Novel strategy to reduce sudden-death risk in the healing phase after myocardial infarction.
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ABSTRACT:
SUBMITTER: Donahue JK
PROVIDER: S-EPMC2742989 | biostudies-literature | 2009 Jan
REPOSITORIES: biostudies-literature
Publications
Novel strategy to reduce sudden-death risk in the healing phase after myocardial infarction.
Circulation 20081222 1
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Project description:AimsThis study assessed associations of minimum final extrastimulus coupling interval utilized within electrophysiology study (EPS) after myocardial infarction (MI) and possible site of origin of induced ventricular tachycardia (VT) with long-term occurrence of spontaneous ventricular tachyarrhythmia and long-term survival.Methods and resultsThis prospective study recruited consecutive patients with left ventricular ejection fraction (LVEF) ≤ 40% who underwent EPS days 3-5 after MI between 2004 and 2017. Positive EPS was defined as sustained monomorphic VT cycle length ≥200 ms for ≥10 s or shorter duration if haemodynamic compromise occurred. Each of the four extrastimuli was shortened by 10 ms at a time, until it failed to capture the ventricle (ventricular refractoriness) or induced ventricular tachyarrhythmia. Outcomes included spontaneous ventricular tachyarrhythmia occurrence and all-cause mortality. Shorter coupling interval length of final extrastimulus that induced VT was associated with higher risk of spontaneous ventricular tachyarrhythmia (P < 0.001). Significantly higher rates of spontaneous ventricular tachyarrhythmia (65.2% vs. 23.2%; P < 0.001) were observed for final coupling interval at EPS <200 ms vs. >200 ms. Right bundle branch block (RBBB) morphology of induced VT, with possible site of origin from the left ventricle, was associated with all-cause mortality [hazard ratio (HR) 3.2, P = 0.044] and a composite of spontaneous ventricular tachyarrhythmia recurrence or mortality (HR 1.8, P = 0.043).ConclusionVentricular tachycardia induced with shorter coupling intervals was associated with higher risk of spontaneous ventricular tachyarrhythymia on follow-up, indicating that the final extrastimulus coupling interval at EPS early after MI should be determined by ventricular refractoriness. Induced VT with possible origin from left ventricle was associated with increased risk of spontaneous ventricular tachyarrhythmia recurrence or death.
| S-EPMC10374980 | biostudies-literature
Project description:ObjectiveInvestigate the association of rs17465637 gene MIAF3 (1q41), rs1376251 gene TAS2R50 (12p13), rs4804611 gene ZNF627 (19p13), rs619203 gene ROS1 (6q22), rs1333049 (9p21), rs10757278 (9p21), rs2549513 (16q23), rs499818 (6p24) associated with myocardial infarction available from the international genome-wide studies with sudden cardiac death (SCD) in a case-control study.MethodsA sample of SCD cases (n=285) was formed using the WHO criteria; the control sample (n=421) was selected according to sex and age. DNA was isolated by phenol-chloroform extraction from the myocardial tissue of SCD cases and blood of control cases. The groups were genotyped for the selected SNPs by real-time PCR using TaqMan probes (Applied Biosystems, United States).ResultsNo statistically significant differences in the genotype and allelic frequencies of studied single nucleotide polymorphisms between sudden cardiac death cases and control were detectable in general group. By separating the groups of sex and age differences in the genotype frequencies of rs1333049, rs10757278 and rs499818 are statistical significance. Genotypes CC of rs1333049 and GG of rs10757278 are associated with an increased sudden cardiac death risk in men (p=0.019, OR=1.7, 95% CI 1.1-2.8; p=0.011, OR=1.8, 95% CI 1.2-2.8, respectively). Genotype AG of rs499818 is associated with an increased sudden cardiac death risk in the women over 50 years old (p=0.009, OR=2.4, 95% CI 1.3-4.6).ConclusionPolymorphisms rs1333049 and rs10757278 are associated with SCD in men and rs499818 in the women aged over 50 years.
| S-EPMC5388015 | biostudies-literature
Project description:Background and aimsRisk stratification of sudden cardiac death after myocardial infarction and prevention by defibrillator rely on left ventricular ejection fraction (LVEF). Improved risk stratification across the whole LVEF range is required for decision-making on defibrillator implantation.MethodsThe analysis pooled 20 data sets with 140 204 post-myocardial infarction patients containing information on demographics, medical history, clinical characteristics, biomarkers, electrocardiography, echocardiography, and cardiac magnetic resonance imaging. Separate analyses were performed in patients (i) carrying a primary prevention cardioverter-defibrillator with LVEF ≤ 35% [implantable cardioverter-defibrillator (ICD) patients], (ii) without cardioverter-defibrillator with LVEF ≤ 35% (non-ICD patients ≤ 35%), and (iii) without cardioverter-defibrillator with LVEF > 35% (non-ICD patients >35%). Primary outcome was sudden cardiac death or, in defibrillator carriers, appropriate defibrillator therapy. Using a competing risk framework and systematic internal-external cross-validation, a model using LVEF only, a multivariable flexible parametric survival model, and a multivariable random forest survival model were developed and externally validated. Predictive performance was assessed by random effect meta-analysis.ResultsThere were 1326 primary outcomes in 7543 ICD patients, 1193 in 25 058 non-ICD patients ≤35%, and 1567 in 107 603 non-ICD patients >35% during mean follow-up of 30.0, 46.5, and 57.6 months, respectively. In these three subgroups, LVEF poorly predicted sudden cardiac death (c-statistics between 0.50 and 0.56). Considering additional parameters did not improve calibration and discrimination, and model generalizability was poor.ConclusionsMore accurate risk stratification for sudden cardiac death and identification of low-risk individuals with severely reduced LVEF or of high-risk individuals with preserved LVEF was not feasible, neither using LVEF nor using other predictors.
