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Journal of Electrocardiology 44 (2011) 7–10www.jecgonline.com

The absence of the ST-segment elevation in acute coronary arterythrombosis: what does not fit, the patient or the explanation?

Ivan Stankovic, MD,⁎ Ivan Ilic, MD, Milos Panic, MD, Alja Vlahovic-Stipac, MD,Biljana Putnikovic, MD, PhD, Aleksandar N. Neskovic, MD, PhD

Department of Cardiology, Clinical Hospital Center Zemun, Belgrade University School of Medicine, Belgrade, Serbia

Received 22 February 2010

Abstract In a few patients with acute proximal thrombotic occlusion of the left anterior descending coronary

⁎ CorrespondingCenter Zemun, 11080

E-mail address: fu

0022-0736/$ – see frodoi:10.1016/j.jelectroc

artery (LAD), tall ischemic T waves never evolve into ST-segment elevation. This was recentlyinaccurately reported as a “novel sign” of proximal LAD occlusion. It has been speculated that theabsence of ST-segment elevation could be attributed to the large area of transmural ischemia, theanatomic variant of Purkinje fibers, or to lack of activation of sarcolemal adenosine triphosphate–potassium channels. This electrocardiographic picture was recently explained by changes in thesubendocardial but not in the epicardial action potential, suggesting subendocardial ischemia as theunderlying mechanism. We present a patient with thrombotic lesion of proximal LAD, staticprecordial ST-segment depression, and tall T waves who underwent primary percutaneousintervention and stent placement. Surprisingly, total thrombotic stent occlusion on the followingday was associated with ST-segment elevation in precordial leads, indeed supporting the concept ofthe regional subendocardial ischemia that was first described more than a decade ago.© 2011 Elsevier Inc. All rights reserved.

Keywords: Subendocardial regional ischemia; ST-segment elevation; Myocardial infarction

In patients with acute proximal thrombotic occlusion ofthe left anterior descending coronary artery (LAD), precordialhyperacute T waves usually evolve rapidly into classicST-segment elevation myocardial infarction (STEMI).1

However, it has been reported that in certain patients withacute thrombotic LAD occlusion, typical ST-segmentelevation (STE) in precordial leads does not occur. Instead,these patients may present with ST-segment depression(STD) at the J point with upsloping ST segments evolvinginto tall, symmetrical T waves in precordial leads.2,3 Thiselectrocardiographic (ECG) pattern was already described in1947 and was termed regional subendocardial ischemia bySclarovsky et al.4,5 According to the latest reports, in smallgroup of patients (about 2% of all anterior STEMI), thisdistinct ECG picture persists and never changes into typicalanteroseptal STEMI pattern in a given patient.2,3 It has beenspeculated that the absence of STE could be due to the largearea of transmural ischemia, the anatomic variant of Purkinjefibers, or to lack of activation of sarcolemal adenosinetriphosphate (ATP)-potassium channels.2,3 This ECG picture

author. Department of Cardiology, Clinical HospitalBelgrade, Serbia.ture.ivan@gmail.com

nt matter © 2011 Elsevier Inc. All rights reserved.ard.2010.05.003

was recently explained by changes in the subendocardial butnot in the epicardial action potential, suggesting subendo-cardial ischemia as the underlying mechanism.6

We present a patient with unusual clinical course thatseriously challenge recently proposed mechanisms for thisphenomenon and indeed supports the concept of the regionalsubendocardial ischemia.

Case report

A 56-year-old man was admitted to the coronary care unitwith burning chest pain lasting for 50 minutes. A 12-leadECG recorded upon admission showed 3 to 4 mm STD at theJ point in precordial leads V3-V6, with upsloping STsegments continuing into tall, symmetrical T waves. Despitebeing consistent with the regional subendocardial ischemia,the ECG changes were recognized as hyperacute T-wavepattern, indicating impending STE in precordial leads.Therefore, the hospital percutaneous coronary intervention(PCI) facility was immediately alerted, while the patient wasgiven nitroglycerin, aspirin, clopidogrel, and unfractionedheparin. The cath lab was ready in 50 minutes, whereas theECG recorded before the procedure did not show progres-sion to STE (Fig. 1A).

Fig. 1. (A) Initial 12-lead ECG showing STD at the J point in precordial leads V3-V6, with upsloping ST segments continuing into tall T waves. Lead aVRdisplays STE, whereas modest reciprocal STD is present in the inferior leads. (B) Coronary angiogram demonstrating thrombotic subocclusive lesion of theproximal LAD coronary artery (arrow).

8 I. Stankovic et al. / Journal of Electrocardiology 44 (2011) 7–10

Coronary angiography identified a culprit critical sub-occlusion of the proximal segment of LAD (Fig. 1B) with adistal TIMI grade 2 flow. In addition, the LAD providedcollateral flow for the right coronary artery (RCA) and

Fig. 2. (A), Electrocardiogram recorded during the attack of chest pain 18 hours afanterior STEMI. (B), Urgent coronary angiogram showing total LAD coronary ar

circumflex artery (LCx), both of which were occluded intheir medial parts. The culprit LAD lesion was treated withsirolimus-eluting coronary stent placement, whereas theRCA and LCx occlusions were left untreated during the

ter LAD stent implantation. Note STE in leads V1-V5, consistent with acutetery occlusion due to acute stent thrombosis (arrow).

