IMAGING IN CARDIOLOGY
Coronary artery spasm: a rare cause of syncope
M.E.W. Hemels, A.C.P. Wiesfeld, F. van den Berg, F. Zijistra, I.C. van Gelder
A
B
.H,^~~~tl-
53-year-old man with no history of (non)cardiac disease and a nonsmoker was admitted to the hospital because of syncope. Sitting in a chair, he had experienced crushing chest pain without palpitations followed by a short loss of consciousness. Thereafter, he had no symptoms at all. The patient was not taking any medication. He had previously experienced chest pain sporadically, which was not related to exercise or cold. Physical examination was within normal limits. Serial electrocardiograms and determination of the cardiac enzymes showed no abnormalities. During ambulatory monitoring neither arrhythmias nor conduction disturbances, ST-segment /T-wave abnormal-
A
Corespondence to: A.C.P. Wiesfeld University Hospital Groningen, Thoraxcenter, Department of Cardiology, P0 Box 30.001, 9700 RB Groningen E-mail: [email protected]
Netherlands Heart Journal, Volume 13, Number 1, January 2005
Figure 1. Twelve-lead electrocardiogram bef-ore and during intravenous isoprenaline. A. Before isoprenaline: sinus rbythm with slight STdeviation in the infmrolateral leads II, III, aVF, Vs and V6 (paper speed I cm=400 ms, 1 cm=l mV). B. During isoprenaline: atrial fibrillation with ST elevation in II, III, aVF and V, and ST depression in I and aVL (paper speed 1 cm=n400ns, I cm=l mV).
ities or a prolonged QT time were observed. During exercise testing at a maximum heart rate of 170 beats/min, maximum blood pressure of 230/90 mmHg and maximum workload of220 Watts, 2 mm ST-segment depression with QT prolongation (until 260 ms) but normally corrected QT 436 ms was observed in leads II, III, aVF, V5 and V6 without any chest pain. Coronary angiography showed no signs of coronary artery disease. Electrophysiological investigation revealed normal conduction and sinus node recovery times. The anterograde Wenckebach point was 360 ms. Neither an atrioventricular reentrant tachycardia nor concealed bypass tract were present. Stimulation in the right ventricular apex during sinus rhythm and basic pacing cycle lengths of 600, 500 and 430 ms with a maximum of two extrasystoles induced no ventricular arrhythmias. Thereafter, isoprenaline (aiming at a heart rate of 110 beats/min) was given intravenously to repeat the stimulation protocol during 21
IMAGING IN CARDIOLOGY
adrenergic stimulation. During infusion the patient reported crushing chest pain. At that moment atrial fibrillation also started. The 12-lead electrocardiogram had changed: ST elevation occurred in II, III and aVF and ST depression in I and aVL, compatible with acute transmural ischaemia in the inferior wall (figure 1B). Isoprenaline was stopped and nitroglycerin was given intravenously, resulting in complete resolution ofthe electrocardiographic abnormalities, suggesting spasm in the proximal right coronary artery. Sinus rhythm restored spontaneously after normalisation of the ST segments. The syncope in our patient may be explained by spasm in the proximal right coronary artery in combination with AF. Bradyarrhythmias or tachyarrhythmias and even sudden death may follow syncope during coronary artery spasm. In our patient several explanations are possible for the occurrence of syncope: a. Ischaemia-induced atrial fibrillation with a rapid ventricular response, resulting in a sudden drop of blood pressure; b. Atrial fibrillation with rapid ventricular response may have aggravated ischaemia and subsequently induced an atrioventricular block; c. Ventricular tachyarrhythmias induced by coronary artery spasm. In patients who experience chest pain during syncope, coronary artery disease should be definitely excluded.' In case ofnormal coronary arteries a spasm provocation test may be warranted. This may include ergonovine or acetylcholine provocation. A provocation test was not considered in the present patient, because we already knew that the coronary anatomy was normal
22
and the electrocardiographic abnormalities during intravenous isoprenaline were typical for transmural ischaemia, hence, could only be explained by spasm. A spasm provocation test would not give any additional clinical significant information. In patients with coronary artery spasm who are treated with calcium antagonists and nitrates, severe complications, such as sudden death or myocardial infarction, are rare.2'3 Also our patient was treated with these drugs, as well as a statin. During six months of follow-up no syncope reoccurred. u References 1
2
3
Guidelines on management (diagnosis and treatment) ofsyncope. Task force on syncope, European Society of Cardiology: Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen PE, et al. EurHeartJ2001;22:1256-306. Freedman SB, Richmond DR, Kelly DT. Long-term follow-up of verapamil and nitrate treatment for coronary artery spasm. Am J Cardiol 1982;50:711-5. Bott-Silverman C, Heupler FA Jr. Natural history of pure coronary artery spasm in patients treated medically. JAm Coll Cardiol 1983;2:200-5.
In this section a remarkable 'image' is presented and a short comment is given. We invite you to send in images (in triplicate) with a short comment (one to two pages at the most) to Mediselect bv, Editorial Office Netherlands Heart Journal, PO Box 63, 3830 AB Leusden, the Netherlands. This section is edited by M.J.M. Cramer.
