Hypertension as a Road to Treatment of Heart Failure with Preserved Ejection Fraction.

PURPOSE OF REVIEW: Hypertension heralds the diagnosis of heart failure (HF) with preserved ejection fraction (HFpEF) in 75-85% of cases and shares many of its adverse outcomes as well as its acute and chronic symptoms. This review provides important new data about the pathophysiology and mechanisms that connect hypertension and HFpEF as well as therapy used in both conditions. RECENT FINDINGS: The traditional model of HFpEF pathophysiology emphasizes the role of hypertension causing increased afterload on the left ventricle (LV), leading to LV hypertrophy (LVH) and subsequent LV diastolic dysfunction. Recent work has provided valuable insights into the mechanisms underlying the transition from hypertension to HFpEF, showing that the pathophysiology extends beyond LVH and diastolic dysfunction. An evolving paradigm suggests that HFpEF is inflammatory in nature with multifactorial pathophysiology, affected by age-related changes and comorbidities. Hypertension shares many of the proinflammatory mechanisms of HFpEF. Furthermore, hypertension precedes HFpEF in the majority of cases. Because of its clinically heterogeneous nature, development of standardized therapies for HFpEF has been challenging. As there are standardized approaches to hypertension, we suggest that similar approaches be used for the treatment of HFpEF, including medical and non-medical therapies. With medical therapies, a treat-to-target blood pressure (BP) strategy could be employed, such as systolic BP < 130 mmHg. With non-medical therapies, approaches to deal with physical inactivity, obesity, and sleep apnea could be used. Due to its heterogeneity, delineation of standardized therapies for HFpEF has been challenging. Focusing on the tremendous overlap of hypertensive heart disease with HFpEF, it is proposed that approaches currently used to guide therapies for hypertension be applied to the treatment of HFpEF.

Preoperative sleep apnea screening protocol reduces medical emergency team activation in patients with atrial fibrillation.

STUDY OBJECTIVES: The association of in-hospital medical emergency team activation (META) among patients with atrial fibrillation (AF) at risk for obstructive sleep apnea (OSA) is unclear. This study evaluates the performance of the DOISNORE50 sleep questionnaire as an OSA screener for patients with AF and determines the prevalence of META among perioperative patients with underlying AF who have a diagnosis or are at risk for OSA. METHODS: A prospective perioperative cohort of 2,926 patients with the diagnosis of AF was assessed for DOISNORE50 questionnaire screening. Propensity-score matching was used to match patients' physical characteristics, comorbidities, length of stay, and inpatient continuous positive airway pressure device usage. META and intensive care unit admissions during the surgical encounter, 30-day hospital readmissions, and 30-day emergency department visits were evaluated. RESULTS: A total of 1,509 out of 2,926 AF patients completed the DOISNORE50 questionnaire and were enrolled in the OSA safety protocol. Following propensity-score matching, there were reduced adjusted odds of META in the screened group of 0.69 (95% confidence interval: 0.48-0.98, P < .001) in comparison to the unscreened group. The adjusted odds of intensive care unit admissions and emergency department visits within 30 days of discharge were statistically lower for the screened group compared with the unscreened group. CONCLUSIONS: Among perioperative AF patients, evidence supports DOISNORE50 screening and implementation of an OSA safety protocol for reduction of META. This study identified decreased odds of META, intensive care unit admissions, and emergency department visits among the screened group. The high-risk and known OSA group showed reduced odds of META following the implementation of an OSA safety protocol. CITATION: Saha AK, Sheehan KN, Xiang KR, et al. Preoperative sleep apnea screening protocol reduces medical emergency team activation in patients with atrial fibrillation. J Clin Sleep Med. 2024;20(5):783-792.

Serum Cotinine and Silent Myocardial Infarction in Individuals Free from Cardiovascular Disease.

Serum cotinine is a sensitive and specific marker of tobacco exposure, including second-hand smoke exposure. We sought to explore the association of tobacco exposure determined by serum cotinine with electrocardiographic silent myocardial infarction (SMI). A total of 7,006 participants (59.0 ± 13.3 years; 52.6% women, 49.7% non-Hispanic whites) without cardiovascular disease from the Third National Health and Nutrition Examination Survey (NHANES III) were included in this analysis. SMI was defined as electrocardiographic evidence of MI in the absence of a history of MI. Multivariable logistic regression analysis was used to examine the association between SMI and serum cotinine tertiles. SMI was detected in 114 (1.63%) of the participants. The prevalence of SMI was higher among those with higher levels of serum cotinine (SMI prevalence was 1.25%, 1.49%, and 2.14% across serum cotinine lower [0.03 to 0.12 ng/ml], middle [0.12 to 1.39 ng/ml], and higher [1.40 to 1890 ng/ml] tertiles, respectively). In a model adjusted for potential confounders, participants within the highest serum cotinine tertile had significantly greater odds of SMI (odds ratio [95% confidence interval]: 2.51 [1.55 to 4.08]) compared with those with serum cotinine levels in the first tertile. Each 10 ng/ml increase in serum cotinine levels was associated with a 2% (p <0.0001) increase in the prevalence of SMI. This association was stronger in white than nonwhite participants (interaction p value = 0.05). In conclusion, elevated serum cotinine levels are associated with SMI. These findings further highlight the risk associated with passive and active smoking on cardiovascular health and underscore the potential utility of serum cotinine in identifying those at risk.