ST Segment Elevations : Always a marker of myocardial infarction ?

Review article

Chairperson :Prof. DR. Chandrasekhara .PM.V.J.Medical College & R.H.

By: Dr. M. Ramesh Babu

About journal

• Indian heart journal .• Volume 65,Number 4, july-august 2013.• G. Coppola a, P. Carita` a, E. Corrado a, A.

Borrelli b, A. Rotolo a, M. Guglielmo a, C. Nugara a, L. Ajello a,*, M. Santomauro c, S. Novo a .

• on behalf of the Italian Study Group of Cardiovascular Emergencies of the Italian Society of Cardiology, University of Palermo , Italy

Introduction

Introduction

Conduction system

6

Introduction

7

E C G

ST segment

• ST segment – interval between depolarization and repolarization of the ventricles.

• ST can be evaluated by using a baseline reference both the PQ and the TP segments.

• PQ segment may be altered by atrial lesions (i.e. valvular diseases, acute pericarditis or atrial infarction).

• In limb leads, the ST segment is isoelectric in >75% of healthy adults.

ST Segment

ST segment <2mm in chest leads

ST segment not more than 0.5 mm in limb leads

ST segment

• The magnitude of ST deviation is related to the amplitude of QRS complex and is higher and more common in young adults of male gender.

• In non-pathological conditions,the elevation can reach even 0.3 mV in V2-V3, while is rarely more than 0.1 mV in the other precordial leads.

• In the MI, ST segment elevation is believed to represent a “current of injury” From damaged cells that are partially depolarized to the healthy myocardium.

ST segment

• In presence of currents of injury, each compensation of the TQ segment induces a displacement of ST segment in a higher position and leads to an elevation.

• The ST segment represents the phase two (plateau) of the action potential (AP): it is possible to suppose that any modification of AP may result in an ST segment deviation.

• In some non-ischemic conditions (such as the Brugada Syndrome), the speed of AP in the epicardial surface seems to be lower than in the endocardial one.

How to measure ST segment?

Abnormalities of ST segment• 1 . Depression of the ST segment.• 2. Elevation of the ST segment.

• Depression of the ST segment• Commonest abnormality mostly marked in V5 and V6 ,

especially V 5.• The basic mechanism giving rise to ST segment depression

is injury to the subendocardial region of the left ventricle.• ST segment force or vector is always deviated towards the

surface of injury.

Forms of ST segment depression

• 1. Horizontally of the ST segment:• One of the earliest sign of coronary insuffiency is the

development of ST segment change horizontally.• The ST segment becomes isoelectric for an

appreciable period , usually 0.12sec or longer.• 2. Upward sloping ST segment:• This is a form of junctional ST segment depression

where only the proximal part of the ST segment – its junction with the QRS complex – is depressed.

Forms of Junctional ST segment

• A hypothetical parabola joining the distal limb of the P wave , the PR segment , the ST segment and the proximal limb of the T wave will be smooth and unbroken.

• It is usually still difficult or impossible to separate the ST segment from the T wave since no ST-T junctional angle has developed.

• A hypothetical parabola will be broken and step- like.• A distinct angle between the ST segment and the T

wave is usually present so that the two can be defined and seperated.

Plane ST segment depression

• Depression of a horizontal ST segment results in plane ST segment depression .

• This is always associated with a sharp angled ST-T junction and hence a clear seperation of the ST segment from the proximal limb of the T wave.

Down – sloping ST segment

• This refers to an ST segment which is already depressed at its proximal origin, and then slopes even further downward.

• Reflects a severe form of impaired coronary blood flow.

• Its a transient form and may occur during the spontaneous attacks of angina pectoris (Heberden’s angina) /precipitated by exercise.

• The greater the depression worse the prognosis.

Elevation of ST segment

• Spontaneous/ exercise induced in following conditions:• Coronary spasm –basic mechanism of prinzmetal’s

angina.• Organic stenosis of the coronary arteries.• Left ventricular aneurysm.• Impaired left ventricular function- common finding in MI

patients.• ST segment elevation is usually the expression of

transmural myocardial injury, which is dominantly epicardial.

• Vector directed to the surface of the injury.

NATURAL VARIANTS

Early repolarization / BER• Benign early repolarization (BER), is a non-

pathological condition,(1% of general population and 48% of patients referred to an emergency point of care for chest pain).

