PMID- 20560000
OWN - NLM
STAT- MEDLINE
DCOM- 20101102
LR  - 20211020
IS  - 1937-5395 (Electronic)
IS  - 1937-5387 (Linking)
VI  - 2
IP  - 4
DP  - 2009 Dec
TI  - The current and emerging role of cardiovascular magnetic resonance imaging in 
      hypertrophic cardiomyopathy.
PG  - 415-25
LID - 10.1007/s12265-009-9136-3 [doi]
AB  - Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiomyopathy with 
      substantial heterogeneity in phenotypic expression and clinical course. 
      Traditionally, two-dimensional echocardiography has been the easiest and most 
      reliable technique for establishing a diagnosis of HCM. However, cardiovascular 
      magnetic resonance (CMR) has emerged as a novel, three-dimensional tomographic 
      imaging technique, which provides high spatial and temporal resolution images of 
      the heart in any plane and without ionizing radiation. As a result, CMR is 
      particularly well suited to provide detailed characterization of the HCM 
      phenotype, including precise assessment of the location and distribution of left 
      ventricular (LV) wall thickening. In this regard, CMR can identify hypertrophy 
      (particularly in the anterolateral free wall and apex), not well appreciated (or 
      underestimated) by two-dimensional echocardiography, with important implications 
      for diagnosis. CMR can also provide detailed characterization of other myocardial 
      structures such as the papillary muscles, which may impact on preoperative 
      management strategies for patients who are candidates for surgical myectomy. 
      Furthermore, CMR enables an accurate assessment of total LV mass, a robust marker 
      of the overall extent of hypertrophy, which may have implications for risk 
      stratification. In addition, a subgroup of HCM patients have normal LV mass (with 
      focal hypertrophy), suggesting that a limited extent of hypertrophy is consistent 
      with a diagnosis of HCM. Finally, following the intravenous administration of 
      gadolinium, first-pass perfusion sequences can identify myocardial perfusion 
      abnormalities, while late gadolinium enhancement (LGE) sequences can characterize 
      areas of myocardial fibrosis/scarring. LGE is associated with systolic 
      dysfunction and likelihood for ventricular tachyarrhythmias on ambulatory Holter 
      monitoring in patients with HCM. However, the precise clinical implications of 
      myocardial perfusion abnormalities and LGE in HCM are still uncertain; this 
      information may have important implications with regard to identifying HCM 
      patients at risk of sudden death and adverse LV remodeling associated with 
      systolic dysfunction. Therefore, at present, CMR provides important information 
      impacting on diagnosis and clinical management strategies in patients with HCM 
      and will likely have an expanding role in the evaluation of patients with this 
      complex disease.
FAU - Maron, Martin S
AU  - Maron MS
AD  - Division of Cardiology, Hypertrophic Cardiomyopathy Center, Tufts Medical Center, 
      Boston, MA, 02111, USA. mmaron@tuftsmedialcenter.org
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20091107
PL  - United States
TA  - J Cardiovasc Transl Res
JT  - Journal of cardiovascular translational research
JID - 101468585
RN  - 0 (Contrast Media)
RN  - AU0V1LM3JT (Gadolinium)
SB  - IM
MH  - Cardiomyopathy, Hypertrophic/*diagnosis/pathology/physiopathology/therapy
MH  - Contrast Media
MH  - Fibrosis
MH  - Gadolinium
MH  - Hemodynamics
MH  - Humans
MH  - *Magnetic Resonance Imaging
MH  - Myocardium/*pathology
MH  - Papillary Muscles/pathology
MH  - Phenotype
MH  - Predictive Value of Tests
MH  - Prognosis
MH  - Severity of Illness Index
MH  - Ventricular Function
EDAT- 2010/06/19 06:00
MHDA- 2010/11/03 06:00
CRDT- 2010/06/19 06:00
PHST- 2009/08/30 00:00 [received]
PHST- 2009/09/28 00:00 [accepted]
PHST- 2010/06/19 06:00 [entrez]
PHST- 2010/06/19 06:00 [pubmed]
PHST- 2010/11/03 06:00 [medline]
AID - 10.1007/s12265-009-9136-3 [doi]
PST - ppublish
SO  - J Cardiovasc Transl Res. 2009 Dec;2(4):415-25. doi: 10.1007/s12265-009-9136-3. 
      Epub 2009 Nov 7.