May 27th, 2010
The Tests Say Intervene, but the Patient Feels Fine
Anju Nohria, MD and James Fang, MD
A 58-year-old asymptomatic man with hypertension and hyperlipidemia was noted to have an abnormal electrocardiogram during his routine annual physical examination. His primary care physician ordered a treadmill stress test.
The patient exercised for 6 minutes and 39 seconds of a standard Bruce protocol, achieving 8.1 METs. He stopped because of dyspnea. His heart rate increased from 63 bpm at rest to 133 bpm at peak exercise; his blood pressure changed from 176/86 to 164/90 mm Hg, respectively. An electrocardiogram showed 3.5-mm horizontal ST-segment depressions — in leads I, II, III, aVF, and V3-6 — that began 5 minutes into the test and resolved 8 minutes into recovery. During exercise, the patient had isolated premature ventricular contractions but no other arrhythmias.
A subsequent myocardial perfusion scan revealed a resting LV ejection fraction of 65% that decreased to 55% during exercise. No regional perfusion defects consistent with scar or ischemia were found.
Cardiac catheterization revealed 3-vessel coronary artery disease with 50% distal left-main disease, 60% ostial and 90% mid left-anterior-descending artery stenoses, an occluded first obtuse marginal branch, 70% proximal right coronary artery disease, and an occluded posterior descending artery. Extensive left-to-left and left-to-right collaterals were identified.
After being referred to a cardiologist, who recommended coronary artery bypass, the patient refused surgery because he was asymptomatic during his routine daily activities. He was treated with aspirin, a beta-blocker, an ACE inhibitor, and a statin.
At re-evaluation 1 year later, the patient reports excellent functional status and no new symptoms of chest pain or dyspnea. Results of a repeat stress test and echocardiogram are essentially identical to the year-old findings.
The patient wants to know whether this is good news or bad news. In other words, have the medications kept him stable and made surgery unnecessary, or is revascularization still advisable because there’s been no improvement?
Questions:
- As the patient asks, are the results of his 1-year evaluation good news or bad news?
- If you recommend revascularization, would you advise surgery or high-risk angioplasty?
Response:
James Fang, MD
Medical therapy and lifestyle changes are generally the primary management strategy for chronic coronary artery disease, and multiple trials have attested to their effectiveness, particularly when symptoms are modest. For example, the COURAGE trial provides reasonable evidence that chronic ischemic heart disease can be managed as successfully with aggressive medical therapy as with revascularization — and the FAME trial indicated that when disease appears intermediate on angiography, ischemic burden is more important than “percent” stenosis in guiding therapy. However, the question in my mind is whether this patient can really be considered asymptomatic. While I might not go so far as to tell the patient his clinical course to date is “bad news,” I would argue that his functional capacity was, in fact, reduced at baseline compared to men his age (given his dyspnea–limited stress test) — and that his burden of ischemia remains significant (as indicated by the decrease in EF with exercise), even after a full year of good medical management. For this reason, I would recommend revascularization.
In terms of the specific procedure, I would recommend surgery over angioplasty, because of the chronically occluded anatomy in more than one vascular territory and the resulting uncertainty about whether “complete” revascularization could be achieved with PCI. Alternatively, I would consider performing only LAD revascularization (PCI), since the effect of the chronically occluded anatomy is attenuated by collateralization. However, I cannot make definitive recommendations about the revascularization strategy without personally reviewing the results of the angiogram. The importance of such a review is exemplified by the fact that many patients did not qualify for randomized trials of CABG versus PCI because their anatomy — when reviewed by both surgeon and interventionalist — clearly indicated one procedure over the other. That said, multiple randomized clinical studies have demonstrated that there are no survival differences between surgery and multivessel PCI, although it should be recognized that both therapeutic strategies continued to improve during the conduct of these trials. Even left main coronary disease is no longer treated exclusively with bypass surgery, although practice patterns differ widely in the U.S. and even more so worldwide.
