Discussion

Dr R. James Valentine (Dallas, Texas). The purpose of this study was to determine the incidence and natural history of incidental renal artery stenoses in the general population of elderly patients. The study methods are sound, and the excellent technical results are commendable. Vascular surgeons should take note of the criterion used to define a hemodynamically significant renal artery stenosis. A peak systolic velocity of 1.8 m/s or more was chosen after many years of laboratory and clinical investigation, and it has been validated with renal arteriography. The Wake Forest group has one of the largest experiences with renal artery disease in the United States. The fact that 99% of their scans were technically satisfactory attests to their expertise in renal artery ultrasound.

The authors did a nice job of sampling the elderly population in the initial study, and recruiting limitations are acknowledged in the manuscript. However, only 14% of the original cohort returned for the second renal artery duplex examination, which represents less than 20% of the survivors in the Cardiovascular Health Study. This brings me to my first question: what happened to the other 80%? After 8 years, important differences may have emerged between the recruited and non-recruited subjects, challenging the notion that the study subjects represent the general population.

My second question relates to the 224 subjects who died after the initial study. At this meeting 13 years ago, we reported that incidental renal artery stenoses represent a marker for coronary artery disease in vascular patients. Did the deceased subjects have a higher incidence of renal artery disease than the survivors?

The take-home message from the present data is this: if you find an incidental renal artery stenosis in an elderly patient, leave it alone. Few lesions will progress. New, hemodynamically significant lesions can be expected to develop in less than 5% of patients. However, new lesions were significantly associated with an increase in diastolic blood pressure and a decrease in renal length. This brings me to my final question: could the affected patients have been identified on the basis of worsening hypertension or rising creatinine?

Dr Jeffrey Pearce. We practice and believe the results of the study support the continued observation and not intervention for incidentally found asymptomatic renal artery lesions, particularly in those patients with normal or well-controlled blood pressure and preserved renal function.

With regard to your first question, you correctly noted that 80% of the surviving participants did not return for a second duplex. With the use of our institution’s GCRC, we attempted to contact all surviving participants. Unfortunately with closure of the CHS and lack of further annual follow-up exams, some of the contact information was inaccurate. Furthermore, many of these octogenarians are now living in nursing facilities, limiting their ability to participate in the exam.

Regarding the question on the prevalence of RVD in those surviving participants, I cannot give you a definitive answer but I might be able to shed some light on the issue. We have previously reported a twofold increase of subsequent cardiovascular events in participants with RVD, even when controlling for prevalent cardiovascular risk factors. Though the presence of RVD did not confer an overall survival disadvantage, we believe these participants are having more cardiac events. Thus, some of them may have succumbed in the study interval due to cardiac disease.

And then finally with regard to your question on patient screening for duplex examinations, we looked critically at those participants that had RVD in this cohort and none of these participants smelled of renovascular disease. None of them had severe hypertension. None of them had renal insufficiency. Therefore, none of these participants would have met our screening criteria, which is for those folks with worsening uncontrolled or severe hypertension or with progressive renal insufficiency.