Heavener T. A,B,D,E,F, Jepson M.A,B,D,E,F, Bushe B.A,B,D,E,F, Thotakura S.B,C,E,F, Chiles ChA,B,D,E,F
Scott & White Medical Center, Temple, TX, United States
A- Conception and study design; B - Collection of data; C - Data analysis; D - Writing the paper;
E- Review article; F - Approval of the final version of the article; G - Other
An ST-segment elevation myocardial infarction represents a time-sensitive cardiac pathology with utmost importance placed upon timely coronary angiography with percutaneous coronary intervention. While emphasis is placed on atherosclerotic or thrombotic coronary occlusion, it is important to recognize other etiologies which may present in a similar fashion. This case demonstrates a 71-year-old female patient with prior coronary artery disease and stenting who presented with acute abdominal pain and elevated cardiac biomarkers as well as ST-segment elevation on initial EKG. Coronary angiography revealed only mild to moderate coronary lesions and patent stents while echocardiography was essential unchanged from prior evaluation. Computed tomography of the abdomen would show findings suggestive of infectious colitis and empiric antibiotics led to full resolution of symptoms. While no definitive cause for her cardiac manifestations was discovered, the authors propose coronary vasospasm or myo-pericarditis as likely etiologies in response to an overwhelming inflammatory state. The case underscores the importance of formulating a comprehensive differential diagnosis during the initial workup of a ST-segment elevation myocardial infarction.
Keywords: colitis, myocarditis, ST segment elevation, coronary vasospasm
Trace Heavener, D.O.
Scott & White Medical Center
2401 S. 31st St.
Temple, TX 76508
Progress in Health Sciences
Vol. 8(1) 2018 pp 226-231
© Medical University of Białystok, Poland
Myocardial ischemia is a mismatch between the oxygen demands of cardiac cells and the oxygen availability. If oxygen demand outstrips supply, the cardiac myocytes experience injury, called myocardial infarction (MI); this commonly manifests as the release of intracellular cardiac enzymes such as troponin. If the supply-demand mismatch is severe enough to cause transmural insult, ST segment elevation may be seen on electrocardiogram (ECG). Prompt diagnosis and treatment for ST-segment myocardial infarction (STEMI) is vital to the preservation of cardiac function. However, there are several known processes, other than MI, coronary atherosclerosis, or acute coronary thrombus, which may cause a presentation consistent with STEMI. These include, but are not limited to, coronary aneurysm , pericarditis , myocarditis , aortic dissection , subarachnoid hemorrhage , pneumonia , chronic obstructive lung disease , cholecystitis , and peritonitis. [7, 9] Furthermore, there are case reports on the correlations between ST segment elevation and ischemic colitis , as well as ST segment elevation and inflammatory (Inflammatory Bowel Disease) colitis.  In our review of the literature, we were unable to find any case reports of acute infectious colitis leading to a STEMI presentation.
We present the case of a 71-year-old female who presented for right upper quadrant abdominal pain, nausea and non-bloody non-bilious emesis. The patient had a medical history significant for coronary artery disease requiring prior drug eluding stent placement over ten years prior, uncontrolled type 2 diabetes mellitus, and heart failure with preserved ejection fraction. She had never smoked and had no known family history of MI. She also noted feeling anxious, short of breath, and had bilateral shoulder pain that was worse on the left.
In the emergency department, her vital signs were within normal limits. ECG revealed ST elevation in leads II, III and aVF, with a troponin level of 0.01 upon presentation (Fig. 1). Given the presentation, consistent with STEMI, she had emergent coronary angiography performed which revealed mild to moderate diffuse coronary disease with patent LAD stents (Fig. 2). An echocardiogram showed normal left ventricular systolic function with an ejection fraction of 50-55%, with no regional wall motion abnormalities, no valvular abnormalities, and no pericardial effusion. Subsequent laboratory work revealed cardiac troponin elevated up to 17.09 at six hours after admission and peaking at 27.44 at hour 14.
The following day she continued to have persistent abdominal pain and developed several loose non-bloody stools. Although a stool polymerase chain reaction test was negative for common diarrheal pathogens, an abdominal and pelvic computer tomography was obtained that showed diffuse inflammatory stranding and wall thickening involving the descending and sigmoid colon concerning for infectious, ischemic, or inflammatory colitis (Fig. 3).