Acute Phase Of Myocardial Infarction Research Articles

Inhibition of the Renin-Angiotensin System Post Myocardial Infarction Prevents Inflammation-Associated Acute Cardiac Rupture.

Inhibition of the renin-angiotensin system (RAS) is beneficial in patient management after myocardial infarction (MI). However, whether RAS inhibition also provides cardiac protection in the acute phase of MI is unclear. Male 129sv mice underwent coronary artery occlusion to induce MI, followed by treatment with losartan (L, 20 and 60mg/kg), perindopril (P, 2 and 6mg/kg), amlodipine (20mg/kg as a BP-lowering agent) or vehicle as control. Drug effects on hemodynamics were examined. Effects of treatments on incidence of cardiac rupture, haematological profile, monocyte and neutrophil population in the spleen and the heart, cardiac leukocyte density, expression of inflammatory genes and activity of MMPs were studied after MI. Incidence of cardiac rupture within 2weeks was significantly and similarly reduced by both losartan (L) and perindopril (P) in a dose-dependent manner [75% (27/36) in vehicle, 40-45% in low-dose (L 10/22, P 8/20) and 16-20% (L 5/32, P 4/20) in high-dose groups, all P < 0.05]. This action was independent of their BP-lowering action, as amlodipine reduced BP to a similar degree without effect on rupture (70%, 21/30). Compared to the control group, high dose losartan and perindopril decreased counts of white blood cells, neutrophils and lymphocytes (all P < 0.05), and inhibited splenic monocyte and neutrophil release into the circulation. Consequently, monocyte, neutrophil and leukocyte infiltration, inflammatory gene expressions (IL-1β, IL-6, MMP9, MCP-1, TNF-α and TGFβ1) and activity of MMP2 and MMP9 in the infarct tissue were attenuated by losartan and/or perindopril treatment (all P < 0.05). RAS inhibition by losartan or perindopril prevented cardiac rupture at the acute phase of MI through blockade of splenic release of monocytes and neutrophils and consequently attenuation of systemic and regional inflammatory responses.

Biochemical markers of type 2 diabetes as a late complication of myocardial infarction: a case-control study.

IntroductionOn average, 19–23% of patients with acute myocardial infarction (MI) suffer from type 2 diabetes mellitus, which is newly diagnosed in a significant number of patients. Both classic carbohydrate metabolism and lipid metabolism may be promising diagnostic markers for insulin resistance in acute coronary syndrome.Material and methodsTwo hundred patients (130 males and 70 females aged 61.4 ±1.12 years) with ST-segment elevation MI were included in the study. Patients were divided into two groups based on manifestations of diabetes: (1) 171 patients without diabetes within 1 year after MI; and (2) 29 patients with manifestations of diabetes. The control group comprised 33 people without diseases of the cardiovascular system and diabetes and was matched by age and gender with patients.ResultsIn patients with an imbalanced adipokine state during the acute phase of MI, we noted an increased concentration of free fatty acids (p > 0.05) and reduced ghrelin levels (p > 0.05) and activation of the proinflammatory and thrombotic potentials of blood plasma. Patients who developed diabetes 1 year after MI showed hospital stays with more pronounced changes in the study parameters.ConclusionsThe most informative biochemical parameters associated with the development of diabetes at 1 year after MI were adiponectin, retinol protein, ghrelin, tumor necrosis factor α, and plasminogen activator inhibitor.

ACUTE MYOCARDIAL INFARCTION IN THE ABSENCE OF CORONARY ARTERY OBSTRUCTION – A COMPLICATION OF ANTICANCER THERAPY WITH CAPECITABINE

The clinical case of acute myocardial infarction during a therapy with capecitabine is considered. Cardiovascular diseases and cardiovascular risk factors were not detected before the anticancer treatment. In a week after start of the fluoropyrimidine therapy, a routine electrocardiography revealed the acute phase of myocardial infarction of the lower localization. The diagnosis was confirmed by biochemical blood tests. The administration of capecitabine was discontinued. An urgent coronary angiography did not find obstruction of the coronary arteries. Thus, according to the results of a standard therapeutic examination of the patient, it was impossible to predict the development of capecitabine-induced cardiovascular toxicity before the start of anticancer therapy, as well as diagnose it clinically.

