Echocardiography and Cardiac Magnetic Resonance in the Assessment of Left-Ventricle Remodeling: Differences Implying Clinical Decision.

Introduction: Transthoracic echocardiography (TTE) and cardiovascular magnetic resonance (CMR) are the most important modalities used in clinical practice to assess cardiac chambers. However, different imaging techniques may affect their results and conclusions. The aim of our study was to compare left-ventricle (LV) remodeling assessed using TTE and CMR in the context of various cardiovascular diseases. Methods: A total of 202 consecutive patients sent for an elective cardiovascular diagnosis were scheduled for a 2D TTE and CMR, performed within 2 weeks. The study group was divided and analyzed based on the clinical indications for CMR, including coronary artery disease, heart failure, native aortic valve regurgitation or paravalvular leak after aortic valve replacement, or cardiomyopathies. Results: The mean LV mass index (LVMi) values calculated using TTE were significantly larger (127.1 ± 44.5 g/m²) compared to the LVMi assessed using CMR (77.1 ± 26.2 g/m²; p < 0.001). The LV end-diastolic volumes assessed using TTE were underestimated for all the study patients (78.6 ± 43 mL vs. 100.5 ± 39 mL; p < 0.0001) and subgroups, but a statistical trend was observed in patients with cardiomyopathy. Those differences in single parameters led to differences in LV remodeling and the final treatment decision. CMR and TTE provided similar conclusions on LV systolic dysfunction in 68% of the patients. Conclusions: Our results showed that the greater the degree of LV remodeling and dysfunction, the greater the difference between the modalities. Therefore, CMR should be introduced into routine clinical practice, especially for patients undergoing LV remodeling, which may change clinical decisions in a considerable number of cases.

Systemic immune- inflammation index predicts post-MI left ventricular remodeling.

AIMS: Previous studies demonstrated that remodeling after successful percutaneous coronary intervention (PCI) depends on the inflammatory response triggered by myocardial infarction (MI). The systemic immune-inflammation index (SII) is a novel inflammation index strongly associated with coronary artery disease. In our study, we sought to determine whether SII could predict Post-MI LV remodeling. METHODS AND RESULTS: The study population included 528 patients (mean age 62.5 ± 10.2, 73% male) diagnosed with STEMI. Based on the increase in LVEDV within the first 12 months after STEMI, patients were divided into two groups. We categorized the ≥ 20% increase in LVEDV among remodelers (257 patients, 49%), and the other 271 patients (51%), as non-remodelers. To determine the relationship between laboratory parameters and LV remodeling, univariate and multivariate logistic regression models were used. In a univariate model, higher hs-CRP and SII values were associated with increased LVEDV. In a multivariate analysis, SII independently correlated with LV remodeling A cut-off value of 613.3 or higher for SII was significantly correlated with LV remodeling based on ROC analysis. CONCLUSION: SII provides an easy-to-calculate and affordable biomarker for cardiovascular diseases. It may be used as a new biomarker to predict LV remodeling in patients with STEMI.

Cardiovascular Interactions of Renin-Angiotensin-Aldosterone System Assessed by Cardiac Magnetic Resonance: The Multi-Ethnic Study of Atherosclerosis.

BACKGROUND: The effects of the renin-angiotensin-aldosterone system in cardiovascular system have been described based on small studies. The aim of this study was to evaluate the relationship between aldosterone and plasma renin activity (PRA) and cardiovascular structure and function. METHODS: We studied a random sample of Multi-Ethnic Study of Atherosclerosis participants who had aldosterone and PRA blood assays at 2003-2005 and underwent cardiac magnetic resonance at 2010. Participants taking angiotensin-converting enzyme inhibitors or angiotensin receptor blockers were excluded. RESULTS: The aldosterone group was composed by 615 participants, mean age 61.6 ± 8.9 years, while the renin group was 580 participants, mean age 61.5 ± 8.8 years and both groups had roughly 50% females. In multivariable analysis, 1 SD increment of log-transformed aldosterone level was associated with 0.07 g/m2 higher left ventricle (LV) mass index (P = 0.04) and 0.11 ml/m2 higher left atrium (LA) minimal volume index (P < 0.01). Additionally, higher log-transformed aldosterone was associated with lower LA maximum strain and LA emptying fraction (P < 0.01). Aldosterone levels were not significantly associated with aortic measures. Log-transformed PRA was associated with lower LV end diastolic volume index (ß standardized = 0.08, P = 0.05). PRA levels were not significantly associated with LA and aortic structural or functional differences. CONCLUSIONS: Higher levels of aldosterone and PRA are associated with concentric LV remodeling changes. Moreover, aldosterone was related to deleterious LA remodeling changes.

