Impact of Optical Coherence Tomography Imaging on Decision-Making During Percutaneous Coronary Intervention in Patients Presented With Acute Coronary Syndromes.

BACKGROUND: Optical coherence tomography (OCT) provides valuable information to guide percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) regarding lesion preparation, stent sizing, and optimization. The aim of the present study was to compare lumen expansion of stent-treated lesions immediately after the procedure for ACS between OCT-guided PCI and angiography-guided PCI.Methods and Results:This study investigated stent-treated lesions immediately after PCI for ACS by using quantitative coronary angiography in 390 patients; 260 patients with OCT-guided PCI and 130 patients with angiography-guided PCI. Before stenting, the frequency of pre-dilatation and thrombus aspiration were not different between the OCT-guided and angiography-guided PCI groups. Stent diameter was significantly larger as a result of OCT-guided PCI (3.11±0.44 mm vs. 2.99±0.45 mm, P=0.011). In post-dilatation, balloon pressure-up (48% vs. 31%, P=0.001) and balloon diameter-up (33% vs. 6%, P<0.001) were more frequently performed in the OCT-guided PCI group. Minimum lumen diameter (2.55±0.35 mm vs. 2.13±0.50 mm, P<0.001) and acute lumen gain (2.18±0.54 mm vs. 1.72±0.63 mm, P<0.001) were significantly larger in the OCT-guided PCI group. Percent diameter stenosis (14±4% vs. 24±10%, P<0.001) and percent area stenosis (15±5% vs. 35±17%, P<0.001) were significantly smaller in the OCT-guided PCI group. CONCLUSIONS: OCT-guided PCI potentially results in larger lumen expansion of stent-treated lesions immediately after PCI in the treatment of ACS compared with angiography-guided PCI.

The changes in biventricular remodelling and function after atrial septal defect device closure and its relation to age of closure.

BACKGROUND: The trans-catheter closure of atrial septal defect (ASD) usually has a rapid impact on biventricular remodelling and functions. Whether the transcatheter closure of ASD at early childhood or at adulthood age would affect the improvement in biventricular dimensions and functions remains an area of active research. RESULTS: This prospective observational study enrolled 70 subjects (50 ASD cases and 20 control subjects). Tissue Doppler imaging (TDI) and strain (S) were performed for the control group and ASD patients at baseline and at 24 h and 1 month after ASD device closure. The total ASD group was subdivided into two subgroups: group-1-children and adolescent with ASD, who underwent transcatheter closure at age ≤ 19 years; group-2-adult who underwent ASD device closure at age > 19 years old. The right and left ventricular global longitudinal systolic strain (RV/LV-GLS) and RV free wall longitudinal strain (RV free wall LS) showed a significant decline after 24 h of device closure (RVGLS-P = 0.001, LVGLS-P = 0.048, RV free wall LS-P < 0.001). However, after a 1-month follow-up, the LVGLS increased in comparison with 24 h changes after device closure (P = 0.038). The baseline mean value of RV free wall LS of G2 was significantly lower than G1 value (P < 0.001). There was no statistically significant difference between the 2 age subgroups regarding biventricular GLS and RV free wall LS changes after device closure. The changes in LV diastolic function immediately and after 1 month of device closure showed a statistically significant change in e' and its delta change value in group-2 in comparison with its baseline values and to group-1 delta changes (P = 0.002, P = 0.011, P = 0.019, respectively). CONCLUSION: The ASD transcatheter closure reduced biventricular global and RV free wall longitudinal systolic strain within 1 day of intervention and was associated with a short-term improvement in the LV-GLSS after a 1-month duration. The progressive increase in LV preload results in its strain growth and reduction in diastolic function after transcatheter ASD closure. The older age at the time of ASD device closure was associated with a significant decrease in the RV free wall LS and septal e' velocity towards abnormality.

Circulating Endothelial Cells and Platelet Microparticles in Mitral Valve Disease With and Without Atrial Fibrillation.

Hypercoagulability in mitral valve disease (MVD), a cause of atrial fibrillation (AF) and stroke, is potentially due to endothelial damage/dysfunction (marked by circulating endothelial cells [CECs]), platelet activation (soluble P-selectin [sPsel], platelet microparticles [PMPs], and soluble CD40 [sCD40]), and oxidized low-density lipoprotein (oxLDL) cholesterol. We measured these variables in 24 patients with MVD as well as in 21 with MVD + AF and compared them with 20 healthy controls (HCs). The CECs and PMPs were measured by flow cytometry; sPsel, oxLDL, and CD40 by enzyme-linked immunosorbent assay. Compared with HCs, sPsel and PMPs were equally higher in MVD and MVD + AF; sCD40 and oxLDL were higher in MVD + AF than in HCs and MVD; and CECs were higher in MVD than in the HCs, with further increases in MVD + AF (all P < .001). We conclude that excess platelet activation is present in MVD regardless of AF, and that increased endothelial damage in MVD is greater when compounded by AF.