WHAT CHANGES IN PERFUSION AND MYOCARDIAL FUNCTION AFTER LATE REVASCULARIZATION OF ACUTE MYOCARDIAL INFARCTION?

Aim. To determine the influence of the time gap between acute myocardial infarction with ST-segment elevation and intracoronary intervention performed later than 2.5 hours on myocardium, we studied indicators of perfusion over time with an aid of SPECT, including intraventricular asynchrony (2–4 days and 6–8 months after stent installation). Materials and method. We observed 22 patients with multivessel coronary lesion. The Russian program with the analysis of perfusion, function and the phase images was used in SPECT synchronized with ECG. Results. Showed that the time gap prior to coronary intervention in the acute phase of myocardial infarction may be directly connected with the increase in impaired perfusion during the end-systole and the severity of pathological intraventricular asynchrony without ECG signs. All patients had significantly decreased wall mobility and intraventricular asynchrony together with increased R-R interval in the late period (after 6–8 months) independently from the coronary intervention time. In patients of group 1 (coronary intervention within 6 hours), focal transmural lesions of myocardium significantly decreased. Conclusion. Late revascularization help decrease intraventricular asynchrony reducing the risk of heart failure in future.

Ranolazine Facilitates Termination of Ventricular Tachyarrhythmia Associated With Acute Myocardial Ischemia Through Suppression of Late INa-Mediated Focal Activity.

Ventricular tachycardia/fibrillation (VT/VF) associated with acute myocardial ischemia is the most common cause of sudden cardiac death, but its underlying mechanisms are incompletely understood. It is hypothesized that late Na+current (INa) contributes to arrhythmogenic activity in ischemic myocardium.Methods and Results:Langendorff-perfused rabbit hearts with regional ischemia in ventricles were optically mapped. Perfusion with ranolazine (10 μmol/L), a selective inhibitor of lateINa, significantly reduced excitation frequency and facilitated termination of VT/VF induced after occlusion of the left main coronary trunk. The activation pattern during ischemic VT/VF was characterized by breakthrough-type excitations (BEs) from multiple origins, predominantly in the ischemic border zone (BZ) and occasional short-lived rotors. Ranolazine perfusion significantly reduced the incidence of BEs in the BZ. Rotors tended to decrease with progression of ischemia and disappeared after ranolazine perfusion. During constant pacing, ranolazine attenuated ischemia-induced shortening of action potentials in the BZ without affecting conduction velocity, probably due toIKrinhibition. In intact hearts without coronary occlusion, ranolazine (10 μmol/L) terminated aconitine-induced VT by inhibiting focal arrhythmogenic activity in the injection site. LateINa-mediated focal arrhythmogenic activity plays important roles in the maintenance of ischemic VT/VF in isolated rabbit hearts. Suppression of lateINaby ranolazine may be a promising therapeutic strategy to reduce arrhythmic death during the acute phase of myocardial infarction.

Predictors and outcomes of new-onset atrial fibrillation in patients with acute myocardial infarction

