Since the release of the "2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8)", much controversy has ensued over the appropriate systolic blood pressure goal for those over the age of 60 years. This guideline suggested liberalizing the target for this population to <150 mmHg, moving away from previous guidelines suggesting a target of <140 mmHg. While some national quality measures have accepted the new relaxed blood pressure goal, the American Heart Association and American College of Cardiology have not. Recently published data show that millions of adults over 60 years of age would be classified as controlled using a threshold of <150 mmHg, but not with a target of <140 mmHg. In addition, emerging randomized trial evidence suggests that targeting a systolic blood pressure well below 140 mmHg is beneficial in older adults. In light of the improved health and vitality of older adults, and the steady decline in cardiovascular and cerebrovascular mortality over recent decades, we do not think it is in good judgment to liberalize the treatment target in adults less than 80 years of age.

T he search for novel clinical markers in order to improve the prediction of cardiovascular disease (CVD) beyond traditional risk factors is an ongoing area of research. Whereas risk factors such as tobacco abuse, hyperlipidemia, and diabetes mellitus are currently used to calculate global CVD risk, 1 they are not equally predictive in all subgroups of race 2 and sex, 3 and they are even less reliable predictors of noncoronary vascular disease, which is more prevalent in nonwhite populations.2 This might be particularly relevant among Latinos, who are among the fastest-growing minority groups, expanding at 4 times the rate of the rest of the United States' population. 4 Although circulating inflammatory biomarkers such as high-sensitivity C-reactive protein (hs-CRP) have been shown to improve CVD risk discrimination, validation cohorts have included just 1% Latino subjects. 5 In addition, elevation in these circulating biomarkers varies significantly with race and ethnicity, 6 so their diagnostic usefulness in the Latino population remains unknown. Recently, the use of physiologic tools such as pulse-wave velocity (PWV) for estimating vascular stiffness has been shown to improve the accuracy of risk stratification. Specifically, a meta-analysis of more than 17,000 patients suggests that the addition of arterial PWV to traditional 10-year CVD risk calculation improves the net reclassification index.7 Notably, the results of this study showed improved risk categorization to the greatest degree among younger individuals and those labeled as having intermediate global risk. Reclassifying intermediate-risk patients as high-or low-risk, when measures of arterial stiffness are taken into account, therefore has potentially important implications for initiating or withholding therapeutic interventions. The role of arterial stiffness in improving CVD prediction is promising; however, to date, it has not been adequately evaluated among populations of lower socioeconomic status.

Introduction: Pulmonary hypertension (PH) was shown in multiple studies to be associated with an increased risk of mortality after transcatheter aortic valve replacement (TAVR). However, it is unclear if echocardiogram derived right ventricular systolic pressure (RVSP) is associated with health status outcomes in surviving patients after TAVR. We explored for an association between baseline RVSP and quality of life in patients before and after undergoing TAVR. Methods: We estimated RVSP by echocardiography using the modified Bernoulli equation in a single-center cohort of patients undergoing TAVR from 2012-2017 . Disease-specific health status was assessed at baseline and 1-month and 12-months after TAVR with the Kansas City Cardiomyopathy Questionnaire-Overall Summary Score (KCCQ-OS). We then explored the association between baseline RVSP and KCCQ-OS before and after TAVR using a linear mixed model with an interaction for time and baseline RVSP and adjusted for baseline mitral valve regurgitation and systolic blood pressure. Results: Among 485 patients who underwent TAVR (mean age 81.7±7.9 years, 54.8% men), baseline RVSP was 42±15 mmHg, and 73% had RVSP >34 mmHg. After TAVR, mean RVSP decreased to 37±13 mmHg at 1 month and 36±14 mmHg at 12 months. Baseline KCCQ-OS was 46±25 and improved to 66.9±23.6 at 1 month and 69.5± 22.6 at 12 months. In the linear mixed model, there was a significant cross-sectional association between baseline RVSP and baseline KCCQ-OS, with higher RVSP associated with worse health status. However, baseline RVSP was not significantly associated with KCCQ-OS at 1 month or 12 months (Figure). Conclusions: RVSP is not associated with worse health status after TAVR. This suggests that while patients with high RVSP are at an increased risk for mortality after TAVR, surviving patients appear to have similar health status as those with normal RVSP.

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