1.DR. ANJANI ECG LOCALISATION OF CULPRIT VESSEL IN ACUTE MI

2. Blood supply of the heart The two coronary arteries, the right coronary artery (RCA) and left coronary artery (LCA), originate from their respective sinuses of Valsalvathe RCA from the right sinus of Valsalva and the LCA from the left sinus of Valsalva. The right sinus of Valsalva is located anteriorly and the left sinus of Valsalva posteriorly and to the left. The third sinus of Valsalva, located posteriorly and to the right, does not give rise to a coronary artery, and is referred to as noncoronary cusp/sinus. There may be variations in the number, shape, and location of coronary ostia or origins of the coronary arteries, most of which are of no clinical significance. 3. RCA The RCA arises from the right sinus of Valsalva, inferior to the origin of the LCA. It courses anteriorly and inferiorly under the right atrial appendage along the right atrioventricular (AV) groove, toward the acute margin of the heart, where it turns posteriorly and inferiorly toward the crux of the heart and divides into the posterior descending coronary artery (PDA) and the posterolateral ventricular branch (PLB) The RCA supplies the right atrium, right ventricle, posterior third of the interventricular septum, and 4. The conus branch arises as the first branch of the RCA The conus branch courses anteriorly and to the right and supplies the pulmonary outflow tract The sinoatrial nodal artery is the second branch that arises from the proximal RCA in 65.4%, immediately distal to the RCA origin. In 16.6% of cases, the sinoatrial nodal artery arises from the LCX This artery courses toward the superior vena cava near the cranial aspect of the interatrial septum. 5. The next branches of the RCA are the marginal branches that supply the right ventricular myocardium. The acute marginal artery comes off the acute margin of the heart and courses anteriorly and to the right, anterior to the right ventricle. The acute marginal branches supply the free wall of the right ventricular myocardium. 6. In 10% to 20% of patients, an acute marginal branch runs on the diaphragmatic surface of the heart to supply the distal posterior interventricular septum. After the RCA gives off the acute marginal branches, it continues in the right AV groove toward the diaphragmatic aspect of the heart. At the crux of the heart, the RCA makes a U-turn and branches into the PDA and PLB 7. The PDA is of variable size and runs along the diaphragmatic surface in the posterior interventricular groove toward the inferior septum. Short septal branches arising perpendicularly from the PDA supply the posterior third of the septum and can connect with the septal branches from the LAD to form a collateral circulation. The PLB runs in the posterior left AV groove and gives off multiple branches that supply the posterior and inferior wall of the left ventricle. 8. Within 1 to 2 cm of the crux, the PLB runs on the diaphragmatic surface of the left ventricle parallel to the PDA to supply the posterolateral diaphragmatic surface of the left ventricle. Here the RCA can serve as a collateral for an occluded LCX. Also close to the crux of the heart, just distal to the PDA origin, the RCA gives rise to a small AV nodal artery that supplies the AV node of the conduction system . The AV nodal artery arises from the LCX in a left dominant system. 9. LMCA LMCA arises from the left sinus of Valsalva . It courses to the left, beneath the left atrial appendage and posterior to the right ventricular outflow tract, before branching into the LAD and the LCX A normal variation in the anatomy is a true trifurcation of the LM, when the middle branch between the LAD and LCX is called the ramus intermedius (RI) 10. LAD The LAD runs anteriorly and inferiorly in the anterior interventricular groove to the apex of the heart, and supplies the anterior and anterolateral wall of the left ventricular myocardium and the anterior two thirds of the interventricular septum. In approximately 82% of cases, the LAD curves around the cardiac apex to supply part of the inferior wall of the left ventricle. 11. In 7%, it may not reach the apex of the heart, and in about 11% of cases, the LAD terminates in the distal anterior interventricular groove or even more proximally. In such cases, the distal territory may be supplied by an unusually long diagonal branch or by RCA branches that traverse the posterior interventricular groove or the inferior surface of the heart, a normal variant. This is one of the potential collateral routes if either the RCA or the LAD is occluded. 