Fa-Chang Yu, Cho-Kai Wu, Shih-Hsien Sung, Yen-Wen Wu, Chih-Chung Hsiao, Kai-Chun Chang, Bing-Hsiean Tzeng, Chia-Ti Tsai, Chung-Lieh Hung
Obesity-associated exertional dyspnea is a major diagnostic blind spot in contemporary heart failure care. In many patients, symptoms reflect overlapping contributions from mechanical ventilatory constraint, low cardiorespiratory fitness, regional cardiac adiposity, peripheral skeletal muscle dysfunction, and occult heart failure with preserved ejection fraction (HFpEF). Diagnosis is frequently delayed because obesity lowers natriuretic peptide concentrations, reduces the sensitivity of resting echocardiography, and overlaps with noncardiac causes of exercise intolerance. Current evidence supports obesity-related HFpEF as a distinct phenotype shaped by visceral and epicardial adiposity, maladaptive adipokine signaling, inflammation, plasma volume expansion, and abnormal exercise hemodynamics. In this context, cardiopulmonary exercise testing (CPET) is best viewed as a mechanistic phenotyping tool that helps refine suspicion, characterize the dominant physiological limitation, and guide further testing when resting evaluation is inconclusive. Emerging anti-obesity therapies have strengthened the clinical importance of recognizing obesity-related HFpEF, but whether treatment-induced benefit is accompanied by improvement in CPET-defined physiology remains uncertain.