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NDT Advance Access originally published online on November 14, 2007
Nephrology Dialysis Transplantation 2008 23(2):601-607; doi:10.1093/ndt/gfm642
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Prognostic significance of renal function in patients undergoing dobutamine stress echocardiography

Stefanos E. Karagiannis1, Harm H.H. Feringa1, Abdou Elhendy2, Ron van Domburg1, Michel Chonchol3, Radosav Vidakovic1, Jeroen J. Bax4, George Karatasakis5, George Athanasopoulos5, Dennis V. Cokkinos5 and Don Poldermans1

1Department of Cardiology, Erasmus MC, Rotterdam, The Netherlands, 2Department of Cardiology, Marshfield Clinic, Marshfield, WI, USA, 3Division of Renal Diseases and Hypertension, University of Colorado, Health Sciences Center, Denver, CO, USA, 4Department of Cardiology, Leiden University, Leiden, The Netherlands and 5First Department of Cardiology, Onassis Cardiac Surgery Centre, Athens, Greece

Correspondence and offprint requests to: Don Poldermans, Department of Cardiology, Room H 923, Erasmus MC, 3015 GD Rotterdam, The Netherlands. Tel: +31-104639222; Fax: +31-104634957; E-mail: d.poldermans{at}erasmusmc.nl



   Abstract
Top
 Abstract
Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Background. Dobutamine stress echocardiography (DSE) is used for risk stratification of patients with suspected coronary artery disease (CAD). However, the prognostic value of DSE among the entire strata of renal function has yet to be determined. We assessed the prognostic value of renal function relative to DSE findings.

Methods. We studied 2292 patients, divided into 729 (32%) patients with normal renal function [creatinine clearance (CrCl) >90 ml/min] and 1563 (68%) with renal dysfunction, classified as mild (CrCl: 60–90 ml/min) in 933, moderate (CrCl: 30–60 ml/min) in 502 and severe (CrCl < 30ml/min) in 128 patients. All patients underwent DSE for the evaluation of known or suspected CAD and were followed for a mean of 8 years.

Results. New wall motion abnormalities during DSE and mildly, moderately and severely abnormal CrCl were powerful independent predictors for all-cause mortality, cardiac death and hard cardiac events (cardiac death and non-fatal myocardial infarction). Kaplan–Meier curves demonstrated that patients with normal DSE and renal dysfunction have greater probability for cardiac death and hard cardiac events compared to those with normal renal function. The warranty of a normal DSE in the presence of moderate renal dysfunction was 15 and 36 months for 10 and 20% risk for cardiac death and hard cardiac events, respectively.

Conclusions. The presence and severity of renal dysfunction has additional independent prognostic value over DSE findings. The low-risk warrantee period after a normal DSE is determined by the severity of renal dysfunction.

Keywords: dobutamine stress echocardiography; prognosis; renal function



   Introduction
Top
 Abstract
 Introduction
Subjects and methods
 Results
 Discussion
 References
 
Cardiovascular disease is the major cause of death in patients with renal dysfunction [1]. In particular, coronary artery disease (CAD) is an important predictor of mortality in chronic renal failure patients [2]. Dobutamine stress echocardiography (DSE) is a widely used non-invasive imaging technique for detection of CAD [3]. Several studies have demonstrated the high predictive value of DSE for long-term cardiac events in patients with normal renal function [4]. It has also been suggested as a tool for risk stratification of patients with chronic renal failure, specifically in patients undergoing evaluation for kidney transplantation [5]. However, the value of wall motion abnormalities (WMA) during DSE among the entire strata of renal function has yet to be determined. The identification of clinical variables that influence prognosis in addition to abnormalities on DSE is important to optimise risk stratification in a given patient. The aim of this observational follow-up study was to assess the prognostic value of renal function relative to DSE findings in patients with known or suspected CAD.