• Possible mechanisms: “hypervagotonia”, “asthenic habitus”, and an early start of the repolarization in the epicardial surface before the end of depolarization in the entire myocardium.

Cont..

• In BER, the ECG shows an elevated ST segment that presents a concave slope in more than one lead.

• A notch (or a little delay) in the terminal portion of the QRS complex, associated with the presence of high and concordant T waves, is also detectable.

• The elevation is usually < 0.2 mV (80-90% of the cases) but in some patients it can reach even 0.5 mV.

Cont.

• Only in 2% of the cases, an elevation >0.5 mV is found.• The highest elevation is usually observed in precordial

leads (fromV2 -V5); if it is confined to limb leads a different diagnosis should be evaluated.

• The aspect of T waves (which are typically tall, peaked and concordant) may resemble that one detected in acute myocardial infarction (AMI), especially in the case of posterior involvement.

• D/D’S:pericarditis.

Cont.

• In patients with acute pericarditis, at least at the beginning, there is a frequent depression of PR segment, especially in V6 with a specular elevation in aVR, not present in BER.

• ST segment elevation is usually more pronounced and prone for dynamic changes in pericarditis than in BER.

LV hypertrophy and hypertrophic cardiomyopathy

• LVH is a very common condition that is associated with ST segment elevation.

• As in LBBB, the repolarization pattern is

discordant to the QRS. The elevation is more commonly observed in leads V2-V3 and is usually <0.3 mV with minor in V4-V6.

cont .

• ECG shows high voltage of R waves in antero-lateral leads associated to Q waves in anterior and inferior leads.

• The T waves, usually being very deep and inverted in V2-V4, may resemble a non-Q AMI. Rarely, a real ST elevation might be seen.

ECG hypertrophic cardiomyopathy

LBBB

• In this condition ST segment and T-waves are usually discordant with the QRS, since they are directed in opposite directions.

• A concordant ST segment shift should always be referred to a myocardial lesion and considered as strongly indicative of MI.

• In discordant ST elevation of the J point 0.5 mV in V1-V2 is strongly suggestive of MI in the presence of LBBB.

• The same ST changes have been observed in 7.3% of a population of 124 patients with LBBB without MI.

LBBB

• In the same group, a direct correlation between QRS amplitude and entity of the ST segment elevation was found.

• Moreover, in LBBB, the QRS/T ratio appears to be more predictive than the amplitude of ST elevation.

• When this ratio is near to or < 1, the probability to an MI is high.

LBBB

Criteria for diagnosing acute AWMI with LBBB:• 1. ST elevation in at least one lead of >1mm

concordant to the positive QRS complex (5 points).• 2. ST depression of >1 mm in V1-V3 (3 points).• 3. discordant ST elevation > 5mm in at least one

leads with a predominant negative QRS (2 points).• A total > or = to 3 points is s/o an acute MI in

presence of LBBB.

LBBB

• An Acute IWMI with LBBB can be diagnosed routinely as there is no masking effect of the LBBB in the inferior leads.

LBBB

Diagnosing old AWMI with LBBB• Presence of LBBB may mask features of old AWMI.• Presence of Q waves in leads V5-V6 ,I or AVL in

presence of LBBB S/O old AWMI.• Notching of 50 ms on the ascending limd of the S

wave of leads V3-V5 ( Cabrera’s sign).• Notching in the upstroke of R wave in leads I, AVL

or V6 ( Champan’s sign) are considered indicators of old AWMI in presence of LBBB.

Artifacts

Leads malpositioning:• Usually, during stress test and in emergency

point of care, even the peripheral electrodes are positioned on the chest (Mason-Likar disposition).

• Sometimes, this kind of disposition may alter the Einthoven Triangle leading to possible alterations of the ST segment.

Artifacts

• During electrical cardioversions or the adminisration of a DC shock by an implantable cardioverter defibrillator, a transient ST segment elevation is rarely observed.

• A consistent ST elevation for more than 2 min may indicate a myocardial lesion

Atrial Flutter 2:1(a) after a DC shock (b).

In Cardiovascular diseases

Pericarditis.• Although pericardium is electrically inactive, its infection

and/or inflammation may affect the external part of epicardium and cause significant ECG modifications.

• In Acute pericarditis :• Earliest sign is tall and symmetrical T waves.• Abnormalities in ST segment – elevated concave upward

ST segment (saddle shaped) with tall and peaked T wave . Vector is towards the injured tissue.

