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Claudio Cuccia

University of Insubria

Publishes on Acute Myocardial Infarction Research, Cardiac Imaging and Diagnostics, Atrial Fibrillation Management and Outcomes. 111 papers and 1.7k citations.

111Publications
1.7kTotal Citations

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Top publicationsby citations

Single-Point Cardiac Troponin T at Coronary Care Unit Discharge after Myocardial Infarction Correlates with Infarct Size and Ejection Fraction
Mauro Panteghini, Claudio Cuccia, Graziella Bonetti et al.|Clinical Chemistry|2002
Cited by 104

BACKGROUND: One of the major concerns in replacing creatine kinase MB (CK-MB) with cardiac troponins is the lack of evidence of the ability of troponins to estimate the size of acute myocardial infarction (AMI). We investigated the ability of a single measurement of cardiac troponin T (cTnT) at coronary care unit (CCU) discharge to estimate infarct size and assess left ventricular (LV) function in AMI patients. METHODS: We studied 65 AMI patients in whom infarct size was estimated by CK-MB peak concentrations and gated single-photon emission computed tomography (SPECT) myocardial perfusion using technetium-99m sestamibi and LV function by SPECT imaging. Measurements of cTnT and SPECT were performed 72 h (median) after admission (range, 40-160 h). SPECT was also repeated 3 months later. RESULTS: We found a significant correlation between cTnT and both the peak CK-MB concentrations (r = 0.76; P <0.001) and the perfusion defect size at SPECT (r = 0.62; P <0.001). cTnT was inversely related to LV ejection fraction (LVEF) assessed both early (r = -0.56; P <0.001) and 3 months after AMI (r = -0.70; P <0.001). cTnT >2.98 micro g/L predicted a LVEF <40% at 3 months with a sensitivity of 86.7%, specificity of 81.4%, and a likelihood ratio for a positive test of 4.7 (95% confidence interval, 4.0-5.4). CONCLUSIONS: A single cTnT measurement at CCU discharge after AMI is useful as a noninvasive estimate of infarct size and for the assessment of LV function in routine clinical setting.

Coronary stents and vascular response to implantation: literature review
Marta Francesca Brancati, Francesco Burzotta, Carlo Trani et al.|Pragmatic and Observational Research|2017
Cited by 48Open Access

Drug-eluting stents (DESs) have minimized the limitations of bare-metal stents (BMSs) after percutaneous coronary interventions. Nevertheless, serious concerns remain about possible late complications of stenting, such as stent thrombosis (ST) and in-stent restenosis (ISR), although the introduction of second-generation DESs seems to have softened the phenomenon, compared to the first-generation ones. ST is a potentially catastrophic event, which has been markedly reduced by optimization of stent implantation, novel stent designs, and dual antiplatelet therapy. The exact mechanism to explain its occurrence is under investigation, and, realistically, multiple factors are responsible. ISR of BMSs has been previously considered as a stable condition with an early peak (at 6 months) of intimal hyperplasia, followed by a regression period beyond 1 year. On the contrary, both clinical and histologic studies of DESs have demonstrated evidence of continuous neointimal growth during long-term follow-up, named "late catch-up" phenomenon. The acknowledgment that ISR is a relatively benign clinical condition has been recently challenged by evidences which reported that patients with ISR can experience acute coronary syndromes. Intracoronary imaging is an invasive technology that allows identifying features of atherosclerotic plaque of stent implanted and of vascular healing after stenting; it is often used to complete diagnostic coronary angiography and to drive interventional procedures. Intracoronary optical coherence tomography is currently considered a state-of-the-art imaging technique; it provides, compared to intravascular ultrasound, better resolution (at least >10 times), allowing the detailed characterization of the superficial structure of the vessel wall. Imaging studies "in vivo," in agreement with histological findings, suggest that chronic inflammation and/or endothelial dysfunction may induce late de novo "neoatherosclerosis" inside both BMSs and DESs. So, neoatherosclerosis has become the prime suspect in the pathogenesis of late stent failure.