Changes in Coronary Plaque Composition in Patients With Acute Myocardial Infarction Treated With High-Intensity Statin Therapy (IBIS-4)

Räber, Lorenz; Koskinas, Konstantinos C.; Yamaji, Kyohei; Taniwaki, Masanori; Roffi, Marco; Holmvang, Lene; Garcia, Hector M.; Zanchin, Thomas; Maldonado, Rafaela; Moschovitis, Aris; Pedrazzini, Giovanni; Zaugg, Serge; Dijkstra, Jouke; Matter, Christian M.; Serruys, Patrick W.; Lüscher, Thomas F.; Kelbæk, Henning; Karagiannis, Alexios; Radu, Maria; Windecker, Stephan

doi:10.1016/j.jcmg.2018.08.024

Cited by 78 publications

(52 citation statements)

References 29 publications

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“…In another study assessing changes in plaque lipid content by means of serial NIRS, intensive statin treatment (rosuvastatin 40 mg) resulted in greater reduction in the maximal lipid core burden index of obstructive coronary lesions compared with standard-of-care lipid-lowering therapy within a short-term (7-week) follow-up 74 . Consistent with these RCT data, observational evidence showed an increase in fibrous cap thickness, reduction in inflammation, and regression of high-risk TCFA to presumably more stable lesion phenotypes in non-culprit lesions of patients with STEMI treated with high-dose rosuvastatin 75 . The effect of the PCSK9i alirocumab on IVUS-, OCT-, and NIRS-defined plaque burden and composition is currently being investigated in the PACMAN-AMI trial (NCT03067844).…”

Section: Effect Of Ldl-c Lowering Therapies On Coronary Plaquessupporting

confidence: 66%

Lipid-lowering therapy and percutaneous coronary interventions

Koskinas

Mach²,

Räber³

2021

EuroIntervention

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Although technological and procedural advances have resulted in substantial improvements in clinical outcomes following percutaneous coronary interventions (PCI), recurrent coronary events may occur despite achieving optimal procedural results. Beyond myocardial revascularisation failure related to anatomical or stent-related factors, adverse cardiovascular events post PCI often arise from non-culprit lesions not treated during index interventions. While stenting treats a focal manifestation of a systemic, progressive disease, the residual risk following an acute coronary syndrome (ACS) or elective PCI is largely related to the systemic pro-atherogenic effects of suboptimally controlled cardiovascular risk factors. Lowering atherogenic lipid levels, in particular low-density lipoprotein cholesterol (LDL-C), can halt the progression of coronary atherosclerosis and improve cardiovascular outcomes to an extent that is proportional to the magnitude of LDL-C reduction. Early (in-hospital) initiation of intensive statin therapy leads to a very early clinical benefit following ACS, and prolonged adherence to optimised lipid-lowering treatment effectively reduces longer-term cardiovascular events following PCI. Therefore, achieving guideline-recommended treatment goals for LDL-C with statins and, if indicated, with the addition of non-statin lipid-lowering drugs should become a priority for all physicians involved in the treatment of patients with coronary heart disease, including comprehensive strategies initiated during the in-hospital care of patients undergoing coronary interventions. This review article summarises current evidence on the role of LDL-C in the development and progression of coronary atherosclerosis, discusses the clinical benefits of intensive lipid-lowering treatments, and presents current guideline recommendations, with emphasis on patients undergoing PCI.

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Section: Effect Of Ldl-c Lowering Therapies On Coronary Plaquessupporting

confidence: 66%

Lipid-lowering therapy and percutaneous coronary interventions

Koskinas

Mach²,

Räber³

2021

EuroIntervention

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“…Some small-to-moderate sample size longitudinal imaging studies have suggested that atherosclerotic plaques of differing maturity frequently co-exist and their morphology may change over time, being able to both gain and lose the features of vulnerability [8][9][10][11][12][13][14] ; even up to three quarters of vulnerable plaques might evolve towards a more stable phenotype while on a high-intensity statin therapy. 13 At present, the clinical consequences of detecting the features of plaque vulnerability remain limited as the positive predictive value of current imaging modalities for the prediction of major adverse cardiac events (MACE) is too low for clinical relevance. However, such limitations have prompted a number of technical advances including both diagnostics and analytics.…”

