FAME or COURAGE: Can we have both?

She came into the office as a 67-year-old postmenopausal female with dyslipidemia on atorvastatin (Lipitor), asking me to "check out" her heart. She takes warfarin for a deep venous thrombosis (DVT) and suspected pulmonary embolism (PE) over 10 years ago, which was unprovoked. She has about 40 pounds to lose around her middle and no definite family history of heart disease. She cannot really tell me about her exercise tolerance because she is sedentary. When she initially developed shortness of breath, for which she had an exhaustive workup including a Mayo Clinic visit, she subconsciously began to avoid doing anything that made her winded. She just assumed her "laziness" was caused by her prior "blood clot." Doing my due-diligence as a cardiovascular healthcare provider, I put her through the usual rigors of cardiovascular risk assessment:

• Resting echo: Normal LVEF and size, diastolic noncompliance, no significant valvular pathology, right ventricular systolic pressure (RVSP) 48 mm Hg.
• Calcium score: Total: 350-260 counts involving the left main coronary artery, no counts in the left anterior descending (LAD) artery, the remaining counts in the proximal circumflex and right coronary artery (RCA).
• Stress nuclear: Moderate distal lateral apical reversibility in a small segment, but only five and a half minutes of bike protocol testing was completed.
• * Lipids: Fairly well-controlled for the average American on Lipitor but with an LDL of 90.
• Postprandial blood sugar at two hours with 75-g Glucola: 170.

We had a couple of discussions by phone and a couple of office visits. We discussed the periprocedural awkwardness of stopping and starting warfarin and the option of a radial-artery approach in order to avoid it. Since her exercise tolerance was poor on little-acknowledged dyspnea, I really couldn't tell whether her symptoms were cardiac (ischemia or diastolic dysfunction), deconditioning, or "leftover" pulmonary vascular bed injury. I was nervous about the left main calcium counts. My tendency to cath in face of ischemia and minimal symptoms in a sedentary patient is fueled by my having been burned twice by that exact scenario. Those two patients failed "optimal medical therapy" in a big way despite having been deemed "stable." In addition, my prior invasive-cardiology mentor, J Davis Talley, always taught me to "worship at the tomb of the open artery," a "weakness" I struggle with on a daily basis. Although I haven't talked with him in many years, as closely as he watches the literature, I'm certain he has morphed his stance on that topic significantly. I wonder what he would have done with this patient.

My patient chose to undergo coronary angiography. To the interventionalist's credit, he resisted the oculostenotic reflex despite a 90% stenosis of the LAD, two diagonal branches that were also 90%, and an RCA of 60%. She walked back into my office with her boyfriend for another discussion as to "what to do now." Her family doctor cited the COURAGE trial, offered a change to rosuvastatin (Crestor), and recommended watchful waiting. The morning I opened the exam room door for her discussion was the morning that Shelley Wood, our managing editor of heartwire, posted the FAME II preliminary data from EuroPCR. It confirmed the suspicions we've all lived with throughout the interventional era but until now, the proof of it had slipped through our fingers. Indeed, we still aren't sure of how firmly we have that proof in our grasp until the data on hard outcomes are completely calculated.

FAME II begs for fractional flow reserve (FFR), but the patient is now back on warfarin and requires we go back through a DVT risk, bridging with enoxaparin (Lovenox), then the risk of "triple therapy" with warfarin, aspirin, and a thienopyridine. At the same time, she is not on the "optimal medical therapy" described by Dr De Bruyne in FAME II, when he stated that "over 86% of patients received beta blockers, 90% received ACE inhibitors, and 93% received statins." I have concerns regarding the lack of OMT because my patient had neither the heart rate nor the blood pressure for addition of a beta blocker or an ACE inhibitor. The day before the preliminary FAME II data were published; I would have folded my hands, admittedly with some reservation, and rested on the laurels of the COURAGE trial. Now, I think the best advice is to proceed on with a flow wire study, notwithstanding the hassles of bridging and juggling INRs. She asked me point blank what I'd do, and I told her that I would undergo a flow wire study if it were my coronary anatomy.

For now, the patient and her significant other are mulling over their options. They seem to be learning toward watchful waiting and a three-month follow-up. I explained that as long as she has 40 pounds of weight to lose, she will not be optimally managed. A failure to perform daily exercise will also contribute to her risk of plaque rupture, further fueled by her mild glucose intolerance. She joked that she had just stopped at Dairy Queen last week and wasn't sure she could give up her ice-cream habit. I worried as she left the office that despite such superbly designed studies, those outcomes could still misadvise us, as they cannot possible take into consideration the very impactful issues of compliance, glucose intolerance, sedentary lifestyle, and the professional and personal interpretations of whether or not the patient is truly symptomatic.

"Heavy is the head who wears the crown" as the decision maker with regard to recommending for or against coronary intervention in the patient without STEMI. In my 21 years of private practice, there have never been so many pieces of the puzzle to consider in this decision-making tree. It seemed so much easier, back in the day when we practiced the "caveman" mentality of "see blocked artery, do blocked artery." The complication rates were low, but the costs of medical therapy were high, and we can no longer afford it. All we can do is weigh the information we have against individual patient characteristics; do what has worked well for the majority of our patients throughout our practice experiences; arm our patients with information on diet, exercise, and the importance of medical compliance; load them up with medications proven to reduce risk; and cath those who worry us. It seems that FAME II may have just taken a whole lot of guesswork out of this formula, and I hope cath labs across the country will adopt this approach if the final calculations in the primary end points are impressive.

