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Delayed Coronary Vasospasm in a Patient with Metastatic Gastric Cancer Receiving FOLFOX Therapy

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Delayed Coronary Vasospasm in a Patient with Metastatic Gastric Cancer Receiving FOLFOX Therapy Delayed Coronary Vasospasm in a Patient with Metastatic Gastric Cancer Receiving FOLFOX Therapy Christopher James Little, MD; Bao Sean Nguyen, MD; and Pamela J. Tsing, MD A 40-year-old man with stage IV gastric adenocarcinoma was found to have coronary artery vasospasm in the setting of recent 5-fluorouracil administration. Christopher Little is a oronary artery vasospasm is a rare to demonstrate this.4,5 The pathophysiology of Resident Physician in Anesthesiology and Bao but well-known adverse effect of 5- 5-FU-induced cardiotoxicity is unknown, but Nguyen is a Resident Phy- Cfluorouracil (5-FU) that can be life threat- adverse effects on cardiac microvasculature, sician in Internal Medicine, ening if unrecognized. Patients typically pres- myocyte metabolism, platelet aggregation, both at UCLA Medical Center in Los Angeles, ent with anginal chest pain and ST elevations and coronary vasoconstriction have all been California. Pamela Tsing on electrocardiogram (ECG) without athero- proposed.3,6 is a Hospitalist Physician at the VA Greater Los An- sclerotic disease on coronary angiography. In the current case, we present a patient geles Healthcare System This phenomenon typically occurs during or with stage IV gastric adenocarcinoma who in California, and Assistant Clinical Professor at the shortly after infusion and resolves within hours complained of chest pain during hospitalization David Geffen School of to days after cessation of 5-FU. and was found to have coronary artery vaso- Medicine at UCLA. In this report, we present an unusual case of spasm in the setting of recent 5-FU adminis- Correspondence: Pamela Tsing coronary artery vasospasm that intermittently re- tration. Following coronary angiography that ([email protected]) curred for 25 days following 5-FU treatment in a showed a lack of atherosclerotic disease, the Fed Pract. 2021;38 (suppl 2). 40-year-old male with stage IV gastric adenocar- patient continued to experience episodes of Published online May 13. cinoma. We also review the literature on typical chest pain with ST elevations on ECG that re- doi:10.12788/fp.0123 presentation and risk factors for 5-FU-induced curred despite cessation of 5-FU and repeated coronary vasospasm, findings on coronary angi- administration of vasodilatory medications. ography, and management options. 5-FU is an IV administered antimetabolite CASE PRESENTATION chemotherapy commonly used to treat solid A male aged 40 years was admitted to the tumors, including gastrointestinal, pancreatic, hospital for abdominal pain, with initial imag- breast, and head and neck tumors. 5-FU in- ing concerning for partial small bowel obstruc- hibits thymidylate synthase, which reduces tion. His history included recently diagnosed levels of thymidine, a key pyrimidine nucleo- stage IV gastric adenocarcinoma complicated side required for DNA replication within tumor by peritoneal carcinomatosis status post initi- cells.1 For several decades, 5-FU has re- ation of infusional FOLFOX-4 (5-FU, leucovo- mained one of the first-line drugs for colorec- rin, and oxaliplatin) 11 days prior. The patient tal cancer because it may be curative. It is the was treated for small bowel obstruction. How- third most commonly used chemotherapy in ever, several days after admission, he de- the world and is included on the World Health veloped nonpleuritic, substernal chest pain Organization’s list of essential medicines.2 unrelated to exertion and unrelieved by rest. Cardiotoxicity occurs in 1.2 to 18% of pa- The patient reported no known risk factors, tients who receive 5-FU therapy.3 Although family history, or personal history of coronary there is variability in presentation for acute artery disease. Baseline echocardiography cardiotoxicity from 5-FU, including sudden and ECG performed several months prior death, angina pectoris, myocardial infarction, showed normal left ventricular function with- and ventricular arrhythmias, the mechanism out ischemic findings. most commonly implicated is coronary artery Physical examination at the time of chest vasospasm.3 The direct observation of active pain revealed a heart rate of 140 beats/min. coronary artery vasospasm during left heart The remainder of his vital signs were within catheterization is rare due its transient nature; normal range. There were no murmurs, rubs, however, several case studies have managed gallops, or additional heart sounds heard on S76 • FEDERAL PRACTITIONER SPECIAL ISSUE • MAY 2021 FIGURE 1 Electrocardiogram Obtained During Patient’s Initial Chest Pain Episode ST elevations can be seen in leads II, III, aVF, V4, V5, and V6, and reciprocal depressions in leads I and