Netherlands Heart Joumal, Volume 13, Number 1, January 2005
Coronary artery spasm: a rare cause of syncope
M.E.W. Hemels, A.C.P. Wiesfeld, F. van den Berg, F. Zijistra, I.C. van Gelder
A
B
.H,^~~~tl-
53-year-old man with no history of (non)cardiac disease and a nonsmoker was admitted to the hospital because of syncope. Sitting in a chair, he had experienced crushing chest pain without palpitations followed by a short loss of consciousness. Thereafter, he had no symptoms at all. The patient was not taking any medication. He had previously experienced chest pain sporadically, which was not related to exercise or cold. Physical examination was within normal limits. Serial electrocardiograms and determination of the cardiac enzymes showed no abnormalities. During ambulatory monitoring neither arrhythmias nor conduction disturbances, ST-segment /T-wave abnormal-
A
Corespondence to: A.C.P. Wiesfeld University Hospital Groningen, Thoraxcenter, Department of Cardiology, P0 Box 30.001, 9700 RB Groningen E-mail: [email protected]
Netherlands Heart Journal, Volume 13, Number 1, January 2005
Figure 1. Twelve-lead electrocardiogram bef-ore and during intravenous isoprenaline. A. Before isoprenaline: sinus rbythm with slight STdeviation in the infmrolateral leads II, III, aVF, Vs and V6 (paper speed I cm=400 ms, 1 cm=l mV). B. During isoprenaline: atrial fibrillation with ST elevation in II, III, aVF and V, and ST depression in I and aVL (paper speed 1 cm=n400ns, I cm=l mV).
ities or a prolonged QT time were observed. During exercise testing at a maximum heart rate of 170 beats/min, maximum blood pressure of 230/90 mmHg and maximum workload of220 Watts, 2 mm ST-segment depression with QT prolongation (until 260 ms) but normally corrected QT 436 ms was observed in leads II, III, aVF, V5 and V6 without any chest pain. Coronary angiography showed no signs of coronary artery disease. Electrophysiological investigation revealed normal conduction and sinus node recovery times. The anterograde Wenckebach point was 360 ms. Neither an atrioventricular reentrant tachycardia nor concealed bypass tract were present. Stimulation in the right ventricular apex during sinus rhythm and basic pacing cycle lengths of 600, 500 and 430 ms with a maximum of two extrasystoles induced no ventricular arrhythmias. Thereafter, isoprenaline (aiming at a heart rate of 110 beats/min) was given intravenously to repeat the stimulation protocol during 21
IMAGING IN CARDIOLOGY
adrenergic stimulation. During infusion the patient reported crushing chest pain. At that moment atrial fibrillation also started. The 12-lead electrocardiogram had changed: ST elevation occurred in II, III and aVF and ST depression in I and aVL, compatible with acute transmural ischaemia in the inferior wall (figure 1B). Isoprenaline was stopped and nitroglycerin was given intravenously, resulting in complete resolution ofthe electrocardiographic abnormalities, suggesting spasm in the proximal right coronary artery. Sinus rhythm restored spontaneously after normalisation of the ST segments. The syncope in our patient may be explained by spasm in the proximal right coronary artery in combination with AF. Bradyarrhythmias or tachyarrhythmias and even sudden death may follow syncope during coronary artery spasm. In our patient several explanations are possible for the occurrence of syncope: a. Ischaemia-induced atrial fibrillation with a rapid ventricular response, resulting in a sudden drop of blood pressure; b. Atrial fibrillation with rapid ventricular response may have aggravated ischaemia and subsequently induced an atrioventricular block; c. Ventricular tachyarrhythmias induced by coronary artery spasm. In patients who experience chest pain during syncope, coronary artery disease should be definitely excluded.' In case ofnormal coronary arteries a spasm provocation test may be warranted. This may include ergonovine or acetylcholine provocation. A provocation test was not considered in the present patient, because we already knew that the coronary anatomy was normal
22
and the electrocardiographic abnormalities during intravenous isoprenaline were typical for transmural ischaemia, hence, could only be explained by spasm. A spasm provocation test would not give any additional clinical significant information. In patients with coronary artery spasm who are treated with calcium antagonists and nitrates, severe complications, such as sudden death or myocardial infarction, are rare.2'3 Also our patient was treated with these drugs, as well as a statin. During six months of follow-up no syncope reoccurred. u References 1
2
3
Guidelines on management (diagnosis and treatment) ofsyncope. Task force on syncope, European Society of Cardiology: Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen PE, et al. EurHeartJ2001;22:1256-306. Freedman SB, Richmond DR, Kelly DT. Long-term follow-up of verapamil and nitrate treatment for coronary artery spasm. Am J Cardiol 1982;50:711-5. Bott-Silverman C, Heupler FA Jr. Natural history of pure coronary artery spasm in patients treated medically. JAm Coll Cardiol 1983;2:200-5.
In this section a remarkable 'image' is presented and a short comment is given. We invite you to send in images (in triplicate) with a short comment (one to two pages at the most) to Mediselect bv, Editorial Office Netherlands Heart Journal, PO Box 63, 3830 AB Leusden, the Netherlands. This section is edited by M.J.M. Cramer.
Netherlands Heart Joumal, Volume 13, Number 1, January 2005
