April 21st, 2011
Will a STICH in Time Save Nine?
Anju Nohria, MD and James Fang, MD
A 57-year-old man with a history of hypertension, hyperlipidemia, and smoking presented with increasing dyspnea on exertion, mild chest discomfort, and lower-extremity edema. Physical exam results were consistent with decompensated heart failure.
Echocardiographic findings:
- left-ventricular ejection fraction (LVEF), 20%
- LV end-diastolic dimension, 6.3 cm
- global hypokinesis (with regional variation affecting the septum, inferior wall, and apex most severely)
- mildly enlarged right ventricle with moderately reduced function
- mitral annular dilatation with at least moderate mitral regurgitation
- moderate tricuspid regurgitation (estimated pulmonary-artery systolic pressure, 30 mm Hg + right-atrial pressure)
An evaluation for the cause of new-onset cardiomyopathy included a left-heart catheterization that revealed 60% left-main disease and an 80% proximal right coronary artery lesion.
Subsequent myocardial perfusion imaging (with Regadenoson positron-emission tomography) revealed a medium-size perfusion defect throughout the inferior and basal inferoseptal walls with moderate reversibility and a small reversible perfusion defect in the LV apex. The patient’s summed stress score (scar + ischemia) was 11; the summed difference score (ischemia) was 4. His resting LVEF was 16%, with an end-systolic volume index of 96 mL/m2. His post-stress LVEF was 18%, with an end-systolic volume index of 100 mL/m2.
The patient was treated with intravenous diuretics and was started on aspirin and a statin. Once he was euvolemic, a low-dose ACE inhibitor and beta-blockers were added. Amiodarone was started after monitoring revealed several runs of nonsustained ventricular tachycardia.
A right-heart catheterization after medical optimization revealed right-atrial pressure of 4 mm Hg, pulmonary-artery pressure of 41/19 mm Hg, and pulmonary capillary wedge pressure of 13 mm Hg. Pulmonary-artery saturation was 66%, with a calculated cardiac output of 3.1 L/minute and a cardiac index of 1.65 L/minute/m2.
Questions:
1. Would coronary revascularization benefit this patient? If so, would you recommend that he undergo surgical revascularization specifically?
2. Do findings from the recently published STICH trial influence your assessment? If so, how?
3. If you proceed with surgery, should it be performed at a ventricular assist device/transplant center?
Response
James Fang, MD
This gentleman has received appropriate care up to this point. I would have taken the same approach. If he remains symptomatic (particularly with angina), revascularization can be offered. In some centers, multivessel/left main PCI could even be entertained. It should be pointed out that this patient would not have been eligible for STICH because of the left main disease. However, the overall approach remains consistent with the STICH trial in that patients crossed over from medicine to surgery if it was felt to be clinically necessary. I generally favor the performance of high risk procedures or surgeries in places where advanced support can be offered.
One final comment: the hemodynamics are a bit curious. The calculated cardiac output is relatively low for that pulmonary artery saturation suggesting that either the hgb concentration was very high or the oxygen consumption used in the calculation may not have been accurate.
Follow-Up
Anju Nohria, MD
The patient was thought to have a combined ischemic and nonischemic cardiomyopathy. Given his low ejection fraction and left-ventricular dilatation, he was considered to be a high-risk candidate for surgical revascularization without clear expectation of benefit. Therefore, he was medically managed and evaluated for cardiac transplantation.
The only notable finding on the patient’s initial evaluation for transplant was continued tobacco use, and listing for transplantation was deferred until he could demonstrate abstinence from smoking for at least 6 months. His initial peak oxygen uptake was 7.4 mL/kg/minute at an adequate work load. After close follow-up and gradual up-titration of his ACE-inhibitor and beta-blocker dosing, peak oxygen uptake had increased (9 months later) to 13 mL/kg/minute.
The patient continues to exhibit NYHA class III symptoms, and his consent for listing as a Status 2 transplantation candidate is now being sought.
