coronary stenting for coronary vasospasm refractory to medical therapy

4
Coronary Stenting for Coronary Vasospasm Refractory to Medical Therapy Andrew Burns, * MBBS (Hons), FRACP , Yuvaraj Malaiapan, MBBS, MRCPI, FRACP , and Ian Meredith, MBBS, PhD, FRACP We describe the case of a 54-year-old male with recurrent chest pain, ST segment eleva- tion, and bradycardia. Coronary vasospasm was confirmed by acetylcholine challenge. After failing medical therapy, stenting of an extensive segment of the right coronary ar- tery has been clinically successful after 24-months follow-up. ' 2007 Wiley-Liss, Inc. Key words: prinzmetal; angina; acetylcholine INTRODUCTION Therapy for coronary vasospasm, originally described as Prinzmetal’s (or variant) angina [1], is primarily pharmacologic with calcium channel antagonists and nitrates used as first line agents [2]. For vasospasm refractory to medical therapy, there have been a lim- ited number of case series of percutaneous intervention with variable results [3,4]. Here we describe a case of coronary vasospasm refractory to medical therapy, which resolved with stenting of an extensive segment of the right coronary artery. CASE REPORT A 54-year-old male of Indian background presented with chest pain and collapse at home. He had a 20 pack-year history of smoking, hypercholesterolemia, asthma, and nasal polyposis. A nontoxic multinodular goitre had been treated with radioactive iodine 13 years previously and his thyroid function had been sta- ble on 100-mcg daily of thyroxine. The initial rhythm strip obtained by the ambulance service demonstrated complete heart block with ST elevation in lead II, however his ECG on arrival at ED was unremarkable except for sinus bradycardia. He developed further chest pain in the emergency depart- ment associated with profound sinus bradycardia and hypotension requiring adrenaline infusion. Repeat ECG (Fig. 1) revealed ST elevation inferiorly and he was given loading doses of Aspirin (300 mg) and Clopidogrel (600 mg), commenced on unfractionated heparin intravenous infusion and transferred to the cardiac catheterization laboratory for emergent left heart catheterization. He was found to have a severe discrete stenosis of the proximal right coronary artery (Fig. 2) which was stented with a 3.0 mm 3 20 mm Taxus stent (Fig. 3). A brief period of complete heart block ensued which required temporary transvenous pacing. He made an uncomplicated recovery from this and was discharged on standard medical therapy. The troponin I peak was 18.17 mcg/L and CK peaked at 850 U/L. During the subsequent 4 months, he represented with two further episodes of chest pain associated with collapse and, on each occasion, he was noted to be hy- potensive and bradycardic requiring atropine when paramedics attended. With each episode transient ST segment elevation and rise in serum troponin I prompted repeat coronary angiography which revealed minimal neointimal proliferation within the stent and no new lesions elsewhere in the right coronary artery. A provocative test for coronary vasospasm was not performed at this stage. Between episodes he had no exertional symptoms. A tentative clinical diagnosis of coronary vasospasm was made and the patient was commenced on high dose calcium channel antagonist (Diltiazem 360 mg) and long acting nitrate (Isosorbide mononitrate 120 mg). After a fourth presentation with chest pain and pro- found bradycardia, an acetylcholine challenge test was undertaken as previously described [5,6] to es- tablish areas of the right coronary artery prone to Monash Heart, Monash Medical Centre, Melbourne, Australia *Correspondence to: Burns Andrew, Cardiac Investigation Unit, St. Vincent’s Hospital, Fitzroy, Victoria, Australia. E-mail: [email protected] This article contains supplementary material available via the Inter- net at http://www.interscience.wiley.com/jpages/1522-1946/suppmat. Received 11 January 2007; Revision accepted 29 January 2007 DOI 10.1002/ccd.21144 Published online 9 April 2007 in Wiley InterScience (www. interscience.wiley.com). ' 2007 Wiley-Liss, Inc. Catheterization and Cardiovascular Interventions 70:379–382 (2007)

Upload: andrew-burns

Post on 06-Jun-2016

218 views

Category:

Documents


2 download

TRANSCRIPT

Page 1: Coronary stenting for coronary vasospasm refractory to medical therapy

Coronary Stenting for Coronary VasospasmRefractory to Medical Therapy

Andrew Burns,* MBBS (Hons), FRACP, Yuvaraj Malaiapan, MBBS, MRCPI, FRACP,and Ian Meredith, MBBS, PhD, FRACP

We describe the case of a 54-year-old male with recurrent chest pain, ST segment eleva-tion, and bradycardia. Coronary vasospasm was confirmed by acetylcholine challenge.After failing medical therapy, stenting of an extensive segment of the right coronary ar-tery has been clinically successful after 24-months follow-up. ' 2007 Wiley-Liss, Inc.

Key words: prinzmetal; angina; acetylcholine

INTRODUCTION

Therapy for coronary vasospasm, originally describedas Prinzmetal’s (or variant) angina [1], is primarilypharmacologic with calcium channel antagonists andnitrates used as first line agents [2]. For vasospasmrefractory to medical therapy, there have been a lim-ited number of case series of percutaneous interventionwith variable results [3,4]. Here we describe a case ofcoronary vasospasm refractory to medical therapy,which resolved with stenting of an extensive segmentof the right coronary artery.

