Key result
In patients with coronary artery disease, diabetes was associated with lower global left ventricular peak systolic longitudinal strain at rest (14.5% vs 17.4%; P=0.0001) and during peak stress.
Why the study?
Does diabetes reduce left ventricular longitudinal strain during dobutamine stress echocardiography in patients with significant coronary artery disease?
Cross-Sectional (n=127)
Does diabetes reduce left ventricular longitudinal strain during dobutamine stress echocardiography in patients with significant coronary artery disease?
Absolute Event Rate: 14.5% vs 17.4%
p-value: p=0.0001
Diabetes independently impairs left ventricular longitudinal strain in patients with coronary artery disease across all stages of dobutamine stress echocardiography, demonstrating a synergistic detrimental effect on myocardial function.
DM-associated strain reduction in CAD during DSE may signal additive risk; leaves open prognostic value and DSE interpretation impact.
Aims: Diabetes (DM) is a strong cardiovascular risk factor modifying also the left ventricular (LV) function that may be objectively assessed with echocardiographic strain analysis. Although the impact of isolated DM on myocardial deformation has been already studied, few data concern diabetics with coronary artery disease (CAD), especially in all stages of dobutamine stress echocardiography (DSE). We compared LV systolic function during DSE in CAD with and without DM using state-of-the art speckle-tracking quantification and assessed the impact of DM on LV systolic strain. Methods and results: DSE was performed in 250 patients with angina who afterwards had coronarography with ≥50% stenosis in the left main artery and ≥70% in other arteries considered as significant. In this analysis, we included 127 patients with confirmed CAD: 42 with DM [DM(+); mean age 64 ± 9 years] and 85 patients without DM [DM(-); mean age 63 ± 9 years]. The severity of CAD and LV ejection fraction (EF) were similar in both groups. Global and regional LV peak systolic longitudinal strain (PSLS) revealed in all DSE phases lower values in DM(+) group: 14.5 ± 3.6% vs. 17.4 ± 4.0% at rest; P = 0.0001, 13.8 ± 3.9% vs. 16.7 ± 4.0% at peak stress; P = 0.0002, and 14.2 ± 3.1% vs. 15.5 ± 3.5% at recovery; P = 0.0432 for global parameters, although dobutamine challenge did not enhance further resting differences. LV EF, body surface area, and diabetes were independent predictors for strain in 16-variable model (R2 = 0, 51, P < 0.001). Conclusion: PSLS although diminished in both groups with CAD was lower in diabetics at all DSE stages, and DM was an independent predictor of this impairment. However, the dobutamine challenge did not deepen the resting differences, suggesting that the direct impact of coronary stenoses effaces the influence of DM during DSE. The comparison with our previous data revealed synergistic, detrimental effect of coexisting CAD and DM on myocardial strain.
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Wierzbowska‐Drabik et al. (2017) conducted a cross-sectional in Coronary artery disease (n=127). Diabetes vs. No diabetes was evaluated on Global left ventricular peak systolic longitudinal strain (PSLS) at rest (p=0.0001). In patients with coronary artery disease, diabetes was associated with lower global left ventricular peak systolic longitudinal strain at rest (14.5% vs 17.4%; P=0.0001) and during peak stress.
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