British Heart Journal, I975, 37, 77I-774.
Syncope in association with Prinzmetal variant angina Richard Harper, Thomas Peter, and David Hunt From the Cardiac Department, The Royal Melbourne Hospital, Victoria, Australia
A case of Prinzmetal variant angina with transient complete atrioventricular block and syncopal episodes following an anteroseptal myocardial infarction is described. The syncopal attacks were not prevented by demand cardiac pacing and were presumably caused by transient severe ischaemia of the left ventricle, with a consequent reduction in cardiac output. The left ventriculogram showed a large anterior dyskinetic area corresponding to the high grade proximal obstruction in the left anterior descending artery demonstrated by coronary angiography. All other coronary vessels appearedfree of disease and it is suggested that the anginal episodes were caused by transient proximal segmental spasm of the right coronary artery. The anginal episodes were successfully prevented by a regimen of two-hourly coronary arterial vasodilator therapy. In I959 Prinzmetal and co-workers (i959) described a variant form of angina in which the chest pain occurred at rest and was not related to physical exertion or emotion. The characteristic feature of this syndrome is the occurrence of an electrocardiographic current of injury pattern during chest pain rather than ST segment depression which is the usual pattern of classical angina. Prinzmetal's variant angina also differs from classical effortinduced angina in that haemodynamic changes do not precede the anginal attacks though impairment of left ventricular function occurs during the actual episode of chest pain and correlates well with the degree of electrocardiographic abnormality (Guazzi et al., I97I). This paper describes a patient with Prinzmetal variant angina who developed a pronounced reduction in cardiac output and syncope during anginal episodes.
Case report A 5o-year-old female patient was admitted to the Coronary Care Unit of the Royal Melboume Hospital in June I973, with a 4-hour history of severe crushing retrostemal chest pain. She had had hypertension for I2 years and a i2-month history of chest pain at rest but not on exertion. The hypertension had been well controlled with methyldopa and hydrochlorothiazide and she was on no other medication. Physical examination revealed a blood pressure of i4olgo nmmHg (i8.61i2.0 kPa) and a pulse rate of 96. Examination of the lung fields revealed fine basal crepitations. Her heart sounds were normal and there was no evidence of thyrotoxicosis or of any neurological abnormality. The electrocardiogram showed extensive anteroseptal infarction.
Twenty-four hours after admission she developed further chest pain lasting 5 minutes, and during this time the electrocardiogram showed complete atrioventricular block, with a ventricular rate of 6o per minute. She returned to sinus rhythm upon cessation of the pain. On the fourth day after admission she had another episode of chest pain associated with transient loss of consciousness. Over the next 24 hours several episodes of chest pain followed by second (Mobitz I) (Fig. i, panel C) and third degree atrioventricular block, with narrow QRS complexes and a ventricular rate of between 40 to 6o beats per minute, were documented. Each time, sinus rhythm returned immediately after relief of the pain. During these episodes, despite a ventricular rate of 40 per minute or more, the patient became drowsy. A temporary pacing wire was inserted and a His bundle electrocardiogram was obtained during sinus rhythm. The AH and HV intervals were go and 40 ms, respectively. Atrial pacing to a rate of I20 beats per minute did not induce chest pain or atrioventricular block and the AH interval increased to I20 ms. In view of the recurrent episodes of complete heart block, a permanent demand pacemaker (Elema I53) was inserted and the patient was given practolol ioo mg twice a day. She was discharged from hospital, but 2 weeks later was readmitted after an episode of severe chest pain and transient loss of consciousness with generalized convulsions and incontinence of urine. On admission she was in sinus rhythm and serial electrocardiograms and enzyme studies did not reveal any evidence of myocardial infarction. She was continuously monitored and on the second day after admission a typical attack was recorded (Fig. I). She developed chest pain which was preceded by significant ST segment elevation in the inferior leads (Fig. i panel B). The PR interval progressively lengthened and the onset of a higher degree of atrioventricular block
772 Harper, Peter, and Hunt
Ais'
.... .........
