Shock-Wave Therapy Improves Myocardial Blood Flow Reserve in Patients with Refractory Angina: Evaluation by Real-Time Myocardial Perfusion Echocardiography

Carregando...
Imagem de Miniatura
Citações na Scopus
7
Tipo de produção
article
Data de publicação
2019
Título da Revista
ISSN da Revista
Título do Volume
Editora
MOSBY-ELSEVIER
Citação
JOURNAL OF THE AMERICAN SOCIETY OF ECHOCARDIOGRAPHY, v.32, n.9, p.1075-1085, 2019
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: Cardiac shock-wave therapy (CSWT) has been demonstrated as an option for the treatment of patients with refractory angina (RA), promoting immediate vasodilatory effects and, in the long-term, neoangiogenic effects that would be responsible for reducing the myocardial ischemic load. The aim of this study was to determine the effects of CSWT on myocardial blood flow reserve (MBFR) assessed by quantitative real-time myocardial perfusion echocardiography in patients with RA. Methods: Fifteen patients (mean age 61.5 +/- 12.8 years) with RA who underwent CSWT during nine sessions, over 3 months of treatment, were prospectively studied. A total of 32 myocardial segments with ischennia were treated, while another 31 did not receive therapy because of technical limitations. Myocardial perfusion was evaluated at rest and after dipyridamole stress (0.84 mg/kg) before and 6 months after CSWT, using quantitative real-time myocardial perfusion echocardiography. Clinical effects were evaluated using Canadian Cardiovascular Society grading of angina and the Seattle Angina Questionnaire. Results: The ischemic segments treated with CSWT had increased MBFR (from 1.33 +/- 0.22 to 1.74 +/- 0.29, P < .001), a benefit that was not observed in untreated ischemic segments (1.51 +/- 0.29 vs 1.54 +/- 0.28, P = .47). Patients demonstrated increased global MBFR (from 1.78 +/- 0.54 to 1.89 +/- 0.49, P = .017). Senn iquantitative single-photon emission computed tomographic analysis of the treated ischemic segments revealed a score reduction from 2.10 +/- 0.87 to 1.68 +/- 1.19 (P = .024). There was improvement in Canadian Cardiovascular Society score (from 3.20 +/- 0.56 to 1.93 +/- 0.70, P < .05) and in Seattle Angina Questionnaire score (from 42.3 +/- 12.99 to 71.2 +/- 14.29, P < .05). No major cardiovascular events were recorded during follow-up. Conclusions: CSWT improved MBFR in ischemic segments, as demonstrated by quantitative real-time myocardial perfusion echocardiography. These results suggest that CSWT has the potential to increase myocardial blood flow, with an impact on symptoms and quality of life in patients with RA.
Palavras-chave
Refractory angina pectoris, Myocardial contrast echocardiography, Shock-wave therapy
Referências
  1. Abdelmoneim SS, 2009, EUR J ECHOCARDIOGR, V10, P813, DOI 10.1093/ejechocard/jep084
  2. Alunni G, 2017, CARDIOVASC REVASCULA, V18, P572, DOI 10.1016/j.carrev.2017.05.006
  3. Berman DS, 2004, J NUCL CARDIOL, V11, P414, DOI 10.1016/j.nuclcard.2004.03.033
  4. Bom MJ, 2014, NETH HEART J, V22, P151, DOI 10.1007/s12471-014-0524-1
  5. Burneikaite G, 2017, CARDIOVASC ULTRASOUN, V15, DOI 10.1186/s12947-017-0102-y
  6. Cassar A, 2014, MAYO CLIN PROC, V89, P346, DOI 10.1016/j.mayocp.2013.11.017
  7. Cerqueira MD, 2002, CIRCULATION, V105, P539, DOI 10.1161/hc0402.102975
  8. Osorio AF, 2007, J AM SOC ECHOCARDIOG, V20, P709, DOI 10.1016/j.echo.2006.11.016
  9. Fukumoto Y, 2006, CORONARY ARTERY DIS, V17, P63, DOI 10.1097/00019501-200602000-00011
  10. Gaibazzi N, 2010, J AM SOC ECHOCARDIOG, V23, P1242, DOI 10.1016/j.echo.2010.09.003
  11. GOULD KL, 1974, AM J CARDIOL, V33, P87, DOI 10.1016/0002-9149(74)90743-7
  12. Ha CH, 2013, INT J CARDIOL, V168, P4168, DOI 10.1016/j.ijcard.2013.07.112
  13. Huang TH, 2016, MOL MED, V22, P850, DOI 10.2119/molmed.2016.00108
  14. Kowatsch I, 2007, J AM SOC ECHOCARDIOG, V20, P1109, DOI 10.1016/j.echo.2007.02.008
  15. Lang RM, 2015, J AM SOC ECHOCARDIOG, V28, P1, DOI [10.1016/j.echo.2014.10.003, 10.1093/ehjci/jev014]
  16. Lim HE, 2000, J AM SOC ECHOCARDIOG, V13, P264, DOI 10.1067/mje.2000.103508
  17. Mannheimer C, 2002, EUR HEART J, V23, P355, DOI 10.1053/euhj.2001.2706
  18. Matskeplishvili ST, 2017, TERAPEVT ARKH, V89, P22, DOI 10.17116/terarkh201789422-28
  19. Mattoso AAA, 2013, J AM SOC ECHOCARDIOG, V26, P539, DOI 10.1016/j.echo.2013.01.016
  20. Meuwissen M, 2001, CIRCULATION, V103, P184
  21. Mozaffarian D, 2015, CIRCULATION, V131, pE29, DOI 10.1161/CIR.0000000000000152
  22. Nakanishi R, 2016, J NUCL CARDIOL, V23, P530, DOI 10.1007/s12350-015-0150-3
  23. Nishida T, 2004, CIRCULATION, V110, P3055, DOI 10.1161/01.CIR.0000148849.51177.97
  24. Oi K, 2008, TOHOKU J EXP MED, V214, P151, DOI 10.1620/tjem.214.151
  25. Pellikka PA, 2007, J AM SOC ECHOCARDIOG, V20, P1021, DOI 10.1016/j.echo.2007.07.003
  26. Peltier M, 2004, J AM COLL CARDIOL, V43, P257, DOI 10.1016/j.jacc.2003.07.040
  27. Porter TR, 2018, J AM SOC ECHOCARDIOG, V31, P241, DOI 10.1016/j.echo.2017.11.013
  28. Santos JMT, 2010, AM J CARDIOL, V105, P243, DOI 10.1016/j.amjcard.2009.09.009
  29. Tsutsui JM, 2005, J AM COLL CARDIOL, V45, P1235, DOI 10.1016/j.jacc.2005.01.024
  30. Tsutsui JM, 2005, CIRCULATION, V112, P1444, DOI 10.1161/CIRCULATIONAHA.105.537134
  31. Uwatoku T, 2007, CORONARY ARTERY DIS, V18, P397, DOI 10.1097/MCA.0b013e328089f19b
  32. Vogel R, 2005, J AM COLL CARDIOL, V45, P754, DOI 10.1016/j.jacc.2004.11.044
  33. Wang J, 2015, EUR J CLIN INVEST, V45, P1270, DOI 10.1111/eci.12546
  34. Wei K, 1998, CIRCULATION, V97, P473
  35. Wu JF, 2016, CIRC-CARDIOVASC IMAG, V9, DOI 10.1161/CIRCIMAGING.116.004129
  36. Yang P, 2013, HEART VESSELS, V28, P284, DOI 10.1007/s00380-012-0244-7