CASE REPORT

A 54-year-old male of Indian background presentedwith chest pain and collapse at home. He had a 20pack-year history of smoking, hypercholesterolemia,asthma, and nasal polyposis. A nontoxic multinodulargoitre had been treated with radioactive iodine 13years previously and his thyroid function had been sta-ble on 100-mcg daily of thyroxine.The initial rhythm strip obtained by the ambulance

service demonstrated complete heart block with STelevation in lead II, however his ECG on arrival at EDwas unremarkable except for sinus bradycardia. Hedeveloped further chest pain in the emergency depart-ment associated with profound sinus bradycardia andhypotension requiring adrenaline infusion. RepeatECG (Fig. 1) revealed ST elevation inferiorly and hewas given loading doses of Aspirin (300 mg) andClopidogrel (600 mg), commenced on unfractionatedheparin intravenous infusion and transferred to thecardiac catheterization laboratory for emergent leftheart catheterization. He was found to have a severediscrete stenosis of the proximal right coronary artery(Fig. 2) which was stented with a 3.0 mm 3 20 mmTaxus stent (Fig. 3). A brief period of complete heart

block ensued which required temporary transvenouspacing. He made an uncomplicated recovery from thisand was discharged on standard medical therapy. Thetroponin I peak was 18.17 mcg/L and CK peaked at850 U/L.During the subsequent 4 months, he represented

with two further episodes of chest pain associated withcollapse and, on each occasion, he was noted to be hy-potensive and bradycardic requiring atropine whenparamedics attended. With each episode transient STsegment elevation and rise in serum troponin Iprompted repeat coronary angiography which revealedminimal neointimal proliferation within the stent andno new lesions elsewhere in the right coronary artery.A provocative test for coronary vasospasm was notperformed at this stage. Between episodes he had noexertional symptoms.A tentative clinical diagnosis of coronary vasospasm

was made and the patient was commenced on highdose calcium channel antagonist (Diltiazem 360 mg)and long acting nitrate (Isosorbide mononitrate 120 mg).After a fourth presentation with chest pain and pro-

found bradycardia, an acetylcholine challenge testwas undertaken as previously described [5,6] to es-tablish areas of the right coronary artery prone to

Monash Heart, Monash Medical Centre, Melbourne, Australia

*Correspondence to: Burns Andrew, Cardiac Investigation Unit, St.

Vincent’s Hospital, Fitzroy, Victoria, Australia.

E-mail: [email protected]

This article contains supplementary material available via the Inter-

net at http://www.interscience.wiley.com/jpages/1522-1946/suppmat.

Received 11 January 2007; Revision accepted 29 January 2007

DOI 10.1002/ccd.21144

Published online 9 April 2007 in Wiley InterScience (www.

interscience.wiley.com).

' 2007 Wiley-Liss, Inc.

Catheterization and Cardiovascular Interventions 70:379–382 (2007)

Page 2: Coronary stenting for coronary vasospasm refractory to medical therapy

spasm with a view to further percutaneous interven-tion. Bilateral femoral arterial access and prophylac-tic temporary femoral transvenous pacing were estab-lished. Continuous monitoring with 12 lead ECG andsimultaneous left ventricular and femoral arterialpressures were undertaken. The ostium of the rightcoronary artery was engaged with an AL2 guidingcatheter and a 0.014-in. balance guidewire waspassed to the distal vessel. Intravascular ultrasound(IVUS) pullback was performed from the distal rightcoronary artery which showed moderately severe pla-que in the mid to distal vessel. Normal saline (0.9%)was initially infused via an over-the-wire balloon

positioned just beyond the ostium of the vessel as acontrol infusion. Subsequently, two 50-mcg aliquotsof acetylcholine were then infused which resulted insevere multifocal spasm (Fig. 4 and Supplementarymovie). This was associated with significant inferiorST segment elevation and completely resolved withinfusion of 200 mcg of GTN. The areas of intensevasospasm correlated with the segments of plaquedemonstrated on IVUS.Given limited experience with extensive stent place-

ment for coronary vasospasm, we elected to continuemedical therapy and to implant a permanent pace-maker with a single ventricular lead. Despite this,

Fig. 1. Twelve lead ECG at initial presentation demonstrating first degree heart block and STsegment elevation in the inferior leads with reciprocal changes in precordial leads.

Fig. 2. Right coronary arteriogram (LAO 308 using AL2 cathe-ter) at first presentation demonstrating apparent severe proxi-mal stenosis (arrow).

Fig. 3. Right coronary arteriogram (LAO 308) at first presenta-tion after 3.0 mm 3 20 mm Taxus stent positioned withinlesion demonstrated in Fig. 2 (arrow). Temporary transvenouspacing in situ.

380 Burns et al.

Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).