12. The LAD gives off septal perforators and diagonal branches. The diagonal branches course along and supply the anterior and anterolateral wall of the left ventricular myocardium. They can vary in size and number, and are sequentially numbered as they arise from the LAD). The septal perforator branches arise at right angles from the LAD and supply the anterior two thirds of the interventricular septum. 13. They are numbered sequentially as they arise from the LAD and are of smaller caliber then diagonal branches and vary in number (one to five) and distribution. The first septal branch is more constant in position than the first diagonal. It may branch early with both branches running parallel within the septum. Occasionally, a septal branch runs parallel to the LAD within the myocardium of the septum. 14. LCX The LCX runs posteriorly and to the left in the left AV groove . It gives rise to obtuse marginal branches that are also numbered sequentially as they arise from the LCX (OM1, OM2, and OM3) The LCx artery is the dominant vessel in 15% of patients, supplying the left PDA from the distal continuation of the LCx. In the remaining patients, the distal LCx varies in size and length, depending on the number of posterolateral branches supplied by the distal RCA. The LCX and its branches supply the lateral and posterolateral wall of the left ventricle. Additional branches of the LCX are small atrial branches that supply the lateral 15. The RI is the most common variation of LCA anatomy, occurring when the LM trifurcates; the branch between the LAD and the LCX is the RI. The RI can supply the myocardial territory of the diagonal branch or the obtuse marginal branch depending on whether it supplies the anterior wall or the lateral wall of the left ventricular myocardium. When large, the RI perfuses a significant portion of the myocardial territory of the diagonal branch and OM1 16. DOMINANCE OF CORONARY CIRCULATION The artery that supplies the inferior portion of the posterior interventricular septum is considered to be the dominant artery. In 80% to 85% of cases, the RCA is dominant; when at the crux of the heart, it gives rise to the PDA and PLB . In a left dominant system, the LCX continues in the posterior left AV groove and gives rise to the PDA and PLB; this is seen in 7% to 8% of the population. In the remaining 7% to 8%, there is a codominant system or balanced circulation in which the RCA gives rise to the PDA and terminates in the posterior interventricular groove; the LCX may also give rise to a PDA with two PDAs running parallel in the interventricular septum, or the LCX may give rise to all posterolateral branches The nondominant artery is usually smaller in size and terminates early in its respective AV groove. 17. SA Nodal Artery is supplied by the RCA in ~60% of patients. In the remaining ~40% the SAN arises from either the LCx or from both the RCA and LCx. AV Nodal Artery is supplied by the PDA branch from the RCA in ~80-90% of patients. In the remainder the AVN arises from the PDA off the LCx in a left-dominant circulation . Bundle of HIS receives a dual blood supply (from the AVN and LAD). Within the septum the HIS divides into right and left bundle branches. 18. Right Bundle Branch is a relatively thin conduction fascicle; it is primarily supplied by septal perforatorsfrom the LAD (it may also receive collaterals from the RCA or LCx). The common Left Bundle Branch divides after a short distance into the LAH (Left Anterior Hemifascicle) and LPH (Left Posterior Hemifascicle). LAH is supplied by septal perforators from the LAD. LAHB (Left Anterior HemiBlock) is commonly seen with acute anterior MI (since the LAH is very susceptible to ischemia with anterior MI). LPH is much thicker and more diffuse than the LAH. The LPH has a dual blood supply (from RCA andLCA). LPHB (Left Posterior HemiBlock) is rare compared to 19. ECG localisation The electrocardiogram (ECG) is a key investigation in diagnosing acute ST-segment elevation myocardial infarction (STEMI). During acute transmural ischaemia, one of the important determinants of the site of coronary artery occlusion is the direction of the vector of ST-segment deviation. The injury vector is always oriented toward the injured area. The lead facing the injury vector head shows ST-segment elevation and the lead facing the vector tail (opposite leads) shows ST segment depression. 