Objective: To examine whether aggressive risk factor modification in chronic kidney disease (CKD) can limit the development of new ischaemia or reduce cardiac events.
Methods: Patients with CKD were randomly assigned to either an aggressive risk factor modification strategy (targeted treatment of hypertension, dyslipidaemia, homocysteine, haemoglobin and phosphate) or standard care. An intention to treat analysis was performed on 152 patients who had baseline dobutamine stress echocardiography (DSE), including 107 who had follow-up DSE. Biochemical parameters, cardiac risk factors and investigations (ECG, two-dimensional echocardiography) were recorded at baseline. New ischaemia was classed as new or worsening stress wall motion abnormality between follow-up and baseline DSE. Patients were followed up for the development of new ischaemia or cardiac death, acute coronary syndrome and non-fatal myocardial infarction over 1.8 years.
Results: The development of new ischaemia was common but not different between the standard and aggressively treated groups (15 (21%) v 18 (23%), p = 0.8). Independent predictors of new ischaemia were older age, abnormal ECG, higher systolic blood pressure and lower serum high density lipoprotein cholesterol, but not treatment arm. The standard and aggressively treated groups did not differ in cardiac event rate (10% v 13%, p = 0.6) or all-cause mortality (10% v 19%, p = 0.2). In patients with an abnormal baseline DSE (non-diagnostic, scar or ischaemia), the event rate was similar (22% v 20%, p = 0.9).
Conclusion: Aggressive risk factor modification in CKD does not limit the development of new ischaemia or reduce cardiac events in patients with an abnormal DSE.
- CKD, chronic kidney disease
- DSE, dobutamine stress echocardiography
- HDL, high density lipoprotein
- LDL, low density lipoprotein
- OR, odds ratio
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Published Online First 10 April 2006
↵* Also the Department of Renal Medicine, Princess Alexandra Hospital, Brisbane, Australia
Supported in part by a project grant (102471) and Centre of Clinical Research Excellence award (219285), National Health and Medical Research Council, Canberra, Australia and funding from the Princess Alexandra Hospital Foundation
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