The two strategies have clear trade-offs that must be considered both in the clinical context and in light of the patient’s preferences. For example, the modest but real risk for early morbidity and mortality with cardiac surgery must be balanced against the crossover rate and need for multiple follow-up procedures with PCI. Furthermore, although continued pharmacologic therapy is a cornerstone of both strategies, absolute compliance with dual-antiplatelet therapy becomes paramount with multiple coronary stents. Whenever possible, patients and their families should be counseled about the risks and benefits of surgery versus PCI. Further risk stratification may be possible based on the recent SYNTAX trial, but formal “SYNTAX scoring” is unlikely to catch on, much in the same way that “TIMI scoring” is rarely done formally in clinical practice when managing NSTEMI.
Follow-Up:
Anju Nohria, MD
The patient was counseled that although it was good news that he had not worsened over the past year, it was bad news that he continued to have a modest exercise capacity and, more importantly, a reduction in his EF with activity, suggesting diminished contractile reserve. The cardiologist once again urged the patient to consider surgery and offered angioplasty if the patient was afraid to undergo a surgical intervention. For the time being, however, the patient has opted to pursue medical therapy unless he experiences symptoms that limit him in his daily activities.
13 Responses to “The Tests Say Intervene, but the Patient Feels Fine”
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The patient made the right call
Considering that with the 3-vessel disease, this patient had neither a decreased ejection fraction or a reversible perfusion defect involving over 10% of his myocardium, there is no real reason to think that he will do better with revascularization. I would first congratulate him on the courage to resist the occulo-stenotic reflex a trap most physicians fall into with zeal. The fact that a statin alone did not result in plaque regression should not be a surprise to anyone. If we want to see regression, we need to raise HDL as well as lower LDL. This would be best accomplished with the addition of high dose fish oil derived omega-3 fatty acid (at least 2gm) and extended release nicotinic acid(at least 1 gm). In addition we should correct the Vit D deficiency that almost certainly exists with adequate D-3 to get the blood level between 50-80. This approach will result in plaque stability and dramatic reduction of coronary events. this benefit will last a lifetime as compared to a bypass which looses all of its value by year ten.
echoing Bill’s comments
I would still track his plaque – baseline and then 6 months then biannually until I can achieve robust plaque regression. I would use proven therapies to achieve that regression, which predicts half the rate of cardiovascular events as in progressors. My first approach in doing this would be to aim for as low an LDL as possible given the evidence that high dose statins prevent more events than low dose statins (Post-CABG, SAGE, TNT, PROVE-IT, A-to-Z Z phase, IDEAL, etc). I would ensure his medical therapy is optimized and consider an aldosterone antagonist if BP was still high. Most importantly I would track his plaque over time. The problem with CABG is that we often consider it to be a final fix to the patient’s problem, and then walk away with the hard job of medical management left not complete.
speaking of non-traditional risk factors…
would anybody prioritize checking a CRP and consider switching to rosuvastatin based on the level?
HSCRP
I might consider an HSCRP of <1 as one of my therapeutic targets until enough time had passed to reassess the atherosclerosis by non-invasive imaging. I would not use it as part of a decision regarding which statin to use.
He has left main coronary disease, with confirmation of hemodynamic significance (reduction in EF with exercise). In addition to optimal medical therapy, he should be referred for coronary revascularization. Given his chronic total occlusions, surgery would most likely result in more complete revascularization than PCI.
“Track the plaque” sounds great…but there’s no reliable way to do so noninvasively.
Show me the DATA
Yes he has L Main disease but it is not obstructive. Triple vessel disease with decreased EF in the resting state results in improved outcomes (in the pre statin era) however to my knowledge, there is no data regarding decreased post stress EF. There is no demonstrable ischemia with spec imaging.. Where is the DATA to say that he will benefit from CABG. EBT calcium imaging has been shown to be a reliable way to track plaque progression, see 2007 AHA expert scientific paper.
Competing Interests: I avoid the need for revascularization by finding coronary disease in the preclinical asymptomatic state using EBT calcium imaging and treat to the goal of calcium progression of less than 15% annually.
patient in the driver seat is the key
I like this case because it presents a high risk patient who is clearly in the driver seat with regard to decision-making. You could make the case for a variety of strategies – and each one has substantial uncertainty associated with it – that is, uncertainty about what net effect it will provide. Even among us there is disagreement about the relative value of revascularization vs some sort of surveillance — and then the target based approach to biomarkers. In the end this patient should hear from physicians with different views and decide on an approach knowing that there is not a simple answer.