| S-EPMC11560274 | biostudies-literature
Project description:BackgroundPatients with a left ventricular ejection fraction ≤ 35% are at increased risk of sudden cardiac death (SCD) within the first months after a myocardial infarction (MI). The wearable cardioverter defibrillator (WCD) is an established, safe and effective solution which can protect patients from SCD during the first months after an MI, when the risk of SCD is at its peak. This study aimed to evaluate the cost-effectiveness of WCD combined with guideline-directed medical therapy (GDMT) compared to GDMT alone, after MI in the English National Health Service (NHS).MethodsA multi-state Markov model, with a hypothetical cohort of 1000 patients, was developed to evaluate WCD + GDMT compared with GDMT alone, over a lifetime time horizon. Model input parameters were obtained from the pivotal randomised controlled trial and literature. The outcomes were costs and quality-adjusted life-years (QALYs), discounted at 3.5% annually, with overall results presented as an incremental cost-effectiveness ratio (ICER).ResultsThe cost-effectiveness analysis demonstrated that WCD + GDMT is potentially a cost-effective option with an ICER of £23,024 per QALY gained, which is in the acceptable willingness to pay threshold (WTP) range of £20,000-£30,000 set by the National Institute for Health and Care Excellence (NICE) in England. Results of probabilistic sensitivity analysis (PSA) indicated that WCD + GDMT has 89.3% and 23% probability of being cost-effective at WTP thresholds of £30,000 and £20,000, respectively.ConclusionsImplementation of WCD in patients post-MI is potentially a cost-effective use of resources for the NHS and improves clinical outcomes amongst adherent patients and in circumstances where implantable cardioverter defibrillators are not indicated by the guidelines.
| S-EPMC11865419 | biostudies-literature
Project description:Whole peripheral blood samples collected into Paxgene tubes from 338 adult participants in the Emory University Cardiovascular Biobank, in Midtown Atlanta. The sample is of mixed cardiovascular function diversity, and is part of a survey of the impact of status of cardiovascular disease on gene expression and clinical attributes. Sample annotations only include gender and proofed ethnicity for purposes of IRB, as well as technical features of the study (plate, phase of study, and RNA quality RIN score). 338 individuals in the Emory Cardiovascular Biobank in Midtown Atlanta., 219 men and 119 women. The age of individulas were between 26 and 85 (mean 62). 333 Caucasian (CAU), 4 African American (AFA), 1 South Asian (SAS).
2014-07-01 | E-GEOD-49925 | biostudies-arrayexpress
Project description:IntroductionThe present study evaluated the application of incorporating non-linear J/U-shaped relationships between mean HbA1c and cholesterol levels into risk scores for predicting acute myocardial infarction (AMI) and non-AMI-related sudden cardiac death (SCD) respectively, amongst patients with type 2 diabetes mellitus.MethodsThis was a territory-wide cohort study of patients with type 2 diabetes mellitus above the age 40 and free from prior AMI and SCD, with or without prescriptions of anti-diabetic agents between January 1st, 2009 to December 31st, 2009 at government-funded hospitals and clinics in Hong Kong. Patients recruited were followed up until 31 December 2019 or their date of death. Risk scores were developed for predicting incident AMI and non-AMI-related SCD. The performance of conditional inference survival forest (CISF) model compared to that of random survival forests (RSF) model and multivariate Cox model.ResultsThis study included 261 308 patients (age = 66.0 ± 11.8 years old, male = 47.6%, follow-up duration = 3552 ± 1201 days, diabetes duration = 4.77 ± 2.29 years). Mean HbA1c and low high-density lipoprotein-cholesterol (HDL-C) were significant predictors of AMI on multivariate Cox regression. Mean HbA1c was linearly associated with AMI, whilst HDL-C was inversely associated with AMI. Mean HbA1c and total cholesterol were significant multivariate predictors with a J-shaped relationship with non-AMI-related SCD. The AMI and SCD risk scores had an area under the curve (AUC) of 0.666 (95% confidence interval (CI) = [0.662, 0.669]) and 0.677 (95% CI = [0.673, 0.682]), respectively. CISF significantly improves prediction performance of both outcomes compared to RSF and multivariate Cox models.ConclusionA holistic combination of demographic, clinical and laboratory indices can be used for the risk stratification of patients with type 2 diabetes mellitus for AMI and SCD.
