If we know that sterile technique is important to reduce infection in the cardiac electrophysiology laboratory when implanting foreign bodies like pacemakers and defibrillators, why do interventional cardiologists feel the risks of implanting foreign bodies like bare-metal or drug-eluting stents are less likely to become infected?
Now let me be clear. I have no data on this subject. Certainly when fevers develop after an angioplasty we might consider stent infection in the differential diagnosis of post-stenting fever. But could subclinical infection without fever be a cause of stent thrombosis? I know that the practice of not wearing surgical masks and hats is common in many cath labs around the country. Yesterday AM in the New York Times we saw yet another cardiologist without a hat or mask while performing an interventional cardiac procedure. Note that the technician assisting the doctor is wearing the mask and hat (and protective goggles).
But take a look at this high-speed picture of the average sneeze:
What kind of critters are spread widely in the lab setting when this occurs? Speech spreads bacteria in a similar fashion.
This is a particularly perplexing problem because localized stent infection just might (and I emphasize the word "might") be a cause of in-stent thrombosis. Since in-stent thrombosis and sudden late clotting of stents has recently come to the forefront of cardiologists' conciousness, as well as the conciousness of medical device companies like Boston Scientific, Medtronic and Cordis, why are we not having this discussion? Admittedly this conjecture is extremely difficult to prove or disprove. Stents are small and fixed into critical blood vessels supplying the heart muscle. Systemic symptoms may NOT be seen because of the tiny size of the devices. (When was the last time you had a fever when a splinter was caught in your foot?) Removing a stent for "culture" is impossible once the device is deployed in the coronary artery (short of open heart surgery and bypass). But fastidious organisms that grow slowly are well-described in the infectious disease and cardiology literature.
Before we start blaming drug-eluting stents as the problem, perhaps we ought to examine our own practices more carefully. Could we be part of the recently-discovered problem with in-stent thrombosis?
Hey, this might be a cool project....