Subclinical Abnormalities of Left Ventricular Myocardial Deformation in Early-Stage Chronic Kidney Disease: The Precursor of Uremic Cardiomyopathy?

https://doi.org/10.1016/j.echo.2008.09.013Get rights and content

Background

Abnormal left ventricular (LV) deformation is an independent predictor of poor cardiovascular outcome in end-stage renal disease. Studies in early-stage chronic kidney disease (CKD) have not been performed despite the known graded inverse relationship between glomerular filtration rate and adverse cardiovascular events.

Methods

Forty patients with CKD stage 2 or 3 and no history of cardiovascular disease or diabetes and 30 healthy controls underwent Doppler myocardial imaging for longitudinal deformation (strain/strain rate).

Results

There were no differences in LV ejection fraction or systolic tissue Doppler velocities between patients with CKD and controls. In CKD, mean global strain (−15% ± 4% vs −17% ± 3%, P <.01) and mean global strain rate were reduced compared with controls (−0.88 ± 0.16 vs −1.06 ± 0.31, P <.05). Peak systolic strain was reduced in the basal lateral (−13.9% ± 0.9% vs −17.9% ± 1.02%, P <.01), basal septal (−17.1% ± 0.8% vs −19.4% ± 0.77%, P <.05), and mid-septal (−16.4% ± 0.78% vs −18.9% ± 0.88%, P <.05) walls with more basal postsystolic shortening (P <.01). Peak systolic strain rate was reduced in the basal lateral, mid-lateral, and mid-septal segments (P <.05).

Conclusion

Conventional measures of systolic function are preserved in early-stage CKD, but systolic deformation is abnormal, consistent with an adverse cardiovascular prognosis.

Section snippets

Materials and Methods

The first 50 patients prospectively recruited into a single-center, prospective, double-blind, placebo-controlled, randomized interventional trial of spironolactone 25 mg once daily compared with placebo (www.clinicaltrials.gov Identifier: NCT00291720) were studied in this prespecified echocardiographic substudy. Patients in the substudy were younger (48 ± 11 years vs 57 years ± 12, P <.01) than the patients subsequently recruited in the study but did not significantly differ in other

Demographic Data

There were no significant differences in demographic data between subjects and controls (Table 1). The cause of CKD was diverse (glomerulonephritis 55%, quiescent vasculitis/systemic lupus erythematosus 30%, adult polycystic kidney disease 8%, other 7%) and confirmed on biopsy in 70% of cases. Fifty-one percent of patients had a history of hypertension as a complication of their renal pathology, but this was well controlled in all patients with an average of 2.1 antihypertensive agents per

Discussion

This is the first study to demonstrate that patients with early CKD have subclinical LV systolic dysfunction with evidence of impaired deformation on echocardiography. These changes are present at a stage when subjects have normal or near normal serum creatinine (mean serum creatinine 1.43 mg/dL) and are consistent with the epidemiologic evidence that early-stage CKD is associated with adverse cardiovascular outcomes with an increase in event rates evident from a GFR as high as ≤ 90 mL/min/1.73

Limitations

The lack of a control group with treated hypertension and normal renal function means that we cannot exclude the impact of hypertension on the functional abnormalities documented in this study. A 5 mm Hg difference in systolic blood pressure was present between patients with CKD and controls, although this was not statistically significant. This was not a study however, of patients with hypertension and incidental renal dysfunction. All patients were recruited from a specialist renal clinic and

Conclusions

Abnormal longitudinal systolic deformation is present in asymptomatic individuals with early CKD without clinical evidence of heart disease. These changes represent the first detectable echocardiographic manifestations of systolic dysfunction in CKD and along with abnormalities of diastolic function may be the precursors of the major alterations in LV geometry and function that are characteristic of ESKD.

Acknowledgments

We thank Susan Maiden, Lesley Fifer, and Helen Jones for help in running the study and Peter Nightingale for statistical support.

References (33)

Cited by (0)

Disclosure: The authors have no conflicts of interests to declare.

Funding Source: This work is supported by the British Heart Foundation.

View full text