Figure 10.1.1

Figure 10.1.2

In the coronary reperfusion era, recognition of true posterior ST-segment elevation myocardial infarction (STEMI) is both crucial and challenging. Overlooking this diagnosis represents a missed opportunity for acute coronary reperfusion by PCI or thrombolytic therapy with the associated benefits of these approaches on mortality and morbidity.

Question 1

Which findings on the initial ECG (Figure 10.1.1) led to emergency coronary angiography?

Answer 1

The initial ECG (Figure 10.1.1) shows anterior ST-segment depression of 1–2 mm in leads V₂–V₄. In a patient with symptoms compatible with myocardial ischemia, this finding is consistent with either anterior ischemia or posterior ST-segment elevation. The latter conclusion is based on evidence that anterior ST depression may be reciprocal to posterior ST elevation, reflecting a true posterior STEMI.¹ The next step in the evaluation was urgent acquisition of a repeat ECG with the electrodes for leads V₄–V₆ relocated (at the level of V₆): to the left posterior axillary line (V₇), the tip of the left scapula (V₈), and just left of the spinal column (V₉), respectively. As shown in Figure 10.1.2, there is marked ST elevation in V₇–V₉, confirming the diagnosis of true posterior STEMI and thereby providing the indication for acute coronary reperfusion.

Question 2

What evidence of potential true posterior MI is not present on the initial ECG (Figure 10.1.1)?

Answer 2

Tall R waves in leads V₁ and V₂, which may be the reciprocal of posterior Q waves, are not present in leads V₁ and V₂ since there were no pathologic Q waves in leads V₇–V₉. The differential diagnosis of tall R waves in leads V₁ and V₂ includes right ventricular enlargement, right bundle branch block, Wolff–Parkinson–White syndrome, and lead misplacement.

Question 3

Which coronary artery is most likely occluded in this patient?

Answer 3

Studies in humans have demonstrated that occlusion of the right coronary artery is associated with ST-segment elevation in leads II, III, and aVF, whereas left circumflex coronary artery occlusion commonly results in ST-segment elevation in the lateral precordial leads and V₇–V₉.^2,3 However, distribution of the coronary arteries can differ and right coronary occlusion may also be associated with true posterior MI. In this patient, posterior MI was due to a total proximal occlusion of the left circumflex artery (Figure 10.1.3). He received PCI to this vessel with excellent results, as shown in Figure 10.1.4.

Figure 10.1.3

Figure 10.1.4

References

1. Amsterdam E, Wenger N, Brindis R, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes. Circulation. 2014;130:e344–e426.

2. Kulkarni A, Brown R, Ayoubi M, et al. Clinical use of posterior electrocardiographic leads: A prospective electrocardiographic analysis during coronary occlusion. Am. Heart J. 1996;131:736–741.

3. Casas R, Marriott H, Glancy L. Value of leads V7-V9 in diagnosing posterior wall acute myocardial infarction and other causes of tall R waves in V1-V2. Am. J. Cardiol. 1997;80:508–509.

Patient History

A 67-year-old male presented to the emergency department with severe epigastric pain radiating to the left chest associated with nausea, vomiting, and diaphoresis. There was no relief with antacids. The patient’s ECG (Figure 10.2.1) revealed a paced cardiac rhythm and showed marked ST segment elevation in leads II, III, and aVF, as well as less ST elevation in leads V₄–V₆ and marked ST depression in leads I and aVL. These findings were consistent with a possible inferior ST-segment elevation MI (STEMI) and the patient underwent coronary angiography with revascularization of the culprit occluded coronary artery by percutaneous coronary intervention (PCI).

Figure 10.2.1

Left ventriculography showed inferior wall hypokinesis. Troponin I was elevated. An ECG one week following the procedure (Figure 10.2.2) revealed considerable resolution of the ST elevations seen in Figure 10.2.1 during the acute process. Thus, the entire clinical presentation confirmed acute myocardial infarction (MI) with total coronary artery occlusion. Note that the patient had a ventricular pacemaker at the time of presentation (Figure 10.2.1) and that he has an atrioventricular (AV) sequential pacer post-MI (Figure 10.2.2).

Figure 10.2.2

Question 1

Which coronary artery was the culprit vessel in this patient?

Answer 1

The patient had an inferior STEMI. It was statistically likely that the culprit vessel was the right coronary artery, which is true for 85%–90% of inferior STEMIs. However, ST elevation in the inferior and lateral leads is consistent with a left circumflex artery occlusion, which coronary angiography demonstrated. The challenge of recognizing STEMI in patients with paced rhythms is similar to that in patients with left bundle branch block (LBBB), i.e., the inherent repolarization abnormalities in paced rhythm and LBBB confound the standard criteria for diagnosing ST elevation MI.

