Abstract 15225: Post-ischemic Myocardial Insulin Resistance Induced by Tnf-α Overproduction Precipitates the Development of Heart Failure After Myocardial Infarction

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Feng Fu ◽  
Jia Li ◽  
Jie Xu ◽  
Yuan Zhang ◽  
Chao Gao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Left Ventricular ◽  
Separate Experiment ◽  
Tnf Α ◽  
Lv Remodeling ◽  
Myocardial Insulin Resistance

Objectives: Clinical evidence has demonstrated a decreased myocardial insulin response in HF patients. However, the role of myocardial insulin resistance and the underlying mechanisms in HF are largely unclear. Methods and Results: Sprague Dawley rats subjected to myocardial infarction (MI) resulted in a progressive left ventricular (LV) remodeling and dysfunction. Echocardiographic assessment showed preserved LV end-systolic dimension (LVESD 0.453 ± 0.027 cm) and ejection fraction (EF 57.03 ± 2.35%) at 1 wk after MI, and evident LV dilation (LVESD 0.612 ± 0.026 cm) and dysfunction (EF 40.21 ± 3.09%) at 4 wk after MI. Myocardial insulin sensitivity decreased significantly at 1 wk after MI as evidenced by reduced insulin-stimulated myocardial fluorodeoxyglucose uptake (Standardized Uptake Value: 2.71 ± 0.42 vs. 5.13 ± 0.51 of sham+insulin, n=6, P <0.01) and GLUT-4 translocation and altered insulin signaling, whereas systemic insulin sensitivity remained unchanged. Mechanistically, myocardial TNF-α production was increased following MI. Treatment with etanercept (a TNF-α inhibitor) post-MI improved myocardial insulin sensitivity, while adenovirus-mediated overexpression of TNF-α resulted in myocardial insulin resistance in non-MI hearts. In addition, TNF-α overexpressed rat hearts exhibited LV dysfunction (EF 41.32 ± 4.21%) and LV dilation as early as 1 wk after MI. Moreover, insulin treatment during the first week following MI suppressed myocardial TNF-α production and increased myocardial insulin sensitivity, resulting in alleviated cardiac dysfunction and remodeling at 4 wk after MI. Importantly, in a separate experiment, cardiomyocyte-specific insulin receptor knockout mice exhibited aggravated post-ischemic LV remodeling and dysfunction compared with littermate controls. Conclusions: Our data provide novel insights that myocardial insulin resistance, independently of systemic insulin resistance, precipitates the development of post-ischemic HF. Myocardial insulin resistance is an early event partly attributed to myocardial TNF-α overproduction following MI. This finding indicates the essential role of myocardial insulin signaling in protection against ischemic HF.

Aging is associated with myocardial insulin resistance and mitochondrial dysfunction

2007 ◽  
Vol 293 (5) ◽  
pp. H3063-H3071 ◽  
Author(s):  
Siva Bhashyam ◽  
Pratik Parikh ◽  
Hakki Bolukoglu ◽  
Alexander H. Shannon ◽  
James H. Porter ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Signaling ◽  
Insulin Action ◽  
Left Ventricular ◽  
Whole Body ◽  
Acid Uptake ◽  
Nonesterified Fatty Acids ◽  
Left Circumflex Artery ◽  
Mitochondrial Structure ◽  
Myocardial Insulin Resistance

