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A Patient in Whom Self-Terminating Ventricular Fibrillation

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A Patient in Whom Self-Terminating Ventricular Fibrillation 568 Br HeartJ 1993;69:568-571 A patient in whom self-terminating ventricular fibrillation was a manifestation of myocardial reperfusion Br Heart J: first published as 10.1136/hrt.69.6.568 on 1 June 1993. Downloaded from Norbert M van Hemel, J Herre Kingma Abstract and cross sectional echocardiography. Self-terminating ventricular fibrillation Additional laboratory examination showed a was recorded in a 47 year old woman normal lipid pattern (serum cholesterol 4f8, without coronary artery or other struc- high density lipoprotein cholesterol 1-23, tural heart disease. Reperfusion was triglycerides 1-24 mmol/l) and the results of a thought to be responsible for the ventric- routine haematological and blood chemistry ular fibrillation because the arrhythmia were normal. During the first day after started while the ST segment was return- admission she showed signs of minor ing to the baseline during an episode of ischaemic brain damage but these disap- silent ischaemia that was probably peared within a week. caused by coronary spasm. This case Graded bicycle stress testing carried out 14 shows that potentially lethal arrhythmias days after cardiac arrest showed a maximal can arise during reperfusion and that exercise tolerance of eight minutes (105 W) ventricular fibrillation during reperfu- without symptoms. At maximal heart rate the sion may be self-terminating. ST segment changes of the 12 lead electro- cardiogram suggested ischaemia (fig 1): pre- (Br Heart3J 1993;69:568-571) mature ventricular extrasystoles were seen only in the recovery phase. This ischaemic pattern disappeared within five minutes after Transient occlusion of a major coronary ves- the maximal workload was achieved. She did sel by spasm leading to subsequent ischaemia not complain of chest pain during stress test- can cause serious ventricular arrhythmias. ing. Right and left heart catheterisation did These ischaemia induced arrhythmias are not show any abnormalities. Coronary arteri- clearly different from the reperfusion arrhyth- ography showed normal arteries and there mia that is caused by the re-establishment of was no evidence of bridging segments. Supine coronary flow to the ischaemic region after bicycle graded exercise testing carried out http://heart.bmj.com/ transient occlusion. 1-3 Occlusion arrhythmias during the invasive study did not provoke are associated with progressive ST segment coronary spasm. Ergometrine (0-1 and 0f2 deviation whereas reperfusion arrhythmias mg) given every five minutes during coronary occur when the ST segment is returning to arteriography did not provoke any ST seg- baseline.'-3 We describe an unusual patient in ment changes, coronary spasm, or ventricular whom self-terminating ventricular fibrillation arrhythmia.4 (VF) was the only manifestation of reperfu- Continuous two channel Holter recording sion after coronary artery spasm. when she was off treatment showed several on October 1, 2021 by guest. Protected copyright. episodes of symptom-free ST segment changes (maximum deviation 3 mm). There Case report was a diurnal pattern with profound On 4 April 1990 a 47 year old woman was ischaemic episodes being more common in admitted to the emergency room after a sud- the morning (8&00-9 00 am) and night den cardiac arrest at rest without any previ- (8 00-9 00 pm), as was reported in patients ous signs or symptoms. Her husband had with angina.35 The increase in sinus rate that started cardiopulmonary resuscitation imme- preceded ST segment deviation was not diately. The paramedical staff on the ambu- remarkable but sinus tachycardia up to 140 lance, which arrived within eight minutes, beats/min was frequently recorded at the time recorded ventricular fibrillation and restored of peak ST segment deviation. The recording sinus rhythm with two 400 DC shocks. The on 21 April 1990 showed an asymptomatic circulation was stabilised within minutes. episode of profound ST segment change at Department of Apart from the cardiac arrest the patient did 20 16. This was followed by recovery of the Cardiology, St not have any other cardiac symptoms. Her ST segment and decrease in sinus rate to the Antonius Hospital, previous medical history was unremarkable baseline value (fig 2). Without Nieuwegein, The warning Netherlands and there was no family history of cardiovas- arrhythmias, ventricular fibrillation started N M van Hemel cular disease. She had smoked 25 cigarettes a four minutes after peak ST segment changes, J Herre Kingma day for many years. Physical examination when abnormal T waves were the only resid- Correspondence to: showed no abnormalities. Blood pressure was ual signs of silent ischaemia. Ventricular fib- Dr N M van Hemel, Department of Cardiology, 130/80 mm Hg. After admission to the coro- rillation causing syncope persisted for 81 St Antonius Hospital, nary care unit an acute myocardial infarction seconds, then organised to become a ventric- Koekoekslaan 1, 3435 CM Nieuwegein, was excluded