Literature DB >> 2888158

Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts.

H F Weisman, B Healy.   

Abstract

Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually reach peak extent within seven to 14 days. Clinical data suggest that infarct expansion occurs in approximately 35% to 45% of anterior transmural myocardial infarctions and to a lesser extent in infarctions at other sites. Although expansion usually develops in large infarcts, the extent of transmural necrosis rather than absolute infarct size predicts its occurrence. Expansion has an adverse effect on infarct structure and function for several reasons. Functional infarct size is increased because of infarct segment lengthening, and expansion results in over-all ventricular dilatation. Thus, patients with expansion of an infarct have poorer exercise tolerance, more congestive heart failure symptoms, and greater early and late mortality than those without expansion. Infarct rupture and late aneurysm formation are two additional structural consequences of infarct expansion. Experimental and clinical data suggest that the incidence and severity of expansion can be modified by interventions. Increased ventricular loading conditions and steroidal and nonsteroidal antiinflammatory agents make expansion more severe. Reperfusion of the infarct segment and pharmacologic interventions that decrease ventricular afterload lessen the severity of expansion. Previous myocardial infarction and preexisting ventricular hypertrophy may also limit the development of infarct expansion. Infarct extension is defined clinically as early in-hospital reinfarction after a myocardial infarction. The pathologic finding of infarct extension is necrotic and healing myocardium of several different recent ages within the same vascular territory. Although this pathologic criterion usually cannot be verified, studies employing invasive and noninvasive assessment of patients with early reinfarction provide evidence that the new myocardial injury is usually in the same vascular risk region as the original infarction. A variety of different criteria have been applied in the clinical diagnosis of infarct extension, and this has resulted in a large range of estimated frequencies from under 10% to as high as 86%. High estimates are found in studies using one or two nonspecific criteria such as ST segment shift or reelevation of total CK. The lowest rates have been found when combinations of criteria are used.(ABSTRACT TRUNCATED AT 400 WORDS)

Entities:  

Mesh:

Substances:

Year:  1987        PMID: 2888158     DOI: 10.1016/0033-0620(87)90004-1

Source DB:  PubMed          Journal:  Prog Cardiovasc Dis        ISSN: 0033-0620            Impact factor:   8.194


  37 in total

1.  Benefits of late reperfusion in the treatment of acute myocardial infarction.

Authors:  Kinji Ishikawa
Journal:  J Thromb Thrombolysis       Date:  2002-06       Impact factor: 2.300

2.  Ventricular remodelling after myocardial infarction.

Authors:  M A Vannan; D J Taylor
Journal:  Br Heart J       Date:  1992-09

3.  Injectable hydrogel properties influence infarct expansion and extent of postinfarction left ventricular remodeling in an ovine model.

Authors:  Jamie L Ifkovits; Elena Tous; Masahito Minakawa; Masato Morita; J Daniel Robb; Kevin J Koomalsingh; Joseph H Gorman; Robert C Gorman; Jason A Burdick
Journal:  Proc Natl Acad Sci U S A       Date:  2010-06-07       Impact factor: 11.205

4.  Left ventricular remodelling after myocardial infarction: importance of residual myocardial viability and ischaemia.

Authors:  C A Visser
Journal:  Heart       Date:  2003-10       Impact factor: 5.994

5.  Image-based left ventricular shape analysis for sudden cardiac death risk stratification.

Authors:  Fijoy Vadakkumpadan; Natalia Trayanova; Katherine C Wu
Journal:  Heart Rhythm       Date:  2014-05-20       Impact factor: 6.343

6.  IGF-1 degradation by mouse mast cell protease 4 promotes cell death and adverse cardiac remodeling days after a myocardial infarction.

Authors:  Thor Tejada; Lin Tan; Rebecca A Torres; John W Calvert; Jonathan P Lambert; Madiha Zaidi; Murtaza Husain; Maria D Berce; Hussain Naib; Gunnar Pejler; Magnus Abrink; Robert M Graham; David J Lefer; Nawazish Naqvi; Ahsan Husain
Journal:  Proc Natl Acad Sci U S A       Date:  2016-06-06       Impact factor: 11.205

Review 7.  Injectable acellular hydrogels for cardiac repair.

Authors:  Elena Tous; Brendan Purcell; Jamie L Ifkovits; Jason A Burdick
Journal:  J Cardiovasc Transl Res       Date:  2011-06-28       Impact factor: 4.132

Review 8.  Inhibition of the renin-angiotensin system after acute myocardial infarction--treat first, select later?

Authors:  A S Hall; R Sapsford; S G Megarry; S G Ball
Journal:  Heart       Date:  1996-11       Impact factor: 5.994

Review 9.  Ischaemic ventricular aneurysms: true or false?

Authors:  M J Davies
Journal:  Br Heart J       Date:  1988-08

10.  MRI evaluation of injectable hyaluronic acid-based hydrogel therapy to limit ventricular remodeling after myocardial infarction.

Authors:  Shauna M Dorsey; Jeremy R McGarvey; Hua Wang; Amir Nikou; Leron Arama; Kevin J Koomalsingh; Norihiro Kondo; Joseph H Gorman; James J Pilla; Robert C Gorman; Jonathan F Wenk; Jason A Burdick
Journal:  Biomaterials       Date:  2015-08-06       Impact factor: 12.479

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.