FIG. i Electrocardiographic tracings of lead III during a typical episode. A) Sinus rhythm before the onset of pain. B) Sinus rhythm with ST segment elevation immediately after the onset of chest pain. C) A 2' (Mobitz I) A V block during chest pain before a permanent pacemaker was inserted. D) Right ventricular pacing during an episode of chest pain: the ST segments of the paced complexes are raised. E) Right ventricular pacing in the absence of chest pain: the ST segment of the paced complexes is isoelectric. was interrupted by the implanted demand pacemaker. Despite a regular pacing rhythm (Fig. i, Panel D)., she
Segmental spasm of the right coronary artery was then postulated as the cause of the anginal episodes and the became unconscious and the blood pressure could not patient was given sorbide nitrate sublingually every 2 be recorded. The episode was transient, the patient hours and was observed for a further io days. During regained consciousness spontaneously, the blood pres- this period no further chest pain occurred and she was sure rose to normal levels, sinus rhythm returned, and discharged on this medication. She remained free of the ST segment returned to the isoelectric line. chest pain on this regimnen for a further 6 months, after Several such episodes occurred under observation, which she was electively admitted to hospital to observe each episode lasting between 3 and 5 minutes. The epi- the effects of reduction of her therapy. Twenty-four sodes could be aborted by prompt administration of hours after withdrawal of the coronary vasodilator sublingual nitroglycerine immediately the chest pain therapy the patient developed a further episode of chest developed. pain and syncope and the 2-hourly sorbide nitrate was A provisional diagnosis of Prinzmetal variant angina immediately resumed, and since then the patient has was made and it was postulated that this was due to a remained free of attacks. critical lesion in the right coronary artery, resulting in atrioventricular block and severe myocardial pump Discussion failure. At cardiac catheterization the left ventriculogram The diagnosis of Prinzmetal variant angina in this showed a moderate sized ventricular cavity, with a large dyskinetic segment of the anterior wall. The left ven- patient was supported by the occurrence of angin tricular end-diastolic pressure was 13 mmHg (1.7 kPa) at rest with preservation of exercise tolerance and from the midchest level. the presence of marked ST segmnent elevation The left coronary angiogram showed a 90 per cent during the chest pain. Since the original description stenosis of the anterior descending artery just beyond of this syndrome by Prinzmetal and co-workers, the first diagonal branch (Fig. 2., Panel A). There were there has been considerable debate as to the underno other obstructive lesions in the left coronary system. The right coronary artery was the dominant vessel and lying mechanism of ischaemic pain. Both postwas free of any significant obstructive lesion (Fig. 2., mortem (Prinzmetal et al., I959; Peretz, i961T; Meriel et al., 1966; Dorra et al., 1968; Rizzon et al., Panel B). The artery to the atrioventricular node was well i969; Silverman and Flamm, I97i) and coronary opacifled and was normnal. During the procedure the angiographic studies (Dorra et al., i968; Gianelly, patient did not experience any chest pain. Mugler, and Harrison, 1968; Whiiting et al., I970;
Syncope in association with Prinzmetal variant angina 773
A
B
FIG. 2 A) Left coronary angiogram in 45° left anterior oblique projection revealing a tight stenosis in the proximal left anterior descending artery, as indicated by the arrow. B). Right coronary angiogram in 450 left anterior oblique projection showing a large vessel without any obstructive lesions. The permanent pacemaker electrode is marked by an arrow.
