Browsing by Subject "Sudden cardiac death"

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  • Aro, Aapo Lauri Aleksi; Phan, Derek; Teodorescu, Carmen; Uy-Evanado, Audrey; Reinier, Kyndaron; Gunson, Karen; Jui, Jonathan; Huikuri, Heikki V.; Chugh, Sumeet S. (2017)
    Delayed QRS transition zone in the precordial leads of the 12-lead electrocardiogram (ECG) has been recently associated with increased risk of sudden cardiac death (SCD), but the underlying mechanisms are unknown. We correlated echocardiographic findings with ECG and clinical characteristics to investigate how alterations in cardiac structure and function contribute to this risk marker. From the ongoing population-based Oregon Sudden Unexpected Death Study (catchment population similar to 1 million), SCD cases with prior ECG available (n = 627) were compared with controls (n = 801). Subjects with delayed transition at V-5 or later were identified, and clinical and echocardiographic patterns associated with delayed transition were analysed. Delayed transition was present in 31% of the SCD cases and 17% of the controls. These subjects were older and more likely to have cardiovascular risk factors and history of myocardial infarction. Delayed transition was associated with increased left ventricular (LV) mass (122.7 +/- 40.2 vs. 102.9 +/- 33.7 g/m(2); P <0.001), larger LV diameter (53.3 +/- 10.4 vs. 49.2 +/- 8.0 mm; P <0.001), and lower LV ejection fraction (LVEF) (46.4 +/- 15.7 vs. 55.6 +/- 12.5%; P <0.001). In multivariate analysis, delayed transition was independently associated with myocardial infarction, reduced LVEF, and LV hypertrophy. The association between delayed transition and SCD was independent of the LVEF (OR 1.57; 95% CI 1.04-2.38; P = 0.032). The underpinnings of delayed QRS transition zone extend beyond previous myocardial infarction and reduced LVEF. Since the association with sudden death is independent of these factors, this novel marker of myocardial electrical remodelling should be explored as a potential risk predictor of SCD.
  • Porthan, Kimmo; Kentta, Tuomas; Niiranen, Teemu J.; Nieminen, Markku S.; Oikarinen, Lasse; Viitasalo, Matti; Hernesniemi, Jussi; Jula, Antti M.; Salomaa, Veikko; Huikuri, Heikki; Albert, Christine M.; Tikkanen, Jani T. (2019)
    Background: Electrocardiographic (ECG) left ventricular hypertrophy (LVH) is an established risk factor for cardiovascular events. However, limited data is available on the prognostic values of different ECG LVH criteria specifically to sudden cardiac death (SCD). Our goal was to assess relationships of different ECG LVH criteria to SCD. Methods: Three traditional and clinically useful (Sokolow-Lyon, Cornell, RaVL) and a recently proposed (Peguero-Lo Presti) ECG LVH voltage criteria were measured in 5730 subjects in the Health 2000 Survey, a national general population cohort study. Relationships between LVH criteria, aswell as their selected composites, to SCD were analyzed with Cox regression models. In addition, population-attributable fractions for LVH criteria were calculated. Results: After a mean follow-up of 12.5 +/- 2.2 years, 134 SCDs had occurred. When used as continuous variables, all LVH criteria except for RaVL were associated with SCD in multivariable analyses. When single LVH criteria were used as dichotomous variables, only Cornell was significant after adjustments. The dichotomous composite of Sokolow-Lyon and Cornell was also significant after adjustments (hazard ratio for SCD 1.82, 95% confidence interval 1.20-2.70, P = 0.006) and was the only LVH measure that showed statistically significant population attributable fraction (11.0%, 95% confidence interval 1.9-19.2%, P=0.019). Conclusions: Sokolow-Lyon, Cornell, and Peguero-Lo Presti ECG, but not RaVL voltage, are associated with SCD risk as continuous ECG voltage LVH variables. When SCD risk assessment/adjustment is performed using a dichotomous ECG LVH measure, composite of Sokolow-Lyon and Cornell voltages is the preferred option. (c) 2018 The Authors. Published by Elsevier B.V.
