PMID- 22464482
OWN - NLM
STAT- MEDLINE
DCOM- 20140402
LR  - 20130731
IS  - 1874-1754 (Electronic)
IS  - 0167-5273 (Linking)
VI  - 167
IP  - 3
DP  - 2013 Aug 10
TI  - Relationship of ECG findings to phenotypic expression in patients with 
      hypertrophic cardiomyopathy: a cardiac magnetic resonance study.
PG  - 1038-45
LID - S0167-5273(12)00279-3 [pii]
LID - 10.1016/j.ijcard.2012.03.074 [doi]
AB  - BACKGROUND: The 12-lead electrocardiogram (ECG) is considered an essential 
      screening tool for hypertrophic cardiomyopathy (HCM). A vast array of ECG 
      abnormalities has been described in HCM, although their relationship to left 
      ventricle (LV) morphology and degree of hypertrophy appears elusive. Aim of this 
      study was to assess the relationship of ECG patterns with the HCM phenotype 
      assessed according to the novel opportunities offered by cardiac magnetic imaging 
      (CMR). METHODS: CMR and 12-lead ECG were performed in 257 HCM patients. Severity 
      of ECG abnormalities was defined by the sum of 9 criteria: abnormal cardiac 
      rhythm, QRS duration >/= 100 ms, Romhilt-Estes score >/= 5, fascicular block (LAHB) 
      and/or bundle-branch block (LBBB or RBBB), ST-T abnormalities, ST-T segment 
      elevation >/= 0.2 mV, prolonged QTc interval, pathological Q waves, absence of 
      normal Q wave. Four ECG groups were identified: normal (0 criteria); mildly 
      abnormal (1-3 criteria); moderately abnormal (4-6 criteria); markedly abnormal 
      (7-9 criteria). RESULTS: There was a direct relationship between severity of ECG 
      abnormalities and HCM phenotype. LV mass index was normal in most patients with 
      normal ECG and progressively increased with each class of ECG score, from 70.9 +/- 
      18.6g/m(2) in patients with normal ECG to 107.1 +/- 55.1g/m(2) among those with 
      markedly abnormal ECG (p=<0.0001). Likewise, the prevalence and extent of late 
      gadolinium enhancement (LGE) increased significantly with the ECG score, from 37% 
      in patients with normal ECG to 93% in patients with markedly abnormal ECG 
      (overall p=0.0012). A normal ECG had a negative predictive accuracy of 96% for 
      markedly increased LV mass (>91 g/m(2) for men and >69 g/m(2) for women), and of 
      100% for maximum LV thickness >/= 30 mm. CONCLUSIONS: In a large HCM cohort, the 
      number and severity of ECG abnormalities were directly related to phenotypic 
      expression as revealed by CMR. Although false negative ECG findings remain a 
      challenge in population screenings for HCM, a normal ECG proved effective in 
      ruling out severe LV hypertrophy, suggesting potential implications for long-term 
      follow-up of HCM patients and family members. A simple score for quantification 
      of ECG abnormalities in HCM patients is proposed.
CI  - Copyright (c) 2012 Elsevier Ireland Ltd. All rights reserved.
FAU - Delcre, Sara Dalila Luisella
AU  - Delcre SD
AD  - Division of Cardiology, Cardinal Massaia Hospital of Asti and Faculty of Medicine 
      University of Turin, Asti, Italy. SDelcre@asl.at.it
FAU - Di Donna, Paolo
AU  - Di Donna P
FAU - Leuzzi, Stefano
AU  - Leuzzi S
FAU - Miceli, Salvatore
AU  - Miceli S
FAU - Bisi, Marta
AU  - Bisi M
FAU - Scaglione, Marco
AU  - Scaglione M
FAU - Caponi, Domenico
AU  - Caponi D
FAU - Conte, Maria Rosa
AU  - Conte MR
FAU - Cecchi, Franco
AU  - Cecchi F
FAU - Olivotto, Iacopo
AU  - Olivotto I
FAU - Gaita, Fiorenzo
AU  - Gaita F
LA  - eng
PT  - Journal Article
DEP - 20120330
PL  - Netherlands
TA  - Int J Cardiol
JT  - International journal of cardiology
JID - 8200291
SB  - IM
MH  - Adult
MH  - Aged
MH  - Cardiomyopathy, Hypertrophic/*diagnosis/*physiopathology
MH  - Cohort Studies
MH  - Electrocardiography/*methods
MH  - Female
MH  - Humans
MH  - Magnetic Resonance Imaging, Cine/*methods
MH  - Male
MH  - Middle Aged
MH  - *Phenotype
OTO - NOTNLM
OT  - Cardiac magnetic resonance
OT  - ECG
OT  - Hypertrophic cardiomyopathy
OT  - Hypertrophy
EDAT- 2012/04/03 06:00
MHDA- 2014/04/03 06:00
CRDT- 2012/04/03 06:00
PHST- 2011/09/28 00:00 [received]
PHST- 2012/02/01 00:00 [revised]
PHST- 2012/03/03 00:00 [accepted]
PHST- 2012/04/03 06:00 [entrez]
PHST- 2012/04/03 06:00 [pubmed]
PHST- 2014/04/03 06:00 [medline]
AID - S0167-5273(12)00279-3 [pii]
AID - 10.1016/j.ijcard.2012.03.074 [doi]
PST - ppublish
SO  - Int J Cardiol. 2013 Aug 10;167(3):1038-45. doi: 10.1016/j.ijcard.2012.03.074. 
      Epub 2012 Mar 30.