   Subjects and methods
Top
 Abstract
 Introduction
 Subjects and methods
Results
 Discussion
 References
 
Study population and baseline measurements
The study population included 2292 consecutive patients with known or suspected CAD who were referred at the Erasmus MC (Rotterdam, The Netherlands) for DSE between 1993 and 2003. Diabetes mellitus was defined as fasting plasma glucose level of ≥126 mg/dl on at least two occasions and/or requirement for insulin or oral hypoglycaemic agents, according to the criteria by the American Diabetes Association [6]. Hypercholesterolemia was defined as total cholesterol of 200 mg/dl or use of a cholesterol-lowering agent. Hypertension was defined as systolic blood pressure of 140 mmHg, diastolic blood pressure of 90 mmHg or use of anti-hypertensive medication. Heart failure was defined according to the New York Heart Association classification.

Renal function assessment
Serum creatinine was assessed by a non-kinetic alkaline picrate (Jaffe) method. Creatinine clearance (CrCl) was estimated with the Cockcroft–Gault [7] equation: CrCl (ml/min) = (140 – age) x weight (kg) ÷ 72 x serum creatinine (mg/dl) (x0.85 for women) and standardized for body surface area using the Dubois formula. This equation has close correlation with the measured CrCl and gives a more accurate assessment of renal function than of serum creatinine alone.

The severity of renal disease was estimated according to the widely used American National Kidney Foundation (NKF) classification of chronic kidney disease (CKD) Stages I–V [8]. These NKF criteria for renal failure are: Glomerular filtration rate (GFR) > 90 ml/min/1.73 m2 (Stage I), GFR > 60–89 ml/min/1.73 m2 (Stage II), GFR > 30–59 ml/min/1.73 m2 (Stage III), and GFR < 30 ml/min/1.73 m2 (Stages IV and V).

By this definition patients were divided into four groups: normal renal function (CrCl > 90 ml/min) and mild (CrCl = 60–90 ml/min), moderate (CrCl = 30–60 ml/min) and severe (CrCl < 30 ml/min) renal dysfunction. The local medical ethics committee approved the study protocol. Patients gave an informed consent to undergo this observational follow-up study and the results were derived from a secondary analysis.

Dobutamine stress echocardiography
The DSE protocol was approved by the local medical ethics committee and was performed in accordance with the well-established protocols [9]. Studies were performed using a Sonos 5500 imaging system (Phillips Medical Systems, Eindhoven, The Netherlands). Patients underwent a resting two-dimensional echocardiographic examination from the standard apical and parasternal views. Images were recorded on videotape and also digitized for comparison of different stages. Dobutamine was then administered intravenously by infusion pump, starting at 5 µg/kg/min, followed by 10 µg/kg/min for 5 min and increasing by 10 µg/kg/min every 3 min to a maximum of 40 µg/kg/min (Stage V), and continued for 6 min. The dobutamine infusion was stopped if a target heart rate (85%) of a theoretic maximal heart rate [men: (220 – age) x 85%; women: (200 – age) x 85%] was achieved. If the target heart rate was not achieved and patients had no symptoms or signs of ischemia, atropine (starting with 0.25 mg, increased to a maximum of 2.0 mg) was given intravenously at the end of Stage V while the administration of dobutamine was continued. During the test, a 12-lead Electrocardiogram (ECG) was recorded every minute. Blood pressure was measured at the end of every dobutamine infusion stage.

The criteria for stopping the test were: (i) achievement of the target heart rate, (ii) severe and extensive new WMA, (iii) horizontal or downsloping ST segment of ECG depression of >0.2 mV measured 80 ms after the J point, or ST-segment elevation of ≥0.2 mV in the absence of Q waves, (iv) symptomatic decline in systolic blood pressure of more than 40 mmHg or a systolic blood pressure ≤ 90 mmHg, (v) hypertension (blood pressure > 240/140 mmHg), (vi) the occurrence of sustained cardiac arrhythmias, (vii) severe angina pectoris and (viii) intolerable adverse effects considered to be the result of dobutamine or atropine. Two experienced investigators performed off-line assessment of echocardiographic images without the knowledge of the patient's clinical and coronary angiography data, but with the knowledge of the doses of dobutamine and atropine used. Interobserver and intraobserver agreement for the analysis of DSE studies were reported previously (92 and 94%, respectively) [10]. Regional function was scored according to a 16-segment, five-point scoring model: 1, normal; 2, mildly hypokinetic; 3, severely hypokinetic; 4, akinetic; 5, dyskinetic. The results of DSE were considered positive if new wall motion abnormalities (NWMA) occurred (i.e. if wall motion in any segment worsened by ≥1 grades during the test, with the exception of akinesis becoming dyskinesis). Wall motion score index (WMSI) (total score divided by the number of segments scored) was calculated at rest, low dose and during peak stress. Digital screen format was used to compare images. When there was disagreement between the two assessors, a third investigator viewed the images without the knowledge of the previous assessments, and a majority decision was reached.

