Left Ventricular Remodeling In Patients Research Articles

Predictive Value of Apoptotic Factor M30 for Negative Left Ventricular Remodeling in Patients Undergoing Primary Percutaneous Coronary Intervention

Background: Left Ventricular Negative Remodeling (LVNR) following Primary Percutaneous Coronary Intervention (PPCI) is an important cause of LV systolic dysfunction due to Irreversible Myocardial Injury (IMI). Both necrosis and apoptosis contribute to IMI and LVNR. We assessed the role of specific apoptotic marker M30 in predicting LVNR in patients of anterior wall ST Elevation Myocardial Infarction (STEMI) undergoing PPCI within 12 hours of symptom onset. Methods: This prospective study was done on 100 consecutive patients of anterior wall STEMI (87 men and 13 women, mean age 52.15±12.08 years) meeting our inclusion and exclusion criteria. Blood sample for M30 was drawn at 24 hours after symptom onset, when it reaches peak level. Transthoracic echo was done in each patient at 24 hours after PPCI and at 6 months. LVNR was defined as ≥20% increase in LV end diastolic volume at 6 months after PPCI. Results: 44 patients (44%) developed LVNR at 6 months post PPCI. Diabetes mellitus (p=0.032), symptom onset to balloon time (p=0.059), CPK-MB (p=0.007) and M30 level (p=0.012) were independent predictors of LVNR. The cutoff value of M30 for predicting LVNR was 81.18u/ml with positive predictive value of 70.4% (AUC 85.3, p<0.001). Conclusion: In patients of anterior wall STEMI undergoing PPCI, the apoptotic marker M30 is useful for early prediction of LVNR. This can assist in better risk stratification of patients after successful PPCI and identify the subgroup of patients who require more intensive medical follow up with antiremodeling drugs to attenuate the development of LVNR.

Effect of Neprilysin Inhibition on Left Ventricular Remodeling in Patients With Asymptomatic Left Ventricular Systolic Dysfunction Late After Myocardial Infarction.

Patients with left ventricular (LV) systolic dysfunction after myocardial infarction are at a high risk of developing heart failure. The addition of neprilysin inhibition to renin angiotensin system inhibition may result in greater attenuation of adverse LV remodeling as a result of increased levels of substrates for neprilysin with vasodilatory, antihypertrophic, antifibrotic, and sympatholytic effects. We performed a prospective, multicenter, randomized, double-blind, active-comparator trial comparing sacubitril/valsartan 97/103 mg twice daily with valsartan 160 mg twice daily in patients ≥3 months after myocardial infarction with a LV ejection fraction ≤40% who were taking a renin angiotensin system inhibitor (equivalent dose of ramipril ≥2.5 mg twice daily) and a β-blocker unless contraindicated or intolerant. Patients in New York Heart Association class ≥II or with signs and symptoms of heart failure were excluded. The primary outcome was change from baseline to 52 weeks in LV end-systolic volume index measured using cardiac magnetic resonance imaging. Secondary outcomes included other magnetic resonance imaging measurements of LV remodeling, change in NT-proBNP (N-terminal pro-B-type natriuretic peptide) and high-sensitivity cardiac troponin I, and a patient global assessment of change questionnaire. From July 2018 to June 2019, we randomized 93 patients with the following characteristics: mean age, 60.7±10.4 years; median time from myocardial infarction, 3.6 years (interquartile range, 1.2-7.2); mean LV ejection fraction, 36.8%±7.1%; and median NT-proBNP, 230 pg/mL (interquartile range, 124-404). Sacubitril/valsartan, compared with valsartan, did not significantly reduce LV end-systolic volume index; adjusted between-group difference, -1.9 mL/m2 (95% CI, -4.9 to 1.0); P=0.19. There were no significant between-group differences in NT-proBNP, high-sensitivity cardiac troponin I, LV end-diastolic volume index, left atrial volume index, LV ejection fraction, LV mass index, or patient global assessment of change. In patients with asymptomatic LV systolic dysfunction late after myocardial infarction, treatment with sacubitril/valsartan did not have a significant reverse remodeling effect compared with valsartan. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03552575.

