definisi ami.pdf

8/14/2019 definisi ami.pdf

1/8

EDUCATIONAL OBJECTIVES: Readers will understand the new denition of acute myocardial infarction (MI)and how to make the diagnosis of acute MI

A new, precise denitionof acute myocardial infarction

ABSTRACT

Several international cardiovascular societies haverevised their diagnostic criteria for acute myocardialinfarction (MI) ( J Am Coll Cardiol 2007; 50:21732188).The cornerstone of diagnosis remains a high level ofclinical suspicion, serial electrocardiograms, and troponinlevels. This article reviews the new denition and theappropriate clinical tools necessary to diagnose acute MIaccurately.

KEY POINTS

The clinical presentation of acute MI varies considerably

from patient to patient. Therefore, one must consider thesymptoms, serial electrocardiographic ndings, and serialbiomarker results in concert.

Troponin I or T is now the preferred biomarker of myo-cardial necrosis. Still, troponin can be elevated in manyconditions other than ischemic heart disease.

Electrocardiographic signs of acute ischemia have beenprecisely dened, but electrocardiography can give false-positive or false-negative results in a number of condi-tions.

MI is now categorized into ve types depending oncause.

CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 76 NUMBER 3 MARCH 2009 159

A (MI)portends important and substantial con-sequences. Angioplasty or brinolytic therapyto open the blocked coronary artery is provento improve the patients chances of survivingwithout consequent morbidity or death. Butthe diagnosis is not always straightforward.The presentation of acute MI can vary wide-ly, and a number of other conditions manyof them equally serious emergenciescanmimic its symptoms, electrocardiographicsigns, and biomarker patterns. In an attempt to improve the accuracy ofthe diagnosis of MI, a multinational task forcemet in 1999 under the auspices of the EuropeanSociety of Cardiology and the American Col-lege of Cardiology. The goal was to develop asimple, clinically oriented denition of MI thatcould be widely adopted. A document was cre-ated and published simultaneously in 2000 inthe European Heart Journal and the Journal ofthe American College of Cardiology.1 These or-ganizations updated their paper in 2007 with anew denition of acute MI to account for ad-vances in diagnosis and management. 2 In this article we will review the new de-

nition and how to make the diagnosis of acuteMI today. Specically, the updated denitionincludes:

Subtypes of acute MIImaging tests supporting the diagnosisBiomarker thresholds after percutaneouscoronary intervention or bypass grafting.

TROPONIN: BETTER THAN CK,BUT NOT PERFECT

The original 2000 paper 1 and the 2007 up-

date2

featured the use of the cardiac bio-

REVIEW

doi:10.3949/ccjm.75a.08092

SHAUN SENTER, MD, MSDepartment of Cardiovascular Medicine,Cleveland Clinic

GARY S. FRANCIS, MDProfessor of Medicine,University of Minnesota

CREDITCME


2/8

160 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 76 NUMBER 3 MARCH 2009

marker troponin, which is considerablymore sensitive and specic for heart damagethan total creatine kinase (CK) or its iso-form, CK-MB. The new, more-sensitive biomarker-baseddenition of MI resulted in more cases of MIbeing diagnosed, and this has attracted theattention and scrutiny of many, especiallypopulation scientists and interventional car-diologists.3 This change has caused some con-troversy, especially when dealing with smallrises in troponin following percutaneous coro-nary intervention. In addition, some confusion over ter-

minology remains. For example, the phrase

troponin leak is often used to describe cas-es in which serum troponin levels rise butthere is no MI. However, most experts be-lieve that a rise and fall in troponin is due to

true myocardial cell death. Troponin I andT are such large molecules that they cannotleak from a cardiac cell unless there hasbeen irreparable cellular damagethat is,cell death. On the other hand, troponin is often el-evated in plasma in conditions other thanovert ischemic heart disease ( TABLE 1).4,5 In mostcases, the mechanism of the increased plasmatroponin level is not clearly understood, butclinical evidence of acute MI is otherwiselacking.

Creatine kinase still has a roleIn some cases, CK and CK-MB may be helpfulin determining the acuity of myocardial ne-crosis, but their use will vary by institution.These biomarkers typically rise 2 to 4 hoursafter the initial event and fall within 24 to 48hours, whereas troponin levels stay elevatedfor days or weeks. Thus, the presence of tro-ponin without CK and CK-MB in the rightclinical context may indicate a past MI that isno longer acute.

