Impact of Treatment With Sacubitril/Valsartan on Erectile Dysfunction in Patients With Heart Failure With Reduced Ejection Fraction.

Sacubitril/valsartan (S/V), an angiotensin receptor-neprilysin inhibitor, has been shown to reduce the risk of cardiovascular death or heart failure hospitalization and relieve symptoms in patients with chronic heart failure with reduced ejection fraction. The objective of this study was to assess the effects of S/V on erectile dysfunction in patients with heart failure with reduced ejection fraction (HFrEF). A prospective, open-label study was conducted with 59 male patients diagnosed with HFrEF and concomitant erectile dysfunction. Patients were treated with S/V for a duration of 1 month. The International Index of Erectile Function (IIEF) questionnaire was used to assess the severity of erectile dysfunction and sexual activities at baseline and follow-up visits. Other clinical parameters, including heart rate, were also monitored. After S/V treatment, a significant improvement was observed in sexual activities at the 1-month follow-up visit. The IIEF score showed a statistically significant increase, indicating a decrease in the severity of erectile dysfunction. However, it should be noted that the numerical increase in the IIEF score did not reach clinical significance. This study suggests that S/V treatment in patients with HFrEF may lead to improvements in sexual activities and a reduction in the severity of erectile dysfunction as measured by the IIEF score.

A Breathtaking Case of Pulmonary Hypertension with Frightening Complications and Intertwining Different Etiologies.

Pulmonary hypertension (PH) is a major health problem with increasing awareness. Although most common cause of PH is left heart disease (Group 2 PH), life-threatening complications occur mostly in Group 1 (pulmonary arterial hypertension) and Group 4 (chronic thromboembolic PH) patients. Although external compression of the left main coronary artery (LMCA) due to pulmonary artery dilatation is rare, it is a life-threatening complication since it causes myocardial ischemia and sudden cardiac death. In addition, PH is more than a single clinical entity due to its complex mechanism in which more than one subgroup may develop over time in the same patient. This complex mechanism challenges us when diagnosing the patient and faces us with life-threatening complications. In this case; we report a pulmonary arterial hypertension patient applied to our clinic with progressive dyspnea and recent angina, after detection of LMCA ostial stenosis, the patient was treated with intravascular ultrasound-guided stent implantation. In the further follow-ups, the patient underwent the pulmonary endarterectomy operation due to the diagnosis of chronic thromboembolic pulmonary hypertension secondary to newly diagnosed primary antiphospholipid syndrome.

Evaluation of primary and accessory respiratory muscles and their influence on exercise capacity and dyspnea in pulmonary arterial hypertension.

BACKGROUND: Skeletal and respiratory muscle disfunction has been described in pulmonary arterial hypertension (PAH), however, involvement of accessory respiratory muscles and their association with symptomatology in PAH is unclear. OBJECTIVES: To assess the primary and accessory respiratory muscles and their influence on exercise tolerance and dyspnea. METHODS: 27 patients and 27 healthy controls were included. Serratus anterior (SA), pectoralis muscles (PM) and sternocleidomastoid (SCM) muscle strength were evaluated as accessory respiratory muscles, maximal inspiratory (MIP) and expiratory pressures (MEP) as primary respiratory muscles, and quadriceps as peripheral muscle. Exercise capacity was evaluated with 6-min walk test (6MWT), dyspnea with modified Medical Council Research (MMRC) and London Chest Activity of Daily Living (LCADL) scales. RESULTS: All evaluated muscles, except SCM, and 6MWT were decreased in patient group (p < 0.01). SA was the most affected muscle among primary and accessory respiratory muscles (Cohen's-d = 1.35). All evaluated muscles significantly correlated to 6MWT (r = 0.428-0.525). A multivariate model including SA, SCM and MIP was the best model for predicting 6MWT (R = 0.606; R2 = 0.368; p = 0.013) and SA strength had the most impact on the 6MWT (B = 1.242; ß = 0.340). None of the models including respiratory muscles were able to predict dyspnea, however PM and SA strength correlated to LCADL total (r = -0.493) and MMRC (r = -0.523), respectively. CONCLUSION: SCM may be excessively used in PAH since it retains its strength. Considering the relationship of accessory respiratory muscles with exercise tolerance and dyspnea, monitoring the strength of these muscles in the clinical practice may help providing better management for PAH.