Recent advances in the way we transmit important clinical educational materials now include email, “cloud” internet data repositories, iPhone and iPad instant access, and similar internet applications. Over the last 2 years, I and my colleagues have formed an interested and active group of cardiac cath lab experts to whom several critical questions are posed, circulated for discussion, and feedback provided to one another via a “list serve” internet email. Dr. David Holmes, current ACC President, recently described these new methods and cited our list serve in his President’s Page, entitled, “Clouds, Science, and Education.”1
One of our recent email ‘conversations’ was extremely interesting and as an example of the power of this tool, I thought I would share it with the CLD readership. Please note that the order in which the comments came back to me as the ‘clearing house’ to assemble this conversation may not be completely correct, but I’m sure you can follow the train of thought.
I just finished a case. I would like the group’s input on a woman with acute chest pain who came to us from an outside hospital in Bozeman, MT, after I was asked to help in the decision-making. ECG had ST elevation in 2, 3, f and V3-6. She is a smoker with positive family history but no other CAD risk factors. Hemodynamics were stable with 3/10 chest pain. Cines [Figures 1-3] show a filling defect in the LMCA [left main coronary artery] with distal occlusion of the LAD [left anterior descending coronary artery]. A TTE [transthoracic echocardiogram] with bubble study was negative with only an apical wall motion abnormality. What are the group’s thoughts on management?
Larry S. Dean, MD
Professor of Medicine and Surgery
Director, UW Medicine Regional Heart Center
From Long Beach, CA:
My view — It’s odd to have inferior lateral STEs [ST-elevations] especially with a normal RCA [right coronary artery] (I confess now I didn’t initially see the LAD cut-off). A mobile filling defect in the LM without evidence of atherosclerotic or other vascular disease suggests thrombus, but from what source? Could this be multiple vessel spasm, first RCA, then LM with clot forming in LM asymptomatic? Check for other regions where clot might go. Check for PFO [patent foramen ovale] and hematologic procoagulant state. Vasculitis is low on my list.
Finally, treatment: I’d start heparin and an anti-spasm regimen, clopidogrel maybe, but likely ASA [aspirin]. Repeat angiogram in week to 10 days for resolution of LM thrombus, but I’m not sure what to do if still there. Great case. Let us have follow up.
From Jacksonville, Florida:
The amputated wraparound LAD might explain the EKG. I would run a drug screen.
From Worchester, MA:
Definitely looks like clot in the LM. I agree that this is most likely embolic (unless you think it came from the catheter) and EKG changes may be from other, more distal emboli that had resolved by the time of the angiogram. Questions of hormone therapy and menstrual cycle timing need to be considered, particularly in a smoker. I rather doubt spasm, but think this is more about clotting. It will be difficult acutely to know the best anticoagulant strategy unless a clear source is identified. Although it will be hard to avoid warfarin, I think. Despite her age, you have to look for a neoplastic process.
Bonnie H. Weiner
From St. Louis, MO:
After a period of time with IIb/IIIa blockers and heparin, repeat angiogram should be done. If [thrombus] still there, IVUS [intravascular ultrasound], definitely! IVUS or instrumentation at this time risks further embolization and myocardial damage, so I wouldn’t do it now. I have seen a similar looking thing in a mid LAD and it turned out to be a calcified, eccentric plaque.
Michael J. Lim, MD, FACC, FSCAI
Director, Division of Cardiology
and J. Gerard Mudd
Cardiac Cath Lab
Saint Louis University
From Worchester, MA:
It sounds like we are fairly split on embolus vs thrombus. Would IVUS help? If there is no plaque disruption, embolus is more likely and it would change therapy and strategy significantly.
Bonnie H. Weiner
From Chicago, IL:
This is probably an ulcerated plaque with adherent thrombus. Part of the thrombus has embolized to the LAD. I would advise IIb/IIIa for 48 hours and anticoagulation, then CABG [coronary artery bypass graft surgery].
Lloyd W. Klein, MD, FACC, FSCAI
Professor of Medicine
Rush Medical College
From New Orleans, LA:
Great case! The LM lesion isn’t an embolus, because it wouldn’t be adherent to the wall in a sessile and pedunculated manner like it is. Part of it definitely embolized to the distal LAD, causing the occlusion and STEMI [ST-elevation myocardial infarction]. Asking how to treat it begs the question of what it is. Coronary CTA [computed tomography angiography] might help. If it’s thrombus, then we all know how to treat it, but might differ as to whether to use catheters and filters, or IV therapy. If it’s NOT thrombus, I would take it out. It’s a life-threatening lesion and I don’t think a sternotomy is too drastic for diagnosis and treatment.
From Durham, NC:
In my view, this is unlikely to be embolic — filling defect would not have stopped where it did given the relationship of the size of the filling defect to the diameter of the LM (i.e., filling defect is smaller than the caliber of the LM). So this suggests adherent thrombus to a small, spontaneous coronary dissection or an erosion (much less likely to be an atherosclerotic ruptured plaque). Then the lesion in the distal LAD is due to embolization of material from the original thrombus in the LM. EKG is consistent with an apical LAD infarct. Acutely, I would have put the patient on a GP IIb/IIIa antagonist plus heparin for 48 hours or so, while starting clopidogrel and aspirin. I would have likely done an intracoronary injection via the guide catheter. Also, I would have been quite reticent to put a wire past the LM filling defect to try to open the LAD — additional embolization (or worse) will be detrimental. As to longer term, conservative medical management (i.e., post-MI rx) seems appropriate. I would keep on clopidogrel for some period of time, aspirin forever. Agree with need for drug screen. I would also screen for common hypercoagulable states. Interesting case!
