• A 72-year-old woman complained of intermittent chest pain for 3dys, which became severe and continuous 4hs before presentation.

Clinical Case(2)

• Her cardiovascular risk factors were NIDDM for 30 yrs, hypertension for ten yrs and dyslipidaemia.

• BP was 148/74 mmHg, and HR was 82/min, whereas the rest of the examination was unremarkable.

Clinical Case(2)

• Normal SR, tall R waves in V1 V3

• R wave >0.04s in V1, V2 and V3

• ST segment depression in V1-V4. • Lateral and inferior leads did not

demonstrate T elevation.

• The EKG done in the ER; what is the diagnosis?

Clinical Case(2)

• Coronary angiography showed an occlusion of the proximal LCxCA

• Distal L-ADA 80% stenosis, a dominant RCA with a 60-70% stenosis in the postero-lateral branch.

• PCA to the proximal LCxCA was performed and balloon angioplasty was also done to the obtuse marginal branch of the LCxCA.

• A good final result with TIMI3 flow was obtained with resolution of chest pain.

Clinical Case(2)

Clinical Case(2)

BEFORE AFTER

• I-PMI occurs in the posterior or postero-basal LV wall, is rare and usually associated with an inf. or lat. MI(1,2).

DISCUSSIONClinical Case(2)

• Incidence has been estimated at 3-4% of all AMI(3).

• ECG of posterior MI as described by Schamroth(4) are:

- R wave ≥0.04s in V1 or V2

- Upright T waves in contiguous right precordial leads

- ST segment depression in V1 V3

• R/S ratio ≥1 in leads V1 and V2. • As MI evolves ST segment depression

decreases and the upright T amplitude increases.

- R wave ≥0.04s in V1 or V2

- Upright T waves in contiguous right precordial leads

- ST segment depression in V1 V3

• R/S ratio ≥1 in leads V1 and V2.

• As MI evolves ST segment depression decreases and the upright T amplitude increases.

EKG criteria

Clinical Case(2)

• Turn ECG upside down and look at it from the back.

• Changes in V1 and V2 which might be over-looked at first glance, will be seen as abnormal Q waves, ST elevation and increased T wave inversion(2).

• R>0.04s and R≥S V1, showed a high specificity (>99%) and a high positive predictive value (91%).

• R≥0.04s and R≥S V2, showed 95% of specificity, and 73% positive predictive value.

Clinical Case(2)

• I-PMI has been found to be always due to LCX occlusion(6).

• In another study, an abnormal R wave in V1 had a 96%specificity for LCxCA vs RCA-related infarction, but a sensitivity of only 21%(7).

• In addition, all patients with LCxCA-related MI andabnormal R wave in lead V1, had multivessel disease(7)

• In spite of these, true posterior MIs are usually well-tolerated(1).

• Conventional ECG, even with correct placement of the electrodes, may miss a true I-PMI

Clinical Case(2)

• The use of additional chest leads on the posteriorthorax between the angle of the scapula and thevertebral column, at the level of the 5th intercostalspace (leads V7-9), will increase the sensitivitythrough detection of Q waves(8).

• Some have questioned whether the conventional 1mm ST elevations in the posterior leads were appropriate and it has been found that the currently-used criterion of 1mm to detect ischaemia is inadequate todemonstrate ST segment elevation in the posteriorleads during LCxCA occlusion.

Clinical Case(2)

Possible mimics of ECG changes in a posteriorMI include other causes of tall R waves in V1:

– Right ventricular hypertrophy - Right bundle branch block - Wolf-Parkinson-White syndrome - Normal variants - Ischaemia of the anterior wall of the LV also

produces ST segment depression in leads V1-3 and this must be differentiated from posterior MI.

Isolated PMIClinical Case(2)

• A 53-year-old man presented to the ED, and he had a 4 ½ hrs history of chest pain radiating to both arms.

• The onset of chest pain occurred while walking and was not relieved by rest.

• Associated symptoms included shortness of breath, nausea and diaphoresis. The patient’s only past medical history was of hypertension, for which he was taking losartan, and no other medications.

