Development Of Left Ventricular Remodeling Research Articles

Prognostic value of triglyceride-glucose index for left ventricular remodeling in nondiabetic ST-elevation myocardial infarction patients.

Background: The triglyceride-glucose (TyG) index is a marker of insulin resistance and is associated with cardiovascular mortality and morbidity. Left ventricular remodeling (LVR) after myocardial infarction (STEMI) is associated with poor prognosis. Methods: This retrospective study included 293 STEMI patients. Echocardiography was performed before discharge and 3months after MI. Results: Compared with the non-LVR group, TyG index value was found to be higher in the LVR group (p<0.001). Logistic regression analysis showed that higher maximal troponin I value, higher calculated TyG index value, higher N-terminal prohormone of brain natriuretic peptide level and the presence of anterior MI were independently associated with the development of LVR. Conclusion: A high TyG index level may contribute to the prediction of LVR in nondiabetic STEMI patients undergoing successful primary percutaneous coronary intervention.

Plasma Exosome miRNAs Profile in Patients With ST-Segment Elevation Myocardial Infarction.

BackgroundCirculating microRNAs (miRNAs) have been found to have different expressions in different phases of acute myocardial infarction. The profiles of plasma exosome miRNAs in patients with ST-segment elevation myocardial infarction (STEMI) at 3–6 months postinfarction are unknown.ObjectiveThe aim of this study was to assess the profiles of plasma exosome miRNAs in patients with STEMI in comparison with healthy volunteers and to select specific exosome miRNAs related to pathophysiological changes post-STEMI.MethodsPlasma and echocardiography parameters were collected from 30 patients 3–6 months after STEMI and 30 healthy volunteers. Plasma exosome miRNAs were assessed by using high-throughput sequence (Illumina HiSeq 2500) and profile of the plasma exosome miRNAs was established in 10 patients and 6 healthy volunteers. The specific exosome miRNAs related to heart diseases were selected according to the TargetScan database. The specificity of the selected exosome miRNAs was evaluated in additional 20 post-STEMI patients and 24 healthy volunteers by using quantitative PCR (qPCR). Left ventricular remodeling (LVR) was defined using the European Association of Cardiovascular Imaging criteria according to echocardiography examination. Correlations between expression of the specific miRNAs and echocardiography parameters of LVR were assessed using the Spearman correlation analysis.ResultsTwenty eight upregulated miRNAs and 49 downregulated miRNAs were found in patients 3–6 months after STEMI (p < 0.01) in comparison with the healthy volunteers. The two least expressed and heart-related exosome miRNAs were hsa-miR-181a-3p (0.64-fold, p < 0.01) and hsa-miR-874-3p (0.50-fold, p < 0.01), which were further confirmed by using qPCR and demonstrated significant specificity in another 20 patients with post-STEMI comparing to 24 healthy volunteers [area under the curve (AUC) = 0.68, p < 0.05; AUC = 0.74, p < 0.05]. The expression of hsa-miR-181a-3p was downregulated in patients with LV adverse remodeling in comparison with patients without LV adverse remodeling and healthy volunteers.ConclusionCirculating exosome miR-874-3p and miR-181a-3p were downregulated in patients with STEMI postinfarction. Exosome hsa-miR-181a-3p might play a potential role in the development of LVR in patients with post-STEMI.

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

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&lt;0.001). GLS cutoff value of &gt;-13.5 was shown to have the best diagnostic accuracy (sensitivity =60.0% &amp; specificity =87.1%) in predicting LV remodeling (AUC 0.816, 95% confidence interval [CI] 0.754-0.877, p&lt;0.001). GCS cutoff value of &gt;-16.21 was shown to have the best diagnostic accuracy (sensitivity =75.0% &amp; specificity =71.4%) in predicting LV remodeling (AUC 0.785, 95%CI 0.719-0.85, p&lt;0.001).Conclusion. Speckle tracking echocardiography either longitudinal or circumferential strain has good sensitivity and specificity in predicting LV remodeling after acute myocardial infarction.