INFARCTION:CELL DEATH DUE TO ISCHEMIA

MI is myocardial cell death due to prolongedischemia. Under the microscope, it can becategorized as coagulation necrosis in whichghost-like cell structures remain after hypoxicinsult (typical of most MIs) or contractionband necrosis with amorphous cells that can-not contract anymore, the latter often a hall-

mark of excessive catecholamine damage orreperfusion injury. Apoptosis occurs in theheart but is technically not considered necro-sis and is thought not to be associated withelevated troponin levels. 6,7 In experiments in animals, cell death canoccur as little as 20 minutes after coronaryartery occlusion, although completion of in-farction is thought to take 2 to 4 hours. Thetime to infarct completion may be longer inpatients with collateral circulation or whenthe culprit coronary artery has intermittent

(stuttering) occlusion. Preconditioning of

TABLE 1

Conditions other than MIthat can elevate troponinAcute neurologic disease, including strokeor subarachnoid hemorrhage

Aortic dissection

Aortic valve disease

Apical ballooning syndrome

Burns, especially if affecting > 30% of body surface area

Cardiac contusion or other trauma including surgery, ablation,cardioversion, debrillation

Congestive heart failureacute and chronic

Critical illness, especially with respiratory failure or sepsis

Drug toxicity or toxins

Extreme exertion

Hypertrophic cardiomyopathy

Inltrative diseases, eg, amyloidosis, hemochromatosis,sarcoidosis, and scleroderma

Inammatory diseases, eg, myocarditis or myocardial extensionof endocarditis or pericarditis

Pulmonary embolism, severe pulmonary hypertension

Renal failure

Rhabdomyolysis with cardiac injury

Tachyarrhythmias, bradyarrhythmias, or heart block

ADAPTED FROM THygEsEN K, ALPERT Js, WHITE HD, ON BEHALF OF THE JOINT EsC/ACCF/AHA/ WHF TAsK FORCE FOR THE REDEFINITION OF MyOCARDIAL INFARCTION. UNIVERsAL DEFINITION

OF MyOCARDIAL INFARCTION. J AM COLL CARDIOL 2007; 50:21732188, WITH PERMIssIONFROM ELsEVIER. HTTP://WWW.sCIENCEDIRECT.COM/sCIENCE/JOURNAL/07351097.

ACUTE MYOCARDIAL INFARCTION


3/8


SENTER AND FRANCIS

myocardial cells with intermittent ischemiacan also inuence the timing of myocardial ne-crosis by protecting against cell death to someextent. Alteration in myocardial demand caninuence the time required for completionof infarction either favorably or unfavorably;hence, reducing myocardial demand is bene-cial in acute MI.

Three pathologic phases of MIMI can be categorized pathologically as acute,healing, or healed. Acute MI. In the rst 6 hours after coro-nary artery occlusion, coagulation necrosiscan be seen with no cellular inltration. After6 hours, polymorphonuclear leukocytes inl-trate the infarcted area, and this may continuefor up to 7 days if coronary perfusion does notincrease or myocardial demand does not de-crease. Healing MI is characterized by mononu-

clear cells and broblasts and the absence ofpolymorphonuclear leukocytes. The entirehealing process takes 5 to 6 weeks and can bealtered by coronary reperfusion. Healed MI refers to scar tissue without cel-lular inltration.

CLINICAL FEATURES VARY WIDELY

Sir William Osler said, Variability is the lawof life, and as no two faces are the same, so notwo bodies are alike, and no two individuals re-

act alike and behave alike under the abnormal

conditions which we know as disease. 8 Just so, patients with acute MI display a

wide variety of presentations, from no symp-toms (about 25%) to severe, crushing chestpain. Discomfort may occur in the upper back,neck, jaw, teeth, arms, wrist, and epigastrium.Shortness of breath, diaphoresis, nausea, vom-iting, and even syncope may occur. Unlike inacute aortic dissection, the discomfort is notusually maximal at its onset: it builds up in acrescendo manner. It is not usually changedby position, but can lessen in intensity uponstanding. The discomfort in the chest is deepand visceral, and typically not well localized.A pressure sensation, air hunger, or gas build-up can be described. The only symptom maybe shortness of breath or severe diaphoresis.The symptoms can last from minutes to hoursand can be relieved by sublingual nitroglyc-erin. Atypical or less-prominent symptomsmay make the diagnosis more difcult in the

elderly, patients with diabetes mellitus, andwomen. The physical examination during acuteMI usually nds no clear-cut distinguishingfeatures. The patient may appear pale anddiaphoretic, and the skin cool to the touch.Heart sounds are generally soft. A fourth heartsound may be audible. Blood pressure may below, but it can vary widely. Tachycardia, par-ticularly sinus tachycardia, and pulmonaryedema are poor prognostic signs. In view of the wide variation in presen-

tations, the history and physical ndings

Variability isthe law of lifeOsler

Acute pericarditis

FIGURE 1. Acute pericarditis with elevation of the ST segment in all leads, often up-sloping (red

arrows), and PR depression in all leads (blue arrows), except for PR elevation in aVR (black arrow).


