Myocardial scar tissue
Myocardial scar tissue is referred to as the final result and pathological correlate of myocardial infarction and develops from the infarcted tissue.
Myocardial scar tissue is also called ‘non-viable myocardium’ even though the latter is a misnomer since it is known that even in myocardial scar tissue there are residual functional cells 1,2.
A prolonged reduction of blood flow results in myocardial cell death. The necrotic myocardial zone will subsequently undergo a healing or remodeling process, starting with an inflammatory response, where the necrotic tissue is degraded and resorbed, followed by a fibrotic phase, where myofibroblasts build up collagenous scar tissue and eventually by a remodeling phase, where the scar matures by the steady increase of collagen cross-linking and myofibroblasts undergo apoptosis 1.
This is a gradual dynamic process occurring over the days and weeks, following myocardial infarction and can be divided into three stages 1:
- inflammatory phase
- fibrotic phase
- remodeling phase
In addition to changes in organization and composition, the infarcted tissue faces changes in tissue geometry, characterized by thinning in the radial and lengthening in a circumferential direction. In addition, decreases in infarct surface area and shrinkage were found during the first three weeks indicative of remodeling mechanisms, which are able to overpower local stresses by scar thinning.
The final end result of this on a microscopic/biochemical level rather complex process is a mature myocardial scar.
Myocardial scar tissue consists mainly of fibrillary collagen 1,2, arranged mainly but not only in circumferential, concentric layers but in a variety of fiber orientations, collagen cross-linking but also surviving cardiomyocytes, which are widely separated by the fibrillary collagen fibers and cells termed myofibroblasts 2.
Myocardial scar tissue can be seen with echocardiography and in CT and in particular, be assessed with cardiac MRI.
- thinning and decreased contrast-enhancement or rather perfusion of the affected myocardial segment
- thinning and wall motion abnormalities of the affected segment
- hypokinesia or akinesia/dyskinesia depending on the transmural extent
- decreased systolic shortening or even lengthening of global longitudinal and circumferential strain parameters
- decreased or negative radial strain
Cardiac MRI or rather late gadolinium enhancement is the gold standard in the depiction of myocardial scar tissue. The increased extracellular volume (ECV) in a tissue mostly consistent of extracellular matrix protein as collagen constitutes an increased volume of distribution for extracellular contrast agents and thus to can be nicely depicted with late gadolinium enhancement or pictured with T1 mapping and extracellular volume (ECV) mapping since gadolinium-based contrast agents experience a prolonged wash-out period in these sort of tissues 3-6.
Scar tissue itself is non-contractile and shows a passive behavior on pressure and during the systolic contraction of the remaining myocardium, which leads to thinning of the affected segment and to akinesia or dyskinesia due to outward bulging and stretching of the scar in a transmurally infarcted segment or to hypokinesia in a subendocardial infarct, where the scar tissue overlying cardiomyocytes still contract.
T2/STIR: normal or hypointense
T2 mapping: normal T2 [ms]
T1 mapping: increased T1 [ms]
Perfusion imaging: perfusion defect also under rest
IRGRE/PSIR: varying degrees of subendocardial up to transmural late gadolinium enhancement (LGE) in the affected area of the myocardium
- 1. Richardson WJ, Clarke SA, Quinn TA, Holmes JW. Physiological Implications of Myocardial Scar Structure. (2015) Comprehensive Physiology. 5 (4): 1877-909. doi:10.1002/cphy.c140067 - Pubmed
- 2. Sun Y, Kiani MF, Postlethwaite AE, Weber KT. Infarct scar as living tissue. (2002) Basic research in cardiology. 97 (5): 343-7. doi:10.1007/s00395-002-0365-8 - Pubmed
- 3. Treibel TA, White SK, Moon JC. Myocardial Tissue Characterization: Histological and Pathophysiological Correlation. (2014) Current cardiovascular imaging reports. 7 (3): 9254. doi:10.1007/s12410-013-9254-9 - Pubmed
- 4. Kim RJ, Fieno DS, Parrish TB, Harris K, Chen EL, Simonetti O, Bundy J, Finn JP, Klocke FJ, Judd RM. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. (1999) Circulation. 100 (19): 1992-2002. doi:10.1161/01.cir.100.19.1992 - Pubmed
- 5. Turkbey EB, Nacif MS, Noureldin RA, Sibley CT, Liu S, Lima JA, Bluemke DA. Differentiation of myocardial scar from potential pitfalls and artefacts in delayed enhancement MRI. (2012) The British journal of radiology. 85 (1019): e1145-54. doi:10.1259/bjr/25893477 - Pubmed
- 6. Ibanez B, Aletras AH, Arai AE, Arheden H, Bax J, Berry C, Bucciarelli-Ducci C, Croisille P, Dall'Armellina E, Dharmakumar R, Eitel I, Fernández-Jiménez R, Friedrich MG, García-Dorado D, Hausenloy DJ, Kim RJ, Kozerke S, Kramer CM, Salerno M, Sánchez-González J, Sanz J, Fuster V. Cardiac MRI Endpoints in Myocardial Infarction Experimental and Clinical Trials: JACC Scientific Expert Panel. (2019) Journal of the American College of Cardiology. 74 (2): 238-256. doi:10.1016/j.jacc.2019.05.024 - Pubmed
- 7. Smiseth OA, Torp H, Opdahl A, Haugaa KH, Urheim S. Myocardial strain imaging: how useful is it in clinical decision making?. (2016) European heart journal. 37 (15): 1196-207. doi:10.1093/eurheartj/ehv529 - Pubmed