CORONARY EMBOLISM: A CAUSE OF NON-ST-ELEVATION MYOCARDIAL INFARCTION
more commonly a coronary thrombus with bystander coronary atherosclerosis 1. If a coronary thrombus is identified, aspiration thrombectomy should be considered to reduce cardiovascular mortality and to identify the thrombus’s origin 4,8 . After managing the acute presentation, one’s attention should focus on determining the etiology of the embolic material. Utilization of transthoracic or esophageal echocardiogram is essential in evaluating causes such as atrial and ventricular thrombus, valvular abnormalities, and anatomic defects 5, 8. Thrombophilia evaluation can be considered outpatient if it will change management; however, inpatient evaluation is often flawed 1,8 . SUMMARY: This case highlights the importance of recognizing non- atherosclerotic causes of non-ST-segment elevation myocardial infarctions. It is important to understand the broad differential of type 2 myocardial infarctions and the predisposing factors that can lead to coronary embolism. The combination of oral contraceptives used to treat dysmenorrhea, in addition to the incidentally noted papillary fibroelastoma, are the most plausible etiologies of the patient’s presentation. Though intravascular ultrasound or optical coherence tomography was not used, in the setting of no traditional risk factors, a lack of antecedent angina or anginal equivalents, and angiographically normal coronary arteries it is most plausible that coronary embolism, rather than a primary plaque rupture event, was responsible for the patient’s presentation. CITATIONS: 1. Al-Taweel O, Sami F, Pinsky S, Wineinger T, Berbarie RF. Coronary Embolism Presenting as NSTEMI in a Patient with Splenectomy. Kans J Med. 2021 Apr 19;14:111-113. doi: 10.17161/ kjm.vol1414823. PMID: 33903812; PMCID: PMC8060067. 2. Busti, A. J. (2015, October 1). The Mechanism of Oral Contraceptive (Birth Control Pill) Induced Clot or Thrombus Formation (DVT, VTE, PE) . Evidence Based Medicine Consult. Retrieved November 11, 2022, from https://www.ebmconsult. com/articles/oral-contraceptive-clotting-factors-thrombosis- dvt-pe 3. De Lemos, J. A., Newby, L. K., & Mills, N. L. (2019, September 6). A Proposal for Modest Revision of the Definition of Type 1 and Type 2 Myocardial Infarction . Circulation. Retrieved November 11, 2022, from https://www.ahajournals.org/doi/full/10.1161/ CIRCULATIONAHA.119.042157 4. Jolly SS, James S, Džavík V, Cairns JA, Mahmoud KD, Zijlstra F, Yusuf S, Olivecrona GK, Renlund H, Gao P, Lagerqvist B, Alazzoni A, Kedev S, Stankovic G, Meeks B, Frøbert O. Thrombus
demonstrated no wall motion abnormalities or pathologic findings. The patient was initiated on dual antiplatelet therapy and started on a heparin infusion. She was subsequently taken to the cardiac catheterization lab. A coronary angiogram demonstrated no coronary artery disease but identified a filling defect in the posterolateral branch of the right coronary artery. The finding was felt to be most consistent with a coronary artery embolism rather than distal embolization of a primary plaque rupture event. Given the patient’s lack of traditional coronary artery disease risk factors, antecedent angina before presentation, family history of premature coronary artery disease, and in the setting of suspected coronary artery embolism on coronary angiogram, a transesophageal echocardiogram was performed to evaluate for predisposing pathologic risk factors. Transesophageal echocardiogram with bubble study demonstrated a mobile echo density on the A2 segment of the mitral valve consistent with potential papillary fibroelastoma. No left atrial appendage thrombus, left ventricular thrombus, or patent foramen ovale were identified. The patient was discharged with standard medical therapy in the setting of a non-ST-segment elevation myocardial infarction and was in good health at the time of outpatient follow-up. DISCUSSION The most common etiology of a non-ST-segment elevation myocardial infarction is a type 1 NSTEMI which results from an atherosclerotic plaque rupture event followed by coronary thrombus formation causing subtotal occlusion and subendocardial ischemia. In the absence of angiographically demonstrated coronary artery disease one’s differential should expand to include causes of type 2 myocardial infarctions. The etiologies of type 2 myocardial infarctions can be divided into primary coronary or secondary causes from acute related illnesses 5. Coronary embolism, an infrequent cause of type 2 myocardial infarction, is responsible for approximately three percent of acute coronary syndrome events according to a retrospective analysis by Shibata et al. Though relatively protected by the acute angle take-off, the coronary arteries remain vulnerable to embolic insults. Understanding the causes of these embolic events can be directly related to Virchow’s triad and anatomic predispositions. Examples of predisposing factors include malignancy, hormonal therapy-induced hypercoagulability, endothelial injury following angioplasty, and stasis of normal flow because of atrial fibrillation or aneurysmal dilation of the left ventricle. Additionally, classic anatomic predispositions include an atrial septal defect and a patent foramen ovale 8 . The initial presentation of coronary embolism is difficult to distinguish from an acute coronary syndrome event secondary to type 1 physiology and is often managed similarly. It is distinguished by coronary angiogram which may demonstrate a heavy thrombus burden without coronary artery disease, or
OMAR LEONARDS, MD, XAVIER DIAZ-HERNANDEZ, MD AND SHAHRUKH KHAN, MS-3
INTRODUCTION Acute myocardial infarctions are a known cause of morbidity and mortality worldwide. The most common acute form is a type 1 myocardial infarction related to atherosclerotic plaque rupture and thrombus formation 1,7 . Though rare, a cause of type 2 myocardial infarction, defined as a supply-demand mismatch of myocardial oxygenation, is a coronary artery embolism, which may be responsible for up to three percent of acute coronary syndrome events 3,5,9 . The most common causes of coronary embolism are atrial fibrillation, prosthetic valve thrombi, infective endocarditis, and iatrogenic causes 5,9 . This manuscript will highlight hypercoagulable states and benign cardiac tumors as a cause of acute coronary syndrome in a patient without typical risk factors. CASE REPORT In July of 2022 a 47-year female with class I obesity, depression, and dysmenorrhea being treated with oral contraceptives, presented with a chief complaint of acute onset bilateral arm pain with associated diaphoresis and nausea while leisurely walking. She denied symptoms of gastroesophageal reflux, emesis, new skin changes, hemoptysis or pleuritic chest pain, dyspnea, recent illnesses such as viral infections, or a family history of premature atherosclerotic coronary artery disease or myocardial infarction. She participated in aerobic and resistance training daily without angina or anginal equivalents.
On initial presentation, the patient’s vital signs were a temperature of 36.1º Celsius, a heart rate of 72 beats per minute, a blood pressure of 107/71, a respiratory rate of 16, and a weight of 90 kilograms. The patient’s physical examination was unremarkable for any pertinent findings. Laboratory evaluation was remarkable for stable iron deficiency anemia, marginal thrombocytosis, brain natriuretic peptide of 9, high sensitivity troponin of 44 that peaked at 10,830 twelve hours after presentation, and a negative urine drug screen. Serial electrocardiograms were performed and demonstrated normal sinus rhythm without ST-T wave abnormalities. A chest radiograph performed at the time of presentation did not demonstrate pulmonary edema or widening of the mediastinum. Point of care ultrasound obtained at the time of consultation and formal transthoracic echocardiogram
FIGURE 1. ECG DEMONSTRATING NORMAL SINUS RHYTHM.
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J LA MED SOC | VOL 175 | SUMMER 2023
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