This patient’s inferior ST elevations were striking with “reciprocal” ST depression in leads I and aVL. These findings together with the patient’s symptoms prompted emergency coronary angiography.

Question 2

Are there criteria for the diagnosis of STEMI in patients with electrically paced cardiac rhythm?

Answer 2

Criteria have been suggested for diagnosis in the setting of pacemaker rhythm:^1,2 (1) ≥5 mm ST elevation in leads with negative QRS complexes; (2) ≥1 mm ST elevations in leads with positive QRS complexes; (3) ≥1 mm ST depression in V₁–V₃ (if these leads are positive). The accuracy of these criteria is limited: sensitivity is poor but the specificity is better in one report: 82%–94%.² As in patients with LBBB, management of these patients should be based on the entire clinical presentation and should not depend solely on the foregoing ECG criteria for STEMI.

References

1. Klimczak A, Wranicz JK, Cygankiewicz I, Chudzik M, Goch JH, Baranowski R. Electorcardiographic diagnosis of acute coronary syndromes in patients with left bundle branch block or paced rhythm. Cardiol. J. 2007;14(2): 207–213.

2. Karumbaiah K and Omar B. ST-elevation myocardial infarction in the presence of biventricular paced rhythm. J. Emerg. Med. 2013;45:e35–e40.

Patient History

This is an ECG (Figure 10.3.1) from a 57-year-old male who presented with an acute coronary syndrome (ACS) with ST elevation 6 months prior. The x-ray showed that the heart was in a normal position. The “cath lab” was activated 4 hours after the onset of pain. A stent was deployed in the middle segment of an occluded left circumflex artery (LCX) (Figure 10.3.2).

Figure 10.3.1 12-lead ECG showing sinus rhythm, normal PR and QT intervals, and normal QRS morphology in the frontal plane. Note a tall and slurred R wave in lead V₁, Rs from leads V₂–V₅ with small QRS in lead V₆, and a positive tall T wave is present in leads V₁–V₅ with slight ST ascent and asymmetric T wave, and qRs pattern in lead V₆.

Figure 10.3.2 Coronary angiography showing LCX occlusion at middle segment (right). No right coronary artery occlusion is seen (left).

Question

What is the location of the myocardial infarction (MI)? Select the correct choice

1. There is no MI. This is a normal ECG with extreme levorotation.

2. Posterior wall. Segment 4 of Cerqueira classification.⁷

3. Lateral wall. Segments of lateral wall of Cerqueira classification.⁷

Interpretation, Answer, and Comments

The correct answer is 3. The ECG shows a normal P wave, PR and QT intervals, and QRS complex. There is no abnormal Q wave in the frontal plane, but there is a low voltage R wave is present in lead I and VL. In the horizontal plane there is a slurred tall R wave in V₁ and Rs from V₂–V₅ with small QRS in V₆, and a positive tall T wave is present in V₁–V₄.

This ECG may not be explained by extreme leftward rotation. The heart at x-ray presents normal position and the ECG of extreme leftward rotation may present unique R in V₂ but not in V₁. Furthermore, in extreme left rotation the QRS axis in the frontal plane is around 0° but not present with a S1, S2, or S3 pattern.¹

Using the classic nomenclature and considering the patient history, the patient would be diagnosed with posterior MI. According to Perloff,² the diagnosis of posterior MI may be made when there is in V₁ R/S>1, that represents a mirror pattern of posterior Q wave (Figure 10.3.3).

Figure 10.3.3 Original drawing of true posterior MI with the QRS morphology according to Perloff (1).

Nowadays thanks to correlation between ECG and contrast-enhanced cardiovascular magnetic resonance,^3–6,8 it has been demonstrated that the prominent R in V₁ corresponds to lateral (and not posterior wall) MI due to occlusion of LCX (Figure 10.3.2). In fact, the so-called “posterior wall” corresponds to an inferobasal segment of the inferior wall.⁷ The low voltage of the R wave in leads I and VL, although without pathological Q wave, suggest lateral wall involvement. Therefore, the correct answer is 3.

Figure 10.3.4 shows a cardiovascular magnetic resonance study where delayed contrast enhancement (i.e., myocardial necrosis) is present at the lateral wall (B and C), while the inferobasal segment and the rest of the inferior wall (A) are, in fact, free of necrosis.

Figure 10.3.4 Contrast-enhanced cardiovascular magnetic resonance showing: A. Long axis view with no inferior wall involvement, B. Short axis view: clear non-transmural extensive lateral involvement, and C. A 4-chamber view that shows the longitudinal extension of lateral infarction.

