What to Do with Epicardial Coronary Artery Abnormalities That do not Result in Myocardial Ischemia?

C.Richard Conti,MD,MACC

1 University of Florida Medical School,Gainesville,FL 32610,USA

Abstract

When epicardial arteries with minimal CAD do not limit flow are found at coronary angiography,all cardiologists agree that aggressive risk factor modification and use of appropriate drugs are warranted.Some consider plaque sealing of minor coronary lesions with balloon angioplasty to prevent future infarction.Others believe that a coronary lesion that does not cause ischemia should not have the plaque sealed but should have FFR and the non-ischemia producing stenosis should be treated with aggressive risk factor modification (DEFER study).Evidence based data e.g.DEFER,relates to populations,not the individual.Thus these data provide guidelines,which are suggestions for decision making.The weight of evidence favors angioplasty/stent for epicardial vessels that result in myocardial ischemia.Sealing of non flow limiting plaques with angioplasty must await further information derived from invasive and non invasive studies.

Keywords: Minimal CAD;plaque sealing

Introduction

The general indication for coronary artery angiography is the need to know the details of the coronary pathology in order to determine if revascularization is a treatment option.

I can think of two questions that relate to patients with asymptomatic epicardial coronary artery stenoses.The first question is,“ Why did the patients undergo stress testing to detect ischemia if they had no symptoms? ” I suppose the presence of multiple risk factors for coronary artery disease could justify the testing.

The second question is “ Why were patients undergoing coronary angiography if they were truly asymptomatic? ” One of the answers comes from the ACIP trial in which some patients had ST segment depression (ischemia) during exercise but had no symptoms.

The Issue

The issue here is what should be done to patients with epicardial coronary plaques that do not limit flow in any way but are found during coronary angiography (minimal CAD) and what is the clinical outcome of patients with epicardial plaques that do not limit flow.

Little et al.reported a retrospective study in which several patients with minimal CAD eventually evolved a myocardial infarction [1].They wished to determine if coronary angiography can predict the site of a future coronary occlusion resulting in a myocardial infarction.The answer to their wish is probably no,since 66% (not 100%) of patients evolved an acute myocardial infarction because of an occlusion of a coronary artery that previously had less than a 50% angiographic coronary stenosis.However,their observations support the concept that “ minor” coronary stenoses can be disrupted and eventually occlude the artery.

All cardiologists agree that aggressive risk factor modification and use of appropriate drugs are important in patients with known coronary disease.Even minor coronary plaques may be rupture prone if they have a thin cap and subcapsular lipid pool in which much of the lipid is LDL cholesterol oxidized by activated macrophages [2].Vigorous bending and twisting of these plaques may be related to their rupture.If this is true,then decreasing the lipid pool (STATINS) preventing oxidation of LDL (? vitamin E) and slowing the force and velocity of contraction of the vessels (B-BLOCKERS) seems helpful for preventing myocardial infarction.

One Point of View

Some consider “ plaque sealing” of minor coronary lesions with balloon angioplasty as a method to prevent future infarction.The rationale for this is that a coronary stenosis subjected to balloon angioplasty probably will not progress to occlusion in most cases.If restenosis does occur,the smooth inner lining of the intimal proliferation virtually precludes endothelial rupture and thrombosis.If endothelial rupture and thrombosis is prevented,then the occurrence of myocardial infarction and death is highly unlikely [3] and PCI/stent can be performed if restenosis occurs.Although there is lack of scientific proof to this approach,some still believe that the prognosis of patients is better if plaques are sealed by angioplasty.No one advocates the use of stents at the time of the plaque sealing.

Another Point of View

In contrast to the above position,Pijls believes that:“ If you have a coronary lesion that is not causing ischemia,the intrinsic risk of the stenosis is lower than the risk of PCI/stent.” He also goes on to indicate that because interventionalists cannot discriminate by angiography (which is lumenography) plaques that are prone to rupture “ stents are placed everywhere and the benefits of placing the stents in the right position is countered by the damage done by placing stents where it is not necessary.” Thus,he believes that fractional flow reserve,which can be determined at the time of catheter-based coronary angiography,should be performed in these questionable lesions.In the DEFER study,diameter stenosis was compared to fractional flow reserve.The message that comes from the DEFER study is that:1.Stenting an ischemia producing lesion makes sense because it decreases symptoms and often also improves outcome.2.Stenting a non-ischemia producing stenosis has no benefit compared to medical treatment either in prognosis or symptom relief [4] but non ischemia producing stenoses should be treated with aggressive risk factor modification.

I think it is appropriate to ask ourselves “ how does evidence-based data from clinical trials relate to individual decisions for percutaneous intervention? ” The answer is that evidence-based data does not necessarily relate to the individual but rather to populations.Decision making is an individual exercise,not population based.The “ n” is one.

Clinical trial evidence provides guidelines (suggestions) for decision making,not inflexible rules.To emphasize that point,the patients reported in the DEFER trial,who had fractional flow reserve ＞ 0.75 had a scatter plot from 25% stenosis to 70% stenosis,and patients who had a fractional flow reserve ＜ 0.75 had a scatter plot of 30% stenosis to 88% stenosis.Although there is a statistically significant difference,there was tremendous overlap of data points in these patients,emphasizing that judgment is still required for decision-making in the individual patient.

Conclusions

There are really two sides to the question which need to be addressed by the cardiologist who makes the clinical decision.All clinicians need to have good judgment,and good judgment comes from evidence,experience,and opinion-based consensus.In this instance,the weight of evidence favors optimum medical therapy,risk factor reduction and angioplasty/stent in stenotic epicardial coronary vessels that result in myocardial ischemia.In patients with coronary lesions that do not result in ischemia,there is also a large amount of experience and opinionbased consensus that using FFR is the right way to proceed.However,for those who believe it is important to perform plaque sealing of all stenoses (ischemia producing or unknown),the procedure should be balloon angioplasty without a stent.

My Position on this Topic

1.Although theoretically attractive,sealing of nonflow limiting plaques must await further information derived from invasive and non-invasive studies.2.Anatomic assessment of coronary stenoses determined by catheter-based angiography should be correlated with functional significance (nuclear studies or physiologic studies using FFR) before any revascularization procedure is attempted.3.My final comment to end this discussion is that judgment is still necessary and that decisions be based on as much data that one can obtain.I favor FFR or IFR of stenoses that may or may not produce ischemia.When there are no data or the data are conflicting,try using common sense.4.All coronary artery stenoses,whether they be minimal or high grade,need to be treated with risk-factor modification therapy.

REFERENCES

1.Little WC,Constantinescu M,Applegate RJ,Kutcher MA,Burrows MT,Kahl FR,et al.Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease? Circulation 1988;78(5 Pt 1):1157- 66.

2.Kolodgie FD,Burke AP,Farb A,Gold HK,Yuan J,Narula J,et al.The thin-cap fibroatheroma:a type of vulnerable plaque:the major precursor lesion to acute coronary syndromes.Curr Opin Cardiol 2001;16(5):285- 92.

3.Kern MJ,Meier B.Evaluation of the culprit plaque and the physiologic significance of coronary atherosclerotic narrowings.Circulation 2001;103(25):3142- 9.

4.Pijls NH,van Schaardenburgh P,Manoharan G,Boersma E,Bech JW,van' t Veer M,et al.Percutaneous coronary intervention of functionally nonsignificant stenosis:5 year follow up of the DEFER study.J Am Coll Cardiol 2007;49(21):2105- 11.