Search

Background: Left ventricular (LV) remodeling takes place after acute myocardial infarction (MI), potentially leading to overt heart failure (HF). Enhanced inflammation may contribute to LV remodeling. Our hypothesis was that the immunomodulating effects of intravenous immunoglobulin (IVIg) would be beneficial in patients with impaired myocardial function after MI by reducing myocardial remodeling and improving myocardial function., Methods: Sixty-two patients with acute MI treated by percutaneous coronary intervention, with depressed LV ejection fraction (LVEF) were randomized in a double-blinded fashion to IVIg as induction therapy and thereafter as monthly infusions or placebo for 26 weeks. The primary end point was changes in LVEF from baseline to 6 months as assessed by MRI., Results: Our main findings were: (i) LVEF increased significantly from 38 ± 10 (mean ± SD) to 45 ± 13% after IVIg and from 42 ± 9 to 49 ± 12% after placebo with no difference between the groups. (ii) The scar area decreased significantly by 3% and 5% in the IVIg and placebo group, respectively, with no difference between the groups. (iii) During the induction therapy (baseline to day 5), IVIg induced both inflammatory (e.g., increase in tumor necrosis factor α and monocyte chemoattractant protein-1) and anti-inflammatory (e.g., increase in interleukin-10 and decrease in leukocyte counts) variables, but during maintenance therapy there were no differences in changes of inflammatory mediators between IVIg and placebo., Conclusions: IVIg therapy after ST elevation MI managed by primary PCI does not affect LV remodeling or function. This illustrates the challenges of therapeutic intervention directed against the cytokine network, to prevent post-MI remodeling., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Background: Early prediction of infarct size directs therapy in patients with acute myocardial infarction (AMI). Global strain by echocardiography describes myocardial deformation and correlates with infarct size. However, peak strain measures deformation at a single time point, whereas ischemia and necrosis influence deformation throughout the heart cycle. It was hypothesized that the measurement of myocardial deformation throughout the heart cycle by mean strain is a more comprehensive expression of myocardial deformation. The aim of this study was to assess the ability of mean strain to predict infarct size and to identify large infarctions at admission and after revascularization in patients with AMI., Methods: Seventy-six patients with AMI were included. Echocardiographic measurements were performed at admission and after revascularization. Myocardial strain was calculated using speckle-tracking echocardiography. Infarct size was measured using contrast-enhanced magnetic resonance imaging ≥3 months after revascularization., Results: There were significant correlations between infarct size and longitudinal global mean strain, longitudinal global strain, and left ventricular ejection fraction (P < .0001), both at admission and after revascularization. The correlations improved after revascularization. Longitudinal global mean strain had the best correlation with infarct size and the best ability to discriminate between different infarct size categories. At admission, a cutoff value of -7.6 had 89% sensitivity, 88% specificity, and an area under the receiver operating characteristic curve of 0.92 for the identification of large infarctions. Prediction of infarct size improved for all parameters after revascularization., Conclusions: Longitudinal global mean strain provides improved early prediction of infarct size in patients with AMI compared with longitudinal global strain and left ventricular ejection fraction.

Background: We assessed the time profiles and prognostic utility of circulating markers of collagen turnover (CTO) following acute myocardial infarction (MI). In contrast to previous studies, no patient had been pre-treated with inhibitors of the renin-angiotensin-aldosterone system (RAAS) at the time of initial assessment., Methods: Plasma levels of N-terminal fragment of type I collagen (PINP), carboxy-terminal telopeptide of type I collagen (ICTP), N-terminal fragment of type III collagen (PIIINP), matrix metalloproteinase-1(MMP-1) and tissue inhibitor of MMPs type-1 (TIMP-1) were assessed in 233 patients following acute MI. The CTO markers were initially assessed prior to treatment by either captopril or losartan, at a median of 3 days following MI. In addition, blood samples were acquired at 1 month, 1 year and 2 years following MI. Development of heart failure symptoms, all-cause and cardiovascular death were recorded as endpoints during two years of follow-up., Results: With the exception of PIIINP, all CTO markers demonstrated significant longitudinal changes following MI. At baseline, ICTP (p<0.0001) and TIMP-1 (p=0.01) levels were significantly elevated in patients who later died compared with survivors. In multivariable analysis only ICTP reached statistical significance as predictor of all cause death (p=0.048). In patients developing symptoms of heart failure during follow-up, ICTP was the only significantly elevated CTO marker (p<0.01)., Conclusion: The present study supports a prognostic role for ICTP in both the acute and chronic phase following MI., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

