Risk Of Sudden Cardiac Death Research Articles

Beyond convention: non-compacted myocardium, ventricular tachycardia, and systolic dysfunction in dextrocardia patients: a case series

Background: Noncompaction of the left ventricle (LVNC) is linked to a higher risk of sudden cardiac death and stroke. Its prevalence ranges from 0.014% to 1.3% in the general population, rising to 7.5% in patients with dextrocardia. Case summary: A male in his late 70s presented with worsening dyspnea and leg swelling, with dextrocardia and frequent extrasystoles. Imaging revealed right-sided pleural effusion, severely reduced ejection fraction, and ventricular and atrial dilatation. He developed sustained monomorphic VT, was treated with amiodarone, had successful coronary stenting, and received an ICD with no further hospital readmissions or ICD events. A second case involved a male in his late 50s who presented with dyspnea. He had dextrocardia with situs inversus, subsegmental pulmonary embolism, and LVNC. He was treated with enoxaparin, medical therapy, and Holter monitoring, which showed mild arrhythmias. He declined ICD placement but remained event-free during the first year of follow-up. Discussion: LVNC is a rare condition resulting from abnormal myocardial development during embryogenesis, leading to a two-layered myocardial structure. Diagnosis is based on imaging criteria. LVNC is linked to arrhythmias, heart failure, and conduction abnormalities, requiring interventions such as ICD placement, arrhythmia monitoring, and genetic testing. Further research is needed on genetic associations and long-term outcomes in dextrocardia patients.

Circulating microRNA as promising biomarkers in hypertrophic cardiomyopathy: can advanced cardiac magnetic resonance unlock new insights in research?

Hypertrophic cardiomyopathy (HCM) is a genetic cardiac disorder associated with an increased risk of arrhythmias, heart failure, and sudden cardiac death. Current imaging and clinical markers are not fully sufficient in accurate diagnosis and patient risk stratification. Although known cardiac biomarkers in blood are used, they lack specificity for HCM and primarily stratify for death due to heart failure in overt cases. Non-coding RNAs, particularly microRNAs, have emerged as promising biomarkers due to their role in regulating gene expression in both healthy and pathological hearts. Circulating microRNA signatures may dynamically reflect the progression of HCM, offering potential utility in diagnosis and disease monitoring as well as inform biologic pathways for innovative therapeutic strategies. However, studying microRNAs in cardiovascular diseases is still in its early stages and poses many challenges. This review focuses on emerging research perspectives using advanced cardiac magnetic resonance techniques. We presume, that the search for circulating miR signatures associated with specific adverse myocardial features observed on cardiac magnetic resonance imaging - such as fibrosis, disarray, and microvascular disease - represents a promising direction in HCM research.

Wearable Cardioverter Defibrillator as a Treatment in Patients with Heart Failure of Various Aetiologies—A Series of Ten Cases Within the BIA-VEST Registry

Background/Objectives: Sudden cardiac death (SCD) remains a major global health concern and represents one of the most common causes of mortality due to cardiovascular diseases. The wearable cardioverter–defibrillator (WCD) is an innovative, non-invasive medical device designed to provide continuous heart monitoring and immediate defibrillation in patients at risk for SCD. The study aimed to assess the efficacy of WCD usage in patients awaiting decision on therapy with implantable cardioverter–defibrillators (ICDs). Methods: We explored the clinical applications, benefits, and limitations of WCD usage within the BIA-VEST registry in Poland over the years 2021–2023. The study included 10 patients with a mean age of 49.1 ± 12.02 years. Results: All patients demonstrated good tolerance and compliance with the LifeVest WCD, wearing it for an average of 93.1 days, about 22.8 h per day (95.7% of the time). No interventions from LifeVests were recorded, and there were no effective, ineffective, or inadequate discharges. After the first follow-up echocardiography, five patients still required ICDs. Due to improved LVEF and overall condition in six out of ten patients undergoing WCD bridge therapy, ICD implantation was finally waived. Conclusions: The WCD acts as a bridge to therapy, such as ICD implantation or cardiac surgery, and may be particularly beneficial for patients with transient or evolving conditions, such as structural heart diseases and life-threatening ventricular arrhythmias.

