BACKGROUND: Intradialytic hypotension (IH) has been long recognized as a common complication during hemodialysis (HD) therapy, but few studies have discussed IH-related myocardial injuries and the long-term prognosis of patients prone to IH (HP). METHODS: We conducted a prospective study on 70 chronic HD patients who had no recent occurrences of acute coronary artery syndrome. The patients were divided into two groups: HP (n = 29) and IH resistant (n = 41). While they underwent HD therapy, we monitored and evaluated their baseline data and their patterns of cardiac troponin I (cTnI), creatine kinase, and creatine kinase isoenzyme MB. RESULTS: The HP and IH-resistant patients had similar baseline cardiac marker levels that did not seem to be influenced by uneventful HD therapy. However, if during HD therapy the patients experienced an episode of symptomatic IH, they were found to have significant increases in the creatine kinase MB activity at the end of HD therapy and in the cTnI levels 44 h following HD. After 12 months, the HP patients with baseline cTnI levels > or =0.20 ng/ml were more likely to experience cardiovascular events or death (adjusted odds ratio 15.0, p = 0.012). CONCLUSIONS: Our study showed that, after symptomatic IH episodes, the HP patients were more likely to suffer occult myocardial injuries. HP patients who have high cTnI levels should be closely monitored for cardiovascular diseases.
BACKGROUND: Intradialytic hypotension (IH) has been long recognized as a common complication during hemodialysis (HD) therapy, but few studies have discussed IH-related myocardial injuries and the long-term prognosis of patients prone to IH (HP). METHODS: We conducted a prospective study on 70 chronic HDpatients who had no recent occurrences of acute coronary artery syndrome. The patients were divided into two groups: HP (n = 29) and IH resistant (n = 41). While they underwent HD therapy, we monitored and evaluated their baseline data and their patterns of cardiac troponin I (cTnI), creatine kinase, and creatine kinase isoenzyme MB. RESULTS: The HP and IH-resistant patients had similar baseline cardiac marker levels that did not seem to be influenced by uneventful HD therapy. However, if during HD therapy the patients experienced an episode of symptomatic IH, they were found to have significant increases in the creatine kinase MB activity at the end of HD therapy and in the cTnI levels 44 h following HD. After 12 months, the HPpatients with baseline cTnI levels > or =0.20 ng/ml were more likely to experience cardiovascular events or death (adjusted odds ratio 15.0, p = 0.012). CONCLUSIONS: Our study showed that, after symptomatic IH episodes, the HPpatients were more likely to suffer occult myocardial injuries. HPpatients who have high cTnI levels should be closely monitored for cardiovascular diseases.
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