With regard to the statin – he is high risk – I would have him on a high dose of a statin or a high potency statin regardless of his LDL or Hs-CRP.
Show Me The Money (aka ischemia)!!
Appropriately, Bill wants to see ischemia to prove that the obstruction is hemodynamically significant. In this case (i.e., left main and three vessel disease), one may not see regional perfusion defects by SPECT, since there is balanced ischemia. However, the decrease in EF with exercise is the proof of ischemia. In addition to optimal medical therapy (with high dose statin), I’d revascularize this patient because he has left main disease with evidence of ischemia.
I don’t disagree
I am forced to admit that this patient would be directed for CABG at our facility however I don’t know that such a recommendation is truly an “evidence based” recommendation as the ischemia is implied but not certain to be macro-vascular. He may have equally bad micro-vascular ischemia which could result in the decreased EF and have no improvement with CABG. I think in light of this hazy DATA, it is appropriate that the patient’s input is respected.
Enjoying discussion greatly
There are multiple means of tracking plaque non-invasively; the question is whether it adds value. In my practice I find a picture highly motivating to the patient (and I don’t always have a cath picture to show them). Patients with documented atheroma regression have only half the rate of c.v. events as patients with progression (Spence et al. Stroke Dec 2002). Looking at upstream risk factors alone – whether they are blood glucose and A1c or lipids – is insufficient in comparison with looking at the disease itself (and its biology), as we know from Framingham that such risk factors will under or overestimate risk in 1 in every 4 patients with events (Wilson et al. Circulation 1998). In violation of previous dogma, atherosclerosis can and will regress with sustain attack of all risk factors, but it is insufficient just to measure risk factors alone – plaque must also be measured. In this case, in addition to statin+/-niacin, I would also recommend some sort of BP-lowering regimen geared to the renin-aldosterone profile, glucose-lowering if necessary, lifestyle modification (consisting of a cretan diet), smoking cessation, and measurement of lipoprotein(a), TSH, and free T4.
Monitoring plaque stability and event rates
Progression of calcified plaque, as measured by EBT imaging, of < 15% annually was associated with a 17 fold reduction in events compared to progression in patients taking lipitor. This was independent of LDL response to lipitor. The higher the initial calcium score, the greater the difference in event rates between stability and progression of plaque. (Arteriosclerosis, Thrombosis, and Vascular Biology 2004;24:1272) A second study found a 13 fold difference across the board regardless of therapeutic status (Raggi, Shaw, Callister, Budoff; JACC 2003) Dan, I can respect a doubling of risk however when you see a 13 to 17 fold increase in risk based on calcium progression, one must stand up and take notice.
monitoring plaque progression
Bill, I was responding to the comment that there is no reliable way to monitor plaque non-invasively. I do not think that carotid plaque area or volume regression is the only way to monitor plaque; CAC is another. You could also do serial ABI testing, or do what nephrologists do – measure protein and microalbuminuria in the urine (which also responds to many of the same interventions that we use in CAD). One advantage of US over CAC is that there is zero radiation burden for US (yes, I know that modern CT has brought the radiation burden down, but it still not zero as in ultrasound). In addition, I have seen patients with CAD who have very little CAC but tremendous carotid atheroma, and vice versa. So perhaps using both techniques is the way to go, given that atherosclerosis is both a focal and systemic disease. Measuring risk factors alone, and patting ourselves on the back when we have reached them, does a grave disservice to patients (many of whom will present with further events).
This individuals first ischemic presentation may be his last. The decreased LV function with exertion in the face of L main and multivessel disease is enough for me to recommend CABG. The patient may choose not to follow this recommendation , but should be educated on the possibilkity of SCD due to his ischemic burden.
High dose/potent statins, B-blocker therapy and antiplatelets should be mainstay. I would also look at ACEI for endothelial effects.