Article, Cardiology

Could contrast-enhanced CT detect STEMI prior to electrocardiogram?

Unlabelled imagecontrast-enhanced CT detect STEMI “>American Journal of Emergency Medicine 33 (2015) 128.e5-128.e7

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Case Report

Could contrast-enhanced CT detect STEMI prior to electrocardiogram??

Abstract

We present here a case in which contrast-enhanced computed tomography (CT) was the first diagnostic tool to detect myocardial hypoperfusion in a patient with atypical symptoms and normal electrocardiogram (ECG) on admission. An ST-segment elevation was detected thereafter on a second ECG realized several minutes after CT with raised troponin levels. Percutaneous coronary intervention was performed after failure of thrombolysis and confirmed occlusion of the left anterior descending artery. Further studies are needed to evaluate the role of high-resolution contrast-enhanced CT with or without coronary angiography in the workup of suspected myocardial infarction in the setting of a normal ECG.

A 79-year-old female patient presented to the emergency depart- ment (ED) at 6:50 PM complaining of severe Epigastric pain with retrosternal burning sensation. Her medical history is marked by an Essential hypertension since 20 years well controlled by candesartan 16 mg daily and furosemide 40 mg twice a day, type 2 diabetes mellitus well controlled with metformin 500 mg daily, and stage 2 chronic renal failure. Actually, she complained of 2 episodes of epigastric pain 12 hours apart. The first one took place at 7 AM in the morning at rest, persisted for several minutes, and was self-limited. The second one occurred at 6:30 PM, also at rest, several minutes after food intake with increasing intensity without any irradiation. It was associated with shortness of breath, abdominal cramping, nausea but no vomiting, and one episode of nonbloody loose stool. No other symptoms were mentioned. On initial physical examination, the patient was in pain, had a blood pressure of 150/72 mm Hg, a pulse of 110 beats/min, and capillary oxygen saturation of 98%. Cardiac examination revealed normal heart sounds with an S4 heard at the apex. Neither jugular distension nor hepatojugular reflux was detected. Pulmonary ausculta- tion revealed slightly audible crackles at the basal lung fields. The abdomen was soft with minimal epigastric tenderness but no Murphy sign, and reduced peristalsis. Rectal examination did not reveal melena or bloody stool. A mild Pitting edema was noticed in the lower extremities without any sign of deep vein thrombosis. In the ED, an electrocardiogram (ECG) performed at 7:10 PM (40 minutes after the onset of the epigastric pain) demonstrated only sinus tachycardia and left-axis deviation, without any other abnormalities (Fig. 1). The arterial blood gas on room air showed only a respiratory alkalosis (pH 7.44, pO2 77 mm Hg, pCO2 30 mm Hg, bicarbonate 22 mmol/L, Arterial oxygen saturation 94.8%). Capillary glucose level was 160 g/dL. Her creatinine

? All authors disclose no conflict of interest.

level was equal to 160 umol/L (reference range between 52 and 98 umol/ L) as well as the urea level at 10.8 mmol/L (reference range between 2.5 and 6.1 mmol/L).The pancreatic tests showed a lipase level of 322 IU (reference range between 27 and 208 IU) with normal amylase level at 80 IU (reference range between 30 and 110 IU), and normal liver function test results. The initial cardiac enzymes were normal (troponin I level b0.05 ng/mL; creatinine phophoskinase [CPK] at 58 IU, reference range between 30 and 135 IU; and CPK-MB b16 IU, reference range b20 IU). The brain natriuretic peptide level was 106 pg/mL (reference range, b100 pg/ mL). No other abnormalities were found on the initial laboratory tests including lactate dehydrogenase, Serum electrolytes, and complete blood count. Chest x-ray showed parahilar pulmonary congestion with no other abnormalities.

An Abdominal computed tomography (CT) angiography was performed at 7:45 PM to rule out a mesenteric infarction. It showed permeable celiomesenteric vessels with no intraluminal thrombus, neither abnormal parietal enhancement nor extravasation of contrast agent through the Small intestines. However, it revealed a hypoper- fusion in the apical myocardial region of the left ventricle with an area of low density (Fig. 2). Given the results of CT scan and the persistence of pain, a second ECG was performed at 8:15 PM, revealing an ST- segment elevation in leads V3-V4-V5 (Fig. 3). Hence, cardiac enzymes were repeated shortly after, with a positive troponin I level of 0.44 ng/mL, a CPK at 83 UI, and CPK-MB at 20 UI. Considering the recent installation of the infarction, the high Creatinine levels and the use of intravenous contrast in prior imaging, thrombolysis with 50 mg of intravenous tenecteplase was deemed to be the most appropriate treatment and was then initiated at 8:30 PM (15 minutes after ST-segment elevation appearing on ECG) in addition to aspirin, heparin, ?-blocker, and statin therapy. It efficiently relieved the pain and decreased the ST elevation by more than 50%. The patient was finally admitted to the coronary unit for observation.

