Quantitative evaluation of ischemic myocardial scar tissue by noncontrast T1 mapping using 3 Tesla MR scanner

2014 ◽  
Author(s):  
Aylin Okur ◽  
Mecit Kantarci ◽  
Yesim Kizrak ◽  
Sema Yildiz ◽  
Berhan Pirimoglu ◽  
...  
Keyword(s):  
Quantitative Evaluation ◽  
T1 Mapping ◽  
Scar Tissue ◽  
Myocardial Scar ◽  
3 Tesla ◽  
Myocardial Scar Tissue

scholarly journals Quantitative evaluation of ischemic myocardial scar tissue by unenhanced T1 mapping using 3.0 Tesla MR scanner

2014 ◽  
Vol 20 (5) ◽  
pp. 407-413 ◽  
Author(s):  
Aylin Okur ◽  
Mecit Kantarci ◽  
Yesim Kizrak ◽  
Sema Yildiz ◽  
Berhan Pirimoglu ◽  
...  
Keyword(s):  
Quantitative Evaluation ◽  
T1 Mapping ◽  
Scar Tissue ◽  
Myocardial Scar ◽  
3.0 Tesla ◽  
Myocardial Scar Tissue

scholarly journals Detection of myocardial scar tissue by M-mode echocardiography.

Circulation ◽  
1978 ◽  
Vol 57 (2) ◽  
pp. 230-237 ◽  
Author(s):  
S Rasmussen ◽  
B C Corya ◽  
H Feigenbaum ◽  
S B Knoebel
Keyword(s):  
Scar Tissue ◽  
Myocardial Scar ◽  
Myocardial Scar Tissue

scholarly journals P1437 Integrated ST segment elevation score as a new predictor of the myocardial scar extent determined with LGE-CMR at 1-month follow-up after STEMI

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
A Mester ◽  
T Benedek ◽  
D Opincariu ◽  
A Benedek ◽  
M Ratiu ◽  
...  
Keyword(s):  
Scar Tissue ◽  
Myocardial Scar ◽  
St Segment Elevation ◽  
Elevation Score ◽  
St Segment ◽  
Myocardial Scar Tissue ◽  
Hs Crp ◽  
Lge Cmr

Abstract Funding Acknowledgements Funded by the research grant PlaqueImage, contract number 26/01.09.2016, SMIS code 103544, by the European Union and the Government of Romania Background The inflammatory response in the acute phase of a myocardial infarction, as well as in later phases contributes to the healing process of the infarcted myocardium and the left ventricular remodeling. Restoration and improvement of LV function highly depends on the magnitude of scar formation. Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging has been validated for an accurate determination of the myocardial scar size and transmurality. The recovery of ST segment elevation is a liable marker of vessel patency following PCI. Purpose The aim of the study was to validate a new integrated score of ST segment elevation score (ISSTE) as a new predictor of the myocardial scar tissue size, in relation with increased inflammatory biomarkers, with the extent of myocardial fibrosis at one month, assessed with LGE-CMR, after STEMI. Methods We included 65 patients with STEMI who underwent urgent revascularization with PCI in the first 12 hours from the onset of symptoms. The ISSTE was determined by summing the ST segment elevation in all registered ECG leads at presentation (ISSTE-1) and at 2 hours (ISSTE-2) after primary PCI. Blood samples were also collected at baseline and day-5 for determination of serum hs-CRP levels. At 1-month follow-up all patients under LGE-CMR (1.5T scanner) for evaluation of the myocardial scar extent (volume, percentage, transmurality). Results ISSTE-2 was significantly correlated with day-5 hs-CRP serum levels (r = 0.546, 95%CI: 0.030-0.832, p = 0.037), although no significant correlations were noted with baseline hs-CRP levels (r= 0.238, p = 0.407). There were no significant correlations between ISSTE-1 score and the myocardial scar percentage (r = 0.241, p = 0.11) or high transmurality volume (r = 0.194, p = 0.21), while ISSTE-2 significantly correlated with myocardial scar mass (r = 0.406, 95%CI: 0.107-0.637 p = 0.007) and high transmurality volume (r = 0.344, 95%CI: 0.0320-0.596, p = 0.0273). The restoration of the ST segment, reflected by the difference between ISSTE-1 and ISSTE -2 is correlated with the infarct size mass (r = 0.336, 95%CI: 0.0307 -0.584, p = 0.027). Conclusion The magnitude of ST segment elevation determined at 2 hours after PCI was associated with the inflammatory response at day 5 after STEMI and it may serve as a predictor for the extent of the myocardial scar tissue determined with LGE-CMR at 1 month following STEMI. The ISSTE-1 score calculated at presentation does not reflect extent of the affected myocardial tissue following PCI.

