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Purpose: Diabetes mellitus (DM) is associated with long-term cardiovascular complications, including ischemic heart disease (IHD). Nonetheless, DM may directly impair myocardial and lung structure and function. The aim of this study was to assess the impact of type 2 DM (T2DM) and glycemic control on cardiopulmonary exercise capacity in patients with IHD. Methods: The study involved a cross-sectional analysis of 91 consecutive patients (57 ± 10 yr, 90% men) who underwent a cardiopulmonary exercise test at the beginning of an exercise-based standard phase-II cardiac rehabilitation program, 2 to 3 mo after an acute coronary syndrome. Association of T2DM with cardiopulmonary exercise test parameters was assessed using multiple linear regression analysis controlling for prespecified potential confounders. Results: There were 26 (29%) diabetic subjects among IHD patients included in the study. After adjustment, T2DM was an independent predictor of a reduced peak oxygen uptake ( JOURNAL/jcprh/04.03/01273116-202005000-00006/6FSM1/v/2023-09-11T074857Z/r/image-gif o 2peak) (P = .005), a reduced pulse O2 trajectory (P = .001), a steeper minute ventilation to carbon dioxide output (VE/ JOURNAL/jcprh/04.03/01273116-202005000-00006/6FSM1/v/2023-09-11T074857Z/r/image-gif co 2) slope (P = .046), and an increased dead space-to-tidal volume ratio (VD/VT) at peak exercise (P = .049). Glycated hemoglobin (HbA1c) levels were significantly associated with a reduced forced expiratory volume in the first second of expiration (FEV1) (P = .013), VE (P = .001), and VT (P = .007). JOURNAL/jcprh/04.03/01273116-202005000-00006/6FSM1/v/2023-09-11T074857Z/r/image-gif o 2peak (P trend < .001), JOURNAL/jcprh/04.03/01273116-202005000-00006/6FSM1/v/2023-09-11T074857Z/r/image-gif o 2 at anaerobic threshold (P trend < .001), and pulse O2 trajectory (P trend < .001) decreased among HbA1c tertiles. Conclusions: Patients with IHD and a previous diagnosis of T2DM had a reduced aerobic capacity and a ventilation- perfusion mismatch compared with nondiabetic patients. Poor glycemic control in men further deteriorates aerobic capacity probably due to ventilatory inefficiency.

BackgroundSmoking has been associated with poorer outcomes in relation to COVID-19. Smokers have higher risk of mortality and have a more severe clinical course. There is paucity of data available on this issue, and a definitive link between smoking and COVID-19 prognosis has yet to be established.MethodsWe included 5224 patients with COVID-19 with an available smoking history in a multicentre international registry Health Outcome Predictive Evaluation for COVID-19 (NCT04334291). Patients were included following an in-hospital admission with a COVID-19 diagnosis. We analysed the outcomes of patients with a current or prior history of smoking compared with the non-smoking group. The primary endpoint was all-cause in-hospital death.ResultsFinally, 5224 patients with COVID-19 with available smoking status were analysed. A total of 3983 (67.9%) patients were non-smokers, 934 (15.9%) were former smokers and 307 (5.2%) were active smokers. The median age was 66 years (IQR 52.0–77.0) and 58.6% were male. The most frequent comorbidities were hypertension (48.5%) and dyslipidaemia (33.0%). A relevant lung disease was present in 19.4%. In-hospital complications such sepsis (23.6%) and embolic events (4.3%) occurred more frequently in the smoker group (p<0.001 for both). All cause-death was higher among smokers (active or former smokers) compared with non-smokers (27.6 vs 18.4%, p<0.001). Following a multivariate analysis, current smoking was considered as an independent predictor of mortality (OR 1.77, 95% CI 1.11 to 2.82, p=0.017) and a combined endpoint of severe disease (OR 1.68, 95% CI 1.16 to 2.43, p=0.006).ConclusionSmoking has a negative prognostic impact on patients hospitalised with COVID-19.

Background Glycemic control, even in non-diabetes mellitus (DM) patients, has been associated with ventilation pump inefficiency leading to an impaired aerobic capacity. Brain natriuretic peptide (BNP) levels have also been correlated with exercise capacity, particularly in patients with heart failure. Purpose Assess the complementary impact of glycated haemoglobin (HbA1c) and BNP levels on cardiopulmonary exercise capacity in patients with ischemic heart disease (IHD). Methods Retrospecive cohort of 91 consecutive patients (57±10 years, 90% men; 29% type 2 DM) who underwent a cardiopulmonary exercise testing (CPX) at the beginning of an standard phase-II cardiac rehabilitation program, 2–3 months after an acute coronary syndrome. Results HbA1c and BNP levels correlated with peak oxygen uptake (VO2), anaerobic threshold (AT) and pulse O2 trajectory (Table). HbA1c correlated with ventilation CPX parameters (Table) and independently predicted minute ventilation (VE) and tidal volume (VT), regardless of age, waist circumference and β-blocker therapy. BNP levels correlated with echocardiographic (LVEF, left atrium size and pulmonary artery systolic pressure) and ventilation-perfusion (V/Q) mismatch parameters (Table), and independently predicted VE/VCO2-slope (P=0.037) regardless of age, echocardiographic parameters and β-blocker therapy. Patients were divided into three groups according to HbA1c levels above or below the DM diagnosis cut-off point (6.5%) and median value of BNP levels (44.6 pg/mL). VO2 and AT significantly decreased with elevated HbA1c and/or BNP levels (Figure). CPX parameters HbA1c (%) BNP (pg/mL) r P value r P value Peak VO2 (mL/min/kg) −0.421 <0.001 −0.295 0.005 VO2 at AT (mL/min/kg) −0.352 0.001 −0.271 0.009 O2 pulse trajectory (mL/beat) −0.345 0.001 −0.235 0.025 Minute ventilation (VE) (L/min)* −0.377 <0.001 – NS Tidal volume (VT) (L)* −0.348 0.001 – NS VE/VCO2-slope – NS 0.375 <0.001 PETCO2 at AT (mmHg) – NS −0.315 0.002 HR/VO2-slope – NS 0.307 0.003 *At peak exercise. NS: Non-significant. Conclusions HbA1c and BNP levels were associated with a reduced cardiopulmonary capacity in IHD patients, mediated by a ventilation impairment and a ventilation-perfusion mismatching, respectively. HbA1c and BNP are independent and additive predictors of cardiopulmonary capacity.