9I. Stankovic et al. / Journal of Electrocardiology 44 (2011) 7–10

index procedure. The chest pain resolved after interventionwhile serum markers of myocardial necrosis were elevated.After PCI, STD with T-wave inversion in precordial leadswas observed.

The next day, 18 hours after stent placement, the patientcomplained of severe chest pain, now associated with STE inprecordial leads, consistent with typical anterior STEMIpattern (Fig. 2A). Urgent coronary angiography revealedtotal thrombotic occlusion (TIMI flow 0) of recentlyimplanted LAD stent (Fig. 2B). The patient underwentsuccessful re-PCI and stenting immediately. For thefollowing 48 hours, the patient received additional heparinand tirofiban. He recovered well and was discharged home6 days later.

Discussion

In 1947, Dressler and Roesler were the first whorecognized hyperacute T waves as the earliest electrocardio-graphic sign of myocardial infarction.4 They also observedthat in the few studied patients, these high T waves did notevolve in STE. Later on, STD and a positive T wave in thesame precordial leads have been described as regionalsubendocardial ischemia5,7 associated with a single-vesseldisease in non-STE acute coronary syndromes with elevatedtroponine levels.8 In most cases, this unusual ECG patternhas been related to the subtotal occlusion of the LAD or totalocclusion of the first diagonal, the first obtusemarginal, or theintermediate side branch.9,10

More recently, Verouden et al inaccurately reported overtSTD at the J point with upsloping ST segments continuinginto tall, symmetrical T waves in the precordial leads as a“novel sign” of proximal LAD occlusion.2,3 However, thisdistinct ECG pattern never changed into STE in theprecordial leads in the reported cohort. The authorsconsidered these patients as having a STEMI and proposedseveral mechanisms to explain the absence of STE.2,3

Interestingly, none of these explanations are in line withunusual clinical course of our patient.

One of the explanations they offered was that the area oftransmural ischemia was very large, such that no injurycurrents were generated toward the precordial leadsproducing STE (vector neutralization). In our patient, aproximal LAD culprit lesion jeopardized a large but the samearea of myocardium at both acute events. Despite this, thepattern of regional subendocardial ischemia at initialpresentation was replaced by STE on the following day,rendering this explanation unlikely.

Other 2 suggested mechanisms appear to be even moredoubtful. The epicardial conduction delay due to theanatomic variant of Purkinje fibers (or any other anatomicvariations) can be ruled out by the fact that both ECGpatterns occurred in the same patient in less than 24 hours.

The same applies to the role of the lack of activation ofsarcolemmal ATP-sensitive potassium (KATP) channels byischemic ATP depletion.

In ischemic myocardium, depleted ATP stores leads toopening of KATP channels, which shortens action potential.

11

This shortening accelerates repolarization of ischemic cells

resulting in an electrical gradient and ischemic current that canbe seen as an elevation of the ST segment on surface ECG.12

It has been shown in animal models that homozygousknockout of the Kir6.2 gene, which encodes the pore-forming subunit of cardiac surface KATP channels, will resultin the absence of STE after LAD ligation in mice heart.13

Different ECG patterns occurring in the same patient withthe same thrombotic culprit lesion in a narrow temporalwindow excludes potential variable gene expressions as aconvincing explanation.

On the other hand, the only difference between the firstand second coronary angiography in our patient was “theprogression” of thrombotic subocclusive lesion of proximalLAD to total thrombotic stent occlusion at the same site aday later. Therefore, a mechanism of disparate ECG patternscould be less sophisticated and merely due to the fact that thepatient had LAD subocclusion in the first instance, whereason the second occasion, there was total LAD occlusion.

It was previously reported that tall peaked T waveswithout STE may indicate subendocardial ischemia inpatients who have chronic total occlusion of the LAD andwell developed collaterals that prevent STE.14 Although ourpatient had the collateral network, collateral vesselsoriginated from LAD and provided the retrograde filling ofthe occluded RCA and LCx arteries.

However, at the time of LAD subocclusion, the residualantegrade flow (TIMI 2) was obviously sufficient to preventtransmural ischemia and STE. Stent thrombosis andconsequent total LAD occlusion with no retrograde fillingfrom RCA and LCx led to transmural ischemia and typicalSTEMI pattern on the following day.

It was suggested that the increased T-wave amplitude inregional subendocardial ischemia pattern is likely due toK-ATP dependent hyperpolarization of the myocytes.15 Ourobservation is supported by a recently published explanationbased on the subendocardial localization of the ischemia andthe resulting behavior of subendocardial and subepicardialaction potentials.6

It appears that observed ECG pattern of STD and tall Twaves in the same precordial leads (regional subendocardialischemia) do not have the same pathophysiological back-ground as high ischemic T waves. In some patients, thepattern do progress to ST elevation, whereas in others, itremains stable.

In conclusion, early recognition of this unusual but notnovel ECG pattern carries important clinical implicationsbecause it strongly indicates the presence of acute coronaryartery thrombosis. Uncommon clinical course of our patientprovided the unique evidence that regional subendocardialischemia is responsible for the dissociation between ST-segment and T-wave orientation in the setting of non-STEacute coronary syndromes.

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