CASE REPORT

Residual angina pectoris after

percutaneous coronary intervention for acute coronary syndrome M. Michels, H. Werner, E. Onderwater, W.J. van der Giessen

Fractional flow reserve (FER) is an important diagnostic tool to guide decision-making in the ardiac catheterisation laboratory and for evaluation of percutaneous coronary interventions (PCI). Especially the pressure pullback curve at maximal hyperaemia is convincing in demonstrating the exact location and severity of a coronary stenosis. This pressure pullback curve can also demonstrate the presence of diffuse disease. We present a case in which FFR with pressure pullback curve seven days after a PCI, which did not result in complete symptom relief, indicates the presence of diffuse disease. Based on this result the patient was treated medically. (NethHeartJ2005;13:315-7.) Keywords: coronary angioplasty, coronary pressure, fractional-flow reserve A 40-year-old female with Sjogren's syndrome and Raynaud's phenomenon and a positive family history for coronary artery disease was referred to our hospital for a PCI because ofunstable angina pectoris (Braunwald class III-B). She had led an active life free of symptoms until two weeks before admission, when she experienced extreme tiredness and substemal chest pain. An exercise test revealed ECG changes compatible with ischaemia. Under treatment with carbasalate calcium and [B-blocker she still experienced thoracic pain and was admitted to a community hospital. On admission the ECG revealed repolarisation abnormalM

M. Michels E. Onderwater WJ. van der Glessen Department of Cardiology, Thorax Centre, Erasmus Medical Centre, Rotterdam H. Wemer Department of Cardiology, Vlietland Hospital, Schiedam

Correspondence to: W.J. van der Giessen Department of Cardiology, Thorax Centre, Erasmus Medical Centre, Dr. Molewaterplein 40, 3015 GD Rotterdam E-mail: [email protected]

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Netherlands Heart Journal, Volume 13, Number 9, September 2005

ities in the inferolateral leads; the cardiac markers were not elevated. A coronary angiogram revealed a bifurcation lesion of the left anterior descending (LAD) and the first diagonal branch (figure 1). The mid and distal part of the LAD showed diffuse disease. The other coronary arteries showed no significant lesions. Systolic left ventricular fimction was normal. The bifurcation lesion was treated with two stents using the 'crush' technique.' During this procedure one taxol-eluting stent was implanted in the LAD (3.0x28 mm Taxus Express 2, Boston Scientific) and the diagonal branch (2.25x20 mm Taxus Express 2, Boston Scientific) and postdilated with kissing balloons (Quantum Maverick balloon 3.0x8 mm and Hayate balloon Pro 2.0x20 mm).

After this procedure the symptoms of the patient improved, but she still experienced angina pectoris, albeit without ECG changes, after mobilisation in the referring hospital. A new coronary angiography was performed seven days after the PCI. The implanted stents were angiographically patent without visible stenosis (figure 2) and the right coronary artery and the left circumflex artery appeared normal. To better evaluate the result of the previous intervention in the LAD we performed an FFR measurement during hyperaemia with intravenous adenosine (140 jg/k/min). The pressure pullback curve during maximal hyperaemia showed a gradually decreasing hyperaemic pressure gradient from the distal LAD to the left main (FFR 0.77), with no sudden change at the site of previous bifurcation treatment (figure 3). Such a linear relation indicates diffuse disease without a localised stenosis treatable by a coronary intervention. It was therefore decided to treat the patient medically with carbasalate calcium, ,-blockade, a calcium antagonist, statins and clopidrogel. After a couple of weeks the patient was symptom free.

Dwcwslon Several aspects of this case were remarkable. First there was diffuse one-vessel disease in a young female, without coronary artery risk factors as hypertension, 315

Residual angina pectoris after percutaneous coronary intervention for acute coronary syndrome

Figure 1. Basline coronavy angiogram in SO projection which shows the bifurcation ksion of the LAD and DI (arrow).

Figure2 Cornatyangiogram ofthe treated LAD/DI bifurcation

(bigarrow) one week afterstentimpkantation. Bothstents are nicely patent, the distal LAD sbows difus sckrosis (litte arrows).

diabetes, smoking or hyperlipidaemia. She had documented Sjogren's syndrome which is unlikely to be an explanation for this diffiuse one-vessel disease, although we could find one report describing such a case.2 Sjogren's syndrome is a chronic inflammatory disorder I&III I ! .!r-. ". I I .. :CiAlr

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taracterised primarily by diminished lacrimal and ivary gland secretions, but internal organ involveent occurs in 25% of the patients.3 Cardiac manistations that have been described are autonomic 4sfunction and neonatal heart block in infants from

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Figure 3. Preure pullback curpe in the LAD duringmaximal lptratmia. The vetical line indicates the start ofpullback from distal to proximal LAD. The upper line represents the gradual decline of FFR. Tbe lower two lines represent the mean values of aortic pressure (uppr) and distal coronary pressure (lower). AJo ber, agradual cesing ofthegap between

dX two values can be obsered.