Aging is associated with insulin resistance, often attributable to obesity and inactivity. Recent evidence suggests that skeletal muscle insulin resistance in aging is associated with mitochondrial alterations. Whether this is true of the senescent myocardium is unknown. Twelve young (Y, 4 years old) and 12 old (O, 11 years old) dogs, matched for body mass, were instrumented with left-ventricular pressure gauges, aortic and coronary sinus catheters, and flow probes on left circumflex artery. Before surgery, all dogs participated in a 6-wk exercise program. Dogs underwent measurements of hemodynamics and plasma substrates before and during a 2-h hyperinsulinemic-euglycemic clamp to measure whole body and myocardial glucose and nonesterified fatty acid uptake. Following the protocol, myocardial and skeletal samples were obtained to measure components of the insulin-signaling cascade and mitochondrial structure. There was no difference in plasma glucose (Y, 90 ± 4 mg/dl; O, 87 ± 4 mg/dl), but old dogs had higher ( P < 0.02) nonesterified fatty acids (Y, 384 ± 48 μmol/l; O, 952 ± 97 μmol/l) and plasma insulin (Y, 39 ± 11 pmol/l; O, 108 ± 18 pmol/l). Old dogs had impaired total body glucose disposition (Y, 11.5 ± 1 mg·kg−1·min−1; O, 8.0 ± 0.5 mg·kg−1·min−1; P < 0.05) and insulin-stimulated myocardial glucose uptake (Y, 3.5 ± 0.3mg·min−1·g−1; O, 1.8 ± 0.3 mg·min−1·g−1; P < 0.05). The impaired insulin action was associated with altered insulin signaling and glucose transporter (GLUT4) translocation. There were myocardial mitochondrial structural changes observed in association with decreased expression of uncoupling protein-3. Aging is associated with both whole body and myocardial insulin resistance, independent of obesity and inactivity, but involving altered mitochondrial structure and impaired cellular insulin action.

Abstract 2668: Critical Role of Granzyme B in Left Ventricular Remodeling after Acute Myocardial Infarction

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hideyuki Kondo ◽  
Yukihiro Hojo ◽  
Yoshioki Nishimura ◽  
Nozomu Takahashi ◽  
Tomokazu Ikemoto ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Regression Analysis ◽  
Plasma Levels ◽  
Granzyme B ◽  
Critical Role ◽  
Left Ventricular ◽  
Volume Index ◽  
Lv Remodeling

Background: Granzyme B is a member of the serine esterase family produced by cytotoxic T lymphocytes (CTLs), and has an important role in cellular apoptosis and extracellular matrix degradation. We hypothesized that granzyme B is involved in left ventricular (LV) remodeling after acute myocardial infarction (AMI). Objectives: To elucidate the role of granzyme B in LV remodeling after AMI. Subjects and methods: We employed 41 patients with the first AMI (mean age: 61.9±8.9 years old). We obtained peripheral blood on day 1, day 7 and day 14 after onset. Plasma levels of apoptosis-related molecules, including tumor necrosis factor α (TNFα), a soluble form of the Fas ligand (sFasL) and granzyme B were measured. We checked the activation of CTLs by flow cytometry. Patients were treated by percutaneous coronary intervention within 12 hours after onset. Successful myocardial reperfusion (TIMI flow grade 2 or 3) was accomplished in all patients. LV end-diastolic volume index (LVEDVI) was calculated on day 1 and 6 months after onset. Results: Plasma levels of TNFα, sFasL and granzyme B increased significantly after the onset of AMI (TNFα; day 1: 1.6±0.47, day 7: 3.3±0.65, day14: 4.0±1.2 pg/ml, p<0.05, sFasL; day 1: 72±5.2, day 7: 86±6.7, day14: 95±7.3 pg/ml, p<0.05, granzyme B; day 1: 63±18.4, day 7: 283±57.8, day14: 210.9±46.3 pg/ml, p<0.001). The percentage of CD69± to CD3+ CD8+ lymphocytes was significantly increased (CD69+/CD3+ CD8+; day 1: 14.5±1.7, day 7: 15.8±1.2, day 14: 19.1±1.4%, p<0.05), suggesting that CTLs were activated after onset. Univariate regression analysis showed a significant positive correlation between plasma granzyme B level on day 14 and fold-increase in LVEDVI (r=+0.45, p<0.01). No significant correlation was observed between TNFα and changes in LVEDVI, or sFasL and changes in LVEDVI. Stepwise multivariate regression analysis showed that the plasma granzyme B level on day 14 is a significant explanatory variable for changes in LVEDVI (β = +0.53, p<0.001). Conclusions: These results first indicate that among proapoptic molecules, granzyme B has a critical role in the progression of LV remodeling after AMI.

