Chronic kidney disease (CKD) is endemic in our population, as is cardiovascular disease. Both carry large risks of major morbidity and mortality. The interaction of these two conditions is complex and the addition of CKD to cardiovascular disease worsens the long term prognosis in the latter.1Chronic kidney disease (CKD) is endemic in our population, as is cardiovascular disease. Both carry large risks of major morbidity and mortality. The interaction of these two conditions is complex and the addition of CKD to cardiovascular disease worsens the long term prognosis in the latter.1
Percutaneous intervention in CKD patients is feasible and relatively easily accomplished from a technical point of view. Early reports suggested an increased risk of restenosis in CKD patients after simple balloon angioplasty. However, in the bare metal stent era, target lesion revascularization (TLR) rates were generally not increased in patients with renal insufficiency. Additionally and importantly, percutaneous revascularization did not ameliorate the increased morbidity and mortality associated with CKD and certain procedural complications were actually increased in these patients, e.g., access site complications, major bleeding and contrast nehropathy. The take home message: the presence of CKD probably is a marker of a high risk subset of cardiac patients. To practicing interventional cardiologists, I doubt this comes as any real surprise!
The introduction of drug-eluting stents (DES) to the arsenal of the interventional cardiologist has resulted in dramatic reduction in TLR in large randomized trials. Based on these pivotal studies and clinical experience, the spectrum of patients undergoing implantation of DES has widened to include many who may not have been candidates for PCI in the “bare-metal era.” Early enthusiasm was somewhat tempered by reports of late stent thrombosis with DES. However, in certain patient and lesion subsets, it seems clear that the benefit of DES implantation in reducing restenosis far outweighs the small but significant risk of late stent thrombosis.
Where does the DES risk/benefit ratio fall in the group of patients with CKD? Do they enjoy the same dramatic antirestenotic benefits as the more general population? Are they at increased risk of adverse outcomes such as late thrombosis or more aggressive restenosis? Will there be an improvement in overall outcome or a worsening? Since there are no specific studies addressing these issues, what information is available?
In the current report, Mishkel et al,2 via a retrospective analysis, confirmed earlier observations by the Taxus IV investigators3 that patients with CKD enjoy the same decrease in TLR as patients with normal renal function at the expense of a modest increase in peri-procedural complications. The benefit was evident for both sirolimus and paclitaxel eluting stents. Although the group of patients with severe renal insufficiency (with or without concomitant dialysis) was small compared with the total patient cohort (88 out of a group of 2,758 total patients), there was no excess of stent thrombosis. This is in contrast to several recent reports suggesting that renal insufficiency per se is a risk factor for stent thrombosis with DES.4,5 One potentially intriguing observation, seen in the current study as well as the Taxus IV paper was that TLR rates actually declined as the degree of renal insufficiency worsened. This may be an artifact of the small patient populations or related to some unknown palliative effect of reduced renal function on DES restenosis. My inclination would be to favor the former as opposed to the latter.
However, as in the bare metal stent era, overall MACE and mortality was adversely affected by the presence of renal insufficiency. These patients do not do as well long term, probably not on the basis of increased restenosis or stent thrombosis, but due to the additive deleterious effects of concomitant kidney and heart disease. Thus, I would not let the presence or absence of CKD strongly influence my stent choice as long as other things (e.g., patient compliance, bleeding risk, lesion type, etc.) are relatively stable.
The bottom line: The presence of CKD identifies a high risk subset of cardiac patients!! From purely the point of view of reducing TLR, the use of DES in CKD patients at high risk for restenosis with bare metal stents appears warranted and justified.
The answer to reducing the increased risk on prognosis that CKD plays will be a lot more complex than a simple stent choice.
1. Gupta R,Birnbaum Y, Uretsky B. The renal patient with coronary artery disease. J Am Coll Cardiol 2004; 44:1343-1353.
2. Mishkel GJ, Varghese JJ, Moore AL, et al. Short- and long-term clinical outcomes of coronary drug-eluting stent recipients presenting with chronic renal disease. J Invasive Cardiol 2007;19:331–337.
3. Halkin A, Mehran R, Casey C, et al. Impact of moderate renal insufficiency on restenosis and adverse clinical events after paclitaxel- eluting and bare metal stent implantation: Results from the Taxus IV Trial. Am Heart J 2005;150 (6):1163–1170.
4. Iakovou I, Schmidt T, Bonizzoni E, et al. Incidence, predictors and outcome of thrombosis after successful implantation of drug-eluting stents. JAMA 2005;293:2126–2130.
5. Kuchulakanti P, Chu W, Torguson R, et al. Correlates and long term outcomes of angiographically proven stent thrombosis with sirolimus- and paclitaxel-eluting stents. Circulation 2006: 113:1108–1113.