Page 3: Coronary stenting for coronary vasospasm refractory to medical therapy

the patient represented on with further collapse andchest pain. Percutaneous intervention with overlappingTsunami stents (3.5 3 30 to mid RCA and 3.0 3 20to distal RCA) was undertaken to the area of severespasm previously demonstrated (Fig. 5). High dosecalcium channel antagonist (Diltiazem 360 mg) andnitrate (Isosorbide mononitrate 120 mg) were contin-

ued. After 24-months follow-up he has remainedasymptomatic.

DISCUSSION

This case illustrates the diagnostic and managementdilemma refractory vasospasm can pose. On initial pre-sentation, the patient was treated according to theguidelines for acute ST elevation myocardial infarctionwith an excellent final angiographic result. However,after subsequent presentations it became apparent thatcoronary vasospasm was the likely diagnosis. Whilethe diagnosis of coronary vasospasm is largely clinical,provocative testing with acetylcholine or ergonovineduring angiography are well described. In this case, anacetylcholine challenge was undertaken in an attemptto guide therapy and revealed a long segment of severespasm.The pathogenesis of coronary vasospasm is poorly

understood. There is evidence for local endothelialdysfunction with increased endothelin activity [7]and decreased flow-dependent coronary vasodilationdue to reduced nitric oxide activity [5]. A more dif-fuse disorder of coronary vasomotility has also beenproposed based on the finding of hyperreactiveresponses to both acetylcholine and nitroglycerinthroughout the coronary arteries of patients with vas-ospsasm [8]. Autonomic nervous system dysfunctionis also implicated by the reproduction of spasm byacetylcholine and the efficacy of sympathetic dener-vation [9].Initial experience with angioplasty alone for refrac-

tory vasospasm was disappointing [10], however in thestenting era, the series of Gaspardone et al. [3] andKhatri et al. [4] and other case reports have shownpromising results in focal vasospasm. In this case, wereport the successful treatment of multifocal coronaryvasospasm with a total of stent length of 70 mm.

REFERENCES

1. Prinzmetal M, Kennamer R, Merliss R. Angina pectoris. I. A

variant form of angina pectoris; preliminary report. Am J Med

1959;27:375.

2. Feldman RL. A review of medical therapy for coronary artery

spasm. Circulation 1987;75(6, Part 2):V96–V102.

3. Gaspardone A, Tomai F, Versaci F, Ghini AS, Polisca P, Crea

F, Chiariello L, Gioffre PA. Coronary artery stent placement in

patients with variant angina refractory to medical treatment. Am

J Cardiol 1999;84:96–98, A8.

4. Khatri S, Webb JG, Carere RG, Dodek A. Stenting for coronary

artery spasm. Catheter Cardiovasc Interv 2002;56:16–20.

5. Kugiyama K, Yasue H, Okumura K, Ogawa H, Fujimoto K,

Nakao K, Yoshimura M, Motoyama T, Inobe Y, Kawano H.

Nitric oxide activity is deficient in spasm arteries of patients

with coronary spastic angina. Circulation 1996;94:266–271.

Fig. 4. Severe distal right coronary spasm (arrow) after infu-sion of 50 mcg acetylcholine into right coronary artery afterfourth presentation with collapse and ST segment elevation.Temporary transvenous pacing in situ.

Fig. 5. Post stenting (Tsunami stents: 3.5 3 30 to mid vesseland 3.0 3 20 to distal RCa, arrows) of most severe segment ofspasm demonstrated on prior acetylcholine challenge (Fig. 4).

Coronary Stenting for Refractory Vasospasm 381

Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).

Page 4: Coronary stenting for coronary vasospasm refractory to medical therapy

6. Quyyumi AA, Mulcahy D, Andrews NP, Husain S, Panza JA,

Cannon RO III. Coronary vascular nitric oxide activity in hyper-

tension and hypercholesterolemia. Comparison of acetylcholine

and substance P. Circulation 1997;95:104–110.

7. Cox ID, Botker HE, Bagger JP, Sonne HS, Kristensen BO, Kaski

JC. Elevated endothelin concentrations are associated with reduced

coronary vasomotor responses in patients with chest pain and nor-

mal coronary arteriograms. J Am Coll Cardiol 1999; 34:455–460.

8. Okumura K, Yasue H, Matsuyama K, Ogawa H, Kugiyama K,

Ishizaka H, Sumida H, Fujii H, Matsunaga T, Tsunoda R. Dif-

fuse disorder of coronary artery vasomotility in patients with

coronary spastic angina. Hyperreactivity to the constrictor effects

of acetylcholine and the dilator effects of nitroglycerin. J Am Coll

Cardiol 1996;27:45–52.

9. Bertrand ME, Lablanche JM, Tilmant PY, Ducloux G, Ware-

mbourg H Jr, Soots G. Complete denervation of the heart (auto-

transplantation) for treatment of severe, refractory coronary

spasm. Am J Cardiol 1981;47:1375–1378.

10. Corcos T, David PR, Bourassa MG, Val PG, Robert J, Mata

LA, Waters DD. Percutaneous transluminal coronary angioplasty

for the treatment of variant angina. J Am Coll Cardiol 1985;5:

1046–1054.

382 Burns et al.

Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).