Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping.

Picard, Michael H.; Wilkins, Gerard T.; Ray, Patricia; Weyman, Arthur E.

doi:10.1161/01.cir.82.2.484

Cited by 110 publications

(29 citation statements)

References 42 publications

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“…The present study was powered in terms of numbers of rats to detect significant difference in cardiac function and remodeling between groups at 6 months, followed by a terminal hemodynamic study, so that longer follow-up is not currently available. The degree of LV dilation may be the most powerful predictor of long-term prognosis in patients after MI (63), and additional studies on rats with heart failure after MI using larger numbers of animals and longer follow-up should clarify the effects of PLN inhibition on arrhythmias and survival. One animal died in the S16EPLN-treated group without evidence of heart failure.…”

Section: Figurementioning

confidence: 99%

Chronic phospholamban inhibition prevents progressive cardiac dysfunction and pathological remodeling after infarction in rats

Iwanaga¹,

Hoshijima²,

Gu³

et al. 2004

J. Clin. Invest.

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Ablation or inhibition of phospholamban (PLN) has favorable effects in several genetic murine dilated cardiomyopathies, and we showed previously that a pseudophosphorylated form of PLN mutant (S16EPLN) successfully prevented progressive heart failure in cardiomyopathic hamsters. In this study, the effects of PLN inhibition were examined in rats with heart failure after myocardial infarction (MI), a model of acquired disease. S16EPLN was delivered into failing hearts 5 weeks after MI by transcoronary gene transfer using a recombinant adeno-associated virus (rAAV) vector. In treated (MI-S16EPLN, n = 16) and control (MI-saline, n = 18) groups, infarct sizes were closely matched and the left ventricle was similarly depressed and dilated before gene transfer. At 2 and 6 months after gene transfer, MI-S16EPLN rats showed an increase in left ventricular (LV) ejection fraction and a much smaller rise in LV end-diastolic volume, compared with progressive deterioration of LV size and function in MI-saline rats. Hemodynamic measurements at 6 months showed lower LV end-diastolic pressures, with enhanced LV function (contractility and relaxation), lowered LV mass and myocyte size, and less fibrosis in MI-S16EPLN rats. Thus, PLN inhibition by in vivo rAAV gene transfer is an effective strategy for the chronic treatment of an acquired form of established heart failure.

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Section: Figurementioning

confidence: 99%

Chronic phospholamban inhibition prevents progressive cardiac dysfunction and pathological remodeling after infarction in rats

Iwanaga¹,

Hoshijima²,

Gu³

et al. 2004

J. Clin. Invest.

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“…Measurements included right and left atrial dimensions, LV dimensions, LV volume, LV ejection fraction (EF), RV function, extent of LV endocardium involved by wall-motion abnormality, LV sphericity index, and mitral valve annular dimensions. 9,10 LV volumes were measured by the method of discs from orthogonal apical views. The sphericity index was calculated as a ratio of the LV midventricular dimension (in the apical 4-chamber view) and the long-axis dimension.…”

Section: Echocardiographymentioning

confidence: 99%

Echocardiographic Predictors of Survival and Response to Early Revascularization in Cardiogenic Shock

et al. 2003

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for the SHOCK Trial Background-Although echocardiography is used in diagnosis and management of myocardial infarction, it has not been established whether specific features of cardiac structure or function early in the course of cardiogenic shock provide prognostic value. The purposes of this substudy of the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK (SHOCK) trial were to describe the echocardiographic features of cardiogenic shock, identify findings on early echocardiograms associated with outcome, examine the interaction of such features with treatment, and determine whether these features could provide insights into the survival benefit observed with early revascularization and guide selection of patients for this strategy. Methods and Results-One hundred seventy-five echocardiograms performed within 24 hours of randomization to the early revascularization (ERV) or initial medical stabilization (IMS) arms of the trial were submitted for quantitative assessment, and 169 were suitable for analysis. The 2 groups were similar in terms of clinical and early echocardiographic characteristics. Mean left ventricular ejection fraction (LVEF) was 31%, and moderate or greater mitral regurgitation (MR) was noted in 39.1%. On multivariate analysis, the only independent predictors of survival were MR severity and LVEF. A survival benefit for the ERV strategy was observed at all levels of LVEF and MR. Conclusions-A wide range of cardiac structural and functional abnormalities exists in patients presenting with acute cardiogenic shock. Both short-and long-term mortality appear to be associated with initial left ventricular systolic function and MR as assessed by echocardiography, and a benefit of ERV is noted regardless of baseline LVEF or MR.

