CardioExchange Archive

A 61-year-old man presented with 6 hours of chest pain and ECG changes consistent with an acute anterior-wall myocardial infarction. His cardiac troponin I was 59 ng/mL. Urgent angiography revealed an occluded LAD and 70% proximal OM1, 70% proximal OM2, and 90% proximal RCA stenoses. He was taken to the catheterization laboratory, where an attempt to open the LAD was complicated by a dissection, resulting in TIMI grade 1 flow. A right heart catheterization revealed elevated filling pressures and a low cardiac output, requiring intraaortic balloon pump (IABP) placement and transfer to a tertiary facility. An echo at the time of transfer revealed an LVEF of 10-15% (LVEDD, 5.3 cm), with global hypokinesis and apical akinesis. A PET scan showed viable myocardium, except in the mid- to distal LAD territory. Attempts to wean the IABP resulted in hypotension and increased mitral regurgitation.

Questions: 

• Would you recommend revascularization of the OM and RCA territories or move directly to ventricular assist device support as a bridge to transplantation?
• If revascularization was the appropriate step, would you recommend percutaneous rather than surgical revascularization, given his recent AMI?
• If VAD was the appropriate decision, would you recommend a PVAD as a bridge to stability or move directly to an implantable LVAD?

Response:
James Fang, MD

High risk cardiac surgery is an increasingly common clinical dilemma in cardiovascular practice and is difficult to study since there is great heterogeneity across scenarios. Therefore, we are often left with decision making based on what we know of physiology and anecdotal clinical experience.

In this gentleman’s case, it appears that in addition to advanced coronary artery disease, dynamic mitral regurgitation is playing an important role. I suspect that his ischemic heart disease, poor ventricular function, and mechanical dyssynchrony from the infarct all contribute to his mitral regurgitation. His need for an IABP would support this line of thought. Finally, he may have significant stunning from his recent infarct and some of his ventricular function may recover spontaneously with time. With all of that in mind, here’s what I’d recommend:

I would favor surgical revascularization and mitral valve repair rather than going straight to VAD since there is likely both stunning and hibernation accounting for the severe LV dysfunction (particularly since the ventricle is not dilated).  His dependence on an IABP and previous PET scan would preclude the need to assess contractile reserve, although knowing his contractile reserve (e.g. dobutamine echo) would be ideal.  Although cardiac surgery is risky in this patient, the need for post-cardiotomy support turns out to be relatively rare unless it is a “salvage” situation.  Both the STS database and INTERMACS registry have noted these dramatic advances in cardiac surgery.

Although PCI is less “traumatic”, there are several reasons to favor CABG/MVA:  a) PCI may not adequately address the issue of dynamic mitral regurgitation, b) clopidogrel will be required for months afterward if DESs are used (complicating post operative procedures, including VAD), c) there may be benefit to placing LAD graft because of watershed myocardial territories despite the lack of PET viability in immediate LAD zone.  That being said, if the patient had multiple comorbities (i.e. advanced age, pulmonary disease, malignancy, etc) that would excessively increase their perioperative risk, then multivessel PCI would be reasonable as a palliative strategy.

PVAD may be preferable if needed at the time of CABG/MVA since it can be placed without need for cardiopulmonary bypass, thus shortening total ischemic time.  Also, since stunning may be important here, removal of a VAD is greatly simplified when a percutaneous device is used.  Finally, PVADs can be used to bridge to surgical VADs, e.g. bridge to a decision.

Follow-Up:
Anju Nohria, MD

The patient was assessed and deemed eligible for left-ventricular assist device (LVAD) therapy and cardiac transplantation. After significant discussion with the patient and his family, the patient was referred for surgical revascularization, with LVAD back-up if needed. The patient arrested upon induction of anesthesia. After 3 minutes of resuscitation, he was emergently placed on cardiopulmonary bypass. Pericardial exposure revealed 200 mL to 300 mL of fresh blood, and relief of the tamponade physiology improved the patient’s hemodynamics. He underwent repair of the left anterior descending (LAD) perforation, 4-vessel bypass with a saphenous vein graft (SVG) to the first diagonal and LAD, SVG to the obtuse marginal branch, and SVG to the posterior descending artery. He also had mitral valve replacement with a Biocor porcine valve.

Postoperatively, the patient required prolonged intra-aortic balloon pump (IABP) support and vasopressor therapy with epinephrine, milrinone, and norepinephrine. He developed coagulase-negative Staphylococcus bacteremia, which required discontinuation of the IABP and antibiotic therapy. He also developed bilateral foot gangrene, requiring bilateral amputation of metatarsals. Multiple screens for heparin-induced antibodies were negative.

The patient was discharged to a rehabilitation facility. A follow-up echo revealed global hypokinesis (EF, 20%; LVEDD, 5.4 cm) with mid-distal anterior, apical, and basal-inferior akinesis. He had a well-seated mitral prosthesis with trivial regurgitation. He is currently tolerating low-dose beta-blocker and ACE-inhibitor therapy.

Conclusion:
James Fang, MD

At first glance, the poor outcome could be viewed as an indictment of the high-risk CABG approach, as opposed to a straight-to-LVAD strategy, but I suggest that the outcome reflects the high-risk nature of any cardiac surgery in unstable heart disease. It is likely that both coronary perforation/tamponade leading to cardiac arrest and postoperative vasoplegia with its attendant morbidity would also have complicated a straight-to-VAD approach.

Bleeding complications of cardiovascular interventions and therapeutics are increasingly recognized as independent predictors of poor outcomes. Recent evidence from ACS trials suggests that bleeding complications rival the index event in morbidity and mortality. In this case, tamponade from the coronary perforation and anticoagulation transformed the operative situation from urgent to salvage, substantially increasing the magnitude of the resultant morbidity and mortality, and would have done so, regardless of procedure. Post-operative vasoplegia commonly complicates heart failure surgery and may be the consequence of prolonged low-output, inflammatory cytokines and long-acting oral vasodilators. Methylene blue has been used in these situations with variable success, and I wonder if it was used in this case.

Cardiac surgery is a high-risk endeavor when there is preoperative hemodynamic or ischemic instability and significant LV dysfunction. Some may view this case as evidence of a clinical equipoise that only a randomized trial can resolve. Although it was logistically difficult, the SHOCK trial demonstrated that such studies are feasible. Would the patient have done better with primary VAD therapy? Would you have enrolled this patient into a randomized, clinical trial of high-risk CABG versus LVAD therapy?