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Journal of Cardiovascular Magnetic Resonance

, 19:50

First Online: 04 July 2017Received: 20 December 2016Accepted: 09 May 2017


BackgroundMyocardial hemorrhage is a frequent complication following reperfusion in acute myocardial infarction and is predictive of adverse outcomes. However, it remains unsettled whether hemorrhage is simply a marker of a severe initial ischemic insult or directly contributes to downstream myocardial damage. Our objective was to evaluate the contribution of hemorrhage towards inflammation, microvascular obstruction and infarct size in a novel porcine model of hemorrhagic myocardial infarction using cardiovascular magnetic resonance CMR.

MethodsMyocardial hemorrhage was induced via direct intracoronary injection of collagenase in a novel porcine model of ischemic injury. Animals N = 27 were subjected to coronary balloon occlusion followed by reperfusion and divided into three groups N = 9-group: 8 min ischemia with collagenase +HEM; 45 min infarction with saline I-HEM; and 45 min infarction with collagenase I+HEM. Comprehensive CMR was performed on a 3 T scanner at baseline and 24 h post-intervention. Cardiac function was quantified by cine imaging, edema-inflammation by T2 mapping, hemorrhage by T2* mapping and infarct-microvascular obstruction size by gadolinium enhancement. Animals were subsequently sacrificed and explanted hearts underwent histopathological assessment for ischemic damage and inflammation.

ResultsAt 24 h, the +HEM group induced only hemorrhage, the I-HEM group resulted in a non-hemorrhagic infarction, and the I+HEM group resulted in infarction and hemorrhage. Notably, the I+HEM group demonstrated greater hemorrhage and edema, larger infarct size and higher incidence of microvascular obstruction. Interestingly, hemorrhage alone +HEM also resulted in an observable inflammatory response, similar to that arising from a mild ischemic insult I-HEM. CMR findings were in good agreement with histological staining patterns.

ConclusionsHemorrhage is not simply a bystander, but an active modulator of tissue response, including inflammation and microvascular and myocardial damage beyond the initial ischemic insult. A mechanistic understanding of the pathophysiology of reperfusion hemorrhage will potentially aid better management of high-risk patients who are prone to adverse long-term outcomes.

KeywordsMyocardial infarction Hemorrhage Inflammation Microvascular obstruction T2 T2* Ischemia reperfusion injury cardiovascular magnetic resonance Abbreviations+HEMHemorrhage without Infarction

AMIAcute Myocardial Infarction

ANOVAAnalysis of Variance

CMRCardiovascular Magnetic Resonance

EDVEnd Diastolic Volume

EFEjection Fraction

ESVEnd Systolic Volume

HandEHematoxylin and Eosin

I+HEMInfarction with Hemorrhage

I-HEMInfarction without Hemorrhage

IR-GREInversion Recovery Gradient Echo Sequence

IRIIschemia-Reperfusion Injury

LADLeft Anterior Descending coronary artery

LGELate Gadolinium Enhancement

LVLeft Ventricle

MVOMicrovascular Obstruction

PBSPhosphate Buffered Saline

SDStandard Deviation

SSFPSteady State Free Precession

STEMIST-Segment Elevation Myocardial Infarction

TTCTriphenyltetrazolium Chloride

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Autor: Nilesh R. Ghugre - Mihaela Pop - Reuben Thomas - Susan Newbigging - Xiuling Qi - Jennifer Barry - Bradley H. Strauss - Gr

Fuente: https://link.springer.com/article/10.1186/s12968-017-0361-7

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