Exosome-Derived microRNAs in Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM), characterized by myocardial hypertrophy and an increased risk of sudden cardiac death, poses a significant health burden worldwide. Recent studies have revealed the involvement of exosome-derived microRNAs (miRNAs) in the pathogenesis of HCM, shedding light on novel regulatory mechanisms in cardiac remodeling and dysfunction. This literature review synthesizes current evidence on the role of exosome-derived miRNAs in HCM. It discusses key miRNAs identified from diverse cellular origins, including cardiomyocytes, stem cells, and conduction cells, elucidating their contributions to hypertrophic signaling pathways, fibrosis, and changes in cellular metabolism. Notable miRNAs highly expressed in exosomes such as miR-1, miR-133, and miR-208 are highlighted for their implications in HCM pathophysiology. Moreover, this review explores the diagnostic and therapeutic potential of exosome-derived miRNAs as biomarkers and therapeutic targets in HCM management. The studies summarized in this review demonstrate that exosome-derived miRNAs play a crucial role in orchestrating the molecular events underlying HCM, offering new insights into disease mechanisms and potential therapeutic avenues. Understanding the intricate interplay between exosome-mediated miRNA communication and HCM pathophysiology holds promise for the development of personalized diagnostic tools and targeted therapies to improve patient outcomes in HCM.

Revisiting ICD Therapy for Primary Prevention in Patients With HeartFailure and Reduced Ejection Fraction.

Implantable cardioverter-defibrillators (ICDs) are recommended to reduce the risk of sudden cardiac death (SCD) in patients with heart failure with reduced ejection fraction (HFrEF). The landmark studies leading to the current guideline recommendations preceded the 4 pillars of guideline-directed medical therapies (GDMTs). Therefore, some have questioned the role of ICDs for primary prevention in current clinical practice. In this paper, the authors provide an overview of the current ICD recommendations, including the instrumental clinical trials, the risk of SCD as observed in clinical trials vs real-world scenarios, disparities in ICD use among different patient populations, the impact of contemporary GDMT on outcomes, and ongoing and future trials and methodologies to help identify patients who are at an increased risk of SCD and who may benefit from an ICD. The authors also propose a pragmatic guidance for clinicians when they engage in the shared decision-making discussions for primary ICD implantation.

Two complex coronary artery abnormalities discovered after an acute coronary syndrome : A case report

BackgroundComplex coronary artery abnormalities (CAA) are rare findings with no established guideline for their management in asymptomatic patients. Case summaryWe report the case of a 49-year-old male patient, with no medical history, who was incidentally diagnosed for two congenital complex CAA during for the management of an acute coronary syndrome without ST elevation.The coronary angiogram showed an acute atheromatous occlusion of the right coronary artery (RCA) that was treated by a drug-eluting stent.Transcatheter angiograms as well as the coronary computed tomography (CT) also revealed an ectopic RCA arising from the left cuspid with an inter-arterial course, and a second left anterior descending artery emerging from the RCA with a retro-pulmonary course.The present acute coronary syndrome was not in relation to his congenital disease but with an atheromatous disease. On 48 months of follow-up, the transthoracic echocardiography is normal and the patient remains asymptomatic despite the risk of sudden cardiac death and myocardial infarction. DiscussionThis case shows that CAA can be clinically silent for a long period of time without any correction. It highlights that ischemia in patients with CAA is not always due to the congenital disease. As patients seemed to remain at SCD risk despite surgical correction, not correcting the CAA might remain an alternative in asymptomatic adult patients.

Cardiovascular Diseases in Public Health: Chromosomal Abnormalities in Congenital Heart Disease Causing Sudden Cardiac Death in Children

Chromosomal abnormalities (CAs) are changes in the number or structure of chromosomes, manifested as alterations in the total number of chromosomes or as structural abnormalities involving the loss, duplication, or rearrangement of chromosomal segments. CAs can be inherited or can occur spontaneously, leading to congenital malformations and genetic diseases. CAs associated with cardiovascular diseases cause structural or functional alterations of the heart, affecting the cardiac chambers, valves, coronary arteries, aorta, and cardiac conduction, thus increasing the likelihood of arrhythmias, cardiac arrest, and sudden cardiac death (SCD). An early diagnosis and the adequate management of chromosomal abnormalities associated with cardiovascular diseases are essential to prevent SCD, which is a serious public health problem today. In our review, we analyzed the structural and functional CAs responsible for congenital heart disease (CHD) that increase the risk of SCD and analyzed the prevention strategies to be implemented to reduce SCD.