Follow-up
During follow-up, the end points of the study were all-cause mortality, cardiac death and hard cardiac events [cardiac death or non-fatal myocardial infarction (MI)]. Clinical information was obtained by outpatient visits, mailed questionnaires, telephone interviews or by reviewing hospital records and the electronic patient database. Survival status was obtained by approaching the referring physician or the municipal civil registries. Cardiac death was defined as death caused by acute MI, cardiac arrhythmias or congestive heart failure (CHF). Sudden unexpected death was included as cardiac death.

Statistics
The t-test was used for continuous variable and chi-square test was used for categorical variables. Characteristics were summarized as percentages for categorical variables and as mean ± standard deviation for continuous variables. Univariate and multivariate analysis of clinical and echocardiographic variables with the end points were assessed using the Cox proportional hazards model. Clinical variables that were tested for univariate significance were sex, prior MI, prior coronary artery bypass grafting (CABG), prior percutaneous coronary intervention (PCI), CHF, typical angina, diabetes, hypertension, high cholesterol and smoking. Only clinical variables with univariate significance and representative DSE variables were considered as selection strategy for model building. Variables were selected in a stepwise forward selection manner with entry and retention set at a significance level of 0.05. The fitted model included age only for the purpose of adjustment; all other models were based on the variables selected in the stepwise algorithm, which were replaced by dichotomous versions to facilitate the ease of clinical use. The risk of a variable was expressed as a hazard ratio (HR) with a corresponding 95% confidence interval (CI). The probability of all-cause mortality, cardiac death and hard cardiac events free survival was calculated by the Kaplan–Meier method and the resulting curves were compared by the log rank test [11,12].



   Results
Top
 Abstract
 Introduction
 Subjects and methods
 Results
Discussion
 References
 
The patients’ demographics and clinical characteristics are presented in Table 1.


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  		Table 1. Study population characteristics

 
According to renal function, the total study population was divided into 729 (32%) patients with normal renal function and 1563 (68%) with renal dysfunction. This was classified as mild in 933 patients, moderate in 502 patients and severe in 128 patients. The overall prevalence of hypertension was 36% (809 patients). The respective percentages for mild, moderate and severe renal dysfunction were 33% (298 patients), 45% (223 patients) and 54% (66 patients). The prevalence of diabetes in these groups was 12, 16, and 21%, respectively.

Patient characteristics and hemodynamic response
During DSE the heart rate increased significantly from rest to peak stress. The target heart rate was reached in 91% of patients. Atropine was administered in 206 patients. The mean maximal dobutamine dose was 38 ± 8 mcg/kg/min. Side-effects included hemodynamically stable sustained ventricular tachycardia (>10 complexes) in 23 (1%) patients, non-sustained ventricular tachycardia (<10 complexes) in 115 patients (5%), atrial fibrillation in 23 patients (1%) and severe hypotension (decrease of systolic blood pressure >40 mmHg) in 23 patients (1%).

The WMSI was 1.47 ± 0.60 at rest and 1.55 ± 0.67 at peak stress. Rest WMA were observed in 1469 (64%) patients and new WMA at peak stress were present in 1546 (68%) patients (Table 2).


