Impact of inflammation-mediated response on pan-coronary plaque vulnerability, myocardial viability and ventricular remodeling in the postinfarction period - the VIABILITY study

Abstract

Introduction:While the role of inflammation in acute coronary events is well established, the impact of inflammatory-mediated vulnerability of coronary plaques from the entire coronary tree, on the extension of ventricular remodeling and scaring, has not been clarified yet.Materials and methods:The present manuscript describes the procedures of the VIABILITY trial, a descriptive prospective single-center cohort study. The main purpose of this trial is to assess the link between systemic inflammation, pan-coronary plaque vulnerability (referring to the plaque vulnerability within the entire coronary tree), myocardial viability and ventricular remodeling in patients who had suffered a recent ST-segment elevation acute myocardial infarction (STEMI). One hundred patients with STEMI who underwent successful revascularization of the culprit lesion in the first 12 hours after the onset of symptoms will be enrolled in the study. The level of systemic inflammation will be evaluated based on the serum biomarker levels (hs-CRP, matrix metalloproteinases, interleukin-6) in the acute phase of the myocardial infarction (MI) and at 1 month. Pan-coronary plaque vulnerability will be assessed based on serum biomarkers known to be associated with increased plaque vulnerability (V-CAM or I-CAM) and at 1 month after infarction, based on computed tomographic angiography analysis of vulnerability features of all coronary plaques. Myocardial viability and remodeling will be assessed based on 3D speckle tracking echocardiography associated with dobutamine infusion and LGE-CMR associated with post-processing imaging methods. The study population will be categorized in 2 subgroups: subgroup 1 - subjects with STEMI and increased inflammatory response at 7 days after the acute event (hs-CRP ≥ 3 mg/dl), and subgroup 2 - subjects with STEMI and no increased inflammatory response at 7 days (hs-CRP < 3 mg/dl). Study outcomes will consist in the rate of post-infarction heart failure development and the major adverse events (MACE) rate.Conclusion:VIABILITY is the first prospective study designed to evaluate the influence of infarct-related inflammatory response on several major determinants of post-infarction outcomes, such as coronary plaque vulnerability, myocardial viability, and ventricular remodeling.

Statins Mitigate Stress-Related Vascular Aging and Atherosclerosis in apoE-Deficient Mice Fed High Fat-Diet: The Role of Glucagon-Like Peptide-1/Adiponectin Axis

“…for the formation of vulnerable plaques (Quesada et al, 2015;Ruddy et al, 2016;Morariu et al, 2019). As mentioned before, chronic stress promoted the progression of atherosclerosis in a mouse model by enhancing inflammation and oxidative stress, and the enhanced inflammation and oxidative stress can also change the characteristics of atherosclerotic plaques and promote ruptures.…”

“…Plaque rupture is the leading cause of acute cardiovascular events, and such ruptures are always due to the formation of vulnerable plaques. An excessive inflammatory response, oxidative stress, and degradation of the ECM are all responsible for the formation of vulnerable plaques ( Quesada et al, 2015 ; Ruddy et al, 2016 ; Morariu et al, 2019 ). As mentioned before, chronic stress promoted the progression of atherosclerosis in a mouse model by enhancing inflammation and oxidative stress, and the enhanced inflammation and oxidative stress can also change the characteristics of atherosclerotic plaques and promote ruptures.…”

Discordance between the Clinical Presentation and Morphology of Myocardial Infarction in a Patient with Acute post-Hemorrhagic Anemia

“… 3 The presence of a non-occlusive thrombus in the right coronary artery seemingly contradicted the anteroseptal localization of the MI, which could be explained by systemic inflammation contributing to the concurrent (pancoronary) vulnerability of multiple atherosclerotic plaques or the additive action of atherothrombosis and the decreased oxygen supply on the development of acute ischemia. 5 It should also be noted that the finding of transmural MI on autopsy is not unexpected, given that according to magnetic resonance imaging and autopsy studies, ECG signs (ST elevation or Q wave) cannot reliably exclude this possibility. 6 , 7 The prevalence of moderate and severe anemia was reported in approximately 12% of T2MI cases, 8 forming a distinct clinical syndrome.…”

Alterações Precoces nas Interleucinas Circulantes e no Risco Inflamatório Residual após Infarto Agudo do Miocárdio

“…Sample size was estimated based on previous studies involving early changes in cytokine titers. 10 , 11 The software SPSS, version 18.0 (IBM, Armonk, New York, USA), was used for statistical analysis. All p-values < 0.05 were considered statistically significant.…”

“…O tamanho amostral foi estimado com base em estudos anteriores envolvendo alterações precoces nos títulos de interleucinas. 10 , 11 O software SPSS, versão 18.0 (IBM, Armonk, Nova Iorque, EUA), foi utilizado para a análise estatística. Valores de p < 0,05 foram considerados estatisticamente significativos.…”