4/8


can raise the suspicion of acute MI, but se-quential electrocardiograms and measure-ments of biomarkers (troponin) are alwaysnecessary.

ELECTROCARDIOGRAPHY:NECESSARY BUT NOT SUFFICIENT

Electrocardiography is a key part of the diag-nostic evaluation of suspected acute MI. As inthe 2000 paper, the 2007 update reiterates thesame classic changes that may be seen on anelectrocardiogram. It should be ordered and

reviewed promptly as soon as the diagnosis issuspected, and repeated frequently if the ini-tial tracing is normal. Although electrocardiography is necessary,it cannot distinguish myocardial ischemia fromMI. In addition, electrocardiography alonecannot reliably be used to diagnose acute MI,as many conditions result in deviation of STsegments and may be misinterpreted as acuteMI. Common examples include acute peri-carditis ( FIGURE 1), early repolarization, hyper-kalemia, left ventricular hypertrophy, and

bundle branch block.9

ST-elevation MI vs non-ST-elevation MICases of acute myocardial ischemia and acuteMI are traditionally divided by electrocardiogra-phy ( TABLE 2) into those in which the ST segmentis elevated ( FIGURE 2) and those in which it is not(FIGURE 3). This dichotomy is useful clinically, aspatients with ST-elevation MI are usually tak-en directly to the catheterization laboratory orgiven brinolytic therapy if they have no con-traindications to it, whereas those with non-ST-elevation MI are brought to the catheterizationlaboratory less urgently, depending on variousassociated risk scores. Changes in the ST segment can be very dy-namic, making sequential tracings very useful.Rhythm disturbances and heart block are alsomore likely to be recorded when using sequen-tial readings.

Pitfalls to electrocardiographic diagnosisThe electrocardiographic diagnosis of acute

MI can be very straightforward or quite subtle,

MI symptomsmay be lessprominent inelderly, female,or diabeticpatients

TABLE 2

Electrocardiographicmanifestations of acutemyocardial ischemia *

ST elevationNew ST elevation at the J point in twocontiguous leads

0.2 mV in leads V2V3 (men) 0.15 mV in leads V2V3 (women) 0.1 mV in other leads

ST depression and T-wave changesNew horizontal or down-sloping ST depression 0.05 mV in two contiguous leads; and/orT inversion 0.1 mV in two contiguous leads

with prominent R wave or R/S ratio > 1

*In absence of left ventricular hypertrophy and left bundlebranch block

REPRINTED FROM THygEsEN K, ALPERT Js, WHITE HD, ON BEHALF OFTHE JOINT EsC/ACCF/AHA/WHF TAsK FORCE FOR THE REDEFINITION

OF MyOCARDIAL INFARCTION. UNIVERsAL DEFINITION OF MyOCAR -DIAL INFARCTION. J AM COLL CARDIOL 2007; 50:21732188, WITH

PERMIssION FROM ELsEVIER. HTTP://WWW.sCIENCEDIRECT.COM/ sCIENCE/JOURNAL/07351097.

TABLE 3

Common pitfalls in diagnosingMI by electrocardiography

False-positive ndingsBenign early repolarizationBrugada syndromeCholecystitisFailure to recognize normal limits for J-pointdisplacement

Lead transposition or use of modied Mason-Likar conguration

Left bundle branch blockMetabolic disturbances such as hyperkalemiaPericarditis or myocarditisPre-excitation

Pulmonary embolismSubarachnoid hemorrhage

False-negative ndingsLeft bundle branch blockLeft ventricular hypertrophyPaced rhythmPrior myocardial infarction with Q waves,persistent ST elevation, or both

REPRINTED FROM THygEsEN K, ALPERT Js, WHITE HD, ON BEHALF OFTHE JOINT EsC/ACCF/AHA/WHF TAsK FORCE FOR THE REDEFINITION

OF MyOCARDIAL INFARCTION. UNIVERsAL DEFINITION OF MyOCAR -DIAL INFARCTION. J AM COLL CARDIOL 2007; 50:21732188, WITH

PERMIssION FROM ELsEVIER. HTTP://WWW.sCIENCEDIRECT.COM/ sCIENCE/JOURNAL/07351097.



5/8


SENTER AND FRANCIS

Possible non-ST-elevation MI

FIGURE 3A. Poor R wave progression (red arrows) with terminally symmetric T waves inleads V 1 through V 6 (blue arrows), which suggests possible myocardial injury; this patienthad positive troponin consistent with non-ST-elevation MI.

