Suppression of Repeatedly Occurring Ventricular

Fibrillation with Nifedipine in Variant

Form of Angina Pectoris

Eiichi KIMURA, M.D., Keiji TANAKA, M.D., Kyoichi MIZUNO, M.D., Yuichiro HONDA, M.D., and Hidehiro HASHIMOTO, M.D.

SUMMARY

It is reported that nifedipine, a newly developed antianginal agent,

was dramatically effective to suppress the repeatedly occurring ventricular

fibrillation in 2 cases of variant form of angina pectoris.

Additional Indexing Words:

Antianginal agent

TTACKS of variant form of angina pectoris are known to be accompanied

by several kinds of arrhythmias in many cases. Among them, ventri-

cular fibrillation is the most serious complication, sometimes leading to the

death of patients. In following 2 cases nifedipine,1) a newly developed an-

tianginal agent, was dramatically effective to suppress the repeatedly oc-

curring ventricular fibrillation in variant form of angina pectoris.

CASE REPORTS

Case 1. A 64-year-old male was suffering from precordial pain lasting 1 to

2 min since December, 1975. He was admitted to the Coronary Care Unit of the

Nippon Medical School Hospital at 6 a.m. on March 9, 1976, because of girdle

sensation in the chest, which occurred during sleep in the early morning on the

same day, persisting for about 60 min.

Fig. 1 shows the ECG taken at the intermittent period, which exhibited the

WPW syndrome of type A pattern. The ECG illustrated in Fig. 2 was recorded

during an anginal attack, in which elevation of the ST segment in Leads II and III is clearly observed. This ST elevation disappeared after 5 min, returning to

the ECG previous to the attack. From these findings the diagnosis of variant

form of angina pectoris associated with WPW syndrome was made.

At 9.12 a.m. on the same day ventricular fibrillation occurred suddenly as

seen in Fig. 3, which was converted to sinus rhythm by countershock. Thereafter

From the Department of Internal Medicine, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113,Japan.

Received for publication February 10, 1977.

736

Vol. 18 No. 5 NIFEDIPINE ON VENTRICULAR FIBRILLATION 737

Fig. 1. ECG of Case 1 taken at the intermittent stage, showing WPW

syndrome of type A pattern.

Fig. 2. ECG of Case 1 taken during an attack, showing ST elevation in

Leads II and III in addition to the WPW pattern.

738 KIMURA, TANAKA, MIZUNO, HONDA, AND HASHIMOTO Jap. Heart J. September, 1977

Fig. 3. Ventricular fibrillation observed in Case 1.

Fig. 4. Clinical course of Case 1 during the period of repeated attacks

of ventricular fibrillation.

he experienced 21 episodes of transient ST elevation and 12 attacks of ventricular fibrillation in spite of the continuous intravenous drip infusion of lidocaine of 2 to 4mg/min. DC defibrillation was required 3 times.

Finally nifedipine of 0.2 mg was given intravenously, whereupon the ventri-cular extrasystole decreased markedly in number, along with complete suppression of ventricular fibrillation, as indicated in Fig. 4. Three hours later oral admin-istration of nifedipine was started with a daily dose of 30 mg. Thereafter neither attack of variant angina nor ventricular fibrillation occurred probably due to the effect of the drug.

Cinecoronary arteriography demonstrated 90% stenosis of the right coronary

Vol. 18 No. 5 NIFEDIPINE ON VENTRICULAR FIBRILLATION 739

Fig. 5. ECG of Case 2 taken during an attack. ST elevation in V1 to V4

is observed in addition to the right bundle branch block.

Fig. 6. ECG of Case 2 showing ventricular fibrillation which disappeared

spontaneously in the latter half of the record.

740 KIMURA, TANAKA, MIZUNO, HONDA, AND HASHIMOTO J ap. Heart J. September, 1977

Fig. 7. ECG of Case 2 taken at the intermittent stage. Neither ST

elevation nor right bundle branch block is observed.

Fig. 8. Clinical course of Case 2 during the period of repeated attacks

of ventricular fibrillation.

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NIFEDIPINE ON VENTRICULAR FIBRILLATION 741

artery just proximal to the branching portion of acute marginal branch. He was discharged on March 6, 1976, without complaints.

