A 76-year-old woman presents with chest pain-which she describes as“muscle tightness”- that began when she awoke in the morning. Thepain is constant, exacerbated by deep inspiration, and accompanied by asubjective sense of slight dyspnea; she rates its severity as 3 on a scale of1 to 10. She denies pain radiation, nausea, diaphoresis, palpitations, andlight-headedness. Her only cardiac risk factors are hypertension and a distanthistory of smoking.
A 76-year-old woman presents with chest pain--which she describes as"muscle tightness"--that began when she awoke in the morning. Thepain is constant, exacerbated by deep inspiration, and accompanied by asubjective sense of slight dyspnea; she rates its severity as 3 on a scale of1 to 10. She denies pain radiation, nausea, diaphoresis, palpitations, andlight-headedness. Her only cardiac risk factors are hypertension and a distanthistory of smoking.Her temperature is 36.2C (97.2F); heart rate, 86 beats per minuteand regular; respiration rate, 18 breaths per minute; and blood pressure,133/54 mm Hg. Her chest is clear. Normal S1 and S2 are audible; no murmurs,rubs, or gallops are noted. The ECG is shown here.Which of the following best explains the ECG findings?A. Acute myocardial infarction (MI).B. Acute myopericarditis.C. Benign early repolarization (BER).D. None of the above.DISCUSSION:
The ECG reveals evidenceof ST-segment elevation, most notablein limb leads I, II, and aVF,and precordial leads V 3 through V6 (Figure 1). Slight PR-segment depressionis also seen in these leads.There is evidence of reciprocalPR-segment elevation and ST-segmentdepression in aVR. T wavesare not prominent.Because of the ST-segment elevation,the computer's interpretationof this tracing is "acute MI." However,the morphology of the ST segmentsis concave, unlike the convexshape commonly seen in MI (Figure2). In addition, the wide distributionof ST-segment changes suggests anonterritorial distribution (that is,one that is not consistent with theanatomic vascular supply of themyocardium); this also makes acuteMI less likely.Concave ST-segment elevationcan be seen in BER. However, inBER, the concave ST-segment elevationis usually most evident in theright and mid precordial leads andis commonly associated with prominentT waves. Here, the ST-segmentelevation is broadly distributed inboth limb and precordial leads, andthe T waves are not prominent.The findings on this ECG aremost consistent with acute myopericarditis(choice B).Pathophysiology of myopericarditis.The underlying causes ofthis diffuse inflammation of the pericardialsac and superficial myocardiuminclude infection (primarilyviral), immunologic disorders, uremia,trauma, malignancy, cardiacischemia, and infarction. Affectedpatients complain of sharp, pleuritic,precordial, or retrosternal pain,which can radiate to the left upperback, shoulder, or arm. The pain isworsened by recumbency, cough,swallowing, and inspiration, and isrelieved by an upright or forwardleaningposition.1In patients with subacute orchronic pericarditis, significant pericardialeffusions may develop or theillness may progress to constrictivepericarditis. In some patients withmyopericarditis, the myocardialcomponent of the presentation(acute pulmonary edema, hypotension,and dysrhythmias) may predominate;that is, the presentationmay be essentially the same as thatof acute myocarditis.Electrocardiographic findings.ECG abnormalities are evident in upto 90% of patients with acute myopericarditis.2 These changes are aresult of repolarization abnormalitiesin the atrium and ventricle that arisefrom epicardial inflammation and injury.The most common changes arein the PR segment (caused by atrialrepolarization) and in the ST segmentand T wave (caused by ventricularrepolarization). Because depolarizationoccurs normally, the Pwave and QRS complex are usuallyunaffected.Classic 4-stage progression.Spodick3,4 described a classic 4-stageevolution of the ECG changes seenin acute myopericarditis. The 4stages of the progression involve differentelements of the ECG (Table):
Fewer than half of patients passthrough all 4 stages, however, andatypical progression is common.Stage 1 abnormalities--particularlyPR depression--are detected morefrequently and are considered"quasi-diagnostic."
