Correlations of the changes in bioptic findings with echocardiographic, clinical and laboratory parameters in patients with inflammatory cardiomyopathy

. 2016 Mar ; 31 (3) : 416-26. [epub] 20141225

Jazyk angličtina Země Japonsko Médium print-electronic

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/pmid25539624
Odkazy

PubMed 25539624
DOI 10.1007/s00380-014-0618-0
PII: 10.1007/s00380-014-0618-0
Knihovny.cz E-zdroje

Patients with myocarditis and left ventricular (LV) dysfunction may improve after standard heart failure therapy. This improvement seems to be related to retreat of myocardial inflammation. The aim of the present study was to assess changes in clinical, echocardiographic and some laboratory parameters and to correlate them with changes in the number of inflammatory infiltrating cells in endomyocardial biopsy (EMB) samples during the 6-month follow-up, and to define predictors of LV function improvement among baseline parameters. Forty patients with biopsy-proven myocarditis and impaired LV function (LV ejection fraction-LVEF <40 %) with heart failure symptoms ≤ 6 months were evaluated. Myocarditis was defined as the presence of >14 mononuclear leukocytes/mm(2) and/or >7 T-lymphocytes/mm(2) in the baseline EMB. The EMB, echocardiography and clinical evaluation were repeated after 6 months of standard heart failure therapy. LVEF improved on average from 25 ± 9 to 42 ± 12 % (p < 0.001); LV end-systolic volume and LV end-diastolic volume (LVEDV) decreased from 158 ± 61 to 111 ± 58 ml and from 211 ± 69 to 178 ± 63 ml (both p < 0.001). NYHA class decreased from 2.6 ± 0.5 to 1.6 ± 0.6 (p < 0.001) and NTproBNP from 2892 ± 3227 to 851 ± 1835 µg/ml (p < 0.001). A decrease in the number of infiltrating leukocytes (CD45+/LCA+) from 23 ± 15 to 13 ± 8 cells/mm(2) and in the number of infiltrating T lymphocytes (CD3+) from 7 ± 5 to 4 ± 3 cells/mm(2) (both p < 0.001) was observed. The decline in the number of infiltrating CD45+ cells significantly correlated with the change in LVEF (R = -0.43; p = 0.006), LVEDV (R = 0.39; p = 0.012), NYHA classification (R = 0.35; p = 0.025), and NTproBNP (R = 0.33; p = 0.045). The decrease in the number of CD3+ cells correlated with the change of systolic and diastolic diameters of the left ventricle (R = -0.33; p = 0.038 and R = -0.45; p = 0.003) and with the change in LVEDV (R = -0.43; p = 0.006). Tricuspid annular plane systolic excursion (TAPSE) (OR 0.61; p = 0.005) and early transmitral diastolic flow velocity (E wave) (OR 0.89; p = 0.002) were identified as predictors of LVEF improvement. Improvements in clinical status, LV function and NTproBNP levels correlated with decrease in the number of infiltrating inflammatory cells. TAPSE and E wave velocity were significant predictors of improvement in multivariate regression. Our observations suggest that contemporary guidelines-based therapy of heart failure is an effective treatment option in patients with recent onset biopsy-proven inflammatory cardiomyopathy.

Zobrazit více v PubMed

Eur Heart J. 2008 Sep;29(17):2073-82 PubMed

Circulation. 2001 Jul 3;104(1):39-45 PubMed

Int J Cardiol. 2008 Mar 28;125(1):85-93 PubMed

Heart Vessels. 2013 Jan;28(1):86-90 PubMed

Eur J Heart Fail. 2005 Jun;7(4):444-52 PubMed

Heart. 2002 Oct;88(4):323-4 PubMed

Eur J Heart Fail. 2002 Aug;4(4):411-7 PubMed

Cardiovasc Drugs Ther. 2007 Jun;21(3):155-60 PubMed

Circulation. 2001 May 8;103(18):2254-9 PubMed

Circulation. 2006 Oct 10;114(15):1581-90 PubMed

Eur J Heart Fail. 2009 Apr;11(4):349-53 PubMed

Eur Heart J. 2009 Aug;30(16):1995-2002 PubMed

Circulation. 2005 Feb 22;111(7):887-93 PubMed

Eur Heart J. 2012 Jul;33(14):1787-847 PubMed

Eur J Heart Fail. 2009 Feb;11(2):119-29 PubMed

J Am Coll Cardiol. 2012 Feb 28;59(9):779-92 PubMed

Eur J Echocardiogr. 2003 Dec;4(4):262-71 PubMed

Heart Vessels. 2014 Jul;29(4):486-95 PubMed

J Heart Lung Transplant. 2010 Oct;29(10):1089-103 PubMed

Int J Cardiol. 2008 Aug 1;128(1):38-41 PubMed

Heart Vessels. 2007 Jan;22(1):48-51 PubMed

Heart Fail Clin. 2005 Oct;1(3):467-74 PubMed

Eur J Echocardiogr. 2006 Mar;7(2):79-108 PubMed

Ital Heart J. 2000 Nov;1(11):758-61 PubMed

Circulation. 2007 Nov 6;116(19):2216-33 PubMed

Eur Heart J. 2007 Jun;28(11):1326-33 PubMed

J Clin Immunol. 2009 Nov;29(6):730-7 PubMed

N Engl J Med. 2009 Apr 9;360(15):1526-38 PubMed

Circulation. 2008 Aug 5;118(6):639-48 PubMed

Circulation. 2003 Feb 18;107(6):857-63 PubMed

Heart Vessels. 2013 Sep;28(5):646-57 PubMed

Clin Chim Acta. 2009 Oct;408(1-2):114-22 PubMed

Trends Mol Med. 2012 Jul;18(7):426-37 PubMed

Heart. 1996 Mar;75(3):295-300 PubMed

Heart. 2001 May;85(5):499-504 PubMed

Prog Cardiovasc Dis. 2010 Jan-Feb;52(4):274-88 PubMed

J Am Coll Cardiol. 2011 Sep 6;58(11):1112-8 PubMed

Circulation. 2013 Oct 15;128(16):e240-327 PubMed

Eur Heart J. 2011 Nov;32(21):2616-25 PubMed

Am J Physiol Heart Circ Physiol. 2004 Jan;286(1):H83-90 PubMed

Dtsch Arztebl Int. 2012 May;109(20):361-8 PubMed

Virchows Arch. 2013 Jul;463(1):1-5 PubMed

Cardiovasc Res. 2001 May;50(2):290-300 PubMed

Cardiovasc Res. 2003 Oct 15;60(1):5-10 PubMed

N Engl J Med. 2000 Mar 9;342(10):690-5 PubMed

Eur Heart J. 2013 Sep;34(33):2636-48, 2648a-2648d PubMed

Circulation. 2006 Oct 24;114(17):1883-91 PubMed

Am Heart J. 1994 Aug;128(2):301-7 PubMed

Int J Cardiol. 2005 Sep 15;104(1):92-100 PubMed

Eur Heart J. 2007 Jun;28(11):1279-80 PubMed

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...