Reperfusion reduces left ventricular dilatation by preventing infarct expansion in the acute and chronic phases of myocardial infarction
Reference (64)
- et al.
Multicenter trial of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) in acute myocardial infarction: effects on infarct size and left ventricular function
J Am Coll Cardiol
(1989) - et al.
Early thrombolysis in acute myocardial infarction: limitation of infarct size and improved survival
J Am Coll Cardiol
(1986) - et al.
Relation between infarct size and left ventricular performance assessed in patients with first acute myocardial infarction randomized to intracoronary thrombolytic therapy or to conventional treatment
Am J Cardiol
(1988) - et al.
Effect of streptokinase on left ventricular modeling and function after acute myocardial infarction: the GISSI (Gruppo Italiano per lo Studio della Streptokinasi Nell'infarto Miocardico) trial
J Am Coll Cardiol
(1989) - et al.
Preservation of global and regional left ventricular function after early thrombolysis in acute myocardial infarction
J Am Coll Cardiol
(1986) - et al.
Acute reduction in functional infarct expansion with late coronary reperfusion: assessment with quantitative two-dimensional echocardiography
J Am Coll Cardiol
(1988) - et al.
Effect of successful intravenous reperfusion therapy on regional myocardial function and geometry in humans a tomographic assessment using two-dimensional echocardiography
J Am Coll Cardiol
(1989) - et al.
Effects of late administration of tissue-type plasminogen activator on left ventricular remodeling and function after myocardial infarction
J Am Coll Cardiol
(1990) - et al.
Early dilation of the infarcted segment in acute transmural myocardial infarction: role of infarct expansion in acute left ventricular enlargement
J Am Coll Cardiol
(1984) - et al.
Patterns of creatine kinase release during acute myocardial infarction after nonsurgical reperfusion: comparison with conventional treatment and correlation with infarct size
J Am Coll Cardiol
(1984)
Plasminogen Activator Italian Multicenter Study (PAIMS): comparison of in travenous recombinant single-chain human tissue-type plasminogen activator (rt-PA) with intravenous streptokinase in acute myocardial infarction
J Am Coll Cardiol
Reperfusion of the infarct-related coronary artery prevents left ventricular expansion above and beyond myocardial salvage
Am Heart J
Infarct artery perfusion and changes in left ventricular volume in the month after acute myocardial infarction
J Am Coll Cardiol
From myocardial salvage to patient salvage in acute myocardial infarction: the role of reperfusion therapy
J Am Coll Cardiol
Acute effects of delayed reperfusion on myocardial infarct shape and left ventricular volume: a potential mechanism of additional benefits from thrombolytic therapy
J Am Coll Cardiol
Time course of left ventricular dilatation after myocardial infarction: influence of infarct-related artery and success of coronary thrombolysis
J Am Coll Cardiol
Patterns of left ventricular dilatation during the six months after myocardial infarction
J Am Coll Cardiol
Increased left ventricular volume following myocardial infarction in man
Am Heart J
Late effects of acute infarct dilatation on heart size: a two dimensional echocardiographic study
Am J Cardiol
Prognosis after recovery for first acute myocardial infarction: determinants of reinfarction and sudden death
Am J Cardiol
Exercise training after anterior Q wave myocardial infarction: importance of regional left ventricular function and topography
J Am Coll Cardiol
Left ventricular remodeling in the year after first anterior myocardial infarction: a quantitative analysis of contractile segment lengths and ventricular shape
J Am Coll Cardiol
Infarct expansion versus extension: two different complications of acute myocardial infarction
Am J Cardiol
Infarct expansion pathologic analysis of 204 patients with a single myocardial infarct
J Am Coll Cardiol
Importance of coronary collateral circulation for kinetics of serum creatine kinase in acute myocardial infarction
Am J Cardiol
Heterogeneity of left ventricular segment wall thickening and excursion in 2-dimensional echocardiogram of normal human subjects
Am J Cardiol
Effect of intravenous streptokinase on left ventricular function and early survival after acute myocardial infarction
N Engl J Med
Limitation of myocardial infarct expansion by reperfusion independent of myocardial salvage
Circulation
Dissociation between infarct reduction and myocardial expansion with reperfusion [Abstract]
J Am Coll Cardiol
Peak creatine kinase as a measure of effectiveness of thrombolytic therapy in acute myocardial infarction
Am J Cardiol
A prospective trial of intravenous streptokinase in acute myocardial infarction (I.S.A.M.). Mortality, morbidity, and infarct size at 21 days
N Engl J Med
The Thrombolysis in Myocardial Infarction (TIMI) Trial. Phase I findings
N Engl J Med
Cited by (31)
Beneficial effect of reperfusion therapy beyond the preservation of left ventricular function in patients with acute ST-segment elevation myocardial infarction
2011, International Journal of CardiologyCitation Excerpt :This has been reported from randomized trials as well [11]. The mechanisms involved in the beneficial effect of early reperfusion therapy might be improved healing of infarct tissue and prevention of ventricular remodeling, prevention of infarct expansion, a positive effect on diastolic function and increased electrical stability [3,4,12–16]. However despite the use of the propensity score for the adjustment of confounders, these and other factors which we did not include in the analysis may have played a major role on outcome and therefore this study remains a hypothesis generating study.
