J INVASIVE CARDIOL 2017;29(7):E86-E87.
Key words: cardiac imaging, coronary atherogenesis, genetics
A 45-year-old woman (twin #1) was admitted to our hospital with 24-hour history of atypical chest pain, but a stress test evidenced cardiac ischemia. Coronary angiography disclosed a proximal obtuse marginal I (OMI) stenosis >80% (Figures 1A and 1B; Video 1), and a drug-eluting stent was successfully implanted (Figure 1C). Remarkably, only 1 week later, her identical twin sister (twin #2) presented with repeated episodes of precordial pain at rest, negative T-waves on electrocardiography, yet normal cardiac enzyme levels. Interestingly, not only did angiography reveal a coronary arterial network almost similar to twin #1, but also a nearly identical OMI stenotic lesion >85%, which was stented as well (Figures 1D-1F; Video 2). Both patients were discharged home in excellent clinical condition and remain asymptomatic to date.
The twins were both housewives, and shared common environmental influences, lifestyles, and dietary habits since their childhood. Twin #1 was hypertensive (poorly adherent with medication), while twin #2 was a heavier smoker (34 pack-years vs 21 pack-years, respectively). Notably, their father died suddenly at age 56.
In the recent era, the clinical impact of habitual dietary and pharmaceutical parameters on coronary artery atherogenic micromilieu has been overemphasized; however, the role of genetics on coronary atherogenesis is emerging and yet to be determined.1 In this respect, observations on monozygotic twins could be of major interest, by examining the impact of identical heredity over environmental parameters on coronary artery disease phenotype.
Cardiac manifestations and angiographic characteristics of coronary artery disease in identical twins have been previously dealt with in a handful of case reports and series; yet, the results were highly controversial.2-4 Our rare case demonstrates striking similarities in both the timing and type of clinical manifestation, as well as in the underlying anatomy and the distribution of coronary artery disease. We therefore conclude that the role of genetics on the development, progression, and destabilization-vulnerability of atheromatous plaque may be dominant. In addition, genetically encoded coronary anatomy patterns may have influenced local rheological characteristics and atheromatous phenotype in our twins. Certainly, case reports are of less clinical value in advancing scientific knowledge and reviewing current therapeutic algorithms in rare diseases. However, our report provides evidence that in the event of premature coronary artery disease in one of a monozygotic twin pair, meticulous evaluation and possibly early coronary angiography may be a rational approach for the asymptomatic counterpart.
See Videos 1 and 2 here.
1. Cirino AL, Ho CY. Genetic testing for inherited heart disease. Circulation. 2013;128:e4-e8.
2. Giknis FL, Holt DE, Whiteman HW, Singh MD, Benchimol A, Dimond EG. Myocardial infarction in twenty-year-old identical twins. Am J Cardiol. 1965;16:122-126.
3. Holmes DR Jr, Kennel AJ, Smith HC, Gordon H, Moore SB. Coronary artery disease in twins. Br Heart J. 1981;45:193-197.
4. Frings A, Mayer B, Bocker W, et al. Comparative coronary anatomy in six twin pairs with coronary artery disease. Heart. 2000;83:47-50.
From the 1Department of Cardiology, General Hospital of Trikala, Thessaly, Greece; and 2Department of Critical Care, University Hospital of Larissa, Thessaly, Greece.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript accepted December 15, 2016.
Address for correspondence: John Papanikolaou, MD, Biopolis, 41110 Larissa, Thessaly, Greece. Email: email@example.com