Cheng et al., I972; Bobba et al., I97I; Dhurandhar co-workers, that continuous haemodynamic moniet al., I972) have indicated that most patients with toring in 4 patients with spontaneous variant this syndrome have a local area of narrowing in a angina did not detect any circulatory changes premajor coronary artery. The degree of obstruction, ceding the anginal attacks (Guazzi et al., I97I). In our patient, the occurrence of transient comhowever, is often insufficient to account for the symptoms at rest (Gianelly et al., I968), particularly plete heart block, with narrow QRS complexes and as exercise tolerance is preserved. Furthermore, the presence of ST segment elevation in the inferior there have been several reports of Prinzmetal leads during chest pain, suggested a critical lesion angina occurring in association with normal cor- in the right coronary artery. The coronary angioonary arteries (Ross and Gorlin, I968; Demany, gram, however, showed a dominant right coronary Tamba, and Zimmerman, I968; Cheng et al., artery which appeared free of any obstructive 1972; Whiting et al., I970; Christian and Botti, lesion. The left anterior descending artery, as I972). For these reasons, coronary artery spasm expected, had a proximal high grade obstruction has been postulated as the precipitating mechanism accounting for the anteroseptal infarction and the in this form of variant angina, but verification of corresponding dyskinetic area on the left ventriculothis concept has been difficult. Recently, however, gram. Thus in this patient, the right coronary artery there have been 3 reports of Prinzmetal variant supplied the major portion of the remaining viable angina in which spasm of the right coronary artery myocardium as well as the atrioventricular node. during chest pain was documented by coronary Therefore, we postulate that this patient had interarteriography (Oliva, Potts, and Pluss, I973; mittent spasm of the proximal right coronary artery Schroeder, Silverman, and Harrison, I974; Kerin producing severe ischaemia of both the left venand Macleod, I974). In all 3 cases the spasm tricle and the atrioventricular node, resulting in appeared unrelated to the catheter tip and when the important reduction in cardiac output with conangiograms were performed in the absence of chest sequent hypotension and syncope. Guazzi and copain, the right coronary artery was normal in 2 workers (Guazzi et al., I97I), using sophisticated cases and had minimal disease in the other case. haemodynamic monitoring methods, have demonThe hypothesis that coronary artery spasm is the strated transient impairment of left ventricular precipitating factor in Prinzmetal variant angina is function including a reduction in cardiac output further supported by the observation of Guazzi and during attacks of variant angina, but this is usually
774 Harper, Peter, and Hunt not severe enough to produce clinical manifestations (MacAlpin, Kattus, and Alvaro, I973). In our case, however, left ventricular function had already been compromised by a large anterior wall infarction and, therefore, a sudden reduction in blood flow in the right coronary artery could be expected to produce a pronounced fall in the cardiac output, with consequent syncope. The diagnosis of coronary artery spasm in this patient is further supported by the satisfactory response to coronary artery vasodilators and the recurrence of symptoms on withdrawal of this therapy. Transient atrioventricular block during classical angina is unusual, but has been reported to occur in association with Prinzmetal variant angina where there has been involvement of the right coronary artery (MacAlpin et al., I973). There have been three reports where a permanent pacing system has been implanted because of high grade atrioventricular block and syncope during episodes of Prinzmetal angina (Bodenheimer et al., I974; Gianelly et al., I968; Whiting et al., 1970). In all cases, atrioventricular conduction between attacks was normal, as was the situation in our patient even when the conducting system was stressed with atrial pacing. Chiche, Haiat, and Steff (I974) have described two patients who developed syncope during episodes of classical (Heberden's) angina. Both patients had evidence of conduction disturbances between anginal episodes and in both patients the syncopal episodes were successfully treated by permanent pacing. Our case illustrates the fact that, in Prinzmetal angina, syncopal episodes are not necessarily prevented by cardiac pacing even when high grade atrioventricular block during an attack of chest pain has been documented. Therefore, we recommend that patients with syncope and atrioventricular block should be monitored in hospital with a temporary pacing electrode and several anginal episodes observed before a decision to pace an individual patient permanently is made. References Bobba, P., Di Guglielmo, L., Vecchio, C., and Montemartina, C. (I97I). Coronarographic pattems in Prinzmetal's variant angina. Acta Cardiologica, 26, 568. Bodenheimer, M., Lipski, J., Donoso, E., and Dack, S. (1974). Prinzmetal's variant angina: a clinical and electrocardiographic study. American Heart Journal, 87, 304. Cheng, T. O., Bashour, T., Kelser, G. A., Weiss, L., and Bacos, J. (I972). Variant angina of Prinzmetal with normal coronary arteriograms: a variant of the variant (abstract). Annals of Internal Medicine, 76, 862.
