Background: Marijuana use is increasing in the United States, and its effect on cardiovascular health is unknown. Purpose: To review harms and benefits of marijuana use in relation to cardiovascular risk factors and clinical outcomes. Data Sources: PubMed, MEDLINE, EMBASE, PsycINFO, and the Cochrane Library between 1 January 1975 and 30 September 2017. Study Selection: Observational studies that were published in English, enrolled adults using any form of marijuana, and reported on vascular risk factors (hyperglycemia, diabetes, dyslipidemia, and obesity) or on outcomes (stroke, myocardial infarction, cardiovascular mortality, and all-cause mortality in cardiovascular cohorts). Data Extraction: Study characteristics and quality were assessed by 4 reviewers independently; strength of evidence for each outcome was graded by consensus. Data Synthesis: 13 and 11 studies examined associations between marijuana use and cardiovascular risk factors and clinical outcomes, respectively. Although 6 studies suggested a meta bolic benefit from marijuana use, they were based on cross-sectional designs and were not supported by prospective studies. Evidence examining the effect of marijuana on diabetes, dyslipidemia, acute myocardial infarction, stroke, or cardiovascular and all-cause mortality was insufficient. Although the current literature includes several long-term prospective studies, they are limited by recall bias, inadequate exposure assessment, minimal marijuana exposure, and a predominance of low-risk cohorts. Limitation: Poor- or moderate-quality data, inadequate assessment of marijuana exposure and minimal exposure in the populations studied, and variation in study design. Conclusion: Evidence examining the effect of marijuana on cardiovascular risk factors and outcomes, including stroke and myocardial infarction, is insufficient. Primary Funding Source: National Heart, Lung, and Blood Institute. (PROSPERO: CRD42016051297)

Atrial arrhythmias, including atrial fibrillation and atrial flutter, are common in patients with pulmonary hypertension and are closely associated with clinical decompensation and poor clinical outcomes. The mechanisms of arrhythmogenesis and subsequent clinical decompensation are reviewed. Practical implications and current evidence for the management of atrial arrhythmias in patients with pulmonary hypertension are summarised.

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Heart failure with preserved ejection fraction (HFpEF) is a prevalent but incompletely understood syndrome. Traditional models of HFpEF pathophysiology revolve around systemic HTN and other causes of increased left ventricular afterload leading to left ventricular hypertrophy (LVH) and diastolic dysfunction. However, emerging models attribute the development of HFpEF to systemic proinflammatory changes secondary to common comorbidities which include HTN. Alterations in passive ventricular stiffness, ventricular-arterial coupling, peripheral microvascular function, systolic reserve, and chronotropic response occur. As a result, HFpEF is heterogeneous in nature, making it difficult to prescribe uniform therapies to all patients. Nonetheless, treating systemic HTN remains a cornerstone of HFpEF management. Antihypertensive therapies have been linked to LVH regression and improvement in diastolic dysfunction. However, to date, no therapies have definitive mortality benefit in HFpEF. Non-pharmacologic management for HTN, including dietary modification, exercise, and treating sleep disordered breathing, may provide some morbidity benefit in the HFpEF population. Future research is need to identify effective treatments, perhaps in more specific subgroups, and focus may need to shift from reducing mortality to improving exercise capacity and symptoms. Tailoring antihypertensive therapies to specific phenotypes of HFpEF may be an important component of this strategy.