The impact of renal denervation treatment on left ventricular remodeling in patients with resistant hypertension

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Agency for Research an Development OnBehalf HIPERDIAB Background Increased blood pressure is considered the major determinant for structural alterations of the left ventricle resulting in increased myocardial mass and pathological remodeling. Renal denervation is a novel treatment for hypertensive patients with promising results on blood pressure levels. Purpose Evaluation of impact of renal denervation treatment on indices of left ventricular remodeling in patients with resistant hypertension. Methods 75 patients with resistant hypertension after a 3-week standardized treatment with Losartan 100 mg, Amlodipine 10 mg and Indapamid 1,5 mg were randomly assigned into three equal groups, depending on medication supplemented to previously administered: IM group - Moxonidine, IIB group - Bisoprolol and IIID group – renal artery denervation (RDN). Patients were assessed by echocardiographic exam at baseline and 6 months follow-up. Renal denervation was performed with a Symplicity Spyral catheter. Results Increased at the baseline in all three groups (170,96 ± 11,69 g/m2 in IM versus 156,5 ± 11,08 g/m2 in IIB and 164,94 ± 9,61 g/m2 in IIID groups) left ventricular mass index at 6 months of evaluation noted a statistically authentic reduction in all three groups, the group of patients treated with Moxonidine and RDN having a comparable and superior effect to the group treated with Bisoprolol (159,02 ± 10,34 g/m2 versus 150,5 ± 10,51 g/m2 and 149,15 ± 9,31 g/m2 in IM, IIB and IIID groups, p > 0,05). Simultaniously with the regression of left ventricular myocardial hypertrophy all three treatment regimens induced the improvement of its geometry, renal denervation group demonstrated a superior effect in ameliorating of this parameter (Tab.). Conclusion The data obtained confirmed the benefit of RDN treatment in patients with resistant hypertension in inducing reverse-remodeling of the LV, the beneficial effect being superior to both pharmacotherapeutic regimens. Geometric pattern of the left ventricle Group IM Group IIB Group IIID χ2 p baseline Concentric remodeling 5 (20%) 5 (20%) 4 (16%) 0,71 > 0,05 Concentric hypertrophy 13 (52%) 15 (60%) 14 (56%) Excentric hypertrophy 7 (28%) 5 (20%) 7 (28%) Normal geometry - - - 6 months Concentric remodeling 3 (12%) 7 (28%) 7 (28%) 4,61 < 0,05 Concentric hypertrophy 13 (52%) 13 (52%) 10 (40%) Excentric hypertrophy 8 (32%) 5 (20%) 5 (20%) Normal geometry 1 (4%) - 3 (12%)

His-purkinje system pacing upgrade improve the heart performances in patients suffering from pacing-induced cardiomyopathy with or without permanent atrial fibrillation

IntroductionThe efficacy and safety of his-purkinje system pacing (HPSP) upgrades in patients with pacing-induced cardiomyopathy (PICM) and atrial fibrillation (AF) are still unknown. Methods and resultsPatients with PICM were continuously enrolled from January 2018 to March 2020. All patients were further divided into AF subgroup and sinus rhythm subgroup. Clinical data including echocardiographic examination parameters, electrocardiogram (ECG) measurements, and New York Heart Association (NYHA) classification, were assessed before and after the procedure. The HPSP upgrades, including his bundle pacing (HBP) and left bundle branch pacing (LBBP) were completed in 34 of 36 (94%) patients, Complications including electrode dislodged, perforation, infection or thrombosis were not observed in the perioperative period. During a mean of 11.52 ± 5.40 months of follow-up. The left ventricular ejection fraction (LVEF) increased significantly (33.76 ± 7.54 vs 40.41 ± 9.06, P < 0.001), and the QRS duration decreased (184.22 ± 23.76 ms vs 120.52 ± 16.67 ms, P < 0.001) after the upgrades. LVEDD reversed from 59.29 ± 7.74 mm to 53.91 ± 5.92 mm (P < 0.001), and the NYHA functional class also improved to 2.00 ± 0.76 from 2.55 ± 0.91 at the first follow-up (P < 0.001). The left atrium (LA) size also slightly decreased compared to the initial state (47.44 ± 7.14 mm VS 45.56 ± 7.78, P = 0.010). BNP significantly decreased from a median value of 458.06(256.35–755.10) to 172.31(92.69–552.14) (P = 0.004). The threshold did not increase significantly (1.18 ± 0.76 mv@0.4 ms vs 1.26 ± 0.91mv @ 0.4 ms, P = 0.581). These improvements in patients with AF were similar with those in patients without AF (P > 0.05). ConclusionsHPSP upgrades improved the heart performance and reversed the left ventricular remodeling in patients suffering from PICM with or without AF, and it should be a promising choice in these patients.

