Howard N. Hodis

TL;DR: Prenatal air pollution exposures, DNA methyl transferase genotypes, and associations with newborn LINE1 and Alu methylation and childhood blood pressure and carotid intima-media thickness in the Children’s Health Study suggest genetic and epigenetic variation may play important roles in downstream cardiovascular consequences of prenatal air pollution exposure.

TL;DR: Cumulated data support a ‘window-of-opportunity’ for maximal reduction of CHD and overall mortality and minimization of risks with HRT initiation before 60 years of age and/or within 10 years of menopause and continued for 6 years or more.

TL;DR: Evaluated subclinical atherosclerosis in different arterial sites in addition to FRS may be useful in targeting subjects for lifestyle and other interventions and is prominent across the spectrum of FRS.

TL;DR: The finding that advanced HIV-related immunosuppression was associated with increased carotid arterial stiffness independent from the effects of traditional atherosclerosis risk factors suggests that the etiologic mechanism underlying reports of an increased cardiovascular disease risk among HIV-infected individuals might involve HIV- related immunOSuppression leading to vascular dysfunction and arterial stiffening.

TL;DR: Suppressing HIV replication below clinical thresholds was associated with less progression of atherosclerosis and the proatherogenic mechanisms of HIV replication and the net CVD benefit of different antiretroviral drugs should be a focus of future research.