Browsing by Subject "Sudden cardiac death"
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Item Ankle-Brachial Index and Risk of Sudden Cardiac Death in the Community: The ARIC Study(American Heart Association, 2024) Suzuki, Takeki; Zhu, Xiaoqian; Adabag, Selcuk; Matsushita, Kunihiro; Butler, Kenneth R.; Griswold, Michael E.; Alonso, Alvaro; Rosamond, Wayne; Sotoodehnia, Nona; Mosley, Thomas H.; Medicine, School of MedicineBackground: Sudden cardiac death (SCD) is a significant global public health problem accounting for 15% to 20% of all deaths. A great majority of SCD is associated with coronary heart disease, which may first be detected at autopsy. The ankle-brachial index (ABI) is a simple, noninvasive measure of subclinical atherosclerosis. The purpose of this study was to examine the relationship between ABI and SCD in a middle-aged biracial general population. Methods and results: Participants of the ARIC (Atherosclerosis Risk in Communities) study with an ABI measurement between 1987 and 1989 were included. ABI was categorized as low (≤0.90), borderline (0.90-1.00), normal (1.00-1.40), and noncompressible (>1.40). SCD was defined as a sudden pulseless condition presumed to be caused by a ventricular tachyarrhythmia in a previously stable individual and was adjudicated by a committee of cardiac electrophysiologists, cardiologists, and internists. Cox proportional hazards models were used to evaluate the associations between baseline ABI and incident SCD. Of the 15 081 participants followed for a median of 23.5 years, 556 (3.7%) developed SCD (1.96 cases per 1000 person-years). Low and borderline ABIs were associated with an increased risk of SCD (demographically adjusted hazard ratios [ HRs ], 2.27 [ 95% CI, 1.64-3.14 ] and 1.52 [ 95% CI, 1.17-1.96 ], respectively) compared with normal ABI. The association between low ABI and SCD remained significant after adjustment for traditional cardiovascular risk factors (HR, 1.63 [ 95% CI, 1.15-2.32 ]). Conclusions: Low ABI is independently associated with an increased risk of SCD in a middle-aged biracial general population. ABI could be incorporated into future SCD risk prediction models.Item APOL1 G3 variant is associated with cardiovascular mortality and sudden cardiac death in patients receiving maintenance hemodialysis of European Ancestry(Karger, 2022) Schwantes-An, Tae-Hwi; Robinson-Cohen, Cassianne; Liu, Sai; Zheng, Neil; Stedman, Margaret; Wetherill, Leah; Edenberg, Howard J.; Vatta, Matteo; Foroud, Tatiana M.; Chertow, Glenn M.; Moe, Sharon M.; Medical and Molecular Genetics, School of MedicineIntroduction: The G1 and G2 variants in the APOL1 gene convey high risk for the progression of chronic kidney disease in African Americans. The G3 variant in APOL1 is more common in patients of European ancestry (EA); outcomes associated with this variant have not been explored previously in EA patients receiving dialysis. Methods: DNA was collected from approximately half of the patients enrolled in the Evaluation of Cinacalcet HCl Therapy to Lower Cardiovascular Events (EVOLVE) trial and genotyped for the G3 variants. We utilized an additive genetic model to test associations of G3 with the EVOLVE adjudicated endpoints of all-cause mortality, cardiovascular mortality, sudden cardiac death (SCD), and heart failure. EA and African ancestry samples were analyzed separately. Validation was done in the Vanderbilt BioVU using ICD codes for cardiovascular events that parallel the adjudicated endpoints in EVOLVE. Results: In EVOLVE, G3 in EA patients was associated with the adjudicated endpoints of cardiovascular mortality and SCD. In a validation cohort from the Vanderbilt BioVU, cardiovascular events and cardiovascular mortality defined by ICD codes showed similar associations in EA participants who had been on dialysis for 2 to <5 years. Discussion/conclusions: G3 in APOL1 variant was associated with cardiovascular events and cardiovascular mortality in the EA patients receiving dialysis. This suggests that variations in the APOL1 gene that differ in populations of different ancestry may contribute to cardiovascular