Chiche, P., Haiat, R., and Steff, P. (I974). Angina pectoris with syncope due to paroxysmal atrioventricular block: role of ischaemia. Report of two cases. British Heart Journal, 36, 577. Christian, N., and Botti, R. E. (I972). Prinzmetal's variant angina pectoris with prolonged electrocardiographic changes in the absence of obstructive coronary disease. American Journal of the Medical Sciences, 263, 225. Demany, M. A., Tambe, A., and Zimmerman, H. A. (I968). Coronary arterial spasm. Diseases of the Chest, 53, 7I4. Dhurandhar, R. W., Watt, D. L., Silver, M. D., Trimble, A. S., and Adelman, A. G. (1972). Prinzmetal's variant form of angina with arteriographic evidence of coronary arterial spasm. American Journal of Cardiology, 30, 902. Dorra, M., Waynberger, M., Nezry, R., and Slama, R. (I968). A propos d'une observation d'angor dit de Prinzmetal a forme syncopale. Archives des Maladies du Coeur et des Vaisseaux, 6i, I043. Gianelly, R., Mugler, F., and Harrison, D. C. (I968). Prinzmetal's variant of angina pectoris with only slight coronary atherosclerosis. California Medicine, Io8, 129. Guazzi, M., Polese, A., Fiorentini, C., Magrini, F., and Bartorelli, C. (I97I). Left ventricular performance and related haemodynamic changes in Prinzmetal's variant angina pectoris. British Heart Journal, 33, 84. Kerin, N., and Macleod, C. A. (I974). Coronary artery spasm associated with variant angina pectoris. British Heart Journal, 36, 224. MacAlpin, R. N., Kattus, A. A., and Alvaro, A. B. (I973). Angina pectoris at rest with preservation of exercise capacity; Prinzmetal's variant angina. Circulation, 47, 946. Meriel, P., Galinier, F., Bounhoure, J. P., Mignon, J. P., and Salvador, M. (I966). Onde monophasique et tachycardie ventriculaire dans l'angor spontane de type Prinzmetal. Archives des Maladies des Coeur et des Vaisseaux, 59, 460. Oliva, P. B., Potts, D. E., and Pluss, R. G. (1973). Coronary arterial spasm in Prinzmetal angina. Documentation by coronary arteriography. New England Journal of Medicine, 288, 745. Peretz, D. I. (I96I). Variant angina pectoris of Prinzmetal. Canadian Medical Association Journal, 85, IIOI. Prinzmetal, M., Kennamer, R., Merliss, R., Wada, T., and Bor, N. (I959). Angina pectoris: a variant form of angina pectoris. American,Journal of Medicine, 27, 375. Rizzon, P., Biasco, G., Bacca, F., Brindicci, G., and Masselli Campagna, G. (I969). Su di un caso di angina variante: studio cinico ed anatomopatologico. Bollettino della Societdi Italiana di Cardiologia, 14, 8I6. Ross, R. S., and Gorlin, R. (I968). Coronary arteriography. Circulation, 37-38, Suppl. III, 67. Schroeder, J. S., Silverman, J. F., and Harrison, D. C. (1974). Right coronary arterial spasm causing Prinzmetal's variant angina. Chest, 55, 573. Silverman, M. E., and Flamm, M. D. (97I). Variant angina pectoris: anatomy findings and prognostic implications. Annals of Internal Medicine, 75, 339. Whiting, R. B., Klein, M. D., Vander Veer, J., and Lown, B. (1970). Variant angina pectoris. New England J'ournal of Medicine, 282, 709.
Requests for reprints to Dr. David Hunt, Cardiac Departnent, Royal Melbourne Hospital, Grattan Street, Parkville, Victoria 3050, Australia.