The cardiac magnetic resonance (CMR) images from a group of patients with myocardial scars and implanted cardioverter-defibrillator (ICD) are divided into a group with low risk of arrhythmias (late incidents) and a group with high risk of arrhythmias (early incidents). Several hundred quantitative features describing sizes, statistics and textures of the segmented and defined areas of the images are computed from manually segmented images in an exploratory analysis. The method used to determine decision regions to discriminate the patients with low risk of arrhythmias from the patient with high risk of arrhythmias is a maximum likelihood estimation based Bayes classifiers described in [1]. The results presented can be interpreted as hypothesis of which features, and combinations of features, that might have discriminative power. A major hypothesis that arises is that there are important textural information in the scarred and non-scarred areas.

Increased circulating chemokines have been reported during acute myocardial infarction and might give prognostic information about future ischemic events. However, data on the chemokine network in relation to infarct size and measures of left ventricular remodeling after successful percutaneous coronary intervention (PCI) are lacking. A total of 42 patients with first-time ST-segment elevation acute myocardial infarction with a single occluded vessel were recruited, and cardiac magnetic resonance was used for serial assessment (2, 7, and 60 days) of infarct size and left ventricular remodeling. The chemokines were analyzed before and after PCI. After PCI, high levels of CCL4, CXCL16, CXCL10, and, in particular, CXCL8 within the first week after PCI correlated positively with the degree of myocardial damage, as reflected by correlations with the maximum troponin T levels and infarct size after 2 months, as assessed by cardiac magnetic resonance, and with impaired myocardial function after 2 months as assessed by cardiac magnetic resonance and neurohormonal methods. In contrast, the plasma levels of CCL3 and CXCL7 during the first week correlated negatively with myocardial dysfunction after 2 months. In conclusion, our findings suggest a role for chemokines in both adaptive and maladaptive responses after myocardial infarction and might support a role for CCL4, CXCL16, CXCL10, and, in particular, CXCL8 in postmyocardial infarction reperfusion and remodeling.

Background: Altered activity of the matrix metalloproteinases (MMP-2 and -9), has been implicated in the left ventricular (LV) remodeling process occurring after myocardial infarction (MI). In the acute phase, a relation between plasma MMP-9 levels and parameters of LV dysfunction has been demonstrated. The relationship in long-term survivors has not been investigated. We studied the relationships of these biochemical markers, and N-terminal pro-B-type natriuretic peptide (N-BNP), with measures of long-term LV remodeling., Methods and Results: Plasma levels of N-BNP, MMP-2, and MMP-9 were measured at randomization, 1 month, 1 year, and > 4 years after complicated AMI. Contrast-enhanced cardiac magnetic resonance (CMR) was performed at 4.4 (+/-0.4) years in 52 clinically stable long-term survivors of the index AMI. We assessed the relationships of plasma N-BNP, MMP-2, and MMP-9 with myocardial scarring, and measures of long-term LV remodeling. Compared with a reference population, N-BNP and MMP-9 levels were increased at all time points from the acute phase until > 4 years after MI. Plasma N-BNP and MMP-9 correlated only in the subacute phase (randomization, mean 3.3 days after MI) days after acute MI (r = 0.38, P = .006). At CMR assessment > or = 4 years, log MMP-9 level was inversely related to LV ejection fraction (P = .002) and nonscarred myocardial mass (P = .008). This relationship was independent of MMP-2. Log N-BNP was related to end diastolic volume index (P = .0002). There was no correlation between log MMP-9 and LV volumes., Conclusion: There is a time-dependent relationship between plasma N-BNP and MMP-9 levels, these peptides correlating only in the acute phase after MI. In long-term follow-up, plasma MMP-9 and N-BNP levels were related to different parameters of LV remodeling. These findings suggest that in long-term survivors of complicated MI, different mechanisms modulate plasma levels of MMP-9 and N-BNP.