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Ncthcriands Heart Journal, Volume 13, Number 9, September 2005

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Residual angina pectoris after percutaneous coronary intervention for acute coronary syndrome

Sjogren's syndrome mothers.4'5 The principal pathological lesion is a lymphocytic infiltration, which is common to all affected organs.6 In a patient with Sjogren's syndrome and severe pulmonary hypertension a lung biopsy showed intimal and medial hypertrophy with narrowing vessel lumina.7 In most cases, however, only much smaller blood vessels are affected, so epicardial coronary involvement is not likely to occur.8

The second remarkable aspect was that she did not become symptom free after treatment ofthe bifurcation lesion. Intracoronary pressure measurement (FFR) revealed that this was due to a significant pressure gradient build-up over the course of the LAD. Measurement of FFR during diagnostic angiography can provide important information for decision-making and for monitoring and evaluating coronary interventions.9'10 FFRis derived from the ratio of the mean distal coronary artery pressure to the aortic pressure during maximal arteriolar vasodilatation with intravenous adenosine. The index is independent ofchanges in systemic blood pressure and heart rate. The normal value of the index is 1.0 and an FFR of less than 0.75 identifies a functionally important stenosis."11"2 In all instances where maximal increase in coronary flow is restricted, FFR can underestimate the severity of the stenosis.9 11 In patients with chest pain and moderate stenosis on coronary arteriography the decision whether the lesion should be treated is generally answered positively ifthe index is less than 0.75. Clinical outcome studies have shown that it is safe to defer PCI of a stenosis if the FFRis >0.75.9Y13 In vessels with several sites suspected of having important stenoses, a pressure pullback curve can be used to identify the exact location and haemodynamic severity of a stenosis. While recording this pressure pullback curve the sensor is pulled back across the artery during maximal hyperaemia induced by an intravenous infusion of adenosine. This continuous infusion is necessary as an intracoronary bolus injection, which is standard practice in most centres, but is too short acting to allow the recording of a pullback curve. In case of a local functionally important stenosis in the diffusely diseased vessel, the pressure pullback curve will show a sudden decrease in the hyperaemic pressure gradient proximal to a lesion that can be treated with a PCI. In the presence of diffiuse disease without a local stenosis, a pressure pullback curve shows a gradually decreasing hyperaemic pressure gradient from the distal coronary artery to the ostium, as in the present case.'4 In the absence of a localised lesion these patients will not benefit from a percutaneous or surgical revascularisation.

Netherlands Heart Journal, Volume 13, Number 9, September 2005

Conclusion We present a case of a patient with persistent angina pectoris on exercise after a successful bifurcation stenting of the LAD and the first diagonal. FFR, using a continuous intravenous infusion of adenosine, with the pressure pullback curve in the LAD during the control coronary angiography showed a decreasing hyperaemic pressure gradient from the distal coronary artery to the coronary ostium including the previously treated LAD/ first diagonal bifurcation. This pressure decline occurred gradually and was not restricted to one single location and therefore this patient could not be helped by a repeat coronary intervention. This case clearly illustrates the value of FFR in decisionmaking in the cardiac catheterisation laboratory. U References 1 2

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Daemen J, Lemos PA, Serruys PW. Multi-lesion 'culotte' and 'crush' bifurcation stenting with sirolimus-eluting stents: long-term angiographic outcome. JInvasive Cardiol 2003;15:653-6. Ingu A, Harada H, Fukada J, Yamamoto N, Ueda M, Sato K, et al. A case report of coronary artery bypass grafting in a patient with Sjogren's syndrome. Kyobu Geka 1996;49:847-50. Asmussen K, Andersen V, Bendixen G, Schiodt M, Oxholm P. A new model for classification of disease manifestations in primary Sjogren's syndrome: evaluation in a retrospective long-term study. JIntern Med 1996;239:475-82. Kovacs L, Paprika D, Takacs R, Kardos A, Virkonyi T, Lengyel C, et al. Cardiovascular autonomic dysfunction in primary

Sjogren's syndrome. Rheumatology2004;43:95-9. Borda E, Leiros CP, Bacman S, Berra A, Sterin-Borda L. Sjogren antibodies modify neonatal cardiac function via MI muscarininc acetylcholine receptor activation. IntJ Cardiol 1999;70:23-32. Daniels T. Labial salivary gland biopsy in Sjogren's syndrome: Assessment as a diagnostic criterion in 362 suspected cases. Arthritis Rheum 1984;27:147-56. Nakagawa N, Osanai S, Ide H, Nishigaki Y, Takahashi S, Nakano H, et al. Severe pulmonary hypertension associated with primary Sjogren's syndrome. Inter Med 2003;42:1248-52. Tektonidou M, Kaskani E, Skopouli F, Moutsopoulos H. Microvascular abnormalities in Sjogren's syndrome: nailfold capillaroscopy. Rheumatology 1999;38:826-30. Pijls NH, De Bruyne B, Peels K, van der Voort PH, Bonnier HJ, Bartunek, et al. Measurement of fractional flow reserve to assess the functional severity of coronary-artery stenoses. NEnglJMed 1996;334:1703-8. Bech G, Pijls N, De Bruyne B, Peels K, Michels H, Bonnier H, et al. Usefulness of fractional flow reserve to predict clinical outcome after balloon angioplasty. Circulation 1999;99:883-8. De Bruyne B, Baudhin T, Melin JA, Pijls N, Sys S, et al. Coronary flow reserve calculated from pressure measurements in humans: validation with positron emission tomography. Circulation 1994; 89:1013-22. De Bruyne B, Paulus WJ, Pijls NH. Rationale and application of coronary transstenotic pressure gradient measurements. Cathet Cardiovasc Diagn 1994;33:250-61. Bech GJW, De Bruyne B, Bonnier HJ, Bartunek J, Wijns W, Peels K, et al. Long-term fbllow-up after deferral of percutaneous transluminal coronary angioplasty of intermediate stenosis on the basis of coronary pressure measurement. JAm Coll Cardiol 1998;31: 841-7.

14 Pijls NH, Kern MJ, Yock PG, De Bruyne B. Practice and potential pitfalls of coronary pressure measurement. Cathet Cardiovasc

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Residual angina pectoris after percutaneous coronary intervention for acute coronary syndrome.

Fractional flow reserve (FFR) is an important diagnostic tool to guide decision-making in the cardiac catheterisation laboratory and for evaluation of...
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