FIGURE 3B. ST depression across the precordium (V 1V6) suggestive of subendocardialinjury (black arrows). An electrocardiogram 12 minutes later showed normalization of these

changes; however, cardiac troponin was positive and consistent with non-ST-elevation MI.

Anterolateral ST-elevation MI

FIGURE 2. Anterolateral ST-elevation MI with ST elevation in V 1 through V 3 indicating infarction

of the anteroseptal myocardium (red arrows), and in V 4 through V 6 and I and aVL indicating lateralwall involvement (blue arrows). Note the reciprocal ST depression in inferior leads, ie, III and aVF(black arrows).

ST changescan bevery dynamic,makingsequentialtracings veryuseful


6/8


and many pitfalls can confound the correctdiagnosis ( TABLE 3). When the diagnosis is indoubt, frequent sequential readings are veryuseful. Prior MI. Q waves or QS complexes, whenthe Q wave is sufciently wide ( 0.03 msec)or deep ( 1 mV), usually indicate a previousMI. However, many nuances that further raiseor lower the suspicion for previous MI need tobe considered. These are beyond the scope ofthis brief review but are available in the 2007update. Posterior MI (or inferobasal MI) ismore difficult to identify than anterior MIand is frequently missed on electrocardiog-

raphy due to the absence of ST elevation

on 12-lead readings. Changes on electro-cardiography that raise the suspicion ofposterior MI are prominent R waves in V 2 with accompanying ST-T depression. Pa-tients with posterior MI are less likely to betaken directly to the catheterization labo-ratory unless ST elevations are seen due toconcomitant infarction involving the infe-rior ( FIGURE 4) or lateral ( FIGURE 5) wall, orunless there is high suspicion for myocar-dial injury based on cardiac enzymes andinformation from the history and physicalexamination. Right ventricular infarction often requiresthe use of right-sided leads, which may reveal

ST elevation in V 4R.

Posterior MIis frequentlymissed due toabsence of STelevation

Inferoposterior ST-elevation MI

FIGURE 4. Inferoposterior ST-elevation MI with ST elevation in II, III, and aVF (red arrows)

indicating injury in the inferior wall in addition to possible involvement of the posteriorwall, as suggested by tall R waves (black arrows) with ST depression and T wave inversions(blue arrows) in V 1 and V 2.

Inferolateral ST-elevation MI

FIGURE 5. Inferolateral ST-elevation MI with ST elevation in II, III, and aVF (red arrows) indi-cating injury in the inferior wall in addition to ST elevation in V 4 through V 6 (blue arrows).



7/8


SENTER AND FRANCIS

ECHOCARDIOGRAPHYIF THE DIAGNOSIS IS IN DOUBT

In many cases, acute MI is suspected on clini-

cal grounds but electrocardiography does notverify an acute process. Troponin levels maynot have had time to rise very much, if at all,or the results may not yet be known. Deci-sions to go to the catheterization laboratoryor to do a computed tomographic scan of thechest to exclude aortic dissection must bemade quickly. Echocardiography is an excellent way toassess wall-motion abnormalities. In the ab-sence of any wall-motion abnormality, a largeST-elevation MI is unlikely. A large wall-mo-tion abnormality would verify the probabilityof ongoing acute MI and thus would help withrapid decision-making. Furthermore, echocardiography can helpdetermine the likelihood that the patienthas aortic dissection or pulmonary embolism,either of which can mimic acute MI but re-quires very different treatment.

CLINICAL CLASSIFICATION OF ACUTE MI

The new classication scheme of the differenttypes of MI is shown in TABLE 4. The new classication scheme does notinclude myocardial necrosis from mechanicalmanipulation of the heart during open heartsurgery, from cardioversion, or from toxicdrugs. As clinicians are aware, it is not unusualto see elevated biomarker levels in a host ofconditions unrelated to acute myocardialischemia or MI. The new classication ofacute MI is most helpful in this regard. It will

likely be even more helpful in guiding treat-ment and management when new ultrasen-sitive troponin assays are widely introducedinto clinical practice.

The new classification also negotiatesthe controversy regarding elevated bio-marker levels following percutaneous cor-onary intervention. In brief, elevation ofbiomarkers is not entirely avoidable evenwith a successful percutaneous coronaryintervention, and furthermore, there is noscientific cutoff for biomarker elevations.

So, by arbitrary convention, the troponin

level must rise to more than three timesthe 99th percentile upper reference limitto make the diagnosis of type 4a MI. Aseparate type 4b MI is ascribed to angio-graphic or autopsy-proven stent thrombo-sis.