Studies of patients with acute myocardial infarction (MI) suggest that anterior transmural infarcts are associated with greater left ventricular (LV) remodeling compared with nontransmural nonanterior infarctions. It is unclear whether this relation also exists in long-term survivors of MI. Cardiac magnetic resonance imaging was used to explore the relation between myocardial scar size, localization, transmurality, and degree of long-term LV remodeling in patients with healed MI. Subjects were recruited from a registry of patients with healed MI who participated in the OPTIMAAL trial. Cardiac magnetic resonance imaging was performed to assess LV mass, volumes, LV ejection fraction, and myocardial scarring, adjusting for myocardial ischemia. Fifty-seven patients (mean age 69 +/- 10 years mean ejection fraction 49 +/- 13%) were studied 4.4 +/- 0.4 years after MI. Anterior scar was found in 19 patients and nonanterior scar in 33, whereas 5 patients did not show myocardial scar. Transmural scar was evident in 36 patients. In the 52 patients with scar, average total scar size was 13 +/- 8% of total LV mass. There was a strong linear relation between scar size and LV end-diastolic volume index (r = 0.81, p <0.0001), end-systolic volume index (r = 0.86, p <0.0001), and LV ejection fraction (r = -0.74, p <0.0001). In multivariate analysis, scar size was the strongest independent predictor of ejection fraction and LV volumes independently of scar localization and transmurality. In conclusion, in the studied cohort, there was a linear relation between scar size and ejection fraction and LV volumes. This relation was independent of scar location and transmurality.

The presence or onset of bundle branch block (BBB) is associated with increased mortality in patients after acute myocardial infarction (AMI). The risk increases with age. We assessed the prognostic power of BBB patterns for predicting clinical outcomes in patients after high-risk AMI. In the OPTIMAAL trial, the effects of losartan versus captopril were compared in 5,477 patients with heart failure and/or evidence of left ventricular dysfunction after MI. The association between clinical outcomes and the presence of left or right BBB at randomization (median 3 days after AMI) or occurring during follow-up (mean 2.7 years) was assessed using Cox regression models. At randomization, 8% of patients (n = 438) showed BBB patterns; 3.7% (n = 203) showed left BBB and 4.3% (n = 235) showed right BBB patterns. In patients with left BBB, there was an increased risk of all-cause death and cardiovascular death. In patients with right BBB, there was increased risk of sudden cardiac death/resuscitated cardiac arrest. During follow-up, another 4.9% (n = 272) developed BBB patterns; 2.8% (n = 153) developed left BBB and 2.17% (n = 119) developed right BBB. Left BBB was associated with increased risk for all-cause death, cardiovascular death, and sudden cardiac death/resuscitated cardiac arrest, whereas right BBB was related to increased risk of sudden cardiac death/resuscitated cardiac arrest. In conclusion, our results confirm and quantify previous observations showing substantially increased mortality in patients with BBB patterns at baseline or occurring soon after AMI.

Purpose: The development of left ventricular systolic dysfunction or heart failure following an acute myocardial infarction (MI) is a powerful marker of an adverse prognosis. Recurrent MI could be an important cause of death, either directly or by provoking arrhythmias., Methods: The OPTIMAAL trial randomized 5477 patients with heart failure or evidence of left ventricular dysfunction following acute MI to losartan or captopril. Over a follow-up of 2.7 years, there were 946 deaths. Of the 180 (19%) of these deaths for which autopsy reports were available, acute MI was found in 57% (102 of 180) of the autopsies. By comparison, an endpoints adjudication committee using clinical data attributed death to acute MI in only 29 cases. An acute MI was found at autopsy in 55% (37 of 67) of the deaths that had been classified as due to an arrhythmia and in 81% (21 of 26) of the deaths classified as due to progressive heart failure. Including autopsy diagnoses, the rate of acute MI in patients who died suddenly was independent of the time elapsed since the index MI, but in patients not classified as dying suddenly, there was a time-related decrease in recurrent MI from 78% in the first 30 days to 30% by the end of follow-up. However, only 19% of patients who died underwent autopsy, so recurrent MI may have been substantially more common and perhaps had a different relation to time since the index MI if more patients had undergone autopsy., Conclusions: In patients with evidence of major cardiac dysfunction after MI, recurrent MI found at autopsy is common and has often not been clinically detected.

An abstract of the study "The Relationship Between N-Terminal B-Type Natriuretic Peptide and Circulating Markers of Extracellular Cardiac Remodelling in Patients Following Complicated Myocardial Infarction," by S. Orn and colleagues is presented.

An abstract of the article "Incidence, Severity and Timing of Neurological Events After a Major Myocardial Infarction," by J. G. F. Cleland and colleagues, is presented.

An abstract of the article "Circulating markers of inflammation are independently related to markers of extracellular cardiac remodelling in patients following acute myocardial infarction," by C. Manhenke and colleagues is presented.

An abstract of the article "Temporal Changes Between Infarct Size and Ejection Fraction Following Primary PCI Assessed by Cardiac Magnetic Resonance," by S. Orn and colleagues is presented.