• Sinus tachycardia.

Acute pericarditis

ST elevation is seen only in contiguous leads (regional lead group such as anterior, inferior or lateral/apical) with a frequent depression in the reciprocal leads.

Cont..

• In sub acute pericarditis:• ST segment will become convex upward with

isoelectric T wave.• In chronic pericarditis :• Low to inverted T waves in most leads.• Diminshed amplitude of all the ECG

deflexions.• Potential electrical alterns.

In Myocarditis

• It is defined as the inflammation of the myocardium.• Clinically ranges from subclinical disease

(asymptomatic ECG abnormalities) to fulminant heart failure presenting as a new onset cardiomyopathy.

• It should be considered in young patients symptomatic for acute, ischemic-like chest pain associated with ECG abnormalities and global (rather than segmental) left ventricular dysfunction on ECHO.

Cont.

• The ECG changes, despite angiographically documented absence of coronary vessels involvement, vary from ST segment upsloping in contiguous leads, T waves inversions, widespread ST segment depressions.

• Increase of the VAT• Rough or irregular deflexions• Pathological q waves• Increased QRS duration• Atypical intraventricular conduction defect.

ECG myocarditis

Aortic dissection

• May sometimes be associated with an ST segment elevation due to the involvement of the ostia of coronary arteries, to cardiogenic shock after tamponade or to pre-existing coronary artery disease.

• In other cases, it is possible to observe a phenomenon called “wandering ST”, which is a marker of the disease progression and is characterized by the transient elevation of the ST segment in some leads that reappears in other leads.

Ventricular aneurysm

• The persistence of the typical pattern of the fully evolved phase of myocardial infarction- Q wave ,raised ST segment and inverted T wave – for 3 months or longer after the acute attack suggests the ventricular aneurysm.

Prinzmetal’s angina• It is associated with elevation of ST segment. • The modifications of ST segment, although transient, are the

same of STEMI, since they result from transmural ischemia.• ECG manifestations:• Elevation ST segment frequently manifests in leads V2-V6

amplitude from 4mm to 40mm.• Higher the elevation higher the severity.• Abnormal T waves – the T wave becomes pointed and

widened.• Abnormal QRS complexes – an increase in the amplitude of

the R wave ,a diminution in the depth of the S wave, intraventricular conduction defects like LBBB and RBBB.

Prinzmetal’s angina

Transient elevation of ST segment in inferior leads in patients symptomatic for chest pain and histamine fish poisoning.

Prinzmetal’s angina

Transient elevation of ST segment in inferior leads in patients symptomatic for chest pain who was going to be transferred in the surgery room for an orthopedic intervention.

Brugada Syndrome and arrhytmogenic right ventricular cardiomyopathy/dysplasia

• Osher and Wolff, for the first time in 1953, described a persistent ST elevation in precordial leads without ischemia or any other possible explanation.

• In 1992, Brugada et al described a syndrome which was characterized by RBBB, ST segment elevation in leads V1 to V3 and sudden cardiac death in subjects <65 years.

Cont.

• The imbalance between inwards and outwards ionic currents at phase I defines the pathological substrate for Brugada.

• This channelopathy is a rare conidition.• Originally, 3 patterns of Brugada syndrome were

described.• But only the type I that is charecterized by a

RBBB pattern, ST segment elevation with coving, can be confused with MI.

Cont.

• In type I Brugada syndrome,- maximum ST elevation-In v1 or V2 , coved ST segment with J point elevation fallowed by negative T wave.

• In type II – saddle back configuration with high takeoff of ST segment ,ending in positive or biphasic T wave without touching baseline.

• In type III – ST segment elevation of <0.1mv with either of the morphologies.

Wolff Parkinson White Sndrome• WPW syndrome is an electrocardiographic syndrome which is

the expression of an anomalous AV conduction pathway , congenital in origin.

ECG changes:• A short PR interval.• A slurred , thickened, initial upstroke of the QRS complex,

which is termed as delta wave.• A relatively normal- narrow- ensuing terminal QRS deflexion.• Slightly widening of the QRS complex as a whole.• Secondary ST segment and T wave changes i.e. changes which

are secondary to the abnormal intraventricular conduction of pre-excition , may be confused with myocardial disease.