Calcium/Calmodulin-Dependent Protein Kinase II Delta Inhibition and Ventricular Remodeling After Myocardial Infarction

After anterior ST-segment elevation myocardial infarction (STEMI), left ventricular (LV) remodeling results in heart failure and death. Calcium/calmodulin-dependent protein kinase II delta (CaMKIId) is a key molecular mediator of adverse LV remodeling. To determine whether NP202, an orally active inhibitor of CaMKIId, prevents LV remodeling in patients after anterior STEMI with early residual LV dysfunction. A randomized, double-blind, placebo-controlled multicenter clinical trial of NP202 vs placebo in patients after primary percutaneous coronary intervention (PCI) for anterior STEMI was performed from November 19, 2015, to August 1, 2018. The study was performed at 32 sites across the US, Australia, and New Zealand. Patients presenting with anterior STEMI who underwent PCI within 12 hours of symptom onset and left ventricular ejection fraction (LVEF) less than 45% on screening echocardiogram 48 hours after primary PCI were included in the study. Baseline cardiovascular magnetic resonance (CMR) imaging was performed within 5 days of the STEMI and before administration of the study drug. Follow-up CMR was performed after 3 months. Data were analyzed from November 19, 2015, to August 1, 2018. Patients were randomly assigned to NP202, 1000 mg, daily for 3 months vs corresponding placebo. The primary end point was change in LV end-systolic volume index (LVESVi) on CMR. Secondary end points were change in LV end-diastolic volume index, change in LVEF, change in infarct size, and change in diastolic function. Safety and tolerability were also assessed. A total of 147 patients (mean [SD] age, 58 [11] years; 129 men [88%]; 130 White patients [88%]) who experienced anterior STEMI treated with primary PCI were randomized to receive NP202 (73 [49.7%]) or placebo (74 [50.3%]). Baseline LVEF was similar between groups. At baseline, patients randomized to NP202 had greater LVESVi (48.2 mL/m2) than that in the placebo group (41.3 mL/m2; P = .03). However, the groups were otherwise well matched. For the primary end point of change in LVESVi from baseline to 3 months, there was no significant difference between the placebo (median [interquartile range] change, -0.60 [-9.28 to 5.99] mL/m2) and NP202 groups (-3.53 [-9.24 to 4.81] mL/m2) (P = .78). There was also no difference in the secondary efficacy end points assessed by CMR. NP202 was well tolerated and demonstrated an acceptable safety profile. Major adverse cardiac and cerebrovascular event rates were similar between groups. Two deaths occurred in each group during the follow-up period. Three months of treatment with NP202 after primary PCI for anterior STEMI with residual LV dysfunction did not improve LV remodeling. The drug was safe and well tolerated. ClinicalTrials.gov Identifier: NCT02557217.

Risk Prediction Model Based on Biomarkers of Remodeling in Patients with Acute Anterior ST-Segment Elevation Myocardial Infarction.

BackgroundThe aim of the present study was to develop a risk prediction model in patients with acute anterior ST-segment elevation myocardial infarction (STEMI).Material/MethodsClinical data from 333 patients with acute anterior STEMI were retrospectively analyzed. Clinical echocardiographic and angiographic data from patients with left ventricular remodeling (LVR) and those without LVR were compared. Factors that influenced risk were identified using multivariate logistic regression analysis. The area under the curve (AUC) of the receiver operating characteristic curve was used to assess the diagnostic performance of the model.ResultsAfter 6-month follow-up, 135 of the patients experienced LVR (LVR group), whereas 198 did not (non-LVR group). Results of multivariate analysis showed that the number of stenosed coronary vessels, left ventricular end-diastolic volume (LVEDV), left ventricular ejection fraction (LVEF), transforming growth factor-beta (TGF-β) at admission, and cardiac troponin I 3 days after admission (3-d cTnI) were all factors predictive of LVR in patients with acute anterior STEMI (all P<0.05). The established prediction model was Y=−20.639+0.711×number of stenosed coronary vessels + 0.137×LVEDV-0.129×LVEF+0.026×TGF-β at admission + 0.162×3-d cTnI. The estimated AUC of this model was 0.978 (95% confidence interval [CI] 0.955–0.991), significantly superior to the single-factor numbers for stenosed coronary vessel of 0.650 (95% CI 0.597–0.702), LVEDV of 0.876 (95% CI 0.836–0.910), LVEF of 0.684 (95% CI 0.631–0.734), TGF-β at admission of 0.696 (95% CI 0.644–0.745), cTnI at admission of 0.913 (95% CI 0.877–0.941), and 3-d cTnI of 0.945 (95% CI 0.914–0.967).ConclusionsThe established model had excellent diagnostic accuracy for predicting LVR in patients with acute anterior STEMI.

Left ventricular blood flow kinetic energy is associated with the six-minute walk test and left ventricular remodelling post valvular intervention in aortic stenosis.