Genetic QT score as a predictor of sudden cardiac death in participants with sleep-disordered breathing in the UK Biobank.

The goal of this study was to evaluate the association between a polygenic risk score (PRS) for QT prolongation (QTc-PRS), QTc intervals and sudden cardiac death (SCD) in participants enrolled in the UK Biobank with and without sleep-disordered breathing (SDB). The QTc-PRS was calculated using allele copy number and previously reported effect estimates for each single nuclear polymorphism SNP. Competing-risk regression models adjusting for age, sex, BMI, QT prolonging medication, race, and comorbid cardiovascular conditions were used for SCD analyses. 500,584 participants were evaluated (56.5 ±8 years, 54% women, 1.4% diagnosed with sleep apnea). A higher QTc-PRS was independently associated with the increased QTc interval duration (p<0.0001). The mean QTc for the top QTc-PRS quintile was 15 msec longer than the bottom quintile (p<0.001). SDB was found to be an effect modifier in the relationship between QTc-PRS and SCD. The adjusted HR per 5-unit change in QTc-PRS for SCD was 1.64 (95% CI 1.16 - 2.31, p=0.005) among those with SDB and 1.04 (95% CI 0.95 - 1.14, p=0.44) among those without SDB (p for interaction =0.01). Black participants with SDB had significantly elevated adjusted risk of SCD (HR=9.6, 95% CI 1.24 - 74, p=0.03). In the UK Biobank population, the QTc-PRS was associated with SCD among participants with SDB but not among those without SDB, indicating that SDB is a significant modifier of the genetic risk. Black participants with SDB had a particularly high risk of SCD.

Protecting Young Hearts: Sports Clearance for Young Patients at Risk for Sudden Cardiac Death

Protecting Young Hearts: Sports Clearance for Young Patients at Risk for Sudden Cardiac Death

Sodium-glucose cotransporter-2 inhibitors and clinical outcomes in patients with hypertrophic cardiomyopathy and diabetes: A population-based cohort study.

Hypertrophic cardiomyopathy (HCM) is associated with a significant risk of arrhythmia and heart failure (HF), yet treatment options for patients with HCM have remained limited. We aimed to investigate the relationship between sodium-glucose cotransporter-2 inhibitor (SGLT2i) use and clinical outcomes among patients with concurrent HCM and diabetes in real-world settings. Using the Korean National Health Insurance Service database, we identified patients with a confirmed diagnosis of HCM and prescriptions for antidiabetic drugs from 2018 to 2022. After propensity matching, we compared 2063 patients who received SGLT2i with 2063 patients who did not for clinical outcomes. The primary outcome was a composite of all-cause death and HF hospitalization. Secondary outcomes included individual outcomes of all-cause death, HF hospitalization, sudden cardiac death, and ischaemic stroke. During a median follow-up period of 3.1 years, patients with HCM on SGLT2i had a significantly lower risk of the primary outcome [hazard ratio (HR) 0.76, 95% confidence interval (CI) 0.67-0.86]. Specifically, SGLT2i use was associated with reduced all-cause mortality (HR 0.56, 95% CI 0.46-0.68) and fewer HF hospitalizations (HR 0.82, 95% CI 0.72-0.94). Additionally, SGLT2i use was linked to a decreased risk of sudden cardiac death (HR 0.50, 95% CI 0.33-0.77) and ischaemic stroke (HR 0.74, 95% CI 0.62-0.88). Subgroup analyses by age, sex, and atrial fibrillation did not reveal any significant interactions. The use of SGLT2i was associated with a decreased risk of adverse clinical outcomes among patients with HCM with concurrent diabetes on antidiabetic drugs. This population-based cohort study examined the association between sodium-glucose cotransporter-2 inhibitors (SGLT2is) and clinical outcomes in patients with hypertrophic cardiomyopathy (HCM) and diabetes. Patients with HCM and diabetes who used SGLT2i had a significantly lower risk of all-cause death and heart failure hospitalization compared with those who did not use SGLT2i.These associations were consistent across various subgroups, including sex, age, atrial fibrillation, and income levels.

Sudden cardiac death after acute myocarditis with arrhythmic presentation: hunting for risk predictors − a systematic review and meta-analysis

BackgroundVentricular arrhythmias (VAs) frequently occur in the acute phase of myocarditis. Possible arrhythmic recurrences and the risk of sudden cardiac death (SCD) in this setting are reasons for concern, and...

