Extreme Nonfasting Remnant Cholesterol vs Extreme LDL Cholesterol as Contributors to Cardiovascular Disease and All-Cause Mortality in 90000 Individuals from the General Population

Abstract BACKGROUND Increased nonfasting remnant cholesterol, like increased LDL cholesterol, is causally associated with increased risk for ischemic heart disease (IHD). We tested the hypothesis that extreme concentrations of nonfasting remnant and LDL cholesterol are equal contributors to the risk of IHD, myocardial infarction (MI), and all-cause mortality. METHODS We compared stepwise increasing concentrations of nonfasting remnant and LDL cholesterol for association with risk of IHD, MI, and all-cause mortality in approximately 90 000 individuals from the Danish general population. During up to 22 years of complete follow-up, 4435 participants developed IHD, 1722 developed MI, and 8121 died. RESULTS Compared with participants with nonfasting remnant cholesterol <0.5 mmol/L (19.3 mg/dL), hazard ratios for IHD ranged from 1.3 (95% CI 1.1–1.5) for remnant cholesterol of 0.5–0.99 mmol/L (19.3–38.2 mg/dL) to 2.4 (1.9–2.9) for remnant cholesterol of ≥1.5 mmol/L (58 mg/dL) (P for trend <0.001). Compared with participants with LDL cholesterol <3.0 mmol/L (115.8 mg/dL), hazard ratios for IHD ranged from 1.3 (1.1–1.5) for LDL cholesterol of 3–3.99 mmol/L (115.8–154 mg/dL) to 2.3 (1.9–2.8) for LDL cholesterol of ≥5 mmol/L (193 mg/dL) (P < 0.001). Corresponding hazard ratios for MI ranged from 1.8 (1.4–2.3) to 3.4 (2.5–4.8) for remnant cholesterol (P < 0.001), and from 1.7 (1.4–2.2) to 4.7 (3.5–6.3) for LDL cholesterol (P < 0.001). Nonfasting remnant cholesterol concentrations were associated stepwise with all-cause mortality ranging from hazard ratio 1.0 (0.9–1.1) to 1.6 (1.4–1.9) (P < 0.001), whereas LDL cholesterol concentrations were associated with decreased all-cause mortality risk in a U-shaped pattern, with hazard ratios from 0.8 (0.7–0.8) to 0.9 (0.8–1.0) (P = 0.002). After mutual adjustment, LDL cholesterol best predicted MI, and remnant cholesterol best predicted all-cause mortality. CONCLUSIONS Both lipoproteins were associated equally with risk of IHD and MI; however, only nonfasting remnant cholesterol concentrations were associated stepwise with increased all-cause mortality risk.

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Increased Remnant Cholesterol Explains Part of Residual Risk of All-Cause Mortality in 5414 Patients with Ischemic Heart Disease

Clinical Chemistry ◽

10.1373/clinchem.2015.253757 ◽

2016 ◽

Vol 62 (4) ◽

pp. 593-604 ◽

Cited By ~ 52

Author(s):

Anne-Marie K Jepsen ◽

Anne Langsted ◽

Anette Varbo ◽

Lia E Bang ◽

Pia R Kamstrup ◽

...

Keyword(s):

