Progression of cardiac dysfunction in patients with atherosclerotic renovascular disease.
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 [beta-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.


CONCLUSIONS
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.
Wright
Julian R
JR
Department of Nephrology, Manchester Royal Infirmary, Manchester, UK.
Shurrab
Ala'a E
AE
Cooper
Anne
A
Kalra
Paul R
PR
Foley
Robert N
RN
Kalra
Philip A
PA
D000368:Aged; D050197:Atherosclerosis / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D018660:Blood Pressure Monitoring, Ambulatory / Q000379:methods; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology* / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000150:complications / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012078:Renal Artery Obstruction / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D014463:Ultrasonography; D014654:Vascular Patency