disease.Item The Association between Nocturnal Cardiac Arrhythmias and Sleep-Disordered Breathing: The DREAM Study(American Academy of Sleep Medicine, 2016-06-15) Selim, Bernardo J.; Koo, Brian B.; Qin, Li; Jeon, Sangchoon; Won, Christine; Redeker, Nancy S.; Lampert, Rachel J.; Concato, John P.; Bravata, Dawn M.; Ferguson, Jared; Strohl, Kingman; Bennett, Adam; Zinchuk, Andrey; Yaggi, Henry K.; Department of Medicine, IU School of MedicineSTUDY OBJECTIVES: To determine whether sleep-disordered breathing (SDB) is associated with cardiac arrhythmia in a clinic-based population with multiple cardiovascular comorbidities and severe SDB. METHODS: This was a cross-sectional analysis of 697 veterans who underwent polysomnography for suspected SDB. SDB was categorized according to the apnea-hypopnea index (AHI): none (AHI < 5), mild (5 ≥ AHI < 15), and moderate-severe (AHI ≥ 15). Nocturnal cardiac arrhythmias consisted of: (1) complex ventricular ectopy, (CVE: non-sustained ventricular tachycardia, bigeminy, trigeminy, or quadrigeminy), (2) combined supraventricular tachycardia, (CST: atrial fibrillation or supraventricular tachycardia), (3) intraventricular conduction delay (ICD), (4) tachyarrhythmias (ventricular and supraventricular), and (5) any cardiac arrhythmia. Unadjusted, adjusted logistic regression, and Cochran-Armitage testing examined the association between SDB and cardiac arrhythmias. Linear regression models explored the association between hypoxia, arousals, and cardiac arrhythmias. RESULTS: Compared to those without SDB, patients with moderate-severe SDB had almost three-fold unadjusted odds of any cardiac arrhythmia (2.94; CI 95%, 2.01-4.30; p < 0.0001), two-fold odds of tachyarrhythmias (2.16; CI 95%,1.47-3.18; p = 0.0011), two-fold odds of CVE (2.01; 1.36-2.96; p = 0.003), and two-fold odds of ICD (2.50; 1.58-3.95; p = 0.001). A linear trend was identified between SDB severity and all cardiac arrhythmia subtypes (p value linear trend < 0.0001). After adjusting for age, BMI, gender, and cardiovascular diseases, moderate-severe SDB patients had twice the odds of having nocturnal cardiac arrhythmias (2.24; 1.48-3.39; p = 0.004). Frequency of obstructive respiratory events and hypoxia were strong predictors of arrhythmia risk. CONCLUSIONS: SDB is independently associated with nocturnal cardiac arrhythmias. Increasing severity of SDB was associated with an increasing risk for any cardiac arrhythmia.Item Fatty acids and other risk factors for sudden cardiac death in patients starting hemodialysis(Karger, 2013) Friedman, Allon N.; Yu, Zhangsheng; Denski, Cheryl; Tamez, Hector; Wenger, Julia; Thadhani, Ravi; Li, Yong; Watkins, Bruce; Medicine, School of MedicineBackground: Little is known about risk factors for sudden cardiac death in hemodialysis patients during the high-risk first year of dialysis. We therefore undertook to identify such risk factors in a nationally representative cohort and were able to include baseline levels of blood fatty acids, some of which influence arrhythmogenicity and sudden cardiac death risk. Design: The study cohort included 100 patients who died of sudden cardiac death during the first year of hemodialysis and 300 frequency-matched controls. Using the elastic net statistical method, numerous demographic and clinical characteristics were included with baseline total serum levels for 11 major fatty acids (model 1) and with serum phospholipid fractions of these same fatty acids (model 2). Final models included only covariates that had a non-zero coefficient. Results: In model 1, serum albumin [odds ratio (95% CI): 0.55 (0.33-0.93); p = 0.03] and total serum long-chain n-3 docosapentaenoic acid [0.70 (0.51-0.97); p = 0.03] were inversely associated with the odds of sudden cardiac death, while the total serum saturated fatty acid level had a direct association [1.01 (1.00-1.02); p = 0.03]. In model 2, serum albumin and docosapentaenoic acid remained inversely associated with sudden cardiac death in a similar manner as in model 1. Pulse pressure also had an inverse association [0.96 (0.93-1.00); p < 0.05]. Conclusions: Several factors, including