Electrocardiographic Characteristics of Brugada Syndrome Type I During Exercise Stress Test.

Brugada syndrome (BS) is a genetic channelopathy characterized by an increased risk of sudden cardiac death (SCD) in the absence of structural heart disease. Prognostic stratification is necessary to determine which patients are candidates for implantable cardioverter defibrillator (ICD). The present study aims to evaluate EKG changes during exercise stress tests in patients with BS and to identify any poor prognosis variables. This was an observational, case-control study. Three comparison groups were created: patients with Type 1 BS with or without prior arrhythmic events (BE and BNoE subgroups) and age- and sex-matched healthy individuals. Patients underwent EST and electrocardiographic variables were analyzed. The study recruited 36 patients with type 1 BS, 12 with prior Event (BE) and 24 without (BNoE). Patients in the BE group, in all postexercise recordings, had lower heart rates, notably in the first minute. A significant difference was also observed in the HR drop in the recovery phase, with a greater drop in relation to maximum HR in the first minute in the group of patients who had events. BS patients with prior events had a lower capacity to increase heart rate at peak effort and a greater proportional drop in the recovery phase. No relationship was observed between the occurrence of arrhythmic events and ST-segment elevation during the exercise test.

Anabolic androgen steroids cardiovascular impact. Literature review

Introduction and Purpose: The use of anabolic steroids is widespread. They can be administered either therapeutically or by individuals looking to enhance their athletic performance. This review aims to summarize the scientific understanding regarding the link between the use of AASs and the incidence of cardiovascular complications. Materials and methods The literature available in PubMed and Google Scholar databases was reviewed using the keywords. Description of the state of knowledge: A lot of studies suggest that AASs can be harmful to the cardiovascular system. It has a wide range of long-term and often irreversible consequences. AASs cause myocardial hypertrophy which results in systolic and diastolic disfunction. They disrupt lipid metabolism, act as vasoconstrictors, and promote the calcification of blood vessel walls, thereby increasing the risk of heart attack and stroke. By promoting blood clotting, they increase the incidence of pulmonary embolism, deep vein thrombosis, and cerebral venous sinus thrombosis. The effect on the occurrence of hypertension is not definitively proven. However, a very dangerous consequence of using anabolic steroids is the increased risk of life-threatening arrhythmias -especially ventricular arrhythmias- which can lead to sudden cardiac death. Conclusion: The use of anabolic steroids increases the risk of arrhythmias, heart attacks, and thromboembolic complications, ultimately leading to a higher risk of sudden cardiac death. However, the cause-and-effect relationship is not always clearly captured, and further research is necessary to draw appropriate conclusions.

Are the cardiovascular benefits and potential risks of physical activity and exercise dependent on race, ethnicity or sex?

Physical activity (PA) is established as a cornerstone of cardiovascular health, however, disparities in participation exist across sociocultural groups, which in turn impacts cardiovascular outcomes. Evidence suggests that while the positive cardiovascular effects of exercise are consistent across populations, notable differences in the magnitude of these benefits exist for racial and ethnic minorities and female sex. Females derive greater protection from PA compared to males, with reduced rates of sudden cardiac death (SCD). This review examines the complex interplay of race/ethnicity and sex on the cardiovascular benefits associated with PA and exercise, cardiovascular adaptations to exercise, and risks of SCD and "excessive" volume of exercise. Understanding these factors is crucial for developing targeted interventions to promote cardiovascular health and offset disparities.

Abstract 4119472: Predictors of Sudden Cardiac Death in Patients with Atrial Fibrillation and No Apparent Risk Factor of Sudden Cardiac Death