The role of macrophage inhibitory factor in the development of left ventricular remodeling after STEMI

The role of macrophage inhibitory factor in the development of left ventricular remodeling after STEMI

Serum Levels of Bone Morphogenetic Proteins 2 and 4 in Patients with Acute Myocardial Infarction.

Background: Bone morphogenetic proteins-2 and -4 (BMPs) have been implicated in left ventricular remodeling (LVR) processes such as an inflammation and fibrogenesis. We hypothesized that this knowledge could be translated into clinics. Methods: We studied the dynamics of serum levels of BMPs, its correlation with markers of LVR and with parameters of echocardiography in patients (n = 31) during the six-month follow-up period after myocardial infarction (MI). Results: Elevated serum levels of BMPs decreased by the six-month follow-up period. BMP-2 decreased from the first day after MI, and BMP-4 decreased from the Day 14. The elevated level of BMP-2 at Day 1 was associated with a lower level of troponin I, reperfusion time and better left ventricular ejection fraction (LV EF) at the six-month follow-up. Elevated serum level of BMP-4 at Day 1 was associated with a lower level of a soluble isoform of suppression of tumorigenicity 2 (sST2), age and reperfusion time. An elevated level of BMP-2 at the six-month follow-up was associated with higher levels of BMP-4, high-sensitivity C-reactive protein (hCRP) and sST2. High serum level of BMP-2 correlated with high levels of hCRP and matrix metalloproteinase (MMP)-9 on Day 7. High serum level of BMP-4 correlated with low levels of hCRP, MMP-9 at Day 3, sST2 at Day 1 and with decreased LV EF on Day 7. The findings of multivariate analysis support the involvement of BMP-2 in the development of post-infarction LVR. Conclusions: Our research translates experimental data about the BMPs in the development of adverse LVR into the clinic. Elevated serum levels of BMPs decreased by the end of the six-month period after MI. BMP-2 decreased from the first day and BMP-4 decreased from Day 14. BMP-2 and BMP-4 were associated with the development of LVR. Their correlations with markers of inflammation, degradation of the extracellular matrix, hemodynamic stress and markers of myocardial damage further support our hypothesis. Diagnostic and predictive values of these BMPs at the development of post-infarction LVR in vivo should be investigated further.

The role of inflammation in driving left ventricular remodeling in a pre-HFpEF model

The incidence of HFpEF continues to increase and ∼2/3 of the patient population are post-menopausal women. Unfortunately, most studies focus on the use of male animal models of remodeling. In this study, however, using female rats to set a model of pre-HFpEF, we provide insights to possible mechanisms that contribute to HFpEF development in humans that will lead us to a better understanding of the underlying pathophysiology of HFpEF.

MicroRNAs in the development of left ventricular remodeling and postmyocardial infarction heart failure.

Acute myocardial infarction (AMI) induces unfavorable left ventricular remodeling (LVR), a complex process that involves molecular, cellular, and geometric alterations leading to important changes in heart structure and function. Heart failure (HF) is a frequent complication of AMI, and it remains a serious clinical, epidemiological, and economic challenge. Despite advances in the therapy and management of HF, many patients still suffer from severe symptoms. The underlying molecular mechanisms of the post‑AMI LVR are not yet fully understood. Numerous studies have indicated that dysregulation in the expression of microRNA (miRNA) molecules leads to changes in several pathological processes in the heart, which are associated with post‑AMI transition from cardiac hypertrophy to HF. In this review, we summarize the current knowledge on the role of miRNAs in the regulation of basic processes, such as excessive myocardial fibrosis, pathological cardiomyocyte hypertrophy, and myocardial cell apoptosis. Moreover, the significance of circulating miRNAs as noninvasive prognostic biomarkers in the prediction of LVR and HF after AMI has also been discussed. In conclusion, miR‑29 family members (miR‑29a and miR‑29b), miR‑150, and miR‑30a‑5p represent different groups of miRNAs, but all of them are involved in the regulation of the fundamental processes associated with post‑AMI left ventricular dysfunction and HF. Furthermore, these miRNA molecules may serve as a potential therapeutic target during disease progression.

