Alternate of arrhythmia, heart block with ECG ST-segment elevation
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《中华医药杂志》英文版 2006年第3期
Correspondence to LONG Yong-jun,Department of Cardiology,Hospital 302 Attached to Aviation Group,Anshun 561000,Guizhou Province,China
Tel:+86-853-3469222E-mail:yong jun-long@163.com
[Abstract]A case of variant angina is reported. Variant angina with alternate of arrhythmia and heart block is extreme rare. The therapy should be directed toward the elimination of all episodes of spasm, not cardiac rhythm disturbances themselves. Long-acting calcium channel blocker is very effective in preventing the attacks of variant angina.
[Key words]variant angina;ventricular arrhythmia;atrioventricular block；calcium channel blocker
INRODUCTION
Variant angina is an uncommon special type of coronary artery disease. Its characteristic clinical manifestation is different from unstable angina and acute myocardial infarction. Ventricular arrhythmias and atrioventricular block develop during the temporary coronary spasm occasionally. The therapeutic approach is rather different.
CASE REPORT
The patient was a 49-year-old female who presented with complaints of recurrent chest discomfort and serious jaw pain for 7 days. On admission, the patient was asymptomatic, there were no abnormal findings on physical examination, ECG, UCG and blood chemical detection. During admission, she experienced similar painful attacks at rest in the early morning with transient ST-segment elevation although she took isosorbide dinitrate 30 mg/day and intravenous nitroglycerin 10 mg /day. ST-segment elevation appeared in leads Ⅱ, Ⅲ, AVF (Figure 1), sometimes, appeared in precordial leads simultaneously during attacks. Each attack did not last more than one minute. As the symptoms receded, the ST-segment elevation disappeared rapidly. Continuous ambulatory ECG monitoring revealed alternate of ventricular arrhythmia, A-V block associated with ECG ST-segment elevation (Figure 2, Figure 3) during a night before the patient waking up. Physical examination of this patient between attacks reveals no abnormalities. Routine laboratory tests, including CKMB and cardiac-specific troponin Ⅰ, were normal. The patient’s symptoms did not response to nitrates. After added to long-acting nifedine 20 mg twice a day, the patient became completely asymptomatic. Selective coronary angiograph showed a severe proximal right coronary artery organic stenosis (Figure 4), but normal left coronary artery. Therefore, a drug eluted stent (Firebird, China) was implanted into the stenotic site of right coronary artery. After successful angioplasty, the patient continued to take long-acting nifedipine. She has been angina-free during follow-up of 3 months.
Figure 1 ECG during an attack revealed ST-segment elevation in leads Ⅱ,Ⅲ and AVF
Figure 2 ECG at 3∶51. in the 3rd day after admission revealed ventricular extrasystole, pairs of ventricular extrasystole, and ventricular tachycardia associated with ST-segment elevation in leads Ⅱ,Ⅲ, AVF and V3~V6
Figure 3 ECG at 7∶38 in the same morning revealed 2∶1 AV block followed ventricular extrasystole, associated with ST elevation in leads Ⅱ,Ⅲ, AVF and V1~V3
Figure 4 Angiograph showed 90% stenosis at proximal right coronary artery
DISCUSSION
Variant angina can be diagnosed most easily by recording an ECG during an episode of rest angina[1~3]. The ST-segment elevation that occurs during an attack disappears promptly as the symptom receded. It must be differentiated from acute myocardial infarction(AMI) and unstable angina because of different therapeutic approach. The discomfort of angina is usually easy to differentiate from the pain of AMI by the duration, and lack of precipitating or alleviating factors. The attack did not last longer than ordinary angina episode (more than 1 minute). The presenting symptoms are usually not remarkable enough to be distinguished immediately from those of unstable angina. Angina at rest occurs with a cyclical pattern, often with attacks occurring in the early morning hours. Ambulatory ECG is useful to confirm the diagnosis of variant angina, and reveal ventricular arrhythmias, heart block caused by myocardial ischemia during angina attack[4~8]. Therefore, therapy for ventricular arrhythmias and heart block should be directed toward the elimination of all episodes of spasm. Variant angina is caused by coronary spasm, usually focal and often at the site of a coronary stenosis. The underlying coronary lesion can vary from a subtotal occlusion to a very mild stenosis, and in some cases the coronary arteries are normal angiographically. In this patient ST elevation appeared in leads Ⅱ,Ⅲ, AVF during attacks, but sometimes appeared at precordial leads simultaneously. Therefore, we speculate that the coronary spasm not only occurred at the right coronary artery but also occurred at left one. The underlying coronary lesion for the right coronary spasm is severe proximal right coronary stenosis, but the left coronary artery is normal angiographically. The therapeutic approach is different between variant angina and acute coronary syndrome including AMI and unstable angina. Beta-adrenergic blockers are harmful to the former because of their propensity to increase the frequency and duration of attacks, but useful to the later. On the other side, calcium channel blockers are very effective in preventing attacks of variant angina, but should be avoid in the later.