Heart Disease ◽

Ischemic Heart Disease ◽

Ldl Cholesterol ◽

Hdl Cholesterol ◽

Hazard Ratio ◽

Residual Risk ◽

Ischemic Heart ◽

Increased Risk ◽

All Cause Mortality ◽

Remnant Cholesterol

Abstract BACKGROUND Increased concentrations of remnant cholesterol are causally associated with increased risk of ischemic heart disease. We tested the hypothesis that increased remnant cholesterol is a risk factor for all-cause mortality in patients with ischemic heart disease. METHODS We included 5414 Danish patients diagnosed with ischemic heart disease. Patients on statins were not excluded. Calculated remnant cholesterol was nonfasting total cholesterol minus LDL and HDL cholesterol. During 35836 person-years of follow-up, 1319 patients died. RESULTS We examined both calculated and directly measured remnant cholesterol; importantly, however, measured remnant cholesterol made up only 9% of calculated remnant cholesterol at nonfasting triglyceride concentrations <1 mmol/L (89 mg/dL) and only 43% at triglycerides >5 mmol/L (443 mg/dL). Multivariable-adjusted hazard ratios for all-cause mortality compared with patients with calculated remnant cholesterol concentrations in the 0 to 60th percentiles were 1.2 (95% CI, 1.1–1.4) for patients in the 61st to 80th percentiles, 1.3 (1.1–1.5) for the 81st to 90th percentiles, 1.5 (1.1–1.8) for the 91st to 95th percentiles, and 1.6 (1.2–2.0) for patients in the 96th to 100th percentiles (trend, P < 0.001). Corresponding values for measured remnant cholesterol were 1.0 (0.8–1.1), 1.2 (1.0–1.4), 1.1 (0.9–1.5), and 1.3 (1.1–1.7) (trend, P = 0.006), and for measured LDL cholesterol 1.0 (0.9–1.1), 1.0 (0.8–1.2), 1.0 (0.8–1.3), and 1.1 (0.8–1.4) (trend, P = 0.88). Cumulative survival was reduced in patients with calculated remnant cholesterol ≥1 mmol/L (39 mg/dL) vs <1 mmol/L [log-rank, P = 9 × 10−6; hazard ratio 1.3 (1.2–1.5)], but not in patients with measured LDL cholesterol ≥3 mmol/L (116 mg/dL) vs <3 mmol/L [P = 0.76; hazard ratio 1.0 (0.9–1.1)]. CONCLUSIONS Increased concentrations of both calculated and measured remnant cholesterol were associated with increased all-cause mortality in patients with ischemic heart disease, which was not the case for increased concentrations of measured LDL cholesterol. This suggests that increased concentrations of remnant cholesterol explain part of the residual risk of all-cause mortality in patients with ischemic heart disease.

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Abstract WP226: The Association of Green Tea and Coffee Consumption With Mortality From Cardiovascular Disease and All Causes Among Persons With and Without History of Stroke or Myocardial Infarction: The JACC Study

Stroke ◽

10.1161/str.51.suppl_1.wp226 ◽

2020 ◽

Vol 51 (Suppl_1) ◽

Author(s):

Masayuki Teramoto ◽

Isao Muraki ◽

Kokoro Shirai ◽

Akiko Tamakoshi ◽

Hiroyasu Iso

Keyword(s):

Myocardial Infarction ◽

Cardiovascular Disease ◽

General Population ◽

Green Tea ◽

Coffee Consumption ◽

Tea Consumption ◽

Food Frequency ◽

All Cause Mortality ◽

History Of

Background: Both green tea and coffee consumption have been associated with lower risks of mortality from cardiovascular disease (CVD) and all causes in general population, but little is known about those impact on persons with history of CVD. We examined the association of those consumption with these mortalities among persons with and without history of stroke or myocardial infarction in general population. Methods: The study subjects were 60,664 participants (896 stroke and 1751 myocardial infarction survivors and 58,017 persons with no history of stroke or myocardial infarction), aged 40-79 years at the baseline (1988-1990), who completed a lifestyle and medical history questionnaire including self-administered food frequency under the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC Study). Results: During the median follow-up of 18.5 years, a total of 12,745 (7,458 men and 5,287 women) deaths including 3,737 CVD deaths were documented. Green tea and coffee consumption were inversely associated with CVD and all-cause mortality among myocardial infarction survivors as well as persons without history of stroke or myocardial infarction. After adjustment for known cardiovascular risk factors, the lower risks of mortality from CVD and all-causes associated with frequent green tea consumption (5-6 and ≥7 cups/day) or coffee consumption (≥2 cups/day) remained statistical. Conclusions: Both green tea and coffee consumption were inversely associated with risks of CVD and all-cause mortality among myocardial infarction survivors and persons without history of stroke or myocardial infarction.

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D-dimer and the incidence of heart failure and mortality after acute myocardial infarction

Heart ◽

10.1136/heartjnl-2020-316880 ◽

2020 ◽

pp. heartjnl-2020-316880 ◽

Cited By ~ 1

Author(s):

Xiaoyuan Zhang ◽

Shanjie Wang ◽

Jinxin Liu ◽

Yini Wang ◽

Hengxuan Cai ◽

...

