STEMI and NSTEMI are two distinct pathophysiological entities

David Rott 1. Department of Medicine Hadassah-Hebrew University Medical Center Mt. Scopus Jerusalem !"#$ %srael &. Hadassah Hebrew University Medical Center Mt. Scopus Jerusalem %srael David Leibowitz 1. &.

'uthor 'ffiliations
Department of Medicine Hadassah-Hebrew University Medical Center Mt. Scopus Jerusalem !"#$ %srael Hadassah Hebrew University Medical Center Mt. Scopus Jerusalem %srael

(el) * !& & #+$ $#&, -a.) * !& ,& #+1 &!#$ E-mail address) drott/,1&.net.il

Montalescot et al.1 recently demonstrated that patients with S(0M% and 1S(0M% have similar in-hospital and lon2-term pro2noses as well as similar independent correlates of outcome3 despite very different in-hospital mana2ement. 's per accepted 2uidelines3 whereas most S(0M% patients underwent emer2ent reperfusion treatment 4e.2. primary 5C% or thrombolysis63 1S(0M% patients hardly ever received this 7ind of therapy.&(his different treatment strate2ies3 however3 are 8ustified by evidence-based medicine as thrombolytic therapy in non-9 wave M% patients showed no benefit over standard therapy.: (he reason for the failure of intravenous thrombolytic therapy to improve clinical outcomes in the absence of 'M% with S(se2ment elevation is most li7ely related to the fact that in S(0M% the culprit artery is usually occluded by a thrombus3 whereas in 1S(0M% the culprit artery is usually patent with a non-occlusive thrombus. (he development of S(0 vs. 1S(0 M% does not appear to be coincidental. ;e have demonstrated that most patients with recurrent M% episodes will have either repeated episodes of S(0M% or 1S(0M% but not both3 su22estin2 predilection of some patients to repeated episodes of occlusive thrombi and others to repeated episodes of non-occlusive thrombi.$ Smo7in2 cessation did not influence this findin2.# %ndividual differences in endo2enous tissue plasmino2en activator levels<activity as well as fibrino2en =%% and 5'%-1 levels3 may e.plain these differences which su22est S(0M% and 1S(0M% are in fact different entities. (herefore3 while we certainly a2ree with the authors that secondary prevention such as a22ressive lipid lowerin23 antiplatelet therapy3 etc. are critical with either type of M%3 it is still important to consider S(0M% and 1S(0M% as distinct entities.
5ublished on behalf of the 0uropean Society of Cardiolo2y. 'll ri2hts reserved. > (he 'uthor &,,!. -or permissions please email) 8ournals.permissions/o.ford8ournals.or2

References

1.

Montalescot ?3 Dallon2eville J3 =an @elle 03 Aouanet S3 @aulac C3 De2randsart '3 =icaut 0 . S(0M% and 1S(0M% ) are they so differentB 1 year outcomes in acute myocardial infarction as
defined by the 0SC<'CC definition 4the C50A' re2istry6. 0ur Heart J &,,!D&+)1$, -1$1!.

&.

@raunwald 03 'ntman 0M3 @easley J;3 Califf AM3 Cheitlin MD3 Hochman JS3 JonesAH3 Eerei a7es D3 Eupersmith J3 Fevin (13 5epine CJ3 Schaeffer J;3 Smith 00 :rd3Steward D03 (herou. 53 ?ib bons AJ3 'lpert JS3 -a.on D53 -uster =3 ?re2oratos ?3HiratG7a F-3 Jacobs 'E3 Smith SC Jr. 'CC<'H'
&,,& 2uideline update for the mana2ement of patients with unstable an2ina and non-S(-se2ment elevation myocardial infarction. J 'm Coll Cardiol &,,&D$,)1:""-1:!$.

:.

0ffects of tissue plasmino2en activator and a comparison of early invasive and conservative strate2ies in unstable an2ina and nonH9 wave myocardial infarction) results of the (%M% %%%@ trial. (hrombolysis %n Myocardial %schemia. Circulation1 $D+ )1#$#-1##".

$. #.

Aott D3 ;eiss '3 Cha8e7-Shaul (3 FeibowitG D . S( deviation patterns in recurrent myocardial

infarctions. 'm J Cardiol &,,"D +)1,-1:.

Aott D3 Salameh S3 ;eiss '3 Cha8e7-Shaul (3 FeibowitG D . Smo7in2 cessation does not alter S( deviation pattern of recurrent myocardial infarctions. %nt J Cardiol&,,!. in press.

