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Creatine kinase isoforms as circulating markers of deterioration in idiopathic dilated cardiomyopathy
M Hossein-Nia1, K Baig, J H Goldman
1Department of Cardiological Sciences, St. George's Hospital Medical School, London, U.K.
Insights
Creatine kinase (CK) measurements, particularly CK-MB isoforms, can identify ongoing myocardial damage in dilated cardiomyopathy (DCM) patients. Elevated CK-MB levels indicate a higher risk of adverse events like sudden death or cardiac transplantation in DCM.
Area of Science:
- Cardiology
- Biochemistry
- Internal Medicine
Background:
- Dilated cardiomyopathy (DCM) can involve persistent myocardial inflammation and damage.
- Current prognostic markers for DCM do not quantify myocardial damage.
Purpose of the Study:
- To assess myocardial damage in DCM by measuring plasma creatine kinase (CK) and its isoenzymes (CK-MM, CK-MB).
- To analyze CK-MM and CK-MB isoforms for objective myocardial damage assessment in DCM patients.
Main Methods:
- 77 DCM patients (49 +/- 14 years) were evaluated, with 29 in NYHA class III/IV.
- Follow-up averaged 27 months, with 50 patients stable and 27 deteriorating.
- Plasma CK, CK-MM, CK-MB levels, and CK-MM/CK-MB isoforms were measured.
Main Results:
- DCM patients showed a higher prevalence of abnormal MB2/MB1 ratios compared to controls (14% vs. 1%, p=0.003).
- Deteriorating DCM patients had higher MB2/MB1 ratios (1.22 vs. 0.85, p=0.01) and abnormal ratios more frequently (30% vs. 6%, p=0.004).
- Elevated CK-MB activity in DCM patients increased the odds of sudden death or transplantation by 3.13-fold (p=0.008).
Conclusions:
- CK measurements, especially CK-MB isoforms, serve as markers for myocardial damage in a subset of DCM patients.
- These markers can aid in identifying persistent myocardial damage in DCM.
- Objective assessment of myocardial damage is crucial for managing DCM patients.
Background:
A proportion of patients with dilated cardiomyopathy (DCM) may have ongoing myocardial damage secondary to viral or immune mediated myocardial inflammation.
Hypothesis:
The prognostic determinants identify patients with decreased survival but do not provide a measure of myocardial damage. To obtain an objective assessment of myocardial damage in DCM, we measured plasma levels of creatine kinase (CK), its isoenzymes (CK-MM and CK-MB), and separated the isoforms of CK-MM and CK-MB.
Methods:
The cohort consisted of 77 consecutive patients (61 men, 16 women) with DCM (World Health Organization criteria), aged 49 +/- 14 years (range 19-60). Patients had been symptomatic for 29 +/- 38 months (range 0.5-200 months) with 48 in New York Heart Association class I/II and 29 in class III/IV at the time of diagnosis. During median follow-up of 27 months from diagnosis (range 0.6-165), 50 patients remained clinically stable and 27 had deteriorated.
Results:
A significantly higher proportion of patients with DCM had abnormal MB2/MB1 ratio compared with normal volunteers (11, 14% vs. 1,1%, p = 0.003). Patients who deteriorated had higher MB2/MB1 ratio, (1.22 +/- 0.62 vs. 0.85 +/- 0.56; p = 0.01), and more frequently had abnormal MB2/ MB1 ratio (8, 30% vs. 3, 6%; p = 0.004) and CK and CK-MM activities (5, 19% vs. 2, 4%; p = 0.03) than those who remained stable. Patients with DCM with high CK-MB activity had 3.13-fold increased odds of sudden death or need for cardiac transplantation (95% confidence interval 1.53-6.40, p = 0.008). Thus, CK measurements, in particular CK-MB isoforms, are markers of myocardial damage in a subset of patients with DCM and could be useful in investigating the possibility of persistent myocardial damage in these patients.