Syncope in association with Prinzmetal variant angina Richard Harper, Thomas Peter, and David Hunt From the Cardiac Department, The Royal Melbourne Hospital, Victoria, Australia
A case of Prinzmetal variant angina with transient complete atrioventricular block and syncopal episodes following an anteroseptal myocardial infarction is described. The syncopal attacks were not prevented by demand cardiac pacing and were presumably caused by transient severe ischaemia of the left ventricle, with a consequent reduction in cardiac output. The left ventriculogram showed a large anterior dyskinetic area corresponding to the high grade proximal obstruction in the left anterior descending artery demonstrated by coronary angiography. All other coronary vessels appearedfree of disease and it is suggested that the anginal episodes were caused by transient proximal segmental spasm of the right coronary artery. The anginal episodes were successfully prevented by a regimen of two-hourly coronary arterial vasodilator therapy. In I959 Prinzmetal and co-workers (i959) described a variant form of angina in which the chest pain occurred at rest and was not related to physical exertion or emotion. The characteristic feature of this syndrome is the occurrence of an electrocardiographic current of injury pattern during chest pain rather than ST segment depression which is the usual pattern of classical angina. Prinzmetal's variant angina also differs from classical effortinduced angina in that haemodynamic changes do not precede the anginal attacks though impairment of left ventricular function occurs during the actual episode of chest pain and correlates well with the degree of electrocardiographic abnormality (Guazzi et al., I97I). This paper describes a patient with Prinzmetal variant angina who developed a pronounced reduction in cardiac output and syncope during anginal episodes.
Case report A 5o-year-old female patient was admitted to the Coronary Care Unit of the Royal Melboume Hospital in June I973, with a 4-hour history of severe crushing retrostemal chest pain. She had had hypertension for I2 years and a i2-month history of chest pain at rest but not on exertion. The hypertension had been well controlled with methyldopa and hydrochlorothiazide and she was on no other medication. Physical examination revealed a blood pressure of i4olgo nmmHg (i8.61i2.0 kPa) and a pulse rate of 96. Examination of the lung fields revealed fine basal crepitations. Her heart sounds were normal and there was no evidence of thyrotoxicosis or of any neurological abnormality. The electrocardiogram showed extensive anteroseptal infarction.
Twenty-four hours after admission she developed further chest pain lasting 5 minutes, and during this time the electrocardiogram showed complete atrioventricular block, with a ventricular rate of 6o per minute. She returned to sinus rhythm upon cessation of the pain. On the fourth day after admission she had another episode of chest pain associated with transient loss of consciousness. Over the next 24 hours several episodes of chest pain followed by second (Mobitz I) (Fig. i, panel C) and third degree atrioventricular block, with narrow QRS complexes and a ventricular rate of between 40 to 6o beats per minute, were documented. Each time, sinus rhythm returned immediately after relief of the pain. During these episodes, despite a ventricular rate of 40 per minute or more, the patient became drowsy. A temporary pacing wire was inserted and a His bundle electrocardiogram was obtained during sinus rhythm. The AH and HV intervals were go and 40 ms, respectively. Atrial pacing to a rate of I20 beats per minute did not induce chest pain or atrioventricular block and the AH interval increased to I20 ms. In view of the recurrent episodes of complete heart block, a permanent demand pacemaker (Elema I53) was inserted and the patient was given practolol ioo mg twice a day. She was discharged from hospital, but 2 weeks later was readmitted after an episode of severe chest pain and transient loss of consciousness with generalized convulsions and incontinence of urine. On admission she was in sinus rhythm and serial electrocardiograms and enzyme studies did not reveal any evidence of myocardial infarction. She was continuously monitored and on the second day after admission a typical attack was recorded (Fig. I). She developed chest pain which was preceded by significant ST segment elevation in the inferior leads (Fig. i panel B). The PR interval progressively lengthened and the onset of a higher degree of atrioventricular block
772 Harper, Peter, and Hunt
Ais'
.... .........