  • Terho, Henri K.; Tikkanen, Jani T.; Kenttä, Tuomas V.; Junttila, Juhani M.; Aro, Aapo L.; Anttonen, Olli; Kerola, Tuomas; Rissanen, Harri A.; Knekt, Paul; Huikuri, Heikki V. (2018)
    Background: Abnormal 12 lead electrocardiogram (ECG) findings and proposing its ability for enhanced risk prediction, majority of the studies have been carried out with elderly populations with prior cardiovascular diseases. This study aims to denote the association of sudden cardiac death (SCD) and various abnormal ECG morphologies using middle-aged population without a known cardiac disease. Methods: In total, 9511 middle-aged subjects (mean age 42 +/- 8.2 years, 52% males) without a known cardiac disease were included in this study. Risk for SCD was assessed after 10 and 30-years of follow-up. Results: Abnormal ECG was present in 16.3% (N = 1548) of subjects. The incidence of SCD was distinctly higher among those with any ECG abnormality in 10 and 30-year follow-ups (1.7/1000 years vs. 0.6/1000 years, P <0.001; 3.4;1000 years vs. 1.9/1000 years, P <0.001). At 10-year point, competing risk multivariate regression model showed HR of 1.62 (95% CI 1.0-2.6, P = 0.05) for SCD in subjects with abnormal ECG. QRS duration 110 ms, QRST-angle > 100', left ventricular hypertrophy, and T-wave inversions were the most significant independent ECG risk markers for 10-year SCD prediction with up to 3-fold risk for SCD. Those with ECG abnormalities had a 1.3-fold risk (95% CI 1.07-1.57, P - 0.007) for SCD in 30-year follow-up, whereas QRST-angle > 100 degrees, LVH, ER 0.1 mV and 0.2 mV were the strongest individual predictors. Subjects with multiple ECG abnormalities had up to 6.6-fold risk for SCD (P <0.001). Conclusion: Several ECG abnormalities are associated with the occurrence of early and late SCD events in the middle-age subjects without known history of cardiac disease. (C) 2018 The Authors. Published by Elsevier B.V.
  • Trachsel, Dagmar S.; Calloe, Kirstine; Mykkänen, Anna K.; Raistakka, Pia; Anttila, Marjukka; Fredholm, Merete; Tala, Martti; Lamminpää, Katariina; Klaerke, Dan A.; Buhl, Rikke (2021)
    Exercise-associated sudden deaths (EASDs) are deaths occurring unexpectedly during or immediately after exercise. Sudden cardiac death (SCD) is one cause of EASD. Cardiac arrhythmias caused by genetic variants have been linked to SCD in humans. We hypothesize that genetic variants may be associated with SCD in animals, including horses. Genetic variants are transmitted to offspring and their frequency might increase within a family. Therefore, the frequency of such variants might increase with the inbreeding factor. Higher inbreeding could have a negative impact on racing performance. Pedigree data and career earnings from racehorses diagnosed with SCD between 2002 and 2017 were compared using non-parametric tests with 1) control horses that died due to catastrophic musculoskeletal injuries and 2) horses that raced during the same period without reported problems. Diagnosis of SCD was based on necropsy reports, including macroscopic and microscopic examinations. Death was registered in the study period for 61 horses. Eleven of these horses were excluded due to missing autopsy reports. In 25 cases, the diagnosis remained unknown and death was possibly caused by cardiac arrhythmia, in two cases cardiac disease was identified, in seven cases a rupture of a major vessel had occurred. In addition, 16 horses died or were euthanized due to severe musculoskeletal injuries. No significant differences in inbreeding coefficients or in career earnings were found between the groups or between horses with EASD compared with other horses racing during the same period. The study provides no evidence for increased inbreeding factor in Finnish racehorses with SCD. (c) 2021 Elsevier Inc. All rights reserved.