Background/Aim. The onset of atrial fibrillation (AF) in the acute phase of myocardial infarction (MI) may be a predictor of poor prognosis. The aim of our study was to examine this relationship. Methods. Six hundred patients were enrolled in the study and divided into two groups. The first group included 48 patients with new-onset AF and the second group of 552 patients without this arrhythmia. Patients with previously registered AF were excluded from the study. We investigated the correlation between new-onset AF and intra-hospital mortality as well as mortality during the follow-up period of 48 months. We also analyzed predictors of this arrhythmia. Results. New-onset AF was registered in 48 (8%) patients. The independent predictors of this arrhythmia were older age, particularly more than 70 years [odds ratio 2.37; 95% confidence interval (CI) 1.23?4.58) and increased body mass index (odds ratio 1.17; 95% CI 1.04?1.33). Patients with new-onset AF had a higher mortality during the hospital course than patients without AF, but this difference was not statistically significant (10.4% vs 5.6%, p = 0.179). Patients with this arrhythmia had also a higher mortality after follow-up period of 48 months than patients without AF (33.3 % vs 17.8%, p = 0.009). Major adverse cardiac and cardiovascular events (MACCE) defined as death, recurrent MI, revascularization, and stroke were more after registered in patients with new-onset AF than in those with no this arrhythmia after follow-up period of 48 months (52.1% vs 33.9%, p = 0.011). However, multivariate Cox's regression analysis demonstrated that new-onset AF was not an independent predictor of mortality during the follow-up period of 48 months (HR 0.68; 95% CI 0.38?1.20; p = 0.182). Conclusion. New-onset AF in patients with MI was associated with a higher mortality as well as MACCE after the follow-up period of 48 months but was not an independent predictor of mortality during this period.

Tetramethylpyrazine and Astragaloside IV Synergistically Ameliorate Left Ventricular Remodeling and Preserve Cardiac Function in a Rat Myocardial Infarction Model.

Tetramethylpyrazine (TMP) and astragaloside IV (AGS-IV) are herbal ingredients that have been demonstrated in animal models to limit infarct size and protect cardiomyocytes in the acute phase of myocardial infarction (MI), yet their long-term cardioprotective effects have not been evaluated. In this study, TMP and/or AGS-IV were administrated to rats for 14 days after MI. Echocardiography revealed that the left ventricular (LV) dimensions and cardiac function were preserved in the MI rats with TMP and AGS-IV treatment, compared with untreated MI rats. Moreover, the LV dimensions and cardiac function in the MI rats with TMP and AGS-IV cotreatment were comparable with the sham-operated rats. In addition, TMP and AGS-IV synergistically inhibited LV fibrosis by attenuating MI-induced collagen deposition and elevation of transforming growth factor β1. TMP and AGS-IV, alone or in synergy, enhanced angiogenesis in the infarcted myocardium and reduced cardiac hypertrophy of the remote myocardium after MI. Furthermore, TMP and AGS-IV mutually upregulated the expression of Sonic hedgehog (Shh), Smoothened, and Glioblastoma-2, the receptor and signal transducer of Shh signaling pathway, in the infarcted myocardium. In summary, in the circumstance of the irreversible ischemic injury, the antifibrotic, and pro-angiogenic properties of TMP and AGS-IV on the nonaffected tissues contribute to the cardioprotection in the healing phase post MI, and the cardioprotective effects are likely to be mediated through the Shh pathway.

Gelatinases A and B and Antioxidant Enzyme Activity in the Early Phase of Acute Myocardial Infarction

Oxidative stress plays important roles in the pathophysiology of acute myocardial infarction (AMI). The aim of this study was to investigate the correlation of the oxidative stress status and matrix metalloproteinase activity in AMI patients in comparison to controls. This study included 136 subjects: 68 patients with AMI (42 males/26 females; mean age 58.5 ± 10.5 years) and 68 controls (37 males/29 females; mean age 60.2 ± 12.4 years). Gelatinases A and B were assayed using gelatin zymography, enzyme activities were obtained spectrophotometrically. Gelatinase A and B activities were increased in the AMI patients’ group compared to the control. Activities of serum superoxide dismutase (SOD) and xanthine oxidase (XO) were significantly higher in AMI patients (106.53 ± 23.45 U/l, P &lt; 0.001 and 158.18 ± 29.59 U/l, P &lt; 0.001) than in the control group (55.99 ± 10.79 U/l and 79.81 ± 7.93 U/l). The activity of catalase (CAT) in the sera of AMI patients was lower (271.31 ± 7.53 U/l, P &lt; 0.005) than in the control group (305.94 ± 97.28 U/l). Plasma glutathione peroxidase (GPx) and glutathione reductase (GR) in AMI patients were significantly higher (582.47 ± 184.81 U/l, P &lt; 0.001 and 59.64 ± 21.88 U/l, P &lt; 0.001) than in the control group (275.32 ± 104.69 U/l and 47.71 ± 20.05 U/l). The present findings demonstrate activation of gelatinases A and B and oxidative stress markers in the early stage of AMI. Gelatinases, detected at high levels in AMI patients only, indicate their noticeable predisposition for becoming additional biomarkers of the early phase of AMI.

