Search Results

1 - 10 of 70 items

  • Author: Imre Benedek x
Clear All Modify Search

Abstract

Acute coronary syndromes are usually triggered by the erosion or rupture of a vulnerable coronary plaque. A vulnerable plaque (VP) is an atheromatous plaque which, after suffering different transformations, is prone to rupture causing an acute coronary event. Such a VP carries inside several biomarkers considered as “signatures of vulnerability”, which, if identified, can prompt timely initiation of therapeutic measures in order to prevent the development of an acute myocardial infarction. The most freqeuntly used techniques for identification of vulnerability markers are computed tomographic angiography (CTA), intravascular ultrasound and optical coherence tomography. Endothelial shear stress (ESS) represents a new promising biomarker associated with plaque vulnerability. Determination of ESS is nowadays possible using noninvasive imaging techniques, based on complex computational post-processing of multiple datasets extracted from CTA images and advanced computational fluid dynamics technologies. The aim of this systematic review was to evaluate the role of the coronary ESS, determined using advanced computational techniques for image post-processing, as a feature associated with CTA-derived biomarkers of atheromatous plaque vulnerability, underlining the conceptual differences between high ESS and low ESS as promotors of vulnerability.

Abstract

Introduction: We aimed to assess the relationships between the persistence of elevated circulating levels of hs-CRP, a powerful inflammatory marker, determined at 30 days after an acute myocardial infarction (AMI), and the characteristics of the pre-existing coronary lesions. Material and methods: The study included 83 consecutive patients 30 days post AMI, who were subjected to coronary angiography and primary PCI. The patients were divided into two groups according to their hsCRP levels at 30 days after AMI: group 1 included 35 low-risk patients, with hsCRP levels <2 mg/l, and group 2 included 48 high-risk patients, with hsCRP levels >2 mg/l. Results: Angiographic analysis revealed the presence of a multivascular disease in 48.5% of the patients in group 1 versus 72.9% of the patients in group 2 (p=0.037). The Syntax scores for groups 1 and 2 were 22.2 +/- 6.6 and 27.07+/-0.94, respectively (p=0.001), and these values were significantly correlated with the hsCRP values (r=0.56, p<0.0001). LAD culprit lesions were found in 47.9% of the patients in group 1 and 20% of the patients in group 2 (p=0.01), and 42.8% of the group 1 patients and 83.3% of the group 2 patients had at least one significant stenosis in the LAD (p=0.0002). The ejection fraction at 30 days was significantly lower in the patients with elevated levels of hsCRP (52.91+/-4.03 vs 49.04+/-5.74, p=0.001), showing an inverse correlation with hsCRP levels (r=-0.52, p<0.0001). Conclusions: A more severe coronary artery disease was associated with am increased inflammatory status in the postinfarction phase, as evidenced by the high levels of circulating hsCRP. hsCRP can help for risk stratification in post AMI patients by identifying the subsets of patients who are at risk based on persistent elevated circulating levels of hsCRP at 30 days after infarction.

Abstract

The aim of our study was to investigate the correlation between volumes of thoracic fat distributed in different compartments and the geometry of vulnerable coronary plaques assessed by coronary computed tomography angiography (CCTA), in patients with acute chest pain.

Methods: This was a non-randomized, observational, single-center study, including 50 patients who presented in the emergency department with acute chest pain who underwent 128-slice single-source CCTA. Plaque geometry was evaluated in transversal and longitudinal planes, and the assessment of adipose tissue was performed using the Syngo.via Frontier (Siemens AG, Healthcare Sector, Forchheim, Germany) research platform.

Results: Eccentric plaques presented a significantly higher incidence of spotty calcification (40% vs. 22%, p = 0.018), whereas positive remodeling, volume of low attenuation plaque, and incidence of napkin-ring sign were not significantly different between the study groups or in ascending versus descending plaques. The volume of pericoronary fat around the plaque was significantly larger near eccentric lesions (707.68 ± 454.08 mm3 vs. 483.25 ± 306.98 mm3, p = 0.046) and descendent plaques (778.26 ± 479.37 mm3 vs. 473.60 ± 285.27 mm3, p = 0.016). Compared to ascending lesions, descendent ones presented a significantly larger volume of thoracic fat (1,599.25 ± 589.12 mL vs. 1,240.71 ± 291.50 mL), while there was no significant correlation between thoracic fat and cross-sectional eccentricity.

Conclusions: The phenotype of plaque distribution and geometry seems to be associated with a higher vulnerability of coronary lesions and may be influenced by the local accumulation of inflammatory mediators released by the pericoronary epicardial adipose tissue.

Abstract

Introduction: According to European guidelines, ST elevation acute myocardial infarction should be treated by immediate reperfusion, if diagnosed within 12 hours from the onset of symptoms. We aimed to show the impact of a well-functioning pre-existing STEMI network in improving the results of a national program dedicated to the invasive treatment of AMI.

Methods: We followed the comparison between primary PCI rates and STEMI-related mortality in two regions, after the introduction of a nationwide program for the interventional treatment of acute myocardial infarction: region A, where the territory has been appropriately prepared via previous organizational measures in the network, and region B, where the territory has not been previously prepared.

Results: In 2011, one year after the initiation of the national program, a primary PCI rate of 12.1%, a thrombolysis rate of 10.1% and a no-reperfusion treatment rate of 77.8% have been found in these new centers for patients arriving <12 h from symptoms onset. This has been reflected in a mortality of 23.07% for “early presentations” in these new centers in 2011. In comparison, data from the territorial hospitals of the registry (only those without cathlab facilities, similar to the new centers) showed in 2011 a 73.85% primary PCI rate, 12.09% thrombolysis rate and a 14.07% conservative treatment rate, reflected in a mortality of 6.81% for “early presentations” in the registry centers.

Conclusions: The national strategy for reduction of STEMI related mortality via implementation of primary PCI, started in 2010, had a significant impact especially in that region where the territory was previously prepared with appropriate organizational efforts, including educational and logistic measures.