PMID- 36529735 OWN - NLM STAT- MEDLINE DCOM- 20230106 LR - 20230106 IS - 1472-6823 (Electronic) IS - 1472-6823 (Linking) VI - 22 IP - 1 DP - 2022 Dec 19 TI - Worsening effect of testosterone deficiency on males with heart failure with preserved ejection fraction. PG - 321 LID - 10.1186/s12902-022-01249-3 [doi] LID - 321 AB - BACKGROUND: Heart failure with preserved ejection fraction (HFpEF)is challenging. Patients usually have normal LV size and ejection fraction. This clinical syndrome develops from a complex interaction of several risk factors that cause organ dysfunction and clinical symptoms. There's evidence that testosterone deficiency is associated with a worse cardiometabolic profile and increased inflammatory markers. We thought that these changes might have an impact on heart failure pathogenesis. We aimed to study the relationship between testosterone level and symptoms in HFpEF. METHODS: We studied 120 male patients with HFpEF. According to New York Heart Association (NYHA), patients were classified into I, II and III classes; class IV patients were excluded. All patients were subjected to clinical and echocardiographic examinations. In addition, we measured serum testosterone, cardio-metabolic profile, intracellular adhesive molecule-1(ICAM-1), P-selectin and nitric oxide (NO) levels. RESULTS: Patients with testosterone deficiency had worse NYHA class and higher BNP P = (0.001). Additionally, they had a significantly worse metabolic profile; higher total cholesterol, triglycerides, LDL cholesterol, fasting insulin and HOMA-IR P = (0.005, 0.001, 0.001, 0.001), respectively. Also, they had higher inflammatory markers and worse endothelial functional parameters; (ICAM-1, NO and P- selectin) P = (0.001). Age, BNP and testosterone deficiency can be used as independent predictors of NYHA class III symptoms with a Testosterone cutoff value of 2.7 ng/ml. CONCLUSION: Testosterone deficiency could be used as an independent predictor of symptom severity in HFpEF, and it aggravates systemic inflammation and endothelial dysfunction in these patients. CI - (c) 2022. The Author(s). FAU - Hamam, Ahmed AU - Hamam A AD - Department of internal medicine, Armed Forces College of Medicine, Cairo, Egypt. FAU - Abou-Omar, Mahmoud AU - Abou-Omar M AD - Cardiovascular medicine department, Faculty of Medicine, Tanta University, Tanta, 31511, Egypt. FAU - Rabah, Hanem AU - Rabah H AD - Faculty of Medicine, Department of medical biochemistry, Tanta University, Tanta, Egypt. FAU - Khattab, Haidy AU - Khattab H AD - Faculty of Medicine Department of medical physiology, Tanta University, Tanta, Egypt. FAU - Alaarag, Ahmed AU - Alaarag A AD - Cardiovascular medicine department, Faculty of Medicine, Tanta University, Tanta, 31511, Egypt. ahmed.elaarag@med.tanta.edu.eg. LA - eng PT - Journal Article DEP - 20221219 PL - England TA - BMC Endocr Disord JT - BMC endocrine disorders JID - 101088676 RN - 126547-89-5 (Intercellular Adhesion Molecule-1) RN - 3XMK78S47O (Testosterone) SB - IM MH - Humans MH - Male MH - Echocardiography MH - *Heart Failure/physiopathology MH - Intercellular Adhesion Molecule-1 MH - Stroke Volume MH - *Testosterone/deficiency PMC - PMC9761962 OTO - NOTNLM OT - HFpEF OT - NYHA class OT - Testosterone COIS- We do not have any conflict of interest to declare. EDAT- 2022/12/19 06:00 MHDA- 2022/12/21 06:00 PMCR- 2022/12/19 CRDT- 2022/12/18 23:14 PHST- 2022/04/21 00:00 [received] PHST- 2022/12/12 00:00 [accepted] PHST- 2022/12/18 23:14 [entrez] PHST- 2022/12/19 06:00 [pubmed] PHST- 2022/12/21 06:00 [medline] PHST- 2022/12/19 00:00 [pmc-release] AID - 10.1186/s12902-022-01249-3 [pii] AID - 1249 [pii] AID - 10.1186/s12902-022-01249-3 [doi] PST - epublish SO - BMC Endocr Disord. 2022 Dec 19;22(1):321. doi: 10.1186/s12902-022-01249-3.