Left ventricular (LV) kinetic energy (KE) assessment by four-dimensional flow cardiovascular magnetic resonance (4D flow CMR) may offer incremental value over routine assessment in aortic stenosis (AS). The main objective of this study is to investigate the LV KE in patients with AS before and after the valve intervention. In addition, this study aimed to investigate if LV KE offers incremental value for its association to the six-minute walk test (6MWT) or LV remodelling post-intervention. We recruited 18 patients with severe AS. All patients underwent transthoracic echocardiography for mean pressure gradient (mPG), CMR including 4D flow and 6MWT. Patients were invited for post-valve intervention follow-up CMR at 3 months and twelve patients returned for follow-up CMR. KE assessment of LV blood flow and the components (direct, delayed, retained and residual) were carried out for all cases. LV KE parameters were normalised to LV end-diastolic volume (LVEDV). For LV blood flow KE assessment, the metrics including time delay (TD) for peak E-wave from base to mid-ventricle (14±48 vs. 2.5±9.75 ms, P=0.04), direct (4.91±5.07 vs. 1.86±1.72 µJ, P=0.01) and delayed (2.46±3.13 vs. 1.38±1.15 µJ, P=0.03) components of LV blood flow demonstrated a significant change between pre- and post-valve intervention. Only LV KEiEDV (r=-0.53, P<0.01), diastolic KEiEDV (r=-0.53, P<0.01) and Ewave KEiEDV (r=-0.38, P=0.04) demonstrated association to the 6MWT. However, Pre-operative LV KEiEDV (r=0.67, P=0.02) demonstrated association to LV remodelling post valve intervention. LV blood flow KE is associated with 6MWT and LV remodelling in patients with AS. LV KE assessment provides incremental value over routine LV function and pressure gradient (PG) assessment in AS.

Greater Left Ventricular Remodeling in Patients with Heartmate 3 Support is Associated with Fewer Heart Failure Readmissions, Gastrointestinal Bleeding and Renal Failure

Purpose While pump thrombosis was markedly reduced with HeartMate 3, other clinical outcomes that impact patient morbidity such as heart failure hospitalization (HFH), gastrointestinal bleeding (GIB) and renal failure remain prevalent. This study aims to explore the association between left ventricular (LV) remodeling and these clinical outcomes. We postulate that a greater reduction in LV end-diastolic diameter (LVEDD) would be associated with greater LV unloading and fewer adverse events. Methods Data on demographics, pre/post-implant LVEDD, and clinical outcomes were retrospectively analyzed in patients with HeartMate 3 implant at our institution from 01/2015-01/2020. The primary composite outcome was HFH, GIB and renal failure requiring dialysis (RRT) at 6 months post-implant. Descriptive statistics are reported. Results 201 patients with HeartMate 3 implant (mean age 58 ± 12 years, 56% destination therapy) had median 9.9 [6, 17] months follow-up. Most were Caucasian (79%) males (77%), with ischemic cardiomyopathy (91%). Arrhythmia (62%), dyslipidemia (55%) and hypertension (53%) were common comorbidities. Overall 23 patients died. The 6-month composite outcome of HFH, GIB and RRT was 35%. A decrease of median 9 [4, 16] mm was noted in post-implant LVEDD from baseline. A reduction in LVEDD of 30% occurred in 138, 47, and 11 patients, respectively. A reduction of Conclusion LVEDD size reduction ≥15% from baseline is associated with improved clinical outcomes. Future studies are warranted to validate these findings, and to understand how to best optimize adequate LV unloading leading to such positive LV remodeling.

Compaired Sacubitril/Valsartan with Benalapril on the Left Ventricular Remordeling of Ami after PPCI: A case-control study

Background: To compare the effect of sacubitril/valsartan with benalapril on left ventricular remodeling in patients with acute myocardial infarction. Materials and Methods: 85 patients with acute ST segment elevation myocardial infarction who were treated with PCI in the Second Affiliated Hospital of Tianjin Medical University. The patients were randomly divided into two groups: the experimental group (sacubitril/valsartan, 25-100mg/d, BID) and the control group (benalapril, 5-10mg, QD). Color Doppler echocardiography was performed after 1 month and 3 months respectively, interventricular septal thickness, septal motion amplitude, left ventricular end diastolic diameter, left ventricular end systolic diameter, posterior wall thickness, posterior wall motion amplitude, LVEF, left ventricular weight, left ventricular weight index, NT Pro-BNP, gender, height, weight, body surface area were collected. In order to evaluate the influencing factors in the process of ventricular remodeling, binary multivariate logistic regression analysis was carried out for the indicators with statistical differences in the conclusions of the above control study. Subgroup analysis was carried out and the samples were divided into four subgroups according to gender,age, initial ejection fraction . Resulst: one month after the treatment of sacubitril/valsartan or benalapril, only the left ventricular end systolic diameter was statistically different between the two groups (P &lt; 0.05), and the other indexes were not statistically different. Three months after treatment with sacubitril/valsartan or benalapril, there were statistical differences in the indexes related to myocardial remodeling between the two groups (P &lt; 0.05). The results of multivariate logistic analysis showed that the index of left ventricular end systolic diameter was statistically significant (or=0.006, 95% CI: 0.733-0.981). Acute myocardial infarction whose LVEF is less than 50%, show sacubitril/valsartan is better than traditional ACEI. Conclusion: sacubitril/valsartan Compared with benalapril is better on left ventricular remodeling in patients with ST segment elevation acute myocardial infarction.

