Comment on “Incidence of Myocardial Infarction After High-Risk Vascular Operations in Adults” by Yen-Yi Juo et al. JAMA Surg. 2017

Question raised by the paper – MI incidence in high risk vascular surgery didn’t decrease despite advanced cardiac care pre-op (2.7% 30 day MI in 2009; 3.1% in 2014).
My comment on this paper – This study only analyzed high risk procedure includes open AAA and infrainguinal bypass. Endovascular intervention was not included so SHOULD NOT BE MENTIONED ANYWHERE IN THE ARTICLE.
This study has poor generalizability. It is retrospective study on a very unspecific database. NSQIP database lacks specifics on location of cross-clamping in aortic cases and detailed perioperative medical management. Study population is predominantly white, and criteria for MI was not specified and only included up to 30 days.
With the advancement of endovascular intervention, more AAA and TAAA are treated with simple or complex EVAR (branched or fenestrated). The more emergency procedure in open AAA cohort reflects the makeup of open procedure for AAAs, as more and more elective cases of AAA are done endovascular. Open aortic procedure are also becoming increasingly complex, as the simple AAAs with adequate infrarenal aneurysm neck size, length, morphology are treated predominantly by EVAR. The leftover ones with aneurysm neck angulation and large diameter, juxtarenal/pararenal AAA, etc comprise the open AAA intervention. Thus, one can extrapolate that the open AAA procedures are becoming higher risk with expected poorer outcomes. It is no surprise that there is significantly higher actual incidence of post-op MI in open AAA repair [3.0%] vs [1.9%] in infrainguinal bypass, which is more of an elective procedure with subacute patient presentation. Therefore, pre-op cardiac workup and optimization are paramount. However, one cannot associate endovascular intervention with poorer outcome. EVAR, if anything, has made repair of AAA and TAAA into a low risk procedure, without the need for general anesthesia or cross clamp, and made even the rupture of AAA a controllable incident. It has made the cases of AAA/TAAA that require open approach more morbid procedure, but broad perspective that include all AAA/TAAA treated open and endovascularly would likely reflect an improvement in long term outcome of these patients.

Back to Basics

Happy 2018 everybody! Hope not many of your flights are getting delayed too much.

Also, you are not going to believe what I am going to blog about this time. I have just completed a rotation in neurology. If you follow this blog, you know that I am pretty gung-ho about vascular surgery. I guess I tend to find inspirations at unexpected places.

I wasn’t used to it at first. Coming in at 7am, pre-rounding on patients for 3+ hours, table rounding with attending for another 1-2 hours, and finally formally rounding on patients who are now taking afternoon naps. This schedule is different from surgery, to say the least. The amount of sitting probably gave me a badonkadonk.

However, nothing is all bad. Neurology rotation was 3-4 weeks of getting back to basic science and pathophysiology. I spent tremendous amount of time looking at new concepts and relearning old ones (pathogenesis of thrombus formation, atherosclerosis, embolism, etc).

Why is it easier to perform endarterectomy on arterial lesion caused by thrombosis versus Takayasu’s (the latter is associated with transmural inflammation so hard to find a plane)?  Why does intracranial vasospasm primarily give posterior headache (Posterior circulation has more sympathetic input)? How come temporal arteritis rarely affect intracranial vessels ( they have extremely thin walls with much less elastic fibers in the media and adventitia and absent vasa vasorum compared to their extracranial counter parts)? Those are few out of the many new basic science concepts I was able to learn and make clinically relevant during my time on neurology. Not only did I gain new knowledge, rotating in a medical subspecially like neurology taught me to always keep an eye out on the basic pathogenesis of every clinical disease. Indeed, medicine helps surgeon (or in my case, surgeon-in-training) quite a bit; much more than I thought.

I was once told by a mentor that to be a good surgeon, you need to know 2 things – pathophysiology and anatomy. It’s nice to brush up on the pathophys, an area that is easily forgotten if you spend a tad too long wandering in the other territories of medicine.