Background: Atrial fibrillation (AF) is associated with sudden cardiac death (SCD). It is known that AF is associated with multiple traditional risk factors of SCD, such as coronary artery disease (CAD), history of myocardial infarction (MI), left ventricular hypertrophy (LVH) and low left ventricular ejection fraction (LVEF). However, AF per se could predispose SCD not mediated by these cardiovascular risk factors, and predictors of SCD in AF patients without these apparent SCD risk factors are unknown. Methods: Using the NTUH iMED database, AF patients without apparent SCD risk factors were longitudinal followed up from Jan. 2010 to Dec. 2021. The primary outcome was implantation of implantable cardioverter defibrillator (ICD) due to SCD. Cox regression was used to identify the predictors of SCD. Results: A total of 11250 AF patients without cardiovascular SCD risk factors and LVEF ≥55 % were longitudinally followed up. We first found CHA2DS2-VASc score did not predict SCD event. We found male gender (hazard ratio [HR ] 1.71 [1.05-2.78 ], p =0.032), hyperthyroidism (HR 3.50 [1.40-8.77 ], p=0.007）and paroxysmal AF (PAF)(HR 2.86 [1.63-5.04 ], p&lt;0.001）were associated with higher SCD risks. We created a AFSCD score using these parameters. We found SCD risk incrementally increased with increasing AFSCD score (p &lt;0.001 for trend). Patients with highest score (5 points) had more than 3-fold SCD risk compared with those with 0-point score (1.18 % person-year vs 0.36 %, p&lt;0.001). The C statistic of AFSCD score was significantly higher than CHA2DS2-VASc score (0.64 [0.57-0.70] vs 0.40 [0.33-0.48], p &lt;0.01). Conclusions: Male gender, hyperthyroid AF and PAF were predictors of incident SCD in AF patients and AFSCD scoring scheme based on these risk factors could possibly be implemented in clinical practice.

Abstract 4134619: A Novel Missense Mutation in TNNT2 Gene in a Lebanese Pedigree With Ebstein Anomaly And Wolf-Parkinson-White Syndrome: A Case Report

Background: Ebstein anomaly (EA) is a rare congenital heart defect occurring in 1.2 to 5 in 100,000 live births, characterized by a downward displacement of the tricuspid valve, thin-walled right ventricle, and tricuspid valve regurgitation. It can present variably from asymptomatic cases to severe symptoms like arrhythmias and right-sided heart failure. EA is often associated with other anomalies such as interatrial communication and mitral valve prolapse. The condition can lead to accessory atrioventricular pathways, frequently resulting in Wolff-Parkinson-White syndrome (WPW), which involves abnormal heart electrical activity and increases the risk of sudden cardiac death. While the genetic basis of EA is not fully understood, it appears to involve multiple genes like FLNA and NKX2-5, MYH6, MYH7 suggesting a complex polygenic inheritance pattern. TNNT2 is known to be associated with Cardiomyopathy but has not been previously associated with EA and WPW. Case: In this report, we present findings from a lebanese family with EA, comprising 2 affected individuals. Whole exome sequencing in the affected individuals identified a pathogenic variant in the TNNT2 gene at coding strain position 260 (a missense mutation: C to T), resulting in the substitution of Proline with Leucine at position 87 in affected individuals (Figure 1). No variants were detected in any other candidate gene examined. Individuals I:1 and II:2 were found to be normal, with no EA findings on echocardiography. Methods: Whole exome sequencing in the patients involved collecting blood samples after obtaining consent. These samples were sent to Centogene lab, where genomic DNA is enzymatically fragmented. The regions of interest are then enriched using DNA capture probes, facilitating detailed genetic analysis. Results: The whole exome sequencing identified a heterozygous missense mutation in both the father and his daughter. This nonsynonymous variant is located on chromosome 1 (GRCh37) in the TNNT2 gene region. The specific variant, NM_001276345.1:c.260C&gt;T p.(Pro87Leu), was found in both individuals. Conclusion: In conclusion, the genetic basis of EA is rather complex and remains poorly understood. It is established that mutations in the TNNT2 gene are linked to several cardiomyopathies, none of them overlap with the described phenotype of our patients. In this report, we therefore confirm the potential role of TNNT2 gene mutation in the genetic basis of familial EA with WPW.

Abstract 4138514: From Treatment to Trigger: A Case of Atomoxetine-Induced Brugada Pattern

