An otherwise healthy 50-year-old woman presented to the emergency department of a satellite hospital complaining of worsening indigestion, nausea, and diaphoresis. A 12-lead electrocardiogram (EKG) showed ST-elevation in the anteroseptal leads. The patient was given full-strength aspirin, ticagrelor 180 mg, and a heparin bolus, then transferred to the main campus for primary percutaneous coronary intervention (PCI). Angiography revealed a 100% stenosis of the ostial proximal left anterior descending (LAD) coronary artery. The pre-intervention Thrombolysis in Myocardial Infarction (TIMI) flow was 0. PCI was performed within the ostial proximal, and mid to distal LAD coronary artery. Angiography showed a large thrombus burden; the vessel was initially predilated with a 2.0 mm x 15 mm over-the-wire (OTW) balloon.
There was no-reflow despite multiple intracoronary adenosine injections. The vessel was predilated using a 3.0 mm x 15 mm non-compliant balloon at 8 atmospheres (atm). With recalcitrant no-reflow, the OTW balloon was advanced into the distal LAD and multiple injections of 300-500 mcg intracoronary adenosine were administered with transient improvement/reconstitution in distal flow. A 3.5 mm x 38 mm zotarolimus-eluting stent was positioned in the ostial proximal LAD coronary artery, and deployed at 11 atm. Angiogram showed recalcitrant no-reflow. Multiple attempts with the 2.0 mm OTW predilation balloon were made (in the mid to distal LAD coronary artery). The OTW balloon was exchanged for a Finecross microcatheter (Terumo) over the exchange-length (300 cm) Prowater wire (Abbott Vascular), and additional intracoronary adenosine (500 mcg) injections were administered in the distal LAD coronary artery. A second 2.75 mm x 38 mm zotarolimus-eluting stent was deployed at 12 atm (overlapping with the proximal stent). This was followed by deployment of a third overlapping 2.5 mm x 12 mm zotarolimus-eluting stent at 12 atm. The stents were postdilated using a 3.5 mm x 20 mm non-compliant balloon at 20 atm. Additional (distal) postdilation was performed using a 3.0 mm x 20 mm non-compliant balloon at 24 atm. The stenosis was successfully reduced from 100% to 0%. During the procedure and while preparing to insert and institute mechanical circulatory support with the Impella CP device (Abiomed), the patient went into pulmonary edema requiring endotracheal intubation and mechanical ventilation. The Impella CP device was successfully inserted and secured in place. A final angiogram showed no residual stenosis or angiographically apparent dissection with TIMI-3 flow.
Disclosure: Dr. Ankur Kalra reports no conflicts of interest regarding the content herein.
Dr. Ankur Kalra can be contacted at firstname.lastname@example.org
BEHIND THE SCENES
Talking with Case Operator Dr. Ankur Kalra
Can you provide more background on this patient and how she came to you?
This patient was young, healthy, with no prior past medical history. For her, this was the presenting manifestation of coronary disease. She was transferred (as a STEMI) from one of our satellite emergency departments that is about an hour away. She started having symptoms — this was a Sunday afternoon case — the night before. She started to feel really unwell, nauseous and diaphoretic, before she showed up in the emergency department early Sunday morning. Symptom onset probably occurred the day before and she was still having symptoms. This was a late presentation of STEMI, which is probably why the LAD was totally occluded and extremely thrombotic.
Her symptoms seem to match symptoms often uniquely experienced by women.
Yes, Levine’s sign and other symptoms usually described in older textbooks were derived from how men described their heart attacks. We (as a community) were naïve to extrapolate all those findings to women until some pioneering work by Dr. Bairey Merz from Cedars-Sinai and the WISE study shed light on the fact that women’s presenting symptoms (when they are having an acute coronary syndrome) are different than the typical symptoms experienced by men.
Can you walk us through the case?
