Journal of Womens Health, Issues and Care ISSN: 2325-9795

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Case Report, J Womens Health Issues Care Vol: 3 Issue: 3

Extensive Coronary Disease in a 24 year Old Woman without Traditional Risk Factors Presenting as Cardiac Arrest

Vikram Agarwal1, Neel Chokshi2, Jincy Thankachen1, Eyal Herzog1and Jacqueline Tamis-Holland1
1Department of Medicine, Division of Cardiology, St. Luke’s-Roosevelt Hospital Center, Mount Sinai Health Systems, New York, New York, USA
2Department of Medicine, Penn Heart and Vascular Center, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA
Corresponding author : Vikram Agarwal, MD
MPH, St Luke’s-Roosevelt Hospital Center, Mount Sinai Health Systems, Division of Cardiology, 1111 Amsterdam Avenue, New York, NY 10025, USA
E-mail: [email protected]
Received: January 21, 2014 Accepted: May 23, 2014 Published: May 26, 2014
Citation: Agarwal V, Chokshi N, Fovino LN, Herzog E, Holland JT (2014) Extensive Coronary Disease in a 24 year Old Woman without Traditional Risk Factors Presenting as Cardiac Arrest. J Womens Health, Issues Care 3:3. doi:10.4172/2325-9795.1000144

Abstract

Extensive Coronary Disease in a 24 year Old Woman without Traditional Risk Factors Presenting as Cardiac Arrest

We report a case of a 24-year-old woman without traditional coronary artery disease risk factors, presenting with cardiac arrest due to extensive coronary atherosclerosis. The patient had been admitted to an outside hospital several months earlier with chest pain, and elevated cardiac enzymes, and was diagnosed with “pericarditis”.