Prasugrel Versus Ticagrelor in Patients With Acute Myocardial Infarction Treated With Primary Percutaneous Coronary Intervention

Background: No randomized head-to-head comparison of the efficacy and safety of ticagrelor and prasugrel has been published in the 7 years since the higher efficacy of these newer P2Y 12 inhibitors were first demonstrated relative to clopidogrel. Methods: This academic study was designed to compare the efficacy and safety of prasugrel and ticagrelor in acute myocardial infarction treated with primary or immediate percutaneous coronary intervention. A total of 1230 patients were randomly assigned across 14 sites to either prasugrel or ticagrelor, which was initiated before percutaneous coronary intervention. Nearly 4% were in cardiogenic shock, and 5.2% were on mechanical ventilation. The primary end point was defined as death, reinfarction, urgent target vessel revascularization, stroke, or serious bleeding requiring transfusion or prolonging hospitalization at 7 days (to reflect primarily the in-hospital phase). This analysis presents data from the first 30 days (key secondary end point). The total follow-up will be 1 year for all patients and will be completed in 2017. Results: The study was prematurely terminated for futility. The occurrence of the primary end point did not differ between groups receiving prasugrel and ticagrelor (4.0% and 4.1%, respectively; odds ratio, 0.98; 95% confidence interval, 0.55–1.73; P =0.939). No significant difference was found in any of the components of the primary end point. The occurrence of key secondary end point within 30 days, composed of cardiovascular death, nonfatal myocardial infarction, or stroke, did not show any significant difference between prasugrel and ticagrelor (2.7% and 2.5%, respectively; odds ratio, 1.06; 95% confidence interval, 0.53–2.15; P =0.864). Conclusions: This head-to-head comparison of prasugrel and ticagrelor does not support the hypothesis that one is more effective or safer than the other in preventing ischemic and bleeding events in the acute phase of myocardial infarction treated with a primary percutaneous coronary intervention strategy. The observed rates of major outcomes were similar but with broad confidence intervals around the estimates. These interesting observations need to be confirmed in a larger trial. Clinical Trial Registration: URL: http://www.ClinicalTrials.gov . Unique identifier: NCT02808767.

SY4-2 - Transvascular Left Ventricular Unloading in the Acute Phase of Myocardial Infarction Markedly Reduces Infarct Size and Prevents Future Heart Failure

SY4-2 - Transvascular Left Ventricular Unloading in the Acute Phase of Myocardial Infarction Markedly Reduces Infarct Size and Prevents Future Heart Failure

MiR-22-5p revealed as a potential biomarker involved in the acute phase of myocardial infarction via profiling of circulating microRNAs.

Acute myocardial infarction (AMI) is a life-threatening episode of coronary artery disease. Recently, circulating myocardial-derived microRNAs (miRNAs) have been reported as potential biomarkers of infarction. The present study aimed to identify differentially expressed miRNAs in patients with ST-segment elevation myocardial infarction that could be potentially dysregulated in response to early myocardial damage. miRNA expression profile analysis was performed using the Serum/Plasma Focus miRNA Polymerase Chain Reaction (PCR) panel of Exiqon A/S (Vedbaek, Denmark) on plasma samples of patients on the first day of AMI (admission) and on samples from the identical patients collected six months following AMI. Selected miRNAs were validated by reverse transcription‑quantitative PCR (RT‑qPCR) using independent patients with AMI and a control group of patients with a stable coronary artery disease. Thirty‑two species of plasma miRNA were differentially expressed (P<0.05) on admission compared with six months following AMI. Subsequent validation in an independent patient group confirmed that miR‑133b and miR‑22‑5p were significantly up‑regulated in the serum of patients with AMI. The receiver operating characteristic (ROC) curve analysis demonstrated a diagnostic utility for miR-22-5p, which has not previously been reported to be associated with AMI. Among the selected miRNAs, miR‑22‑5p represents a novel promising biomarker for the diagnosis of AMI.

