Worsening effect of testosterone deficiency on males with heart failure with preserved ejection fraction

Hamam, Ahmed; Abouomar, Mahmoud A.; Rabah, Hanem; Khattab, Haidy; Alaarag, Ahmed

doi:10.1186/s12902-022-01249-3

Cited by 2 publications

(1 citation statement)

References 43 publications

(41 reference statements)

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“…For example, the microRNA miR-181c is differentially expressed in patients with diabetes and comorbid HFpEF, and overexpression of miR-181c has been associated with proinflammatory conditions [ 42 ]. Similarly, testosterone has demonstrated anti-inflammatory effects [ 43 ], and testosterone deficiency has been associated with HFpEF in males with a cardio-metabolic profile [ 44 ]. This proinflammatory state contributes to impaired autophagy of vascular smooth muscle cells and endothelial cells, increased interstitial fibrosis, and stiff cardiomyocytes [ 39 , 45 ].…”

Section: Discussionmentioning

confidence: 99%

Obesity and metabolic syndrome in patients with heart failure with preserved ejection fraction: a cross-sectional analysis of the Veradigm Cardiology Registry

Bae,

Kallenbach,

Nelson

et al. 2024

BMC Endocr Disord

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Background The proportion of heart failure patients with preserved ejection fraction has been rising over the past decades and has coincided with increases in the prevalence of obesity and metabolic syndrome. The relationship between these interconnected comorbidities and heart failure with preserved ejection fraction (HFpEF) is still poorly understood. This study characterized obesity and metabolic syndrome among real-world patients with HFpEF. Methods We identified adults with heart failure in the Veradigm Cardiology Registry, previously the PINNACLE Registry, with a left ventricular ejection fraction measurement ≥ 50% between 01/01/2016 and 12/31/2019. Patients were stratified by obesity diagnosis and presence of metabolic syndrome (≥ 3 of the following: diabetes, hypertension, hyperlipidemia, and obesity). We captured baseline demographic and clinical characteristics and used multivariable logistic regression to examine the odds of having cardiac (atrial fibrillation, coronary artery disease, coronary artery bypass surgery, myocardial infarction, and stroke/transient ischemic attack) and non-cardiac (chronic kidney disease, chronic liver disease, and peripheral artery disease) comorbidities of interest. The models adjusted for age and sex, and the main covariates of interest were obesity and metabolic burden score (0–3 based on the presence of diabetes, hypertension, and hyperlipidemia). The models were run with and without an obesity*metabolic burden score interaction term. Results This study included 264,571 patients with HFpEF, of whom 55.7% had obesity, 52.5% had metabolic syndrome, 42.5% had both, and 34.3% had neither. After adjusting for age, sex, and burden of other metabolic syndrome-associated diagnoses, patients with HFpEF with obesity had lower odds of a diagnosis of other evaluated comorbidities relative to patients without obesity. The presence of metabolic syndrome in HFpEF appears to increase comorbidity burden as each additional metabolic syndrome-associated diagnosis was associated with higher odds of assessed comorbidities except atrial fibrillation. Conclusion Obesity was common among patients with HFpEF and not always co-occurring with metabolic syndrome. Multivariable analysis suggested that patients with obesity may develop HFpEF in the absence of other driving factors such as cardiovascular disease or metabolic syndrome.

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