘healthy’ subset (i.e. absence of medical comorbidities). A confirmatory analysis was conducted with a subgroup sample that also had HRV derived from a resting ECG 10’-protocol obtained during the same time period. Results: The ‘healthy’ subset included 543 participants. Mean age was 40 ± 14y, 41% were male, 74% self-referred as white and mean body-mass-index was 24 ± 3kg/m 2 . Time domain HRV measures showed significant differences by age-decade and by sex. Higher values were observed for males across almost all age-groups. Parasympathetic associated variables (rMSSD and pNN50) showed a U-shaped distribution and reversal increase above 60y. Sympathetic-parasympathetic balance variables (SDNN, SDANN) decreased linearly by age. Race differences were no significant. We compared time domain variables with complete data (Holter and resting ECG) between ‘healthy’ versus ‘unhealthy’ groups. Higher HRV values were shown for the ‘healthy’ subset compared with the ‘unhealthy’ group. Conclusion: HRV measures vary across age and sex. A U-shaped pattern and a reversal increase in parasympathetic variables may reflect an age-related autonomic dysfunction even in healthy individuals that could be used as a predictor of disease development.

In the MESA cohort, OSA measures associate with elevated neutrophil counts and increases in overnight mean HR. These data link innate immune dysregulation with OSA and provide a potential pathophysiologic pathway between CVD and OSA.