Why thrombolysis angina ?

is

contraindicated

in

unstable

September 1,3 &,,+ by dr s ven7atesan %ntra coronary thrombosis is the sine Iua non of acute coronary syndrome 4 @oth S(0M% and 1S(0M%.6 @ut thrombolysis is the specific therapy in S(0M% and is contraindicated in 1S(0M%<U'.

Why is this apparent paradox ? What is basic differnce between UA and A ! ?

%n S(0M% there is a sudden J total occlusion of a coronary artery usually by a thrombus with or without a plaIue .(he immediate aim is to open up the blood vessel . 0very minute is important as myocardium under2oes a continuous process ischemic necrosis. So thrombolysis

4or more specifically fibrinolysis should be attempted immediately6 .(he other option is primary an2ioplasty3 which will not be discussed here. (he thrombus in S(0M% is A@C J fibrin rich and often called a red clot. 1umber of fibrinolytic a2ents li7e strepto7inase3 (issue palsmino2en activator34(5'6 Aeteplace3 (ene7teplace etc have been tested and form the cornerstone of S(0M% mana2ement.(he untoward effect of stro7e durin2 thrombolysis is well reco2nised 3 but usully the ris7 benefit ratio favors thrombolyis in most situations e.cept in very elderly and previous history of stro7e or bleedin2 disorder.

Unstable an2ina is a close companion of S(0M% . Many times it precedes S(0M% often called preinfarction an2ina. Durin2 this phase blood flow in the coronary artery becomes slu22ish 2radually3and patients develop an2ina at rest .@ut unli7e S(0M% there is never a total occlusion and myocardium is viable but ischemic3 and emer2ency salva2in2 of myocardium is not a therapeutic aim but prevention of M% becomes an aim. %t is a parado. of sorts 3 even thou2h thrombus is present in U' 3 %t has been learnt by e.perience thrombolytic a2ents are not useful in preventin2 an M% . Why thrombolysis is not useful in UA ? 1. %n unstable an2ina mechanical obstruction in the form of plaIue fissure<rupture is more common than completely occludin2 thrombus. So lysis becomes less important. &. 0ven if the thrombus is present 3 it is often intra plaIue or intra lesional and the luminal pro8ection of thrombus is reduced and hence thromolytic a2ents have limited area to act. -urther in U'<1S(0M% since it is a slow and 2radual occlusion 4Unli7e sudden J total occlusion in S(0M%6 the platelets 2et mar2inalised and trapped within the plaIue .Hence in U' thrombus is predominantly white. Cften3 a central platelet core is seen over which fibrin clot may also be formed. 'll available thrombolytic a2ents act basically as a fibrinolytic a2ents3 and so it finds difficult to lyse the platelet rich clot.(here is also a small ris7 of these a2ents lysin2 the fibrin cap and e.posin2 underlyin2 platelet core and tri22er a fresh thrombus.(his has

:.

$.

been documented in many trials4 (%M% :b to be specific6 So if we thrombolyse in U' 3 there could be a ris7 of recurrent 'CS episodes in the post thrombolytic phase. #. U' is a semi emer2ency where there is no race a2ainst time to salva2e myocardium .'dministerin2 a stro7e prone thrombolytic a2ent tilts the ris7 benefit ratio a2ainst it. 'mon2 U'3 there is a si2nificant 2roup of secondary <perioperative U' due to increased demand situations. Here there is absolutely no role for any thromolytic a2ents3 the simple reason is 3 there is no thrombus to 2et lysed. Many of the U' patient revascualarisation directly. have multivessel C'D and mi2ht reIuire sur2ical

".

!.

