21 research outputs found

    Restenosis is not associated with stent length in a pig model of coronary stent implantation

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    Background: The aim of this study was to determine if stent length is by itself a risk factor for intimal proliferation and restenosis. Long lesions represent an independent risk factor for restenosis after coronary stent implantation. A longer stented segment might result in a higher probability of restenosis. Methods: Twenty-two 7-month-old male farm pigs underwent implantation of two steel stents, one short (8 mm length) and one long (16 mm length), in the right coronary artery. The pigs were sacrificed 28 days after stent implantation and histomorphometric analysis of the coronary arteries was performed for neointimal area proliferation and area stenosis evaluation. Results: Seventeen short stents and 19 long stents were finally implanted. There were no differences in neointimal proliferation (1.84 ± 0.64 mm2 vs. 1.81 ± 0.94 mm2, p = 0.84), area stenosis (40 ± 9% vs. 41 ± 19%, p = 0.86) and lumen area (2.96 ± 1.30 mm2 vs. 2.51 ± ± 1.18 mm2, p = 0.21) between the short stent group and the long stent group, respectively. Conclusions: These data suggest that stent length by itself does not influence restenosis extent in the porcine model

    Left ventricular deformation mechanics over time in patients with thalassemia major with and without iron overload

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    Background: Myocardial iron overload in patients with thalassemia major (TM) is one of the most important complications. The purpose of the study was to identify advanced echocardiography parameters for early identification of myocardial dysfunction during follow-up of patients with TM. Methods: Forty TM patients who were 41 ± 5 years old were included in the study and divided into two groups according to cardiac magnetic resonance T2* results (Group 1: Τ2* > 25 ms, Group 2: Τ2* ≤ 25 ms). Liver T2* parameters were also measured. Conventional and deformational echocardiographic parameters were measured at baseline and approximately 2 years later. Results: Thirty-two patients had Τ2* = 34 ± 4 ms (Group 1), and 8 had Τ2* = 17 ± 9 ms (Group 2). Blood consumption was 185 ± 60 and 199 ± 37 ml/kg/yr (p = 0.64), and liver T2* was 4 ± 5 and 17 ± 21 ms (p = 0.01) in Groups 1 and 2, respectively. At baseline, Group 1 had better left ventricular global longitudinal strain (GLS) (− 22 ± 3 vs. − 18 ± 5, p = 0.01) and similar left ventricular ejection fraction (LVEF) (62 ± 5% vs. 58 ± 10%, p = 0.086) than Group 2. At the 28 ± 11-month follow-up, LVEF, GLS, and T2* values in Group 1 (63 ± 3%, − 21 ± 3%, 34 ± 4 ms) and Group 2 (56 ± 11%, − 17 ± 4%, 17 ± 9 ms) did not change significantly compared to their corresponding baseline values. In 8 patients from Group 1, a worsening (> 15%) in LS (p = 0.001) was detected during follow-up, with a marginal reduction in LVEF. Conclusions: GLS seems to be an efficient echocardiographic parameter for detecting hemochromatosis-related cardiac dysfunction earlier than LVEF. It also seems to be affected by other factors (free radical oxygen, immunogenetic mechanisms or viral infections) in a minority of patients, underscoring the multifactorial etiology of cardiomyopathy. © 2021, The Author(s)

    Effects of levosimendan on circulating pro-inflammatory cytokines and soluble apoptosis mediators in patients with decompensated advanced heart failure.

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    This randomized, placebo-controlled trial showed that levosimendan administration causes a significant reduction of circulating proinflammatory cytokine interleukin-6 and soluble apoptosis mediators, such as soluble Fas and Fas ligand in patients with decompensated heart failure. These immunomodulatory effects may lead to improvement of symptoms and echocardiographic markers of cardiac contractile performance in these patients

    Endothelin system and atrial fibrillation post-cardiac surgery

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    Objective: We investigated the relation between the endothelin system and atrial fibrillation. Background: Endothelin has been implicated in the pathophysiology of atrial fibrillation, but the exact role of A- and B-receptors is unknown. Methods: We obtained right atrial biopsies from patients in sinus rhythm and preserved left ventricular function, undergoing off-pump coronary artery bypass grafting. The expression of endothelin, A- and B-receptors was measured using real time reverse-transcribed polymerase chain reaction. Results: We studied 52 patients (45 male, mean age 66±1 years, mean ejection fraction 52±1%). During a 5-day post-operative period, persistent atrial fibrillation occurred in 15 patients (28.8%). Endothelin mRNA expression was comparable in patients who subsequently developed atrial fibrillation and in those maintaining sinus rhythm. However, the former group displayed down-regulation of endothelin A- (by approximately 60%, p=0.0059) and of B-receptors (by approximately 40%, p=0.0084). The decreased endothelin A-receptor expression could predict atrial fibrillation occurrence (Wilks λ=0.86, F=6.16, p=0.017). Conclusion: Decreased endothelin A- and B-receptor expression is associated with atrial fibrillation after bypass surgery. © 2008 Springer Science+Business Media, LLC

    Comparison of frequency of calcified versus non-calcified coronary lesions by computed tomographic angiography in patients with stable versus unstable angina pectoris.

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    Item does not contain fulltextComputed tomographic coronary angiography (CTCA) can noninvasively identify calcified and noncalcified coronary plaques. The aim of this study was to compare the phenotypes of all plaques and of culprit plaques between patients with unstable angina pectoris (UAP) and those with stable angina pectoris (SAP), because plaque characteristics may differ between these patients. In 110 patients with UAP and 189 with SAP from a multicenter study comparing 64-slice CTCA with conventional coronary angiography, the number and phenotypes (noncalcified, mixed, and calcified) of coronary plaques were compared. In a subanalysis in 50 patients with UAP and 64 with SAP, culprit plaque characteristics, including culprit plaque cross-sectional area relative to total vessel cross-sectional area, culprit plaque length, remodeling index, and spotty calcification, were determined. Odds ratios for the presence of UAP, adjusted for clinical variables and the total number of plaques, were calculated for plaque characteristics on CTCA. Although the number of plaques was similar for patients with UAP and those with SAP, plaques in patients with UAP were more frequently noncalcified than in patients with SAP. The odds ratio for UAP was 1.3 (95% confidence interval [CI] 1.1 to 1.5) per noncalcified plaque. In the culprit plaque subanalysis, odds ratios for UAP were 0.99 (95% CI 0.96 to 1.01) per millimeter culprit plaque length, 2.7 (95% CI 1.2 to 6.4) for noncalcified culprit plaque, and 1.06 (95% CI 0.99 to 1.13) per percentage relative culprit plaque cross-sectional area. No significant relation was found between remodeling index or spotty calcification and UAP. In conclusion, noncalcified plaques and large noncalcified culprit plaques are more frequently found in patients with UAP than in those with SAP
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