Antihypertensive drug side effects was associated with drug adherence but only excessive urination and decrease in sexual drive significantly predicted lower adherence. These symptoms could be used as markers to screen out patients at high risk of non-adherence.

Experimental studies conducted on animal and human endothelium suggested that higher systolic blood pressure (SBP) variability reduces bioavailability of nitric oxide and increases vascular smooth muscle cell proliferation. These vascular wall changes could stiffen the arterial wall. Using data from the Multi-Ethnic Study of Atherosclerosis, we investigated the association between long-term SBP variability and ten-year percent change in arterial stiffness among 1122 individuals (mean age 57 years, 46% Males at baseline) who were not taking anti-hypertensive medications. Within-individual standard deviation (SD), variability independent of the mean (VIM), and coefficient of variation (CV) of SBP across 5 visits were used to capture long-term SBP variability. Carotid arterial stiffness was measured using distensibility coefficient (DC) and Young’s elastic modulus (YEM) at baseline and after a mean of 9.5 years of follow-up (visit 5). In a multivariate linear regression model, individuals in the 5th quintile as compared to those in the 1st quintile of SD, VIM, and CV of SBP had a 9.8% (95% CI: −17.0%, −2.7%), 6.4% (95% CI: −13.2%, 0.4%), and 8.7% (95% CI: −15.4%, −1.9%) higher decline in DC and a 27.5% (95% CI: 15.8%, 39.3%), 25.8% (95% CI: 14.7%, 36.9%), and 27.9% (95% CI: 16.8%, 39.1%) higher progression in YEM, respectively, after ten years of follow-up. Linear trends in the decline of DC and progression of YEM were observed across the quintiles of SBP variability indices. These findings suggest that higher long-term SBP variability may be a risk factor for arterial stiffness progression independent of mean BP.

This study questions the classic view that DBP is more able to identify future CVD events than SBP in all individuals younger than 50 years. In young adulthood, SBP in black individuals and DBP in white individuals were the most robust indicators of future CVD. In middle-age, SBP in both races identified risk of incident CVD.

The aims of this study are to assess the relationships of visit-to-visit blood pressure (BP) variability in young adulthood to hippocampal volume and integrity at middle age. We used data over eight examinations spanning 25 years collected in the Coronary Artery Risk Development in Young Adults (CARDIA) Study of black and white adults (age 18–30 years) started in 1985–1986. Visit-to-visit BP variability was defined as by standard deviation (SDBP) and average real variability (ARVBP, defined as the absolute differences of BP between successive BP measurements). Hippocampal tissue volume standardized by intracranial volume (%) and integrity assessed by fractional anisotropy (FA) were measured by 3-Tesla MRI at the Year 25 examination (n=545, mean age 51 years; 54% women; and 34% African Americans). Mean systolic BP (SBP)/diastolic BP (DBP) levels were 110/69 mmHg at Year 0 (baseline), 117/73 mmHg at Year 25, and ARVSBP and SDSBP were 7.7 and 7.9 mmHg, respectively. In multivariable-adjusted linear models, higher ARVSBP was associated with lower hippocampal volume (unstandardized regression coefficient [standard error] with 1 SD higher ARVSBP: −0.006 [0.003]), and higher SDSBP with lower hippocampal FA (−0.02 [0.01]; all P<0.05), independent of cumulative exposure to SBP during follow-up. Conversely, cumulative exposure to SBP and DBP was not associated with hippocampal volume. There was no interaction by sex or race between ARVSBP or SDSBP with hippocampal volume or integrity. In conclusion, visit-to-visit BP variability during young adulthood may be useful in assessing the potential risk for reductions in hippocampal volume and integrity in midlife.

