Clinical study—ILate effects of acute infarct dilation on heart size: a two dimensional echocardiographic study☆
References (20)
- et al.
Infarct expansion versus extension. Two different complications of acute myocardial infarction
Am J Cardiol
(1978) - et al.
Risk stratification after acute myocardial infraction
Am J Cardiol
(1978) - et al.
Heart size and ten year survival after uncomplicated myocardial infarction
Am Heart J
(1969) - et al.
Regional cardiac dilatation after acute myocardial infarction. Recognition by two-dimensional echocardiography
N Engl J Med
(1979) - et al.
Expansion of transmural myocardial infarction: a pathophysiological factor in cardiac rupture
Circulation
(1979) - et al.
Two-dimensional echocardiographic recognition of myocardial injury in man: comparison with post mortem studies
Circulation
(1981) Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Great Vessels
- et al.
The initial chest x-ray in acute myocardial infarction. Prediction of early and late mortality and survival
Circulation
(1980) Heart Disease
- et al.
Left ventricular size after acute myocardial infarction. Serial changes and their prognostic significance
Circulation
(1975)
Cited by (251)
Evolution of reperfusion post-infarction ventricular remodeling: New MRI insights
2013, International Journal of CardiologyCitation Excerpt :Expansion is distortion of the ventricletopography caused by alterations of the infarcted segment and without newly infarcted tissue [5]. These studies are mainly based on histochemistry, ECG or echocardiography and principally examined by ex-vivo triphenyl tetrazolium chloride (TTC-) staining [5], expansion of ST-elevation or ventricular silhouettes and dyskinesia/akinesia [6,7], but are not able to assess the actual infarct size quantitatively. SPECT and contrast enhanced CMR allows delineation of the acute necrotic infarct zone and late fibrotic infarct scar.
Ischemia/Infarction
2012, Heart Failure ClinicsCitation Excerpt :Although infarct expansion was first described in autopsied hearts of patients who died within approximately 10 days after transmural MI,14 subsequent studies using two-dimensional echocardiographic imaging established that infarct expansion is an early event that is detectable while patients are still alive, thus making early diagnosis possible.15 Other serial two-dimensional echocardiographic studies showed that the early regional infarct expansion was a major cause of global LV dilation and impaired functional status in patients post-MI.16,17 In the pathologic study, 50% of the patients who died within 30 days had infarct expansion, which was most severe in those with large, transmural, and anterior MI.14
CT for evaluation of myocardial cell therapy in heart failure: A comparison with CMR imaging
2011, JACC: Cardiovascular ImagingCitation Excerpt :This animal study was conducted without any medical therapy given to patients after MI. Therefore, the chronic MIs expanded and the infarct size increased in the placebo group, consistent with results from a clinical study using noninvasive imaging techniques conducted in the early 1980s (34). With modern medical therapy, decreases in infarct size are anticipated in chronic MI, as shown in a recent CMR study (35).
Mechanistic insights into ischemic mitral regurgitation: Echocardiographic and surgical implications
2011, Journal of the American Society of EchocardiographyAlterations in Ventricular Structure. Role of Left Ventricular Remodeling
2011, Heart FailureLeft ventricular remodeling in heart failure: Current concepts in clinical significance and assessment
2011, JACC: Cardiovascular ImagingCitation Excerpt :The term ventricular remodeling refers to alteration in ventricular architecture, with associated increased volume and altered chamber configuration, driven on a histologic level by a combination of pathologic myocyte hypertrophy, myocyte apoptosis, myofibroblast proliferation, and interstitial fibrosis (1–3).
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This study was supported in part by National Institutes of Health Grant 2R01 HL-19232, Specialized Center of Research Grant 5PO-HL-17655, Bethesda, Maryland and a Grant in Aid from the American Heart Association, Dallas, Texas and its Maryland Affiliate, Baltimore, Maryland.
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Present address: Division of Cardiology, The New York Hospital-Cornell Medical Center, New York, New York. Dr. Erlebacher was a Fellow of the American Heart Association, Maryland Affiliate 1979–1980.