Keyword(s):

Myocardial Infarction ◽

Heart Failure ◽

Acute Myocardial Infarction ◽

Plaque Rupture ◽

Risk Of Death ◽

Increased Risk ◽

Clinical Covariates ◽

All Cause Mortality ◽

D Dimer

ObjectiveD-dimer might serve as a marker of thrombogenesis and a hypercoagulable state following plaque rupture. Few studies explore the association between baseline D-dimer levels and the incidence of heart failure (HF), all-cause mortality in an acute myocardial infarction (AMI) population. We aimed to explore this association.MethodsWe enrolled 4504 consecutive patients with AMI with complete data in a prospective cohort study and explored the association of plasma D-dimer levels on admission and the incidence of HF, all-cause mortality.ResultsOver a median follow-up of 1 year, 1112 (24.7%) patients developed in-hospital HF, 542 (16.7%) patients developed HF after hospitalisation and 233 (7.1%) patients died. After full adjustments for other relevant clinical covariates, patients with D-dimer values in quartile 3 (Q3) had 1.51 times (95% CI 1.12 to 2.04) and in Q4 had 1.49 times (95% CI 1.09 to 2.04) as high as the risk of HF after hospitalisation compared with patients in Q1. Patients with D-dimer values in Q4 had more than a twofold (HR 2.34; 95% CI 1.33 to 4.13) increased risk of death compared with patients in Q1 (p<0.001). But there was no association between D-dimer levels and in-hospital HF in the adjusted models.ConclusionsD-dimer was found to be associated with the incidence of HF after hospitalisation and all-cause mortality in patients with AMI.

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Multimorbidity, mortality, and physical activity

Chronic Illness ◽

10.1177/1742395316644306 ◽

2016 ◽

Vol 12 (4) ◽

pp. 272-280 ◽

Cited By ~ 12

Author(s):

Paul D Loprinzi ◽

Ovuokerie Addoh ◽

Chelsea Joyner

Keyword(s):

Physical Activity ◽

Mortality Risk ◽

Physical Inactivity ◽

Self Report ◽

Minimal Effect ◽

Increased Risk ◽

All Cause Mortality ◽

The Government ◽

Physician Diagnosis

Objectives Multimorbidity and physical inactivity are individually associated with increased mortality risk, but the possibility for physical activity to moderate the multimorbidity–mortality relationship has yet to be investigated. Methods Data from the 1999–2006 NHANES were employed, with 16,091 participants constituting the analytic sample. Participants were followed through 2011, including a median follow-up of 99 months. Physical activity was assessed via self-report with multimorbidity assessed from physician diagnosis. Results After adjustment, for every 1 morbidity increase, participants had a 23% increased risk of all-cause mortality (HR = 1.23; 95% CI: 1.19–1.28; p < 0.001). Multimorbidity mostly remained associated with all-cause mortality across all levels of physical activity, with the exception of those achieving four times the dose of the government guidelines. Discussion With the exception of those who engaged in high levels of self-reported physical activity, physical activity had a minimal effect on the multimorbidity–mortality relationship.

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Association of BMI, comorbidities and all-cause mortality by using a baseline mortality risk model

PLoS ONE ◽

10.1371/journal.pone.0253696 ◽

2021 ◽

Vol 16 (7) ◽

pp. e0253696

Author(s):

Jia Li ◽

Gyorgy Simon ◽

M. Regina Castro ◽

Vipin Kumar ◽

Michael S. Steinbach ◽

...

Keyword(s):

Body Mass ◽

Mortality Risk ◽

Risk Model ◽

Risk Groups ◽

Baseline Risk ◽

Increased Risk ◽

Wide Range ◽

Baseline Mortality ◽

All Cause Mortality

Objective The association of body mass index (BMI) and all-cause mortality is controversial, frequently referred to as a paradox. Whether the cause is metabolic factors or statistical biases is still controversial. We assessed the association of BMI and all-cause mortality considering a wide range of comorbidities and baseline mortality risk. Methods Retrospective cohort study of Olmsted County residents with at least one BMI measurement between 2000–2005, clinical data in the electronic health record and minimum 8 year follow-up or death within this time. The cohort was categorized based on baseline mortality risk: Low, Medium, Medium-high, High and Very-high. All-cause mortality was assessed for BMI intervals of 5 and 0.5 Kg/m2. Results Of 39,739 subjects (average age 52.6, range 18–89; 38.1% male) 11.86% died during 8-year follow-up. The 8-year all-cause mortality risk had a “U” shape with a flat nadir in all the risk groups. Extreme BMI showed higher risk (BMI <15 = 36.4%, 15 to <20 = 15.4% and ≥45 = 13.7%), while intermediate BMI categories showed a plateau between 10.6 and 12.5%. The increased risk attributed to baseline risk and comorbidities was more obvious than the risk based on BMI increase within the same risk groups. Conclusions There is a complex association between BMI and all-cause mortality when evaluated including comorbidities and baseline mortality risk. In general, comorbidities are better predictors of mortality risk except at extreme BMIs. In patients with no or few comorbidities, BMI seems to better define mortality risk. Aggressive management of comorbidities may provide better survival outcome for patients with body mass between normal and moderate obesity.

