Author:
Ruddy Stella,Marzo Vincenzo Di,Ngueta Gerard
Abstract
ABSTRACTBackgroundPulse pressure (PP) and mean arterial pressure (MAP) have been well-established as markers of cardiovascular risk in clinical settings. We aimed to determine the impact of cannabis use on both PP and MAP in U.S. adults and to assess the modifying role of sex.MethodsWe abstracted data from the 2009 to 2018 National Health and Nutrition Examination survey (NHANES). Cannabis use was assessed by NHANES professionals in adults aged 18 to 59 years by using computer-assisted self-interviews. We defined PP as the difference between systolic and diastolic BP, and MAP as diastolic BP plus one third of PP. We used multivariable linear models to estimate the covariates-adjusted associations and assessed effect modification by including sex×exposure interaction terms into the model.ResultsThe mean age of the study population (n=8,942) was 35.0±11.9 years, with 51% female (n=4,551). Mean±SD PP and MAP were 46±13 mm Hg and 82±13 mm Hg, respectively. We found a significant interaction between sex and cannabis use in relation to PP (P=0.0878) and no interaction when modeling MAP (P=0.2084). The mean difference of PP between cannabis users and never-users increased with the frequency of use per week, being +4.5 mm Hg (P=0.0004) in those who reported 1 use/week, +4.9 mm Hg (P<0.0001) for 2-3 uses/week and +4.9 mm Hg (P<0.0001) for ≥ 4 uses/week. In females, only those who reported ≥ 4 uses/week showed a higher PP (+3.1 mm Hg;P=0.0050) compared with never-users.ConclusionsIn US adults aged 18 to 59 years, cannabis use is associated with widening of PP in males.CLINICAL PERSPECTIVESWhat is new?We first investigated the cannabis use in relation to PP and MAP and found that cannabis use is associated with widened PP in sex-specific manner.What are the clinical implications?Further evidence from cohort studies is required before it can be firmly concluded that cannabis use is linked to increased PP. Patients should stop cannabis use to optimize treatments with reduction of PP as specific therapeutic target.
Publisher
Cold Spring Harbor Laboratory