Predicting one-year left ventricular mass index regression following transcatheter aortic valve replacement in patients with severe aortic stenosis: A new era is coming.

Aortic stenosis (AS) is the most common valvular heart disease in the western world, particularly worrisome with an ever-aging population wherein postoperative outcome for aortic valve replacement is strongly related to the timing of surgery in the natural course of disease. Yet, guidelines for therapy planning overlook insightful, quantified measures from medical imaging to educate clinical decisions. Herein, we leverage statistical shape analysis (SSA) techniques combined with customized machine learning methods to extract latent information from segmented left ventricle (LV) shapes. This enabled us to predict left ventricular mass index (LVMI) regression a year after transcatheter aortic valve replacement (TAVR). LVMI regression is an expected phenomena in patients undergone aortic valve replacement reported to be tightly correlated with survival one and five year after the intervention. In brief, LV geometries were extracted from medical images of a cohort of AS patients using deep learning tools, and then analyzed to create a set of statistical shape models (SSMs). Then, the supervised shape features were extracted to feed a support vector regression (SVR) model to predict the LVMI regression. The average accuracy of the predictions was validated against clinical measurements calculating root mean square error and R 2 score which yielded the satisfactory values of 0.28 and 0.67, respectively, on test data. Our work reveals the promising capability of advanced mathematical and bioinformatics approaches such as SSA and machine learning to improve medical output prediction and treatment planning.

Maternal hemodynamic profile during pregnancy and in the post-partum in hypertensive disorders of pregnancy and fetal growth restriction.

BACKGROUND: Maternal cardiovascular changes, occurring since the beginning of pregnancy, are necessary for normal placentation and regular evolution of pregnancy. OBJECTIVE: This study aimed to compare the hemodynamic profiles and cardiac remodeling of women with hypertensive disorders of pregnancy and either appropriate for gestational age fetuses or growth-restricted fetuses, women with normotensive pregnancies complicated by fetal growth restriction, and women with uncomplicated pregnancies, during pregnancy and the postpartum period. STUDY DESIGN: A prospective longitudinal case-control design was used for this study. Over the study period, 220 eligible women with singleton pregnancies were selected for the analysis and divided into 4 groups: (1) hypertensive disorders of pregnancy with appropriate for gestational age fetuses; (2) hypertensive disorders of pregnancy with fetal growth restriction; (3) normotensive fetal growth restriction; and (4) controls. Ultrasound fetal biometry and fetoplacental Doppler velocimetry were performed at recruitment. Maternal hemodynamic assessment using transthoracic echocardiography was performed at the time of recruitment by a dedicated cardiologist blinded to maternal clinical data. The same assessments were performed in 104 patients at 32 weeks (interquartile range, 24-40) after delivery by the same cardiologist. RESULTS: During pregnancy, women in the hypertensive-disorders-of-pregnancy-fetal-growth-restriction group showed significantly lower cardiac output and increased compared with those in the control group. These values were associated with concentric remodeling of the left ventricle owing to relatively increased wall thickness, which was not accompanied by an increase in left ventricular mass. Isolated fetal growth restriction presented similar but less important hemodynamic changes; however, there was no change in relative wall thickness. At postpartum follow-up, the hemodynamic parameters of women in the hypertensive-disorders-of-pregnancy-fetal-growth-restriction and isolated-fetal-growth-restriction groups reverted to values similar to those of the control group. Only 8.3% of women in these groups experienced hypertension even in the postpartum period, and asymptomatic stage-B cardiac failure was observed for 17% at echocardiography. In the group of women with hypertensive disorders of pregnancy and appropriate for gestational age fetuses, cardiac output increased as in normal pregnancies, but total vascular resistance was significantly higher; hypertension then occurred, along with ventricular concentric hypertrophy and diastolic dysfunction. At postpartum follow-up, women in the hypertensive-disorders-of-pregnancy-appropriate-for-gestational-age-fetus group showed significantly higher mean arterial pressure, total vascular resistance, and left ventricular mass compared with those in the control group. Persistent hypertension and asymptomatic stage-B cardiac failure were observed in 39.1% and 13% of women in the former group, respectively. CONCLUSION: Pregnancies with hypertensive disorders of pregnancy and fetal growth restriction and normotensive pregnancies with fetal growth restriction were associated with the hemodynamic profile of lower heart rate and cardiac output, most likely because of abnormal adaptation to pregnancy, as confirmed by abnormal changes from pregnancy to the postpartum period. The heart rates and cardiac output of women in the hypertensive-disorders-of-pregnancy-appropriate-for-gestational-age-fetus group showed changes opposite to those observed in the hypertensive-disorders-of-pregnancy-fetal-growth-restriction and fetal-growth-restriction groups. Obesity and other metabolic risk factors, significantly prevalent in women in the hypertensive-disorders-of-pregnancy-appropriate-for-gestational-age-fetus group, predispose to hypertension and cardiovascular diseases during pregnancy and the postpartum period, potentially offering a window for personalized prevention. Such preventive strategies could differ in women with hypertensive disorders of pregnancy and fetal growth restriction characterized by poor early placental development.