Circulating MicroRNAs as Novel Potential Biomarkers for Left Ventricular Remodeling in Postinfarction Heart Failure.

Circulating microRNAs (miRNAs) have been proposed as potential biomarkers for left ventricular remodeling in postinfarction heart failure (HF). However, the diagnostic reproducibility of the use of circulating miRNAs may be affected by the temporal expression of miRNAs following myocardial infarction (MI). In the current study, using a MI-induced HF rat cohort (4-, 8-, and 12-week post-MI groups), we investigated the temporal expression of plasma miRNAs during the development of left ventricular remodeling. The plasma miRNA expression profile was obtained using miRNA sequencing. The expression of candidate miRNAs in plasma and tissues was examined with real-time PCR. Target genes of candidate miRNAs were predicted using a parallel miRNA-messenger RNA expression profiling approach. The value of plasma miRNAs as biomarkers for left ventricular remodeling was evaluated in patients with postinfarction HF (n = 32) and control patients with stable angina and without significant coronary lesions and HF (n = 16) with real-time PCR. Although the expression levels of miR-20a-5p, miR-340-5p, and let-7i-5p were temporally regulated in plasma, myocardium, and peripheral blood mononuclear cells, the expression levels of plasma miRNAs, especially miR-20a-5p, were associated with the development of left ventricular remodeling in the postinfarction HF rat cohort. The target genes of these 3 miRNAs were associated with the mechanistic target of rapamycin, nuclear factor-κB, tumour necrosis factor, apoptosis, and p53 signaling pathways. Additionally, the plasma levels of miR-20a-5p, miR-340-5p, and let-7i-5p were significantly increased in patients with postinfarction HF. However, only the expression levels of miR-20a-5p presented significant positive correlations with left ventricular internal end diastolic dimension and left ventricular end diastolic volume. In conclusion, the expression levels of plasma miR-20a-5p were significantly associated with the degree of left ventricular dilatation, and plasma miR-20a-5p may be a potential biomarker for postinfarction left ventricular remodeling.

The Relationship between Plasma ADAMTS 7 Level and Left Ventricular Remodeling after Acute Myocardial Infarction

AbstractBackground: Left Ventricular (LV) dysfunction is the single strongest predictor of mortality following ST elevation myocardial infarction and is one of the most frequent and deadly complications of non ST elevation myocardial infarc-tion. Degradation of Extracellular Matrix (ECM) causes progressive thinning and dilatation of infarct zone and con-tributes to serious complication as ventricular dilatation, dysfunction, aneurysm and even rupture. The matrix metallo-proteinase-mediated degradation and remodeling of ECM plays an essential role in these disease processes.Aim of the Study: It was to evaluate the relationship between plasma ADAMTS 7 level and left ventricular remod-eling after acute myocardial infarction.Patients and Methods: This study was carried on fifty cases that were divided into two main categories according to their health status. Diseased group included twenty five patients diagnosed as acute myocardial infarction with newly S-T segment elevation. Based on their echocardiographic examination, patients were classified into two groups patients; a group of 16 patients with ejection fraction of more or equal 40 (group I; G1) and 9 patients with an ejection fraction of less than 40 (group II; G2). Control group included twenty five apparently healthy persons serving as controls (group III; G 3). All studied cases were subjected to detailed clinical history, thorough clinical examination, Electrocardiogram (ECG), trans-thoracic Echocardiography (ECHO), routine laboratory investigation included: Cardiac markers, renal function tests, liver function tests, lipid profile, serum elec-trolytes, complete blood picture and special laboratory inves-tigation: Plasma adamts-7 levels measurement by ELISA technique.Results: There was statistically significant increase in ADAMTS 7 concentration in group II (patients with ejection fraction _40) and group III (controls), while there was no statistically significant difference between group I and group III. There was a statistically significant negative correlation between ADAMTS 7 concentration and both ejection fraction and fractional shortening in acute myocardial infarction patients. While there was a statistically significant positive correlation between ADAMTS 7 concentration and both left ventricular end diastolic diameter and left ventricular end systolic diameter in acute myocardial infarction patients.Conclusion: The results of this research showed that there was a significant increase in the mean value of ADAMTS 7 levels in patients with ejection fraction _40%, so it may be used as a strong predictor for the development of left ventricular remodeling after acute myocardial infarction and this may be of a great value as a therapeutic target.