Keywords: Cardiac; Ischemia, Coronary disease; Woman; Risk

Keywords

Cardiac; Ischemia, Coronary disease; Woman; Risk

Introduction

A 24-year-old Caucasian female was brought to the emergency department (ED) by emergency medical service (EMS) following a ventricular fibrillation cardiac arrest.
On the day of presentation, the patient had complained of intermittent chest pain radiating to the neck and arm. Several hours after the onset of pain, the patient’s roommate heard her fall, and subsequently found her non-responsive and pulseless. She performed basic cardio-pulmonary-resuscitation until EMS arrived 5 minutes later.
On evaluation by EMS, the patient was noted to be in ventricular fibrillation. She underwent defibrillation with restoration of sinus rhythm and was intubated for airway protection. A 12 lead electrocardiogram (ECG) showed ST-elevation in the lateral leads with reciprocal ST-depression in the anterior and inferior leads (Figure 1). In the ED, the patient was unresponsive with abnormal flexion to painful stimuli and a Glasgow coma scale score of 5. On physical examination the patient was noted to be lean and athletic (BMI – 22.7 kg/m2). The rest of physical exam was otherwise unremarkable. Emergency coronary angiography revealed extensive and severe coronary atherosclerosis with a 60% stenosis of the mid Left Anterior Descending artery, a total occlusion of the first Diagonal branch, a 95% lesion of a large Ramus, a total occlusion of the proximal Left Circumflex artery with faint filling of the distal vessels by collaterals and a 70% stenosis of the Right Posterior Descending artery (Figure 2). Ventriculography revealed severe hypokinesis of the antero-lateral and infero-lateral basal segments, and apical akinesis, with an ejection fraction (EF) of 35%. A cutting balloon angioplasty of the Diagonal vessel was performed with restoration of TIMI 3 flow (Figure 3). A hypothermia cooling catheter was placed in the femoral vein and therapeutic hypothermia was initiated.
Figure 1: Initial electrocardiogram after the electrical cardio version of the ventricular fibrillation in the field.
Figure 2: Right anterior oblique cranial view of the left coronary system showing severe ostial stenosis of the ramus as well complete occlusion of the first diagonal vessel.
Figure 3: Right anterior oblique cranial view post balloon angioplasty of the first diagonal vessel.
Her past medical history was notable for a hospitalization with chest pain 5 months earlier. Evaluation at that admission reportedly showed non specific ST-segment changes on ECG, mildly elevated troponins, and normal wall motion on echocardiography. She was diagnosed with ‘pericarditis’ and treated with non steroidal antiinflammatory agents with relief of her symptoms; she did not receive any further intervention. There was no other significant past medical or surgical history or childhood illnesses. The patient had been taking oral contraception for one year. She occasionally consumed alcohol, with no history of tobacco or recreational drug use. There was no family history of premature coronary artery disease. Prior to admission the patient was noted to have good exercise capacity.
The patient had a peak serum troponin I level of 10.1 ng/mL, with a peak serum creatine kinase of 1286 IU/L with CK-MB index of 9.1. Cholesterol profile showed total cholesterol of 139 mg/dL, HDL of 49 mg/dL, LDL (calculated) of 25 mg/dL, and triglycerides of 282 mg/ dL. Her lipid profile at the previous and index admissions have been described in Table 1. Her hemoglobin A1C at admission was noted to be 5.3%. In light of the patient’s extensive CAD, she underwent further testing for possible etiologies of premature atherosclerosis. An auto-antibody screen revealed the presence of a high titer (1:320) of antinuclear antibodies (ANA) with a homogeneous pattern. Subsequent measurement of ANA subtypes, including, anti-double strand DNA antibodies, anti-Ro, anti-La, and anti-Smith antibodies were unremarkable. Serum complement levels were within normal range. A hypercoagulability work up showed normal protein C levels with slightly low serum protein S (38%); patient was negative for the factor II prothrombin gene mutation, and for activated protein C resistance (i.e. factor V Leiden), with Russell viper’s venom test being negative for lupus anticoagulant antibody. In addition the serum homocysteine was within normal range. The normal iron studies confirmed the absence of hemochromatosis. Additional laboratory testing including a basic metabolic panel, liver function panel, full coagulation profile, thyroid panel, and urine toxicology screen were all unrevealing. The admission transthoracic echo demonstrated a diffusely hypokinetic ventricle with an EF of 15%. A repeat echo two days post intervention showed an EF of 40% with severe hypokinesis of the lateral, infero-lateral, and inferior walls
Table 1: Lipid profiles at baseline and index admission.
Following therapeutic hypothermia the patient became increasingly more alert and conversive and had movement of all her extremities. Her neurological status conversive, to improve and she was discharged home on post infarction day 10, with aggressive medical management and plans for future elective intervention as an outpatient.

Discussion

To our knowledge, this is the youngest case of a pre-menopausal woman presenting with cardiac arrest from extensive coronary atherosclerosis (CAD) and acute myocardial infarction (MI) in the absence of traditional (or even unusual) cardiac risk factors. The incidence of acute MI from CAD in young women is uncommon although the prognosis remains worse than young men with acute MI [1]. In the GUSTO trial, only 16 of 10,286 enrolled female patients (0.16%) were less than 30 years old. 11 of these 16 patients were referred for coronary angiography, of which 8 of these 11 had significant CAD. (Personal communication, Christopher Granger, MD).
The majority of cases of premature CAD noted in female patients have been associated with traditional cardiac risk factors, metabolic syndrome or secondary causes [1-3]. Lawesson, et al. demonstrated that almost 80% of young females with acute MI had at least one CAD risk factor [2]. While Turhan, et al. reported that 73% of women with premature CAD were found to have the metabolic syndrome [3]. Acute MI in a young individual should therefore prompt evaluation for disease entities that may predispose these patients to premature atherosclerosis, a hypercoaguable state or coronary vasospasm. The differential diagnosis includes vasculitis, familial dyslipidemias, embolic disease or a hypercoagulable state. Other than the nonspecific elevation of ANA titers, the initial evaluation for these entities in our patient failed to show evidence for any of these conditions. In addition, in our patient, it is likely that the patient’s previous admission was a manifestation of her extensive CAD. This illustrates the importance of recognizing the potential for true atherosclerotic disease in patients with a serious cardiac presentation irrespective of the patient’s age, cardiac risk factors, or sex.

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