  • Sánez Tähtisalo, Heini (Helsingfors universitet, 2017)
    Sydän- ja verisuonisairauksien syntyyn vaikuttavat sekä ympäristötekijät että perimä. EKG kuvaa sydämen sähköistä toimintaa. Mitattaviin osiin jaetun EKG:n rinnalla sydänperäiseen äkkikuolleisuuteen vaikuttavien geenitekijöiden tunnistaminen mahdollistaisi riskipotilaiden tunnistamisen ennen vakavia sydänperäisiä häiriöitä sekä ennaltaehkäisevän lääketieteellisen hoidon kohdentamisen. Tässä kandidaattipolymorfismitutkimuksessa selvitettiin onko sydämen toimintaan osallistuvien beeta1 – ja beeta2 –adrenoreseptorien (ADRB1 ja ADRB2) tai angiotensiinikonvertaasientsyymin (ACE) geenien keskeisillä polymorfismeilla vaikutusta EKG:n piirteisiin. Potilasaineistona oli GENRES-tutkimukseen osallistuneet verenpainetautia sairastavat miehet (n=186). Polymorfismien vaikutusta QT-aikaan ja T-aallon muodostumiseen etsittiin nelivaiheisella lineaarisella regressiomallilla. Analyysien keskeisimpinä tuloksina havaittiin tilastollisesti merkitsevä ADRB1 Gly49 –alleelin QT-aikaa lyhentävä vaikutus ja ADRB1 Gly389 –alleelin QT-aikaa pidentävä vaikutus. ADRB2 Gly16Arg- ja Gln27Glu-vaihteluiden yhteys T-aallon muodostumiseen jäi olemattomaksi tai heikoksi. ACE I/D:n deleetio-polymorfismi viittaa tutkimuksen perusteella T-aallon muutoksiin, jotka ovat yhdistettävissä lisääntyneeseen äkilliseen sydänperäiseen kuolleisuuteen. Tämän tutkielman havainnot viittaavat siis useampiin mahdollisiin polymorfismien ja EKG-muuttujien välisiin yhteyksiin ja kannustavat tarkempiin jatkotutkimuksiin yhteyden kliinisen merkityksen arvioimiseksi.
  • Holkeri, Arttu; Eranti, Antti; Haukilahti, M. Anette E.; Kerola, Tuomas; Kenttä, Tuomas V.; Tikkanen, Jani T.; Rissanen, Harri; Heliövaara, Markku; Knekt, Paul; Junttila, M. Juhani; Aro, Aapo L.; Huikuri, Heikki V. (2020)
    BACKGROUND Early repolarization (ER) has been linked to the risk of sudden cardiac death (SCD) in the general population, although controversy remains regarding risks across various subgroups. OBJECTIVE The purpose of this study was to investigate whether age and sex influence the prognostic significance of ER. METHODS We evaluated the 12-lead electrocardiograms of 6631 Finnish general population subjects age >= 30 years (mean age 50.1 +/- 13.9 years; 44.5% men) for the presence of ER (J-point elevation >= 0.1 mV in >= 2 inferior/lateral leads) and followed them for 24.4 +/- 10.3 years. We analyzed the association between ER and the risk of SCD, cardiac death, and ad-cause mortality in subgroups according to age (= 50 years) and sex. RESULTS ER was present in 367 of the 3305 subjects age = 50 years. ER was not associated with any of the endpoints in the entire study population. After adjusting for clinical factors, ER was associated with SCD (hazard ratio [HR] 1.88; 95% confidence interval [CI] 1.16-3.07) in subjects CONCLUSION ER is associated with SCD in subjects younger than 50 years, particularly in women, but not in subjects 50 years and older.
  • Schröder, Linda C.; Holkeri, Arttu; Eranti, Antti; Haukilahti, M. Anette E.; Kerola, Tuomas; Kenttä, Tuomas V.; Noponen, Kai; Seppänen, Tapio; Rissanen, Harri; Heliövaara, Markku; Knekt, Paul; Junttila, M. Juhani; Huikuri, Heikki V.; Aro, Aapo L. (2022)
    Background: Poor R-wave progression (PRWP) is a common clinical finding on the standard 12-lead electrocardiogram (ECG), but its prognostic significance is unclear. Objective: The purpose of this study was to examine the prognosis associated with PRWP in terms of sudden cardiac death (SCD), cardiac death, and all-cause mortality in general population subjects with and without coronary artery disease (CAD). Methods: Data and 12-lead ECGs were collected from a Finnish general population health examination survey conducted during 1978–1980 with follow-up until 2011. The study population consisted of 6854 subjects. Main end points were SCD, cardiac death, and all-cause mortality. PRWP was defined as R-wave amplitude ≤ 0.3 mV in lead V3 and R-wave amplitude in lead V2 ≤ R-wave amplitude in lead V3. Results: PRWP occurred in 213 subjects (3.1%). During the follow-up period of 24.3 ± 10.4 years, 3723 subjects (54.3%) died. PRWP was associated with older age, higher prevalence of heart failure and CAD, and β-blocker medication. In multivariate analyses, PRWP was associated with SCD (hazard ratio [HR] 2.13; 95% confidence interval [CI] 1.34–3.39), cardiac death (HR 1.75; 95% CI 1.35–2.15), and all-cause mortality (HR 1.29; 95% CI 1.08–1.54). In the subgroup with CAD, PRWP had a stronger association with cardiac mortality (HR 1.71; 95% CI 1.19–2.46) than in the subgroup without CAD, while the association with SCD was significant only in the subgroup with CAD (HR 2.62; 95% CI 1.38–4.98). Conclusion: PRWP was associated with adverse prognosis in the general population and with SCD in subjects with CAD.