on the basis of electrocardiogra- ular flutter (300 beats/min) with a torsades de The Netherlands phy, serum creatine kinase concentrations, pointes pattern which lasted 17 seconds. This A patient in whom self-terminating ventricularfibrillation was a manifestation ofmyocardial reperfusion 569 Figure 1 %/I Electrocardiographic I rrlv changes during graded exer- cise testing. Leads I to III, aVR to aVF are shown in panels A, B, C, and leads Vl to V6 in D, E, F. Panels A and D display the Br Heart J: first published as 10.1136/hrt.69.6.568 on 1 June 1993. Downloaded from resting 12 lead ECG pre- ceding stress testing. Biphasic P waves in leads II and III suggest an abnormal site of supraventricular impulse V3 formation. Slight STseg- ment elevation in leads II, III, aVF, V2 to V6 may be categorised as "early repo- larisation". Panels B and E show abnormal ST seg- ments at maximally aVR 11 V4 achieved heart rate of 180 min- (100% ofpredicted value). ST segment depres- sion suggesting ischaemia is clearly visible in leads II, aVF, V3 to V6, while ST segment elevation is present in aVR. Note the appear- ance ofnormal P waves during exercise. Panels C and F display absence of V6 ischaemic ST segments dur- ing exercise during treat- ment with calcium .,I . : antagonists at a maximal heart rate of 180 min-'. A B C D E F Figure 2 Holter recording HR showing self-limiting ven- tricularfibrillation. This (min -1) one lead recording (paper 8.10 100 8.16 speed 6-5 mmls) shows the 90 pm development ofgradual and t0 4 4 pm profound ST depression (8 16 pm) and the return 90 8.11 110 8.17 |4~44~A4 http://heart.bmj.com/ ofthe ST segment to the baseline (8 21 pm) and A4 finally residual negative T ,4~44 waves. Without preceding 100 8.12 130 '4 44*L4r 8.18 arrhythmias ventricularfib- rillation emerged and termi- nated spontaneously after a 8.19 phase ofventricularflutter 110 II 8.13 100 with a torsades de pointes pattern. Finally sinus rhythm resumed after a 8.14 60 8.20 on October 1, 2021 by guest. Protected copyright. long sinus arrest and an 110 episode of transient atri- oventricular block. 90 8.15 80 4 8.21 8.22pm 8.24 8.26 0 5 10 15 20 25 30 570 van Hemel, Herre Kingma arrhythmia terminated spontaneously and manner which enhances the dispersion of was followed by long sinus pauses until, after refractory periods and the facilitation of reen- a transient third atrioventricular block, nor- trant arrhythmias.'6 Abnormal responses to a mal sinus rhythm resumed. After she recov- and ,B adrenergic receptor stimulation'7 and ered consciousness the patient cleaned up superoxide radical formation during urine in her room before she asked for help ischaemia'8 could also influence arrhythmoge- Br Heart J: first published as 10.1136/hrt.69.6.568 on 1 June 1993. Downloaded from from the nursing staff, who only then became nesis. aware of this serious cardiac event. Though coronary artery spasms could not The most likely diagnosis was self- be provoked in our patient, who did not have terminating ventricular fibrillation caused by coronary atherosclerosis, the Holter recording asymptomatic ischaemia that was precipitated showed several painless ischaemic episodes by coronary spasm. Treatment with calcium suggestive of coronary spasm. Ventricular fib- antagonists was given to prevent coronary rillation started at the time the spasm was spasm. Successive Holter recordings and relieved (shown by normalisation of the ST bicycle stress tests (fig 1) showed no new segment) and reperfusion occurred. Tzivoni attacks of ischaemia, coronary spasm, or et al" described reperfusion ventricular fibril- ventricular arrhythmias. After a two year of lation in a patient without coronary artery follow up the patient is still taking nifedipine disease, but VF was preceded by chest pain (80 mg daily), and lives a normal life without and direct current shock was immediately symptomatic arrhythmia, dizziness, or syncope. applied. Crozier et al'2 reported on the resus- citation of two patients with ventricular fibril- lation and ventricular asystole, respectively, Discussion without preceding chest pain. Coronary arte- Spasm of coronary arteries exposes the riography showed normal arteries in both myocardium to the double hazard of transient patients. It is not clear whether ischaemia due ischaemia and subsequent reperfusion. to occlusion or reperfusion played a part in Postmortem studies in cases of sudden car- these cases. These observations show that diac death showed minor recent coronary symptomatic and life-threatening ventricular thrombi or plaque fissuring causing <50% arrhythmias are much rarer after episodes of luminal occlusion in half of those examined.6 coronary spasm than after symptomatic In the remainder, lethal arrhythmias were a ischaemia.3 possible cause of sudden death.7 In those Self-terminating VF is unusual; presum- without obstructive coronary artery disease ably it occurs only when there is rapid and coronary spasm is likely to be important in complete re-establishment of prexisting nor- inducing ischaemia and the associated subse- mal electrophysiological properties in the quent reperfusion.
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