http://www.cnr.it/ontology/cnr/individuo/prodotto/ID109290

Inflammatory activation during maximal physical effort predicts specific membrane damage of cardiomyocytes (Abstract/Comunicazione in atti di convegno)

Type

Prodotto della ricerca (Classe)
Abstract/Comunicazione in atti di convegno (Classe)

Label

Inflammatory activation during maximal physical effort predicts specific membrane damage of cardiomyocytes (Abstract/Comunicazione in atti di convegno) (literal)

Anno

2010-01-01T00:00:00+01:00 (literal)

Alternative label

Pastormerlo L. E.; Cabiati M.; Caselli C.; Del Ry S.; Giannessi D.; Passino C.; Emdin M. (2010)
Inflammatory activation during maximal physical effort predicts specific membrane damage of cardiomyocytes
in Heart Failure Congress 2010, berlin, Germany
(literal)

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Pastormerlo L. E.; Cabiati M.; Caselli C.; Del Ry S.; Giannessi D.; Passino C.; Emdin M. (literal)

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In: HF congress - Heart Failure Congress 2010 (berlin, Germany, 29 May-1 June 2010). Abstract, vol. 9 article n. S263. uropean Journal of Heart Failure Supplements, 2010. (literal)

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Background: Elevated concentrations of cardiac troponin I (TnI) and heart-type fatty acid-binding protein (H-FABP) identify patients with chronic heart failure (CHF) and ongoing myocardial damage (OMD) who are at increased risk for future cardiac events. Chronic inflammation has been advocated to justify CHF progression, possibly related to the development of OMD. We hypothesized that maximal exercise test could be useful to sensitize the assessment of OMD and its possible correlation with inflammatory status. Methods: The serum concentrations of H-FABP, a sensitive marker of membrane damage of cardiomyocytes, TnI, marker of myofibrillar damage and TNFa, as marker of inflammation, were measured in 20 patients with CHF (mean EF 35%±9, NYHA I vs II 50% vs 50%, 50% with ischaemic CHF, 50% primitive, on optimal medical therapy) before, at peak exercise, 1 h and 4 h after a maximal cardiopulmonary stress test. Results: Physical effort caused a significant rise in H-FABP (3.5±1 ng/ml, 1 hour after effort vs. 2.9±0.9 ng/ml at basal condition, p=0.05) and TnI (10 patients had at basal condition TnI values above 0.04 ng/L, the cut-off considered as prognostic in literature, while 4 h after maximal exercise, 15 (75%) patients had values higher). No correlations were evident between basal nor exertional values of TnI and H-FABP. Basal TNFa did not predict OMD. Interestingly TNFa at peak exercise was the only predictor of H-FABP 1 h after stress (r=0.619 p0.001), but not of TnI. Conclusions: Assessment of OMD following maximal exercise stress test could identify a subgroup of CHF patients with myocardial damage not evident in resting conditions. Inflammatory activation seems more associated with membrane rather than myofibrillar damage as indicated by H-FABP and TnI respectively. (literal)

Note