The main purpose of this study was to investigate the cardiovascular responses during exercise in patients with non-insulin-dependent diabetes mellitus (NIDDM)-complicated myocardial infarction (MI). There were 120 MI subjects. Sixty of them who had NIDDM (DM group) were matched with 60 non-NIDDM patients (non-DM group) for peak oxygen uptake (VO
2), age, weight, height, body mass index (BMI), creatine kinase-MB (CK-MB), and ejection fraction (EF). These patients performed cardiopulmonary exercise testing using a ramp treadmill protocol; exercise was performed 1 month after the onset of MI. VO
2, and oxygen (O
2) pulse at the anaerobic threshold (AT) were investigated to measure temporal changes in exercise tolerance. At the respiratory compensation point (RCP), tidal volume (TV) was measured as an index for pulmonary capillary wedge pressure (PCWP), end tidal CO
2 (ETCO
2) was measured as an index of reserved cardiac output, and the ventilatory equivalent for CO
2 (VE/VCO
2) was measured as an index of ventilation efficiency. There were no significant differences between the two groups with respect to EF, O
2pulse, and HR at rest. However, HR increased with regard to exercise time (defined as and HR slope). TV, and ETCO
2 at the RCP were significantly lower, and VE/VCO
2 at the RCP was significantly higher, for the DM group than for the non-DM group. No significant correlation was found between hemoglobin A1c (HbA1c) and, AT or peak VO
2. Patients with NIDDM-complicated MI had impaired submaximal cardiopulmonary responses to exercise, even while their cardiac function at rest and peak VO
2 were similar to those of the non-DM group. These findings suggest that ventilation-perfusion mismatch decreased cardiac output reserve, and increased PCWP during exercise. In addition, the non-DM group has an impaired exercise performance not associated with the degree of glycemic control provided that it is not an extremely serious case.
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