Interventricular Septum Thickness for the Prediction of Coronary Heart Disease and Myocardial Infarction in Hypertension Population: A Prospective Study.

The aim of the present study was to evaluate the prognostic value of interventricular septum thickness (IVSd) on the incidence of cardiovascular diseases. Based on the general population in Northeast China, 10,349 participants were successfully followed up for echocardiography over a median follow-up time of 4.66 years, among which 4801 were hypertensive. Coronary heart disease (CHD) and myocardial infarction (MI) incidence were followed up. Cox proportional hazards models were used to estimate the association of the baseline IVSd with adverse outcomes. IVS hypertrophy increased incident rates of CHD and MI compared with normal IVSd in the overall population and in the female sex-stratification group. In males, IVS hypertrophy had parallel increase rates of CHD (all p < 0.05). Kaplan−Meier analysis showed that IVS hypertrophy could predict CHD and MI incidence and CHD-free and MI-free survival. Multivariable Cox analysis revealed that IVS hypertrophy was correlated with CHD incidence (HR = 1.155, 95% CI = 1.155−2.861, p = 0.01) and MI incidence (HR = 2.410, 95% CI = 1.303−4.458, p = 0.005). In women, IVS hypertrophy was independently associated with CHD and MI incidence (all p < 0.05). Our prospective cohort study illustrated that IVS hypertrophy detected by echocardiography has a prognostic significance for CHD and MI. Therefore, the early detection of IVSd should be conducted to avoid adverse outcomes in further clinical practice.

Wnt11 in regulation of physiological and pathological cardiac growth.

Wnt11 regulates early cardiac development and left ventricular compaction in the heart, but it is not known how Wnt11 regulates postnatal cardiac maturation and response to cardiac stress in the adult heart. We studied cell proliferation/maturation in postnatal and adolescent Wnt11 deficient (Wnt11-/-) heart and subjected adult mice with partial (Wnt11+/-) and complete Wnt11 (Wnt11-/-) deficiency to cardiac pressure overload. In addition, we subjected primary cardiomyocytes to recombinant Wnt proteins to study their effect on cardiomyocyte growth. Wnt11 deficiency did not affect cardiomyocyte proliferation or maturation in the postnatal or adolescent heart. However, Wnt11 deficiency led to enlarged heart phenotype that was not accompanied by significant hypertrophy of individual cardiomyocytes. Analysis of stressed adult hearts from wild-type mice showed a progressive decrease in Wnt11 expression in response to pressure overload. When studied in experimental cardiac pressure overload, Wnt11 deficiency did not exacerbate cardiac hypertrophy or remodeling and cardiac function remained identical between the genotypes. When subjecting cardiomyocytes to hypertrophic stimulus, the presence of recombinant Wnt11 together with Wnt5a reduced protein synthesis. In conclusion, Wnt11 deficiency does not affect postnatal cardiomyocyte proliferation but leads to cardiac growth. Interestingly, Wnt11 deficiency alone does not substantially modulate hypertrophic response to pressure overload in vivo. Wnt11 may require cooperation with other noncanonical Wnt proteins to regulate hypertrophic response under stress.

