Arquivos Brasileiros de Cardiologia (Mar 2006)

Cardioversão elétrica e lesão miocárdica: avaliação pelos novos marcadores de injúria cardíaca Electrical cardioversion and myocardial injury: evaluation by new cardiac injury markers

  • Elizabete Silva dos Santos,
  • Marcos Paulo Pereira,
  • Luiz Minuzzo,
  • Dalmo A. R. Moreira,
  • Rui Ramos,
  • Álvaro Avezum,
  • Ari Timerman,
  • Leopoldo S. Piegas

DOI
https://doi.org/10.1590/S0066-782X2006000300006
Journal volume & issue
Vol. 86, no. 3
pp. 191 – 197

Abstract

Read online

OBJETIVO: Avaliar, através da evolução dos novos marcadores bioquímicos de injúria cardíaca, se a cardioversão elétrica (CVE) causa lesão miocárdica. MÉTODOS: Foram avaliados 76 pacientes (P) submetidos a CVE eletiva de fibrilação atrial ou flutter atrial. Medidas de creatinafosfoquinase (CPK), CKMB-atividade e dosagem de CKMB-massa (M), mioglobina e troponina I cardíaca (cTnI) foram determinadas antes e após 6 e 24 horas da CVE. RESULTADOS: A CVE resultou um sucesso em 58 P (76,3%). A carga cumulativa (CC) foi de até 350 joules (J) em 36 P, de 500 a 650 J em 20 P e de 900 a 960 J em 20 P, com energia média aplicada de 493 J (± 309). A cTnI permaneceu dentro da normalidade nos 76 P. Com o aumento da CC, ocorreu elevação de CPK (> valor de p = 0,007), CKMB-atividade (> valor de p = 0,002), CKMB-M (> valor de p = 0,03) e mioglobina (> valor de p = 0,015). Correlação positiva foi observada entre a CC e picos de CPK (r = 0,660; p OBJECTIVE: Evaluate, based on the evolution of new biochemical markers of cardiac damage, if electrical cardioversion (ECV) causes myocardial injury. METHODS: Seventy-six patients (P) submitted to elective ECV for atrial fibrillation or atrial flutter were evaluated. Creatine phosphokinase (CPK), CK-MB activity, CK-MB mass, myoglobin and cardiac troponin I (cTnI) were measured before, and 6 and 24 hours after ECV. RESULTS: ECV was successful in 58 P (76.3%). Cumulative energy (CE) was up to 350 joules (J) in 36 P, from 500 to 650 J in 20 P and from 900 to 960 J in 20 P; the mean energy delivered being 493 J (± 309). The levels of cTnI remained within normal limits in all 76 P. The increase of cumulative energy led to an elevation of CPK levels (> p value = 0.007), CK-MB activity (> p value = 0.002), CK-MB mass (> p value = 0.03), and myoglobin (> p value = 0.015). A positive correlation between the cumulative energy and CPK peaks was observed (r = 0.660; p < 0.001), CK-MB activity (r = 0.429; p < 0.0001), CK-MB mass (r = 0.265; p = 0.02), and myoglobin (r = 0.684; p < 0.0001), as well as between the number of shocks and the CPK peaks (r = 0.770; p < 0.001), CK-MB activity (r = 0.642; p < 0.0001), CK-MB mass (r = 0.430; p < 0,0001), and myoglobin (r = 0.745; p < 0.0001). CONCLUSION: ECV does not cause myocardial injury detectable by cTnI measurement. Elevations of CPK, CK-MB activity, CK-MB mass and myoglobin result from skeletal muscle injury and are positively correlated with the CE delivered or with the number of shocks.

Keywords