20. Ischaemia at a distance Vs reciprocal changes Patients with ST elevation in one territory often have ST depression in other territories. The additional ST deviation may represent acute ischaemia due to coronary artery disease in non infarct related arteries (ischaemia at a distance) or may represent pure "mirror image" reciprocal changes. Most of the common patterns of remote ST depression probably represent reciprocal changes and not ischaemia at a distance. 21. AWMI In anterior myocardial infarction, ST depression in the inferior leads is reciprocal to involvement of the basal anterolateral region, supplied by the first diagonal branch and represented by ST elevation in leads I and aVL. 22. IWMI In patients with IWMI, ST depression in aVL is a pure reciprocal change and is found in almost all patients, and ST depression in V1V3 probably do not represent ischaemia at a distance, but rather reciprocal changes due to more posterior, inferoseptal, apical, or lateral left ventricular involvement. In contrast, among patients with IWMI, ST depression in V4V6 is associated with concomitant LAD stenosis or three vessel disease. Thus, presence of an atypical pattern of ST depression, and especially ST depression in leads V4V6 in IWMI may signify ischaemia at a distance. 23. In some circumstances, both types of ST depression may be present. In acute myocardial infarction due to occlusion of the D1, in addition to ST elevation in leads I, aVL and V2, there is usually reciprocal ST depression in the inferior leads. The reciprocal ST depression is associated with negative T wave. In contrast, in this type of myocardial infarction if there is ST depression in leads V3V5, it signifies subendocardial involvement. This type of ST depression is associated with tall peaked T waves. 24. IWMI The leads showing the greatest magnitude of ST elevation are, in descending order: leads III, aVF, and II. Caused by occlusion of RCA (80%) or LCX In addition to ST elevation in the inferior leads , reciprocal ST depression in lead aVL is seen in almost all patients with acute inferior myocardial infarction. 25. ECG confirmation of the infarct related artery during acute inferior myocardial infarction may be particularly valuable when coronary angiography indicates lesions in both the right and left circumflex coronary arteries 26. Features favouring RCA as the culprit lesion: ST elevation in LIII > LII (as injury vector is directed to right in RCA occlusion) ST depression in aVL > ST depression in L1 with ST depression > 1 mm in LI and aVL RVMI suggested by ST elevation in V3R,V4R (as RV branch arises from proximal RCA, right ventricular injury cancels reciprocal ST depression in V1,V2 in acute IWMI) ratio of ST depression in V3 to ST elevation in LIII3 in aVL 27. Proximal RCA occlusion: RVMI ratio of ST depression in V3 to ST elevation in LIII 1.2 ST depression in aVL is less frequent; isoelectric or elevation of ST in LI and aVL is more frequent (as lesion is proximal to OM1, injury to anterosuperior base leads to the absence of these reciprocal changes) S:RLII) ST elevation >1 mm in V4R with an upright T (most sensitive sign of RVMI). This sign is rarely seen more than 12 hours after the infarction QS or QR in V3R and/or V4R but has less predictive accuracy than ST elevation in these leads. Occasionally, ST-segment elevation in V2 and V3 results from acute right ventricular infarction, resembling anterior infarction; this occurs only when the injury to the left inferior wall is minimal. Usually, the concurrent inferior wall injury suppresses this anterior ST-segment elevation resulting from right ventricular injury. 31. LATERAL APICAL MYOCARDIAL ZONE In patients with acute inferior myocardial infarction, ST elevation in leads V5 and V6 is thought to indicate extension of the infarct to the lateral aspect of the cardiac apex; however, there is as yet no direct evidence for this. The cause of such an extension may be occlusion of either the left circumflex or a right coronary artery with a posterior descending or posterolateral branch that extends to the lateral apical zone. Tsuka and coworkers found that ST elevation in lead V6 during inferior acute myocardial infarction was associated with a larger infarct size, a greater frequency of major cardiac arrhythmias, and a higher incidence of pericarditis during the patients hospital 32. PWMI The standard 12-lead ECG is a relatively