[Show abstract][Hide abstract] ABSTRACT: 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.
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.
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.
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.
[Show abstract][Hide abstract] ABSTRACT: Background:
Glycemic variability (GV) is associated with coronary plaque rupture at the culprit lesion in acute myocardial infarction (AMI). The present study determined the relationship between GV and coronary plaque vulnerability in the non-culprit vessel.Methods and Results:The present prospective study involved 46 patients with first-episode acute coronary syndrome (ACS) who underwent optical coherence tomography in the non-culprit vessel. The relationship between GV, assessed with continuous glucose monitoring system, and the presence of thin-cap fibroatheroma (TCFA) at the non-culprit plaque with mild-to-moderate stenosis in the non-culprit vessel, was assessed. GV was quantified using mean amplitude of glycemic excursion (MAGE). Patients were divided into tertiles according to MAGE. TCFA was observed in 13 (28%) of the 46 patients. Fibrous cap thickness was thinner (MAGE tertiles: high, 80±40 µm; intermediate, 152±122 µm; low, 155±102 µm; P=0.01), and TCFA was more common (MAGE tertiles: high, 50%; intermediate, 27%; low, 7%; P=0.03) in patients with high MAGE. On multivariate logistic analysis high MAGE was the only significant determinant of TCFA, independent of coronary risk factors (OR, 5.000; P=0.021), homeostasis model assessment of insulin resistance, and hemoglobin A1c(OR, 5.674; P=0.018).
High MAGE measured early after the onset of first-episode ACS correlated with thinner fibrous cap thickness and higher prevalence of TCFA at the non-culprit plaque in the non-culprit vessel.
[Show abstract][Hide abstract] ABSTRACT: Although rapid progression (RP) of coronary artery disease (CAD) has been shown to be a powerful predictor of cardiovascular events, predictors of RP are not fully understood in patients with acute coronary syndrome (ACS).Methods and Results:We prospectively investigated the clinical impact of glycemic variability (GV), as determined on continuous glucose monitoring system (CGMS), on RP of non-culprit lesions in 88 patients with ACS. RP was deﬁned as ≥10% diameter reduction in a pre-existing stenosis ≥50%; ≥30% diameter reduction in a stenosis <50%; development of a new stenosis ≥30% in a previously normal segment; or progression of any stenosis to total occlusion. Patients were classified into 2 groups according to the presence (progressor, n=20) or absence (non-progressor, n=68) of RP. All patients were equipped with a CGMS during the stable phase, and mean amplitude of glycemic excursion (MAGE) was calculated as a marker of GV. Mean MAGE was significantly higher in progressors than in non-progressors (55±19 mg/dl vs. 37±18 mg/dl, P<0.01). On multiple logistic regression analysis, MAGE was an independent predictor of RP (odds ratio, 1.06 per 1 mg/dl; P<0.01).
MAGE early after the onset of ACS is a predictor of RP of non-culprit lesions.
[Show abstract][Hide abstract] ABSTRACT: AimsNon-invasive positive pressure ventilation rapidly improves the symptoms of acute heart failure (AHF). A portion of patients, however, are forced to be intubated even though intubation is associated with serious complications, and hypercapnia is often observed in AHF requiring intubation. The purpose of this study is to examine the clinical profile and management of hypercapnia in AHF patients.Methods and resultsWe examined the arterial blood gas analysis in 193 consecutive AHF patients (73 ± 12 years, 61% men) at admission. Many patients (n = 129, 66.8%) had already been treated with oxygen by the ambulance staff. Hypercapnia (PaCO2 at admission >45 mmHg) and hypocapnia (PaCO2 < 35 mmHg) were observed in 33.7% and 32.6%, respectively. Whereas 16 (24.6%) hypercapnic patients were intubated, there were only one (1.5%) normocapnic and no hypocapnic patients intubated. Patients with hypercapnia are more likely to be in the New York Heart Association Class IV (96.9% vs. 78.9%, P < 0.001), to have acute onset within 6 h (50.8% vs. 25.0%, P < 0.001), and to have radiographic pulmonary oedema (84.6% vs. 57.8%, P < 0.001) than those with hypo-normocapnia. Hypercapnia was more frequent in patients with acute cardiogenic pulmonary oedema than in those with acute decompensated heart failure (51.9% vs. 23.6%, P < 0.001). At discharge, hypercapnia was observed in 17.8% of patients who were hypercapnic at admission.Conclusion
Hypercapnia emerged in AHF acutely and transiently, was associated with immediate airway intervention, and was possibly involved in the pathophysiology of acute pulmonary oedema. Patients with acute onset dyspnoea should have their respiratory status carefully managed. These pathophysiological findings are expected to be utilized in treating or preventing AHF.
[Show abstract][Hide abstract] ABSTRACT: Background:
Impaired glucose metabolism plays an important role in patients with acute myocardial infarction, but the clinical significance of glycemic variability (GV) early after the onset of ST-segment elevation myocardial infarction (STEMI) remains to be fully elucidated.
Methods and results:
We prospectively investigated the clinical impact of GV, as determined by a continuous glucose monitoring system (CGMS), on left ventricular remodeling (LVR) assessed by cardiac magnetic resonance imaging (CMR) in 69 patients (63±13 years, 59 men) with a first reperfused STEMI within 12 h of onset. All patients were equipped with a CGMS when in a stable phase after admission and underwent repeat CMR at baseline and 7 months follow-up. Patients were divided into 2 groups according to the mean amplitude of glycemic excursions (MAGE). Patients in the upper tertile of MAGE were categorized as group High (H) and the other two-thirds as group Low (L). LVR was deﬁned as an absolute increase in left ventricular end-diastolic volume index of ≥20%. LVR more frequently occurred in group H than in group L (56% vs. 11%, P<0.001). Multivariate analysis showed the higher MAGE group was an independent predictor of LVR in the chronic phase (odds ratio, 13.999; 95% confidence interval, 3.059 to 64.056; P=0.001).
MAGE early after the onset of STEMI identified patients with LVR in the chronic phase.
[Show abstract][Hide abstract] ABSTRACT: 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).
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.