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Left main and saphenous vein graft spasm: an unusual association
International Journal of Cardiology 99 (2005) 133 – 134 www.elsevier.com/locate/ijcard
Letter to the Editor
Left main and saphenous vein graft spasm: an unusual association Italo Porto *, Francesco Burzotta, Rocco Mongiardo, Filippo Crea Istituto di Cardiologia, Dipartimento di Medicina Cardiovascolare, Universita` Cattolica del Sacro Cuore, Largo F. Vito, 8, 00168 Roma, Italy Received 10 August 2003; accepted 26 October 2003 Available online 4 July 2004
Abstract We present a case of left main spasm which was associated with spasm of a saphenous vein graft. This case emphasizes the importance of excluding an excessive vasoconstrictory response in patients treated with percutaneous coronary interventions. D 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Coronary artery spasms; Saphenous vein graft; Angina
Coronary artery spasm is an infrequent but important cause of unstable angina [1]. Its incidence among patients undergoing diagnostic coronary angiography for suspected ischaemic syndromes is about 3– 4% [2]. Spasm of left main stem (LMS) is very rare and may represent a serious pitfall for the interventional cardiologist [3]. We report on unusual association of LMS spasm and vein graft spasm. A 60-year-old man with a history of hypercholesterolemia, hypertension and smoking habit presented to our department with a history of anginal chest pain at rest during the last 2 weeks. After hospitalization, he exhibited two prolonged episodes of chest pain associated to mild transient ST segment depression in the anterior leads and slight elevation of cardiac enzymes. Diagnostic coronary angiography showed a long severe stenosis of LMS, involving the left anterior descending artery (LAD) ostium, an ectatic proximal LAD, a critical stenosis of the first obtuse marginal branch (OM1) and of the proximal right coronary artery (RCA). Nitrates were not injected in the LMS, as arterial pressure was low and the patient was already on i.v. nitrates. Thus, he underwent surgical revascularization: the left internal mammary artery (LIMA) was anastomized to mid LAD and two saphenous vein grafts (SVGs) were anastomized to mid RCA and OM1. The patient was discharged without complications and remained symptom free for 3 months on medical therapy with beta blockers, aspirin and statin. An exercise treadmill
* Corresponding author. E-mail address: [email protected] (I. Porto). 0167-5273/$ - see front matter D 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2003.10.061
test one month after surgery was negative for inducible myocardial ischemia. At three months, the patient was admitted after a prolonged episode of severe rest angina. ECG was unremarkable, but a slight Troponin I elevation was noted. He was treated with i.v. nitrates, beta blockers, aspirin and ticlopidine. Repeated coronary angiography showed a small diameter LIMA with impaired anterograde flow (TIMI 1), and a patent SVG to OM1. LMS was unchanged (Fig. 1). How-
Fig. 1. Coronary angiography in LAO caudal view, showing long severe stenosis in the LMS, involving the LAD ostium, an ectatic proximal LAD, and a critical stenosis of proximal OM1.
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Fig 2. Coronary angiography in LAO caudal view, showing a marked reduction in severity of the LMS stenosis, with persistence of an intermediate stenosis in the ostial LAD and a general vasodilation of the left coronary system.
