www.elsevier.com/locate/ajem

American Journal of Emergency Medicine (2012) 30, 637.e1–637.e4

Case Report

Concurrent pulmonary embolism and acute coronarysyndrome with dynamic electrocardiographic changes

Abstract

Concomitant occurrence of pulmonary embolism andacute coronary syndrome is rare. The early diagnosis andtreatment of acute coronary syndrome with right ventricularmyocardial ischemia during acute pulmonary embolism(APE) are crucial. The irreversible right ventricular myocar-dial dysfunction is a major risk factor for mortality fromAPE. In this case report, we present a 66-year-old femalepatient with APE who had a significant right coronary artery(RCA) lesion, which was successfully treated with angio-plasty and stent implantation.

Acute pulmonary embolism (APE) is a relatively frequentcardiovascular emergency that generally appears with chestpain and shortness of breath. The overall inhospital mortalityrate of APE has been reported to be 7% to 11% and raises to25% among those with shock and to 65% among those withcardiopulmonary arrest [1,2]. Life-threatening severe rightventricular dysfunction may develop because of acuteobstruction of pulmonary arterial bed. Irreversible functionalimpairment of right ventricle is a major risk factor formortality. Therefore, acute coronary syndromes (ACSs),which accompany APE and affect the right ventriclefunctions in particular, should be determined and treated inthe early period.

In the present case, a patient diagnosed with APE wassuccessfully treated by percutaneous intervention of theRCA for the concurrent ACS.

A 66-year-old woman was admitted to our emergencydepartment with complaints of shortness of breath andburning chest pain for 4 hours. She also described swellingand pain in her left leg that occurred after a 4-hour bus tripa week ago. She was transferred to the coronary care unitfor the differential diagnosis of the chest pain. On herphysical examination, blood pressure was 180/100 mm Hg,and heart rate was 104 beats per minute and regular. Therespiratory rate was 30 per minute, and oxygen saturationwas 90% in room air. Her electrocardiogram (ECG)revealed a sinus rhythm with incomplete right bundle-branch block, negative T waves, and 0.5-mm ST-segmentdepression in leads V1 to V6 (Fig. 1). Bedside transthoracic

0735-6757/$ – see front matter. Crown Copyright © 2012 Published by Elsevier

echocardiographic examination revealed an enlarged rightventricle with akinetic mid and basal segments andhyperkinetic apical segment (McConell's sign). Therewas moderate tricuspid insufficiency, and the estimatedpulmonary artery pressure was 45 mm Hg. Because of theabsence of shock or resistant hypotension, fibrinolytictherapy for APE was not considered, and she wasscheduled for elective multislice computed tomography(MSCT) imaging. She was treated initially with enoxapar-ine (0.1 mg/kg, BID), acetylsalicylic acid (300 mg/d),and metoprolol (50 mg/d). Biochemical analysis showedincreased D-dimer (2500 ng/mL), troponin I levels (1.2 U/L),and normal creatinine kinase/creatinine kinase-MB levels.On the second day of her hospitalization, she had burningchest pain that impaired hemodynamic stability (systolicblood pressure, 80-90 mm Hg) and was accompanied byparoxysmal atrial fibrillation (PAF) (Fig. 2). Because the PAFepisodes became frequent and impaired the hemodynamicstability, coronary angiography was performed to eliminatean acute coronary event. Coronary angiography revealed60% to 70% tubular narrowing of the mid segment of the leftanterior descending artery (LAD) and 95% to 99% narrowingof the mid proximal segment of the RCA (Fig. 3A).Percutaneous transluminal coronary angioplasty (PTCA)was performed for the severe obstruction in RCA. Theobstruction in the RCA was dilated via a 2.0 × 14 mmmercury balloon (Abbott Laboratories, Abbott Park, IL), anda 2.75 × 16 mm bare metal stent (20 atm, 3.3 mm; Flexmaster[JoMed GmbH, Rangendirgen, Germany]) was implanted(Fig. 3-B). After the intervention, the patient was hemody-namically stable, and the MSCT pulmonary angiography wasperformed 3 days after the procedure. Multislice computedtomography imaging showed diffuse thrombus in both of themain pulmonary arteries extending through to the distalsegment (Fig. 4). Doppler ultrasound examination alsoshowed thrombus in the deep femoral vein of the left lowerextremity. On the fifth day, PTCA was performed for thelesion in LAD. The patient was discharged on the eighth daywith warfarin, acetylsalicylic acid, clopidogrel, atorvastatin,metoprolol, and ramipril.

