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Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
Working Groups goals is to stimulate and disseminate scientific knowledge in different fields of cardiology.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
An interesting case of a young woman presenting the typical features of the syndrome caused by a functional paraganglioma intimate with the aorta and vena cava has been published (3); similar cases of TT syndrome have been reported with adrenal phaeochromocytoma.
Two recent papers reported the findings from endomyocardial biopsies taken during the acute phase of the disease. Both showed histological patterns compatible with strong adrenergic stimulation. In one study 9 patients were biopsied and contraction band necrosis (in 4) and mononuclear cell infiltration (in 3), were documented, associated with elevated levels of norepinephrine and epinephrine peaking on admission (744±52 and 140±166 pg/mc respectively) (4).
Moreover a disproportion between a severely reduced uptake at the ventricular apex on F-18FDG PET image and a slightly reduced uptake of 201 Tl was noted, showing a metabolic defect much more severe than perfusion abnormality (4). Another study performed in TT patients showed intracellular vacuoles of glycogen, disorganisation of contractile and cytoskeletal proteins, while signs of oncotic and apoptotic cell death were absent (5).
After functional recovery of ventricular contractility all described alterations appeared nearly completely reversed. These alterations were interpreted as resulting from catecholamine excess followed by microcirculatory dysfunction and direct cardiotoxicity. A further study performed in 11 consecutive TT patients demonstrated an absence of improvement in contractile performance of the akinetic ventricular wall to low-dose dobutamine infusion (6); a response distinctly different from that expected in an ischemic stunned myocardium, and interpreted as compatible with a catecholamine mediated cardiac toxicity.
1. Elliott P, Andersson B, Arbustini E, et al. Classification of the cardiomyoathies: a position statement from the European society of cardiology working group on myocardial and pericardial diseases. Eur Heart J. 2008;29(2):270-6.
2. Wittstein IS. Apical-ballooning syndrome. Lancet 2007; 370: 545-6
3. Van Spall HCG, Roberts DJ, Sawka Am et al. Not a broken heart . Lancet 2007; 370: 628.
4. Yoshida T, Hibino T, Kako N, et al. A pathophysiologic study of Tako-Tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography. Eur Heart J 2007 ; 28 : 2598-2604.
5. Nef HM, Möllmann H, Kostin S, et al. Tako-Tsubo cardiomyopathy: intraindividual structural analysis in the acute phase after functional recovery. Eur Heart J 2007; 28: 2456-64
6. Fujiwara S, Takeishi Y, Isoyama S, et al. Responsiveness to dobutamine in patients with left ventricular apical ballooning syndrome. Am J Cardiol 2007; 100; 1600-1603.
7. Brutsaert DL, Tako-Tsubo cardiomyopathy. Eur J Heart Failur 2007; 9: 854
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