The association of glutathione S-transferase T1 and M1 deletions with myocardial infarction

Glutathione S-transferases (GSTs) are the family of enzymes involved in the second line of defense against oxidative stress (OS). The lack of GSTT1/GSTM1 enzyme quantity or activity, due to the presence of homozygous deletion compromises antioxidative defense resulting in OS. OS is the critical mechanism in the pathophysiology of atherosclerosis, coronary artery disease, and myocardial infarction (MI). The increase in reactive oxygen species together with the process of apoptosis plays a role in left ventricular remodeling (LVR) after MI. The associations of GSTT1 and GSTM1 gene polymorphisms with the risk of MI are inconsistent. The aim was to analyze the association of GSTT1/GSTM1 null genotypes with first MI and LVR 8 months after the MI. The study involved 330 controls and 438 consecutive patients with symptoms and signs of first MI. The subgroup of 150 MI patients was prospectively followed up for 6 months. Evidence of maladaptive LVR was obtained by 2D Doppler echocardiography 3–5 days and 6 months after the MI. A multiplex polymerase chain reaction was used to detect the deletion in GSTT1 and GSTM1 genes. GSTM1 null genotype was significantly and independently associated with first MI (adjusted OR = 1.45 95% CI 1.03–2.03, p = 0.03). Association of double null genotypes with maladaptive LVR in patients 6 months after the first MI was no longer significant after adjustment for factors that differed significantly between patients with and without maladaptive LVR. This study demonstrated the association of GSTM1 null genotypes with the risk of MI in the Serbian population.

Left Ventricular Remodeling Risk Predicted by Two-Dimensional Speckle Tracking Echocardiography in Acute Myocardial Infarction Patients with Midrange or Preserved Ejection Fraction in Western Romania.

BackgroundPatients with acute myocardial infarction (AMI) are at high risk for left ventricular (LV) remodeling and heart failure. We aimed to study whether LV strains (S) and strain rates (SR) could predict cardiac remodeling in patients with AMI having a midrange or preserved LV ejection fraction (EF) following a percutaneous coronary intervention (PCI) within the first 12 hours from the onset of symptoms.Patients and MethodsThis is a case-control observational study including patients admitted for their first AMI, either with ST-segment elevation (STEMI) or without ST elevation (NSTEMI), with an LVEF > 40% after a successful PCI. Echocardiography was repeated after 6 months, and the patients were divided into two groups, according to whether LV remodeling was determined on echocardiography.ResultsOf the 253 AMI patients (mean 66 aged ± 13 years), including 185 males (73%), 61 (24%) presented signs of LV remodeling. In univariate logistic regression analysis, age, male sex, smoking history, hypertension, hypercholesterolemia, Killip class, renal function, peak creatine phosphokinase - MB level, 2- and 3-vessel coronary artery disease (CAD), and several echocardiographic parameters were significantly associated with LV remodeling (P<0.05). In multivariate logistic regression analysis harmed (H) LS and SR, Killip class, 3-vessel CAD, and LV end-diastolic volume were outlined as independent predictors for LV remodeling. Receiver operating characteristic curve analyses showed that HLS and HLSR were the most powerful independent predictors for LV remodeling (P<0.001), with an area under the curve (AUC) of 0.85 (sensitivity 83%; specificity 84%; p <0.001) and 0.77 (sensitivity 93; specificity 61%; p <0.001), respectively. The identified cut-off values for predictor variables were HLS< −11%, and HLSR< −0.65s−1.ConclusionWe concluded that 2D-STE was the best method to evaluate LV remodeling in patients with AMI and midrange or preserved LVEF following myocardial revascularization by a PCI.

Can Moderate Patient Prosthesis Mismatch Be Tolerated in a Selected Group of Patients with Aortic Valve Replacement?