insensitive tool for detecting PWMI Usually caused by LCx occlusion but may also be seen in dominant RCA occlusion. ST-segment elevation in the posterior chest leads V7 through V9 > 0.5 mm in a case of IWMI ST segment depression in leads V1 and V2 (reciprocal changes) in a case of IWMI suggests concomitant posterior wall MI Abnormal R in V1 (0.04 in duration and/or R/S ratio > 1 in the absence of preexcitation or RVH), with inferior or lateral Q waves, isolated - occlusion of a dominant LCx without collateral circulation 33. Isolated ST elevation in leads V7V9 without ST elevation in the inferior leads occurs in only 4% of patients with acute myocardial infarction and is usually due to left circumflex coronary artery occlusion 34. In inferior myocardial infarction due to proximal right coronary artery occlusion with concomitant right ventricular infarction, posterior wall injury may be masked because the two opposed electrical vectors may cancel each other (that is, ST elevation in leads V1V3 with right ventricular infarction and reciprocal ST depression in these same leads with concurrent posterior infarction). 35. AWMI The amount of LV myocardium at risk of infarction in a case of AWMI depends largely on the site of occlusion in the course of LAD. Therefore knowing the site of LAD occlusion with the help of ECG criteria in the emergency room is of immense help. LAD occlusion may lead to a very extensive AWMI, or only septal, apical-anterior or mid-anterior MI depending on the location of occlusion. Proximal LAD occlusion has been documented as an independent predictor of worse outcome related to increased mortality and recurrent MI and distal LAD occlusion is considered to have a favourable outcome. Thus, an early identification of proximal LAD occlusion has crucial value not only from an academic standpoint, but also from a therapeutic point of view. 36. AWMI Precordial lead (V1-V6) ST-segment elevation in patients with symptoms suggestive of ACS indicates STEMI due to LAD occlusion. ST segment changes in other precordial and frontal leads depends on the presence of ischaemia in three vectorially opposite areas, namely (i) basal septal area perfused by proximal septal branch; (ii) basolateral area perfused by 1st diagonal, and (iii) inferoapical area, when distal LAD wraps around apex 37. During acute AWMI, the maximal ST-segment elevation is best recorded in V2 or V3 (V1 V4) In descending order: V2, V3, V4, V5, aVL, V1, and V6 V2 is the most sensitive lead to record ST-segment elevation (sensitivity 99%) and to identify the culprit lesion at the LAD. Lead V1 captures electrical phenomena from the right paraseptal area, which has dual blood supply by the septal branches of the LAD and by a conal branch of the RCA. So patients with AWMI usually have no ST elevation in V1. 38. Rarely, ST elevation in V1V4 signifies proximal RCA occlusion with concomitant right ventricular infarction RVMI that produces ST elevation in leads V1V4 can be distinguished from anterior MI by ST elevation in lead V1 greater than in lead V2, ST elevation in the right precordial leads V3R and V4R, ST depression in lead V6, and ST elevation in the inferior leads II, III, and aVF. The magnitude of ST elevation in lead V1 correlates better with the magnitude of ST elevation in lead V3R than with lead V2, suggesting that ST elevation in lead V1 reflects the right ventricle more than the left ventricle. 39. In the case of RVMI, the ST segment is directed ant.ly and more than +90 to the right (producing downward displacement of ST segment in LI) while in the case of AS LVMI the vector is also anterior but located from -30 to -90 to the left in frontal plane ( producing an elevation of ST segment in LI) 40. Anterosuperior myocardial zone: The high anterolateral wall at the base of the LV is supplied by D1 of LAD , OM1 of LCX , occ. Ramus intermedius The lead that directly faces this zone is aVL. ST elevation in L1 and aVL(part.) in AWMI indicates LAD occlusion proximal to D1 very specific but low sensitivity.This is acc. by ST depression in inferior leads(reciprocal changes) Patients with a long LAD artery that wraps around the cardiac apex have concomitant injury to the inferiorapical and anterosuperior walls of the left ventricle. When this happens, no ST elevation may be seen in either anterosuperior leads (that is, I, aVL) or inferior leads (that is, II, III, aVF) because the opposing forces cancel each other 41. Proximal LAD