Left ventricular diastolic early and late filling quantified from 4D flow magnetic resonance imaging.

PURPOSE: The purpose of this study was to investigate the value of 4D flow MRI for mitral filling measurements, using transthoracic echocardiography (TTE) and 2D flow MRI as references, as well as identify relationships with age and left ventricle (LV) remodeling in healthy volunteers. MATERIAL AND METHODS: Fifty healthy volunteers (22 men, 28 women; mean age, 51.3 ± 16.9 [SD] years; age range: 20-80 years) prospectively underwent TTE and MRI on the same day. 4D flow volume acquisition was done at 3T with reconstructed spatial/temporal resolutions: 1 × 1.48 × 2.38 mm3/34 ms. Early (E) and late (A) flow rate and maximal velocity peaks were measured from 4D flow data with three strategies: static planes at 1) the mitral valve leaflets tip (4DLT) and 2) annulus (4Dann); and 3) while tracking the annulus through time (4Dtrack). RESULTS: 4DLT- and 4Dtrack-derived E/A ratios were in good agreement with 2D flow and TTE estimates with a superiority over maximal velocities (4DLT: r = 0.71 and r = 0.66; 4Dtrack: r = 0.74 and r = 0.71, respectively) of flow rates (4DLT: r = 0.89 and 0.72; 4Dtrack: r = 0.91 and 0.76, respectively). Measurements of 4DLT and 4Dtrack were highly reproducible (ICC = 0.89 and 0.95, respectively) and significantly correlated with age and LV remodeling (4DLT: r = -0.76 and ρ = -0.49; 4Dtrack: r = -0.79 and ρ = -0.51, respectively). CONCLUSION: E/A ratio can be accurately measured using 4D flow MRI either at a fixed mitral leaflet tip location or through annulus plane time-resolved tracking.

Left ventricle reverse remodeling in chronic aortic regurgitation patients with dilated ventricle after aortic valve replacement.

BACKGROUND: Aortic valve replacement (AVR) for chronic aortic regurgitation (AR) with a severe dilated left ventricle and dysfunction leads to left ventricle remodeling. But there are rarely reports on the left ventricle reverse remodeling (LVRR) after AVR. This study aimed to investigate the LVRR and outcomes in chronic AR patients with severe dilated left ventricle and dysfunction after AVR. METHODS: We retrospectively analyzed the clinical datum of chronic aortic regurgitation patients who underwent isolated AVR. The LVRR was defined as an increase in left ventricular ejection fraction (LVEF) at least 10 points or a follow-up LVEF ≥ 50%, and a decrease in the indexed left ventricular end-diastolic diameter of at least 10%, or an indexed left ventricular end-diastolic diameter ≤ 33 mm/m2. The changes in echocardiographic parameters after AVR, survival analysis, the predictors of major adverse cardiac events (MACE), the association between LVRR and MACE were analyzed. RESULTS: Sixty-nine patients with severe dilated left ventricle and dysfunction underwent isolated AVR. LV remodeling in 54 patients and no LV remodeling in 15 patients at 6-12 months follow-up. The preoperative left ventricular dimensions and volumes were larger, and the EF was lower in the LV no remodeling group than those in the LV remodeling group (all p < 0.05). The adverse LVRR was the predictor for MACE at follow-up. The mean follow-up period was 47.29 months (range 6 to 173 months). The rate of freedom from MACE was 94.44% at 5 years and 92.59% at 10 years in the remodeling group, 60% at 5 years, and 46.67% at 10 years in the no remodeling group. CONCLUSIONS: The left ventricle remodeling after AVR was the important predictor for MACE. LV no remodeling may not be associated with benefits from AVR for chronic aortic regurgitation patients with severe dilated LV and dysfunction.

Regression of Q waves and clinical outcomes following primary PCI in anterior STEMI.