Introduction: Brugada syndrome is an inherited cardiac disorder characterized by specific ECG patterns, notably the coved-type ST-segment elevation in the right precordial leads (V1-V3), leading to an increased risk of sudden cardiac death. This condition often stems from mutations in the SCN5A gene, which impair cardiac sodium channel function. The manifestation of Brugada Pattern, showing typical ECG findings without clinical criteria like sudden cardiac arrest or syncope, is significant. We highlight a case where atomoxetine, a selective norepinephrine reuptake inhibitor used for ADHD, unveiled a type 1 Brugada pattern. Case Presentation: A 26-year-old male with a history of ADHD on atomoxetine only presented to the emergency department with sudden substernal chest pain radiating to his left arm. His initial ECG showed right bundle branch block and type 1 Brugada pattern (Figure.1). Despite normal troponin levels and a negative coronary CT angiography, the patient's ECG abnormalities raised concerns. With no personal or familial history of arrhythmia or SCD and no other medications, atomoxetine was suspected as the trigger. Upon discontinuation, the patient's ECG type 1 Brugada pattern resolved (Figure. 2), and he remained asymptomatic with a normal Holter monitor at a 1-month follow-up. Discussion: Brugada syndrome is marked by dynamic ECG abnormalities, which can surface due to triggers like fever, certain medications, and electrolyte imbalances. Atomoxetine, an ADHD treatment and selective norepinephrine reuptake inhibitor, affects the human cardiac sodium channel (hNav1.5), encoded by the SCN5A gene. This interaction can disrupt heart action potentials, leading to conditions like long QT syndrome and Brugada pattern, by slowing cardiomyocyte depolarization and conduction. Its effect on hNav1.5 resembles that of antidepressants like Fluoxetine, increasing the risk of Brugada pattern. In our case, a patient's type 1 Brugada pattern, with no underlying heart disease or family history, pointed to atomoxetine as the cause. Discontinuing the drug resolved the ECG abnormalities. Conclusion: This case emphasizes the importance of assessing cardiovascular risk before prescribing atomoxetine, especially in individuals at risk for cardiac sodium channel dysfunctions. Immediate intervention and monitoring are critical to prevent severe arrhythmias.

Abstract 4136788: Lipoprotein(a) Levels and the Risk of Ventricular Arrhythmia: Insights from a Comprehensive Retrospective Cohort Study

Background: Sustained ventricular arrhythmias (VAs) are associated with an elevated risk of sudden cardiac death (SCD). Lipoprotein(a) (Lp[a]) is a recognized risk factor for atherosclerotic cardiovascular disease (ASCVD), which in turn associated with increased risk of VAs. However, whether Lp(a) is linked with VAs independent of ASCVD remains unknown. Objective: To examine the association of Lp(a) with VAs in a population-based, retrospective cohort study utilizing data from the TriNetX Research Network. Methods: We conducted a retrospective analysis of the data from 89 healthcare organizations within the TriNetX Research Network. Patients over 18 years old with available serum Lp(a) measurement were included. Participants were divided into two cohorts based on their Lp(a) levels: cohort 1 (Lp(a) ≤75 nmol/L), and cohort 2 (Lp(a) ≥76 nmol/L). Follow-up time to VA occurrence was calculated from the time of Lp(a) level measurement within each cohort. The composite endpoint was the incidence of VAs to include ventricular tachycardia, ventricular fibrillation, ventricular flutter, or cardiac arrest due to underlying cardiac conditions. We compared the two cohorts using Kaplan-Meier survival analysis along with cox proportional hazard regression analysis after propensity score matching. Results: 50,752 patients were included in cohort 1 and 24,474 in cohort 2. After propensity score matching, both cohorts had 23,668 patients. In cohort 1, 307 patients experienced VAs, compared to 303 in cohort 2 (Table 1). The mean age was 53.3 ± 15.7 years, with 53.35% of participants being female, 10.75% being Black, and 69.89% being White. The Kaplan-Meier survival analysis showed a higher survival probability at the end of the study period for the Lp(a) ≤75 compared to the Lp(a) ≥76 cohort (95.11% vs 85.35%, p=0.002). The hazard ratio (HR) for VA was 0.768 (95% CI: 0.652-0.904, p = 0.002), indicating that lower Lp(a) levels are associated with reduced VA risk. Conclusion: This study shows that increased Lp(a) levels are independently associated with a higher incidence of VA. Future research should focus on the mechanisms underlying the relationship between Lp(a) levels and VA, and whether Lp(a) reduction can reduce the risk of VA and other cardiovascular outcomes.