Effect of NF-κB inhibitor on Toll-like receptor 4 expression in left ventricular myocardium in two-kidney-one-clip hypertensive rats.

To investigate the effects of an inhibitor of NF-κB, PDTC (pyrrolidine dithiocarbamate), on TLR4 (Toll-like receptor 4) expression in the left ventricle of Goldblatt hypertension rats. Goldblatt rat model of two-kidney, one-clip (2K1C) hypertension was established in 70 healthy male rats. The rats were randomly divided into sham operation group (S group, n=20), non-drug intervention hypertension group (H group, n=25), and PDTC intervention group (P group, n=25). P group was injected with PDTC. The clip was inserted in the left renal artery of H group and P group (2K1C). Eight weeks after the operation, the rats were sacrificed and the samples of the left ventricle were collected. The concentration of AngII in the left ventricle was assessed by radioimmunoassay. RT-PCR was used to examine the mRNA expression of TLR4 in the left ventricle. Immunohistochemistry was adopted to examine the location of TLR4 and NF-κB in the myocardium. Victoria blue-Ponceau staining of Cardiac collagen was used to evaluate the degree of myocardial fibrosis. Eight weeks after the operation, caudal SBP, meridional end-systolic stress, left ventricular mass index, relative wall thickness, cardiac fibrosis degree, and the concentration of AngII in the left ventricle in P group were significantly lower than those in H group (p<0.01). In cardiac myocytes of S group and P group, TLR4 expression was diffused and presumably cytoplasmic. TLR4 mRNA expression in P group was significantly lower than that of H group (p<0.01). PDTC not only inhibited the activation of NF-κB, but decreased TLR4 expression and AngII content, indicating that the inflammatory signals and oxidative stress mediated by TLR4/NF-κB are involved in the occurrence and development of left ventricular remodeling. Intervention with TLR4/NF-κB and anti-inflammatory and anti-oxidative therapy may be a new target to reverse left ventricular remodeling.

The predictive value of M30 and oxidative stress for left ventricular remodeling in patients with anterior ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention.

Left ventricular (LV) remodeling is an important pathophysiological event that develops following acute myocardial infarction and causes LV systolic dysfunction. Mechanisms such as apoptosis, necrosis, and oxidative stress play an important role in LV remodeling. This study aimed to determine the relationship between the development of LV remodeling and the apoptosis marker M30 in patients with anterior ST-segment elevation myocardial infarction (STEMI) who were treated with primary percutaneous coronary intervention (PCI). This retrospective study included 255 consecutive patients (210 men, 45 women, mean age 54.9±11.8 years) with anterior STEMI who were treated with primary PCI. Blood samples were obtained from each patient at admission and 24 h after admission for measurements of M30, M65, oxidative parameters, and biochemical parameters. Transthoracic echocardiography was performed in each patient within 24 h of infarction and 6 months after infarction. LV remodeling was defined as greater than or equal to 20% increase in end-diastolic volume 6 months after primary PCI. The patients were divided into two groups on the basis of 6 months of post-primary PCI follow-up findings: LV remodeling group and non-LV remodeling group. In all, 60 patients received LV remodeling and 195 did not receive LV remodeling at 6 months after primary PCI. Total oxidative stress, M30 and M65 levels, and the oxidative stress index were significantly higher and the total antioxidant capacity and M65/M30 ratio were lower in the LV remodeling group (P<0.05, for all). Brain natriuretic peptide, M30, and oxidative stress index were independent predictors of LV remodeling (P<0.05 for all). Receiver operating characteristic curve analysis showed that the M30 cut-off value for predicting LV remodeling was 144.9 U/l (80% sensitivity and 77% specificity, P<0.001). In patients with anterior STEMI treated with primary PCI, the apoptosis marker M30 might be useful for predicting LV remodeling and subsequent LV systolic dysfunction.