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“…Once the MI is well established and the damage irreversible, it is important to limit adverse left ventricular (LV) remodeling to reduce the risk of heart failure. Indeed, the extent of LV dilation is the most powerful predictor of long-term prognosis post-MI (22).…”

mentioning

confidence: 99%

Effects of pre-, peri-, and postmyocardial infarction treatment with losartan in rats: effect of dose on survival, ventricular arrhythmias, function, and remodeling

Pourdjabbar¹,

Parker²,

Nguyen³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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. Effects of pre-, peri-, and postmyocardial infarction treatment with losartan in rats: effect of dose on survival, ventricular arrhythmias, function, and remodeling. Am J Physiol Heart Circ Physiol 288: H1997-H2005, 2005. First published November 11, 2004 doi:10.1152/ajpheart.00671.2004.-Angiotensin receptor blockers (ARBs) reduce adverse left ventricular (LV) remodeling and improve LV function and survival when started postmyocardial infarction (MI). ARBs also reduce ventricular arrhythmias during ischemia-reperfusion injury when started pre-MI. No information exists regarding their efficacy and safety when started pre-MI and continued peri-and post-MI. We evaluated whether the ARB losartan improves the outcome when started pre-MI and continued peri-and post-MI. Male Wistar rats (n ϭ 502) were treated for 7 days pre-MI with losartan at a high dose (30 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ), progressively increasing dose (3 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 increased to 10 mg ⅐ kg Ϫ1 ⅐ day Ϫ110 days and 30 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 20 days post-MI), or no treatment. Ambulatory systolic blood pressure and Holter monitoring were performed for 24 h post-MI. Echocardiography was done 30 days post-MI, and LV remodeling, cardiac hemodynamics, and fetal gene expression were assessed 38 days post-MI. High-dose losartan reduced 24-h post-MI survival compared with the progressive dose and control (21.9% vs. 36.6% and 38.1%, P ϭ 0.033 and P ϭ 0.009, respectively). This was associated with greater hypotension in the high dose and no change in ventricular arrhythmias in all groups. In 24-h post-MI survivors, the progressive dose group had reduced mortality from 24 h to 38 days (8.5% vs. 28.6% for control vs. 38.9% for high dose, P ϭ 0.032 and P ϭ 0.01, respectively). Survivors of both losartan groups demonstrated improved LV remodeling, cardiac hemodynamics, preserved GLUT-4, and reduced cardiac fetal gene expression. Pretreatment with ARBs does not reduce 24-h post-MI ventricular arrhythmias or survival, and high doses increase mortality by causing excessive hypotension. In 24-h post-MI survivors, progressively increasing doses of losartan have multiple beneficial effects, including improved survival.angiotensin II receptor blockers; heart failure; infarction; remodeling; hypotension DURING THE ACUTE PHASE of a myocardial infarction (MI), ventricular arrhythmias are the principle cause of death. Indeed, nearly 70% of patients dying of an acute MI die suddenly before arriving to the hospital (10). Safe and effective reduction in peri-MI arrhythmias is thus an essential strategy in improving peri-MI survival. Once a patient reaches the hospital, the major goal of therapy is reestablishing cardiac perfusion to limit MI size. Once the MI is well established and the damage irreversible, it is important to limit adverse left ventricular (LV) remodeling to reduce the risk of heart failure. Indeed, the extent of LV dilation is the most powerful predictor of long-term prognosis post-MI (22).The acute phase of the MI is characterized by neurohumoral activation, a proc...

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Natural history of left ventricular size and function after acute myocardial infarction. Assessment and prediction by echocardiographic endocardial surface mapping.

Cited by 110 publications

References 42 publications

Chronic phospholamban inhibition prevents progressive cardiac dysfunction and pathological remodeling after infarction in rats

Chronic phospholamban inhibition prevents progressive cardiac dysfunction and pathological remodeling after infarction in rats

Echocardiographic Predictors of Survival and Response to Early Revascularization in Cardiogenic Shock

Effects of pre-, peri-, and postmyocardial infarction treatment with losartan in rats: effect of dose on survival, ventricular arrhythmias, function, and remodeling

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