In this study, we aimed to determine the incidence of patient prosthesis mismatch (PPM) and its effects on ejection fraction (EF), gradients, and late survival. 200 patients who underwent isolated mechanical AVR between March 2013 and May 2016 were retrospectively evaluated based on patient records. 200 patients were included in the study. No PPM was detected in 42 (21%) patients, moderate PPM in 122 (61%), and severe PPM in 36 (18%) patients. A significant decrease was found in all groups in terms of mean valve gradients and LVMI (preoperative LVMI compared with postoperative LVMI at the 12th month) (P < .001). A 30% decrease in mean LVMI in the no PPM and moderate PPM groups and a 20% decrease in the severe PPM group were detected at the 6th month. In our postoperative data, we found that EF was preserved, the transvalvular gradient reduced, and LVMI decreased. There was no difference in mortality rates between the control (no PPM) group and the moderate PPM group. Taking into account our patient groups, we can say that no-to-moderate PPM has no major effect on left ventricular remodeling in patients with preserved left ventricular functions.

Association Between Intermittent Hypoxia and Left Ventricular Remodeling in Patients With Obstructive Sleep Apnea-Hypopnea Syndrome.

The present study was undertaken to examine the association between intermittent hypoxia and left ventricular (LV) remodeling and explore which parameter of intermittent hypoxia is most relevant to LV remodeling in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS). Two hundred eighty six patients underwent polysomnographic examination were enrolled. Based on apnea-hypoxia index (AHI), patients were divided into no, mild, moderate and severe OSAHS groups. Between-group differences in LV remodeling and the association between parameters of intermittent hypoxia and LV remodeling was evaluated. Patients with severe OSAHS were more likely to have hypertension, and higher values of LV mass (LVM) and LVM index (LVMI). In univariate regression analysis, male, body mass index (BMI), systolic and diastolic blood pressure (BP), statins, antihypertensive drugs, creatinine, and parameters of intermittent hypoxia (AHI, obstructive apnea index [OAI], lowest oxygen saturation [LSpO2], oxygen desaturation index [ODI], time spent below oxygen saturation of 90% [TS90%], and mean nocturnal oxygen saturation [MSpO2]) were associated with LVMI. After multivariate regression analyses, only male gender, BMI, systolic BP, creatinine, and ODI remained significantly associated with LVMI. Compared to those without LV hypertrophy (LVH), patients with LVH had higher ODI. Compared to patients with normal LV, concentric remodeling and eccentric LVH, those with concentric LVH had higher ODI. In conclusion, intermittent hypoxia was significantly associated with left ventricular remodeling; and among various parameters of intermittent hypoxia, ODI was the most relevant to LV remodeling.

Effects of Nano-Protein Complexes on Apoptosis of Myocardial Infarction Cells Based on Complex Curve Analysis.

Myocardial infarction is one of the common types of coronary heart disease in the clinic. Its morbidity, lethality and disability are high, and it has become a serious threat to human health. At present, it is shown that in the early stage of acute myocardial infarction, myocardial cells are mainly apoptotic, suggesting that effectively blocking myocardial apoptosis in the early stage of myocardial infarction is of great significance for reducing tissue necrosis in the infarcted area. Recent studies have shown that NG nano-protein complexes have a better therapeutic effect on acute myocardial infarction and can inhibit left ventricular remodeling in patients with acute myocardial infarction. However, there are few studies on the effect of NG nano-protein complexes on myocardial cell apoptosis after ischemia. This study used a rat model of acute myocardial infarction to analyze its effect on apoptotic proteins of myocardial cells in rats with acute myocardial infarction in order to provide a certain theoretical basis for its clinical application. In this study, 45 SD rats were randomly divided into a sham operation group, a myocardial infarction group, and a NG nano-protein complex group, with 15 in each group. The sham operation group only underwent thoracotomy, and received normal saline gavage postoperatively; the myocardial infarction group and the NG nano-protein complex group were ligated to the left anterior descending coronary artery of the rat to establish an acute myocardial infarction model, and were performed separately treatment with saline and NG nanoprotein complexes. Finally, we conclude that this nano-protein complex can significantly reduce the expression level of myocardial apoptosis-related proteins in rats with acute myocardial infarction, and is of great significance in inhibiting the apoptosis of acute myocardial infarction cells.

The expression of myeloperoxidase in thrombi is associated with reduced heme oxygenase-1 induction and worse left ventricular remodeling in patients with acute ST-elevation myocardial infarction.