blood content of docosapentaenoic acid and saturated fatty acids, were associated with the odds of sudden cardiac death during year one of hemodialysis. These results raise the possibility that dietary modification may reduce sudden death risk.Item Interassociation Consensus Statement on Cardiovascular Care of College Student-Athletes(American College of Cardiology Foundation, 2016-04) Hainline, Brian; Drezner, Jonathan; Baggish, Aaron; Harmon, Kimberly G.; Emery, Michael S.; Myerburg, Robert J.; Sanchez, Eduardo; Molossi, Silvana; Parsons, John T.; Thompson, Paul D.; Kinesiology, School of Physical Education and Tourism ManagementCardiovascular evaluation and care of college student-athletes is gaining increasing attention from both the public and medical communities. Emerging strategies include screening of the general athlete population, recommendations of permissible levels of participation by athletes with identified cardiovascular conditions, and preparation for responding to unanticipated cardiac events in athletic venues. The primary focus has been sudden cardiac death and the utility of screening with or without advanced cardiac screening. The National Collegiate Athletic Association convened a multidisciplinary task force to address cardiovascular concerns in collegiate student-athletes and to develop consensus for an interassociation statement. This document summarizes the task force deliberations and follow-up discussions, and includes available evidence on cardiovascular risk, pre-participation evaluation, and the recognition of and response to cardiac arrest. Future recommendations for cardiac research initiatives, education, and collaboration are also provided.Item Inverse relationship between long chain n-3 fatty acids and risk of sudden cardiac death in patients starting hemodialysis(Elsevier, 2013) Friedman, Allon N.; Yu, Zhangsheng; Tabbey, Rebeka; Denski, Cheryl; Tamez, Hector; Wenger, Julia; Thadhani, Ravi; Li, Yong; Watkins, Bruce; Medicine, School of MedicineExperimental and clinical evidence suggests that long-chain n-3 fatty acids may protect against sudden cardiac death, the leading cause of mortality in hemodialysis patients. Here we investigated whether long-chain n-3 fatty acids have a protective relationship with sudden cardiac death in 100 patients who died of sudden cardiac death during the first year of starting hemodialysis and 300 patients who survived. Individuals were selected from a nationally representative cohort of over 1000 US hemodialysis units in 2004-2005. The odds of sudden cardiac death were calculated by quartile of long-chain n-3 fatty acid levels over the first year. There was a significant inverse relationship between long-chain n-3 fatty acids and the risk of sudden cardiac death even after adjusting for relevant comorbid conditions, biochemical values, and dietary fats. The odds of sudden cardiac death at 1 year for the second, third, and fourth quartile groups of long-chain n-3 fatty acids were 0.37, 0.22, and 0.20, respectively, compared with the lowest quartile. This significant inverse relationship was maintained even during the highest-risk first few months on hemodialysis. Thus, long-chain n-3 fatty acids are strongly and independently associated with a lower risk of sudden cardiac death in hemodialysis patients throughout the first year of hemodialysis.Item Myocardial Repolarization Dispersion and Autonomic Nerve Activity in a Canine Experimental Acute Myocardial Infarction Model(Elsevier, 2014-01) Piccirillo, Gianfranco; Moscucci, Federica; D’Alessandro, Gaetana; Pascucci, Matteo; Rossi, Pietro; Han, Seongwook; Chen, Lan S.; Lin, Shien-Fong; Chen, Peng-Sheng; Magrì, Damiano; Department of Neurology, IU School of MedicineBackground Evidence from a canine experimental acute myocardial infarction (MI) model shows that until the seventh week after MI the relationship between stellate ganglionic nerve and vagal nerve activities (SGNA/VNA) progressively increases. Objective We evaluated how autonomic nervous system activity influences temporal myocardial repolarization dispersion at this period. Methods We analyzed