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An analysis of the impact of fluid overload and fluid depletion for all-cause and cardiovascular mortality

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfy396 ◽

2019 ◽

Vol 34 (8) ◽

pp. 1385-1393 ◽

Cited By ~ 3

Author(s):

Dimitrie Siriopol ◽

Mihaela Siriopol ◽

Stefano Stuard ◽

Luminita Voroneanu ◽

Peter Wabel ◽

...

Keyword(s):

Mortality Risk ◽

Fluid Overload ◽

Reference Group ◽

Volume Status ◽

Time Varying ◽

Dialysis Fluid ◽

Fluid Status ◽

Increased Risk ◽

All Cause Mortality

Abstract Background Both baseline fluid overload (FO) and fluid depletion are associated with increased mortality risk and cardiovascular complications in haemodialysis patients. Fluid status may vary substantially over time, and this variability could also be associated with poor outcomes. Methods In our retrospective cohort study, including 4114 haemodialysis patients from 34 Romanian dialysis units, we investigated both all-cause and cardiovascular mortality risk according to baseline pre- and post-dialysis volume status, changes in pre- and post-dialysis fluid status during follow-up (time-varying survival analysis), pre–post changes in volume status during dialysis and pre-dialysis fluid status variability during the first 6 months of evaluation. Results According to their pre-dialysis fluid status, patients were stratified in the following groups: normovolaemic with an absolute FO (AFO) compartment between −1.1 and 1.1 L, fluid depletion with an AFO below −1.1 L, moderate FO with an AFO compartment >1.1 but <2.5 L and severe FO with the AFO compartment >2.5 L. Baseline pre-dialysis FO and fluid depletion patients had a significantly elevated risk of all-cause mortality risk {hazard ratio [HR] 1.53 [95% confidence interval (CI) 1.22–1.93], HR 2.04 (95% CI 1.59–2.60) and HR 1.88 (95% CI 1.07–3.39) for moderate FO, severe FO and fluid depletion, respectively}. In contrast, post-dialysis fluid depletion was associated with better survival [HR 0.71 (95% CI 0.57–0.89)]. Similar results were found when using changes in pre- or post-dialysis fluid status during follow-up (time-varying values): FO patients had an increased risk of all-cause [moderate FO: HR 1.39 (95% CI 1.11–1.75); severe FO: HR 2.29 (95% CI 2.01–3.31] and cardiovascular (CV) mortality [moderate FO: HR 1.34 (95% CI 1.05–1.70); severe FO: HR 2.34 (95% CI 1.67–3.28)] as compared with normohydrated patients. Using pre–post changes in volume status during dialysis, we categorized the patients into six groups: Group 1, AFO <−1.1 L pre- and post-dialysis; Group 2, AFO between −1.1 and 1.1 L pre-dialysis and <−1.1 L post-dialysis (the reference group); Group 3, AFO between −1.1 and 1.1 L pre- and post-dialysis; Group 4, AFO >1.1 L pre-dialysis and <−1.1 L post-dialysis; Group 5, AFO >1.1 L pre-dialysis and between −1.1 and 1.1 L post-dialysis; Group 6, AFO >1.1 L pre- and post-dialysis. Using the baseline values, only patients in Groups 1, 5 and 6 maintained an increased risk for all-cause mortality as compared with the reference group. Additionally, CV mortality risk was significantly higher for patients in Groups 5 and 6. When we applied the time-varying analysis, patients in Groups 1, 5 and 6 had a significantly higher risk for both all-cause and CV mortality risk. In the last approach, the highest risk for the all-cause mortality outcome was observed for patients with high-amplitude fluctuation during the first 6 months of evaluation [HR 2.75 (95% CI 1.29–5.84)]. Conclusion We reconfirm the association between baseline pre- and post-dialysis volume status and mortality in dialysis patients; additionally, we showed that greater fluid status variability is independently associated with higher mortality.

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γ-Glutamyltransferase Variability and the Risk of Mortality, Myocardial Infarction, and Stroke: A Nationwide Population-Based Cohort Study

Journal of Clinical Medicine ◽

10.3390/jcm8060832 ◽

2019 ◽

Vol 8 (6) ◽

pp. 832 ◽

Cited By ~ 2

Author(s):

Hye Soo Chung ◽

Ji Sung Lee ◽

Jung A. Kim ◽

Eun Roh ◽

You Bin Lee ◽

...

