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No relation between coronary artery disease or electrocardiographic markers of disease in middle age and prenatal exposure to the Dutch famine of 1944–5
  1. L H Lumey1,
  2. Lauren H Martini1,
  3. Merle Myerson1,2,
  4. Aryeh D Stein3,
  5. Ronald J Prineas4
  1. 1Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA
  2. 2Cardiovascular Disease Prevention program, St Luke's-Roosevelt Hospital Center, Columbia University, New York, New York, USA
  3. 3Hubert Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, Georgia, USA
  4. 4Division of Public Health Sciences, Wake Forest University School of Medicine, Winston Salem, North Carolina, USA
  1. Correspondence to Dr L H Lumey, Department of Epidemiology, Mailman School of Public Health, Columbia University, 722 West 168th Street, New York, NY 10032, USA; lumey{at}columbia.edu

Abstract

Objective and Setting Associations between prenatal famine and coronary artery disease (CAD) have been examined before with inconsistent results. For further evaluation, we examined multiple cardiac risk markers in adult men and women with prenatal exposure to the Dutch famine of 1944–5.

Design Birth cohort study of 407 men and women with prenatal famine exposure, 344 born before or after the famine as time controls, and 324 unexposed siblings as family controls. Study subjects underwent standardised interviews and clinical examinations at age approximately 58 years.

Outcome Measures CAD events from medical history and medical and electrocardiographic (ECG) markers of CAD risk, including 10-year (Framingham) estimates for myocardial infarction and coronary heart disease death, major and minor ECG abnormalities, ECG estimates of left ventricular hypertrophy and left ventricular mass, cardiac autonomic neuropathy measures including the QT index, resting heart rate, heart rate variability from subsequent N–N intervals, and ECG markers of minor T-wave abnormalities, changes in QRS/T frontal plane angle and ST-segment.

Results No increase was seen in CAD risk (HR 1.17; 95% CI 0.73 to 1.88), Framingham risk (OR 1.14; 95% CI 0.90 to 1.44) or in ECG outcomes, adjusting for age and sex. Left ventricular mass estimated with body size was elevated by 3.78 g (95% CI 0.91 to 6.64) after prenatal famine, but showed a 0.65 g decrease (95% CI −2.63 to 1.34) when adjusted for body mass index.

Conclusions We see no relation between prenatal famine and adult CAD, Framingham risk, or any ECG predictors of increased cardiac disease risk.

  • Allied specialities
  • arrhythmias
  • atrial fibrillation
  • cardiac autonomic nervous system
  • cohort study
  • coronary artery disease
  • DOHaD
  • electrocardiography
  • epidemiology
  • Framingham CHD risk score
  • imaging and diagnostics
  • prenatal exposure delayed effects
  • prenatal nutrition
  • psychology/psychiatry
  • public health
  • quality of care and outcomes
  • risk factors
  • sick sinus syndrome
  • subclinical ECG abnormalities
  • sudden adult death syndrome

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Footnotes

  • Funding Funding was provided by the US National Institutes of Health (R01 HL-067914).

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval Ethics approval was provided by Columbia University (USA) and Leiden University (Netherlands) review boards.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement Enquiries are welcome for collaborations on future analyses.

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