BACKGROUND: Pathological Q waves are correlated with infarct size, and Q-wave regression is associated with left ventricular ejection fraction improvement. There are limited data regarding the association of Q-wave regression and clinical outcomes. Our main objective was to assess the association of pathological Q wave evolution after reperfusion with clinical outcomes after anterior STEMI. METHODS: Standard 12-lead electrocardiograms (ECGs) were recorded in 780 anterior STEMI patients treated with primary percutaneous coronary intervention (PCI) from the CIRCUS trial. ECGs were recorded before and 90 min following PCI, as well as at hospitalization discharge and 12 months of follow-up. The number of classic ECG criteria Q waves was scored for each ECG. Patients were classified in the Q wave regression group if they had regression of at least one Q wave between the post-PCI, the discharge and/or one year ECGs. Patients were classified in the Q wave persistent group if they had the same number or greater between the post-PCI, the discharge and/or 1 and one year ECGs. All-cause death and heart failure events were assessed for all patients at one year. RESULTS: There were 323(43%) patients with persistent Q waves (PQ group), 378(49%) patients with Q wave regression (RQ group) and 60(8%) patients with non-Q wave MI (NQ group). Infarct size as measured by the peak creatine kinase was significantly greater in the PQ group compared to the RQ and NQ groups (4633 ±â€¯2784 IU/l vs. 3814 ±â€¯2595 IU/l vs. 1733 ±â€¯1583 IU/l respectively, p < 0.0001). At one year, there were 22 deaths (7%) in the PQ-group, 15 (4%) in the RQ-group and none in the NQ-group (p = 0.04). There was a 4-fold increase in the risk of death or heart failure in the PQ compared to the NQ group (HR 4.7 [1.1; 19.3]; p = 0.03), but there was no significant difference between NQ and RQ groups (HR 3.3 [0.8; 13.8]; p = 0.09). CONCLUSION: In a population of anterior STEMI patients, persistent Q waves defined according to the classic ECG criteria after reperfusion was associated with a 4-fold increase in the risk of heart failure or death compared to non-Q-wave MI, while Q-wave regression was associated with significantly lower risk of events.

Targeting the Autophagy-Lysosome Pathway in a Pathophysiologically Relevant Murine Model of Reversible Heart Failure.

The key biological "drivers" that are responsible for reverse left ventricle (LV) remodeling are not well understood. To gain an understanding of the role of the autophagy-lysosome pathway in reverse LV remodeling, we used a pathophysiologically relevant murine model of reversible heart failure, wherein pressure overload by transaortic constriction superimposed on acute coronary artery (myocardial infarction) ligation leads to a heart failure phenotype that is reversible by hemodynamic unloading. Here we show transaortic constriction + myocardial infarction leads to decreased flux through the autophagy-lysosome pathway with the accumulation of damaged proteins and organelles in cardiac myocytes, whereas hemodynamic unloading is associated with restoration of autophagic flux to normal levels with incomplete removal of damaged proteins and organelles in myocytes and reverse LV remodeling, suggesting that restoration of flux is insufficient to completely restore myocardial proteostasis. Enhancing autophagic flux with adeno-associated virus 9-transcription factor EB resulted in more favorable reverse LV remodeling in mice that had undergone hemodynamic unloading, whereas overexpressing transcription factor EB in mice that have not undergone hemodynamic unloading leads to increased mortality, suggesting that the therapeutic outcomes of enhancing autophagic flux will depend on the conditions in which flux is being studied.

Impact of percutaneous ventricular septal defect closure on left ventricular remodeling and function.

