The results of our study further strengthen the evidence that lifestyle modification and pharmacotherapy for CV risk factors are effective in improving sexual function in men with ED.

Statin therapy is associated with significant improvement in both peripheral and coronary endothelial function. The current study supports a role for statin therapy in patients with endothelial dysfunction.

Morbid obesity remains most common cause of high output failure. The prevalence of the obesity is growing when two-thirds of American adults already are overweight or obese. Obesity is the risk factor for heart disease and eventually leads to heart failure. High output heart failure is common in obese patients and is characterized by high cardiac output, decreased systemic vascular resistance, and increased oxygen consumption. It often occurs in patients with chronic severe anemia, hyperthyroidism, pregnancy, arterial-venous fistulas, and liver disease. However, the pathogenesis of obesity-related high output heart failure is not fully understood. The clinical management of obesity-related high output heart failure follows conventional heart failure regimens due to lack of specific clinical recommendations. This article reviews the possible pathophysiological mechanisms and causes that contribute to obesity-related high output heart failure. This review also focuses on the implications for clinical practice and future research involved with omics technologies to explore possible molecular pathways associated with obesity-related high output heart failure.

Background The usefulness of right heart catherization (RHC) has long been debated, and thus, we aimed to study the real‐world impact of the use of RHC in cardiogenic shock. Methods and Results In the Nationwide Readmissions Database using International Classification of Diseases, Tenth Revision ( ICD‐1 0 ), we identified 236 156 patient hospitalizations with cardiogenic shock between 2016 and 2017. We sought to evaluate the impact of RHC during index hospitalization on management strategies, complications, and outcomes as well as on 30‐day readmission rate. A total 25 840 patients (9.6%) received RHC on index admission. The RHC group had significantly more comorbidities compared with the non‐RHC group. During the index admission, the RHC group had lower death (25.8% versus 39.5%, P <0.001) and stroke rates (3.1% versus 3.4%, P <0.001). Thirty‐day readmission rates (18.7% versus 19.7%, P =0.04) and death on readmission (7.9% versus 9.3%, P =0.03) were also lower in the RHC group. After adjustment, RHC was associated with lower index admission mortality (odds ratio, 0.69; 95% CI, 0.66–0.72), lower stroke rate (odds ratio, 0.81; 95% CI, 0.72–0.90), lower 30‐day readmission (odds ratio, 0.83; 95% CI, 0.78–0.88), and higher left ventricular assist device implantations/orthotopic heart transplants (odds ratio, 6.05; 95% CI, 4.43–8.28) during rehospitalization. Results were not meaningfully different after excluding patients with cardiac arrest. Conclusions RHC use in cardiogenic shock is associated with improved outcomes and increased use of downstream advanced heart failure therapies. Further blinded randomized studies are required to confirm our findings.

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