7 Responses to “Will a STICH in Time Save Nine?”
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Sounds like a mixed ischemic and nonischemic cardiomyopathy. I would start with optimal medical management. Should angina increase at any time, I would pursue mechanical revascularization. A treadmill exercise stress echo would be done on escalated medical therapy. If there is any suggestion for global ischemia, such as failure of end-systolic volumes to decrease with exercise, revasularization would be suggested. (I am not certain how to interpret the LV response to regadenoson). This would likely be CABG in light of the left main and would be done at a facility where percutaneous LV support is availabe.
I suspect LV function and symptoms will dramatically improve with OMT alone. This would include spironolactone. Amiodarone would not be a long term agent for asymptomatic NSVT. Consideration of an ICD would be made after about 6 months if EF remains low.
I do not think my approach would have been different before STICH. My major concern is the physiological significance of the left main stenosis. The STICH trial does lend more confidence in this approach.
Competing interests pertaining specifically to this post, comment, or both:
None
According to the eligibility criteria, patients were “eligible for medical therapy alone if they did not have a stenotic lesion leading to a loss of 50% or more of the diameter of the left main coronary artery”. His LM stenosis being 60%, would he qualify for the medical therapy alone arm of the trial and would we be able to use the findings of STICH to embark upon medical therapy alone? Additionally, after medical optimization, this gentleman has a cardiac index that is less than <1.8 L/min per m2 (cardiogenic shock), another exclusion criteria.
He may represent the group of patients who would derive benefit from revascularization via CABG prior to consideration of other advanced HF therapies.
Competing interests pertaining specifically to this post, comment, or both:
None
Neither medical therapy alone nor CABG is a magic pill or procedure. Medical therapy is effective, but with a 40% mortality rate at 5 years, it is not a cure and requires frequent reassessment. Patients and physicians do not need to rush the decision for CABG. If after careful review, however, there is a decision to take an up-front risk, I believe there will be a modest but clinically meaningful chance of improving long-term survival.
Getting him to stop smoking would seem to me be critical here. He is a poor operative risk. Therefor medical therapy first.
Competing interests pertaining specifically to this post, comment, or both:
none
I agree with Dr Powell. This patient with mixed ischemic and nonischemic (hypertensive?) cardiomyopathy would benefit from medical optimization and assessment of the physiologic significance of his coronary disease, such as by FFR. Stich doesn’t contribute significantly to my approach to this patient, though I may have not performed a viability study. Revacularization with CABG or PCI would depend on the type of lesions (syntax score), physiologic significance, and response of treatment to medical therapy.
A caveat- FFR to assess for lesion specific ischemia in patients with regional/global cardiomyopathic dysfunction(of whatever etiology) would be of uncertain validity.
This patient has severe CHF according to the estimated EF in Echo, also has global LV dysfx , while on catheterization he does not have non reversible ischemia ( suggesting he did not have an MI ) but he has reversible ischemia in the inferior and basal inferoseptal walls and especially in the apex region.
Clinically he has signs of right heart failure ( peripheral edema )and left ( dyspnea on exertion) .
I would treat the patient paralel in some ways –
First , improve medical treatment – lower blood pressure( according to the JNC 7 ) , and optimizing CHF treatment( concerning amiodarone , I would have kept it in the begining as Amiodarone causes hemodynamic effects, as a result of its direct effect on smooth muscle and its calcium channel and alpha adrenergic blockade; it dilates coronary arteries and increases coronary blood flow. Amiodarone also causes peripheral arterial vasodilatation and decreases systemic blood pressure and afterload, go to(GESICA and CHF-STAT) .
second- I would try to revasculate with stent to LT MAIN and RCA- improving especialy the perfusion in the apex region might inprove the EF . So repeat the Echo afterwards .
Third -if afterwards , no improvement in the EF , I would have introduced ICD .