• He had a 30 pack-year smoking history.

Clinical Case(3)

• BP 177/102mmHg, HR 72b/m RR 20 breaths/min, T. 36,5°C.

• Prompted by the ST depres- sion and typical presentation for MI, a reading for post.leads V7 through V9 was immediately obtained and demonstrated ST elevation

• Standard management including M.O.N.A. and heparin

• ED ECG showed downsloping ST depression mostly prominent in leads V1 V4 and tall R wave in V3 (not in V1/V2)

Clinical Case(3)

• A cardiology consultation was obtained, and the pt was taken promptly to the Cath. Lab, whereas Troponin I and other laboratory values were pending at that time.

• Cath. revealed total occlusion of the LCA, a normal LDA, a normal left main artery, a 60% proximal lesion of a small branch of the LCA and luminal irregularities in LDA.

• Pt underwent uncomplicated stenting of the LCA, and

a subsequent Echo evaluation identified moderate to severe posterior wall hypokinesis and was otherwise unremarkable.

Clinical Case(3)

• Pt’s initial troponin I level was 1.4 ng/mL (range 0.0–1.2 ng/mL) with a peak of 172 ng/mL 7 hours after presentation. Five hours after presentation a single CK measurement was obtained and was 3730 U/L with a CK-MB of 191 ng/mL (relative index 5.1%).

• The only complication identified during hospitalization was a single uncomplicated episode of hematemesis.

• The pt otherwise did well and was discharged home on hospital day 4.

Clinical Case(3)

• No EKG ST elevat nor tall R V1 or V2

• EKG reveal ST depression in V1 and V2 and an up-right T wave in V2

• ST elev. in leads V8 and V9.• True incidence is unknown but has reported

between 0% to 12% (6,7,9,13,18) when posterior leads V7 through V9 is obtained

• Identif. pts with I-PMI with standard EKG could be challenging(1,2,10,12–14) due to the location of the AMI(1,2,14)

Clinical Case(3)

Clinical Case(3) Introduction

• Posterior wall of LV is typically supplied by the left Cx coronary artery (1) and is a challenging area of the heart in which to identify acute ischemia and MI.

• During transmural AMI, the characteristic ST-segment elevations seen in other areas of the heart are not seen in isolated posterior myocardial infarctions (IPMI) on standard 12-lead EKG (1,2)

• If A-IPMI were identified promptly in the emergency department (ED), these patients could be considered for thrombolytic therapy or immediate interventional Cath. Lab. (3–6)

• Recently a consensus report from the ACC that was endorsed by the American College of Emergency Physicians (16) use the presence of tall R waves (typically defined as an R/S ratio ≥ 1 in V1 and V2 to define posterior MI with ST depression and carachteristic symptoms .

• Few techniques have been developed to identify IPMI, including the use of posterior leads V7, V8 and V9 (3–10) body surface mapping (11,12) and the development of specific EKG criteria other than ST elevation (13-15)

• We present a case of an acute I-PMI in which the ECG lacked tall R waves in leads V1 and V2 and the use of posterior leads identified ST-segment elevation that changed pt management resulting in the pt going promptly to the Cath. Lab.

Clinical Case(3)

• Current diagnostic criteria for acute I-PMI include: horizontal STsegment depression, tall R waves, and prominent upright T waves in V1, V2 and/or V3 (1,2)

Discussion

• In this case we had down-sloping ST segments and lacked tall R waves in V1 and V2, an up-right T wave in V2 and a tall R wave in V3 were present. It has been suggested that tall R waves in anterior leads (V1, V2 and V3) are simply the electrical equivalent of Q waves in the posterior leads (V7, V8 and V9)(1,2)

• If this were the case, these two findings would always occur simultaneously on a 15-lead ECG (a 12-lead ECG + posterior leads).

• Correlation between anterior R waves, posterior Q waves, and the time course of their development in I-PMI needs further study.

Clinical Case(1)

Clinical Case(1-2)