title: Clinical implication of left precordial T wave inversions in the presence of complete right bundle branch block.
abstract: This study was designed to elucidate whether left precordial negative T waves are electrocardiographic indicators for the diagnosis of hypertrophic cardiomyopathy (HCM) even in the presence of complete right bundle branch block (CRBBB). In 7 consecutive patients with CRBBB accompanied by negative T waves in at least one of the left precordial leads (V4, V5, V6, maximal negativity; 1.06 +/- 0.40 mVol) (left precordial negative T wave group) and in 15 randomly selected CRBBB patients without left precordial T wave inversions (control group), echocardiography was performed to rule out underlying diseases causing left ventricular overload and to identify candidates for magnetic resonance (MR) imaging. None had anginal pain indicating ischemic heart disease. When 2-dimensional echocardiography indicated left ventricular hypertrophy with wall thickness > or = 15 mm, the magnitude and distribution of hypertrophy were scrutinized on contiguous left ventricular MR short-axis images. The diagnostic criterion of HCM was the demonstration of hypertrophy with a wall thickness of 20 mm or more on the left ventricular MR short-axis images. All patients in the left precordial negative T wave group had negative T waves in both I (negativity; 0.27 +/- 0.17 mVol) and aVL (negativity; 0.23 +/- 0.14 mVol), whereas none in the control group did. The diagnostic criterion for HCM was fulfilled in six patients in the left precordial negative T wave group. However there were no patients who fulfilled the criterion in the control group. Negative T waves were recorded in the I (negativity; 0.30 +/- 0.17 mVol), aVL (negativity; 0.25 +/- 0.14 mVol), V4 (negativity; 1.03 +/- 0.46 mVol), V5 (negativity; 0.83 +/- 0.37 mVol) and V6 leads (negativity; 0.31 +/- 0.31 mVol) in all patients with HCM, while they were recorded in only 6% of the patients without HCM. In conclusion, the existence of left precordial negative T waves in the presence of CRBBB strongly indicates HCM.
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Suzuki
authors.forename: W S
authors.initials: WS
authors.lastname: Shin
authors.forename: R
authors.initials: R
authors.lastname: Shimamoto
authors.forename: T
authors.initials: T
authors.lastname: Yamazaki
authors.forename: T
authors.initials: T
authors.lastname: Tsuji
authors.forename: Y
authors.initials: Y
authors.lastname: Murakawa
authors.forename: T
authors.initials: T
authors.lastname: Nakajima
authors.forename: T
authors.initials: T
authors.lastname: Toyo-oka
authors.forename: J
authors.initials: J
authors.lastname: Nishikawa
authors.forename: K
authors.initials: K
authors.lastname: Ohotomo
authors.forename: R
authors.initials: R
authors.lastname: Nagai
authors.forename: M
authors.initials: M
authors.lastname: Omata
mesh_terms: D002037:Bundle-Branch Block / Q000175:diagnosis / Q000503:physiopathology*; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications; D004562:Electrocardiography; D006801:Humans; D008279:Magnetic Resonance Imaging; D009206:Myocardium / Q000473:pathology