"o fibrinolytic agents are contraindicated in UA so what is the next step ? (he emer2ence of intensive and a22ressive platelet-lytic a2ents. ' combination of aspirin3 clopido2rel3 heparin3 2lycoprotien &b :a anta2onist formed the ma8or therapeutic protocol in these patients.0ven thou2h these are called antiplalet a2ents some of them li7e &b<:a anta2onist eptifibatide3 tirofiban3 and many times even heparin has a potential to dissolve a thrombus. So technically one can call these a2ents as thrombolytic a2ents. What are the unresolved issues? 0ven thou2h clinical trials have convincin2ly shown thrombolytic a2ents have no use in U' .(here is a na22in2 belief (H'( there could be 2roup of patients with U' 3 still mi2ht benefit from thrombolysis as total occlusions have been documented in some cases with U'.(his is especially true in peri-infarction unstable an2ina 45re J post6 as there is a fluctuation between total and subtotal occlusions 6 .@ut bed side reco2nition of this population is very difficult. Many would consider this issue as redundant now3 since most of these patients are ta7en up for emer2ency revascularisations why thrombolytics are contraindicated in #"$% ! & Unstable Angina? 'n interestin2 J intelli2ent3 clinically important IuestionK 1owadays3 the first choice in all the cases of M% is early interventional procedure. Durin2 my &# years of clinical carrier as an intensivist in emer2ency cardiolo2y3 % have hardly seen a patient bein2 stabiliGed after havin2 thrombolytic therapy3 instead the increase in the overall morbidity J delayed stability as well as cardiovascular complications are a matter of serious concern. (his mi2ht be e.plained as follows in short. 16 'lthou2h thrombolytics are effective3 their action is not tar2et specific. &6 (hence these are bound to cause si2nificant J serious hemorrheolo2ical disturbances3 li7e micro J macrovascular end or2an hemorrha2es leadin2 to multior2an failure. :6 0ven in patients of S(0M%3 the thrombolytic therapy should be considered only if there are no options or non availability of interventional cardiolo2ical procedures in remote areas3 J the symptoms are not more than si. hours duration. $6 'n important J immediate complication of thrombolytic therapy is the possibility of emer2ent reperfusion arrhythmias which mi2ht be fatal. 4Dr. E. 'shutosh 5osts) :1!$ Joined) &!<:<&,1& Fast 5ost) 11<11<&,1:6 Unstable an2ina and non-S( elevation 4non-9 wave6 myocardial infarction 41S(0M%6 are part of the continuum of acute coronary syndrome 4'CS6 that also includes S( elevation M%. (wo observations constitute the rationale for consideration of the use of fibrinolytic a2ents in the treatment of unstable an2ina or acute 1S(0M%) (he important role of intraarterial thrombus formation in this disorder (he efficacy of fibrinolysis in the mana2ement of acute S( elevation 49 wave6 M% 4S(0M%6.

%n S(0M%3 fibrinolytic a2ents offer a trade-off between reduced mortality and increased incidence of intracerebral bleedin2. %n this settin23 the net benefit is e.pressed as a difference between these two events. (he choice of dose and the means of administration. Diagnosis 'eart Attac( %f a heart attac7 is suspected3 you should be admitted to hospital immediately. Lou will usually be admitted to an acute cardiac care unit 4'CCU6 so the dia2nosis can be confirmed and treatment be2in. 0lectrocardio2raph 40C?6 'n electrocardio2raph 40C?6 is an important test in suspected heart attac7s. 'n 0C? should be carried out within 1, minutes of bein2 admitted to hospital. 'n 0C? measures the electrical activity of your heart. 0very time your heart beats3 it produces tiny electrical si2nals. 'n 0C? machine records these si2nals onto paper3 allowin2 your doctor to see how well your heart is functionin2. 'n 0C? is painless and ta7es about five minutes to perform. Durin2 the test3 electrodes 4flat metal discs6 are attached to your arms3 le2s and chest. ;ires from the electrodes are connected to the 0C? machine3 which records the electrical impulses. (here are two reasons why an 0C? is so important) it helps confirm the dia2nosis of a heart attac7 it helps determine what type of heart attac7 you have had3 which will help determine the most effective treatment for you (ypes of heart attac7 Heart attac7s can be classified by a measurement 7nown as the S( se2ment. (he S( se2ment is an electrical measurement recorded by an 0C?. %t corresponds to the level of dama2e inflicted on the heart. (he hi2her the S( se2ment3 the 2reater the dama2e li7ely. 'cute coronary syndrome ' heart attac7 is a form of acute coronary syndrome 4'CS6D which is where there is a si2nificant bloc7a2e in the coronary arteries. (here are three main types of 'CS) S( se2ment elevation myocardial infarction 4S(0M%6 non-S( se2ment elevation myocardial infarction 41S(0M%6 unstable an2ina (he three types are described in more detail below. S( se2ment elevation myocardial infarction 4S(0M%6 ' S(0M% is the most serious type of heart attac7. %n this type of heart attac73 a prolon2ed interruption to the blood supply3 resultin2 from a total bloc7a2e of the coronary artery3 can cause e.tensive dama2e to a lar2e area of the heart. ' S(0M% is what most people thin7 of when they hear the term heart attac7. 1on-S( se2ment elevation myocardial infarction 41S(0M%6 'n 1S(0M% can be less serious than a S(0M%. (his is because the supply of blood to the heart is only partially bloc7ed3 rather than completely bloc7ed. 's a result3 a smaller section of the heart is dama2ed. However3 1S(0M% is still re2arded as a serious medical emer2ency. Unstable an2ina Unstable an2ina is the least serious type of 'CS althou2h3 li7e 1S(0M%3 it is still re2arded as a medical emer2ency. %n unstable an2ina3 the blood supply to the heart is still seriously restricted3 but there is no permanent dama2e so the heart muscle is preserved. Cther tests ' number of other tests can be used to assess the state of your heart and chec7 for related complications. However3 because heart attac7s are medical emer2encies3 some tests are usually only carried out once your initial treatment has be2un and your condition has been stabilised.