REFERENCES
1. Waters DD. Diagnosis and management of patients with unstable anginaI.In:Fuster V,edr.Hurst’s The Heart. 10th ed , St.Louis:McGraw-Hill ,2000, Chapter 41.
2. Gersh BJ.Other Manifestations of Coronary Artery Disease. In:E Braunwald,ed.Heart Disease, A Textbook of Cardiovascular Medicine. 6th ed.Philadelphia:W.B.Saunders Co,2001,1324-1329.
3. Topol EJ.Textbook of Cardiovascular Medicine,2nd ed.Philadelphia:Lippincott Williams & wilkins, 2003, 322.
4. Bayes de Luna A, Carreras F, Cladellas M, et al.Holter ECG study of the electrocardiographic phenomena in Prinzmetal angina attacks with emphasis on the study of ventricular arrhythmias. J Electrocardiol,1985,18:267.
5. Kaski JC, Tousoulis D, McFadden E, et al.Variant angina pectoris. Role of coronary spasm in the development of fixed coronary obstructions.Circulation, 1992, 85: 619 - 626.
6. Sun H, Mohri M, Shimokawa H, et al.Coronary microvascular spasm causes myocardial ischemia in patients with vasospastic angina.JACC,2002,39(5): 847 - 851.
7. Robertson RM, Wood AJJ, Vaughn WK, Robertson D. Exacerbation of vasotonic angina by propranolol. Circulation,1982,65:281-285.
8. Morikami Y, Yasue H. Efficacy of slow-release nifedipine on myocardial ischemia episodes in variant angina pectoris. Am J Cardiol,1991,68:580-584.
1 Department of Cardiology, Hospital 302 Attached to Aviation Group, Anshun561000,Guizhou Province, China
2 Institute of Cardiovascular Disease of Guizhou Province, Guiyang 550001,Guizhou Province,China
(Editor Emilia)(LONG Yong-jun1, CHEN Zhi-)
Tel:+86-853-3469222E-mail:yong jun-long@163.com
[Abstract]A case of variant angina is reported. Variant angina with alternate of arrhythmia and heart block is extreme rare. The therapy should be directed toward the elimination of all episodes of spasm, not cardiac rhythm disturbances themselves. Long-acting calcium channel blocker is very effective in preventing the attacks of variant angina.
[Key words]variant angina;ventricular arrhythmia;atrioventricular block；calcium channel blocker
INRODUCTION
Variant angina is an uncommon special type of coronary artery disease. Its characteristic clinical manifestation is different from unstable angina and acute myocardial infarction. Ventricular arrhythmias and atrioventricular block develop during the temporary coronary spasm occasionally. The therapeutic approach is rather different.
CASE REPORT
The patient was a 49-year-old female who presented with complaints of recurrent chest discomfort and serious jaw pain for 7 days. On admission, the patient was asymptomatic, there were no abnormal findings on physical examination, ECG, UCG and blood chemical detection. During admission, she experienced similar painful attacks at rest in the early morning with transient ST-segment elevation although she took isosorbide dinitrate 30 mg/day and intravenous nitroglycerin 10 mg /day. ST-segment elevation appeared in leads Ⅱ, Ⅲ, AVF (Figure 1), sometimes, appeared in precordial leads simultaneously during attacks. Each attack did not last more than one minute. As the symptoms receded, the ST-segment elevation disappeared rapidly. Continuous ambulatory ECG monitoring revealed alternate of ventricular arrhythmia, A-V block associated with ECG ST-segment elevation (Figure 2, Figure 3) during a night before the patient waking up. Physical examination of this patient between attacks reveals no abnormalities. Routine laboratory tests, including CKMB and cardiac-specific troponin Ⅰ, were normal. The patient’s symptoms did not response to nitrates. After added to long-acting nifedine 20 mg twice a day, the patient became completely asymptomatic. Selective coronary angiograph showed a severe proximal right coronary artery organic stenosis (Figure 4), but normal left coronary artery. Therefore, a drug eluted stent (Firebird, China) was implanted into the stenotic site of right coronary artery. After successful angioplasty, the patient continued to take long-acting nifedipine. She has been angina-free during follow-up of 3 months.
