[Air pollution, noise and hypertension : Partners in crime]. / Luftverschmutzung, Lärm und Hypertonie : Komplizen im Verbrechen.

Air pollution and traffic noise are two important environmental risk factors that endanger health in urban societies and often act together as "partners in crime". Although air pollution and noise often co-occur in urban environments, they have typically been studied separately, with numerous studies documenting consistent effects of individual exposure on blood pressure. In the following review article, we examine the epidemiology of air pollution and noise, especially regarding the cardiovascular risk factor arterial hypertension and the underlying pathophysiology. Both environmental stressors have been shown to lead to endothelial dysfunction, oxidative stress, pronounced vascular inflammation, disruption of circadian rhythms and activation of the autonomic nervous system, all of which promote the development of hypertension and cardiovascular diseases. From a societal and political perspective, there is an urgent need to point out the potential dangers of air pollution and traffic noise in the American Heart Association (AHA)/American College of Cardiology (ACC) prevention guidelines and the European Society of Cardiology (ESC) guidelines on prevention. Therefore, an essential goal for the future is to raise awareness of environmental risk factors as important and, in particular, preventable risk factors for cardiovascular diseases.

Etiologies and predictors of mortality in an all-comer population of patients with non-ischemic heart failure.

BACKGROUND: Despite progress in diagnosis and therapy of heart failure (HF), etiology and risk stratification remain elusive in many patients. METHODS: The My Biopsy HF Study (German clinical trials register number: DRKS22178) is a retrospective monocentric study investigating an all-comer population of patients with unexplained HF based on a thorough workup including endomyocardial biopsy (EMB). RESULTS: 655 patients (70.9% men, median age 55 [45/66] years) with non-ischemic, non-valvular HF were included in the analyses. 489 patients were diagnosed with HF with reduced ejection fraction (HFrEF), 52 patients with HF with mildly reduced ejection fraction (HFmrEF) and 114 patients with HF with preserved ejection fraction (HFpEF). After a median follow-up of 4.6 (2.5/6.6) years, 94 deaths were enumerated (HFrEF: 68; HFmrEF: 8; HFpEF: 18), equating to mortality rates of 3.3% and 11.6% for patients with HFrEF, 7.7% and 15.4% for patients with HFmrEF and 5.3% and 11.4% for patients with HFpEF after 1 and 5 years, respectively. In EMB, we detected a variety of putative etiologies of HF, including incidental cardiac amyloidosis (CA, 5.8%). In multivariate logistic regression analysis adjusting for age, sex and comorbidities only CA, age and NYHA functional class III + IV remained independently associated with all-cause mortality (CA: HRperui 3.13, 95% CI 1.5-6.51; p = 0.002). CONCLUSIONS: In an all-comer population of patients presenting with HF of unknown etiology, incidental finding of CA stands out to be independently associated with all-cause mortality. Our findings suggest that prospective trials would be helpful to test the added value of a systematic and holistic work-up of HF of unknown etiology.