Sudden coronary death, fatal acute myocardial infarction and widespread coronary and myocardial inflammation

Abbate, Antonio; Bussani, Rossana; Liuzzo, Giovanna; Biondi‐Zoccai, Giuseppe; Barresi, Elena; Mellone, Pasquale; Sinagra, Gianfranco; Dobrina, Aldo; De-Giorgio, Fabio; Sharma, Ranjit; Bassan, Fabio; Severino, Anna; Baldi, Feliciano; Biasucci, Luigi M.; Pandolfi, Franco; Silvestri, Furio; Vetrovec, G W; Baldi, Alfonso; Crea, Filippo

doi:10.1136/hrt.2007.115329

Cited by 32 publications

(23 citation statements)

References 17 publications

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“…In addition to that study, we also found a significant correlation between remote ECV and both CRP and fibrinogen, and a trend towards a significant correlation between remote native T1 and fibrinogen. The correlation between inflammatory markers and remote tissue characteristics suggests a link between remote edema and inflammation, which seems to be supported by previous findings from histological and imaging studies [2, 3, 32]. However, studies comparing CMR with histology in the same group of patients are needed to validate this hypothesis.…”

Section: Discussionsupporting

confidence: 74%

Changes in remote myocardial tissue after acute myocardial infarction and its relation to cardiac remodeling: A CMR T1 mapping study

et al. 2017

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ObjectivesTo characterize the temporal alterations in native T1 and extracellular volume (ECV) of remote myocardium after acute myocardial infarction (AMI), and to explore their relation to left ventricular (LV) remodeling.MethodsForty-two patients with AMI successfully treated with primary PCI underwent cardiovascular magnetic resonance after 4–6 days and 3 months. Cine imaging, late gadolinium enhancement, and T1-mapping (MOLLI) was performed at 1.5T. T1 values were measured in the myocardial tissue opposite of the infarct area. Myocardial ECV was calculated from native- and post-contrast T1 values in 35 patients, using a correction for synthetic hematocrit.ResultsNative T1 of remote myocardium significantly decreased between baseline and follow-up (1002 ± 39 to 985 ± 30ms, p<0.01). High remote native T1 at baseline was independently associated with a high C-reactive protein level (standardized Beta 0.32, p = 0.04) and the presence of microvascular injury (standardized Beta 0.34, p = 0.03). ECV of remote myocardium significantly decreased over time in patients with no LV dilatation (29 ± 3.8 to 27 ± 2.3%, p<0.01). In patients with LV dilatation, remote ECV remained similar over time, and was significantly higher at follow-up compared to patients without LV dilatation (30 ± 2.0 versus 27 ± 2.3%, p = 0.03).ConclusionsIn reperfused first-time AMI patients, native T1 of remote myocardium decreased from baseline to follow-up. ECV of remote myocardium decreased over time in patients with no LV dilatation, but remained elevated at follow-up in those who developed LV dilatation. Findings from this study may add to an increased understanding of the pathophysiological mechanisms of cardiac remodeling after AMI.

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Section: Discussionsupporting

confidence: 74%

Changes in remote myocardial tissue after acute myocardial infarction and its relation to cardiac remodeling: A CMR T1 mapping study

et al. 2017

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“…The reason for this observation is not quite clear. Unspecific myocardial inflammation12 31 caused by HHV6 infection may have resulted in a coronary vasomotility disorder enabling the occurrence of coronary vasospasm. However, there is some evidence that HHV6 can also lead to vascular injury 35.…”

Section: Discussionmentioning

confidence: 99%

Coronary vasospasm as the underlying cause for chest pain in patients with PVB19 myocarditis

Yılmaz

Mahrholdt

Athanasiadis

et al. 2008

Heart

160

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“…Nitrates and calcium channel antagonists may alleviate ischemia due to vasospasm. Yet, we need to identify the molecular alterations responsible for SMC hyperreactivity, as many patients do not respond satisfactorily to standard doses of vasodilators 93 . Knowledge of the post-receptor mechanisms responsible for SMC hyperreactivity and epicardial coronary spasm might enable the development of new therapeutic options for patients who present poor clinical response to nonspecific vasodilator therapy.…”

Section: Plaque Without Thrombusmentioning

confidence: 99%

Acute Coronary Syndromes

2017

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Well into the 21st century, we still triage acute myocardial infarction based on the presence or absence of ST segment elevation, a century-old technology. Meanwhile, we have learned a great deal regarding the pathophysiology and mechanisms of acute coronary syndromes (ACS) at clinical, pathological, cellular, and molecular levels. Contemporary imaging studies have shed new light into the mechanisms of ACS. This review discusses these advances and their implications for clinical management of the ACS for the future. Plaque rupture has dominated our thinking about ACS pathophysiology for decades. Yet, current evidence suggests that a sole focus on plaque rupture vastly oversimplifies this complex collection of diseases, and obscures other mechanisms that may mandate different management strategies. We propose to segment coronary artery thrombosis due to plaque rupture into cases with or without signs of concomitant inflammation. This distinction may have substantial therapeutic implications as direct anti-inflammatory interventions for atherosclerosis emerge. Coronary artery thrombosis due to plaque erosion may be on the rise in an era of intense lipid lowering. Identification of patients with of ACS due to erosion may permit a less invasive approach to management than the current standard of care. We also now recognize ACS that occur without apparent epicardial coronary artery thrombus or stenosis. Such events may arise from spasm, microvascular disease, or other pathways. Emerging management strategies may likewise apply selectively to this category of ACS. We advocate this more mechanistic approach to the categorization of ACS to provide a framework for future tailoring, triage, and therapy for patients in a more personalized and precise manner.

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Sudden coronary death, fatal acute myocardial infarction and widespread coronary and myocardial inflammation

Abstract: The study shows the presence of a lymphocytic infiltrate in both coronary arteries and myocardium and a proinflammatory phenotype shift in the myocardium associated with acute coronary thrombosis in patients dying suddenly, shortly, or even late after coronary thrombosis.

Cited by 32 publications

References 17 publications

Changes in remote myocardial tissue after acute myocardial infarction and its relation to cardiac remodeling: A CMR T1 mapping study

Changes in remote myocardial tissue after acute myocardial infarction and its relation to cardiac remodeling: A CMR T1 mapping study

Coronary vasospasm as the underlying cause for chest pain in patients with PVB19 myocarditis

Acute Coronary Syndromes

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