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AimsWe used virtual histology-intravascular ultrasound (VH-IVUS) to evaluate the relation between coronary plaque characteristics and no-reflow in acute coronary syndrome (ACS) patients.Methods and resultsA total of 190 consecutive ACS patients were imaged using VH-IVUS and analysed retrospectively. Angiographic no-reflow was defined as TIMI flow grade 0, 1, and 2 after stenting. Virtual histology-intravascular ultrasound classified the colour-coded tissue into four major components: fibrotic, fibro-fatty, dense calcium, and necrotic core (NC). Thin-cap fibroatheroma (TCFA) was defined as focal, NC-rich (≥10% of the cross-sectional area) plaques being in contact with the lumen in a plaque burden ≥40%. Of the 190 patients studied at pre-stenting, no-reflow was observed in 24 patients (12.6%) at post-stenting. The absolute and %NC areas at the minimum lumen sites (1.6 ± 1.2 vs. 0.9 ± 0.8 mm2, P < 0.001, and 24.5 ± 14.3 vs. 16.1 ± 10.6%, P = 0.001, respectively) and the absolute and %NC volumes (30 ± 24 vs. 16 ± 17 mm3, P = 0.001, and 22 ± 11 vs. 14 ± 8%, P < 0.001, respectively) were significantly greater, and the presence of at least one TCFA and multiple TCFAs within culprit lesions (71 vs. 36%, P = 0.001, and 38 vs. 15%, P = 0.005, respectively) was significantly more common in the no-reflow group compared with the normal-reflow group. In the multivariable analysis, %NC volume was the only independent predictor of no-reflow (odds ratio = 1.126; 95% CI 1.045–1.214, P = 0.002).ConclusionIn ACS patients, post-stenting no-reflow is associated with plaque components defined by VH-IVUS analysis with larger NC and more TCFAs.

If patients with SF were continued on combination antiplatelet therapy irrespective of ischemic symptoms, there would occur a low rate of major adverse cardiac events, especially cardiac death associated with SF.

Diabetic patients with ACS have more plaques with characteristics of plaque vulnerability, different composition of plaques, and have increased inflammatory status compared with nondiabetic patients with ACS.

Background Hypokalemia increases the vulnerability to ventricular fibrillation (VF). We hypothesize that the apamin-sensitive small conductance calcium-activated potassium current (IKAS) is activated during hypokalemia and that IKAS blockade is proarrhythmic. Methods and Results Optical mapping was performed in 23 Langendorff perfused rabbit ventricles with atrioventricular block and either right ventricular (RV) or left ventricular (LV) pacing during normokalemia or hypokalemia. Apamin prolonged the action potential duration (APD) measured to 80% repolarization (APD80) by 26 ms [95% confidence interval, CI, 14–37] during normokalemia and by 54 ms [CI, 40 to 68] during hypokalemia (P=0.01) at 1000 ms pacing cycle length (PCL). In hypokalemic ventricles, apamin increased the maximal slope of APD restitution, the PCL threshold of APD alternans, the PCL for wavebreak induction and the area of spatially discordant APD alternans. Apamin significantly facilitated the induction of sustained VF (from 3/9 hearts to 9/9 hearts, P=0.009). Short term cardiac memory was assessed by the slope of APD80 versus activation time. The slope increased from 0.01 [CI, −0.09 to 0.12] at baseline to 0.34 [CI, 0.23 to 0.44] after apamin (P<0.001) during RV pacing, and from 0.07 [CI, −0.05 to 0.20] to 0.54 [CI, 0.06 to 1.03] after apamin infusion (P=0.045) during LV pacing. Patch-clamp studies confirmed increased IKASin isolated rabbit ventricular myocytes during hypokalemia (P=0.038). Conclusions Hypokalemia activates IKAS to shorten APD and maintain repolarization reserve at late activation sites during ventricular pacing. IKAS blockade prominently lengthens the APD at late activation sites and facilitates VF induction.