Studying Dynamic Features in Myocardial Infarction Progression by Integrating miRNA-Transcription Factor Co-Regulatory Networks and Time-Series RNA Expression Data from Peripheral Blood Mononuclear Cells

Myocardial infarction (MI) is a serious heart disease and a leading cause of mortality and morbidity worldwide. Although some molecules (genes, miRNAs and transcription factors (TFs)) associated with MI have been studied in a specific pathological context, their dynamic characteristics in gene expressions, biological functions and regulatory interactions in MI progression have not been fully elucidated to date. In the current study, we analyzed time-series RNA expression data from peripheral blood mononuclear cells. We observed that significantly differentially expressed genes were sharply up- or down-regulated in the acute phase of MI, and then changed slowly until the chronic phase. Biological functions involved at each stage of MI were identified. Additionally, dynamic miRNA–TF co-regulatory networks were constructed based on the significantly differentially expressed genes and miRNA–TF co-regulatory motifs, and the dynamic interplay of miRNAs, TFs and target genes were investigated. Finally, a new panel of candidate diagnostic biomarkers (STAT3 and ICAM1) was identified to have discriminatory capability for patients with or without MI, especially the patients with or without recurrent events. The results of the present study not only shed new light on the understanding underlying regulatory mechanisms involved in MI progression, but also contribute to the discovery of true diagnostic biomarkers for MI.

Left Ventricular Mechanics in Functional Ischemic Mitral Regurgitation in Acute Inferoposterior Myocardial Infarction.

Ischemic mitral regurgitation (MR) is an established adverse prognostic factor after myocardial infarction (MI). Functional ischemic mitral regurgitation in acute phase of MI remains under‐investigated due to its often transient and dynamic nature. We aimed to assess left ventricular (LV) mechanics by speckle‐tracking echocardiography in acute inferoposterior MI and ischemic mitral regurgitation (MR).MethodsSixty‐nine patients with no structural cardiac valve abnormalities and first acute inferoposterior MI were prospectively enrolled into the study. Two‐dimensional transthoracic echocardiography for regional myocardial function and valve assessment was performed within 48 hours of presentation after reperfusion therapy (percutaneous coronary intervention). Based on degree of MR, patients were divided into no significant MR (NMR) group (N = 34, with no or mild (grade 0–I) MR) and ischemic MR (IMR) group (N = 35, with grade ≥2 MR). Thirty‐five age‐ and gender‐matched healthy individuals served as a normal reference group. Offline 2D speckle tracking analysis was performed with GE EchoPAC software.ResultsLV ejection fraction and longitudinal myocardial deformation parameters were significantly better in healthy subjects, but did not differ between both study groups. All circumferential myocardial deformation parameters were significantly worse in IMR group compared to healthy subjects and NMR group. Global, basal, and mid‐ventricular radial strain was significantly lower in IMR group compared to both—healthy subjects and NMR group.ConclusionIschemic mitral regurgitation in acute inferoposterior MI is associated with worse radial and circumferential LV deformation parameters assessed by 2D speckle tracking echocardiography.

Hyponatremia at discharge as a predictor of 12-month clinical outcomes in hospital survivors after acute myocardial infarction.