ever, an occlusive, diffuse spasm of the SVG to RCA was noted, associated with chest pain and ST segment depression. Spasm was resistant to intracoronay nitrates administration and partially responded to high dose diltiazem (not shown). Injection of contrast medium into LMS had confirmed the presence of a long, severe stenosis. However, the intracoronary injection of nitrates and diltiazem resulted in a striking reduction of LMS stenosis severity, to as low as 30 –40% (Fig. 2). No coronary intervention was performed on the LMS. The patient was started on 360 mg daily of oral dialtiazem in addition to aspirin and statin. At six-month follow up, the patient was pain free and a treadmill test was negative at high workload. This case highlights the relevance of coronary spasm in the management of acute coronary syndromes [1]. Indeed, the first clinical presentation of this patient (episodes of severe prolonged chest pain promptly resolved by sublingual nitrates) was probably caused by spasm at the site of a subcritical LMS stenosis. In the angiographic evaluation of patients with LMS narrowing, nitrates are often not administered, due to the rare
occurrence of a spontaneous vasospasm of the left main stem, to the low likelihood of catheter induced left main spasm, and to the possible detrimental lowering of the systemic arterial pressure. Indeed, there are only sporadic reports of spontaneous or catheter induced LMS spasm [3,4]. Yet, as shown by this case, nitrate administration may unmask the dynamic nature of an apparently fixed stenosis. Of note, i.v. nitrates may be insufficient to completely resolve coronary spasm superimposed to a subcritical stenosis, thus leading to questionable therapeutic choices. Another intriguing feature of this case is spasm at the site of a vein graft a few months after surgery. This is, again, a rather infrequent event [5,6], probably because patients with vasospastic angina do not usually undergo coronary bypass surgery. Furthermore, early after surgery, smooth muscle cells layer in venous grafts is rather thin. The causes of smooth muscle cells hyperreactivity responsible for coronary spasm in men are still largely speculative [1]. Coronary spasm is associated with a high prevalence of migraine and Raynaud’s phenomenon [1], thus supporting the idea that SMC hyperreactivity is not limited to coronary circulation. This case suggests that SMC hyperreactivity may also be present in venous segments, although its clinical relevance remains to be established.
References [1] Maseri A. Ischemic Heart Disease. New York: Churchill Livingstone; 1995. [2] Paraham WA, Kern MJ. The disappearing coronary stenosis: reemphasizing the importance of excluding coronary vasospasm before coronary intervention. Catheter Cardiovasc Interv 2002;11:224 – 8. [3] Jain D, Kurowski V, Reppel M, Katus HA, Richardt G. Severe, resistant spasm of the left main coronary artery—a serious pitfall. J Invasive Cardiol 2000;12:327 – 9. [4] Persin GA, Matthai Jr WH. Catheter-induced spasm of the left main coronary artery. J Invasive Cardiol 2000;12:158 – 61. [5] Kafka H, FitzGibbon GM, Leach AJ. Aortocoronary vein graft spasm during angiography. Can J Cardiol 1995;11:211 – 6. [6] Webb JG, Aldridge HE, Fulop J, Haq A. Aortocoronary saphenous vein graft spasm inducing ventricular fibrillation. Am Heart J 1989; 117:485 – 6.
Letter to the Editor
Left main and saphenous vein graft spasm: an unusual association Italo Porto *, Francesco Burzotta, Rocco Mongiardo, Filippo Crea Istituto di Cardiologia, Dipartimento di Medicina Cardiovascolare, Universita` Cattolica del Sacro Cuore, Largo F. Vito, 8, 00168 Roma, Italy Received 10 August 2003; accepted 26 October 2003 Available online 4 July 2004
Abstract We present a case of left main spasm which was associated with spasm of a saphenous vein graft. This case emphasizes the importance of excluding an excessive vasoconstrictory response in patients treated with percutaneous coronary interventions. D 2004 Elsevier Ireland Ltd. All rights reserved. Keywords: Coronary artery spasms; Saphenous vein graft; Angina
Coronary artery spasm is an infrequent but important cause of unstable angina [1]. Its incidence among patients undergoing diagnostic coronary angiography for suspected ischaemic syndromes is about 3– 4% [2]. Spasm of left main stem (LMS) is very rare and may represent a serious pitfall for the interventional cardiologist [3]. We report on unusual association of LMS spasm and vein graft spasm. A 60-year-old man with a history of hypercholesterolemia, hypertension and smoking habit presented to our department with a history of anginal chest pain at rest during the last 2 weeks. After hospitalization, he exhibited two prolonged episodes of chest pain associated to mild transient ST segment depression in the anterior leads and slight elevation of cardiac enzymes. Diagnostic coronary angiography showed a long severe stenosis of LMS, involving the left anterior descending artery (LAD) ostium, an ectatic proximal LAD, a critical stenosis of the first obtuse marginal branch (OM1) and of the proximal right coronary artery (RCA). Nitrates were not injected in the LMS, as arterial pressure was low and the patient was already on i.v. nitrates. Thus, he underwent surgical revascularization: the left internal mammary artery (LIMA) was anastomized to mid LAD and two saphenous vein grafts (SVGs) were anastomized to mid RCA and OM1. The patient was discharged without complications and remained symptom free for 3 months on medical therapy with beta blockers, aspirin and statin. An exercise treadmill
* Corresponding author. E-mail address: [email protected] (I. Porto). 0167-5273/$ - see front matter D 2004 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2003.10.061
test one month after surgery was negative for inducible myocardial ischemia. At three months, the patient was admitted after a prolonged episode of severe rest angina. ECG was unremarkable, but a slight Troponin I elevation was noted. He was treated with i.v. nitrates, beta blockers, aspirin and ticlopidine. Repeated coronary angiography showed a small diameter LIMA with impaired anterograde flow (TIMI 1), and a patent SVG to OM1. LMS was unchanged (Fig. 1). How-
Fig. 1. Coronary angiography in LAO caudal view, showing long severe stenosis in the LMS, involving the LAD ostium, an ectatic proximal LAD, and a critical stenosis of proximal OM1.