BACKGROUND: Ventricular septal defect (VSD) is the most common congenital heart disease. In patients with large VSD, left side chambers are subjected to volume overload with subsequent chambers dilatation and eccentric left ventricular hypertrophy. Percutaneous closure of VSD has been shown to be an effective method with equal safety and efficacy when compared to surgery. The effect of VSD closure on LV remodeling has been mainly assessed in patients treated with surgery and to date published data remain scarce. Therefore, we aim to evaluate the effect of percutaneous VSD closure on different LV parameters. RESULTS: Seventeen patients (median age 6 years (IQR 4.75-8 years), 70.6% females) who underwent percutaneous VSD closure were enrolled in the study. Sixteen patients (94%) had perimembranous VSD, and one patient had muscular VSD. The procedure was successful in all patients with no major complications. Nit Occlud® Lê coil device was implanted in 16 patients (94%), and one patient received Amplatzer PDA duct occlude device. At 6-months follow-up, there was a significant reduction in indexed LV dimensions [LVEDD/BSA (median 46.5 mm/m2 vs. 42.9 mm/m2, p = 0.03), LVESD/BSA (median 31.7 mm/m2 vs. 26.7 mm/m2, p = 0.02)], indexed LV volumes [LVEDV/BSA (median 52.6 ml/m2 vs. 37.3 ml/m2, p = 0.02), LVESV/BSA (median 31.7 ml/m2 vs. 23.3 ml/m2, p = 0.02)] and indexed LV mass (median 62.4 gm/m2 vs. 57.9 ml/m2, p = 0.01). There was a significant reduction in LVEDD Z-score (p = 0.01) and LVESD Z-score (p = 0.04). There was no significant change in LV EF. CONCLUSIONS: Percutaneous VSD closure is associated with improvement of various LV parameters with consequential favorable LV remodeling and function.

Too much of a good thing in ischemic mitral: lessons for surgeons and cardiologists.

No abstract present.

Influence of sodium ferulate on miR-133a and left ventricle remodeling in rats with myocardial infarction.

To explore the influence of sodium ferulate (SF) on miR-133a and left ventricle remodeling (LVR) in rats with myocardial infarction (MI). The left coronary artery was ligated to create 36 ischemia-reperfusion (IR) rat models that were randomly divided into mock surgical group (MSG) (not ligated), model group (MG), and sodium ferulate group (SFG). After the successful modeling, SFG was intravenously injected with SF at the dose of 10 mg/kg, and the other two groups were injected with the same volume of normal saline. After 28 days, cardiac hemodynamic indices of all groups were measured; the myocardial infarction size (MIS), left ventricular mass index (LVMI), and collagen volume fraction (CVF) were calculated, the content of serum malondialdehyde (MDA) and activities of catalase (CAT), superoxide dismutase (SOD) and glutathione catalase (GSH-px) were detected by ELISA, and miR-133a expression in myocardial tissues of the left ventricle (LV) was detected by RT-qPCR. SF improved the cardiac hemodynamic indices of rat model and reduced the MIS, LVMI and CVF. SF decreased the serum MDA level and increased the serum CAT, SOD and GSH-px levels in rat model. SF increased the expression of miR-133a in myocardial tissue of rat model. Therefore, SF could effectively reduce the myocardial injury of IR rats and improve the LVR. Its mechanism may be related to the antioxygenation and upregulation of miR-133a.

Mitral Plasticity: The Way to Prevent the Burden of Ischemic Mitral Regurgitation?

The ischemic impairment of the left ventricular contractility, followed by an adverse remodeling leading to the displacement of the papillary muscles (PMs), increased tethering forces and loss of valve competence has been the long-term accepted definition of ischemic mitral regurgitation (IMR). Over the years, different approaches of management have attempted to address valve regurgitation, nevertheless failing to achieve satisfactory outcomes. Recent studies have observed some structural and molecular changes of the mitral valve (MV), challenging the concept of a bystander passive to the subvalvular involvement. Indeed, the solely mechanical stretch of the PMs, as in the dilated left ventricle because of the aortic valve regurgitation, is not enough in causing relevant MV regurgitation. This setting triggers a series of structural changes called "mitral plasticity," leaflets increase in their size among others, ensuring an adequate systolic area closure. In contrast, the ischemic injury not only triggers the mechanical stretch on the subvalvular apparatus but is also a powerful promotor of profibrotic processes, with an upregulation of the transforming growth factor (TGF)-ß signaling pathway, leading to a MV with exuberant leaflet thickness and impaired mobility. In this article, we revise the concept of IMR, particularly focusing on the new evidence that supports dynamic changes in the MV apparatus, discussing the consequent clinical insights of "mitral plasticity" and the potential therapeutic implications.

Effect of high-intensity interval training on cardiac structure and function in rats with acute myocardial infarct.

