Assessement of left ventricular mechanical dispersion and global longitudinal strain in prognosis of adverse cardiac remodeling in patients after ST-segment elevation myocardial infarction

ST elevation myocardial infarction (STEMI) remains to have high risk of mortality even in patients after successful percutaneous intervention (PCI). One of the mains reasons of worthening prognosis is heart failure (HF) because of adverse cardiac remodelling (ACR). The role of left ventricular global longitudinal strain (LVGLS) and mechanical dispersion (LV MD) in prediction of ACR for STEMI patients still remained unclear.

The aim of the study was to estimate role of LVMD and LVGLS as predictors for ACR in patients after STEMI who had successful PCI after 12 months.

119 STEMI patients who consent to participate in the study were enrolled. All of them had no previous myocardial infarction, atrial fibrillation/flutter, severe comorbidities, poor acoustic windows, HF with reduced ejection fraction. Clinical, hemodynamic, ECG, transthoracic echocardiography with Doppler and speckle-tracking (LVMD and LVGLS) parameters were measured in acute period and after 12 months. The levels of circulating biomarkers were measured during few days after STEMI. ACR was determined as an increase in LV EDV >10% and/or LV ESV >10% at 365 days (±14 days) follow-up period.

Results: A total of 119 patients with STEMI after successful PCI with TIMI III were included in the study. They were mainly male (88.2%) with an average age of 59 years. Enrolled patients were divided into 4 groups according LVMD level.

The univariate log regression analysis displayed markers that were found to be predictors for ACR. Multivariate log regression analysis revealed that LVGLS >–8%, high level of LVMD and NT-proBNP >953 pg/mL were independent predictors for ACR.

ROC analysis demonstrated that all three predictive models based on LVMD (AUC=0.84. p<0.001, Sensitivity 80.8%, specificity 87.5%, cutoff point =68 msc), LVGLS (AUC=0.62; p<0.001, Sensitivity 82.0%, specificity 66.7%, cutoff point =–8%) and NT pro-BNP (AUC=0.60. p<0.001, Sensitivity 78.2%, specificity 73.5%, cutoff point =953 pmol/mL) allowed to identify STEMI patients in acute period with high risk of ACR.

The addition of LVMD to the basal prognostic model (NT-proBNP >953 pg/mL) significantly improved the discriminative potency of the predictive model (AUC 0.84 (0.72-0.90), p=0.001, NRI Median 95% CI =0.54, p=0.018, IDI Median 95% CI =0.53, p=0.042), while LV GLS did not yield it neither alone (AUC 0.62 (0.58-0.69), p=0.49, NRI Median 95% CI =0.30, p=0.25, IDI Median 95% CI =0.04, p=0.62), nor with adding it to the basal model (AUC 0.83 (0.73-0.91), p=0.001, NRI Median 95% CI =0.52, p=0.02, IDI Median 95% CI =0.052, p=0.044). The only LVMD became an independent marker of ACR predicting improving the discriminative potency of NT-proBNP.

Conclusion: Our study revealed that LVMD and LVGLS might be useful in prediction of ACR in patients with STEMI after PCI after 12 months follow-up period. But an independent marker of ACR in our prognostic model became only LVMD.