Analysis of apical remodeling in gated myocardial perfusion SPECT imaging in ischemic cardiomyopathy
2008, Journal of Nuclear CardiologyCitation Excerpt :This sign appeared in 75% of the patients in our series who had a DP. Generally speaking, left-ventricular remodeling develops secondary to extensive transmural myocardial infarction,13-18 and is arbitrarily divided into an early phase (within the first 72 hours) and a late phase (>72 hours).19 The early phase includes expansion of the infarcted area, occasionally causing myocardial rupture or ventricular aneurysm.
Relationship Between Systolic Pulsed Wave Tissue Doppler Parameters and Both Invasive and Noninvasive Reperfusion Criteria in Patients with Acute Anterior Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention
2008, Journal of the American Society of EchocardiographyCitation Excerpt :On the other hand, patients with MBG 0 or 1 showed significant deterioration of systolic PTD parameters in the infarct-related walls. Because of the possible failure of myocardial reperfusion in these patients, they possibly demonstrate a larger infarct size with more deleterious infarct extension and infarct expansion,15 resulting in functional deterioration of systolic motion in the infarct-related segments. Patients with TIMI 3 flow demonstrated a similar trend, yet the differences between the first and the second reading were not statistically significant in some of the examined walls.
Patients with hibernating myocardium show altered left ventricular volumes and shape, which revert after revascularization: Evidence that dyssynergy might directly induce cardiac remodeling
2006, Journal of the American College of CardiologyEffect of antecedent systemic hypertension on subsequent left ventricular dilation after acute myocardial infarction (from the Survival and Ventricular Enlargement trial)
2004, American Journal of CardiologyCitation Excerpt :By demonstrating a graded increase in the risk of LV dilation with poor BP control among hypertensives at baseline and during follow-up, our analyses provide additional support to the notion that inadequate BP control may be causally related to greater LV dilation after AMI. Several studies have associated larger myocardial infarcts,1,19 transmural myocardial infarctions,1 anterior wall myocardial infarctions,20,21 and preexisting LV hypertrophy14 with an increased risk of LV dilation after AMI and reported that coronary reperfusion,22 captopril use,23 and β-blocker use24 decrease the risk of LV dilation after AMI. In the present investigation, we accounted for the disparity in the distribution of these key factors, associated with hypertension and/or proved to influence remodeling after AMI, in multivariable analyses.
Postinfarctional remodeling: Increased dye intensity in the myocardial risk area after angioplasty of infarct-related coronary artery is associated with reduction of ventricular volumes
2001, Journal of the American College of CardiologyCitation Excerpt :No correlations were found for the other variables. Left ventricular remodeling is the final result of chronic changes in shape and structure and is characterized by progressive enlargement (23–26), a process in which the infarct size and the perfusion status of the IRA (27–29)are considered to be the most important factors. In recent years, clinicians’ attention has been focused (1–4)on the role of microcirculation preserved within the infarcted area, which is able to influence postinfarctional remodeling.