I want what all cardiologists want for our patients. We want them to be safe, and we want them to have a good quality of life. We must acknowledge that we cannot just hang our hats on mortality reduction alone as our guide. We need to analyze as much data as possible to continue our quest to advise our patients we well as possible. At the end of the day, I do not want to be labeled as COURAGEOUS or FAMOUS.

For the sake of my patients, I just want to be right.

See also:

FAME II: FFR pinpoints stable CAD patients who fare worse with OMT

Medical therapy takes COURAGE: No benefit of PCI over optimal drugs for preventing events in stable CAD

Your comments

	FAME or COURAGE: Can we have both?
	# 1 of 8	May 25, 2012 03:45 (EDT)
	Baxter Montgomery, MD, FACC	This patient clearly needs a nutritional intervention.  Her true disease state isn't CAD.  Her disease state is her poor lifestyle.  More specifically, her poor diet.  If she were to consume a more nutritionally excellent diet she could reverse her heart disease and minimize the need for medications.  A nutritionally execellent diet can result in a comprehensive improvement in her health.  See attached data: http://www.drbaxtermontgomery.com/about/benefits/
	# 2 of 8	May 27, 2012 05:47 (EDT)
	Deepak Garg FRCP FSCAI	Excellent example of how FAME II will help  that perhaps only AD/D territory should have revacularisation for a better outcome and prevent a significant anterior event. Triple therapy/ IGT probably would bring CABG as the preferred option but surgeon wil not like her for BMI which brings in the tedious job we have with patients still being casual and humorous about what responsibility they themselves carry to improve their life style-  to allow evicence based therapies. She and her partner should focus on this issue in the 3 months they have.    DG
	# 3 of 8	May 27, 2012 12:35 (EDT)
	Walid Saber	This patient has 2 vessel CAD with normal LV function.  AS an Interventionalist I would say that 90% LAD described here does not need FFR.  In addition if it was proximal LAD ( which was not described here), then there is a mortality benefit for revascularization, not just symptom relief.
	# 4 of 8	May 29, 2012 06:41 (EDT)
	Dr YVC REDDY, MD DM MRCP FACC FCSI	Since this lady has symptoms with documented ischemic defect on perfusion scan at low - moderate workload, and angiography documenting 90% severe LAD stenosis (accepting correct estimation), she would need PCI for LAD. If the LAD stenosis were borderline (50%-70%) or if the symptoms were not there or if the stress perfusion scan were equivocal, there would have been a role for FFR in LAD. Or else, we would be advising FFR in every lesion in every scenario, the so-called "FFRmania" or "FFRabuse". Appropriateness of PCI is an important issue and FFR should be utilised in scenarios where the indication for PCI is equivocal. ....
	# 5 of 8	May 29, 2012 07:50 (EDT)
	Albert Fink MD	Re: FAME II- Isn't it curious how an open labeled trial confirms something that we've long suspected? Let's wait for the real data but the design of the trial lumping in the soft endpoint -unplanned hospitialization and urgent revacularization- with hard endpoints as the primary outcome metric is a disturbing  trend in industry sponsored trials  and especially so in this unblinded trial.
	# 6 of 8	June 3, 2012 04:51 (EDT)
	Brett Forge	Even if she wasn't on warfarin and she had stable angina and severe double vessel disease, there is no evidence that revascularisation will prevent death of heart attack. 33% of pts in COURAGE had triple vessel disease, all the pts in MASS II had multi vessel disease. FAME simply shows that if you do FFR then there is a 1/10 chance of avoiding an 'urgent' revascularisation. A soft endpoint which is irrelevant in this pt whose life is at stake. Medical treatment needs to be optimised. It is likely that when she went on lipitor her disease stopped progressing. That is why she came to you for a cardiac workup rather than complaining of her SOB. When her LDL is down to 68 with aggressive LLT, diet and an execise program her symptoms will slowly start to improve.   So even if it were not for the warfarin she should have a program of opimal medical therapy. However adding the problems of dual anti platelet therapy to warfarin is simply unconscionable in a stable patient where the risk of serious bleeding is close to 20% in the first year in some studies.  I also feel the initial workup which involves a heavy dose of radiation with Thallium and CT calcium is inappropriate, now you wish to add an angio with stenting. I would have performed a conventional stress test which could have been followed by a CT coronary angiogram. Then follow up with medical therapy would be appropriate.  Such an approach saves a large amount of money, a heavy dose of radiation and also provides the ideal management for this lady.
	# 7 of 8	June 4, 2012 02:06 (EDT)
	garry holland	In the DEFER study, fractional flow reserve was used to determine the need for stenting in patients with intermediate single vessel disease.In those patients with a stenosis with a FFR of less than 0.75, outcome was significantly worse. In patients with a FFR of 0.75 or more however, stenting did not influence outcomes. This suggests that FFR is a useful tool to gauge decision-making in this setting.this pt has 2VD!!!!!.....also i believe it is quite funny that $ are an issue here as ..if you go back in and do the FFR ...havn't you wasted more $ ....you could have done the FFR the first time and had the consent to do stenting depending on the result and if not then CABG asap.....now more $ are going to be used up making a decision to re-enter (+ XXX Dr visits etc) and i dont think this poor pt has time (time is myocardium) to play around with. ode to the' caveman' forget the $...whats a life worth.
	# 8 of 8	June 4, 2012 10:44 (EDT)
	Colin Rose	Exactly. Presumably this patient had been on Lipitor for years but still developed advanced coronary atherosclerosis. So take a hint; atherosclerosis is not caused by a deficiency of statins which should never be prescribed for primary prevention. Atherosclerosis caused by junk food and/or tobacco addictions which are only aggravated by the moral hazard effect of statins. OMT must include significant, documented lifestyle change, proven to reverse atherosclerosis, before considering "revascularizaton".

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