ARVC/D

• Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a genetically determined heart muscle disorder that is characterized by the fibro-fatty replacement of right ventricle myocardium in the so called “triangle of dysplasia”.

• The disease has a variable expression but even in its concealed form individuals are often asymptomatic but may be at risk of sudden cardiac death especially during exertion.

Cont.

• The (major and minor) criteria for the diagnosis, which are based on structural, histological, ECG, arrhythmic and familial features, have been recently revised.

• Notably, in subjects with ARVC/D, there is often an elevation of ST segment which is similar to that detectable in Brugada syndrome and represent a challenge in differentiating between a real Brugada syndrome or an acute ischemia.

ECG ARVC/D

Arrhythmogenic right ventricular cardiomyopathy/dysplasia.

Pulmonary diseases

• PTE: Obstruction of the blood flow through the lungs leads to an increased pressure overload in the right chambers.

• Major PTE results whenever the combination of embolism size and underlying cardiopulmonary status interact to produce hemodynamic instability.

Cont.

• As the result of pressure overload in the right ventricle, the ECG usually shows tachycardia/atrial fibrillation, right bundle branch block and/or the pattern S1Q3T3, which is considered suggestive,even if not specific.

• Occasionally, an STsegment elevation in right precordial leads is also possible.

• The evidence of Q waves in DIII and aVF (but not in DII) without ST elevation in the same leads may allow to differentiate a PTE from an MI.

Pulmonary thromboembolism

Acute pulmonary embolism

• ECG changes:• Low amplitude deflexions.• Rt. Arterial enlargement.• Rt. Ventricular enlargement.• Rt. Ventricular Myocardial ischaemia.• Rt. Ventricular myocardial injury.• RBBB.• Arterial tachyarrthmias.

ECG changes in frontal leads

• S1,Q3,T3 Pattern.• S-T segment depression in standard leads I and II.• A “ stair case “ ascent of the ST segment in leads I and II,

consists of flattening of the initial part of the ST segment and T wave,fallowed by a more or less sharp rise and then again flattening of the terminal portion of T.

• Rt. Axis deviation.• RBBB.• Tall peaked P waves in lead II.

S1 Q3 T3• S1 (LEAD I) is a frequent manifestation of acute pulmonary

embolism.• Usually changes in few hours to a deep and narrow deflexion.• This may regress within 24 hrs or return normal gradual over

weeks.• A deep prominent q wave in lead III – is an important

component of triad of APE.• Q wave forms q R complex, q S complex does not forms.• This q wave does not fullfill pathological q wave criteria.• T wave inversion in lead III is almost always associated with the

S1 Q3 abnormality.

SI SII SIII Syndrome

• As a normal variant in healthy individuals who have no evidence of heart disease.

• As an expression of RV dominance like in TOF, pulmonary atresia, cor pulmonale, transposition of great vessels.

• In Anterior wall MI especially apical wall infarction.

• In straight back syndrome – a congenital anomaly the upper dorsal vertebral column is lost.

Atelectasis and pulmonary metastases

• Atelectasis is the collapse of lung tissue and results in reduced (or absent) gas exchange and oxygen absorption to healthy tissue.

• The ECG with ST segment elevation usually shows development of a deep S wave in lead I and a new Q wave in lead III.

• The T waves are, however, normal and the classic “SIQ3T3 pattern” observed in patients with PTE is not present.

• Pulmonary hypertension may be able to overload the right ventricle and results in ST segment changes in inferior leads.

• Pulmonary metastases are another cause of ST segment alterations in patients without cardiac artery diseases.

Gastrointestinal diseases

• Acute pancreatitis • Differentiation of acute pancreatitis from an acute coronary

syndrome is difficult.• Pancreatitis itself may indeed produce minor transient ECG

changes that frequently involve T waves (inversions) or ST segment (depression).

• However, sometimes typical changes, such as ST segment elevation without underlying cardiac pathology may be recorded.

• The metabolic abnormalities, such as hypocalcemia, hypernatremia, hypokalemia, hypomagnesemia and insulin-induced hypoglycemia that often characterize the acute pancreatitis,may be involvedin the genesis of these electrocardiographic features.

Cont.

• ST segment elevation and in particular coronary vasospasm, exacerbation of prior coronary artery disease or formation of thrombus in the coronary arteries due to the increased platelet adhesiveness or to coagulopathy induced by pancreatic enzyme.