occlusion 42. ST depression in aVL in AWMI indicates LAD occlusion distal to D1 ST elevation in L1,aVL and V2 with iso electric or ST depression in V3 and V4 indicates isolated D1 occlusion In contrast, a LAD artery occlusion proximal to the first diagonal branch results in ST elevation extending beyond lead V2V3 and occasionally, to V4V6 ST elevation in L1,aVL with reciprocal ST depression in V2 indicates LCX occlusion(as it supplies more posteriorly) 43. ST depression in the inferior leads II, III, and aVF during acute AWMI indicates injury to the high anterolateral wall and does not signify inferior wall ischaemia. Such reciprocal ST depression in the inferior leads indicates LAD occlusion proximal to the first D1branch. However, in patients with a long LAD artery that wraps around the cardiac apex, proximal LAD artery occlusion may not produce reciprocal ST depression in the inferior leads because of extension of the infarction to the inferoapical wall. 44. Several ECG criteria have been reported to indicate a LAD artery occlusion proximal to the first septal perforator branch: (1) ST elevation in lead aVR (2) right bundle branch block (3) ST depression in lead V5 and (4) ST elevation in lead V1 >2.5mm Birnbaum et al found no association between ST elevation in lead V1 and LAD artery occlusion proximal to the first septal branch in one series. Criteria reported to indicate a LAD artery occlusion distal to the first septal perforator branch include abnormal Q waves in leads V4V6 45. Lateral and apical myocardial zones: Anteroseptal pattern with ST elavation confined to V1-V3 indicates LAD occlusion In contrast, isolated ST elevation in leads V4V6, without ST elevation in leads V1V3 is usually due to an occlusion of the left circumflex artery or distal diagonal branch rather than the main LAD artery. It is plausible that in patients with extensive anterior myocardial infarction (ST elevation in leads V1V6), the injury extends to the distal anterolateral wall and cardiac apex due to a long LAD artery and/or prominent diagonal branches,whereas patients with an anteroseptal pattern (ST elevation confined to leads V1V3) have a short LAD artery or large obtuse marginal branches or ramus intermediate branch that supply these anterolateral and apical zones. However, there have been no investigations to determine whether there are differences in coronary anatomy between patients with an anteroseptal versus an extensive anterior myocardial infarction ECG pattern 46. Inferior myocardial zone: During acute anterior myocardial infarction, injury may extend to the inferior wall, as evidenced by ST elevation in leads II, III, and aVF, if the LAD artery wraps around the cardiac apex. However, anterior myocardial infarction that is caused by a LAD artery occlusion proximal to the first diagonal branch does not manifest such an anterior and inferior injury pattern because of cancellation of opposing vectors 47. Indicators of proximal LAD occlusion on surface ECG are ST-segment elevation in V1-V3 and aVL and aVR and ST-segment depression of >1 mm in lead aVF ST-segment depression in V5 disappearance of preexistent septal Q waves in lateral leads (direction of ST-segment vector is upward, toward leads V1, aVL, and aVR, and away from the inferior leads) New QRBBB in V1 is a specific but insensitive 48. Occlusion of the LAD beyond the origin of the first diagonal branch: ST-segment elevation in leads V1, V2, and V3 without significant inferior ST-segment depression LAD occlusion distal to the origin of the first diagonal branch, in a vessel that wraps around the apex to supply the inferoapical region of the left ventricle: ST-segment elevation in leads V1, V2, and V3 with concomitant elevation in the inferior leads 49. BOTTOM LINE Regarding Simultaneous Acute Inf. + Ant. ST Elevation:Simultaneous inferior ST elevation may occur in as many as 15% of patients with acute anterior MI. Some of these patients have a "wraparound" LAD but others may have a proximal RCA occlusion as the "culprit artery". Clues to whether the "culprit artery" is proximal RCA vs 'wraparound' LAD include: i) ST elevation in III > II(suggests prox RCA); ii) ST elevation in V1 > V3 (suggests prox RCA); - or - iii) progressively more ST elevation as one moves from V1-toward-V4 (suggests 'wraparound' LAD). 