Hyponatremia in the early phase of acute myocardial infarction (AMI) is a well-known predictor of poor prognosis. However, little is known about the clinical implication of sodium levels at discharge in hospital survivors after AMI. The study included 1290 consecutive patients (64±12years; 877 men) who survived the index hospitalization after AMI. We determined the 12-month mortality rates of these patients. Patients who died during the 12-month follow-up had lower sodium levels at discharge than those who had survived (137±6 vs. 139±4mmol/L; P<0.014). Hyponatremia at discharge, defined as a serum sodium level ≤135mmol/L, was present in 210 patients (16.3%). In the Cox-proportional hazard model, hyponatremia at discharge (hazard ratio, 2.264; 95% confidence interval, 1.119-4.579; P=0.023) was an independent predictor of 12-month mortality. Moreover, hyponatremia at discharge had an incremental prognostic value over conventional risk factors (χ 2=7, P=0.007), and conventional risk factors and log N-terminal Pro-B-type natriuretic peptide combined (χ 2=5, P=0.021). In the subgroup analysis, the 12-month mortality of patients with hyponatremia at discharge was significantly higher than in those without, irrespective of age, Killip class, left ventricular ejection fraction, percutaneous coronary intervention at index hospitalization, and prescription of diuretics at discharge. Hyponatremia at discharge is an independent predictor of 12-month mortality in hospital survivors after AMI.

Omentin-1 levels in patients with premature coronary artery disease, metabolic syndrome and healthy controls. Short communication.

Omentin-1 is an adipokine which could have a protective role against the manifestation of atherosclerosis. Only limited data are available on omentin-1 serum values in patients with premature clinical manifestations of atherosclerosis. We tested omentin-1 in human serum by ELISA method in 61 individuals with a premature manifestation of coronary artery disease (CAD), 40 patients with metabolic syndrome and 40 healthy control subjects. Omentin-1 serum levels were significantly lower in patients with CAD (103.1±62.7 mg/L) compared to metabolic syndrome (668.2±339.6 mg/L) and healthy subjects (623.0±373.5 mg/L) (P < 0.01). In CAD patients, omentin-1 serum levels did not differ between patients sampled in the acute phase of myocardial infarction (n = 28; 110.3±82.4 mg/L) and in the chronic phase several months or years after myocardial infarction (n = 33; 97.0±39.3 mg/L) (P = 0.41). We found a weak positive correlation between omentin-1 and body mass index (r = 0.21, P = 0.014). No significant correlation was found between peak cardiac troponin T and omentin-1 (correlation coefficient r = 0.118, P = 0.406). Serum omentin-1 seems to be a useful biomarker of coronary artery disease across the whole age spectrum.

TCF7L2 polymorphism is associated with low nitric oxide release, endothelial dysfunction and enhanced inflammatory response after myocardial infarction

BackgoundThe favorable effects of insulin during myocardial infarction (MI) remain unclear due to the divergence between mechanistic studies and clinical trials of exogenous insulin administration. The rs7903146 polymorphism of the transcription factor 7-like 2 (TCF7L2) gene is associated with attenuated insulin secretion. MethodsIn non-diabetic patients with ST-elevation MI (STEMI), using such a model of genetically determined down-regulation of endogenous insulin secretion we investigated the change in plasma insulin, C-peptide, interleukin-2 (IL-2), C-reactive protein (CRP), and nitric oxide (NOx) levels between admission (D1) and the fifth day after MI (D5). Coronary angiography and flow-mediated dilation (FMD) were performed at admission and 30days after MI, respectively. Homeostasis Model Assessment estimated insulin secretion (HOMA2%β) and insulin sensitivity (HOMA2%S). ResultsAlthough glycemia did not differ between genotypes, carriers of the T-allele had lower HOMA2%β and higher HOMA2%S at both D1 and D5. As compared with non-carriers, T-allele carriers had higher plasma IL-2 and CRP at D5, higher intracoronary thrombus grade, lower FMD and NOx change between D1 and D5 and higher 30-day mortality. ConclusionIn non-diabetic STEMI patients, the rs7903146 TCF7L2 gene polymorphism is associated with lower insulin secretion, worse endothelial function, higher coronary thrombotic burden, and higher short-term mortality. General significanceDuring the acute phase of MI, a lower capacity of insulin secretion may influence clinical outcome.