| S-EPMC8279628 | biostudies-literature
Project description:Patients at a high risk for sudden cardiac death (SCD) without previous history of cardiovascular disease remain a challenge to identify. Atherosclerosis and prothrombotic states involve inflammation and non-cardiac tissue damage that may play active roles in SCD development. Therefore, we hypothesized that circulating proteins implicated in inflammation and tissue damage are linked to the future risk of SCD. We conducted a prospective nested case-control study of SCD cases with verified myocardial infarction (N = 224) and matched controls without myocardial infarction (N = 224), aged 60 ± 10 years time and median time to event was 8 years. Protein concentrations (N = 122) were measured using a proximity extension immunoassay. The analyses revealed 14 proteins significantly associated with an increased risk of SCD, from which two remained significant after adjusting for smoking status, systolic blood pressure, BMI, cholesterol, and glucose levels. We identified leukotriene A4 hydrolase (LTA4H, odds ratio 1.80, corrected confidence interval (CIcorr) 1.02-3.17) and hepatocyte growth factor (HGF; odds ratio 1.81, CIcorr 1.06-3.11) as independent risk markers of SCD. Elevated LTA4H may reflect increased systemic and pulmonary neutrophilic inflammatory processes that can contribute to atherosclerotic plaque instability. Increased HGF levels are linked to obesity-related metabolic disturbances that are more prevalent in SCD cases than the controls.
| S-EPMC9499415 | biostudies-literature
Project description:Although numerous therapies are widely applied clinically and stem cells and/or biomaterial based in situ implantations have achieved some effects, few of these have observed robust myocardial regeneration. The beneficial effects on cardiac function and structure are largely acting through paracrine signaling, which preserve the border-zone around the infarction, reduce apoptosis, blunt adverse remodeling, and promote angiogenesis. Ionic extracts from biomaterials have been proven to stimulate paracrine effects and promote cell-cell communications. Here, the paracrine stimulatory function of bioactive ions derived from biomaterials is integrated into the clinical concept of administration and proposed "ion therapy" as a novel strategy for myocardial infarction. In vitro, silicon- enriched ion extracts significantly increase cardiomyocyte viability and promote cell-cell communications, thus stimulating vascular formation via a paracrine effect under glucose/oxygen deprived conditions. In vivo, by intravenous injection, the bioactive silicon ions act as "diplomats" and promote crosstalk in myocardial cells, stimulate angiogenesis, and improve cardiac function post-myocardial infarction.
| S-EPMC6325593 | biostudies-literature
Project description:BackgroundThe majority of sudden cardiac deaths (SCDs) occur in low-risk populations often as the first manifestation of cardiovascular disease (CVD). Biomarkers are screening tools that may identify subclinical cardiovascular disease and those at elevated risk for SCD. We aimed to determine whether the total to high-density lipoprotein cholesterol ratio, high-sensitivity cardiac troponin I, NT-proBNP (N-terminal pro-B-type natriuretic peptide), or high-sensitivity C-reactive protein individually or in combination could identify individuals at higher SCD risk in large, free-living populations with and without cardiovascular disease.MethodsWe performed a nested case-control study within 6 prospective cohort studies using 565 SCD cases matched to 1090 controls (1:2) by age, sex, ethnicity, smoking status, and presence of cardiovascular disease.ResultsThe median study follow-up time until SCD was 11.3 years. When examined as quartiles or continuous variables in conditional logistic regression models, each of the biomarkers was significantly and independently associated with SCD risk after mutually controlling for cardiac risk factors and other biomarkers. The mutually adjusted odds ratios for the top compared with the bottom quartile were 1.90 (95% CI, 1.30-2.76) for total to high-density lipoprotein cholesterol ratio, 2.59 (95% CI, 1.76-3.83) for high-sensitivity cardiac troponin I, 1.65 (95% CI, 1.12-2.44) for NT-proBNP, and 1.65 (95% CI, 1.13-2.41) for high-sensitivity C-reactive protein. A biomarker score that awarded 1 point when the concentration of any of those 4 biomarkers was in the top quartile (score range, 0-4) was strongly associated with SCD, with an adjusted odds ratio of 1.56 (95% CI, 1.37-1.77) per 1-unit increase in the score.ConclusionsWidely available measures of lipids, subclinical myocardial injury, myocardial strain, and vascular inflammation show significant independent associations with SCD risk in apparently low-risk populations. In combination, these measures may have utility to identify individuals at risk for SCD.
| S-EPMC7995996 | biostudies-literature
Project description:Whole peripheral blood samples collected into Paxgene tubes from 338 adult participants in the Emory University Cardiovascular Biobank, in Midtown Atlanta. The sample is of mixed cardiovascular function diversity, and is part of a survey of the impact of status of cardiovascular disease on gene expression and clinical attributes. Sample annotations only include gender and proofed ethnicity for purposes of IRB, as well as technical features of the study (plate, phase of study, and RNA quality RIN score).
2014-07-01 | GSE49925 | GEO