Abstract 1651: Exercise Improves Aging-associated Myocardial Insulin Resistance by Enhancing Mitochondrial Function in an eNOS Dependent Mechanism

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Qiu X Li ◽  
Quan J Zhang ◽  
Hai F Zhang ◽  
Kun R Zhang ◽  
Jia Li ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Mitochondrial Function ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Enos Expression ◽  
Adult Heart ◽  
Aging Heart ◽  
Myocardial Insulin Resistance

Objective . This study sought to determine whether exercise reduces aging-associated myocardial insulin resistance, with a specific focus on the role of eNOS and its relation to mitochondria. Methods . Aging male Sprague-Dawley rats (24 months) were subjected to swim training (60 min/d, 5 d/wk, 9 wk) or assigned as sedentary control. The myocardial contraction, myocardial glucose uptake, mitochondrial function, and eNOS signaling were determined. Results. Aging rats had myocardial insulin resistance as shown by decreased insulin-induced glucose uptake (0.22±0.05 μmol/min/g in aging heart vs.1.29 ± 0.13 μmol/min/g in adult heart, n=8, P <0.01) and attenuated insulin’s positive inotropic role as evidenced by reduced left ventricular developed pressure (90±12 mmHg in aging heart vs. 155±14 mmHg in adult heart, P <0.01). Mitochondrial function was decreased in aging hearts as manifested by the attenuated maximum O 2 consumption by FCCP (1.85±0.39 μmol/min/g in aging hearts vs. 3.72±0.40 μmol/min/g in adult hearts, P <0.01). This was accompanied with the reduced insulin-induced O 2 consumption (1.37±0.31 μmol/min/g in aging heart vs. 2.35±0.31 μmol/min/g in adult heart, P <0.01). In addition, eNOS expression and its phosphorylation by insulin were reduced by 1.2- and 2.3-fold in aging heart, respectively ( P <0.01). Swim training upregulated eNOS expression by 72% ( P <0.01), facilitated eNOS phosphorylation by insulin ( P <0.01), and improved myocardial insulin sensitivity as shown by enhanced glucose uptake by insulin ( P <0.01). Moreover, mitochondrial function was facilitated as manifested by the enhanced O 2 consumption by insulin ( P <0.05), and maximum O 2 consumption ( P <0.01) following swim training. Pretreatment with Cavtratin, an eNOS inhibitor, abolished exercise-improved mitochondrial response to insulin, blocked exercise-improved myocardial insulin sensitivity and the positive inotropic response to insulin in aging heart. Conclusion . These results demonstrate that impaired eNOS signaling and subsequent mitochondrial depression is a major mechanism contributes to aging-associated myocardial insulin resistance, and that exercise improves insulin sensitivity by restoring eNOS signaling and enhancing mitochondrial function.

Accelerated LV remodeling after myocardial infarction in TIMP-1-deficient mice: effects of exogenous MMP inhibition

2005 ◽  
Vol 288 (1) ◽  
pp. H149-H158 ◽  
Author(s):  
John S. Ikonomidis ◽  
Jennifer W. Hendrick ◽  
Andrea M. Parkhurst ◽  
Amanda R. Herron ◽  
Patricia G. Escobar ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ejection Fraction ◽  
Left Ventricular ◽  
Wild Type ◽  
End Diastolic Volume ◽  
Coronary Ligation ◽  
Lv Remodeling ◽  
And Function ◽  
Deficient Mice

Alterations in matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) have been implicated in adverse left ventricular (LV) remodeling after myocardial infarction (MI). However, the direct mechanistic role of TIMPs in the post-MI remodeling process has not been completely established. The goal of this project was to define the effects of altering endogenous MMP inhibitory control through combined genetic and pharmacological approaches on post-MI remodeling in mice. This study examined the effects of MMP inhibition (MMPi) with PD-166793 (30 mg·kg−1·day−1) on LV geometry and function (conductance volumetry) after MI in wild-type (WT) mice and mice deficient in the TIMP-1 gene [TIMP-1 knockout (TIMP1-KO)]. At 3 days after MI (coronary ligation), mice were randomized into four groups: WT-MI/MMPi ( n = 10), TIMP1-KO-MI/MMPi ( n = 10), WT-MI ( n = 22), and TIMP1-KO-MI ( n = 23). LV end-diastolic volume (EDV) and ejection fraction were determined 14 days after MI. Age-matched WT ( n = 20) and TIMP1-KO ( n = 28) mice served as reference controls. LVEDV was similar under control conditions in WT and TIMP1-KO mice (36 ± 2 and 40 ± 2 μl, respectively) but was greater in TIMP1-KO-MI than in WT-MI mice (48 ± 2 vs. 61 ± 5 μl, P < 0.05). LVEDV was reduced from MI-only values in WT-MI/MMPi and TIMP1-KO-MI/MMPi mice (42 ± 2 and 36 ± 2 μl, respectively, P < 0.05) but was reduced to the greatest degree in TIMP1-KO mice ( P < 0.05). LV ejection fraction was reduced in both groups after MI and increased in TIMP1-KO-MI/MMPi, but not in WT-MI/MMPi, mice. These unique results demonstrated that myocardial TIMP-1 plays a regulatory role in post-MI remodeling and that the accelerated myocardial remodeling induced by TIMP-1 gene deletion can be pharmacologically “rescued” by MMP inhibition. These results define the importance of local endogenous control of MMP activity with respect to regulating LV structure and function after MI.