On the contrary, Figure 10.3.5 shows a typical example of inferolateral MI (QR in II, III, aVF, and R/S >1 in V₁). See the correlation with contrast-enhanced cardiovascular magnetic resonance. In old terminology, this would be diagnosed as inferoposterior MI.

Figure 10.3.5 Electrocardiographic and cardiovascular magnetic resonance images of an inferolateral infarction. Q waves of necrosis are present in leads II, III, and aVF (inferior necrosis); an R ≥ S morphology is present in lead V₁ (lateral necrosis). Contrast-enhanced cardiovascular magnetic resonance (four-chamber, long- and short-axis views) clearly shows an inferolateral necrosis.

Figure 10.3.6 explains that in cases of MI of lateral wall the necrosis vector (yellow) faces lead V₁ and records a prominent R in this lead. In case of necrosis of the inferobasal segment (former “posterior wall”), the blue vector faces leads V₃ and V₄ and the surface ECG cannot record any characteristic pattern because this lead already presents an RS pattern in normal conditions.^4,7

Figure 10.3.6 Schematic drawing of the transverse plane of the thorax viewed from below. The infarction vector produced by involvement of the wall formerly termed posterior (blue arrow) is directed toward leads V₃ and V₄, while the infarction vector generated by the lateral wall (yellow arrow) is directed toward leads V₁ and V₂.

Figure 10.3.7 shows the three typical patterns of R wave in lead V₁ (exclusive R wave often with slurs, R>S, and low voltage r/s >0.5 compared with rS seen in case of inferior MI.

Figure 10.3.7 A comparison between different types of lateral MI showing a tall R wave in V₁ with R/S > 1 or at least > 0.5 if S wave is very small.

Conclusions

For decades, a prominent R wave (R, Rr, RS) in a right precordial lead (V₁) has been considered a key criterion for the diagnosis of posterior MI. This conclusion has been accepted as a dogma since the paper of Perloff published more than 50 years ago.² Now it is time to consider the end of this dogma.⁹ After ECG cardiovascular magnetic resonance correlations performed 10 years ago, various papers^3–6,8 argued that, in the absence of conditions that modified QRS shape such as right ventricular hypertrophy, complete right bundle-branch block, or Wolff–Parkinson–White syndrome, the appearance of a prominent R wave in V₁ in the course of ACSs indicates a lateral MI. This lateral MI is usually larger and more transmurally extended than when a prominent R wave in the right precordial leads is absent; therefore, this conclusion should be considered as a standard of scientific guidelines.⁹

References

1. Bayés de Luna A. Clinical Electrocardiography. West Sussex, UK: Wiley-Blackwell; 2012.

2. Perloff JK. The recognition of strictly posterior myocardial infarction by conventional scalar electrocardiography. Circulation. 1964;30:706–718.

3. Bayés de Luna A, Cino JM, Pujadas S, et al. Concordance of electrocardiographic patterns and healed myocardial infarction location detected by cardiovascular magnetic resonance. Am. J. Cardiol. 2006;97:443–451.

4. Bayés de Luna A, Wagner G, Birnbaum Y, et al. International Society for Holter and Noninvasive Electrocardiography. A new terminology for left ventricular walls and location of myocardial infarcts that present Q wave based on the standard of cardiac magnetic resonance imaging: A statement for healthcare professionals from a committee appointed by the International Society for Holter and Noninvasive Electrocardiography. Circulation. 2006;114:1755–1760.

5. Rovai D, Di Bella G, Rossi G, et al. Q-wave prediction of myocardial infarct location, size and transmural extent at magnetic resonance imagining. Coron. Artery Dis. 2007;18:381–389.

6. Van Der Weg K, Bekkers SC, Winkens B, et al. Evaluation of the electrocardiogram in identifying and quantifying lateral involvement in nonanterior wall infarction using cardiovascular magnetic resonance imaging. J. Electrocardiol. 2012;45(5):478–484.

7. Cerqueira MD, Weissman NJ, Dilsizian V, et al. American heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association. Circulation. 2002;105:539–542.

8. Goldwasser D, Senthilkumar A, Bayés de Luna A, et al. Lateral MI explains the presence of prominent R wave (R ≥ S) in V1. Ann. Noninvasive Electrocardiol. 2015;20(6):570–577.

9. Bayés de Luna A, Rovai D, Pons LLado G, et al. The end of an electrocardiographic dogma: A prominent R wave in V1 is caused by a lateral not posterior myocardial infarction-new evidence based on contrast-enhanced cardiac magnetic resonance-electrocardiogram correlations. Eur. Heart J. 2015;36:959–964.

Patient History

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