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  		Table 2. DSE results according to renal function

 
Long-term follow-up
During a mean long-term follow up of 8 years, 553 patients (24%) died, which included 86 (12%) patients with normal CrCl, 192 (21%) with mild renal dysfunction, 209 (42%) with moderate and 66 (52%) with severe renal dysfunction. Cardiac death occurred in 317 patients (14%); the respective numbers among the strata of CrCl was 42 for normal CrCl (6% of normal), 109 for mild renal dysfunction (12% of mild), 133 for moderate (26% of moderate) and 33 for severe renal dysfunction patients (26% of severe). One hundred (4%) patients suffered non-fatal MI. Overall, 417 (18%) patients had at least one hard cardiac event.

Predictors of all-cause mortality, cardiac death and hard cardiac events
Table 3 summarizes the hazard ratios after multivariate analysis for predictors of all-cause mortality, cardiac death and hard cardiac events either unadjusted or adjusted for age and clinical variables with univariate significance, i.e. prior MI, prior CABG, prior PCI, CHF, diabetes, hypertension, high cholesterol and smoking. Ischemia during DSE and mildly, moderately and severely abnormal CrCl were powerful independent predictors for all end points.


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  		Table 3. Multivariate analysis for the end points of all-cause mortality, cardiac death and hard cardiac events (cardiac death or non-fatal MI)a

 
The incremental values (all p < 0.001) per 30 ml/min decrease of CrCl over new WMA during DSE for the end points of all-cause mortality, cardiac death and hard cardiac events and the respective improvements in global {chi}2 are shown in Figure 1.


Figure 1
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  		Fig. 1. Incremental value of a 30 ml/min decrease of CrCl over NWMA during DSE for the end points of all-cause mortality, cardiac death and hard cardiac events (cardiac death + MI).

 
Kaplan–Meier curves for the end point of all-cause mortality in patients with normal DSE, rest WMA, new WMA and more than four abnormal segments during DSE among the entire strata of renal function are shown in Figure 2 (all p < 0.001).


Figure 2
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  		Fig. 2. Kaplan–Meier curves for all-cause mortality in patients with normal DSE, rest WMA, NWMA and more than four abnormal segments in DSE and according to renal function, for a period of 8 years.

 
Figure 3 demonstrates the Kaplan–Meier curves for cardiac death and hard cardiac events in patients with normal DSE among the entire strata of renal function (p < 0.001 for moderate renal dysfunction). Patients with normal DSE and mainly moderate renal dysfunction have greater probability for both cardiac death and hard cardiac events compared to those with normal renal function.


Figure 3
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  		Fig. 3. Kaplan–Meier curves for cardiac death and hard cardiac events in patients with normal DSE and according to renal function, for a period of 8 years. Patients with normal DSE and renal dysfunction have greater probability for both cardiac death and hard cardiac events compared to those with normal renal function. The warranty of a normal DSE in the presence of moderate renal dysfunction was 15 and 36 months for 10 and 20% risk, respectively.

 
Kaplan–Meier curves for cardiac death and hard cardiac events in patients with new WMA and more than four abnormal segments during DSE among the entire strata of renal function are demonstrated in Figure 4 (all p < 0.001).


Figure 4
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  		Fig. 4. Kaplan–Meier curves for cardiac death and hard cardiac events in patients with NWMA and more than four abnormal segments in DSE and according to renal function, for a period of 8 years.

 


   Discussion
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
References
 
This study showed the predictive value of renal function relative to DSE findings during a long-term mean follow-up of 8 years. Ischemia during DSE was an independent predictor of mortality and hard cardiac events among the entire strata of renal function (Table 2). The global {chi}2 increased significantly when CrCl was added to the model (Figure 1). The degree of renal dysfunction was an additional determinant of survival and hard events among patients with normal as well as those with abnormal DSE (Figures 2–4). Based on survival curves, we suggest that patients with moderate renal dysfunction and normal DSE at baseline represent the highest risk group and should repeat the DSE every 15 and 36 months. This suggestion derives from the Kaplan–Meier curve (Figure 3) showing that 10% of patients with moderate renal dysfunction in 15 months and 20% of these patients in 36 months do have a cardiac event, i.e. cardiac death alone or hard cardiac event.

