Genetic Susceptibility of Myocardial Infarction

Zdravkovic, Slobodan; Wienke, Andreas; Pedersen, Nancy L.; Fairé, Ulf dé

doi:10.1375/twin.10.6.848

Cited by 23 publications

(19 citation statements)

References 29 publications

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“…In particular, onset of CAD before age 42 years is rare and atypical. Our results are broadly consistent with previous findings on the heritability of cardiac death,11 angina,36 and MI12 in Swedish twins, and sex differences in heritability of precursors of CAD 26…”

Section: Commentsupporting

confidence: 93%

Major Depression and Coronary Artery Disease in the Swedish Twin Registry

Kendler

Gardner²,

Fiske³

et al. 2009

Arch Gen Psychiatry

127

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Context Major depresssion (MD) and coronary artery disease (CAD) frequently co-occur. The mechanisms of comorbidity are uncertain. Objective To clarify sources of MD-CAD comorbidity. Design Major depression was assessed at the time of the personal interview, and CAD from hospital discharge records and death certificates. Setting Swedish population-based twin registry. Participants The study included 30 374 twins with a mean age of 57 years. Main Outcome Measure Modified DSM-IV diagnosis of MD or diagnosis of CAD. Results Lifetime association between MD and CAD was modest (odds ratio, ~1.3). In time-dependent Cox analyses, onset of CAD produced concurrent and ongoing hazard ratios for MD of 2.83 and 1.75. These risks increased if the diagnosis of CAD was restricted to myocardial infarction. Onset of MD increased the concurrent and ongoing hazard ratios for CAD to 2.53 and 1.17. The ongoing CAD risk was strongly associated with depressive severity and recurrence. Twin models showed that the modest comorbidity between MD and CAD in women arose primarily from shared genetic effects, although the genetic correlation was small (+0.16). In men, the source of comorbidity was moderated by age, being environmental in older members and largely genetic in younger members of the sample. Conclusions Although the MD-CAD relationship across the lifespan is modest, time-dependent models reveal stronger associations. The sustained effect of CAD onset on MD risk is much stronger than vice versa. The effect of MD on CAD is largely acute, and the longer-term effects are apparently mediated via depressive recurrence. When examined separately, in men, environmental effects, which are often acute, play a large role in MD-CAD comorbidity, whereas in women, chronic effects, which are in part genetic, are more important. In men, genetic sources of MD-CAD comorbidity are more important in younger members of the sample.

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Section: Commentsupporting

confidence: 93%

Major Depression and Coronary Artery Disease in the Swedish Twin Registry

Kendler

Gardner²,

Fiske³

et al. 2009

Arch Gen Psychiatry

127

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“…Previous twin studies have found that coronary heart disease deaths, myocardial infarction and angina pectoris have a substantial hereditary component 22 23. Most recently, advances in bioinformatics and high-throughput genomic technology have facilitated the completion of several genome-wide association studies (GWAS) to search for susceptibility genes for CAD 24.…”

Section: Discussionmentioning

confidence: 99%

Measurement of heritability of myocardial blood flow by positron emission tomography: the Twins Heart Study

Votaw

Faber

et al. 2012

Heart

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Objective To estimate the heritability of myocardial blood flow (MBF) and coronary flow reserve (CFR) measured with positron emission tomography (PET). Design Cross-sectional twin study. Setting General clinical research centre of a university hospital at Atlanta, USA. Patients A sample of 180 middle-aged (mean±SD 55±2.9 years) male twins, including 107 monozygotic and 73 dizygotic twins. Main outcome measures All twins underwent imaging of MBF with PET 13NH3 at rest and after adenosine stress during a single imaging session. Structural equation modelling was used to estimate the heritability of MBF at rest and during adenosine stress, as well as of CFR. Results The basal MBF (mean±SD) was 0.69±0.20 ml/min/g, and the MBF during adenosine stress was 1.70±0.49 ml/min/g; the CFR was 2.62±0.99. There was substantial heritability for MBF both at rest (0.48, 95% CI 0.29 to 0.64) and during adenosine stress (0.51, 95% CI 0.29 to 0.68), as well as CFR (0.48, 95% CI 0.26 to 0.65). Conclusions For the first time, a substantial genetic contribution to the interindividual variation in MBF and CFR measured with PET in middle-aged men has been demonstrated. The data suggest that a fruitful direction for future work would be the identification of genetic variants for early atherosclerotic stages assessed by PET imaging.

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“…Estimates of mean monozygotic twin discordance rates from the literature and the TwinsUK cohort for a series of common diseases, such as colon cancer and breast cancer [32], rheumatoid arthritis (RA) [33,34], osteoarthritis (OA) [35], psoriasis [36], cardiovascular disease (CVD) and myocardial infarction (MI) [37], type 1 diabetes [38,39], type 2 diabetes [38,40], autism and autism spectrum disorders (ASD) [41-44], and schizophrenia [45]. …”

Section: Disease-discordant Twin Ewasmentioning

confidence: 99%