Key result
Stenotic CAD linked to ~7% lower early diastolic strain rate, indicating subtle myocardial dysfunction.
Why the study?
Identification of the transmural extent of myocardial necrosis and degree of non-viability after acute myocardial infarction is clinically important but challenging with current methods.
Does resting segmental strain rate imaging differentiate patients with stenotic coronary artery disease from those without CAD among individuals with chronic chest pain?
Observational (n=598)
No
Does resting segmental strain rate imaging differentiate patients with stenotic coronary artery disease from those without CAD among individuals with chronic chest pain?
Answers are grounded in this paper and cite their sources.
Resting segmental early diastolic strain rate (SRe) can identify subtle regional myocardial dysfunction in patients with stable CAD, offering better discriminatory value than global longitudinal strain.
OBJECTIVES: The aim of this study was to determine if strain rate imaging (SRI) correlates with the transmural extent of myocardial infarction (MI) measured by contrast-enhanced magnetic resonance imaging (Ce-MRI). BACKGROUND: Identification of the transmural extent of myocardial necrosis and degree of non-viability after acute MI is clinically important. METHODS: Tissue Doppler echocardiography with SRI and Ce-MRI were performed in 47 consecutive patients with a first acute MI between days 2 and 6 and compared to 60 age-matched healthy volunteers. Peak myocardial velocities and peak myocardial deformation strain rates were measured. Location and size of the infarct zone was confirmed by Ce-MRI using the delayed enhancement technique with a 16-segment model. RESULTS: Contrast-enhanced MRI identified transmural infarction in 21 patients, non-transmural infarction in 15 (mean transmurality of infarct 72.3 +/- 10.6%), and another 11 patients with subendocardial infarction (<50% transmural extent of the left ventricular wall). Peak systolic strain rate (SRs) of the transmural infarction segments was significantly lower compared to normal myocardium or with non-transmural infarction segments (both p < 0.0005). A cutoff value of SRs >-0.59 s(-1) detected a transmural infarction with high sensitivity (90.9%) and high specificity (96.4%), and -0.98 s(-1) >SRs >-1.26 s(-1) distinguished subendocardial infarction from normal myocardium with a sensitivity of 81.3% and a specificity of 83.3%. CONCLUSIONS: Peak myocardial deformation by SRI can differentiate transmural from non-transmural MI, and it allows noninvasive determination of transmurality of the scar after MI and thereby the extent of non-viable myocardium.
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Zhang et al. (2005) conducted an observational in Chronic chest pain with suspected stable CAD and acute MI (n=598). Stenotic coronary artery disease (PCI or CABG indicated) vs. Non-stenotic coronary arteries (No-CAD) was evaluated on Resting early diastolic strain rate (SRe) without artefacts (p=< 0.001).
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