Acute cholecystitis

• Acute cholecystitis is another acute abdominal condition,which can produce an ST segment elevation that mimics AMI.

• Gallbladder distension is able to increase heart rate, arterial blood pressure and plasma renin levels

Drug induced ST segment elevation

• Many drugs may have cardiac effects through various mechanisms.

• Some drugs can have a “direct” effect by stimulating cardiac receptors or by inducing anatomic damage or inflammation.

• Some others may “indirectly” interfere with the activity of autonomous nervous system.

• A lot of cardiac side effects and ECG modification can be associated with drug consumption.

Cont.

• When an ST segment elevation (or an ECG modification) without a clear clinical setting is detected, the presence of a drug interaction should be always excluded.

• For example, clozapine, which intensively acts on nervous system, may cause hypotension,tachycardia, ST displacement (depression and/or elevation) and myocarditis.

• In such cases, clozapine should be no longer administrated.

Elevation of ST segment during treatment with clozapine.

Digitalis effect• Digitalis effects on myocardial repolarization, consists of 4 ECG changes.• 1. Effect on ST segment- characteristic inverse check mark configuration

of the S-T segment manifests in leads which have dominantly upright QRS complexes, i.e. in leads with tallest R waves.

• When this inverse check mark effect on ST segment appears in leads with the tallest R waves as well as in leads with dominantely negative QRS deflexions s/o digitalis toxity.

• Therapuetic administation of digitalis diminishes the magnitude of the T wave but does not change its direction.

• With digitalis toxicity T wave amplitude diminishes and also changes the direction.

• Shortening of Q-T interval.• Abnormal cardiac rhythms ( II deg. A-v block and ven.extrasystoles, v.t).

Potassium effect (hyperkalaemia)

• Progressive diminution and eventual disappearance of the P wave.

• Widening of the QRS complex.• A bizarre intraventricular conduction defect like RBBB.• Tall , widened and characteristically shaped T wave. The

proximal limb of T wave is steeper than distal limb.• With high k+ levels ST segment disappers and becomes

the ascending limb of the S wave forms continous vertical line with proximal limb of T wave.

• Virtual disappearance of the ST segment.

Hypokalaemia

• Progressive diminution with eventual diaspearance of the T wave.

• Progressive increase in the amplitude of the U wave.

• First and second degree AV block (wenckenbach type).

• Depression of the ST segment. The depression may be horizontal or concave – upward.

Calcium effect(Hypocalcemia)

• Prolongation of Q-T interval due increase in duration (0.50-0.60 sec).

• Elongation ST segment that has increased horizontally and duration (0.3-0.34) ends in a T wave.

• T wave occasionally become inverted, sometimes deeply and increased in amplitude.

Hypercalcaemia

• Shortening of the Q-T interval.• Shortening of the ST segment , virtually

disappears and incorporated into the T wave.• The ST segment sometimes slightly elevated

and gives rise to a impression of epicardial injury.

Hemorrhagic cerebrovascular disease

• ECG changes are usually observed in patients with acute cerebrovascular pathology such as strokes or subarachnoid hemorrhages.

• Subarachnoid hemorrhage is generally due to the rupture of an aneurysm and is characterized by headache, rushing, nausea and loss of consciousness.

• The sympathetic neuronal activation, which is consequent to the increase of intracranial pressure, seems to play an important pathogenic role.

• The ECG modifications may sometimes resemble an MI.

Cont.• The most common abnormalities are prolongation of QT interval,

inversion of T waves and appearance of abnormal U wave.• The literature has reported cases of ST segment elevation in

absence of coronary artery disease; they are probably related to the catecholamine effect on myocytes or to spasm of the epicardial coronary arteries, which at least may even cause a real myocardial ischemia.

• This situation may be also seen in pheochromocytoma, cocaine abuse or emotional stress.

• Sometimes the subarachnoid hemorrhage may also induce an ST segment elevation without the release of markers of myocardial necrosis nor anatomical necrosis, as confirmed by the autopsy.

• Elevation of ST segment during treatment with clozapine.

ECG during acute subarachnoid hemorrhage

Myocardial infarction

• Myocardial infarction results in ischaemia, injury and necrosis.

• Infarction process evolves through 3 phases:• 1. hyperacute phase• 2. fully evolved phase• 3. chronic stabilized phase.

