
Hariom Tyagi
Lokpriya Hospital,
India
Abstract Title: Near simultaneous presentation of coronary artery disease in identical twins
Biography:
Dr. Hariom Tyagi has completed his MD (MEDICINE) (2001-2004) from GSVM Medical College, CSJM University, Kanpur, Uttar Pradesh, India and DM (CARDIOLOGY) (2010-2013) Rabindranath Tagore Medical College, Udaipur, University of Health Sciences, Rajasthan, India. I have 18+ year’s experienced as a Senior Interventional Cardiologist. I have routinely been performing complex angioplasties including, primary PCI, left main bifurcation, graft PCI, and CTO. Along with it, he has experience of performing more than 5000 Coronary angiography above 1000 Coronary angioplasties, Competent in IVUS and FFR for routine PCIs, more than 100 permanent pacemaker implemented [including dual chamber pacemakers, ICD,CRT], more than 100 Valvuloplasties, more than 30 ASD device and PDA (device and coil) closure and numerous peripheral angioplasties.
Research Interest:
Background: Cardiovascular diseases, in particular coronary artery disease (CAD), remain the leading cause of morbidity and mortality in the world. The development of coronary artery disease having a strong genetic component. In our presentation, there is a pair of monozygotic identical twins presenting near simultaneously with coronary heart disease and identical atherosclerotic lesions. To date there are only 10 cases series of CAD in identical twins.
Methods:
Case-I: A 70 years old male presented here with C/O heaviness in chest, sweating, associated with generalized weakness since 1 day prior to admission. At the time of admission, ECG revealed Q-wave & ST-T changes in inferolateral leads and ECHO suggestive of Adequate LV systolic function, LVEF=55%, Mild MR. Patient was diagnosed as a case of CAD/ACS/ACUTE IWMI (LP).
Case-II: A 70 years old male presented here with C/O angina on exertion, dyspnea on exertion, uneasiness, associated with generalized weakness since 10-15 day prior to admission. At the time of admission, ECG revealed Non specific changes and ECHO suggestive of Adequate LV systolic function, LVEF=55%, Mild MR. H/o TMT +ve. Patient was diagnosed as a case of CAD/AOE-II/DOE-II/TMT+ve.
Results: Case-I: The patient was taken for CAG which revealed LAD: Type III vessel, mid 40-50% disease, LCX: Co-dominant, ostioproximal minimal disease, OM2: Proximal 80-90% disease, L-PDA: 90% disease, RCA: Co-dominant, mid 100% occlusion. In same sitting taken for PTCA to RCA (culprit vessel) by Radial route & in second sitting, PTCA to OM done. Post PTCA period was uneventful & discharged in satisfactory condition. Case-II: The patient was taken for CAG which revealed LAD: Type III vessel, proximal 40-50% disease, distal 70% disease, LCX: Co-dominant, proximal 40-50% disease, mid 50-60% disease, OM1: Ostioproximal 90% disease, L-PDA: Proximal 80% disease, RCA: Co-dominant, proximal to mid 60-70% disease, distal 90% calcified. Patient was taken for PTCA to RCA by Radial route. Post PTCA period was uneventful & discharged in satisfactory condition.
Conclusion: The genetics of CAD are complex and while some Mendelian disorders contribute of CAD, most manifestations result from a multifactorial interplay between genetic factors. Similarities between the twins are fascinating, near simultaneous onset, and similar coronary lesions. There is the suggested predominance of genetic risk factors. This risk is about 20 time higher that of representative individual of the general public. The result of this study shows that the genetic effect is greatest other then environmental factors. The other features observed have also been reported and a high index of suspicion of CAD should exist even in asymptomatic twins if a coronary event has occurred in the other.