Dynamics of left ventricular mechanics in patients with stable ischemic heart disease after coronary artery stenting

The aim of this study was to assess dynamics of left ventricular (LV) mechanics after coronary artery stenting in patients with stable ischemic heart disease. The analysis was performed in 52 stable ischemic heart disease patients (age of 58.16±8.94 years) with left ventricular (LV) ejection fraction (EF) of 55% and more. Percutaneous coronary intervention (PCI) was performed in all patients according to indications. Syntax score did not exceed 22. Two-dimensional echocardiography and Speckle Tracking Imaging were performed to assess the LV global longitudinal strain (GLSLV), global rotation, global rotation rate at systole and early diastole at the basal, apical, and papillary muscle levels, twist, untwist and torsion before and during the first week after PCI. Cardiac-specific enzymes including troponin I and creatine phosphokinase-MB (CPK-MB) were evaluated before, 6 and 24 hours after PCI in all patients. Cut-off value of CPK-MB and Troponin I for acute coronary syndrome were 25 U/L and more and 0.5 ng/mL and more, respectively. Normal GLSLV was found in 22 patients. GLSLV was decreased (less than -18%) in 30 patients. The patients with decreased GLSLV before PCI had delayed peak LV global rotation the levels of papillary muscles and the apex. The worsening of GLSLV after PCI was found in 24 (46.15%) patients and the improvement of GLSLV was detected in 28 (53.85%) patients. The values of the global rotation, global rotation rate at systole and early diastole, twist, untwist and torsion of LV did not differ in patients with positive and negative GLSLV dynamics. In patients with abnormal GLSLV before PCI and with its worsening after PCI, there was a decrease in time to peak of LV global rotation rate in early diastole at the basal level (509.50±68.28 ms, Ме=505.50 ms vs. 479.88±49.54 ms, Ме=488.00 ms; р=0.04), an increase in the time to peak of LV global apical rotation rate in systole (246.13±164.19 ms; Ме=89.50 ms vs 126.14±52.31 ms; Ме=126.00; U=9.50, Zadj=2.09; р=0.03), and a decrease in global apical rotation rate in early diastole (-17.70±22.25; Ме=-23.52 vs -52.65±24.11; Ме=-45.94; U=5.00, Zadj=2.60; р=0.009). We found a significant increase in Troponin I 24 h and CPK-MB 6 and 24 h after PCI in patients who had GLSLV worsening after PCI, but it did not exceed cut-off value for acute coronary syndrome. Conclusions. (1) There is GLSLV worsening in 46.15% patients after PCI. (2) GLSLV worsening after PCI in stable CAD patients is associated with an increase in cardiac-specific enzymes after PCI and GLSLV worsening caused by the coronary microembolization during PCI. (3) An increase in the time to peak of LV global rotation rate in systole at the levels of papillary muscles and the apex is an early marker of worsening of cardiac mechanics. (4) In patients with abnormal GLSLV before PCI and with its worsening after PCI, the time to peak of LV global apical rotation rate in systole was increased and global apical rotation rate in early diastole was decreased.