scholarly journals Value of contrast-enhanced, balanced cine-MR sequences in the assessment of apparent infarct size after acute myocardial infarction: A prospective comparison with delayed-enhancement sequences

2005 ◽  
Vol 22 (6) ◽  
pp. 765-771 ◽  
Author(s):  
Jean-Pierre Laissy ◽  
Fabien Hyafil ◽  
Valérie Huart ◽  
Jean-Michel Serfaty ◽  
Sylvie Chillon ◽  
...  
2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Nunohiro ◽  
S Kuwasaki ◽  
T Fukushima ◽  
S Furudono ◽  
H Suenaga ◽  
...  

Abstract The involvement of cholesterol crystals (CCs) in plaque progression and destabilization of atherosclerotic plaques has been recently recognized. However, little is known about CCs and myocardial salvage in the Acute myocardial infarction (AMI) patients. This study aimed to evaluate the association between the existence of CCs at the site of culprit coronary artery and myocardial salvage index (MSI).To investigate, we applied the diagnostic resources of Optical Coherence Tomography (OCT). Methods This study included 53 AMI patients (90% with STEMI) who underwent primary PCI within 24h of onset. 53 STEMI patients underwent magnetic resonance imaging (CMR) of 5th days and 3 months after PCI. Infarct size was measured on delayed-enhancement imaging, and area at risk was quantified on T2-weighted imaging. MSI was calculated as [area at risk − infarct size] × 100/area at risk. 3 months CMR with contrast-enhanced imaging of late gadolinium enhancement-LGE. Patients were divided 2 groups according to the existence of CCs at the site of culprit coronary artery. Results CCs occurs in 26 of 53 (49%). Acute 5th days risk area (13.5±4.1 vs 12.6±4.9, P=0.48) and 3months infarct size (5.3±3.5 vs 7.0±3.2, P=0.066) were not significant between CCs and no CCs group. But salvage index were significantly lower in patients with CCs group (47.7±17.5% vs 60.1±20.2%, P=0.021) Conclusion Salvage index in patients that CCs were found by the OCT analysis, remain low after AMI. This study demonstrates the potential correlation between the myocardial salvage and vulnerable morphological features of culprit lesion to the presence of CCs with AMI patients.


Radiology ◽  
2006 ◽  
Vol 240 (2) ◽  
pp. 529-536 ◽  
Author(s):  
Gilbert L. Raff ◽  
William W. O'Neill ◽  
Ralph E. Gentry ◽  
Ammar Dulli ◽  
Kostaki G. Bis ◽  
...  

1999 ◽  
Vol 82 (S 01) ◽  
pp. 68-72 ◽  
Author(s):  
Alessandro Sciahbasi ◽  
Eugenia De Marco ◽  
Attilio Maseri ◽  
Felicita Andreotti

SummaryPreinfarction angina and early reperfusion of the infarct-related artery are major determinants of reduced infarct-size in patients with acute myocardial infarction. The beneficial effects of preinfarction angina on infarct size have been attributed to the development of collateral vessels and/or to post-ischemic myocardial protection. However, recently, a relation has been found between prodromal angina, faster coronary recanalization, and smaller infarcts in patients treated with rt-PA: those with preinfarction angina showed earlier reperfusion (p = 0.006) and a 50% reduction of CKMB-estimated infarct-size (p = 0.009) compared to patients without preinfarction angina. This intriguing observation is consistent with a subsequent observation of higher coronary recanalization rates following thrombolysis in patients with prodromal preinfarction angina compared to patients without antecedent angina. Recent findings in dogs show an enhanced spontaneous lysis of plateletrich coronary thrombi with ischemic preconditioning, which is prevented by adenosine blockade, suggesting an antithrom-botic effect of ischemic metabolites. Understanding the mechanisms responsible for earlier and enhanced coronary recanalization in patients with preinfarction angina may open the way to new reperfusion strategies.A vast number of studies, globally involving ≈17,000 patients with acute myocardial infarction, have unequivocally shown that an infarction preceded by angina evolves into a smaller area of necrosis compared to an infarct not preceded by angina (Table 1) (1). So far, preinfarction angina has been thought to have cardioprotective effects mainly through two mechanisms: collateral perfusion of the infarctzone (2-4), and ischemic preconditioning of the myocardium (5-7). Here we discuss a further mechanism of protection represented by improved reperfusion of the infarct-related artery.


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