QJM Advance Access originally published online on August 10, 2009
QJM 2009 102(10):695-704; doi:10.1093/qjmed/hcp105
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Progression of cardiac dysfunction in patients with atherosclerotic renovascular disease
From the 1Department of Nephrology, Manchester Royal Infirmary, Manchester, 2Department of Nephrology, 3Department of Cardiology, Salford Royal Hospital, Salford, UK, 4Department of Cardiology, Portsmouth Hospitals NHS Trust, Portsmouth, UK and 5Nephrology Analytical Services, USRDS, Minneapolis, MN, USA
Address correspondence to Dr Philip A. Kalra, Consultant Nephrologist, Hope Hospital, Stott Lane, Salford, M6 8HD, UK. email: philip.kalra{at}srft.nhs.uk
Received 16 January 2009 and in revised form 12 July 2009
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Abstract |
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Background: Patients with atherosclerotic renovascular disease (ARVD) are at increased risk of heart disease because of the association with hypertension, coronary artery disease, cardiac failure and chronic kidney disease (CKD). A previous echocardiographic cross-sectional study showed that only 5% of patients with ARVD had normal cardiac structure and function at baseline. In this longitudinal study of the same patient cohort the progression of cardiac dysfunction and factors which predict declining cardiac function in patients with ARVD were delineated.
Methods: Seventy-nine patients were available for baseline analysis, but 16 withdrew from follow-up during the study. Forty-three patients (27M and 16F, age at study entry [mean ± SD] 69.7 ± 8.0 years) who were managed conservatively and 8 (age 69.8 ± 5.7) who were managed with renal revascularization underwent echocardiography and 24 h ambulatory blood pressure investigations at baseline and 12 months thereafter. The two data sets were interrogated to determine changes in blood pressure and cardiac status (morphological and functional); baseline factors which predicted such changes were ascertained. Twelve patients underwent baseline investigation but did not complete follow-up because of death (nine patients) or requirement of dialysis (three patients).
Results: Conservatively managed patients: At 12 months eGFR, (38.6 ± 18.3 vs 35.0 ± 18.5 ml/min; P = 0.001) had fallen whilst proteinuria had increased (0.3 ± 0.4 vs 0.6 ± 0.8 g/24 h; P = 0.001). Despite no increase in the number of blood pressure medications there was a fall in blood pressure between baseline and follow-up investigations (140.0 ± 16.5/75.3 ± 11.8, MAP 98.6 ± 12.3 mmHg vs 135.7 ± 16.1/69.6 ± 9.1, MAP 92.5 ± 10.2 mmHg; P < 0.001 for diastolic blood pressure and MAP). At 12 months, there was an increase in the number of patients with LVH (72.9% vs 81.4%). There were increases in left ventricular dimensions [left ventricular end diastolic diameter (5.1 ± 0.8 vs 5.5 ± 0.8 cm; P = 0.009), and left ventricular end diastolic volume (140.9 ± 39.5 vs 163.3 ± 61.0 ml; P = 0.01)]. There was no significant relationship of these changes in cardiac parameters to anatomical severity of renal artery disease but patients with severe renal dysfunction at baseline had an increase in left ventricular dilatation at follow-up. Linear regression analysis revealed an association between elevated time-averaged PTH and LV dilatation [β-coefficient and 95% confidence intervals, 0.18 (0.04, 0.32); P = 0.01]. Revascularization: No significant changes in any biochemical or echocardiographic parameters were seen between baseline and 1 year investigations in this small sub-group.
Conclusion: Patients with ARVD exhibit a high prevalence of LVH at diagnosis and progressive left ventricular dilatation over the first year after diagnosis. This dilatation is associated with severe renal impairment at baseline and not associated with anatomical severity of renal artery disease.