Perfusion Computed Tomography for the Assessment of Myocardial Viability — a Case Series

Abstract Myocardial viability plays an important role in preventing the development of left ventricular remodeling following an acute myocardial infarction. A preserved viability in the infarcted area has been demonstrated to be associated with a lower amplitude of the remodeling process, while the extent of the non-viable myocardium is directly correlated with the amplitude of the remodeling process. A number of methods are currently in use for the quantification of the viable myocardium, and some of them are based on the estimation of myocardial perfusion during pharmacologic stress. 64-slice Multi-detector Computed Tomography (MDCT) during vasodilator stress test, associated with CT Coronary Angiography (CCTA) has a high diagnostic accuracy in evaluating myocardial perfusion. In this article, we present a sequence of 3 clinical cases that presented with symptoms of myocardial ischemia, who underwent 64-slice MDCT imaging at rest and during adenosine stress test, in order to assess the extent of the hypoperfused myocardial areas. Coronary artery anatomy and the Coronary Calcium Score was assessed for all 3 patients by performing CT Coronary Angiography. The combination of CT Angiography and adenosine stress CT myocardial perfusion imaging can accurately detect atherosclerosic lesions that cause perfusion abnormalities, compared with the combination of invasive angiography and single-photon emission computed tomography (SPECT).

Circulating MicroRNA-146a and MicroRNA-21 Predict Left Ventricular Remodeling after ST-Elevation Myocardial Infarction

Objectives: MicroRNA (miR)-146a and miR-21 have been reported to participate in inflammatory reactions and fibrosis. Excessive inflammation and cardiac fibrosis may play important roles in the development of left ventricular remodeling (LVR). This study assessed whether miR-146a, miR-21 and other biomarkers could predict LVR after myocardial infarction (MI). Methods: Circulating miR-146a, miR-21 and other biomarker levels were measured in 198 patients with acute MI 5 days after primary percutaneous coronary intervention (PCI). All patients were assessed by transthoracic echocardiography on day 5 and 1 year after primary PCI. Results: Concentrations of circulating miR-146a, miR-21, C-reactive protein, creatine kinase MB type and troponin I, as well as estimated glomerular filtration rate (eGFR) and left ventricular ejection fraction (LVEF), were significantly higher in patients with than in those without LVR (p < 0.05). Multivariate logistic regression analysis showed that circulating miR-146a (odds ratio, OR = 2.127, p < 0.0001), miR-21 (OR = 1.119, p < 0.0001), eGFR (OR = 0.939, p = 0.0137) and LVEF (OR = 0.802, p = 0.0048) were independent predictors of LVR development. The area under the curve for the combination of miR-146a and miR-21 was significantly higher than for either alone. Conclusion: Circulating miR-146a and miR-21 may be novel biomarkers predictive of LVR after acute MI. Their combination may better predict LVR than either alone.

Left atrial volume index as a predictor of left ventricular remodeling in patients with anterior STEMI treated with primary PCI

Abstract Background Left ventricular remodeling (LVR) after myocardial infarction (MI) is associated with adverse cardiovascular events. Left atrial volume index (LAVI) was emerged as a prognostic factor for cardiovascular outcome. The aim of the study was to assess the value of measuring LAVI at discharge as a predictive factor for the development of LVR after anterior ST-elevation MI (STEMI) treated with primary percutaneous coronary intervention (PPCI). Methods The study included 100 consecutive patients with first anterior STEMI successfully treated with primary percutaneous coronary intervention (PPCI). Echocardiographic evaluation was performed at the time of discharge and at 6 months. LVR was defined as >20% increase in LVEDVI at 6 months compared with that at discharge. Results The prevalence of LVR was 31%. Patients who developed LVR had higher LVESVI at baseline, lower EF%, higher WMSI, higher LAVI, and longer time to perfusion. Multivariable logistic regression analysis showed that LAVI was the only predictive factor for LVR (p = 0.003, 95% CI = 1.87–19.7). ROC curve analysis showed that LAVI was predictive for LVR with a cut-off value 38 ml/m2 (sensitivity 96.8% and specificity 77%, p = 0.001, 95% CI = 0.93–0.99). Conclusion LAVI is a simple and non-invasive echocardiographic marker that can predict the development of LVR in patients with anterior STEMI treated with PPCI.