From Los Angeles, CA:
The angiograms did not open, but from the description, I have the following thoughts: Does she have migraines? If so, does she take triptans? Coronary artery spasm is seen in both [conditions]. PFO is not ruled out by TTE. She needs a TCD [transcranial Doppler]. Are cocaine or marijuana involved? We have a case report of marijuana with anterior MI and low platelet count. What is her platelet count? An IVUS would identify atheroma in a smoker.
From Richmond, VA:
I think patient showered emboli thru a probable PFO. My recommendation would be to heparinize +/- IIb/ IIIa and bring back to lab in 3 days. Patient needs evaluation for PFO. I would not try to suck clot out, as it might embolize.
George W. Vetrovec, MD
Medical College of Virginia Campus
Virginia Commonwealth University
From Los Angeles, CA:
Plaque erosion in LM is likely, as she is a smoker. EKG is consistent with a wraparound LAD.
For management: “marinate” the thrombus with heparin and eptifibatide for 48 hours and then re-image. I had a case of massive thrombus in an SVG [saphenous vein graft] during my fellowship at the MGH [Massachusetts General Hospital] in which we marinated the thrombus and when we took another look 2 days later, the clot had completely resolved.
William M. Suh, MD
David Geffen School of Medicine at UCLA
From Ocala, FL:
It looks like thrombus, especially since the distal LAD is cut off (accounting for the ECG changes from apical injury or infarction). The etiology is likely embolic in the setting of otherwise normal-looking coronary arteries. I would recommend discontinuation of all hormonal therapy and smoking, start a workup for hypercoagulable state, fully anticoagulate for 7 days (with DAPT [dual antiplatelet therapy]), and repeat coronary angiography at that time. If no correctable unifying diagnosis is identified, I would recommend therapy indefinitely with warfarin and low-dose aspirin.
From New York City, NY:
I think it’s most likely an in situ thrombus due either to plaque erosion or possibly a focal spontaneous dissection. She may have an underlying vasculopathy. Assuming she’s not menstruating, I would treat with DAPT + eptifibatide for 4-5 days, then re-angiogram. At some point, IVUS will be critical. Perform a hypercoagulability and connective tissue disease work up, stop smoking and hormones, look for PFO, etc.
Gregg W. Stone MD
New York, NY
From New York City [Upper East Side]:
Last one in has advantage of everybody else’s opinion. I think she has CAD [coronary artery disease]. It looks like her PDA [posterior descending artery] has mild disease in the proximal 1/2 and the OMs [obtuse marginal] don’t taper normally. It could easily have been a low-grade but angry plaque in the LM with associated thrombus, some of which went to the distal LAD. Unlikely to be embolus as it wouldn’t have stopped in the mid-LM; it would have lodged in at the bifurcation. However, excluding PFO is reasonable to do. Likewise, a hematologic screen is a good idea, but I’m betting it’s normal, especially if she’s on oral contraceptives.
I would: (1) use heparin or bivalirudin + GPI [glycoprotein IIb/ IIIa inhibition] for 48 hours, then restudy with IVUS if clot is resolved. If not, repeat anticoagulant treatment another 48 hrs, then get IVUS. If the filling abnormality persists or you find a very nasty lesion there, wouldn’t hesitate to TCAB [thoracic coronary artery bypass] a LIMA [left internal mammary artery] to LAD. Suspect she’ll have mild LM lesion under the clot that could be safely managed with anti-platelet therapy. She goes home on ASA, prasugrel, ARB [angiotensin receptor blocker], BB [beta blocker], and varenicline (Chantix). Stop oral contraceptives meds if being used.
Kirk N. Garratt MSc MD
Lenox Hill Hospital
What Happens Now?
In summary, it is evident that there is no single answer from the acute clinical question, but the value of considering these many views leads the readers down a thoughtful and carefully examined course of management and future treatment. Since there remain several unknowns, we cannot say with certainty what the right answer is at this time, but I hope the value of this conversation and its contents from the many experts will help address this and other clinical conundrums in the future in your lab.
PS: Here’s the follow-up from Dr. Dean:
I really appreciate everyone’s input on the case. I elected to stop after the diagnostic procedure, so no aspiration, IVUS, etc. She was placed on IV heparin with abciximab for 12 hours, ASA and clopidogrel. The CK peaked at 1199, MB 207, troponin 9.53. EF [ejection fraction] was 65% with apical severe hypokinesis. She returned to the lab 4 days later [Figures 4-5]. At this point, the plan is to treat her with dual antiplatelet therapy plus warfarin for 4 weeks and then re-image. I suspect there will be complete resolution. Her coagulation evaluation is still pending, but she was not on any drugs that would increase her risk of thrombosis. I think this is a textbook case of plaque erosion. I may do an IVUS on restudy just to see how much plaque she has.
(By the way, this is the second case like this I have had in the past 6 weeks. The other case was in the LAD with a large clot burden, and we did AngioJet and stented her. IVUS after thrombectomy had minimal plaque.)
I’m sure we all learned something. Thanks!
- Holmes, Jr., D. President’s Page: Clouds, Science, and Education. J Am Coll Cardiol 2011; 57:2376–2378, doi:10.1016/j.jacc.2011.05.003
Disclosure: Dr. Kern reports that he is a speaker for Volcano Therapeutics and St. Jude Medical, and is a consultant for Merit Medical and InfraReDx, Inc.