In patientswith myopericarditis, this isusually less than 5 mm and occurssimultaneously throughout all limband precordial leads (I, II, III, aVF,aVL, and V
) with theexception of aVR and V
(in whichreciprocal ST-segment depressionis often seen). There is usually noclear territorial distribution; however,in postinfarct myopericarditis,in which inflammation may be localized,findings can be focal (eg, in theinferior distribution). The elevatedST segments seen in myopericarditisare concave or obliquely flat ontheir initial upslope, with an indistinctJ point. The T waves remainconcordant without flattening orinversion.It can be difficult to differentiatebetween the ST-segment elevationassociated with acute myopericarditisand ST-segment elevationof other origins, such as that seenin BER, acute MI, or ischemia.However, close examination revealsuseful distinctions.The elevated ST segments inBER are similar in morphology tothose seen in myopericarditis, withan initial concave upslope and indistinctJ point. However, ST-segmentelevation in BER is limited primarilyto the precordial leads and is mostprominent in the right precordialleads. In BER, the J point is minimallyelevated and T waves areprominent. In myopericarditis, boththe J point and ST-segment elevationare more pronounced; T wavesare less prominent. This differencecan be assessed through use of theST:T ratio (ratio of ST-segmentelevation to T-wave amplitude) inlead V
. Using the PR segment asbaseline, measure ST-segment elevation(at the J point) and T-waveamplitude. An ST:T ratio of 0.25or greater suggests myopericarditis,while a ratio of less than 0.25 suggestsBER
In acute MI, the initial morphologyof ST segments is often convexor obliquely flat. Moreover, the distributionof ST-segment elevation isusually territorial. T-wave inversionoften occurs along with ST-segmentelevation in acute MI, whereas inmyopericarditis, it occurs only afterresolution of the ST-segment abnormalities.The presence of Q wavessuggests acute MI, while PR-segmentdepression suggests myopericarditis.Finally, the ECG abnormalitiesevolve over a much shorter timein acute MI (hours to a few days)than in myopericarditis.
This isusually transient, but it may be theearliest and most specific sign ofacute myopericarditis. Like ST-segmentelevation, PR-segment depressionoccurs diffusely in the limband precordial leads (most prominentlyin II, V
, and V
. ), except foraVR and V
, which may have reciprocalelevation (
). In assessingthe PR segment, it is importantto use the TP segment as baseline;otherwise any depression maybe misinterpreted as ST-segmentelevation.
T-wave inversionsare encountered diffusely laterin the progression of myopericarditis,after ST-segment elevations haveresolved. This stage often does notoccur or is not detected.
Therhythm most commonly associatedwith acute myopericarditis is normalsinus rhythm or sinus tachycardia.Because of the proximity of the sinusnode to the pericardium, it was previouslythought that the inflammationcould precipitate atrial fibrillationor flutter. However, recent studiessuggest that the sinus node is virtuallyimmune to surrounding inflammation.
While myopericarditis canoccur in conjunction with dysrhythmias(most commonly supraventriculardysrhythmias), these disturbancesare generally attributable to underlyingcardiac disease.
Outcome of this case.
Thispatient's ECG shows classic signs ofstage 1 myopericarditis. There areST-segment elevations--most prominentin leads I, II, aVF, and V
--with a concave morphology.PR-segment depressionsare seen in the same leads, withoutprominent T waves. In lead aVR,there is evidence of reciprocalPR-segment elevation and ST-segmentdepression.The patient was admitted, andacute MI was ruled out. An echocardiogramrevealed a small pericardialeffusion but was otherwise unremarkable.Her symptoms and ECGabnormalities resolved, and she recovereduneventfully.
Shabetai R. Acute myopericarditis.
Chan TC, Brady WJ, Pollack M. Electrocardiographicmanifestations: acute myopericarditis.
J Emerg Med.
Spodick DH. Diagnostic electrocardiographic sequencesin acute pericarditis-significance of PRsegment and PR vector changes.
Spodick DH. Differential diagnosis of acute pericarditis.
Prog Cardiovas Dis.
Ginzton LE, Laks MM. The differential diagnosisof acute pericarditis from the normal variant: newelectrocardiographic criteria.
Marinella MA. Electrocardiographic manifestationsand differential diagnosis of acute myopericarditis.
Am Fam Physician.
Baljepally R, Spodick DH. PR-segment deviationas the initial electrocardiographic responses inacute myopericarditis.
Am J Cardiol.
Spodick DH. Significant arrhythmias duringmyopericarditis are due to concomitant heart disease.
J Am Coll Cardiol.