Acute pulmonary embolism is an urgent clinical condi-tion resulting from acute obstruction of pulmonary artery andthe branches as well. The patients with acute massive pul-monary embolism (PE) that progresses to shock and hypo-tension due to severe right heart failure die in a short time

Inc. All rights reserved.

Fig. 1 Electrocardiographic findings at the time of admission to the hospital: sinus rhythm, incomplete right bundle-branch block, 0.5-mmST-segment depression, and negative T waves in leads V1 to V6 and negative T wave in D3.

637.e2 Case Report

[3]. Inhospital mortality rate among overall APE cases isreported to be 7% to 11%, whereas it was 25% in those withshock and 65% in those with cardiopulmonary arrest [1,2]

Acute coronary syndrome concomitant with APE is quiterare, and it is difficult to diagnose because of similar clinicalfindings and symptoms. Acute coronary events observed inthe course of APE can be evaluated in 3 parts in the guidanceof the literature.

The first one is the right ventricular ischemia or infarctiondeveloped due to the increased right ventricular afterloadthat is secondary to massive pulmonary embolus. In thesecases, in general, no significant coronary artery obstructionthat might lead to the right ventricular ischemia has beendetermined [4,5]. However, based on the autopsies of 6cases with massive PE accompanied by isolated rightventricle myocardial infarction, coronary arteries weredetermined to be normal in 1 case, whereas significantobstruction was determined in the right or left coronaryarteries of the remaining 5 cases. It was stated that theseobstructions might partly be responsible for the rightventricle necrosis in APE [6].

Paradoxical coronary embolism is the other rare cause ofACS that accompanies APE. Myocardial infarction second-ary to APE has been reported in the patients who hadnot been diagnosed with patent foramen ovale (PFO) before[7-9]. Thrombus that resembles embolus was observed in thecoronary arteries on coronary angiographies performed inthese patients because of the changes in ST-T segmentobserved on ECG in the course of APE. Patent foramenovale, which allows thrombus to pass into the left atriumfrom the right atrium, thereafter, into the coronary arterysystem, was determined on echocardiographic examinations.

The third cause that leads to ACS in APE is the presenceof severe obstruction in coronary arteries. A patient whounderwent coronary angiography because of acute chestpain and elevated troponin levels in the course of APE andwho was performed a percutaneous coronary interventionfor the significant obstruction in LAD has been reported inthe literature [10]. In the present case, percutaneouscoronary intervention was performed to the significantobstruction in the RCA, which led to ACS. Vasospasm dueto increased catecholaminergic discharge and the activation

Fig. 2 Paroxysmal atrial fibrillation that accompanied chest pain and hypotension on the second day of hospitalization.

Fig. 3 A, The image of 95% to 99% tubular narrowing in the mid proximal segment of the RCA. B, The image after PTCA andstent implantation.

637.e3Case Report

References

Fig. 4 The image of diffuse thrombus extending through to thedistal segment in both main pulmonary arteries in the MSCTpulmonary angiography.

637.e4 Case Report

of coagulation system are likely the causes of preexistingcoronary artery obstruction to become symptomatic. Sys-tolic functions of the right ventricular myocardium, whichhave been affected in APE, have worsened because of theincrease in the severity of the obstruction in RCA.Disappearance of the arrhythmias and the hypotensionafter percutaneous revascularization process performed inthe present case revealed the importance of acute coronaryevents in the course of APE and raised the thought that theyshould be diagnosed and treated as soon as possible.

Electrocardiographic findings in APE are generallynormal but neither sensitive nor specific. Sinus tachycardiaand nonspecific changes of ST-segment and T wave are themost frequently encountered findings. Inversion of T wavesin precordial derivations that include right ventricularoverload, S1Q3T3 pattern, transient right bundle-branchblock, sudden atrial fibrillation, and other atrial arrhythmiasare the strong ECG changes that indicate PE [11]. In thepresent case, there were incomplete right bundle-branchblock, Q waves, and T wave inversion in D3 that indicatesright ventricular overload. These ECG findings are thechanges that are expected to be present in APE. T wavechanges in anterior derivations may be either nonspecificchanges encountered in APE or ischemic changes developeddue to the obstruction in LAD. Furthermore, frequent PAFattacks observed in this case may be due to the increasedsympathetic activity in APE; however, it should be kept inmind that they might also occur because of the acuteischemic coronary events in the patients with chest pain.