  • Kentta, Tuomas V.; Nearing, Bruce D.; Porthan, Kimmo; Tikkanen, Jani T.; Viitasalo, Matti; Nieminen, Markku S.; Salomaa, Veikko; Oikarinen, Lasse; Jula, Antti; Kontula, Kimmo; Newton-Cheh, Chris; Huikuri, Heikki V.; Verrier, Richard L. (2016)
    BACKGROUND Heterogeneity of depolarization and repolarization underlies the development of lethal arrhythmias. OBJECTIVE We investigated whether quantification of spatial depolarization and repolarization heterogeneity identifies individuals at risk for sudden cardiac death (SCD). METHODS Spatial R-, J-, and T-wave heterogeneity (RWH, JWH, and TWH, respectively) was analyzed using automated second central moment analysis of standard digital 12-lead electrocardiograms in 5618 adults (2588, 46% men; mean +/- SEM age 50.9 +/- 0.2 years), who took part in the epidemiological Health 2000 Survey as representative of the entire Finnish adult population. RESULTS During the follow-up period of 7.7 +/- 0.2 years, a total of 72 SCDs occurred (1.3%), with an average yearly incidence rate of 0.17% per year. Increased RWH, JWH, and TWH in left precordial leads (V-4-V-6) were univariately associated with SCD (P <.001 for each). When adjusted with standard clinical risk markers, JWH and TWH remained independent predictors of SCD. Increased TWH (>= 102 mu V) was associated with a 1.7-fold adjusted relative risk for SCD (95% confidence interval [CI] 1.0-2.9; P = .048) and increased JWH (>= 123 mu V) with a 2.0-fold adjusted relative risk for SCD (95% CI 1.2-3.3; P = .006). When both TWH and JWH were above the threshold, the adjusted relative risk for SCD was 2.9-fold (95% CI 1.5-5.7; P = .002). When RWH (>= 470 mu V), JWH, and TWH were all above the threshold, the adjusted relative risk for SCD was 3.2-fold (95% CI 1.4-7.1; P = .009). CONCLUSION Second central moment analysis of standard resting 12-lead electrocardiographic morphology provides an ultrarapid means for the automated measurement of spatial RWH, JWH, and TWH, enabling analysis of high subject volumes and screening for SCD risk in the general population.
  • Holkeri, Arttu; Eranti, Antti; Haukilahti, M. Anette E.; Kerola, Tuomas; Kenttä, Tuomas V.; Noponen, Kai; Seppänen, Tapio; Rissanen, Harri; Heliövaara, Markku; Knekt, Paul; Junttila, M. Juhani; Huikuri, Heikki V.; Aro, Aapo L. (2021)
    Background: Negative T-waves are associated with sudden cardiac death (SCD) risk in the general population. Whether flat T-waves also predict SCD is not known. The aim of the study was to examine the clinical characteristics and risk of SCD in general population subjects with flat T-waves. Methods: We examined the electrocardiograms of 6750 Finnish general population adults aged ≥30 years and classified the subjects into 3 groups: 1) negative T-waves with an amplitude ≥0.1 mV in ≥2 of the leads I, II, aVL, V4–V6, 2) negative or positive low amplitude T-waves with an amplitude <0.1 mV and the ratio of T-wave and R-wave <10% in ≥2 of the leads I, II, aVL, V4–V6, and 3) normal positive T-waves (not meeting the aforesaid criteria). The association between T-wave classification and SCD was assessed during a 10-year follow-up. Results: A total of 215 (3.2%) subjects had negative T-waves, 856 (12.7%) flat T-waves, and 5679 (84.1%) normal T-waves. Flat T-wave subjects were older and had more often cardiovascular morbidities compared to normal T-wave subjects, while negative T-wave subjects were the oldest and had most often cardiovascular morbidities. After adjusting for multiple factors, both flat T-waves (hazard ratio [HR] 1.81; 95% confidence interval [CI] 1.13–2.91) and negative T-waves (HR 3.27; 95% CI 1.85–5.78) associated with SCD. Conclusions: Cardiovascular risk factors and disease are common among subjects with flat T-waves, but these minor T-wave abnormalities are also independently associated with increased SCD risk.