Associations with antihypertensive medication classes and progression of arterial stiffness have not been studied in a prospective multi-ethnic cohort. All participants had hypertension at baseline, defined as blood pressure ≥140/90 mmHg or use of antihypertensive medications. Medication use and blood pressure were assessed at 5 time points. Young’s elastic modulus and distensibility coefficient of the right common carotid artery were obtained by ultrasound at baseline and after a mean (standard deviation) follow up period of 9.4 (0.5) years. Associations with changes in Young’s elastic modulus and distensibility coefficient, baseline antihypertensive medication use, number of visits each medication class were reported, and blood pressure control (<140/90 mmHg) were assessed using multiple linear regression models. At baseline, participants (n=1206) were mean age 63.2 (9.0) years (55% female; 35% African-American, 19% Hispanic, 12% Chinese). Mean systolic blood pressure was 136.5 (20.6) mmHg. Greater progression of arterial stiffness was associated with older age, African-American ethnicity, and baseline calcium channel blocker use. There were no other associations between changes in Young’s elastic modulus or distensibility coefficient and use of other medication classes (all p>0.4). Achieving blood pressure control (<140/90 mmHg) at all visits was associated with slower progression of arterial stiffness (Young’s elastic modulus β=−790.1 mmHg, p=0.01, distensibility coefficient: β=7.34×10−4 mmHg−1, p=0.001). Blood pressure control, rather than use of any particular antihypertensive medication class, was associated most strongly with slowing arterial stiffness progression. Over nearly a decade of follow-up, no consistent associations between any specific antihypertensive medication class and progressive carotid arterial stiffening were identified.

No abstract

Self-reported medication adherence is known to overestimate true adherence. However, little is known about patient factors that may contribute to the upward bias in self-reported medication adherence. The Objective of this study is to examine whether demographic, behavioral, medication, and mood factors are associated with being a false positive self-reported adherer (FPA) to antihypertensive drug treatment. We studied 175 patients (mean age: 50 years; 57% men) from primary care clinics starting antihypertensive drug treatment. Self-reported adherence was measured with the medication adherence report scale (MARS) and by the number of drug doses missed in the previous week/month and compared to pill count adherence (PCAR) as gold standard. Data on adherence, demographic, behavioral, medication, and mood factors were collected at baseline and every three months up to 1 year. FPA was defined as being non-adherer by PCAR and adherer by self-report. Mixed effect logistic regression was used for the analysis. Twenty percent of participants were FPA. Anxiety increased (odds ratio -OR: 3.00; P=0.01), while smoking (OR: 0.40; P=0.03), and drug side effects (OR: 0.46, P=0.03) decreased the probability for FPA by MARS. An educational below completed high school increased the probability of being a FPA as measured by missing doses in the last month (OR: 1.66; P=0.04) and last week (OR: 1.88; P=0.02). The validity of self-reported adherence varies significantly according to drug side effects, behavioral factors, and patient’s mood. Careful consideration should be given to the use of self-reported measures of adherence among patients likely to be false-positive adherers.

Elastic arteries stiffen via 2 main mechanisms: (1) load-dependent stiffening from higher blood pressure and (2) structural stiffening due to changes in the vessel wall. Differentiating these closely coupled mechanisms is important to understanding vascular aging. MESA (Multi-Ethnic Study of Atherosclerosis) participants with B-mode carotid ultrasound and brachial blood pressure at exam 1 and exam 5 (year 10) were included in this study (n=2604). Peterson and Young elastic moduli were calculated to represent total stiffness. Structural stiffness was calculated by adjusting Peterson and Young elastic moduli to a standard blood pressure of 120/80 mm Hg with participant-specific models. Load-dependent stiffness was the difference between total and structural stiffness. Changes in carotid artery stiffness mechanisms over 10 years were compared by age groups with ANCOVA models adjusted for baseline cardiovascular disease risk factors. The 75- to 84-year age group had the greatest change in total, structural, and load-dependent stiffening compared with younger groups ( P <0.05). Only age and cessation of antihypertensive medication were predictive of structural stiffening, whereas age, race/ethnicity, education, blood pressure, cholesterol, and antihypertensive medication were predictive of increased load-dependent stiffening. On average, structural stiffening accounted for the vast majority of total stiffening, but 37% of participants had more load-dependent than structural stiffening. Rates of structural and load-dependent carotid artery stiffening increased with age. Structural stiffening was consistently observed, and load-dependent stiffening was highly variable. Heterogeneity in arterial stiffening mechanisms with aging may influence cardiovascular disease development.