Association of dietary iron restriction with left ventricular remodeling after myocardial infarction in mice

Several epidemiologic studies have reported that body iron status and dietary iron intake are related to an increased risk of acute myocardial infarction (MI). However, it is completely unknown whether dietary iron reduction impacts the development of left ventricular (LV) remodeling after MI. Here, we investigate the effect of dietary iron restriction on the development of LV remodeling after MI in an experimental model. MI was induced in C57BL/6 J mice (9-11 weeks of age) by the permanent ligation of the left anterior descending coronary artery (LAD). At 2 weeks after LAD ligation, mice were randomly divided into two groups and were given a normal diet or an iron-restricted diet for 4 weeks. Sham operation without LAD ligation was also performed as controls. MI mice exhibited increased LV dilatation and impaired LV systolic function that was associated with cardiomyocyte hypertrophy and interstitial fibrosis in the remote area, as compared with the controls at 6 weeks after MI. In contrast, dietary iron restriction attenuated LV dilatation and impaired LV systolic function coupled to cardiomyocyte hypertrophy and interstitial fibrosis in the remote area. Importantly, cardiac expression of cellular iron transport proteins, transferrin receptor 1 and divalent metal transporter 1 was increased in the remote area of MI mice compared with the controls. Dietary iron restriction attenuated the development of LV remodeling after MI in mice. Cellular iron transport might play a role in the pathophysiological mechanism of LV remodeling after MI.

Echocardiographic Datasets Showing Development of Cardiac Remodelling in Rats at Different Time-points after Acute Myocardial Infarction

A B S T R A C T The simulation of the time course of development of heart failure after an acute myocardial infarction requires large, open-access datasets. In this report, we present large echocardiographic datasets of cardiac function in rats after myocardial infarction at two different time points (2 and 13 weeks). We present measurements that show the deterioration of global left ventricular (LV) function, regional function, development of LV dilation, reactive hypertrophy and changes in LV geometry. We present in addition measurements showing the degree of cardiac injury assessed by the area and weight of the scar tissue. These data represent the progressive nature of cardiac remodelling and could be used to build computational models to predict the development of heart function deterioration based on the extent of myocardial injury and the development of LV remodelling.

Prevention of electrocardiographic left ventricular remodeling by the angiotensin receptor blocker olmesartan in patients with type 2 diabetes.

To assess the ability of olmesartan (OLM) to prevent or delay left ventricular remodeling and hypertrophy in patients with type 2 diabetes. This prespecified ECG substudy of Randomised OlmesArtan and Diabetes MicroAlbuminuria Prevention (ROADMAP), which compared OLM with placebo, assessed the signs of left ventricular remodeling in patients with a 12-lead ECG at baseline and after at least 2 years. Cornell voltage QRS duration product (primary objective), Cornell voltage index and Sokolow-Lyon index were assessed. In total, 9418 ECG recordings and 1513 patients from ROADMAP were analyzed (placebo, n = 736; OLM, n = 777). Quartiles defined by baseline Cornell voltage QRS duration product were assessed and the proportion of patients in the highest quartile (≥200 mVms) increased from 24.0 to 26.5% in the placebo group and decreased from 25.5 to 22.3% in the OLM group [odds ratio (OR) 0.598 (95% confidence interval [CI] 0.440-0.813); P = 0.0011]. The OR did not change after adjustment for baseline parameters. By the end of study, 38.7% of patients in the placebo group and 34.7% in the OLM group shifted from a lower to a higher quartile or remained in the highest quartile of Cornell voltage QRS duration product [OR 0.797 (95% CI 0.637-0.996); P = 0.0465]. This translated into a 20.3% risk reduction with OLM and suggested OLM attenuated the progression of left ventricular remodeling versus placebo. OLM substantially delayed the development of left ventricular remodeling in type 2 diabetes. This effect was not explained by the differences in blood pressure control. Thus, OLM delayed the onset of microalbuminuria, as well as the ECG signs of cardiac structural adaptation in type 2 diabetes.