autonomic nerve activity as well as QT and RR variability from recordings previously obtained in 9 dogs. From a total 48 short-term electrocardiographic segments, 24 recorded before and 24 seven weeks after experimentally-induced MI, we obtained three indices of temporal myocardial repolarization dispersion: QTe (from q wave T to wave end), QTp (from q wave to T wave peak) and Te (from T wave peak to T wave end) variability index (QTeVI, QTpVI, TeVI). We also performed a heart rate variability power spectral analysis on the same segments. Results After MI, all the QT variables increased QTeVI (median [interquartile range]) (from - 1.76[0.82] to −1.32[0.68]), QTeVI (from −1.90[1.01] to −1.45[0.78]) and TeVI (from −0.72[0.67] to −0.22[1.00]), whereas all RR spectral indexes decreased (p<0.001 for all). Distinct circadian rhythms in QTeVI (p<0.05,) QTpVI (p<0.001) and TeVI (p<0.05) appeared after MI with circadian variations resembling that of SGNA/VNA. The morning QTpVI and TeVI acrophases approached the SGNA/VNA acrophase. Conversely, the evening QTeVI acrophase coincided with another SGNA/VNA peak. After MI, regression analysis detected a positive relationship between SGNA/VNA and TeVI (R2: 0.077; β: 0.278; p< 0.001). Conclusion Temporal myocardial repolarization dispersion shows a circadian variation after MI reaching its peak at a time when sympathetic is highest and vagal activity lowest.Item Perspective: a dynamics-based classification of ventricular arrhythmias(Elsevier, 2015-05) Weiss, James N.; Garfinkel, Alan; Karagueuzian, Hrayr S.; Nguyen, Thao P.; Olcese, Riccardo; Chen, Peng-Sheng; Qu, Zhilin; Department of Medicine, IU School of MedicineDespite key advances in the clinical management of life-threatening ventricular arrhythmias, culminating with the development of implantable cardioverter-defibrillators and catheter ablation techniques, pharmacologic/biologic therapeutics have lagged behind. The fundamental issue is that biological targets are molecular factors. Diseases, however, represent emergent properties at the scale of the organism that result from dynamic interactions between multiple constantly changing molecular factors. For a pharmacologic/biologic therapy to be effective, it must target the dynamic processes that underlie the disease. Here we propose a classification of ventricular arrhythmias that is based on our current understanding of the dynamics occurring at the subcellular, cellular, tissue and organism scales, which cause arrhythmias by simultaneously generating arrhythmia triggers and exacerbating tissue vulnerability. The goal is to create a framework that systematically links these key dynamic factors together with fixed factors (structural and electrophysiological heterogeneity) synergistically promoting electrical dispersion and increased arrhythmia risk to molecular factors that can serve as biological targets. We classify ventricular arrhythmias into three primary dynamic categories related generally to unstable Ca cycling, reduced repolarization, and excess repolarization, respectively. The clinical syndromes, arrhythmia mechanisms, dynamic factors and what is known about their molecular counterparts are discussed. Based on this framework, we propose a computational-experimental strategy for exploring the links between molecular factors, fixed factors and dynamic factors that underlie life-threatening ventricular arrhythmias. The ultimate objective is to facilitate drug development by creating an in silico platform to evaluate and predict comprehensively how molecular interventions affect not only a single targeted arrhythmia, but all primary arrhythmia dynamics categories as well as normal cardiac excitation-contraction coupling.Item Recognizing and Managing Myocarditis Following Covid-19 Vaccination: Mitigating Risk of Sudden Cardiac Death in Athletes(Elsevier, 2022) Kauth, Mark; Kovacs, Richard J.; Medicine, School of MedicineBackground: Myocarditis is a risk for sudden cardiac death (SCD) in athletes, and its recognition and appropriate management are of paramount importance for safe return to athletic activity. Myocarditis has been reported as a complication of the mRNA COVID-19 vaccines, especially in young males. It is not known whether prior COVID-19 infection increases risk for myocarditis after vaccination. We present a case of a young athletic male previously infected with COVID-19, who developed myocarditis after a second dose of the Pfizer mRNA COVID-19 vaccine. Case: A 19-year-old healthy male presented to the ED. He described anterior squeezing chest pain without association with activity or rest, and lateral chest pain exacerbated by movement. 