BACKGROUND: Exercise training is beneficial for cardiac rehabilitation. Nevertheless, few study focused on the role of high-intensity interval training (HIIT) in cardiac repair. The current study aimed to elucidate the effect of HIIT on cardiac rehabilitation and the involved mechanisms after acute myocardial infarction (MI). METHODS: A total of 65 male rats underwent coronary ligation or sham operation and were randomly assigned to 4 groups: sham (n = 10), sedentary (MI-Sed, n = 12), moderate-intensity continuous training (MI-MCT, n = 12) and HIIT (MI-HIIT, n = 12). One week after MI induction, adaptive training starts follow by formal training. After the experiment, cardiac functions were determined by echocardiography and hemodynamic measurements. Changes in infarct size, collagen accumulation, myofibroblasts, angiogenesis, inflammation level, endothelin-1 (ET-1), and renin-angiotensin-aldosterone system (RAAS) activities were measured. Data were analyzed by one-way ANOVA. RESULTS: After MI, cardiac structure and function were significantly deteriorated. However, post-MI HIIT for 8 weeks had significantly ameliorated left ventricular end-diastolic pressure (LVEDP), LV systolic pressure (LVSP), and maximum peak velocities of relaxation (-dP/dtmax). Moreover, it preserved cardiac functions, reduced infarct size, protected the myocardium structure, increased angiogenesis and decreased the myofibroblasts and collagen accumulation. HIIT for 4 weeks had no effect on LVEDP, -dP/dtmax, infarct size and angiogenesis. Additionally, it induced inflammation response and repressed ET-1 and RAAS activities were found in myocardium and peripheral circulation after HIIT. CONCLUSION: Our results suggested that post-MI HIIT had a positive role in cardiac repair, which might be linked with the induction of inflammation and inhibition of ET-1 and RAAS activities.

Effect of a Weight Loss Program on Biochemical and Immunological Profile, Serum Leptin Levels, and Cardiovascular Parameters in Obese Dogs.

This study aimed to investigate the effects of a weight loss program (WLP) on biochemical and immunological profile, and cardiovascular parameters in a cohort of dogs with naturally occurring obesity. Eleven obese dogs [body condition scoring (BCS), ≥7/9] were enrolled into the study and underwent clinical and cardiovascular examination, and blood testing before (T0) and after 6 months (T1) of WLP. Eleven normal weight (BCS, 4/5) healthy dogs were used as a control (CTR) group. Compared to the CTR group, at T0 obese dogs expressed higher serum leptin concentrations (p < 0.0005) that significantly decreased after weight loss (p < 0.005) but remained higher than the CTR group. Furthermore, obese dogs showed considerably lower levels (p < 0.0005) of regulatory T cell (Treg) compared to the CTR group, but they did not change after weight loss at T1. In obese dogs, tumor necrosis factor (TNF)-α and interleukin (IL)-6 concentrations were substantially reduced at T1 (p < 0.0001 and p < 0.005). Regarding the cardiovascular parameters, only one obese dog was hypertensive at T0, and systolic blood pressure values showed no significant differences at the end of the WLP. The ratio of interventricular septal thickness in diastole to left ventricle internal diameter in diastole (IVSd/LVIDd) was significantly greater in obese dogs at T0 than in the CTR group (p < 0.005). It decreased after weight loss (p < 0.05). In obese dogs, troponin I level significantly reduced with weight loss (p < 0.05), while endothelin-1 level did not differ statistically. The results suggest that the immune dysregulation in the presence of high leptin levels and reduced number of Treg could affect obese dogs as well as humans. Based on our findings, we may speculate that a more complete immune-regulation restore could be obtained by a greater reduction in fat mass and a longer-term WLP. Finally, left ventricular remodeling may occur in some obese dogs. However, in canine species, further studies are needed to investigate the impact of obesity and related WLP on cardiovascular system.

Efficacy of IntraCoronary Erythropoietin Delivery BEfore Reperfusion-Gauging Infarct Size in Patients with Acute ST-segment Elevation Myocardial Infarction (ICEBERG).