GW25-e0719 High Brachial-ankle pulse wave velocity is a conditional factor for the development of left ventricular remodeling: population based nested case-control study

GW25-e0719 High Brachial-ankle pulse wave velocity is a conditional factor for the development of left ventricular remodeling: population based nested case-control study

Association between Multilayer Left Ventricular Rotational Mechanics and the Development of Left Ventricular Remodeling after Acute Myocardial Infarction

The identification of patients at risk for developing left ventricular (LV) remodeling after acute myocardial infarction (AMI) has crucial prognostic implications. The aims of this study were (1) to investigate the relationship between peak subepicardial and subendocardial twist and infarct transmurality, as assessed using contrast-enhanced magnetic resonance imaging, and (2) to evaluate the association between peak subepicardial and subendocardial twist and LV remodeling 6 months after AMI. A total of 213 patients with ST-segment elevation AMIs who underwent three-dimensional echocardiography for LV volumes and functional assessment and two-dimensional speckle-tracking analysis for the evaluation of LV twist (subendocardial vs subepicardial) were retrospectively included. A subgroup of 40 patients underwent magnetic resonance imaging within 2 months for infarct size quantification. Peak subepicardial twist was strongly related to infarct size (number of segments with transmural scar: r(2) = 0.526, P < .001; total scar score: r(2) = 0.515, P < .001) compared with peak subendocardial twist (number of segments with transmural scar: r(2) = 0.379, P < .001; total scar score: r(2) = 0.331, P < .001). In the overall population, 44 patients (21%) developed significant LV remodeling at 6-month follow-up (LV end-systolic volume increase ≥ 15%). These patients showed significantly more impaired peak subepicardial and subendocardial twist at baseline compared with patients without LV remodeling (4.5 ± 1.3° vs 9.4 ± 3.5°, P < .001; 7.0 ± 3.2° vs 12.9 ± 5.8°, P < .001, respectively). Importantly, peak subepicardial twist (odds ratio, 0.241; 95% confidence interval, 0.134-0.431; P < .001) and peak troponin T (odds ratio, 1.152; 95% confidence interval, 1.006-1.320; P = .041) were independently associated with the development of LV remodeling. Peak subepicardial twist strongly reflects infarct transmurality as assessed with magnetic resonance imaging and is independently associated with LV remodeling after AMI.

Left ventricular remodelling after acute myocardial infarction: Impact of clinical, echocardiographic parameters and polymorphism of angiotensinogen gene

The development of left ventricular remodelling after acute myocardial infarction is a predictor of heart failure and mortality. The purpose of the present study was to assess whether the polymorphism of angiotensinogen (AGT) gene with threonine (T) instead of methionine (M) at amino acid 235 in exon 2 (M235T) had effects on cardiac remodelling after acute myocardial infarction. One hundred and forty-one patients (mean age 56.4±11.1 years) with a first acute myocardial infarction were enrolled. Within 24-72 hours of the onset of the symptoms and at a four month period two-dimensional echocardiography was performed. Remodelling was defined as a 20% increase from the baseline in left ventricular end-diastolic volume. The genotypes of the study group were compared with the reference group (n=1010) genotypes. AGT M235T polymorphism was determined using polymerase chain reaction amplification. At follow-up, 49 patients (34.7%) were classified as having left ventricular remodelling. Anterior localization of the infarct (p=0.008), leucocyte count at admission (p=0.040), global left ventricular longitudinal strain (p=0.021) and MM genotype of AGT (p=0.024) were independent predictors of ventricular remodelling after myocardial infarction. Anterior wall infarction, increased leucocyte count, decreased longitudinal strain of left ventricular and polymorphism of AGT M235T may predict remodelling after myocardial infarction.