0321 : Cardiogenic shock in acute myocardial infarction. The experience of the military hospital. About (7)0 cases

Cardiogenic shock remains the leading cause of death in the acute phase of myocardial infarction (MI); it is the result of myocardial and / or mechanical failure complication. The aim of our study was to investigate the epidemiological, clinical and support of a serie of patients hospitalized for MI complicated by cardiogenic shock as well as the immediate and late prognosis. It was a single-center retrospective study of 70 patients hospitalized in the service of cardiology of the military hospital for myocardial infarction complicated by cardiogenic shock, between 2005 and 2012. The mean age was 63 ± 10 years, 80% were men. The majority of myocardial infarction were anteriors. On admission 41% were in left ventricular failure, and 59% in shock. Thrombolysis was performed in 51% of patients. Angiography had identified a single truncal achieved in 28% of cases, bi -vessel in 44% of cases and tri- truncal in 28% of cases. The transcoronary angiolpasty was primary in 27% of cases and of rescue in 73% of cases. Revascularization was complete in 37% of cases. The success rate of TCA was 85%. The majority of bare stents were used (83%). The mean LVEF was 49 ± 14.4%. 70% of patients received vasopressor therapy with a mean duration of 3.5 days. IABP was placed in 2 patients with an average duration of 2 days. The average of hospital stay was 7 ± 8 days. Hospital mortality was 47%, occurring on average in the sixth day of hospitalization (6±9 days). We found that renal failure, late onset of shock, hyperglycemia, leukocytosis, use of vasopressors, and the anterior territory of MI were significantly predictive of hospital mortality. Despite significant advances in the treatment of myocardial infarction, particularly techniques of reperfusion, therapeutic drug, and the advent of several circulatory support techniques, mortality of cardiogenic shock in acute phase of myocardial infarction remains high. The author hereby declares no conflict of interest

0337 : Predictors of early mortality in acute myocardial infarction complicated by cardiogenic shock

The most serious complication during myocardial infarction (MI) is cardiogenic shock. It's the result of myocardial and/or mechanical failure complication. The aim of our study was to investigate the epidemiological and clinical characteristics of a serie of patients hospitalized for MI complicated by cardiogenic shock as well as the predictive factors of early mortality. It was a single-center retrospective study of 70 patients hospitalized in the service of cardiology of the military hospital for myocardial infarction complicated by cardiogenic shock, between 2005 and 2012. The mean age was 63±10 years, 80% were men. Cardiovascular risk factors were as follows: 89% were smokers, 62% presented diabetes mellitus, 50% had hypertension, 40% had dyslipidemia and 10% had a family history of coronary artery disease. 24% of patients had renal insuffisancy. 39% were admitted before the 6th hour from beginning of chest pain, 12% were admitted between the 6th and the 12th hour and 45% were admitted beyond the 12th hour. On admission 41% were in left ventricular failure, and 59% in shock. The majority of myocardial infarction (45%) were anteriors. Angiography had identified a single truncal achieved in 28% of cases, bi- vessel in 44% of cases and tri- truncal in 28% of cases. The trans-coronary angiolpasty (TCA) was primary in 27% of cases and of rescue in 73% of cases. Revascularization was complete in 37% of cases. The mean LVEF was 49±14.4%. The average of hospital stay was 7±8 days. Hospital mortality was 47%, occurring on average in the sixth day of hospitalization (6±9 days). We found that renal failure, late onset of shock, hyperglycemia, leukocytosis, use of vasopressors, and the anterior territory of MI were significantly predictive of hospital mortality. Despite advances in the treatment of myocardial infarction, particularly reperfusion techniques, and medical care in intensive care units, cardiogenic shock mortality in acute phase of myocardial infarction remains high. Renal failure, late onset of shock, hyperglycemia and the anterior territory of MI were the major predictive of hospital mortality. A multidisciplinary approach including medical actors and pre-hospital centers specialized in the treatment of this condition is actually necessary. The author hereby declares no conflict of interest