FIG. i Electrocardiographic tracings of lead III during a typical episode. A) Sinus rhythm before the onset of pain. B) Sinus rhythm with ST segment elevation immediately after the onset of chest pain. C) A 2' (Mobitz I) A V block during chest pain before a permanent pacemaker was inserted. D) Right ventricular pacing during an episode of chest pain: the ST segments of the paced complexes are raised. E) Right ventricular pacing in the absence of chest pain: the ST segment of the paced complexes is isoelectric. was interrupted by the implanted demand pacemaker. Despite a regular pacing rhythm (Fig. i, Panel D)., she
Segmental spasm of the right coronary artery was then postulated as the cause of the anginal episodes and the became unconscious and the blood pressure could not patient was given sorbide nitrate sublingually every 2 be recorded. The episode was transient, the patient hours and was observed for a further io days. During regained consciousness spontaneously, the blood pres- this period no further chest pain occurred and she was sure rose to normal levels, sinus rhythm returned, and discharged on this medication. She remained free of the ST segment returned to the isoelectric line. chest pain on this regimnen for a further 6 months, after Several such episodes occurred under observation, which she was electively admitted to hospital to observe each episode lasting between 3 and 5 minutes. The epi- the effects of reduction of her therapy. Twenty-four sodes could be aborted by prompt administration of hours after withdrawal of the coronary vasodilator sublingual nitroglycerine immediately the chest pain therapy the patient developed a further episode of chest developed. pain and syncope and the 2-hourly sorbide nitrate was A provisional diagnosis of Prinzmetal variant angina immediately resumed, and since then the patient has was made and it was postulated that this was due to a remained free of attacks. critical lesion in the right coronary artery, resulting in atrioventricular block and severe myocardial pump Discussion failure. At cardiac catheterization the left ventriculogram The diagnosis of Prinzmetal variant angina in this showed a moderate sized ventricular cavity, with a large dyskinetic segment of the anterior wall. The left ven- patient was supported by the occurrence of angin tricular end-diastolic pressure was 13 mmHg (1.7 kPa) at rest with preservation of exercise tolerance and from the midchest level. the presence of marked ST segmnent elevation The left coronary angiogram showed a 90 per cent during the chest pain. Since the original description stenosis of the anterior descending artery just beyond of this syndrome by Prinzmetal and co-workers, the first diagonal branch (Fig. 2., Panel A). There were there has been considerable debate as to the underno other obstructive lesions in the left coronary system. The right coronary artery was the dominant vessel and lying mechanism of ischaemic pain. Both postwas free of any significant obstructive lesion (Fig. 2., mortem (Prinzmetal et al., I959; Peretz, i961T; Meriel et al., 1966; Dorra et al., 1968; Rizzon et al., Panel B). The artery to the atrioventricular node was well i969; Silverman and Flamm, I97i) and coronary opacifled and was normnal. During the procedure the angiographic studies (Dorra et al., i968; Gianelly, patient did not experience any chest pain. Mugler, and Harrison, 1968; Whiiting et al., I970;
Syncope in association with Prinzmetal variant angina 773
A
B
FIG. 2 A) Left coronary angiogram in 45° left anterior oblique projection revealing a tight stenosis in the proximal left anterior descending artery, as indicated by the arrow. B). Right coronary angiogram in 450 left anterior oblique projection showing a large vessel without any obstructive lesions. The permanent pacemaker electrode is marked by an arrow.
