8416 Spontaneous Coronary Artery Dissection Due to Estrogen Containing Oral Contraceptive Pills: A Case Report

Abstract Disclosure: M. Parvez: None. T. Khattak: None. A. Kavarthapu: None. K. Pulivarthi: None. Introduction: Spontaneous coronary artery dissection (SCAD) is defined by the separation of layers within the coronary artery wall, resulting in the creation of a false channel. It is a rare but significant contributor to acute coronary syndrome (ACS), especially in individuals who are young and generally healthy. The exact cause remaining uncertain. In this report, we present a case involving a young woman who had a history of using OCPs and experienced SCAD, underlining the plausible connection between hormonal birth control and this uncommon cardiovascular condition. Case Presentation: A 24-year-old female with class III obesity, hypothyroidism, and major depressive disorder presented with 12 hours of progressive substernal pain. She described the pain as tightness, severe, radiating to the right shoulder with no associated aggravating or relieving factors. The patient reported that she has been taking 1 mg norethindrone acetate and 20 mcg ethinyl estradiol for the past 1 year for an irregular menstrual cycle. She denied the use of illicit drugs. There was no family history of cardiac disease, sudden cardiac death, or genetic disorder. Upon arrival, her vital signs were as follows: blood pressure, 157/100 mmHg; heart rate 77, SpO2, 98% on room air; and body mass index, 51.96. The physical examination findings were unremarkable. EKG demonstrated nonspecific ST-T changes in the anterior and inferior leads, and echocardiography revealed an estimated LVEF of 30-35% with septum, apical lateral segment, and apex wall motion abnormalities. Labs were significant for elevated Troponin I 2.29 and ProBNP 221. Rheumatological workup results were negative. A diagnosis of NSTEMI was made and she was immediately taken for cardiac catheterization, there was 100% occlusion of proximal left anterior descending artery. IVUS of the LAD showed a mid-LAD bridge and proximal SCAD as the cause of occlusion. Otherwise, the LM and LAD were free of atherosclerosis or other diseases. A percutaneous coronary interventional device was deployed to the lesion within the proximal LAD. The stenosis was successfully reduced from 100% to 0%, and DES was placed. The pre-intervention TIMI flow was 0, and the Post-intervention TIMI flow was 3. She was initiated on goal directed medical therapy and was discharged with LifeVest. Discussion: SCAD is a rare but fatal cause of acute coronary syndrome. The incidence has been estimated at 0.1-4% of ACS cases. OCPs are known to cause thrombosis, but not SCAD. SCAD is typically observed in young or middle-aged females. Reports have shown an increased number of cases during pregnancy and the peripartum period. Our patient was taking an estrogen-containing OCPs and developed SCAD. However, the cause of SCAD in an increased estrogen state is not well understood. In conclusion, further research is needed to understand its pathophysiology and risks. Presentation: 6/3/2024