I could easily wire the lesion. Her lesion was at the ostium of the left anterior descending coronary artery, right where it originates from the left main coronary artery. What was surprising was that even after several attempts at balloon dilatation, there was absolutely no flow. No-reflow occurs in about 2% of cases, and is suggestive that this was a late presentation, because the acute thrombus had time to organize and the entire vessel became thrombotic. Routine aspiration thrombectomy is not indicated in STEMI any longer, following two large randomized, controlled trials, TASTE and TOTAL. However, this was not a routine case and we did try to aspirate thrombus. We did about four rounds of aspiration with an aspiration catheter. Even after having aspirated some of the thrombus, however, we were not able to establish flow. We went in with an over-the-wire balloon, exchanged it with a microcatheter that was distal in the coronary, and started giving industrial doses of adenosine to improve microvascular flow. The microcatheter allowed us to inject dye and see the vessel was healthy distally, but the dye was hanging in the vessel, so we knew the microvascular flow was very poor. At that point, we had to make a decision whether to leave this alone or keep working. The patient started to become sicker on the table. She was agitated, short of breath, and her oxygen saturation and blood pressure were dropping. Her end diastolic pressure was high. We had to emergently call anesthesia and intubate her, and initiate mechanical circulatory support. In the midst of all this, we wanted to make sure we were not losing wire position in the LAD, because that would be a disaster. To pharmacologically manage this lesion, we had given industrial doses of adenosine. Our activated clotting time on heparin was also therapeutic; it was over 300 seconds. We bolused and then started an infusion of eptifibatide, a glycoprotein IIb/IIIa antagonist that is not routinely used in STEMIs, but in this case, we did so, because of the significant thrombotic burden. Despite all the pharmacology on board, there was still no flow. At this point, starting from the ostium of the LAD, all the way down the entire length of the vessel, we deployed three stents. Even after creating a channel with the first stent, there was still no flow. We stented distal to the first stent, and then stented again, distal to the second stent, ending up with three overlapping stents across the length of the LAD. Multiple post dilations were done with non-compliant balloons to make sure these stents were well apposed. We finished the case with TIMI-3 flow. The entire duration of the case took almost 6 hours and we were not able to establish flow until the very last stent. Our team was comprised of a technologist, a nurse, a fellow and myself, trying to do as much as we could to get this patient home. One could hear a sigh of relief in the room when everyone saw TIMI-3 flow at the end.
No-reflow can be a huge challenge.
The general idea is to improve flow by improving microvascular function. Usually this is attempted by administering industrial doses of adenosine, nitroprusside, or a calcium channel blocker. IIb/IIIa antagonists are administered, the activated clotting time is kept therapeutic, and aspiration thrombectomy is performed to get rid of as much thrombotic burden as possible. It challenges patience and nerves, and there were many occasions I asked myself, “How far am I going to go, and when am I going to stop?” We kept going. We saw the vessel had flow distally by injecting contrast through the microcatheter. We wanted to avoid a full metal jacket, i.e., stenting starting from the beginning of the vessel all the way to the end, but I think that is what was required in this case. The patient went to the ICU, intubated and with the Impella left ventricular assist device, which was in place for 24 hours. The entire anterior wall was not moving on echocardiogram the following day. It was surprising that she came to the lab hemodynamically stable, probably because she had a huge right coronary artery. I think she survived because there was flow in the right coronary and that vessel was not diseased. Even the left circumflex was not diseased. She had severe single-vessel disease.
[At the time of this interview] this patient has been in the hospital for a few weeks, but her hospital course was complicated by hospital-acquired pneumonia and cardiac conduction disease. She had intermittent heart block that may require a pacemaker. But she is stable, on oral medications, and is asymptomatic.
Can you address how radiation safety was handled in this long case?
We practice radiation safety mechanisms in the lab and we want to do cases which are radiation compliant. Radiation safety is always on our minds. We were beyond the threshold dose. Such cases are fortunately few and far between. In the latter half of the case, we did go down to 7 and a half frames per second from 15 frames per second. Typically, I use a lot of “fluoro save;” I don’t cine unless I need it, because that is 10x the radiation. We were cautious with the table height, and the proximity of the flat-panel detector to the patient, and also in making sure that we were collimating.
Any final thoughts?
University Hospitals (UH) does an incredible job in taking care of a very sick patient population. Many patients unfortunately have had a tough life and are sick. They need to be taken care of. I have been working at UH only a few months, but have found it to be very fulfilling, because cases are very challenging.
Obviously, this case teaches you many things. It humbles you, challenges you, and makes you grow. I am glad for this patient that we could get her home, because that is what really matters: how the patient does at the end.