BackgroundMyeloperoxidase (MPO) secreted by neutrophils is the enzyme that kills bacteria and other pathogens. Acute myocardial infarction (AMI) is usually caused by thrombosis in response to vulnerable plaque rupture. Circulating MPO was found to be associated with increased mortality in AMI patients. However, the relationship between MPO in thrombi and the prognosis of AMI patients remains unknown.HypothesisMPO expression in thrombi is associated with the prognosis of patients who underwent primary percutaneous coronary intervention (PCI) after AMI.MethodsThis study included 41 consecutive patients with acute ST‐elevation myocardial infarction, who successfully underwent primary PCI, during which we collected thrombi remaining in the culprit artery using aspiration catheters. These thrombus samples were fixed, and immunohistochemical staining against MPO and heme oxygenase‐1 (HO‐1) was conducted. Enrolled patients were divided into two groups based on the induction of thrombotic MPO, which was quantified using Image J software.MethodsWe observed that increased MPO was associated with lower left ventricular ejection fraction (LVEF) and worse LV remodeling in AMI patients. Instead, patients with decreased thrombotic MPO induction had a considerable improvement in LVEF 1 month after discharge (54.4 ± 2.0% vs. 61.1 ± 2.3%, p < 0.01). In the MPO group, a reduction in the thrombotic HO‐1 level contributed to the development of adverse LV remodeling. Logistic regression showed that MPO was a considerable risk factor for adverse LV remodeling (adjusted OR 3.70, p < 0.05).ConclusionMPO expression in thrombi is associated with reduced LVEF and deteriorated LV remodeling in AMI patients, which may be due to HO‐1 suppression in thrombi.

Left Ventricular Remodeling in Patients with Primary Aldosteronism: A Prospective Cardiac Magnetic Resonance Imaging Study.

ObjectiveThis study used cardiac magnetic resonance imaging (MRI) to compare the characteristics of left ventricular remodeling in patients with primary aldosteronism (PA) with those of patients with essential hypertension (EH) and healthy controls (HCs).Materials and MethodsThis prospective study enrolled 35 patients with PA, in addition to 35 age- and sex-matched patients with EH, and 35 age- and sex-matched HCs, all of whom underwent comprehensive clinical and cardiac MRI examinations. The analysis of variance was used to detect the differences in the characteristics of left ventricular remodeling among the three groups. Univariable and multivariable linear regression analyses were used to determine the relationships between left ventricular remodeling and the physiological variables.ResultsThe left ventricular end-diastolic volume index (EDVi) (mean ± standard deviation [SD]: 85.1 ± 13.0 mL/m2 for PA, 75.9 ± 14.3 mL/m2 for EH, and 77.3 ± 12.8 mL/m2 for HC; p = 0.010), left ventricular end-systolic volume index (ESVi) (mean ± SD: 35.2 ± 9.8 mL/m2 for PA, 30.7 ± 8.1 mL/m2 for EH, and 29.5 ± 7.0 mL/m2 for HC; p = 0.013), left ventricular mass index (mean ± SD: 65.8 ± 16.5 g/m2 for PA, 56.9 ± 12.1 g/m2 for EH, and 44.1 ± 8.9 g/m2 for HC; p < 0.001), and native T1 (mean ± SD: 1224 ± 39 ms for PA, 1201 ± 47 ms for EH, and 1200 ± 44 ms for HC; p = 0.041) values were higher in the PA group compared to the EH and HC groups. Multivariable linear regression demonstrated that log (plasma aldosterone-to-renin ratio) was independently correlated with EDVi and ESVi. Plasma aldosterone was independently correlated with native T1.ConclusionPatients with PA showed a greater degree of ventricular hypertrophy and enlargement, as well as myocardial fibrosis, compared to those with EH. Cardiac MRI T1 mapping can detect left ventricular myocardial fibrosis in patients with PA.

Predictive value of early cardiac mri functional and geometric indexes on adverse left ventricular remodelling in anterior STEMI patients. A report from the CIRCUS study

Post-infarction adverse left ventricular (LV) remodelling is strongly associated with subsequent heart failure events. The conicity index, sphericity index and LV global functional index (LVGFI) are new LV remodelling indexes assessed by cardiac magnetic resonance (CMR). The aim of our study was to assess their predictive value on one-year adverse LV remodelling in patients with anterior myocardial infarction. CMR studies were performed in 129 anterior ST-elevated myocardial infarction (STEMI) patients (58 ± 12 years, 78%men) from the randomized CIRCUS trial (CMR sub-study) treated with the primary percutaneous coronary intervention (PCI) and were followed for the occurrence of major adverse cardiovascular events (MACE) (death or hospitalization for heart failure). The conicity index, sphericity index, LVGFI, infarct size (IS) and microvascular obstruction (MVO) were assessed by CMR performed 5 ± 2 days after coronary reperfusion. Adverse LV remodelling was defined as an increase in LV end-diastolic volume ≥ 15% by transthoracic echocardiography at 1 year. Adverse LV remodeling occurred in 27% of patients in one year. IS and MVO were significantly predictive of adverse LV remodelling (OR = 1.03, CI 95% [1.02–1.05], P < 0.001 and OR = 1.12, CI 95% [1.05–1.22] P < 0.001, respectively). Among the newly tested indexes, only LVGFI was significantly predictive of adverse LV remodelling (OR = 1.10, CI 95% [1.03–1.16], P = 0.001). In multivariate analysis, only IS remained an independent predictor of adverse LV remodeling at 1 year (OR = 1.05, CI 95% [1.02–1.08], P < 0.001). LVGFI and IS were associated with the occurrence of MACE (OR = 1.21; CI 95% [1.08–1.37], P < 0.001 and OR = 1.02; CI 95% [1.00–1.04], P = 0.018 respectively). However, the conicity and sphericity indexes were not associated with MACE ( Fig. 1 ). LVGFI was associated with adverse LV remodelling and MACE at one year after anterior STEMI. However, this relationship and its predictive value in on top of infarct size remain hypothesis-generating at this stage. Further studies are needed to explore the relationship of all these remodelling indices with adverse outcomes in larger populations of MI patients.

