Left ventricular mass in normotensive subjects with autosomal dominant polycystic kidney diseaseBMJ 1994; 309 doi: https://doi.org/10.1136/bmj.309.6969.1617 (Published 17 December 1994) Cite this as: BMJ 1994;309:1617
- Anand K Saggar-Malik,
- Constantinos G Missouris,
- Jaswinder S Gill,
- Donald R J Singer,
- Nirmala D Markandu,
- Graham A MacGregor
- Blood Pressure Unit and Department of Cardiological Sciences, St George's Hospital Medical School, London SW17 0RE, lecturer in medicine, research fellow, lecturer in cardiology, lecturer in medicine, senior research assistant, professor of cardiovascular medicine.
- Correspondence to: Dr Saggar-Malik.
- Accepted 29 September 1994
Autosomal dominant polycystic kidney disease increases the risk of premature cardiovascular disease and sudden death.1 One possible mechanism may be left ventricular hypertrophy, which exacerbates cardiac risk in patients with other types of disease. We assessed whether disproportionate cardiac hypertrophy occurs in polycystic kidney disease.
Subjects, methods, and results
Asymptomatic, untreated subjects with normal renal function and no history of hypertension were selected from our polycystic register. Fourteen out of 23 eligible white subjects were recruited (10 women and four men, mean age 32 (SD 12) years (range 16-55), mean supine blood pressure 122/76 mm Hg (range 144-103/86-59)). These were age and sex matched with 14 unrelated, white, healthy volunteers (mean age 33 (SD 13) years (range 18-58), mean blood pressure 116/ 70 mm Hg (range 140-89/86-60)). All subjects had a serum creatinine concentration below 120 μmol/l and a creatinine clearance above 80 ml/min. The study was approved by the hospital ethics committee.
Subjects were studied on their usual diets. They collected a urine sample over 24 hours for determination of electrolyte and creatinine concentrations. Blood pressure was the mean of five readings with an ultrasound sphygmomanometer (Arteriosonde, Roche). Blood was taken for measurement of plasma renin activity and concentrations of aldosterone and angiotensin II after subjects had been sitting for 10 minutes. Echocardiograms (Hewlett Packard, 2.5 MHz transducer) were read by two cardiologists blinded to clinical details. Left ventricular mass index was calculated using the American Society of Echocardiography convention corrected for body surface area. Data, expressed as geometric means (SD), were analysed, after log transformation if appropriate, using Student's t test for paired observations. Correlations were assessed by linear regression.
Left ventricular mass index was 23% greater (95% confidence interval 11 to 34) in the polycystic subjects (81 (7)) than in the controls (68 (11), P<0.01; figure), an increase not explained by differences in body surface area, renal function, physical activity, or race. No subject had any cardiac valvar defects, and there were no significant differences in urinary sodium excretion over 24 hours, renin activity, or concentrations of aldosterone, natriuretic peptide, or angiotensin II between the groups (data not shown). Blood pressure was higher in the polycystic subjects (122/76 (12/9) mm Hg) than the controls (116/70 (17/8) mm Hg; P=0.22/0.06), but it did not correlate with ventricular mass index in either group. There was no relation between absolute or percentage differences in blood pressure and ventricular mass index between the groups.
We found an increased left ventricular mass index in normotensive subjects with polycystic kidney disease and normal renal function compared with controls. Some previous studies of left ventricular mass in adults with polycystic kidney disease have been confounded by poor matching of controls or by a history of hypertension with or without renal impairment,2 3 conditions which can increase ventricular mass. As our polycystic subjects had slightly raised blood pressure we calculated the expected increase in left ventricular mass index. For a 10 mm Hg increase in systolic pressure this was 4%4 and for a 6 mm Hg increase in systolic or diastolic pressure 2.2% (1% to 3%) and 4.5% (3% to 6%) respectively.5
This small difference in blood pressure therefore probably does not explain the large increase in ventricular mass index. As we did not measure ambulatory blood pressure, we cannot exclude a role for differences in diurnal blood pressure as explanation for our findings. No differences in circadian blood pressure were found however, in young, non-uraemic polycystic patients.2
Activation of the renin system may lead to ventricular enlargement. In our study, however, there was no difference in sodium intake or in the activity of the renin system between the groups. An alternative mechanism for the increase is the defect of extracellular matrix that is believed to occur in polycystic kidney disease.
Since left ventricular hypertrophy is associated with ventricular ectopy, even in normotensive patients, our finding of a large increase in left ventricular mass in normotensive polycystic subjects early in the course of the disease provides a possible mechanism for sudden cardiac death in this common disease and reinforces the need for early assessment of possible risk factors in subjects at risk within affected families.
We thank Drs J B Eastwood, A J Eisenger, and M R Bending for allowing us to study their patients; Dr J J Morton for measuring angiotensin II; Dr P Vallance and Professor D Johnston for access to Medical Research Council data; and Dr M Bland for his statistical advice. DRJS was a British Heart Foundation Intermediate Research Fellow (F201) and AKS-M holds the Williams Fellowship of the University of London.