Isolated T Wave Inversion in Lead aVL: An ECG Survey and a Case Report.

Background. Computerized electrocardiogram (ECG) analysis has been of tremendous help for noncardiologists, but can we rely on it? The importance of ST depression and T wave inversions in lead aVL has not been emphasized and not well recognized across all specialties. Objective. This study's goal was to analyze if there is a discrepancy of interpretation by physicians from different specialties and a computer-generated ECG reading in regard to a TWI in lead aVL. Methods. In this multidisciplinary prospective study, a single ECG with isolated TWI in lead aVL that was interpreted by the computer as normal was given to all participants to interpret in writing. The readings by all physicians were compared by level of education and by specialty to one another and to the computer interpretation. Results. A total of 191 physicians participated in the study. Of the 191 physicians 48 (25.1%) identified and 143 (74.9%) did not identify the isolated TWI in lead aVL. Conclusion. Our study demonstrated that 74.9% did not recognize the abnormality. New and subtle ECG findings should be emphasized in their training so as not to miss significant findings that could cause morbidity and mortality.

The neglected lead on electrocardiogram: T wave inversion in lead aVL, nonspecific finding or a sign for left anterior descending artery lesion?

BACKGROUND: The electrocardiogram (ECG) is the most important diagnostic tool for acute myocardial infarction (AMI). T wave inversion (TWI) in lead aVL has not been emphasized or well recognized. OBJECTIVE: This study examined the relationship between the presence of TWI before the event and mid-segment left anterior descending (MLAD) artery lesion in patients with AMI. METHODS: Retrospective charts of patients with acute coronary syndrome between the months of January 2009 and December 2011 were reviewed. All patients with MLAD lesion were identified and their ECG reviewed for TWI in lead aVL. RESULTS: Coronary angiography was done on 431 patients. Of these, 125 (29%) had an MLAD lesion. One hundred and six patients (84.8%) had a lesion > 50% and 19 patients (15.2%) had a lesion < 50%. Of the 106 patients who had a MLAD lesion > 50%, 90 patients (84.9%) had TWI in lead aVL and one additional lead. Of the 19 patients who had an MLAD lesion < 50%, 8 patients (42.1%) had TWI in lead aVL and one additional lead. Isolated TWI in lead aVL had an overall sensitivity of 76.7% (95% confidence interval [CI] 0.65-0.86), a specificity of 71.4% (95% CI 0.45-0.88), a positive predictive value of 92%, a negative predictive value of 41.7%, a positive likelihood ratio of 2.7 (95% CI 1.16-6.22), and negative likelihood ratio of 0.32 (95% CI 0.19-0.58) for predicting a MLAD lesion of > 50% (p = 0.0011). CONCLUSIONS: TWI in lead aVL might signify a mid-segment LAD lesion. Recognition of this finding and early appropriate referral to a cardiologist might be beneficial. Additional studies are needed to validate this finding.

Does angiotensin-converting enzyme inhibitor use exacerbate hereditary angioedema?

BACKGROUND: Approximately 2% of angioedema (AE) patients have a hereditary or an acquired deficiency of the complement 1 (C1) esterase inhibitor (C1 INH) gene. Some case reports indicate an association between angiotensin-converting enzyme inhibitor (ACEI) use and exacerbation of hereditary AE (HAE). OBJECTIVE: The aim of this retrospective study is to investigate the association between HAE and ACEI use in a larger patient population. METHODS: A retrospective chart review of patients who presented with AE and patients with diagnostic serum assays for functional C1 INH, C1 INH antigenic protein, C1q, C1q immune complex (C1q IC), and complement 4 (C4) regardless of medical complaint. Descriptive statistics were used to analyze the data. RESULTS: A total of 1594 patients had complement levels measured (136 C1 INH, 55 C1q, 10 C1q IC, and 1500 C4), of which 156 (9.7%) patients presented with AE. Angiotensin-converting enzyme inhibitor use was documented in 747 (47%) patients. Low C1 INH was detected in one patient with recurrent AE who was not taking ACEI. Another patient who presented with recurrent AE was found to have systemic lupus erythematosus with abnormal C4, C1q, and C1q IC, but normal C1 INH. A low C4 level was present in 94 patients, 4 of which had AE. CONCLUSIONS: The risk of exacerbating HAE by ACEI might be present, but we did not find any association in this retrospective study. Further studies are needed to determine the existence of this association.