The majority of older patients who develop heart failure (HF), particularly older women, have a preserved left ventricular ejection fraction (HFpEF). Patients with HFpEF have severe symptoms of exercise intolerance, poor quality‐of‐life, frequent hospitalizations, and increased mortality. The prevalence of HFpEF is increasing and its prognosis is worsening. However, despite its importance, our understanding of the pathophysiology of HFpEF is incomplete, and drug development has proved immensely challenging. Currently, there are no universally accepted therapies that alter the clinical course of HFpEF. Originally viewed as a disorder due solely to abnormalities in left ventricular (LV) diastolic function, our understanding has evolved such that HFpEF is now understood as a systemic syndrome, involving multiple organ systems, likely triggered by inflammation and with an important contribution of aging, lifestyle factors, genetic predisposition, and multiple‐comorbidities, features that are typical of a geriatric syndrome. HFpEF is usually progressive due to complex mechanisms of systemic and cardiac adaptation that vary over time, particularly with aging. In this review, we examine evolving data regarding HFpEF that may help explain past challenges and provide future directions to care patients with this highly prevalent, heterogeneous clinical syndrome.

Active smoking is a widely accepted risk factor for cardiovascular disease and is recognized as a major public health problem. Passive smoking, also known as secondhand smoke exposure (SHSE), is thought to have similar cardiovascular consequences and the risk has been postulated to be equivalent to that of active smoking. A major component of this risk involves the connection with chronic hypertension. There are several population-based observational studies investigating the relationship between SHSE and chronic hypertension, all of which demonstrate a positive association. Given that SHSE appears to be a risk factor for chronic hypertension, SHSE should also be a risk factor for hypertensive end-organ disease. Many studies have sought to investigate this relationship, but this has yet to be fully elucidated. In this review, we focus on the current evidence regarding the association between SHSE and hypertension as well as exploration of the links between SHSE and hypertensive end-organ damage.

Purpose of Review We reviewed the effects of hypertension and the means to prevent and treat it across the spectrum of a woman’s lifespan and identified gaps in sex-specific mechanisms contributing to hypertension in women that need to be addressed. Recent Findings Hypertension continues to be an important public health problem for women across all life stages from adolescence through pregnancy, menopause, and older age. There remain racial, ethnic, and socioeconomic differences in hypertension rates not only overall but also between the sexes. Blood pressure cutoffs during pregnancy have not been updated to reflect the 2017 ACC/AHA changes due to a lack of data. Additionally, the mechanisms behind hypertension development in menopause, including sex hormones and genetic factors, are not well understood. Summary In the setting of increasing inactivity and obesity, along with an aging population, hypertension rates are increasing in women. Screening and management of hypertension throughout a women’s lifespan are necessary to reduce the burden of cardiovascular disease, and further research to understand sex-specific hypertension mechanisms is needed.

In a subgroup of 337 participants (mean age 64±9 years; 45% women) from the SPRINT (Systolic Blood Pressure Intervention Trial), where participants were randomly assigned to intensive treatment (target systolic blood pressure <120 mm Hg) versus standard treatment (<140 mm Hg), we examined the effect of intensive blood pressure lowering on indexes of aortic stiffness. Carotid-femoral pulse wave velocity, a validated global measure of aortic stiffness, was measured by echo-guided Doppler at baseline and 18-month follow-up visit. Aortic elastance, distensibility, and compliance were measured by cardiac magnetic resonance imaging. During follow-up, the intensive treatment produced a mean between-group reduction in systolic blood pressure of 12.7 mm Hg (95% CI, 11.1–14.3 mm Hg). During follow-up, intensive treatment significantly attenuated the increase in carotid-femoral pulse wave velocity compared with standard treatment (adjusted follow-up least square mean=9.0 m/s [95% CI, 8.7–9.3] versus 10.0 m/s [9.6–10.3]; P <0.001), an effect that persisted even after adjusting for mean arterial pressure. Intensive treatment also decreased the aortic elastance index (least square mean, 1.38 mm Hg/mL per m ² [95% CI, 1.34–1.41] versus 1.48 mm Hg/mL per m ² [95% CI, 1.44–1.51], P =0.002) compared with standard treatment. No significant between-group differences were observed for aortic distensibility and compliance. We conclude that intensive treatment significantly attenuated increases in carotid-femoral pulse wave velocity and aortic elastance index. Attenuation of increases in aortic stiffness may be one of the mechanisms contributing to the benefit of intensive blood pressure treatment observed in SPRINT. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01206062.