The new guidelines also suggest that tro-ponin values be more than ve times the 99thpercentile of the normal reference range dur-ing the rst 72 hours following coronary arterybypass graft surgery (CABG) when consider-ing a CABG-related MI (type 5). Whenevernew pathologic Q waves appear in territoriesother than those identied before the pro-cedure, MI should be considered, especiallyif associated with elevated biomarkers, newwall-motion abnormalities, or hemodynamicinstability.

Thus, the diagnosis of acute MI now has

TABLE 4

Clinical classication of MI

Type 1Spontaneous myocardial infarction (MI) related to ischemia due toa primary coronary event such as plaque erosion and/or rupture,ssuring, or dissection

Type 2MI secondary to ischemia due to either increased oxygen demandor decreased supply, eg, coronary artery spasm, coronary embolism,anemia, arrhythmias, hypertension, or hypotension

Type 3Sudden unexpected cardiac death, including cardiac arrest, oftenwith symptoms suggestive of myocardial ischemia, accompaniedby presumably new ST elevation, new left bundle branch block, or

evidence of fresh thrombus in a coronary artery by angiographyand/or at autopsy, but death occurring before blood samples couldbe obtained or at a time before the appearance of cardiacbiomarkers in the blood

Type 4aMI associated with percutaneous coronary intervention

Type 4bMI associated with stent thrombosis as documented byangiography or at autopsy

Type 5MI associated with coronary artery bypass grafting

REPRINTED FROM THygEsEN K, ALPERT Js, WHITE HD, ON BEHALF OF THE JOINT EsC/ACCF/AHA/ WHF TAsK FORCE FOR THE REDEFINITION OF MyOCARDIAL INFARCTION. UNIVERsAL DEFINITION

OF MyOCARDIAL INFARCTION. J AM COLL CARDIOL 2007; 50:21732188, WITH PERMIssIONFROM ELsEVIER. HTTP://WWW.sCIENCEDIRECT.COM/sCIENCE/JOURNAL/07351097.


8/8


widely accepted global criteria that distinguishvarious types of acute MI that occur under mul-tiple circumstances. It is expected that describ-ing the type of acute MI according to the new

criteria will further enhance our understandingof the event, its proper management, and itsprognosis.

REFERENCES 1. The Joint European Society of Cardiology/American

College of Cardiology Committee . Myocardial infarctionredeneda consensus document of the Joint EuropeanSociety of Cardiology/American College of CardiologyCommittee for the Redenition of Myocardial Infarction.J Am Coll Cardiol 2000; 36:959969.

2. Thygesen K, Alpert JS, White HD, on behalf of the JointESC/ACCF/AHA/WHF Task Force for the Redenition ofMyocardial Infarction . Universal denition of myocardial

infarction. J Am Coll Cardiol 2007; 50:21732188. 3. Roger VL, Killian JM, Weston SA, et al . Redenition of

myocardial infarctionprospective evaluation in thecommunity. Circulation 2006; 114:790797.

4. Jaffe AS, Babuin L, Apple FS . Biomarkers in acute cardiacdisease. J Am Coll Cardiol 2006; 48:111.

5. French JK,White HD . Clinical implications of the new de-nition of myocardial infarction. Heart 2004; 90:99106.

6. James TN . The variable morphological coexistence ofapoptosis and necrosis in human myocardial infarction:signicance for understanding its pathogenesis, clinicalcourse, diagnosis and prognosis. Coron Artery Dis 1998;9:291307.

7. Sobel BE, LeWinter MM . Ingenuous interpretation ofelevated blood levels of macromolecular markers of myo-cardial injury: a recipe for confusion. J Am Coll Cardiol2000; 35:13551358.

8. Osler W . Aequanimitas: With Other Addresses to MedicalStudents, Nurses and Practitioners of Medicine. Osler Wil-liam Edition: 3, revised. Philadelphia: Blakistons, 1932.

9. Wang F, Asinger RW, Marriott HJ . ST-segment elevation inconditions other than acute myocardial infarction. N EnglJ Med 2003; 349:21282135.

ADDRESS : Shaun Senter, MD, MS., Cleveland Clinic Heart andVascular Institute, J132-7, 9500 Euclid Avenue, Cleveland, OH,44195; e-mail [email protected].

Copyright CompliancePermission to reproduce articles from the Cleveland Clinic Journal ofMedicine may be obtained from:Copyright Clearance Center1-800-982-3887, ext. 2862marketing @copyright.comwww.copyright.com

CME ANSWERSAnswers to the credit test on page 206 of this issue

1B 2D 3E 4A 5D 6A 7E 8A


definisi ami.pdf

Documents