@lood tests Dama2e to your heart from a heart attac7 causes certain proteins to slowly lea7 into your blood. 0nGymes are special proteins that help re2ulate chemical reactions that ta7e place in your body. %f you have had a suspected heart attac73 a sample of your blood will be ta7en so it can be tested for these heart proteins 47nown as cardiac mar7ers6. Lour protein levels will be measured throu2h a series of blood samples ta7en over the course of a few days. (his will allow dama2e to your heart to be assessed3 and also help determine how well you are respondin2 to treatment. Chest M-ray ' chest M-ray can be useful if dia2nosis of a heart attac7 is uncertain and there are other possible causes of your symptoms3 such as a poc7et of air trapped between the layers of your lun2s 4pneumothora.6. ' chest M-ray can also be used to chec7 whether complications have arisen from the heart attac73 such as a build-up of fluid inside your lun2s 4pulmonary oedema6. 0chocardio2ram 'n echocardio2ram is a type of ultrasound scan that uses sound waves to build up a picture of the inside of your heart. (his can be useful to identify e.actly which areas of the heart have been dama2ed and how this dama2e has affected your heartNs function. Coronary an2io2raphy Coronary an2io2raphy can help determine whether a bloc7a2e or narrowin2 has occurred in the coronary arteries and3 if so3 to locate the e.act location of the bloc7a2e or narrowin2. (he test involves insertin2 a thin tube3 7nown as a catheter3 into one of the blood vessels in your 2roin or arm. (he catheter is 2uided into your coronary arteries usin2 M-rays. ' special fluid3 7nown as a contrast a2ent3 is pumped throu2h the catheter. (his fluid shows up on M-rays. Studyin2 how it flows around and throu2h your heart can help locate the site of any bloc7a2e or narrowin2. ' coronary an2io2ram is often performed 8ust before sur2ery because the results can help 2uide the efforts of the sur2eon. See treatin2 a heart attac7 for more information. #"$% ! 1on-S( Se2ment 0levation Myocardial %nfarction 41S(0M%6 is one of the three types of 'cute Coronary Syndrome 4'CS63 and li7e all 'CS3 1S(0M% should be considered a medical emer2ency. 1S(0M% is identical to unstable an2ina e.cept for one thin2. %n 1S(0M%3 in contrast to unstable an2ina3 cardiac enGyme blood tests are abnormal3 indicatin2 that at least some actual cell dama2e is occurrin2 to heart muscle cells. -undamentally3 however3 in every other way 1S(0M% and unstable an2ina are identical. (hey both indicate that a plaIue has ruptured in a coronary artery3 that the ruptured plaIue and the associated blood clot are producin2 partial bloc7a2e of the artery3 and that the heart muscle supplied by that artery is in 2rave dan2er of sustainin2 irreversible dama2e. %n other words3 the imminent ris7 of a OfullO myocardial infarction3 with irreversible death of part of the heart muscle3 is very hi2h in both 1S(0M% and unstable an2ina. (he symptoms3 the clinical circumstances3 and the treatment of 1S(0M% are identical to those of unstable an2ina.Lou can read about those aspects of 1S(0M% here. Source) (hy2esen3 E3 'lpert3 JS3 ;hite3 HD3 et al. Universal definition of myocardial infarction) Eristian (hy2esen3 Joseph S. 'lpert and Harvey D. ;hite on behalf of the Joint 0SC<'CC-<'H'<;H- (as7 -orce for the Aedefinition of Myocardial %nfarction. 0ur Heart J &,,!D &+)&#&#.