2. Sgarbossa EB, Pinski SL, Gates KB,Wagner GS; GUSTO-1 Investigators. Early electrocardiographic diagnosis of acutemyocardial infarction in the presence of ventricular paced rhythm. Am J Cardiol. 1996;77(5):423-424.
The authors analyzed data from GUSTO-1. They looked at all patients in the study who had a paced rhythm and were diagnosed with AMI and included in the GUSTO trial. Many physicians, however, have been reluctant to make this diagnosis and to enter a patient with chest pain and a paced rhythm into a thrombolytic trial. Consequently, only 32 patients (0.1%) with pacemakers were included in GUSTO-1, which is much lower than the percentage of patients with CP and AMI who have a ventricular pacemaker. We do not know the incidence of (and therefore the pre-test probability of) AMI in patients with CP and a pacemaker and this study provides no helpful data in that regard. Fifteen of these 32 patients were excluded because their rhythms were not generated by the pacer. The ECG’s of the 17 remaining AMI patients were matched with 17 patients with pacers, stable CAD and no CP. The ECG criteria developed by Sgarbossa et al. (246) for LBBB were then tested on patients and controls. Results, as follows, were similar to those in the LBBB study.· --ST elevation >/= 5 mm in one lead with a predominantly negative QRS was the only criterion that had statistical significance and high specificity (positive likelihood ratio = 4.41).
Additional findings that could be useful but were not statistically significant:· --ST elevation >/= 1mm in leads with predominantly positive QRS (sensitivity 53%, specificity 88%).· --ST depression of >/= 1mm in one of leads V1-V3 (sensitivity 29%, specificity 82%).
3. Khan ZU, Chou TC. Right ventricular infarction mimicking acute anteroseptal left ventricular infarction. Am Heart J 1996; 132:1089-1093.
The authors studied 4 patients whose concurrent inferior and RV AMI mimicked inferior and anteroseptal LV AMI and found that the ECG’s of all patients showed ST elevation not only in V1, but also in V2-V3. More surprising still was the development of Q-waves in V1-V3 without the presence of anterior AMI.
4. Geft IL, Shah PK, Rodriguez L, et al. ST elevations in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol. 1984;53(8):991-996.
These authors used angiography and scintigraphy to study 69 patients with ST elevation in V1-V5 and found that the RCA was occluded, the LAD was open, and the RV was the area of infarct in 5 patients (7%). In cases of anterior AMI due to LAD occlusion, ST elevation was least in V1 and maximal in V2 to V4, whereas in RV AMI, ST elevation was highest in V1-V2 and decreased toward V5. RV AMI’s were also associated with inferior ST elevation.
Pseudoanteroseptal MI in LBBB
5. Smith SW, HeegaardW, Bachour FA, BradyWJ. Acute myocardial infarction with left bundle-branch block: disproportional anterior ST elevation due to right ventricular myocardial infarction in the presence of left bundle-branch block. Am J Emerg Med. 2008;26(3):342-347.
We reported here a case of precordial and inferior ST elevation in LBBB that was due to inferior and RV STEMI.