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Background: Blood glucose variability is receiving considerable attention as a new risk factor for coronary artery disease. This study aimed to investigate the association between blood glucose variability and coronary plaque tissue characteristics. Methods: In 57 patients with acute coronary syndrome, integrated backscatter intravascular ultrasound (IB-IVUS) and gray-scale IVUS were performed before balloon dilatation or stent implantation in the culprit vessels. Standard IVUS indices were evaluated for volume index (volume/length), and plaque components were measured by IB-IVUS for percent tissue volume. In addition to conventional glucose indicators, blood glucose variability in a stable state was determined by calculating the mean amplitude of glycemic excursions (MAGE) using a continuous glucose monitoring system. Results: Higher MAGE values were significantly correlated with larger percent plaque volumes (r = 0.32, p = 0.015), and increased lipid (r = 0.44, p = 0.0006) and decreased fibrous (r = -0.45, p = 0.0005) plaque components. In contrast, HbA1c or fasting plasma glucose values were not significantly correlated with plaque volumes and percent plaque components. Homeostasis model assessment of insulin resistance values were positively correlated with vessel (r = 0.35, p = 0.007) and plaque (r = 0.27, p = 0.046) volumes, but not with percent plaque components. In multiple regression analysis, higher MAGE values were independently associated with increased lipid (β = 0.80, p = 0.0035) and decreased fibrous (β = -0.79, p = 0.0034) contents in coronary plaques. Conclusions: Among all glucose indicators studied, only higher blood glucose variability was an independent determinant of increased lipid and decreased fibrous contents with larger plaque burden, suggesting blood glucose variability as one of the important factors related to coronary plaque vulnerability. [ABSTRACT FROM AUTHOR]

Aims We sought to compare the morphological features of non-culprit plaques with >50% diameter stenosis in patients with acute coronary syndromes (ACS) with those of culprit plaques in patients with ACS and stable angina pectoris (SAP) using optical coherence tomography (OCT) and integrated backscatter intravascular ultrasound (IB-IVUS). Methods and results A total of 150 culprit and non-culprit coronary plaques (non-culprit vessels) in 150 patients with coronary artery disease were interrogated by OCT before percutaneous coronary intervention (PCI). Patients were categorized as follows: 73 culprit plaques in patients with ACS (ACS-C), 32 non-culprit plaques in patients with ACS (ACS-NC), and 45 culprit plaques in patients with SAP. The fibrous cap thickness was thinner in the ACS-C and ACS-NC groups than in the SAP group and was thinnest in the ACS-C group (ACS-C vs. ACS-NC vs. SAP, 60 vs. 82 vs. 114 µm, P < 0.001). IB-IVUS sub-analysis of 95 patients demonstrated that% lipid volume was greater and % fibrous volume was lower in the ACS-NC group than those in the SAP group (ACS-C vs. ACS-NC vs. SAP, 56.3 ± 11.0 vs. 59.9 ± 11.2 vs. 50.1 ± 13.9%, P < 0.05 and 39.5 ± 9.0 vs. 35.0 ± 9.0 vs. 43.9 ± 11.3%, P < 0.01, respectively). Conclusion Plaques of non-culprit vessels in patients with ACS had a thinner fibrous cap and a higher percentage of lipid content than culprit plaques in patients with SAP. However, the fibrous cap thickness was thinner in the culprit lesions in patients with ACS than in the non-culprit lesions in patients with ACS, while plaque compositions were not significantly different between the groups. [ABSTRACT FROM AUTHOR]

Pacemaker. QT interval (QTI) may change when cardiac junction is improved by optimizing the AV delay. QTI is used as the sensor for rate responsive pacemakers. Evoked (e)QTI is measured as the time duration from the ventricular pace-pulse to the T sense point, which is the steepest point of the intracardiac T wave. The relationship between AV delay and eQTI and cardiac function was studied in 13 patients (74.2 ± 9.3 [SD] years old) with an implanted QT-driven DDDR pacemaker. A special pacemaker software module was downloaded into the pacemaker memory for eQTI data logging. AV delay was set at 100, 120, 150, 180, 210, and 240 ms. Cardiac output (CO) was measured by' continuous Doppler echocardiography eQTI was 343.3 ± 22.5, and 343.4 ± 23.2 ms (P < 0.01. repeated ANOVA) and CO was 4.2 ± 0.8, 4.6 ± 0.8, and 4.2 ± 0.8 L/min (P < 0.0001, repeated ANOVA) when AV delay was set at the AV delay shortened by one step (AV[-]) and prolonged by one step (AV[+]) from the AV delay at which QT interval was maximum (AV[max]) in seven patients, in whom the peak AV delay at which the eQTI was maximal could be identified. eQTI decreased from 345.1 ± 20.9 to 339.4 ± 21.1 ms (P < 0.0001) and CO decreased from 4.4 ± 1.4 to 4.1 ± 1.3 L/min (P <0.005) when AV delay was prolonged from AV(max) to AV(+) in all patients. eQTI decreased from 345.1 ± 22.5 to 343.3 ± 22.4 ms (P < 0.0005) and CO decreased from 4.6 ± 0.8 to 4.2 ± 0.8 L/min (P < 0.05) when AV delay was shortened from AV(max) to AV(-) in seven patients. Thus, CO was maximal when AV delay was set at the AV delay at which eQTI was maximal. In conclusion, the optimal AV delay can be predicted from the eQTI sensed by an implanted pacemaker. and automatic setting of the optimal A V delay can be achieved by the QT sensor of an implanted pacemaker. [ABSTRACT FROM AUTHOR]