Survival and Function of Bioengineered Cardiac Grafts

Circulation ◽  
1999 ◽  
Vol 100 (suppl_2) ◽  
Author(s):  
Ren-Ke Li ◽  
Zhi-Qiang Jia ◽  
Richard D. Weisel ◽  
Donald A. G. Mickle ◽  
Angel Choi ◽  
...  
Keyword(s):  
Tissue Culture ◽  
Subcutaneous Tissue ◽  
Scar Tissue ◽  
Myocardial Scar ◽  
Fetal Rat ◽  
Myocardial Scar Tissue ◽  
And Function ◽  
Cardiac Graft

Introduction —Patients with congenital heart disease frequently require graft material for repair of cardiac defects. However, currently available grafts lack growth potential and are noncontractile and thrombogenic. We have developed a viable cardiac graft that contracts spontaneously in tissue culture by seeding cells derived from fetal rat ventricular muscle into a biodegradable material. We report our investigations of the in vitro and in vivo survival and function of this bioengineered cardiac graft. Methods and Results —A cardiomyocyte-enriched cell inoculum derived from fetal rat ventricular muscle was seeded into a piece of Gelfoam (Upjohn, Ontario, Canada), a biodegradable gelatin mesh, to form the graft. For in vitro studies, growth patterns of the cells within the graft were evaluated by constructing growth curves and by histologic examination; in in vivo studies, the graft was cultured for 7 days and then implanted either into the subcutaneous tissue of adult rat legs or onto myocardial scar tissue in a cryoinjured rat heart. Five weeks later, the graft was studied histologically. The inoculated cells attached to the gelatin mesh and grew in 3 dimensions in tissue culture, forming a beating cardiac graft. In both the subcutaneous tissue and the myocardial scar, blood vessels grew into the graft from the surrounding tissue. The graft implanted into the subcutaneous tissue contracted regularly and spontaneously. When implanted onto myocardial scar tissue, the cells within the graft survived and formed junctions with the recipient heart cells. Conclusions —Fetal rat ventricular cells can grow 3-dimensionally in a gelatin mesh. The cells in the graft formed cardiac tissue and survived and contracted spontaneously both in tissue culture and after subcutaneous implantation. Future versions of this bioengineered cardiac graft may eventually be used to repair cardiac defects.

Revascularization of Myocardial Scar Tissue Following Prostaglandin E1-Therapy in Patients with Ischemic Heart Disease

2003 ◽  
Vol 199 (3) ◽  
pp. 129-136 ◽  
Author(s):  
Mohammad Reza Mehrabi ◽  
Nermin Serbecic ◽  
Forouzan Tamaddon ◽  
Kurt Huber ◽  
Richard Pacher ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Prostaglandin E1 ◽  
Scar Tissue ◽  
Myocardial Scar ◽  
Ischemic Heart ◽  
Myocardial Scar Tissue

scholarly journals Tuberculous myocarditis presenting as a refractory ventricular tachycardia of biventricular origin

2012 ◽  
Vol 7 (2) ◽  
pp. 60-66 ◽  
Author(s):  
MP Gautam ◽  
G Sogunuru ◽  
G Subramanyam ◽  
RC Viswanath
Keyword(s):  
Ventricular Tachycardia ◽  
Clinical Symptoms ◽  
Scar Tissue ◽  
Myocardial Scar ◽  
Hemodynamic Compromise ◽  
Lv Dysfunction ◽  
Long Run ◽  
Myocardial Scar Tissue ◽  
Life Threatening ◽  
Artery Disease

Ventricular tachycardia (VT) is one of the difficult clinical problems for the physician. Its evaluation and treatment are complicated because of its life-threatening nature and urgent need of rapid management. Any process that creates myocardial scar tissue could be the substrate for ventricular tachycardia. The coronary artery disease is the most common cause of myocardial scar. The dilated cardiomyopathies, hypertrophic cardiomyopathy, right ventricular dysplasia, Chagas disease, sarcoidosis, myocarditis including tubercular and other chronic granulomatous conditions and surgical incisions in the ventricle also can create myocardial scar and can lead to ventricular tachycardia. Occasionally, the arrhythmia may be well-tolerated, but in most of the situations it is associated with grave, life-threatening hemodynamic compromise. Regardless of the arrhythmia mechanism, the severity of clinical symptoms and hemodynamic compromise determines the urgency with which VT must be treated. Rarely, patients present with repetitive runs of nonsustained or sustained VT despite the medical treatment and poorly respond to the conventional treatment. Such refractory VT may cause a tachycardia-induced cardiomyopathy in long run. In such cases, long-term management also include looking beyond the VT and work up for the possible and treatable cause of VT. Here we are presenting a case report of a young patient with tubercular myocarditis who has presented to us with recurrent ventricular tachycardia of both right bundle and left bundle branch block morphology and LV dysfunction. A review of literature has been carried out on causes and management of refractory VT.Journal of College of Medical Sciences-Nepal, 2011, Vol-7, No-2, 60-66DOI: http://dx.doi.org/10.3126/jcmsn.v7i2.6686

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