Acute pulmonary embolism with ST-segment elevation in the inferior leads

Abstract

ST-segment elevation (STE) in the right precordial leads is a remark-able and relatively common electrocardiographic (ECG) sign of moderatetosevereacutepulmonaryembolism(APE) [1–4].Someofthesecasesareaccompanied by STE in the inferior leads [2]. However, it is an unusualphenomenon to detect STE con fined to the inferior leads (in the absenceof acute occlusive coronary artery) [5]. We present here a case of STEconfined to the inferior leads as the only ECG manifestation of APE anddiscuss the possible intrinsic mechanism.A79-year-oldmalewithoutpriorcardiovascularhistoryadmittedtotheemergencydepartmentduetodyspneaandchestdiscomfortforthelast two days.Hehad brain surgery 15 days prior to remove a meningi-oma. The ECG (Fig. 1A) before brain surgery was normal. At admission,blood pressure (BP) was 110/60 mm Hg. Next ECG (Fig. 1B) showednew S-wave in lead I, incomplete right bundle branch block (RBBB)and minor STE in leads aVR and V1–V2. Under the presumption ofacute coronary syndrome, an emergent coronary angiography wasperformed showing minor atherosclerosis in the left anterior and cir-cumflex coronary arteries. One day later, the dyspnea was aggravatedwithoxygendesaturationandBPdroppedto90/55mmHg.SubsequentECG (Fig. 1C) showed STE in the inferior leads, resolution of the STEin leads aVR and V1–V2, higher R′-wave in leads V1–V2 and widerQ-wave in lead III (in comparison to Fig. 1B). An echocardiogramshowedright ventricular (RV) enlargement, freewall hypokinesia,flat-ten of the interventricular septum, and severe tricuspid regurgitation.APE was highly suspected and a CT pulmonary artery angiographyconfirmedbilateralpulmonaryarterialthrombus.Thrombolytictherapywas initiated but patient's condition rapidly deteriorated into cardio-genic shock dying few hours later. The ECG (Fig. 1D) obtained duringcardiogenic shock showed STE in the inferior leads and reappearanceof STE in leads V1–V3. The last ECG (Fig. 1E) was recorded beforedeath showing STE in leads aVR, III and V1–V3, ST-segment depression(STD) in leads I and V5–V6, QR sign in lead V1 and negative T-wave inleads V1–V3.The mechanisms to explain STE in APE include the following:(i) concomitant occlusive coronary artery with/without paradoxicalcoronary artery embolism via atrial sepal defect or patent foramenovale [3], and (ii) RV transmural ischemia due to hypotension, hypox-emia, pulmonary artery hypertension and catecholamine surge [2,3].STE in the right precordial leads with or without STE in the inferiorleads is an important ischemic pattern of APE reflecting transmural RVischemia [2,6]. Our case and a case reported by Emren et al. [5] withSTE confined to the inferior leads presented without significant coro-nary artery disease. We speculate that STE confined to the inferiorleads may result from transmural RV ischemia. Fig. 1B clearly showedSTE in the right precordial leads, which is a typical ischemic pattern inAPE. However, when the STE occurred in the inferior leads as inFig. 1C, simultaneous resolution of STE in the right precordial leadswas observed. In inferior STE myocardial infarction, STD can be foundin the right precordial leads and may be an electrical mirror phenome-non [7]. Hence, we speculate that STE in the inferior leads can counter-actSTEintherightprecordialleads.STEconfinedtotheinferiorleadsinAPE is a response to a speci fic degree of RV transmural ischemia. Whenthetransmuralischemiadegreeincreases,STEmayreappearintherightprecordial leads. Just as in Fig. 1D and E, when the patient's conditiondeteriorated, STE depicted in the inferior and right precordial leads.Our group previously described three specific ECG patterns in APE,indicating different manifestations of myocardial ischemia: (i) STE inleadaVR withconcomitantSTDinleadsIandV4toV6(LVsubendocar-dial ischemia), (ii) STE in leads V1 to V3/V4 with or without STE in theinferior leads (RV transmural ischemia) and (iii) STE in leads III and/orV1/V2 with concomitant STD in leads V4/V5 to V6 (LV subendocardialischemia with concomitant RV transmural ischemia) [2]. APE shouldbe highly suspected in patients with specific ischemic patterns withconcomitant RV strain pattern, such as S1Q3 and/or abnormal QRSmorphology in lead V1 including notched S-wave, RBBB and Qr sign [2].In conclusion, STE confined to the inferior leads can be a transientECG manifestation in APE. It is important to recognize the dynamic