Four hours after the end of thrombolysis, the patient felt once again the same epigastric pain and was urgently transferred to the percutaneous coronary intervention unit. A Significant stenosis was observed on the Left anterior descending artery and percutaneous coronary angioplasty, and a drug-eluting stent was placed in the left anterior descending artery. Echocardiography realized the second day showed a hypokinetic myocardial apex with preserved cardiac function. The patient finally left the hospital in good conditions with a prescribed therapy of ticagrelor, aspirin, ?-blocker, a statin, and an angiotensin receptor blocker.

Chest pain is the second most common complaint in the ED and one of the most intriguing symptoms because of to its relation to several factors including pulmonary, esophageal, and aortic emer- gencies as well as acute coronary syndromes [1]. Although

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128.e6 C. Sabbagh et al. / American Journal of Emergency Medicine 33 (2015) 128.e5128.e7

Fig. 1. Normal ECG finding realized 40 minutes after the onset of pain.

prompt recognition of ACS is essential to allow rapid intervention, differentiating it from other etiologies, which account for more than 70% of acute nontraumatic chest pain, could be difficult mainly because clinical evaluation is frequently unreliable, especially in women, and the electrocardiogram may show a normal result in ACS [1-3]. For instance, CT scanning, which is available in most hospital

Fig. 2. Contrast-enhanced CT realized 75 minutes after the onset of pain showing on the arterial pHase (a) and on portal phase (b) hypodense myocardium of the left ventricular apex (white arrow) compared with adjacent normal myocardium (black arrow).

centers, has been used to rule out non-ACS etiologies of chest pain [4]. However, with technology improvement and better imaging resolu- tion, more and more reports have been able to detect myocardial infarction (MI) on conventional CT as an area of decreased ventricular myocardial enhancement in a specific coronary arterial distribution [4-6]. In a retrospective study undergone by Gosalia et al. [3] on 18 patients, contrast-enhanced CT had a sensitivity of 83% and a specificity of 95% for detecting MI. Also, with multislice spiral tomography, radiologist could differentiate between unstable angina and MI, with Perfusion defect detected in only 10% for the former but up to 95% for the latter. Also, larger transmural defects were found in ST-segment elevation MI (STEMI) compared to non-STEMI [7]. In all these studies, however, patients had CT scan at least 1 day after installation of chest pain, and we did not find in the literature any report about imaging shortly after chest pain occurrence and before ECG changes installation. This report is the first to present a possible role of contrast-enhanced CT in detecting STEMI prior to installation of ECG changes and enzyme level elevation. Further studies are needed to evaluate the role of high-resolution contrast-enhanced CT scanning with or without coronary angiography in the workup of suspected MI in the setting of a normal ECG finding.

Chadi Sabbagh Mayda Rahi

Emergency Department, Hotel Dieu de France Teaching Hospital

Saint Joseph University

Beirut, Lebanon

Maria Baz Fadi Haddad

Internal Medicine Department Hotel Dieu de France Teaching Hospital

Saint Joseph University

Beirut, Lebanon

Omar Helwe Noel Aoun

radiology department, Hotel Dieu de France Teaching Hospital

Saint Joseph University

Beirut, Lebanon

Tony Ibrahim Hematology-Oncology Department Hotel Dieu de France Teaching Hospital

Saint Joseph University

Beirut, Lebanon

C. Sabbagh et al. / American Journal of Emergency Medicine 33 (2015) 128.e5128.e7 128.e7

Fig. 3. Second ECG realized 105 minutes after the onset of pain revealing ST-segment elevation in precordial leads V3, V4, and V5 (black arrows).

Lynn Abdo, MD Internal Medicine Department Saint Antoine Hospital

Pierre-et-Marie-Curie University

Paris, France

Corresponding author. Internal Medicine Department

Saint Antoine Hospital Pierre-et-Marie-Curie University 184rue du Faubourg-Saint-Antoine 75571 Paris cedex 12, France

Tel.: +33 787946081

E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2014.06.039

References

  1. Hollander JE, Chase M. Evaluation of chest pain in the emergency department. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on May 07, 2013).
  2. Goodacre S, Thokala P, Carroll C, Stevens JW, Leaviss J, Al Khalaf M, et al. Systematic review, meta-analysis and economic modelling of Diagnostic strategies for Suspected acute coronary syndrome. Health Technol Assess 2013;17:1-18.
  3. Gosalia A, Haramati LB, Sheth MP, Spindola-Franco H. CT detection of acute myocardial infarction. AJR Am J Roentgenol 2004;182:1563-6.
  4. Panagiotidis E, Price G, Harland S, Bomanji J, Kayani I. Myocardial uptake of 99mTc-HDP and reduced perfusion on CT in subacute myocardial infarction. Clin Nucl Med 2014;39:117-20.
  5. Arnett JH, Mohajer K, Okon SA. Evidence of acute myocardial infarction on CT. Br J Radiol 2007;80:219-21.
  6. Ichinose T, Yamase M, Yokomatsu Y, Kawano Y, Konishi H, Tanimoto K, et al. Acute myocardial infarction with myocardial perfusion defect detected by contrast- enhanced computed tomography. Intern Med 2009;48:1235-8.
  7. Veselova TN, Ternovoi SK. Informative value of multislice spiral computed tomography in identifying myocardial perfusion defect in patients with acute myocardial infarction. Ter Arkh 2013;85:16-21.

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