Slowly resolving global myocardial inflammation/oedema in Tako-Tsubo cardiomyopathy: evidence from T2-weighted cardiac MRI
- Christopher Neil1,2,
- Thanh Ha Nguyen1,2,
- Angela Kucia3,4,
- Benjamin Crouch1,
- Aaron Sverdlov1,2,
- Yuliy Chirkov1,2,
- Gnanadevan Mahadavan1,2,
- Joseph Selvanayagam5,
- Dana Dawson6,
- John Beltrame1,2,
- Christopher Zeitz1,2,
- Steven Unger1,2,
- Thomas Redpath6,
- Michael Frenneaux6,
- John Horowitz1,2
- 1The Queen Elizabeth Hospital, Adelaide, Australia
- 2The University of Adelaide, Adelaide, Australia
- 3The Lyell McEwin Hospital, Adelaide, Australia
- 4The University of South Australia, Adelaide, Australia
- 5Flinders Medical Centre, Adelaide, Australia
- 6The University of Aberdeen, Aberdeen, UK
- Correspondence to Professor John Horowitz, Cardiology Unit, The Queen Elizabeth Hospital, 28 Woodville Road, Woodville South, SA 5011, Australia; john.horowitz{at}adelaide.edu.au
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Contributors CJN, patient recruitment, data collection and analysis, writing. THN, patient recruitment, data collection and analysis, writing. AMK, patient recruitment, data collection, writing. BC, data analysis. AS, patient recruitment, writing. YC, data collection, writing. GM, patient recruitment, data analysis, writing. JS, patient recruitment, writing. DD, data analysis, writing. JB, data collection, writing. CZ, patient recruitment, writing. SU, data collection, writing. TR, data analysis, writing. MF, data analysis, writing. JH, patient recruitment, data analysis, writing.
- Accepted 23 March 2012
- Published Online First 11 July 2012
Abstract
Objective Tako-Tsubo cardiomyopathy (TTC) is associated with regional left ventricular dysfunction, independent of the presence of fixed coronary artery disease. Previous studies have used T2-weighted cardiac MRI to demonstrate the presence of periapical oedema. The authors sought to determine the distribution, resolution and correlates of oedema in TTC.
Patients 32 patients with TTC were evaluated at a median of 2 days after presentation, along with 10 age-matched female controls. Extent of oedema was quantified both regionally and globally; scanning was repeated in patients with TTC after 3 months. Correlations were sought between oedema and the extent of hypokinesis, catecholamine release, release of N-terminal prohormone of B-type natriuretic peptide (NT-proBNP), and markers of systemic inflammatory activation (high-sensitivity C-reactive protein and platelet response to nitric oxide).
Results In the acute phase of TTC, T2-weighted signal intensity was greater at the apex than at the base (p<0.0001) but was nevertheless significantly elevated at the base (p<0.0001), relative to control values. Over 3 months, T2-weighted signal decreased substantially, but remained abnormally elevated (p<0.02). The regional extent of oedema correlated inversely with radial myocardial strain (except at the apex). There were also direct correlations between global T2-weighted signal and (1) plasma normetanephrine (r=0.39, p=0.04) and (2) peak NT-proBNP (r=0.39, p=0.03), but not with systemic inflammatory markers.
Conclusions TTC is associated with slowly resolving global myocardial oedema, the acute extent of which correlates with regional contractile disturbance and acute release of both catecholamines and NT-proBNP.
- Tako-Tsubo cardiomyopathy
- oedema
- cardiovascular MRI
- N-terminal proBNP
- allied specialties
- psychology/psychiatry
- depression
- myocardial disease
- myocardial ischaemia and infarction (IHD)
- imaging and diagnostics
- heart failure
- endothelium
- basic science
- free radicals
- oxidative stress
- cardiac function
- tissue doppler
- cardiomyoplasty
- cardiac ultrasound
- coronary angiography
- exercise echocardiography
- cardiac remodelling
- CT scanning
- echocardiography-exercise
- syndrome x
- myocardial viability
- coronary artery disease
- gender
- coronary artery disease
- spasm
- coronary physiology
- coronary flow
- angina treatment
- microvascular
- MRI
- heart failure treatment
- hypertrophic cardiomyopathy
- endothelial function
- nitrites
- oxidative stress
- heart failure treatment
- cardiomyopathy hypertrophic
Footnotes
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Funding This study was supported in part by a research grant from the National Health and Medical Research Council of Australia. CJN was the recipient of an Australian Postgraduate Award scholarship and a CVL Cardiovascular and Lipid research grant. THN held a University of Adelaide Endeavour International Postgraduate Research Scholarship.
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Competing interests None.
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Ethics approval Ethics approval was provided by HREC, TQEH, Adelaide, Australia.
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Provenance and peer review Not commissioned; internally peer reviewed.
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Data sharing statement Imaging or clinical data could be shared, were a collaborative agreement in place with the requesting party.