Cheng et al., I972; Bobba et al., I97I; Dhurandhar co-workers, that continuous haemodynamic moniet al., I972) have indicated that most patients with toring in 4 patients with spontaneous variant this syndrome have a local area of narrowing in a angina did not detect any circulatory changes premajor coronary artery. The degree of obstruction, ceding the anginal attacks (Guazzi et al., I97I). In our patient, the occurrence of transient comhowever, is often insufficient to account for the symptoms at rest (Gianelly et al., I968), particularly plete heart block, with narrow QRS complexes and as exercise tolerance is preserved. Furthermore, the presence of ST segment elevation in the inferior there have been several reports of Prinzmetal leads during chest pain, suggested a critical lesion angina occurring in association with normal cor- in the right coronary artery. The coronary angioonary arteries (Ross and Gorlin, I968; Demany, gram, however, showed a dominant right coronary Tamba, and Zimmerman, I968; Cheng et al., artery which appeared free of any obstructive 1972; Whiting et al., I970; Christian and Botti, lesion. The left anterior descending artery, as I972). For these reasons, coronary artery spasm expected, had a proximal high grade obstruction has been postulated as the precipitating mechanism accounting for the anteroseptal infarction and the in this form of variant angina, but verification of corresponding dyskinetic area on the left ventriculothis concept has been difficult. Recently, however, gram. Thus in this patient, the right coronary artery there have been 3 reports of Prinzmetal variant supplied the major portion of the remaining viable angina in which spasm of the right coronary artery myocardium as well as the atrioventricular node. during chest pain was documented by coronary Therefore, we postulate that this patient had interarteriography (Oliva, Potts, and Pluss, I973; mittent spasm of the proximal right coronary artery Schroeder, Silverman, and Harrison, I974; Kerin producing severe ischaemia of both the left venand Macleod, I974). In all 3 cases the spasm tricle and the atrioventricular node, resulting in appeared unrelated to the catheter tip and when the important reduction in cardiac output with conangiograms were performed in the absence of chest sequent hypotension and syncope. Guazzi and copain, the right coronary artery was normal in 2 workers (Guazzi et al., I97I), using sophisticated cases and had minimal disease in the other case. haemodynamic monitoring methods, have demonThe hypothesis that coronary artery spasm is the strated transient impairment of left ventricular precipitating factor in Prinzmetal variant angina is function including a reduction in cardiac output further supported by the observation of Guazzi and during attacks of variant angina, but this is usually
774 Harper, Peter, and Hunt not severe enough to produce clinical manifestations (MacAlpin, Kattus, and Alvaro, I973). In our case, however, left ventricular function had already been compromised by a large anterior wall infarction and, therefore, a sudden reduction in blood flow in the right coronary artery could be expected to produce a pronounced fall in the cardiac output, with consequent syncope. The diagnosis of coronary artery spasm in this patient is further supported by the satisfactory response to coronary artery vasodilators and the recurrence of symptoms on withdrawal of this therapy. Transient atrioventricular block during classical angina is unusual, but has been reported to occur in association with Prinzmetal variant angina where there has been involvement of the right coronary artery (MacAlpin et al., I973). There have been three reports where a permanent pacing system has been implanted because of high grade atrioventricular block and syncope during episodes of Prinzmetal angina (Bodenheimer et al., I974; Gianelly et al., I968; Whiting et al., 1970). In all cases, atrioventricular conduction between attacks was normal, as was the situation in our patient even when the conducting system was stressed with atrial pacing. Chiche, Haiat, and Steff (I974) have described two patients who developed syncope during episodes of classical (Heberden's) angina. Both patients had evidence of conduction disturbances between anginal episodes and in both patients the syncopal episodes were successfully treated by permanent pacing. Our case illustrates the fact that, in Prinzmetal angina, syncopal episodes are not necessarily prevented by cardiac pacing even when high grade atrioventricular block during an attack of chest pain has been documented. Therefore, we recommend that patients with syncope and atrioventricular block should be monitored in hospital with a temporary pacing electrode and several anginal episodes observed before a decision to pace an individual patient permanently is made. References Bobba, P., Di Guglielmo, L., Vecchio, C., and Montemartina, C. (I97I). Coronarographic pattems in Prinzmetal's variant angina. Acta Cardiologica, 26, 568. Bodenheimer, M., Lipski, J., Donoso, E., and Dack, S. (1974). Prinzmetal's variant angina: a clinical and electrocardiographic study. American Heart Journal, 87, 304. Cheng, T. O., Bashour, T., Kelser, G. A., Weiss, L., and Bacos, J. (I972). Variant angina of Prinzmetal with normal coronary arteriograms: a variant of the variant (abstract). Annals of Internal Medicine, 76, 862.