However, regarding all-cause mortality patients with both moderate and severe renal dysfunction and normal DSE represent similar high-risk groups (Figure 2).

Comparison to previous studies
The American Society of Transplantation has reported guidelines for the pre-transplant evaluation of patients with severe renal dysfunction [13]. They included the use of non-invasive cardiac stress testing; however, it remained unclear which test to use due to the lack of firm support for a single test. Some studies have suggested that DSE is superior to exercise ECG for diagnosis of CAD in patients with renal dysfunction [14] and also has prognostic value in this setting [14]. The theoretical advantages of DSE in renal dysfunction include maintained sensitivity and specificity in hypertension [18] and bundle branch block [19].

It is known that early renal failure is associated with changes in traditional and non-traditional cardiovascular risk factors [2]. The avoidance of coronary angiography and potentially nephrotoxic contrast material is also critical in these patients. Therefore, given its safety and low cost, DSE could be used as a screening tool in detecting occult CAD before the development of MI or sudden cardiac death in patients with renal dysfunction [20].

A previous study has shown that the accuracy for detecting CAD and the prognostic implications of positive results of DSE in patients with renal dysfunction appear similar to the general population [Table 2, Figure 1).

Although the prognosis of patients with renal dysfunction and normal DSE was better than for patients with new WMA, the event rate remained substantial for all end points. This could be explained by the high-risk profile of our population and by the known high prevalence of cardiac events in patients with renal failure even in the absence of CAD at baseline because uremia itself provides an atherogenic milieu [17].

In two of the largest prognostic series, the prognostic value of a normal DSE in renal dysfunction appears to be limited to about 2 years [4,21]. We have shown in an even larger study population with a longer follow-up period that the predictive value of a normal DSE in the presence of moderate renal dysfunction is limited to 15 and 36 months for 10 and 20% risk for cardiac event respectively.

In conclusion, we found that renal dysfunction has additional independent prognostic value over DSE findings, irrespective of the presence and severity of WMA. The low-risk period after a normal DSE is determined by the presence of moderate mainly renal dysfunction.



   Acknowledgments
 
Conflict of interest statement. None declared.



   References
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 

  1. Sarnak MJ, Levey AS, Schoolwerth AC, et al. A statement from American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention. Kidney disease as a risk factor for development of cardiovascular disease. Circulation (2003) 108:2154–2169.[Free Full Text]
  2. Hostetter TH. Chronic kidney disease predicts cardiovascular disease. N Engl J Med (2004) 351:1344–1346.[Free Full Text]
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  8. Levey AS, Coresh J, Balk E, Kausz AT, Levin A, Steffes MW, Hogg RJ, Perrone RD, Lau J, Eknoyan G. National Kidney Foundation Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification. Ann Intern Med (2003) 139:137–147.[Abstract/Free Full Text]
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  10. Arnese M, Cornel JH, Salustri A, et al. Prediction of improvement of regionalleft ventricular function after surgical revascularization: a comparison of low dose dobutamine echocardiography with 201Tl single-photon emission computed tomography. Circulation (1995) 91:2748–2752.[Abstract/Free Full Text]
  11. Fleiss JL. Statistical Methods for Rates and Proportions. (1981) 2nd edn. New York: Wiley.
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  14. Sharma R, Pellerin D, Gaze DC, et al. Dobutamine stress echocardiography and the resting but not exercise electrocardiograph predict severe coronary artery disease in renal transplant candidates. Nephrol Dial Transplant (2005) 20:2207–2214.[Abstract/Free Full Text]
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  17. Rakhit DJ, Armstrong KA, Beller E, et al. Risk stratification of patients with chronic kidney disease: results of screening strategies incorporating clinical risk scoring and dobutamine stress echocardiography. Am Heart J (2006) 152:363–370.[CrossRef][Web of Science][Medline]
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Received for publication: 20.12.06
Accepted in revised form: 22. 8.07


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