  • Tikkanen, Jani T.; Kentta, Tuomas; Porthan, Kimmo; Anttonen, Olli; Eranti, Antti; Aro, Aapo L.; Kerola, Tuomas; Rissanen, Harri A.; Knekt, Paul; Heliövaara, Markku; Holkeri, Arttu; Haukilahti, Anette; Niiranen, Teemu; Hernesniemi, Jussi; Jula, Antti; Nieminen, Markku S.; Myerburg, Robert J.; Albert, Christine M.; Salomaa, Veikko; Huikuri, Heikki V.; Junttila, M. Juhani (2022)
    BACKGROUND QRS duration and corrected QT (QTc) interval have been associated with sudden cardiac death (SCD), but no data are available on the significance of repolarization component (JTc interval) of the QTc interval as an independent risk marker in the general population. OBJECTIVE In this study, we sought to quantify the risk of SCD associated with QRS, QTc, and JTc intervals. METHODS This study was conducted using data from 3 population cohorts from different eras, comprising a total of 20,058 individuals. The follow-up period was limited to 10 years and age at baseline to 30-61 years. QRS duration and QT interval (Bazett's) were measured from standard 12-lead electrocardiograms at baseline. JTc interval was defined as QTc interval - QRS duration. Cox proportional hazards models that controlled for confounding clinical factors identified at baseline were used to estimate the relative risk of SCD. RESULTS During a mean period of 9.7 years, 207 SCDs occurred (1.1 per 1000 person-years). QRS duration was associated with a significantly increased risk of SCD in each cohort (pooled hazard ratio [HR] 1.030 per 1-ms increase; 95% confidence interval [CI] 1.017-1.043). The QTc interval had borderline to significant associations with SCD and varied among cohorts (pooled HR 1.007; 95% CI 1.001-1.012). JTc interval as a continuous variable was not associated with SCD (pooled HR 1.001; 95% CI 0.996-1.007). CONCLUSION Prolonged QRS durations and QTc intervals are associated with an increased risk of SCD. However, when the QTc interval is deconstructed into QRS and JTc intervals, the repolarization component (JTc) appears to have no independent prognostic value.
  • Aro, Aapo L.; Rusinaru, Carmen; Uy-Evanado, Audrey; Reinier, Kyndaron; Phan, Derek; Gunson, Karen; Jui, Jonathan; Chugh, Sumeet S. (2017)
    Background: Syncope has been associated with increased risk of sudden cardiac arrest (SCA) in specific patient populations, such as hypertrophic cardiomyopathy, heart failure, and long QT syndrome, but data are lacking on the risk of SCA associated with syncope among patients with coronary artery disease (CAD), the most common cause of SCA. We investigated this association among CAD patients in the community. Methods: All cases of SCA due to CAD were prospectively identified in Portland, Oregon (population approximately 1 million) as part of the Oregon Sudden Unexpected Death Study 2002-2015, and compared to geographical controls. Detailed clinical information including history of syncope and cardiac investigations was obtained from medical records. Results: 2119 SCA cases (68.4 +/- 13.8 years, 66.9% male) and 746 controls (66.7 +/- 11.7 years, 67.0% male) were included in the analysis. 143 (6.8%) of cases had documented syncope prior to the SCA. SCA cases with syncope were > 5 years older and had more comorbidities than other SCA cases. After adjusting for clinical factors and left ventricular ejection fraction (LVEF), syncope was associated with increased risk of SCA (OR 2.8; 95%CI 1.68-4.85). When analysis was restricted to subjects with LVEF >= 50%, the risk of SCA associated with syncope remained significantly elevated (adjusted OR 3.1; 95%CI 1.68-5.79). Conclusions: Syncope was associated with increased risk of SCA in CAD patients even with preserved LV function. These findings suggest a role for this clinical marker among patients with CAD and normal LVEF, a large subgroup without any current means of SCA risk stratification. (C) 2016 Published by Elsevier Ireland Ltd.