R40 Predicting Improved Left Ventricular Remodelling in Patients That Undergo SAVR and TAVR

Left ventricular (LV) remodelling is associated with adverse outcomes in patients with aortic stenosis, and is poorly correlated with echocardiographic measurements. We predict the effects of surgical (SAVR) and transcatheter (TAVR) aortic valve replacement in patients with severe AS on LV remodelling using CMR tissue tracking, and non-contrast T1 mapping.

Early myocardial remodeling after aortic valve replacement

Background: Aortic valve disease leads to eccentric or concentric left ventricular (LV) hypertrophy and changes in the left ventricle function. The goal of aortic valve replacement (AVR) is to alleviate the pressure and volume overload on the left ventricle, allowing myocardial remodeling and regression of LV mass. Objectives: The objective of this study was to assess early LV remodeling in patients with severe aortic valve stenosis and/or moderate-to-severe aortic regurgitation after AVR. Materials and Methods: This prospective study was conducted in the department of cardiovascular and thoracic surgery between January 2015 and February 2016. All patients undergoing AVR exclusively over 1 year were included in the study. Patients were assessed at 1 week, 6 weeks, 3 months, and 6 months after AVR by transthoracic echocardiography. Peak and mean pressure gradients across aortic valve, LV ejection fraction, fractional shortening, LV dimensions, and LV mass along with other parameters were measured in the pre- and postoperative period. Results: A total of 33 patients with different lesions who underwent AVR were evaluated. All but one child (aged 12 years) were adults with a median age of 52 years ± 14.6 years including 21 males and 12 females. The LV mass index (LVMI) regression occurred over time in all cases. Mean LVMI decreased to 149.20 ± 53.7 g/m2 at 1 week and 120.8 ± 45.49 g/m2 at 6 weeks of AVR from its baseline value of 180.8 ± 58.9 g/m2 (P < 0.001). Six patients who were followed up to 1 year had mean LVMI 122.46 ± 50.0 g/m2. Conclusion: Marked reduction in LV mass was discerned after AVR as early as 1 week and further reduction continued up to 6 weeks; however, regression thereafter was not statistically significant.

Rationale and methods of a randomized trial evaluating the effect of neprilysin inhibition on left ventricular remodelling.

AimsIn patients at high risk of heart failure following myocardial infarction (MI) as a result of residual left ventricular systolic dysfunction (LVSD), the angiotensin receptor neprilysin inhibitor sacubitril/valsartan may result in a greater attenuation of adverse left ventricular (LV) remodelling than renin angiotensin aldosterone system inhibition alone, due to increased levels of substrates for neprilysin with vasodilatory, anti‐hypertrophic, anti‐fibrotic, and sympatholytic effects.MethodsWe designed a randomized, double‐blinded, active‐comparator trial to examine the effect of sacubitril/valsartan to the current standard of care in reducing adverse LV remodelling in patients with asymptomatic LVSD following MI. Eligible patients were ≥3 months following MI, had an LV ejection fraction ≤40% as measured by echocardiography, were New York Heart Association functional classification I, tolerant of an angiotensin‐converting enzyme inhibitor or angiotensin receptor blocker at equivalent dose of ramipril 2.5 mg twice daily or greater, and taking a beta‐blocker unless contraindicated or intolerant. Patients were randomized to sacubitril/valsartan (target dose 97/103 mg twice daily) or valsartan (target dose 160 mg twice daily). The primary endpoint will be change in LV end‐systolic volume indexed for body surface area measured using cardiac magnetic resonance imaging over 52 weeks from randomization. Secondary endpoints include other magnetic resonance imaging‐based metrics of LV remodelling, biomarkers associated with LV remodelling and neurohumoral activation, and change in patient well‐being assessed using a patient global assessment questionnaire.ConclusionsThis trial will investigate the effect of neprilysin inhibition on LV remodelling and the neurohumoral actions of sacubitril/valsartan in patients with asymptomatic LVSD following MI.