50. LMCA stenosis Typical ECG findings in severe LMCA stenosis or occlusion include ST-segment elevation in lead aVR more than V1 with either widespread ST-segment depression or anterior ST elevation. Yamaji et al described an aVR ST-segment of >0.05 mV elevation present in 88% of the LMCA obstruction group compared with 46% in the left anterior descending artery. 51. Grading of ischaemia Shortly after occlusion of a coronary artery, serial ECG changes are detected by leads facing the ischaemic zone Grade I ischaemia: the T waves become tall, symmetrical, and peaked Grade II ischaemia: there is ST elevation , without distortion of the terminal portion of the QRS Grade III ischaemia: changes in the terminal portion of the QRS complex appear. These changes include an increase in the amplitude of the R waves and disappearance of the S waves. 52. Differentiation between viable and necrotic myocardium at the ischemic area at risk Q waves were traditionally considered as a sign of myocardial necrosis It has been suggested that Q waves that appear within six hours from onset of symptoms do not signify irreversible damage, do not preclude myocardial salvage by thrombolytic therapy transient and disappear later. Several authors have found early Q waves to be associated with larger ischaemic zone and ultimate infarct size. 90 minutes after thrombolytic therapy, TIMI flow grade III is achieved less often in patients with than without abnormal Q waves on presentation 53. Early inversion of the T waves, along with ST elevation resolution, is a sign of reperfusion Wong et al reported that 90 minutes after thrombolytic therapy, TIMI flow grade III was seen less often in patients presented with ST elevation and negative T waves than in those with positive T waves Therefore, ST elevation with negative T waves, especially if it occurs in patients presenting more than two hours of onset of symptoms, might be a sign of a more advanced stage of myocardial infarction with lesser chance of achieving successful reperfusion and higher mortality. It might be a sign that irreversible damage has already 54. PRESENCE OF OLD MYOCARDIAL INFARCTION Presence of abnormal Q waves in leads without ST elevation is suggestive of old myocardial infarction. However, pathological Q waves in leads with ST elevation do not necessarily mean old myocardial infarction or completion of the present acute myocardial infarction. 55. THANK YOU 56. Acute INFERIOR Infarction: Sinus Bradycardia and 1st, 2nd, or 3rd degree AV block may all be seen with acute inferior MI. When they occur early (within the first ~6 hours) increased vagal tone is the most common mechanism. As a result Atropine (sometimes in low dose) tends to be very effective if treatment is needed. Complete (3) AV block with acute inferior MI is generally at the level of the AV Node. As a result the QRS isusually narrow and the escape rate acceptable (between 40-60/min) such that the patient may not be symptomatic even when AV block is complete. Edema of the AV node (rather than increased vagal tone) is the mechanism of AV block that develops later (after 12-24 hours). Atropine is much less likely to work in such cases although AV block usually still resolves on its own over days-to- weeks as edema subsides (permanent pacing is usually not needed) 57. Acute ANTERIOR Infarction Vagal tone is not implicated (Atropine is therefore unlikely to work). Sinus Tachycardia is typically seen with acute anterior MI (due to enhanced sympathetic tone and/orassociated heart failure). This may respond to cautious use of IV beta-blockers. Conduction system damage is due to septal necrosis. Risk of complications is greatest with LMain orproximal LAD occlusion (prior to S-1 takeoff ). 1st Degree AV Block may also be seen with anterior MI (not due to AV nodal ischemia but rather from HIS involvement). 2nd Degree AV Block with anterior MI is typically Mobitz II. The QRS is wide because the level of block isbelow the AV Node. Atropine is ineffective and pacing is essential (since complete AV block or ventricular standstill may abruptly occur). New RBBB with anterior MI is a sign of severe conduction system damage. There may be bifascicular block (usually RBBB/LAHB but occasionally with extensive necrosis RBBB/LPHB). PACING (both temporary and permanent) is much more likely to be needed with anterior MI. Additivedefects (ie, RBBB plus 1st degree; RBBB/LAHB) will increase risk of complete AV block. Development of severe conduction disturbance with acute anterior MI is a poor prognostic sign (indicative of extensive myocardial necrosis = high risk of cardiogenic shock).