Case 2. A 65-year-old male had the first attack of anginal pain on June 20, 1976. He was admitted to the Coronary Care Unit of the Nippon Medical School Hospital at 1.50 a.m. on June 24 because of anginal attack which occurred 11.00

p.m. of the previous day.On admission the patient was still complaining of severe chest pain and the

ECG showed the right bundle branch block pattern with ST elevation in V1 through V4, as seen in Fig. 5. Immediately after admission an attack of ventricular fibrilla-tion occurred, but it was eliminated by countershock. Thereafter he experienced 3 episodes of ventricular fibrillation, which terminated spontaneously without using defibrillator. One of these episodes is illustrated in Fig. 6. Fig. 7 shows the ECG at the intermittent period, in which both the right bundle branch block and ST elevation disappeared. However, Q deflection was observed in V2, suggesting the remnant of previous myocardial infarction.

As seen in Fig. 8, attack of chest pain and transient ST elevation occurred repeatedly. Lidocaine was thought ineffective, because the 4th attack of ventricular fibrillation occurred during its intravenous drip infusion. Then, nifedipine of 0.4 mg was given intravenously at 6.30 a.m. Thereafter, chest pain, ventricular fibrilla-tion and ventricular extrasystoles were completely suppressed, although only one brief episode of ST elevation occurred. The deep Q wave and persisting ST eleva-tion, however, appeared in leads V1 to V4 at 6.50 p.m. on the same day, indicating development of anteroseptal infarction. After hospitalization for 13 weeks, the

patient was discharged without any complaints. Cinecoronary arteriography was not carried out, because agreement of the patient was not obtained.

DISCUSSION

It is indisputable that Case 1 was suffering from variant angina, although it was complicated with WPW syndrome. On the other hand, Case 2 cannot be regarded simply as variant angina, because Q deflection was present in V2 at the intermittent period. According to the recent opinions, however, variant angina is ascribed to the coronary spasm and it is not inconceivable that coronary spasm can occur in some branch even when old myocardial infarction is present. In the present case, the symptoms and signs are almost in accordance with variant angina except the presence of Q deflection in V2. It is justifiable, therefore, that this case is regarded as a type of variant angina as far as the relationships between coronary hemodynamic changes and ef-fects of the drugs concern.

Nifedipine is an antianginal agent developed very recently and par-ticularly effective on variant form of angina pectoris according to our experi-ences.2) It was dramatically effective in the above described cases and attack of ventricular fibrillation was completely eliminated, although intravenous lidocaine did not prevent the occurrence of the attack.

742 KIMURA, TANAKA, MIZUNO, HONDA, AND HASHIMOTO J ap. Heart J. September, 1977

Such findings lead us to the concept that this drug has some electrophy-

siological actions on the cardiac automaticity or conduction. Although the

properties of this drug have not been examined in detail, Taira and his col-leagues3),4) demonstrated in animal experiments that nifedipine has no effect

on A-V conduction in practical sense. Therefore, it is more reasonable to

consider that nifedipine was effective on ventricular fibrillation indirectly

through its antianginal action. In other words, effect of this drug should be

attributed to the action to improve the myocardial ischemia which is causative

of ventricular fibrillation.

Although the prognosis of variant angina is said usually favorable, some

patients succumb to ventricular fibrillation which occurs abruptly in associa-tion with the attack. In this regard the effectiveness of nifedipine for preven-

tion of this serious complication must be highly appreciated.

REFERENCES

1. Kimura E, Mabuchi G, Kikuchi H: The clinical effect of 4-(2'-nitrophenyl)-2,6-dimethyl-3,5-dicarbomethoxyl-1,4-dihydropyridine (BAY a 1040) on angina pectoris evaluated by se-

quential analysis. Arzneim-Forsch 22: 365, 19722. Hosoda S, Kimura E: Efficacy of nifedipine in the variant form of angina pectoris. 3rd

International Adalat Symposium. Excerpta Medica, Amsterdam, Oxford, p 195, 19763. Taira N, Motomura S, Narimatsu A, Iijima T: Experimental pharmacological investigations

of effects of nifedipine on atrioventricular conduction in comparison with those of other coro-nary vasodilators. 2nd International Adalat Symposium. Springer-Verlag, Berlin, Heidel-berg, New York, p 40, 1975

4. Narimatsu A, Taira N: Effects on atrio-ventricular conduction of calcium-antagonistic coro-nary vasodilators, local anesthetics and quinidine injected into the posterior and the anterior septal artery of the atrio-ventricular node preparation of the dog. Naunyn-Schmiedberg's Arch Parmacol 294: 169, 1976