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Background: Racial disparities in access to advanced therapies for heart failure (HF) patients are well documented, although the reasons remain uncertain. We sought to determine the association of race on utilization of ventricular assist device (VAD) and transplant among patients with access to care at VAD centers and if patient preferences impact the effect. Methods: We performed an observational cohort study of ambulatory chronic systolic HF patients with high-risk features and no contraindication to VAD enrolled at 21 VAD centers and followed for 2 years in the REVIVAL study (Registry Evaluation of Vital Information for VADs in Ambulatory Life). We used competing events cause-specific proportional hazard methodology with multiple imputation for missing data. The primary outcomes were (1) VAD/transplant and (2) death. The exposures of interest included race (Black or White), additional demographics, captured social determinants of health, clinician-assessed HF severity, patient-reported quality of life, preference for VAD, and desire for therapies. Results: The study included 377 participants, of whom 100 (26.5%) identified as Black. VAD or transplant was performed in 11 (11%) Black and 62 (22%) White participants, although death occurred in 18 (18%) Black and 36 (13%) White participants. Black race was associated with reduced utilization of VAD and transplant (adjusted hazard ratio, 0.45 [95% CI, 0.23–0.85]) without an increase in death. Preferences for VAD or life-sustaining therapies were similar by race and did not explain racial disparities. Conclusions: Among patients receiving care by advanced HF cardiologists at VAD centers, there is less utilization of VAD and transplant for Black patients even after adjusting for HF severity, quality of life, and social determinants of health, despite similar care preferences. This residual inequity may be a consequence of structural racism and discrimination or provider bias impacting decision-making. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01369407.

The role of adventitia-derived reactive oxygen species (ROS) in vascular disease and impaired vascular relaxation is not clear. Based on robust adventitial ROS generation and effects on MAPK involvement in vascular dysfunction, we hypothesized that adventitia-derived ROS hydrogen peroxide (H(2)O(2)) impairs vascular relaxation through activation of medial smooth muscle p38 MAPK. By using a novel in vivo model, the adventitial surface of rat carotid arteries was bathed in situ for 90 min with vehicle, angiotensin II (AngII; 500 nM), AngII+H(2)O(2)-scavenger catalase (3,000 U/ml), AngII+p38 MAPK inhibitor SB203580 (10 μM), or AngII+superoxide dismutase (SOD; 150 U/ml). After these in vivo treatments, ex vivo tone measurements on isolated vessels revealed that periadventitial application of AngII impaired both acetylcholine-induced (endothelium-dependent) and sodium nitroprusside-induced (endothelium-independent) relaxations. In vivo coincubation with catalase or SB203580 significantly improved, but SOD exacerbated AngII-induced impairment of in vitro endothelium-dependent and -independent vascular relaxations. Western blots of vascular media, separated from the adventitia, demonstrated increased medial p38 MAPK activation and decreased medial phosphatase SHP-2 activity in AngII-treated vessels. These effects were reversed by in vivo periadventitial addition of catalase. These findings provide the first evidence that adventitia-derived H(2)O(2) participates in vascular dysfunction through p38 MAPK activation and SHP-2 inhibition.

Patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) have low levels of physical activity (PA). Increased PA has health benefits including improved quality of life. This study aimed to identify patient-perceived barriers to PA that correlate with objectively measured PA in this population. We performed a cross-sectional survey of 40 patients with PAH and CTEPH. Participants rated how often 15 barriers interfere with being physically active on a 5-point Likert Scale. The primary outcome measure was PA quantified using the Fitbit Zip activity tracker for two weeks. The primary independent variables were the 15 barriers and a summary score (total average barriers). Separate multivariable linear regressions were performed to assess the association between the 15 barriers and the summary score and PA adjusting for age, sex, and PAH etiology. Of the participants, 85% (34/40) had valid step counts and were included. Of these 34, 85% (n = 29) were female and 91% (n = 31) had PAH. The median (interquartile range [IQR]) number of daily steps was 3913 (2309–6313). The barriers endorsed most strongly were lack of self-discipline, lack of energy, and lack of interest. In the multivariable analysis, a 1-unit increase in perceived lack of interest, lack of enjoyment, and lack of skills was associated with a significant decrease in step counts of -1414 steps (95% confidence interval [CI] = (−2580 – −248), −1458 steps (−2404 – −511), and −1533 steps (−2910 – −156), respectively. Counseling and interventions aimed at increasing PA in patients with PAH should address interest, enjoyment, and skill development.