Abstract 4134896: Clinical and Echocardiographic Markers for the Prediction of Incident Atrial Arrhythmias in Hypertrophic Cardiomyopathy

Introduction: Hypertrophic cardiomyopathy (HCM), in addition to increasing the risk for heart failure and sudden cardiac death, augments the risk for atrial fibrillation (AF) and atrial flutter (AFL). We aimed to identify clinical and echocardiographic risk factors that are predictive of incident AF/AFL in HCM patients. Methods: This retrospective study included 99 HCM patients from University of Chicago without prior AF/AFL, followed for a median of 3.2 years (IQR: 11.5 months-6.9 years). Clinical data were obtained via chart review; echocardiographic findings were obtained using AI software (Us2.ai) with measurements audited by a level III echocardiography reader. Statistical testing included Chi-square/Fisher’s exact (categorical variables) and T-test/Wilcoxon rank sum (continuous variables). Univariate and multivariate Cox regressions assessed predictive value of risk factors for AF/AFL. Results: 18 HCM patients (18%) developed AF/AFL ( Table 1 ). On univariate analysis, older age (HR 1.06, 95%CI 1.02-1.11, p=0.002), hypertension (HR 8.32, 95%CI 1.10-63.20, p=0.04), diabetes (HR 3.90, 95%CI 1.51-10.03, p=0.005), prior stroke (CVA, HR 3.81, 95%CI 1.34-10.86, p=0.012), and NYHA class II-IV (HR 8.48, 95%CI 2.97-24.21, p&lt;0.001) predicted AF/AFL. E/A (p=0.04), E/e’ (p=0.028), MV-A (p=0.022), and LVEF (p=0.02) were also significant predictors ( Figure 1 ). LVEF (HR 0.92, 95%CI 0.87-0.98, p=0.013) remained a significant predictor of AF/AFL on multivariate analysis controlling for age, hypertension, diabetes, CAD, CVA, and NYHA class. Conclusions: Traditional risk factors including age, hypertension, diabetes, CVA, and NYHA class are significant predictors of incident AF/AFL in HCM patients, highlighting the need for comprehensive risk factor evaluation. Even after adjustment for these clinical markers, LVEF independently predicts new AF/AFL in HCM patients, underscoring the importance of routine echocardiographic assessment for risk stratification in this patient population.

Abstract 4115652: Effect of the sodium-glucose co-transporter 2 inhibitor, Dapagliflozin, on ventricular repolarization electrocardiographic parameters: DAPA-ECG study

Background: In patients with type 2 diabetes (T2D), hyperglycemia and glycemic variability lead to prolongation and greater heterogeneity of ventricular repolarization, manifested on the electrocardiogram through an increase in QT, QTc, TpeakTend (TpTe) intervals and the TpTe/QT ratio, increasing the risk of potentially malignant arrhythmias. Dapagliflozin has demonstrated efficacy in reducing cardiovascular events in T2D patients and in the risk of serious ventricular arrhythmias and sudden cardiac death. However, the exact mechanisms by which dapagliflozin confers this protection have not yet been fully elucidated. Goals/Aims: The main objective of the study was to evaluate the impact of dapagliflozin on the TpTe interval of patients with T2D, and secondarily, it examined its impact on various electrocardiographic parameters such as the QT and QTc intervals, the TpTf/QT ratio, QT dispersion, J-T peak interval, QRS-T angle and heart rate. Methods: This randomized, prospective, multicenter and open-label study involved 174 patients with T2D, divided into two groups: one treated with dapagliflozin and the other with optimized medical therapy without iSGLT2. Clinical, electrocardiographic, laboratory and echocardiographic evaluations were carried out at the beginning and after three months. The statistical analysis included means, standard deviations, quartiles, and frequencies, with 95% confidence intervals, using Chi-square (or Fisher) and t-test (or Mann-Whitney) for initial differences, and a linear mixed-effects model to evaluate the results, adopting a significance level of 0.05. Results: The TpTe interval was significantly reduced in the dapagliflozin group from 76.87 ± 12.47 to 67.80 ± 10.34 (p&lt;0.001), and the QTc interval reduced from 424.07 ± 30.76 to 411.26 ± 25.31 (p=0.022). The TpTe/QT ratio in the dapagliflozin group was shortened from 0.20 ± 0.03 to 0.18 ± 0.02 (p&lt;0.001). Both groups showed reductions in mean blood glucose and HbA1c, with a greater decrease observed in the control group. No significant changes were recorded in other variables analyzed. Conclusion: In patients with T2D, dapagliflozin significantly reduced the duration of the TpTe and QTc intervals, in addition to the TpTe/QT ratio. These findings indicate a decrease in ventricular electrical remodeling with a potential cardioprotective effect of dapagliflozin, which would partly explain its benefits in reducing potentially malignant ventricular arrhythmias and sudden cardiac death.