Fully evolved phase

• The infarcted regions consists of a central core of necrosis ,surrounded by injured tissue,which in turn is surrounded by a zone of ischaemic tissue.

• The myocardial necrosis is represented by a QS complex.

• The myocardial injury is represented by an elevated and coved or convex- upward ST segment.

• The myocardial ischaemia is reflected by an inverted , symmetrical and pionted T wave which is increased in magnitude.

Myocardial necrosis

• 1.QS complex : is totally negative QRS complex, with no ensuring positivity.

• QS complexes of myocardial necrosis are evident in leads V2-V4.

• Necrotic tissue is electrically inert and cannot be activated or depolarized.it constitutes a transmural infarction ,an electrical ‘hole’ or ‘window’ within the muscle wall.

• QRS vectors are directed away from a necrotic or infracted myocardium.

Myocardial necrosis

• 2. A Q r complex is the manifestation of a deep wide pathological Q wave which is fallowed by a small r wave.

• This terminal positivity reflects the depolarization of remaining viable myocardial tissue in the infarcted ventricular wall.

• This will occur when the infarction results in endocardial or epicardial rinds of necrosis.

• 3.Attentuation of R wave amplitude without associated pathological Q wave is a frequent manifestation with MI, yet tends to be a neglected diagnostic parameter.

ECG effects of myocardial injury

• Myocardial injury is reflected by deviation of the ST segment , deviated towards the surface of the injured tissue- epicardial surface.

• The ST segment in the fully evolved phase of the infarction are coved or convex upward.

• Reciprocal and indicative changes:• The coved and elevated ST segments of an acute

myocardial infarction are termed indicative changes.• The depressed ST segments associted with an acute

myocardial infarction are termed reciprocal changes.

ECG effects of myocardial ischaemia

• Myocardial ischaemia is reflected in leads oriented to the ischeamic region by inverted, symmetrical and pointed T waves which are frequently also increased in magnitude.

• T wave vector is directed away from the region of myocardial ischaemia.

Hyperacute phase of myocardial infarction

• The hyperacute phase of MI occurs before the fully evolved phase and usually within a few hours of the onset of the infarction.

• ECG changes:• 1. increased ventricular activation time.• 2. increased amplitude of the R wave.• 3. slope elevation of the ST segment.• 4. tall and widened T waves.

Cont.• Increased ventricular activation time: i.e. delay in

the onset of the intrinscoid deflexion- the time from beginning of the QRS complex to the apex of the R wave.

• Time is delayed beyond 0.45sec – 0.6sec.• This is illustrated in leads AVL , V5 and V6.• Increased amplitude of the R wave:• R wave becomes taller , particularly noticeable in

cases of the hyperacute phase of inferior wall MI (leads II,III,AVF).

• The increased ventricular activation time and tall R wave are due to acute injury block.

Cont.• Slope elevation of the ST segment:• The ST segment straight upward sloping then becomes

elevated.• The very earliest sign of this manifestation may merely be a

straightening of the ST segment without any elevation.• Tall and widened T waves:• The T wave becomes very tall and wide , it exceeds the

amplitude of associated R wave.• The monophasic deflexion , it is difficult to separate all 3

deflexions( R, ST and T waves ).• Reciprocal ST segment depression usually occurs in leads to

the uninjured surface.• Prinzmetal’s angina may have identical presentation to the

hyperacute phase of MI. (resolves within 20 min.).

Cont.

• Significance of hyperacute phase:• During this phase that the complication of

primary ventricular fibrillation is most likely to occur.

• Indication for intense vigilance and coronary care monitoring.

• The greater the elevation of the ST segment , and taller the T wave , the more potentially critical situation.

cont

• Chronic stabilized phase:• The elevated ST segment gradually returns to

the baseline , becoming predominantly isoelectric once again.

• The inverted T wave gradually regains its positivity.

• The QRS complex may regain some of its previous positivity.

Sub endocardial infarction

• ECG findings are not as definitive or clear-cut as that of transmural or even epicardial infarction.

• The diagnosis is made by clinico- ECG correlation.• Clinico-biochemical correlation.• In ECG depressed ST segment with deeply inverted

T waves in mid,lateral precordial and in standard leads I and II.

• These abnormal changes persist for several days.

conclusions

• ST segment is a important marker for MI but also a significant finding in lot of other diseases.

Thank you