Logo of thij
Tex Heart Inst J. 2005; 32(1): 78–80.

Cardiogenic Shock Caused by Severe Coronary Artery Spasm Immediately after Coronary Stenting

Aaron Wong, MBBS, Alfred Cheng, MD, Charles Chan, MB, ChB, and Yean-Leng Lim, MBBS, PhD

Department of Cardiology (Drs. Chan, Lim, and Wong), National Heart Centre, Singapore; Department of Cardiology (Dr. Cheng), Tan Tock Seng Hospital, Singapore

Abstract

Coronary artery spasm is common during percutaneous coronary intervention and is easily relieved by intracoronary administration of vasodilators. We report the case of a patient who had severe, protracted, generalized spasm of the entire left coronary artery system during coronary artery stenting. The spasm, which was unresponsive to intracoronary vasodilators administered via guiding catheter, resulted in pulmonary edema and cardiogenic shock. Local injection of nitroglycerin via a transit catheter in the coronary artery eventually resolved the spasm and reversed the cardiogenic shock. To our knowledge, this is the 1st report of such a case in the English-language medical literature.

Key words: Angina pectoris/etiology, angioplasty, percutaneous coronary/adverse effects, cardiogenic shock, coronary vasospasm, coronary stenting, heart catheterization/adverse effects, nitroglycerin/therapeutic use, vasoconstriction

Due to mechanical stimuli, coronary vasospasm in the treated vessel is a common occurrence during percutaneous coronary intervention (PCI), especially after balloon dilation or coronary stent deployment.1 The administration of intracoronary vasodilators in this situation is usually sufficient to relieve the spasm. We report the case of a patient in whom intense coronary spasm of both the left anterior descending coronary artery (LAD) and the circumflex artery (LCX) occurred during coronary artery stenting of the LAD. The spasm was unresponsive to conventional therapy and resulted in cardiogenic shock.

Case Report

In September 2001, a 67-year-old woman with cardiovascular risk factors of hypertension and hyperlipidemia was admitted to Tan Tock Seng Hospital, Singapore, for symptoms of unstable angina. Electrocardiography (ECG) on admission showed widespread T wave inversion in the anterior and lateral leads. She also had hyperthyroidism and was taking carbimazole. The angina subsided after the administration of intravenous nitrates and heparin, with no elevation of creatinine kinase (CK) or troponin T. Two days later, coronary angiography showed single-vessel disease with 100% occlusion of the mid LAD.

Percutaneous coronary intervention was performed 4 days later, and initial coronary angiography showed a recanalized LAD with an 80% residual diameter stenosis (Fig. 1). The lesion was pre-dilated with a 2.5 x 15-mm balloon catheter, followed by deployment of a 3.0 x 18-mm Bx Velocity[TM] coronary artery stent (Cordis Corporation, a Johnson & Johnson company; Miami Lakes, Fla) in the mid LAD. Selective angiography after stenting showed severe spasm of the entire LAD (including the diagonal branches) and the left circumflex artery (LCx), with almost complete obliteration of the vessel lumens (Fig. 2). The patient experienced severe chest pain, which correlated with ST elevation in the inferior and anterior ECG leads. Her blood pressure fell to 70/50 mmHg. Despite the administration of intracoronary nitrates and verapamil, and re-dilation of the LAD with the balloon catheter, there was no improvement in the blood pressure or coronary spasm. The patient developed frank pulmonary edema and required mechanical ventilation, inotropic support, and intra-aortic balloon pump (IABP) support. The spasm of the LAD and LCx was eventually relieved with local delivery of nitrates, via a Rapid Transit[TM] catheter (Cordis Corporation) positioned in the distal LAD (Fig. 3).

The patient experienced 2 more episodes of chest pain while she was recovering in the coronary care unit; these episodes were associated with gross ST segment elevation in the inferior and posterior ECG leads (Fig. 4). The ECG changes and symptoms resolved promptly with the administration of intravenous nitrates. The patient was started on a long-term oral calcium channel blocker. The CK-MB and troponin T levels were mildly elevated after the procedure.

Seven days after coronary angioplasty, the patient was well and was discharged from the hospital. When last seen in June 2004, she had experienced no recurrence of symptoms, and the left ventricular ejection fraction was normal on echocardiography.

Discussion

Coronary artery spasm is the cause of variant angina, which generally occurs when a patient is at rest; it is usually transient.2 Coronary artery spasm has also been suggested as a cause of typical angina pectoris, myocardial infarction, malignant arrhythmias, sudden death, and even cardiac rupture.3,4 It has been postulated that a sudden, intense, localized contraction of smooth muscle cells around a vulnerable plaque in patients with atherosclerosis can cause the plaque to rupture, and thus lead to platelet aggregation and thrombus formation. Acute myocardial infarction associated with coronary artery spasm, with or without underlying coronary artery disease, has been widely reported in the medical literature.5 --7

The occurrence of spasm in multiple coronary arteries during angiography is rarely reported. Maseri's group8 and Bell and colleagues9 reported a total of 4 cases of simultaneous spasm of multiple coronary arteries. The occurrence of stunned myocardium after simultaneous spasm of multiple coronary arteries has also been reported, with symptoms of mild heart failure and reversible regional wall motion abnormalities of the left ventricle as shown on echocardiography.10 Coronary spasms in these case reports were transient and had no notable consequences. However, occasionally, coronary artery spasm can be persistent and refractory to conventional treatment, and may require PCI or even coronary artery bypass grafting.

