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European Heart Journal Advance Access originally published online on February 16, 2006
European Heart Journal 2006 27(9):1128-1129; doi:10.1093/eurheartj/ehi806
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Gatekeeper for coronary angiography: reply

Poul F. Høilund-Carlsen

Department of Nuclear Medicine
Odense University Hospital
DK-5000 Odense C
Denmark
Tel: +45 65411397
fax: +45 65906192
E-mail address: pfhc{at}ouh.fyns-amt.dk

Allan Johansen

Department of Nuclear Medicine
Odense University Hospital
DK-5000 Odense C
Denmark

Werner Vach

Department of Statistics
J.B. Winsløws Vej 9B, 2.DK-5000 Odense C
Denmark

Torben Haghfelt

Department of Cardiology
Odense University Hospital
DK-5000 Odense C
Denmark

We thank Geluk and Zijlstra for their kind words as well as their considerations and proposals. The latter hits right into the heart of the issue: should one stick to the ‘anatomic’ paradigm urging us to detect and treat coronary stenoses and calcifications rather than follow the ‘physiological’ approach to examine for and potentially treat the hypoperfusion, often but not always, caused by stenoses?

Following the first paradigm, a sensitivity of 81% for obstructive coronary artery disease (CAD) and may be even one of 95% for three-vessel disease should be considered suboptimal in what Geluk and Zijlstra term a not-low-risk population. In their opinion, this speaks of using a costly technique such as electron beam computed tomography as a filter detecting coronary calcifications, i.e. a late manifestation of CAD, because the absence of calcifications implies a high negative predictive value with regard to CAD.

However, from a physiological point of view, the reasoning by Geluk and Zijlstra is somewhat upside down. If accepting that angina pectoris is caused by myocardial hypoperfusion or ischaemia, one should primarily prevent, detect, and treat this condition rather than stenoses per se which do, far from always, cause reduced perfusion. Secondly, one should examine whether or not regional myocardial ischaemia is reversible, as revascularization is ineffective in patients with irreversible or fixed perfusion defects.1 Consequently, it is only when reversible ischaemia has been documented that invasive treatment and preceding catheterization is justified, especially if one considers the cost and risk associated with these procedures.2,3 Therefore, MPS is preferable as gatekeeper rather than angiography or ECBT because none of these methods provides information on ischaemia or hypoperfusion. The often used argument that MPS may overlook three-vessel or left main disease is hardly relevant because in our intermediate risk population (in which MPS is generally considered most useful2,4), we ‘overlooked’ severe coronary disease in only 1.1%.3 In addition, it has been shown years ago, before the advent of modern medical treatment, that it is only a minority of patients with three-vessel or left main disease who will live longer with coronary revascularization than without, namely patients with depressed left ventricular function.5,6 All our patients with normal perfusion and ‘overlooked’ severe CAD had a normal ejection fraction.

Absence of coronary calcium on EBCT may have a high negative predictive value for the presence of obstructive CAD but not for the atherosclerotic process, which is rational to detect and treat if reversible ischaemia is present. In fact, with the advent of non-invasive angiography with 64-slice CT, we fear that the search for coronary calcification will spread and intensify like a steppe fire and lead to even more catheterizations and revascularizations unless MPS (and the presence of reversibility and not coronary calcium) is used as filter early in the work-up process.

References

  1. Johansen A, Høilund-Carlsen PF, Christensen HW, Vach V, Møldrup M, Haghfelt T. Use of myocardial perfusion imaging to predict the effectiveness of coronary revascularisation in patients with stable angina pectoris. Eur J Nucl Med Mol Imaging 2005; 32: 1363–1370. Published online ahead of print April 12, 2005.[CrossRef][Medline]
  2. Des Prez RD, Shaw LJ, Gillespie RL, Jaber WA, Noble GL, Soman P, Wolinsky DG, Williams KA. Cost-effectiveness of myocardial perfusion imaging: a summary of the currently available literature. J Nucl Cardiol 2005; 12: 750–759.[CrossRef][Web of Science][Medline]
  3. Høilund-Carlsen PF, Johansen A, Christensen HW, Vach W, Møldrup M, Bartram P, Veje A, Haghfelt T. Potential impact of myocardial perfusion scintigraphy as gatekeeper for invasive examination and treatment in patients with stable angina pectoris: observational study without post-test referral bias. Eur Heart J 2006; 27: 29–34. Published online ahead of print September 23, 2005.[Abstract/Free Full Text]
  4. Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS, Ferguson TB, Fihn SD, Fraker TD, Gardin JM, O'Rourke RA, Pasternak RC, Williams SV. ACC/AHA 2002 Guideline update for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999. Guidelines for the Management of Patients with Chronic Stable Angina) 2002. www.acc.org/clinical/guidelines/stable/stable.pdf (22 January 2006).
  5. Alderman EL, Bourassa MG, Cohen LS, Davis KB, Kaiser GG, Killip T, Mock MB, Pettinger M, Robertson TL. Ten-year follow-up of survival and myocardial infarction in the randomized Coronary Artery Surgery Study. Circulation 1990; 82: 1629–1646.[Medline]
  6. Takaro T, Peduzzi P, Detre KM, Hultgren HN, Murphy ML, van der Bel-Kahn J, Thomsen J, Meadows WR. Survival in subgroups of patients with left main coronary artery disease. Veterans Administration Cooperative Study of Surgery for Coronary Arterial Occlusive Disease. Circulation 1982; 66: 14–22.[Abstract/Free Full Text]

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This Article
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