Echocardiographic indices related with acute coronary anatomy in acute phase of myocardial infarction: our experience

Inferior acute myocardial infarction (IAMI) is often associated with right ventricle involvement (RVAMI). Echocardiogram (Echo) shows the ischemic involvement of the right ventricle with an initial dilatation (RVD) and segmental cinetic abnormalities (RVSCS). During RVAMI the normal convexity of the interatrial septum (IAS) toward right atrium is inverted (IASI). 53 patients with IAMI were studied with ECG, echo and hemodinamic monitoring by a Swan-Ganz catheter. Echo was early performed and patients were subdivided into three groups: 1. IAMI with RVSCS and/or RVD with IASI (12 patients); 2. IAMI with RVSCS and/or RVD without IASI (8 patients); 3. IAMI without VSCS, RVD IASI (33 patients). ECG showed RV involvement only in A and B groups (ST-T segment elevation more than 2 mm in V3 r - V5 r). Echo-Doppler showed no statistically differences between the two groups on RV protodiastolic pression; no hemodinamic differences between the two groups (p = n.s.); no statistically differences in central venous pressure, right ventricular pressure, cardiac output, wedge pressure. Complications (arrhytmias, heart failure, ipotension, pericarditis, 3rd A-V block) were so subdivided: group A: 6 patients (50%); group B: 2 patients (24%); group C: 4 patients (12%) with statistical significance (p<0.03) between all three groups. Coronarography showed that in group A significative lesions were localized in the proximal tract of the right coronary and/or in the proximal tract of the circumflex coronary; on the contrary in B and C groups the lesions were localized in medium and distal tract of the two vessels. Mortality at six months was 41 % in group A (5 patients); 20 % in group B (2 patients); 6 % in group C (2 patients), with p<0.01 between all three groups. Echo after six months showed IASI only in two patients of group A. Patients with IASI revealed complications (residual angina, ventricular ipercinetic arrytmias). IASI in patients with IAMI and RVAMI seems to identify a group with higher risk in developing complications and with a more adverse prognosis.

Soluble galectin-3 is associated with premature myocardial infarction.

Inflammatory responses are pivotal in the initiation and development of premature atherosclerotic lesions. Galectin-3 represents a valuable biomarker for both progression and destabilization of atherosclerotic lesions. This study aims to assess the involvement of galectin-3 in premature myocardial infarction. In this multicentre case-control study, we assessed circulating galectin-3 levels in 144 patients comprising 72 consecutive survivors of acute myocardial infarction (≤ 40 years) and 72 hospital controls frequency matched for age, gender and centre. Patients with acute myocardial infarction showed significantly higher galectin-3 levels as compared to controls in the acute phase of acute myocardial infarction (2552 ± 1992 vs. 1666 ± 829 pg/mL; P < 0·001) as well as in the stable phase 1 year after the index event (3692 ± 1774 vs. 1666 ± 829 pg/mL; P < 0·001). Circulating galectin-3 was significantly and independently associated with premature myocardial infarction in the logistic regression analysis (acute phase: adj. OR per 1-SD change 2·03, 95% CI 1·30-3·19; P = 0·002; stable phase: adj. OR of 6·54 (95% CI 2·56-16·68; P < 0·001). Moreover, we observed a significant correlation between circulating galectin-3 and leucocyte count (r = 0·35, P < 0·001), non-HDL cholesterol (r = 0·23, P = 0·014) and HDL cholesterol (r = -0·29, P = 0·002). We demonstrated that elevated levels of circulating galectin-3 are strongly associated with premature myocardial infarction. Galectin-3 might serve as link between dyslipidaemia as driving force of plaque formation with inflammation as initiator of plaque rupture in patients with premature acute myocardial infarction.