Chiche, P., Haiat, R., and Steff, P. (I974). Angina pectoris with syncope due to paroxysmal atrioventricular block: role of ischaemia. Report of two cases. British Heart Journal, 36, 577. Christian, N., and Botti, R. E. (I972). Prinzmetal's variant angina pectoris with prolonged electrocardiographic changes in the absence of obstructive coronary disease. American Journal of the Medical Sciences, 263, 225. Demany, M. A., Tambe, A., and Zimmerman, H. A. (I968). Coronary arterial spasm. Diseases of the Chest, 53, 7I4. Dhurandhar, R. W., Watt, D. L., Silver, M. D., Trimble, A. S., and Adelman, A. G. (1972). Prinzmetal's variant form of angina with arteriographic evidence of coronary arterial spasm. American Journal of Cardiology, 30, 902. Dorra, M., Waynberger, M., Nezry, R., and Slama, R. (I968). A propos d'une observation d'angor dit de Prinzmetal a forme syncopale. Archives des Maladies du Coeur et des Vaisseaux, 6i, I043. Gianelly, R., Mugler, F., and Harrison, D. C. (I968). Prinzmetal's variant of angina pectoris with only slight coronary atherosclerosis. California Medicine, Io8, 129. Guazzi, M., Polese, A., Fiorentini, C., Magrini, F., and Bartorelli, C. (I97I). Left ventricular performance and related haemodynamic changes in Prinzmetal's variant angina pectoris. British Heart Journal, 33, 84. Kerin, N., and Macleod, C. A. (I974). Coronary artery spasm associated with variant angina pectoris. British Heart Journal, 36, 224. MacAlpin, R. N., Kattus, A. A., and Alvaro, A. B. (I973). Angina pectoris at rest with preservation of exercise capacity; Prinzmetal's variant angina. Circulation, 47, 946. Meriel, P., Galinier, F., Bounhoure, J. P., Mignon, J. P., and Salvador, M. (I966). Onde monophasique et tachycardie ventriculaire dans l'angor spontane de type Prinzmetal. Archives des Maladies des Coeur et des Vaisseaux, 59, 460. Oliva, P. B., Potts, D. E., and Pluss, R. G. (1973). Coronary arterial spasm in Prinzmetal angina. Documentation by coronary arteriography. New England Journal of Medicine, 288, 745. Peretz, D. I. (I96I). Variant angina pectoris of Prinzmetal. Canadian Medical Association Journal, 85, IIOI. Prinzmetal, M., Kennamer, R., Merliss, R., Wada, T., and Bor, N. (I959). Angina pectoris: a variant form of angina pectoris. American,Journal of Medicine, 27, 375. Rizzon, P., Biasco, G., Bacca, F., Brindicci, G., and Masselli Campagna, G. (I969). Su di un caso di angina variante: studio cinico ed anatomopatologico. Bollettino della Societdi Italiana di Cardiologia, 14, 8I6. Ross, R. S., and Gorlin, R. (I968). Coronary arteriography. Circulation, 37-38, Suppl. III, 67. Schroeder, J. S., Silverman, J. F., and Harrison, D. C. (1974). Right coronary arterial spasm causing Prinzmetal's variant angina. Chest, 55, 573. Silverman, M. E., and Flamm, M. D. (97I). Variant angina pectoris: anatomy findings and prognostic implications. Annals of Internal Medicine, 75, 339. Whiting, R. B., Klein, M. D., Vander Veer, J., and Lown, B. (1970). Variant angina pectoris. New England J'ournal of Medicine, 282, 709.
Requests for reprints to Dr. David Hunt, Cardiac Departnent, Royal Melbourne Hospital, Grattan Street, Parkville, Victoria 3050, Australia.