Elevated troponin levels in APE have been found to beassociated with mortality [12]. Rapid and severe increase inright ventricle pressure leads to myocardial ischemia in rightventricle as well as troponin release. In this case, troponinlevel was determined to be increased at the time of

admission. This elevation resulted either from the increasein right ventricular pressure or from the right ventricularischemia because of ACS.

It should be kept in mind that acute coronary events mightaccompany APE, which progresses with severe impairment inright ventricular function, in the presence of refractory atrialarrhythmia and chest pain. Early diagnosis and treatment aremandatory, particularly in patients who have coronary arteryinvolvement that leads to right ventricular ischemia.

Ahmet Yildiz MDCem Bostan MDFatih Akin MD

Alev Arat Ozkan MDTevfik Gurmen MD

Istanbul University, Institute of CardiologyIstanbul 34096, Turkey

E-mail address: drayildiz@yahoo.com

doi:10.1016/j.ajem.2011.02.006

[1] Stein PD, Kayali F, Olson RE. Estimated case fatality rate ofpulmonary embolism, 1979 to 1998. Am J Cardiol 2004;93(9):1197-9.

[2] Guidelines on diagnosis and management of acute pulmonaryembolism. Task Force on Pulmonary Embolism, European Societyof Cardiology. Eur Heart J 2000;21:1301-36.

[3] Kasper W, Konstantinides S, Geibel A, Oischewski M, Heinrich F,Grosser KD, et al. Management strategies and determinants ofoutcome in acute major pulmonary embolism: results of a multicenterregistry. J Am Coll Cardiol 1997;30:1165-71.

[4] Jerjes Sánchez C, Gutiérrez-Fajardo P, Ramírez-Rivera A, García-Mollinedo Mde L, Hernández Chávez G. Acute infarct of the rightventricle secondary to a massive pulmonary thromboembolism. ArchInst Cardiol Mex 1995;65(1):65-73.

[5] Mittal SR, Arora H. Pulmonary embolism with isolated rightventricular infarction. Indian Heart J 2001;53(2):218-20.

[6] Coma-Canella I, Gamallo C, Martinez Onsurbe P, Lopez-Sendon J.Acute right ventricular infarction secondary to massive pulmonaryembolism. Eur Heart J 1988;9(5):534-40.

[7] Budavari AI, Glenn TJ, Will KK, Askew JW, Fortuin FD. A case ofsimultaneous pulmonary embolism and acute myocardial infarctionsecondary to a previously undiagnosed patent foramen ovale. J HospMed 2009;4(5):E5-E9.

[8] Uchida S, Yamamoto M, Masaoka Y, Mikouchi H, Nishizaki Y. Acase of acute pulmonary embolism and acute myocardial infarctionwith suspected paradoxical embolism after laparoscopic surgery. HeartVessels 1999;14(4):197-200.

[9] Haghi D, Sueselbeck T, Papavassiliu T, Haase KK, Borggrefe M.Paradoxical coronary embolism causing non-ST segment elevationmyocardial infarction in a case of pulmonary embolism. Z Kardiol2004;93(10):824-8.

[10] Wozakowska-Kapłon B, Bzymek RM, Gutkowski W. Acute coronarysyndrome following massive pulmonary embolism in a 81-year-oldwoman with thrombophilia. Kardiol Pol 2008;66(5):543-7.

[11] Livaditis IG, Paraschos M, Dimopoulos K. Massive pulmonaryembolism with ST elevation in leads V1-V3 and successfulthrombolysis with tenecteplase. Heart 2004:90.

[12] Kostantinides S. Pulmonary embolism: impact of right ventriculardysfunction. Curr Opin Cardiol 2005;20:496-501.

本文献由“学霸图书馆-文献云下载”收集自网络，仅供学习交流使用。

学霸图书馆（www.xuebalib.com）是一个“整合众多图书馆数据库资源，

提供一站式文献检索和下载服务”的24 小时在线不限IP

图书馆。

图书馆致力于便利、促进学习与科研，提供最强文献下载服务。

图书馆导航：

图书馆首页 文献云下载 图书馆入口 外文数据库大全 疑难文献辅助工具