Abstract 566: Critical Role of Ghrelin in Ventricular Remodeling after Acute Myocardial Infarction

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hideyuki Kondo ◽  
Yukihiro Hojo ◽  
Yoshioki Nishimura ◽  
Nozomu Takahashi ◽  
Tomokazu Ikemoto ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Remodeling ◽  
Critical Role ◽  
Left Ventricular ◽  
Volume Index ◽  
Enzyme Linked Immunosorbent Assay ◽  
Lv Remodeling ◽  
Total Ghrelin

Background: Ghrelin is a novel growth hormone (GH)-releasing peptide, originally isolated from the stomach, which has been identified as an endogenous ligand for the GH secretagogues receptor (GHS-R). Previous studies revealed that chronic administration of ghrelin suppresses cardiac sympathetic activity and prevents left ventricular (LV) remodeling after acute myocardial infarction (AMI). However clinical role of ghrelin after AMI is still not clear. We examined the role of ghrelin in LV remodeling after AMI. Objectives: To elucidate the role of ghrelin in LV remodeling after AMI. Subjects and methods: We employed patients with the first AMI (n=41, mean age 61.9±8.9 years old). We obtained peripheral blood on 1, 7, 14 days and 6 months after the onset. Plasma total ghrelin levels were measured by enzyme-linked immunosorbent assay. Patients were treated by percutaneous coronary intervention within 12 hours after onset. Successful myocardial reperfusion (TIMI flow grade 2 or 3) was accomplished in all patients. To analyze LV remodeling, all patients submitted to two serial left ventriculographies carried out on the day of admission and 6 months after the onset (mean 199±13 days). LV volume index (LVEDVI) was calculated by QCA-CMS software. Results: Plasma total ghrelin levels increased after the onset of AMI (day 0: 28.4±6.4, day 7: 75.1±12.2, day 14: 89.9±14.8 pg/ml, 6months: 46.5±6.6 fmol/ml, p<0.001). There was a significant positive correlation between plasma ghrelin levels on day 14 after the onset and changes in LVEDVI (r=+0.53, p<0.001). The stepwise multivariate regression analysis showed that the plasma ghrelin level on day 14 is a significant explanatory variable for the changes in LVEDVI (F=8.77, p<0.01, β=+0.40). Conclusions: The elevation of Ghrelin levels might be a compensatory mechanism to prevent LV remodeling. These results first indicate that ghrelin has a critical role in the progression of left ventricular remodeling after AMI.

Abstract 1342: The NF-kappaB P50 Subunit Protects Against Remodeling and Cardiac Dysfunction Following Myocardial Infarction

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Leo Timmers ◽  
J Karlijn van Keulen ◽  
Imo I Hoefer ◽  
Joost P Sluijter ◽  
Marie Jose Goumans ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Molecular Mechanisms ◽  
Interstitial Fibrosis ◽  
Systolic Dysfunction ◽  
Protective Role ◽  
Left Ventricular ◽  
Lv Remodeling ◽  
Nf Kappab