134
I. Porto et al. / International Journal of Cardiology 99 (2005) 133–134
Fig 2. Coronary angiography in LAO caudal view, showing a marked reduction in severity of the LMS stenosis, with persistence of an intermediate stenosis in the ostial LAD and a general vasodilation of the left coronary system.
ever, an occlusive, diffuse spasm of the SVG to RCA was noted, associated with chest pain and ST segment depression. Spasm was resistant to intracoronay nitrates administration and partially responded to high dose diltiazem (not shown). Injection of contrast medium into LMS had confirmed the presence of a long, severe stenosis. However, the intracoronary injection of nitrates and diltiazem resulted in a striking reduction of LMS stenosis severity, to as low as 30 –40% (Fig. 2). No coronary intervention was performed on the LMS. The patient was started on 360 mg daily of oral dialtiazem in addition to aspirin and statin. At six-month follow up, the patient was pain free and a treadmill test was negative at high workload. This case highlights the relevance of coronary spasm in the management of acute coronary syndromes [1]. Indeed, the first clinical presentation of this patient (episodes of severe prolonged chest pain promptly resolved by sublingual nitrates) was probably caused by spasm at the site of a subcritical LMS stenosis. In the angiographic evaluation of patients with LMS narrowing, nitrates are often not administered, due to the rare
occurrence of a spontaneous vasospasm of the left main stem, to the low likelihood of catheter induced left main spasm, and to the possible detrimental lowering of the systemic arterial pressure. Indeed, there are only sporadic reports of spontaneous or catheter induced LMS spasm [3,4]. Yet, as shown by this case, nitrate administration may unmask the dynamic nature of an apparently fixed stenosis. Of note, i.v. nitrates may be insufficient to completely resolve coronary spasm superimposed to a subcritical stenosis, thus leading to questionable therapeutic choices. Another intriguing feature of this case is spasm at the site of a vein graft a few months after surgery. This is, again, a rather infrequent event [5,6], probably because patients with vasospastic angina do not usually undergo coronary bypass surgery. Furthermore, early after surgery, smooth muscle cells layer in venous grafts is rather thin. The causes of smooth muscle cells hyperreactivity responsible for coronary spasm in men are still largely speculative [1]. Coronary spasm is associated with a high prevalence of migraine and Raynaud’s phenomenon [1], thus supporting the idea that SMC hyperreactivity is not limited to coronary circulation. This case suggests that SMC hyperreactivity may also be present in venous segments, although its clinical relevance remains to be established.
References [1] Maseri A. Ischemic Heart Disease. New York: Churchill Livingstone; 1995. [2] Paraham WA, Kern MJ. The disappearing coronary stenosis: reemphasizing the importance of excluding coronary vasospasm before coronary intervention. Catheter Cardiovasc Interv 2002;11:224 – 8. [3] Jain D, Kurowski V, Reppel M, Katus HA, Richardt G. Severe, resistant spasm of the left main coronary artery—a serious pitfall. J Invasive Cardiol 2000;12:327 – 9. [4] Persin GA, Matthai Jr WH. Catheter-induced spasm of the left main coronary artery. J Invasive Cardiol 2000;12:158 – 61. [5] Kafka H, FitzGibbon GM, Leach AJ. Aortocoronary vein graft spasm during angiography. Can J Cardiol 1995;11:211 – 6. [6] Webb JG, Aldridge HE, Fulop J, Haq A. Aortocoronary saphenous vein graft spasm inducing ventricular fibrillation. Am Heart J 1989; 117:485 – 6.