Reduced pressure-volume response to exercise may reflect subclinical myocardial disease in type 2 diabetes

Background: The predictive value of negative exercise stressechocardiography in subjects with type 2 diabetes (T2DM) isless than in those without T2DM. A reduced end-systolic pressure-volume(SP/ESV) response may identify at risk pts, but the pathophysiologyof this finding has not been determined. We sought to identifyif the abnormal SP/ESV response reflected subclinical diabeticheart disease. Methods: Myocardial dysfunction was sought with resting andexercise echo in 168 apparently healthy T2DM (97 men, 55 ±10 y). Ischemia was excluded by ExE. Conventional data, tissuevelocity, strain and strain rate were acquired at baseline andpeak stress from 6 basal segts in conventional apical views.{Delta}SP/ESV was calculated as [(peak stress systolic blood pressure/peakstress end systolic volume index) -(rest systolic blood pressure/restend systolic volume index)]. Results: Post exercise, 83 subjects showed a {Delta}SP/ESV ≤12 mmHg/ml/m2.These patients were noted to have significantly lower restingdiastolic tissue velocity, lower peak heart rates on exerciseand poorer exercise capacity than those with {Delta}SP/ESV > 12mmHg/ml/m2 [Table]. There were no significant differences betweenthe groups in terms of age, BMI, fasting glucose and systolicstrain or strain rate. In a logistic regression model incorporatingdiastolic tissue velocity, peak heart rate and exercise capacity,all were significant univariate correlates of {Delta}SP/ESV, althoughexercise capacity was the strongest (OR= 0.88, p= 0.02). Conclusions:{Delta}SP/ESV index correlates with resting diastolictissue velocity, peak heart rate and exercise capacity, allof which have known prognostic implications in T2DM. The systolicresponse to stress may provide information analogous to thatprovided by diastolic dysfunction as a marker of subclinicaldisease. © 2009 American Heart Association, Inc

Contribution of autonomic dysfunction to abnormal exercise blood pressure in type 2 diabetes mellitus

Objectives: The purpose of this study was to compare the presence and severity of autonomic dysfunction in type 2 diabetes mellitus patients, with and without exaggerated blood pressure responses to exercise

Usefulness of at rest and exercise hemodynamics to detect subclinical myocardial disease in type 2 diabetes mellitus

Patients with type 2 diabetes mellitus (T2DM) might have subclinical myocardial dysfunction identified at rest or unmasked during exercise. We examined the correlates of the myocardial exercise response in patients with T2DM. Myocardial dysfunction was sought during at rest and exercise echocardiography in 167 healthy patients with T2DM (97 men, 55 +/- 10 years). Myocardial ischemia was excluded using stress echocardiography. Standard echocardiography and color tissue Doppler imaging measures (early diastolic tissue velocity [Em], strain, and strain rate) were acquired at baseline and peak stress. The calibrated integrated backscatter was calculated from the at rest parasternal long-axis view. The longitudinal diastolic functional reserve index after exercise was defined as Delta Em [1 - (1/Em(base))]. The clinical, anthropometric, and metabolic data were collected at rest and stress. Subclinical myocardial dysfunction at baseline (n = 24) was independently associated with weight (odds ratio [OR] 1.02, p = 0.04) and hemoglobin A1c (OR 1.36, p = 0.03). This group displayed an impaired exercise response that was independently associated with a reduced exercise capacity (OR 0.84, p = 0.034) and longitudinal diastolic functional reserve index (OR 0.69, p = 0.001). Inducible myocardial dysfunction (stress E

Reduced end-systolic pressure-volume ratio response to exercise: A marker of subclinical myocardial disease in type 2 diabetes

Background-Limitations in the predictive value of negative exercise echocardiography in type 2 diabetes mellitus has been linked to a reduced end-systolic pressure-volume response (ESPVR). We sought whether abnormal ESPVR reflected subclinical diabetic heart disease by examining the association between the ESPVR and markers of myocardial dysfunction and to establish if the change (Delta) or peak systolic blood pressure/end-systolic left ventricular volume ratio (SP/ESV) is a better marker of contractile reserve in type 2 diabetes mellitus

Biomarker and imaging responses to spironolactone in subclinical diabetic cardiomyopathy

Subclinical diabetic cardiomyopathy (DCM) is frequent in asymptomatic subjects with type 2 diabetes (T2DM). We sought the response of functional and fibrosis markers to therapy in a trial of aldosterone antagonism for treatment of DCM.Biochemical, anthropometric, and echocardiographic data were measured in 225 subjects with T2DM. Myocardial function was evaluated with standard echocardiography and myocardial deformation; ischaemia was excluded by exercise echocardiography. Calibrated integrated backscatter and post-contrast T1 mapping from cardiac magnetic resonance imaging were used to assess myocardial structure. Amino-terminal propeptides of pro-collagen type I (PINP) and III (PIIINP), the carboxy-terminal propeptide of pro-collagen type I (PICP) and transforming growth factor beta-1 were measured from peripheral blood or urine to assess myocardial collagen turnover.Diastolic dysfunction was identified in 81 individuals, of whom 49 (25 male, age 60 ± 10 years) were randomized to spironolactone 25 mg/day or placebo therapy for 6 months. Groups were well-matched at baseline. Spironolactone therapy was associated with improvements in diastolic filling profile (Δpeak E wave velocity -4 ± 15 vs. 9 ± 10 ms, P = 0.001; ΔE/A ratio -0.1 ± 0.3 vs. 0.2 ± 0.2, P < 0.001) and cIB values (-21.2 ± 4.5 dB vs. -18.0 ± 5.2 dB, P = 0.026; ΔcIB -5.1 ± 6.8 vs. -1.3 ± 5.2, P = 0.030). ΔcIB was independently associated with spironolactone therapy (β = 0.320, P = 0.026) but not Δblood pressure. With intervention, pro-collagen biomarkers (ΔPINP P = 0.92, ΔPICP P = 0.25, ΔPIIINP P = 0.52, and ΔTGF-β1 P = 0.71) and T1 values (P = 0.54) remained similar between groups.Spironolactone-induced changes in myocardial structure and diastolic properties in DCM are small, and are unassociated with changes in collagen biomarkers or T1 values