Previous clinical studies have shown inconsistent results regarding the effect of erythropoietin in ST-segment elevation myocardial infarction (STEMI). This study investigated whether directed intracoronary infusion of darbepoetin-α into ischemic myocardium before reperfusion would reduce infarct size or post-infarct remodeling in STEMI patients.Eighty STEMI patients received one of the following treatments simultaneously with the first balloon inflation: intracoronary darbepoetin-α 300 µg (n = 40) or saline (n = 40), administered via the over-the-wire balloon system. The primary endpoint was infarct size estimated by serial cardiac enzyme levels after procedure. The secondary endpoints were (1) infarct size and proportion of salvaged myocardium measured with cardiac magnetic resonance (CMR) at baseline; (2) post-infarct remodeling (PIR), defined as an increase in left ventricular end-diastolic volume more than 20% at 4 months compared to the baseline on CMR; and (3) composite cardiovascular endpoints assessed at 4 months.The peak CK-MB [median 270.0 (interquartile range 139.8-356.3) versus 231.5 (131.0-408.5) ng/mL, P = 0.55] and troponin-I [128.5 (63.5-227.8) versus 109.0 (43.8-220.0) ng/mL, P = 0.52) ] did not differ between the darbepoetin-α and control group. Fifty-seven patients completed the baseline and 4-month follow-up CMR. There were no differences in infarct size [30.6 (18.1-49.8) versus 31.5 (22.5-47.3) cm3, P = 0.91), proportion of salvaged myocardium [26.7% (15.9-42.6%) versus 35.8% (22.4-48.8%), P = 0.12) or PIR (8.0% versus 6.7%, P = 0.62) between the two groups. Composite cardiovascular outcomes did not differ between the two groups.In conclusion, administration of intracoronary darbepoetin-α before reperfusion did not reduce infarct size or post-infarct remodeling in STEMI patients.

Epicardial fat amount is associated with the magnitude of left ventricular remodeling in aortic stenosis.

Both genetic and environmental factors interact to control left ventricular (LV) remodeling in the context of aortic stenosis (AS). Epicardial adipose tissue (EAT) is a specific visceral adipose tissue with paracrine properties in close contact with the myocardium. We sought to assess determinants of EAT amount and its association with the magnitude and pattern of LV remodeling in patients suffering from severe AS. Between January 2014 and September 2017, we prospectively explored consecutive patients referred to our Heart Valve Center for SAVR presenting with severe AS and normal left ventricular ejection fraction (> 50%). Comprehensive transthoracic echocardiography (TTE) including assessment of LV remodeling and EAT amount were performed. 202 patients were included. EAT was significantly larger in elderly, diabetic and obese patients. EAT thickness was correlated positively with indexed LV mass in AS (r2 = 0.21; p < 0.0001) as well as severe LV remodeling pattern. Importantly, this observation persisted after adjustment for other factors associated with LV remodeling (ß ± SE = 1.74 ± 0.34; p < 0.0001). Large amounts of EAT are positively and independently associated with more pronounced and severe LV remodeling in severe AS. Further exploration regarding the impact of functional properties of EAT on LV remodeling is required.

Persistently elevated plasma heart-type fatty acid binding protein concentration is related with poor outcome in acute decompensated heart failure patients.

BACKGROUND: The aim of the study was to determine clinical and prognostic role of repeated heart-type fatty acid binding protein (hFABP) measurements in acute decompensated HF (ADHF) patients. METHODS: In seventy-seven ADHF patients (III and IV NYHA class, mean age 70 ±â€¯12.7 years, mean left ventricle ejection fraction [LVEF] 29.73 ±â€¯13.3%) plasma hFABPs concentrations (SunRed Biological Technology) were measured twice - on admission and at discharge (mean time of hospitalization 10.7 ±â€¯4.9 days). Combined end point (CEP), assessed after mean 9.2 ±â€¯7.3 months, was defined as death or the need of HF re-hospitalization. RESULTS: Median hFABP concentration on admission was significantly lower than at discharge. hFABP concentrations on admission significantly correlated with echocardiographic parameters of LV remodeling. Among fifty-six patients (72.7%) who reached CEP, significantly higher admission and discharge hFABP concentrations were found. Patients with plasma discharge hFABP concentrations higher than 7.8 ng/mL were at higher risk of CEP (log-rank test, p = 0.01). Logistic stepwise regression analysis revealed discharge hFABP, LVEF and left ventricle mass index independent and significant predictors of CEP (p < 0.05). CONCLUSIONS: In ADHF patients plasma hFABP admission concentrations are related with LV remodeling. Persistently elevated hFABP concentrations have prognostic value, as may reflect continuous myocardial damage despite effective treatment and clinical improvement.