Keyword(s):

Myocardial Infarction ◽

Hazard Analysis ◽

Population Based ◽

Hazard Ratios ◽

Risk Of Mortality ◽

Increased Risk ◽

Cardiometabolic Disorders ◽

All Cause Mortality ◽

Korean National Health Insurance ◽

Related Mortality

Although it has been suggested that the γ-glutamyltransferase (GGT) level is an indicator of cardiometabolic disorders, there is no previous study to evaluate the implication of GGT variability on the development of myocardial infarction (MI), stroke, all-cause mortality, and cardiovascular disease (CVD)-related mortality. GGT variability was measured as the coefficient variance (GGT-CV), standard deviation (GGT-SD), and variability independent of the mean (GGT-VIM). Using the population-based Korean National Health Insurance Service-Health Screening Cohort, we followed 158,736 Korean adults over a median duration of 8.4 years. In multivariable Cox proportional hazard analysis, the risk of mortality, MI, and stroke showed a stepwise increase according to the quartiles of GGT-CV, GGT-SD or GGT-VIM. In the highest quartile of GGT-CV compared to the lowest quartile after adjusting for confounding variables including mean GGT, the hazard ratios (HRs) for incident MI, stroke, mortality, and CVD-related mortality were 1.19 (95% confidence interval (CI), 1.06–1.34; p < 0.001), 1.20 (95% CI, 1.10–1.32; p < 0.001), 1.41 (95% CI, 1.33–1.51; p < 0.001), and 1.52 (95% CI, 1.30–1.78; p < 0.001), respectively, which were similar or even higher compared with those associated with total cholesterol variability. This is the first study to demonstrate that high GGT variability is associated with increased risk of MI, stroke, all-cause mortality, and CVD-related mortality in the general population.

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Visit-to-visit variability of serum uric acid measurements and the risk of all-cause mortality in the general population

Arthritis Research & Therapy ◽

10.1186/s13075-021-02445-7 ◽

2021 ◽

Vol 23 (1) ◽

Author(s):

Xue Tian ◽

Anxin Wang ◽

Yingting Zuo ◽

Shuohua Chen ◽

Licheng Zhang ◽

...

Keyword(s):

Uric Acid ◽

General Population ◽

Serum Uric Acid ◽

Cox Proportional Hazard ◽

Increased Risk ◽

All Cause Mortality ◽

Alternative Measures ◽

Average Real Variability ◽

Longitudinal Variability

Abstract Background Evidence on longitudinal variability of serum uric acid (SUA) and risk of all-cause mortality in the general population is limited, as many prior studies focused on a single measurement of SUA. Methods A total of 53,956 participants in the Kailuan study who underwent three health examinations during 2006 to 2010 were enrolled. Variability of SUA was measured using the coefficient of variation (primary index), standard deviation, average real variability, and variability independent of the mean. Cox proportional hazard regressions were used to calculate the hazard ratio (HR) and 95% confidence interval (CI) for the association of variability of SUA with subsequent risk of all-cause mortality, considering its magnitude and the direction and across different baseline SUA categories. Results Over a median follow-up of 7.04 years, 2728 participants died. The highest variability of SUA was associated with an increased risk of all-cause mortality, the HR was 1.33 (95% CI, 1.20–1.49) compared with the lowest variability. In this group, both a large fall (HR, 1.28; 95% CI, 1.14–1.44) and rise (HR, 1.18; 95% 1.05–1.32) in SUA were related to risk of all-cause mortality. These associations were similar across different baseline SUA categories. Consistent results were observed in alternative measures of SUA variability. Moreover, individuals with higher variability in SUA were more related to common risk factors than those with stable SUA. Conclusions Higher variability in SUA was independently associated with the risk of all-cause mortality irrespective of baseline SUA and direction of variability in the general population.