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confidence: 99%

Vulnerable plaques and patients: state-of-the-art

Tomaniak

Katagiri

Modolo

et al. 2020

European Heart Journal

131

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Despite advanced understanding of the biology of atherosclerosis, coronary heart disease remains the leading cause of death worldwide. Progress has been challenging as half of the individuals who suffer sudden cardiac death do not experience premonitory symptoms. Furthermore, it is well-recognized that also a plaque that does not cause a haemodynamically significant stenosis can trigger a sudden cardiac event, yet the majority of ruptured or eroded plaques remain clinically silent. In the past 30 years since the term ‘vulnerable plaque’ was introduced, there have been major advances in the understanding of plaque pathogenesis and pathophysiology, shifting from pursuing features of ‘vulnerability’ of a specific lesion to the more comprehensive goal of identifying patient ‘cardiovascular vulnerability’. It has been also recognized that aside a thin-capped, lipid-rich plaque associated with plaque rupture, acute coronary syndromes (ACS) are also caused by plaque erosion underlying between 25% and 60% of ACS nowadays, by calcified nodule or by functional coronary alterations. While there have been advances in preventive strategies and in pharmacotherapy, with improved agents to reduce cholesterol, thrombosis, and inflammation, events continue to occur in patients receiving optimal medical treatment. Although at present the positive predictive value of imaging precursors of the culprit plaques remains too low for clinical relevance, improving coronary plaque imaging may be instrumental in guiding pharmacotherapy intensity and could facilitate optimal allocation of novel, more aggressive, and costly treatment strategies. Recent technical and diagnostic advances justify continuation of interdisciplinary research efforts to improve cardiovascular prognosis by both systemic and ‘local’ diagnostics and therapies. The present state-of-the-art document aims to present and critically appraise the latest evidence, developments, and future perspectives in detection, prevention, and treatment of ‘high-risk’ plaques occurring in ‘vulnerable’ patients.

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“…Although dyslipidemia is a major determinant of long-term clinical outcomes in AMI patients, many recent studies have focused on high-dose statin therapy, rather than the important role of RASI. [ 26 , 27 ] The SMILE (Survival of Myocardial Infarction Long-term Evaluation) trial [ 28 ] and its post hoc analysis [ 29 ] demonstrated that compared with the placebo and normocholesterolemic group, the early treatment with zofenopril was more effective in reducing morbidity and mortality in AMI and hypercholesterolemia patients (relative risk reduction = 43%, P = .034). Despite these previous studies that have proven the beneficial effects of RASIs in diabetes and dyslipidemia, there exist limited comparative data on the long-term major clinical outcomes of RASI therapy in diabetic and dyslipidemic AMI patients.…”

Section: Discussionmentioning

confidence: 99%

Impacts of renin–angiotensin system inhibitors on two-year clinical outcomes in diabetic and dyslipidemic acute myocardial infarction patients after a successful percutaneous coronary intervention using newer-generation drug-eluting stents

et al. 2020

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This study investigated the impacts of renin–angiotensin system inhibitors (RASIs) on 2-year clinical outcomes in diabetes and dyslipidemic acute myocardial infarction (AMI) patients after a successful percutaneous coronary intervention (PCI) using newer-generation drug-eluting stents (DESs). A total of 16,997 AMI patients were enrolled, and divided into four groups based on the presence or absence of diabetes and dyslipidemia as follows: diabetes –/dyslipidemia –(group A, 11,132 patients), diabetes +/dyslipidemia – (group B, 3,860 patients), diabetes –/dyslipidemia + (group C, 1,328 patients), and diabetes +/dyslipidemia + (group D, 677 patients). The clinical endpoint was the occurrence of major adverse cardiac events (MACEs), the composite of total death, recurrent myocardial infarction (re-MI), and any repeat revascularization, including target lesion revascularization (TLR), target vessel revascularization (TVR), and non-target vessel revascularization (non-TVR). After RASIs therapy, the cumulative incidences of MACEs (adjusted hazard ratio [aHR], 1.330; 95% confidence interval [CI], 1.022–1.732; P = .034), any repeat revascularization (aHR, 1.584; 95% CI, 1.092–2.298; P = .015), TLR, and TVR were significantly higher in group B than group C. However, the cumulative incidences of all-cause death, cardiac death, re-MI, and non-TVR were similar in groups B and C. In this study, under the newer-generation DESs era, repeat revascularization rate reduction benefit of RASIs therapy in diabetic AMI patients was lesser than that in dyslipidemic AMI patients. However, larger randomized controlled studies are needed to confirm these results in the future.

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Changes in Coronary Plaque Composition in Patients With Acute Myocardial Infarction Treated With High-Intensity Statin Therapy (IBIS-4)

Cited by 78 publications

References 29 publications

Lipid-lowering therapy and percutaneous coronary interventions

Lipid-lowering therapy and percutaneous coronary interventions

Vulnerable plaques and patients: state-of-the-art

Impacts of renin–angiotensin system inhibitors on two-year clinical outcomes in diabetic and dyslipidemic acute myocardial infarction patients after a successful percutaneous coronary intervention using newer-generation drug-eluting stents

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