To our knowledge, severe coronary spasm causing pulmonary edema and cardiogenic shock has not been reported in the English-language medical literature. The spasm in the left coronary arterial system in our patient was unusual because it was generalized (involving the whole length of both arteries, including the branches), intense (causing almost complete obliteration of the vessel lumen), and protracted (unrelieved with intracoronary vasodilators). The territory involved in the spasm was equivalent to acute left main occlusion. Consequently, the patient developed pulmonary edema and cardiogenic shock that required mechanical ventilation, inotropic support, and IABP support. Whether the right coronary artery was also involved during the generalized spasm is unknown. The LCx in our patient was a large and dominant artery, and could account for the ST segment elevation in the inferior ECG leads.

Various factors have been associated with coronary spasm, including vigorous exercise, coronary ectasia, and endothelial nitric oxide synthase (eNOS) gene polymorphisms, as well as smoking and the use of alcohol and cocaine. Although thyrotoxicosis has been associated with coronary spasm,11 the results of a thyroid function test in our patient were within normal limits. We postulate that our patient was hypersensitive to smooth muscle cell constrictor stimuli, and therefore extremely prone to coronary spasm.12 This tendency was evidenced by the occurrence of spasm after the initial balloon dilation and by the development of several episodes of chest pain while the patient was in the ward after the procedure. These signs and symptoms were associated with gross ST-segment elevation on ECG, and were relieved by nitroglycerin administration. The deployment of a slightly oversized stent in our patient could also have triggered the generalized spasm.

Intracoronary administration of vasodilators through a guiding catheter was ineffective in our patient, because reduced blood flow prevented the drugs from reaching the site of the spasm. Local intracoronary administration of vasodilators through the Rapid Transit catheter minimized the systemic effects of the drugs and ensured their delivery distally, which proved to be effective in our patient. This technique of local administration of vasodilators should be attempted for relief of coronary artery spasm in patients who are unresponsive to conventional therapy.7

Conclusion

Coronary artery spasm is common during PCI procedures; however, severe, generalized, prolonged spasm in 2 major coronary arteries during coronary artery stenting, with resultant cardiogenic shock, has not been previously reported. Distal local intracoronary administration of vasodilators via the Rapid Transit catheter was successful in relieving the spasm in our patient and may be useful for other patients in a similar situation.

Footnotes

Address for reprints: Aaron Wong, MBBS, Department of Cardiology, National Heart Center, 17 Third Hospital Avenue, Singapore 168752. E-mail: http://www.central.gov/redirect3.cgi?&&reftype=extlink&artid=555830&iid=18544&jid=92&&Aaron_WONG@nhc.com.sg

Dr. Lim is now at the Centre for Cardiovascular Therapeutics, Victoria, Australia, and Dr. Cheng is at Mount Elizabeth Medical Centre, Singapore.

References
1.
Fischell T. Coronary artery spasm after percutaneous transluminal coronary angioplasty: pathophysiology and clinical consequences. Cathet Cardiovasc Diagn 1990;19:1 --3.
2.
Prinzmetal M, Kennamer R, Merliss R, Wada T, Bor N. Angina pectoris. I. A variant form of angina pectoris; preliminary report. Am J Med 1959;27:375 --88.
3.
Hillis LD, Braunwald E. Coronary-artery spasm. N Engl J Med 1978;299:695 --702.
4.
Maseri A, L'Abbate A, Baroldi G, Chierchia S, Marzilli M, Ballestra AM, et al. Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of "preinfarction" angina. N Engl J Med 1987;299: 1271 --7.
5.
Vincent GM, Anderson JL, Marshall HW. Coronary spasm producing coronary thrombosis and myocardial infarction. N Engl J Med 1983;309:220 --3.
6.
Lip GY, Ray KK, Shiu MF. Coronary spasm in acute myocardial infarction. Heart 1998;80:197 --9.  
7.
Rashid H, Marshall RJ, Diver DJ, Breall JA. Spontaneous and diffuse coronary artery spasm unresponsive to conventional intracoronary pharmacological therapy: a case report. Catheter Cardiovasc Interv 2000;49:188 --91.  .
8.
Maseri A, Pesola A, Marzilli M, Severi S, Parodi O, L'Abbate A, et al. Coronary vasospasm in angina pectoris. Lancet 1977;1:713 --7.
9.
Bell MR, Lapeyre AC 3rd, Bove AA. Angiographic demonstration of spontaneous diffuse three vessel coronary artery spasm. J Am Coll Cardiol 1989;14:523 --7.
10.
Fournier C, Boujon B, Herbert JL, Zamani K, Grimon G, Blondeau M. Stunned myocardium following coronary spasm [published erratum appears in Am Heart J 1991;122: 1796]. Am Heart J 1991;121(2 Pt 1):593 --5.
11.
Nakano T, Konishi T, Takezawa H. Vasospastic angina in thyrotoxicosis ---case reports. Angiology 1987;38:717 --22.
12.
Maseri A, Davies G, Hackett D, Kaski JC. Coronary artery spasm and vasoconstriction. The case for a distinction. Circulation 1990;81:1983 --91.
Figures and Tables
Fig. 1 Before coronary intervention, a coronary angiogram of the left coronary artery (right anterior oblique caudal projection) shows a recanalized mid LAD with significant residual stenosis.
Fig. 2 After stenting, coronary angiography shows generalized, severe spasm of the whole left coronary system except for the stented segment in the anteroposterior caudal projection.
Fig. 3 The final angiographic results are shown after administration of nitroglycerin through the Rapid Transit[TM] catheter positioned in the distal left anterior descending coronary artery.
Fig. 4 While the patient is at rest and experiencing chest pain, electrocardiography shows ST elevation and ST depression in the inferior and anterior leads, respectively, and 1st-degree heart block.