Introduction Left ventricular (LV) remodeling leads to congestive heart failure and is a main determinant of morbidity and mortality following myocardial infarction (MI). To further improve the treatment of post infarct LV remodeling, a better understanding of the molecular mechanisms involved in this complicated process is required. The nuclear factor (NF)- κB family (p50, p52, p65) usually forms dimers that regulate DNA transcription in response to a variety of stimuli including pro-inflammatory cytokines, oxidative stress and also ischemia. Inhibition of NF- κB has been shown to reduce heart failure following MI in rats. The specific role of the different NF- κB subunits during LV remodeling, however, has not been clarified thus far. In this study, we elucidate the role of the NF- κB p50 subunit in post infarct LV remodeling. Methods and Results MI was induced in wild type C57Bl6 mice and NF- κB p50 KO mice. Without affecting infarct size (45.4 ± 4.3 vs. 42.5 ± 4.6%; p=0.461), the absence of NF- κB p50 increased the extent of LV remodeling (EDV: 175 ± 13 vs. 107 ± 11 μl; p=0.005) and aggravated systolic dysfunction (LVEF: 16.1 ± 1.5 % vs. 24.7 ± 3.7%; p=0.045) 28 days following MI as assessed by magnetic resonance imaging (9.4 T). In the non-infarcted myocardium, interstitial fibrosis (1.53 ± 0.28 vs. 1.05 ± 0.15 grayvalue/μm 2 ; p=0.042) and hypertrophy (426 ± 51 vs. 251 ± 12 μm 2 /cardiomyocyte; p=0.018) were increased in NF-κB p50 KO mice. In the infarct area, however, collagen density was decreased (15.11 ± 1.16 vs. 27.28 ± 4.93 grayvalue/μm 2 ; p=0.028), which was accompanied by increased TNF-alpha mRNA expression (0.086 ± 0.04 vs. 0.026 ± 0.015; p=0.046) and increased MMP9 activity (0.31 ± 0.03 vs. 0.19 ± 0.03; p=0.049) Conclusion These data provide evidence for a protective role of NF- κB p50 in post infarct maladaptive LV remodeling, most likely by reducing inflammatory cytokine production and matrix degradation.

The role of macrophage migration inhibitory factor in predicting left ventricular remodeling in patients with acute myocardial infarction

2021 ◽  
Author(s):  
T. Y. Storozhenko ◽  
M. P. Kopytsya ◽  
I. R. Vishnevska ◽  
L. L. Pietienova
Keyword(s):  
Myocardial Infarction ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Left Ventricular ◽  
Macrophage Migration ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment ◽  
Lv Remodeling

Objective — to assess the role of circulating markers of inflammation and macrophage migration inhibitory factor (MIF) in the development of left ventricular (LV) remodeling 6 months after acute ST‑segment elevation myocardial infarction (STEMI). Materials and methods. The study involved 120 patients after STEMI and successful primary percutaneous coronary intervention (PCI). Transthoracic echocardiography with Doppler was performed within 24 — 48 hours after PCI and after 6 months of follow‑up to assess LV remodeling. The levels of MIF and inflammatory markers were measured before and after PCI. All patients were divided into two groups according to the median MIF level < 2501 pg/ml (first group, n = 60) and > 2501 pg/ml (second group, n = 60). Results. Patients with the high levels of circulating MIF had a higher frequency of complications in the hospital and long‑term periods (p = 0.024), including newly diagnosed heart failure or decompensation with hospitalizations. High MIF levels in patients of the second group were accompanied by a significant enlargement of end‑diastolic and end‑systolic LV volumes (p = 0.028; p = 0.031, respectively), the development of secondary mitral regurgitation (p = 0.024) and decreased LV systolic function (p = 0.037). MIF threshold values for predicting remodeling > 2694 pg/ml (sensitivity 69.2 %, specificity 71.4 %, AUC = 0.714; 95 % CI  0.509 — 0.870; p = 0.0375) and LV dysfunction > 2484 pg/ml (sensitivity 90.0 %, specificity 58.0 %, AUC = 0.782; 95 % CI  0.675 — 0.867, p = 0.0003) were determined using ROC analysis. According to the results of univariate and multivariate analysis, levels of MIF (p = 0.028) and soluble suppressor of tumorigenesis‑2 (p = 0.042) were most significant predictors of LV remodeling. A correlation between the levels of MIF and white blood cells count (r = 0.33, p = 0.0001), C‑reactive protein (r = 0.19, p = 0.032), troponin (r = 0.44, p = 0.002) has been established. Conclusions. An early increase of MIF levels is associated with the development of adverse structural and functional changes in left ventricle of patients after acute ST‑segment elevation myocardial infarction.

