Key result
Comorbid type 2 diabetes in HFpEF is linked to ~23% lower peak VO2.
Why the study?
Exercise capacity and its predictors in HFpEF patients with comorbid type 2 diabetes mellitus remain not clearly understood.
Does comorbid T2DM reduce exercise capacity and hemodynamic response in patients with HFpEF?
Case-Control (n=149)
No
Does comorbid T2DM reduce exercise capacity and hemodynamic response in patients with HFpEF?
Absolute Event Rate: 11.6% vs 15.1%
p-value: p=<0.001
Comorbid T2DM in patients with HFpEF is associated with significantly reduced exercise capacity, heart rate response, and peripheral oxygen extraction compared to HFpEF without T2DM.
Comorbid T2DM may further impair exercise capacity in HFpEF; hypothesis-generating for targeted interventions.
Background Type 2 diabetes mellitus (T2DM) is a frequently observed complication in patients with heart failure with preserved ejection fraction (HFpEF). Although a characteristic finding in such patients is a decrease in objective exercise capacity represented by peak oxygen uptake (peakVO 2 ), exercise capacity and its predictors in HFpEF with T2DM remain not clearly understood. This case–control study aimed to investigate the association between exercise capacity and hemodynamics indicators and T2DM comorbidity in patients with HFpEF aged 65–80 years. Methods Ninety-nine stable outpatients with HFpEF and 50 age-and-sex-matched controls were enrolled. Patients with HFpEF were classified as HFpEF with T2DM (n = 51, median age, 76 years) or without T2DM (n = 48, median age, 76 years). The peakVO 2 and ventilatory equivalent versus carbon dioxide output slope (VE vs VCO 2 slope) were measured by cardiopulmonary exercise testing. The peak heart rate (HR) and peak stroke volume index (SI) were measured using impedance cardiography, and the estimated arteriovenous oxygen difference (peak a-vO 2 diff) was calculated with Fick's equation. The obtained data were compared among the three groups using analysis of covariance adjusted for the β-blocker medication, presence or absence of sarcopenia, and hemoglobin levels in order to determine the T2DM effects on exercise capacity and hemodynamics in patients with HFpEF. Results In HFpEF with T2DM compared with HFpEF without T2DM and the controls, the prevalence of sarcopenia, chronotropic incompetence, and anemia were significantly higher (p < 0.001). The peakVO 2 (Controls 23.5 vs. without T2DM 15.1 vs. with T2DM 11.6 mL/min/kg), peak HR (Controls 164 vs. without T2DM 132 vs. with T2DM 120 bpm/min), peak a-vO 2 (Controls 13.1 vs without T2DM 10.6 vs with T2DM 8.9 mL/100 mL), and VE vs VCO 2 slope (Controls 33.2 vs without T2DM 35.0 vs with T2DM 38.2) were significantly worsened in patients with HFpEF with T2DM (median, p < 0.001). There was no significant difference in peak SI among the three groups. Conclusions Our results suggested that comorbid T2DM in patients with HFpEF may reduce exercise capacity, HR response, peripheral oxygen extraction, and ventilation efficiency. These results may help identify cardiovascular phenotypes of HFpEF complicated with T2DM and intervention targets for improving exercise intolerance.
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Sugita et al. (2023) conducted a case-control in Heart failure with preserved ejection fraction (HFpEF) (n=149). Type 2 diabetes mellitus (T2DM) comorbidity vs. HFpEF without T2DM and healthy controls was evaluated on Peak oxygen uptake (peakVO2) in mL/min/kg (p=<0.001). Comorbid type 2 diabetes in patients with HFpEF significantly reduced peak oxygen uptake to 11.6 mL/min/kg compared to 15.1 mL/min/kg in those without diabetes.
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