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Effect of Digoxin Therapy on Mortality in Patients With Atrial Fibrillation: An Updated Meta-Analysis

Frontiers in Cardiovascular Medicine ◽

10.3389/fcvm.2021.731135 ◽

2021 ◽

Vol 8 ◽

Author(s):

Xiaoxu Wang ◽

Yi Luo ◽

Dan Xu ◽

Kun Zhao

Keyword(s):

Atrial Fibrillation ◽

Meta Analysis ◽

Cochrane Library ◽

Clinical Effects ◽

Hazard Ratios ◽

Risk Of Mortality ◽

Increased Risk ◽

All Cause Mortality ◽

The Cochrane Library

Background: Whether digoxin is associated with increased mortality in atrial fibrillation (AF) remains controversial. We aimed to assess the risk of mortality and clinical effects of digoxin use in patients with AF.Methods: PubMed, Embase, and the Cochrane library were systematically searched to identify eligible studies comparing all-cause mortality of patients with AF taking digoxin with those not taking digoxin, and the length of follow-up was at least 6 months. Hazard ratios (HRs) with 95% confidence intervals (CIs) were extracted and pooled.Results: A total of 29 studies with 621,478 patients were included. Digoxin use was associated with an increased risk of all-cause mortality in all patients with AF (HR 1.17, 95% CI 1.13–1.22, P < 0.001), especially in patients without HF (HR 1.28, 95% CI 1.11–1.47, P < 0.001). There was no significant association between digoxin and mortality in patients with AF and HF (HR 1.06, 95% CI 0.99–1.14, P = 0.110). In all patients with AF, regardless of concomitant HF, digoxin use was associated with an increased risk of sudden cardiac death (SCD) (HR 1.40, 95% CI 1.23–1.60, P < 0.001) and cardiovascular (CV) mortality (HR 1.27, 95% CI 1.08–1.50, P < 0.001), and digoxin use had no significant association with all-cause hospitalization (HR 1.13, 95% CI 0.92–1.39, P = 0.230).Conclusion: We conclude that digoxin use is associated with an increased risk of all-cause mortality, CV mortality, and SCD, and it does not reduce readmission for AF, regardless of concomitant HF. Digoxin may have a neutral effect on all-cause mortality in patients with AF with concomitant HF.Systematic Review Registration:https://www.crd.york.ac.ukPROSPERO.

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Association Between Silent Myocardial Infarction and Long‐Term Risk of Sudden Cardiac Death

Journal of the American Heart Association ◽

10.1161/jaha.120.017044 ◽

2021 ◽

Vol 10 (1) ◽

Author(s):

Yun‐Jiu Cheng ◽

Yu‐He Jia ◽

Feng‐Juan Yao ◽

Wei‐Yi Mei ◽

Yuan‐Sheng Zhai ◽

...

Keyword(s):

Myocardial Infarction ◽

Sudden Cardiac Death ◽

Cardiac Death ◽

Population Attributable Fraction ◽

Cardiovascular Health Study ◽

Primary Study ◽

Hazard Ratios ◽

Increased Risk ◽

Silent Myocardial Infarction

Background Although silent myocardial infarction (SMI) is prognostically important, the risk of sudden cardiac death (SCD) among patients with incident SMI is not well established. Methods and Results We examined 2 community‐based cohorts: the ARIC (Atherosclerosis Risk in Communities) study (n=13 725) and the CHS (Cardiovascular Health Study) (n=5207). Incident SMI was defined as electrocardiographic evidence of new myocardial infarction during follow‐up visits that was not present at the baseline. The primary study end point was physician‐adjudicated SCD. In the ARIC study, 513 SMIs, 441 clinically recognized myocardial infarctions (CMIs), and 527 SCD events occurred during a median follow‐up of 25.4 years. The multivariable hazard ratios of SMI and CMI for SCD were 5.20 (95% CI, 3.81–7.10) and 3.80 (95% CI, 2.76–5.23), respectively. In the CHS, 1070 SMIs, 632 CMIs, and 526 SCD events occurred during a median follow‐up of 12.1 years. The multivariable hazard ratios of SMI and CMI for SCD were 1.70 (95% CI, 1.32–2.19) and 4.08 (95% CI, 3.29–5.06), respectively. The pooled hazard ratios of SMI and CMI for SCD were 2.65 (2.18–3.23) and 3.99 (3.34–4.77), respectively. The risk of SCD associated with SMI is stronger with White individuals, men, and younger age. The population‐attributable fraction of SCD was 11.1% for SMI, and SMI was associated with an absolute risk increase of 8.9 SCDs per 1000 person‐years. Addition of SMI significantly improved the predictive power for both SCD and non‐SCD. Conclusions Incident SMI is independently associated with an increased risk of SCD in the general population. Additional research should address screening for SMI and the role of standard post–myocardial infarction therapy.

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