scholarly journals Progranulin induces adipose insulin resistance and autophagic imbalance via TNFR1 in mice

2015 ◽  
Vol 55 (3) ◽  
pp. 231-243 ◽  
Author(s):  
Bo Zhou ◽  
Huixia Li ◽  
Jiali Liu ◽  
Lin Xu ◽  
Qinyue Guo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Mammalian Target Of Rapamycin ◽  
Tumor Necrosis Factor Receptor ◽  
Mitochondrial Activity ◽  
Causative Role ◽  
Important Regulator

Progranulin (PGRN) has recently emerged as an important regulator for insulin resistance. However, the direct effect of PGRN in vivo and the underlying role of progranulin in adipose insulin resistance involving the autophagy mechanism is not fully understood. In this study, mice treated with PGRN for 21 days exhibited the impaired glucose tolerance and insulin sensitivity, remarkable adipose autophagy as well as attenuated insulin signaling via inhibition of mammalian target of rapamycin (mTOR) pathway. Furthermore, blockade of tumor necrosis factor receptor 1 (TNFR1) by TNFR1BP-Fc injection resulted in the restoration of impaired insulin sensitivity and insulin signaling induced by PGRN. Consistent with these findings in vivo, PGRN treatment induced defective insulin signaling, abnormal autophagic and mitochondrial activity in cultured adipocytes, while such effects were nullified by the blockade of TNFR1. In addition, PGRN-deficient adipocytes were more refractory to tunicamycin- or dexamethasone-induced insulin resistance, indicating the causative role of the TNFR1 pathway in the action of PGRN. Collectively, our findings support the notion that PGRN is a key regulator of insulin resistance and that PGRN may mediate its effects, at least in part, by inducing autophagy via the TNFR1-dependent mechanism.

scholarly journals Role of Speckle Tracking in the Evaluation of Left Ventricular Remodeling After Streptokinase Infusion in Patients with Acute Anterior Myocardial Infarction

2020 ◽  
Vol 16 (6) ◽  
pp. 876-880
Author(s):  
Sh. I. Farag ◽  
Kh. E. El-Rabbat ◽  
M. A. El-Awadi ◽  
A. M. Sabry
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Diagnostic Accuracy ◽  
Speckle Tracking ◽  
Left Ventricular ◽  
Cutoff Value ◽  
Group I ◽  
Lv Remodeling ◽  
Streptokinase Infusion

Background. Left ventricular (LV) remodeling is an adverse consequence after acute myocardial infarction.Aim. To assess the role of speckle tracking in the evaluation of LV remodeling after streptokinase infusion in patients with acute anterior ST-segment elevation myocardial infarction (STEMI).Material and methods. A total of 200 patients with first acute anterior STEMI received streptokinase as a reperfusion therapy were included. Conventional echocardiography and speckle tracking were performed within 3 days of admission and 3 months later. According to the development of LV remodeling, patients were classified into two groups. Group (I) patients with LV remodeling (60 patients) and group (II) patients without remodeling (140 patients).Results. Patients with LV remodeling had lower global longitudinal (GLS) and circumferential (GCS) strain values (-13.19±4.57 vs. -18.90±4.23 % and -13.16±4.27 vs. -17.16±3.3 %, respectively, p<0.001). GLS cutoff value of >-13.5 was shown to have the best diagnostic accuracy (sensitivity =60.0% & specificity =87.1%) in predicting LV remodeling (AUC 0.816, 95% confidence interval [CI] 0.754-0.877, p<0.001). GCS cutoff value of >-16.21 was shown to have the best diagnostic accuracy (sensitivity =75.0% & specificity =71.4%) in predicting LV remodeling (AUC 0.785, 95%CI 0.719-0.85, p<0.001).Conclusion. Speckle tracking echocardiography either longitudinal or circumferential strain has good sensitivity and specificity in predicting LV remodeling after acute myocardial infarction.

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