aVL. cardiac auscultation. Chest pain was not re- Treatment producible to palpation or positional in nature. Following catheterization, the patient returned An ECG demonstrated dynamic inferolateral to the medical intensive care unit, where he ST elevations with reciprocal changes in leads continued to report intermittent episodes of I and aVL (Figure 1). A bedside echocardio- chest pain with ST elevations. In the following gram showed hypokinesis of the septal wall. days, he was started on isosorbide mononi- Troponin-I returned below the detectable level. trate 150 mg daily and amlodipine 10 mg daily. The patient was taken for emergent coronary Although these vasodilatory agents reduced the catheterization, which demonstrated patent epi- frequency of his chest pain episodes, intermit- cardial coronary arteries without atherosclerosis, tent chest pain associated with ST elevations on a left ventricular ejection fraction of 60%, and a ECG continued even with maximal doses of iso- right dominant heart (Figures 2 and 3). Ventricu- sorbide mononitrate and amlodipine. Adminis- logram showed normal wall motion. Repeat tro- tration of sublingual nitroglycerin during chest ponin-I several hours after catheterization was pain episodes effectively relieved his chest pain. again below detectable levels. Given the severity and frequency of the patient’s Given the patient’s acute onset of chest pain chest pain, the oncology consult team recom- and inferolateral ST elevations seen on ECG, mended foregoing further chemotherapeutic the working diagnosis prior to coronary cath- treatment with 5-FU. erization was acute coronary syndrome. The differential diagnosis included other causes of Outcome life-threatening chest pain, including pulmo- Despite holding 5-FU throughout the patient’s nary embolism, pneumonia, aortic dissection, hospitalization and treating the patient with an- myopericarditis, pericardial effusion, cardiac tianginal mediations, frequent chest pain epi- tamponade, or coronary artery vasospasm. sodes associated with ST elevations continued Computed tomography (CT) angiography of to recur until 25 days after his last treatment with the chest was not consistent with pulmonary 5-FU (Figure 4). The patient eventually expired embolism or other acute cardiopulmonary pro- during this hospital stay due to cancer-related cess. Based on findings from coronary angiog- complications. raphy and recent exposure to 5-FU, as well as resolution followed by recurrence of chest pain DISCUSSION and ECG changes over weeks, the most likely Coronary artery vasospasm is a well-known diagnosis after coronary catheterization was complication of 5-FU that can be life threatening coronary artery vasospasm. if unrecognized.6-8 As seen in our case, patients MAY 2021 • FEDERAL PRACTITIONER SPECIAL ISSUE • S77 FOLFOX Therapy FIGURE 2 Left Coronary Artery System fusional administration of 5-FU is thought to be associated with a higher rate of cardiotoxicity and a higher tumor response rate.9 Most cases of coronary vasospasm occur either during infusion of 5-FU or within hours to days after completion. The median time of presentation for 5-FU-induced coronary ar- tery vasospasm is about 12 hours postinfusion, while the most delayed presentation reported in the literature is 72 hours postinfusion.6,8 De- layed presentation of vasospasm may result from the release of potent vasoactive metabo- lites of 5-FU that accumulate over time; there- fore, infusional administration may accentuate this effect.6,9 Remarkably, our patient’s chest pain episodes persisted for 25 days despite treatment with anti-anginal medications, high- Patent left anterior descending and left cir- lighting the extent to which infusional 5-FU can cumflex arteries. produce a delay in adverse cardiotoxic effects FIGURE 3 Right Coronary Artery System and the importance of ongoing clinical vigilance after 5-FU exposure. Vasospasm alone does not completely ex- plain the spectrum of cardiac toxicity attributed to 5-FU administration. As in our case, coronary angiography during symptomatic episodes often fails to demonstrate coronary vasospasm.8 Ad- ditionally, ergonovine, an alkaloid agent used to assess coronary vasomotor function, failed to induce coronary vasospasm in some patients with suspected 5-FU-induced cardiac toxicity.10 The lack of vasospasm in some patients with 5-FU-induced cardiac toxicity suggests multiple independent effects of 5-FU on cardiac tissue that are poorly understood. In the absence of obvious macrovascular ef- fects, there also may be a deleterious effect of 5-FU on the coronary microvasculature that may Patent right coronary artery, posterior descend- result in coronary artery vasospasm. Though cor- ing artery, and posterolateral extension. onary microvasculature cannot be directly visu- alized, observation of slowed coronary blood typically present with anginal chest pain relieved
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