6-8 months prior, he tested positive for COVID-19 infection via RT-PCR saliva test with symptoms that included rhinorrhea, cough, anosmia, ageusia, and mild chest pain. Symptoms resolved spontaneously. He later received two doses of the Pfizer vaccine, with second dose given 10 days prior to presentation. Vital signs and physical exam were normal. ECG showed 0.5-1mm ST segment elevation in the inferior and lateral leads. Troponin-I was elevated and peaked at 3.61 ng/mL, CBC, comprehensive metabolic panel, TSH, and C-reactive protein were normal. CT angiogram of the chest was normal. Transthoracic echocardiogram demonstrated normal left ventricular systolic function, normal wall motion, and no pericardial effusion. Decision-making: This patient was clinically diagnosed with myocarditis. He was treated with ibuprofen and beta blocker with improvement. Cardiac magnetic resonance imaging with and without gadolinium demonstrated minimal T2 signal elevation, but did reveal late gadolinium enhancement of 25-75% of the inferior and lateral walls. Athletic activity was restricted for 3-6 months and follow-up testing is yet to be completed. Conclusion: Although rare, myocarditis is a recognized complication following COVID-19 mRNA vaccination. Risk may be increased in younger male patients, and those previously infected with COVID-19. It is important to anticipate this complication of vaccination in the competitive athlete population, to mitigate risk of SCD.Item Relaxin Inhibits Ventricular Arrhythmia and Asystole in Rats With Pulmonary Arterial Hypertension(Frontiers Media, 2021-07-06) Martin, Brian; Vanderpool, Rebecca R.; Henry, Brian L.; Palma, Joshua B.; Gabris, Beth; Lai, Yen-Chun; Hu, Jian; Tofovic, Stevan P.; Reddy, Rajiv P.; Mora, Ana L.; Gladwin, Mark T.; Romero, Guillermo; Salama, Guy; Medicine, School of MedicinePulmonary arterial hypertension (PAH) leads to right ventricular cardiomyopathy and cardiac dysfunctions where in the clinical setting, cardiac arrest is the likely cause of death, in ~70% of PAH patients. We investigated the cardiac phenotype of PAH hearts and tested the hypothesis that the insulin-like hormone, Relaxin could prevent maladaptive cardiac remodeling and protect against cardiac dysfunctions in a PAH animal model. PAH was induced in rats with sugen (20 mg/kg), hypoxia then normoxia (3-weeks/each); relaxin (RLX = 0, 30 or 400 μg/kg/day, n ≥ 6/group) was delivered subcutaneously (6-weeks) with implanted osmotic mini-pumps. Right ventricle (RV) hemodynamics and Doppler-flow measurements were followed by cardiac isolation, optical mapping, and arrhythmia phenotype. Sugen-hypoxia (SuHx) treated rats developed PAH characterized by higher RV systolic pressures (50 ± 19 vs. 22 ± 5 mmHg), hypertrophy, reduced stroke volume, ventricular fibrillation (VF) (n = 6/11) and bradycardia/arrest (n = 5/11); both cardiac phenotypes were suppressed with dithiothreitol (DTT = 1 mM) (n = 0/2/group) or RLX (low or high dose, n = 0/6/group). PAH hearts developed increased fibrosis that was reversed by RLX-HD, but not RLX-LD. Relaxin decreased Nrf2 and glutathione transferases but not glutathione-reductase. High-dose RLX improved pulmonary arterial compliance (measured by Doppler flow), suppressed VF even after burst-pacing, n = 2/6). Relaxin suppressed VF and asystole through electrical remodeling and by reversing thiol oxidative stress. For the first time, we showed two cardiac phenotypes in PAH animals and their prevention by RLX. Relaxin may modulate maladaptive cardiac remodeling in PAH and protect against arrhythmia and cardiac arrest.