Figure 1 ECG during an attack revealed ST-segment elevation in leads Ⅱ,Ⅲ and AVF
Figure 2 ECG at 3∶51. in the 3rd day after admission revealed ventricular extrasystole, pairs of ventricular extrasystole, and ventricular tachycardia associated with ST-segment elevation in leads Ⅱ,Ⅲ, AVF and V3~V6
Figure 3 ECG at 7∶38 in the same morning revealed 2∶1 AV block followed ventricular extrasystole, associated with ST elevation in leads Ⅱ,Ⅲ, AVF and V1~V3
Figure 4 Angiograph showed 90% stenosis at proximal right coronary artery
DISCUSSION
Variant angina can be diagnosed most easily by recording an ECG during an episode of rest angina[1~3]. The ST-segment elevation that occurs during an attack disappears promptly as the symptom receded. It must be differentiated from acute myocardial infarction(AMI) and unstable angina because of different therapeutic approach. The discomfort of angina is usually easy to differentiate from the pain of AMI by the duration, and lack of precipitating or alleviating factors. The attack did not last longer than ordinary angina episode (more than 1 minute). The presenting symptoms are usually not remarkable enough to be distinguished immediately from those of unstable angina. Angina at rest occurs with a cyclical pattern, often with attacks occurring in the early morning hours. Ambulatory ECG is useful to confirm the diagnosis of variant angina, and reveal ventricular arrhythmias, heart block caused by myocardial ischemia during angina attack[4~8]. Therefore, therapy for ventricular arrhythmias and heart block should be directed toward the elimination of all episodes of spasm. Variant angina is caused by coronary spasm, usually focal and often at the site of a coronary stenosis. The underlying coronary lesion can vary from a subtotal occlusion to a very mild stenosis, and in some cases the coronary arteries are normal angiographically. In this patient ST elevation appeared in leads Ⅱ,Ⅲ, AVF during attacks, but sometimes appeared at precordial leads simultaneously. Therefore, we speculate that the coronary spasm not only occurred at the right coronary artery but also occurred at left one. The underlying coronary lesion for the right coronary spasm is severe proximal right coronary stenosis, but the left coronary artery is normal angiographically. The therapeutic approach is different between variant angina and acute coronary syndrome including AMI and unstable angina. Beta-adrenergic blockers are harmful to the former because of their propensity to increase the frequency and duration of attacks, but useful to the later. On the other side, calcium channel blockers are very effective in preventing attacks of variant angina, but should be avoid in the later.
REFERENCES
1. Waters DD. Diagnosis and management of patients with unstable anginaI.In:Fuster V,edr.Hurst’s The Heart. 10th ed , St.Louis:McGraw-Hill ,2000, Chapter 41.
2. Gersh BJ.Other Manifestations of Coronary Artery Disease. In:E Braunwald,ed.Heart Disease, A Textbook of Cardiovascular Medicine. 6th ed.Philadelphia:W.B.Saunders Co,2001,1324-1329.
3. Topol EJ.Textbook of Cardiovascular Medicine,2nd ed.Philadelphia:Lippincott Williams & wilkins, 2003, 322.
4. Bayes de Luna A, Carreras F, Cladellas M, et al.Holter ECG study of the electrocardiographic phenomena in Prinzmetal angina attacks with emphasis on the study of ventricular arrhythmias. J Electrocardiol,1985,18:267.
5. Kaski JC, Tousoulis D, McFadden E, et al.Variant angina pectoris. Role of coronary spasm in the development of fixed coronary obstructions.Circulation, 1992, 85: 619 - 626.
6. Sun H, Mohri M, Shimokawa H, et al.Coronary microvascular spasm causes myocardial ischemia in patients with vasospastic angina.JACC,2002,39(5): 847 - 851.
7. Robertson RM, Wood AJJ, Vaughn WK, Robertson D. Exacerbation of vasotonic angina by propranolol. Circulation,1982,65:281-285.
8. Morikami Y, Yasue H. Efficacy of slow-release nifedipine on myocardial ischemia episodes in variant angina pectoris. Am J Cardiol,1991,68:580-584.
1 Department of Cardiology, Hospital 302 Attached to Aviation Group, Anshun561000,Guizhou Province, China
2 Institute of Cardiovascular Disease of Guizhou Province, Guiyang 550001,Guizhou Province,China
(Editor Emilia)(LONG Yong-jun1, CHEN Zhi-)