1146 BRIEF REPORTS

FIGURE 1. Left coronary angiogram in the right anterior oblique pro- jection. Note the 80% diameter left main stem stenosis (arrow). This angiogram was performed after the administration of intracoronary nitroglycerin.

dominal examination revealed uterine enlargement consis- tent with a pregnancy of 12 to 14 weeks.

The resting electrocardiogram revealed nonspecific ST- T-wave changes. During spontaneous chest pain, at bed rest, there was 4 mm of ST-segment depression throughout the precordial leads associated with ventricular ectopic ac- tivity.

Cardiac catheterization demonstrated a left ventricular end-diastolic pressure of 10 mm Hg. Angiography disclosed a 90% diameter reduction of the left main coronary artery with collateral flow from the right coronary artery to the left circumflex artery. The right coronary artery was normal. Repeat catheterization the next day, after the institution

of high-dose oral nitrate therapy, disclosed an 80% diameter reduction of the left main coronary artery after intracoronary nitroglycerin (Fig. 1). The total radiation dose to the lower abdomen was 0.010 rem.

The patient continued to have frequent episodes of angina at rest despite isosorbide dinitrate (20 mg orally and 20 mg sublingually every 3 hours) alternating at 90 minutes with topical nitroglycerin (3 inches every 3 hours). CABG was subsequently performed, with grafts to the left anterior de- scending artery, left circumflex artery and left obtuse mar- ginal artery. Cardiopulmonary bypass time was 90 minutes. Convalescence after surgery was uneventful. Subsequently, the pregnancy was uneventful and the patient gave birth to a full-term 3.2-kg girl who was normal.

CAD in pregnancy may be difficult to recognize. Manifestations of chest discomfort during pregnancy are likely to be ascribed to gastrointestinal, abdominal or nonspecific cause. Although one is reluctant to per- form coronary angiography in a pregnant patient, shielding of the abdomen with monitoring of the fetal dosage and utilization of the brachial rather than the femoral approach, as was done in our patient, allows the study to be performed, when necessary, without sig- nificant radiation exposure. Although CABG has not previously been reported during pregnancy, in this patient with severe left main coronary narrowing, we believe that it was life saving and resulted in a normal full-term pregnancy.

References

1. Ginz B. Myocardial infarction in pregnancy. J Obstet Gynecol 1970;77: 610-615.

2. Husalnl MH. Myocardial infarction during pregnancy; report of two cases with a review of the literature. Postgrad Mad J 1971;47:660-665,

Electrocardiographic Events Before, During and After Acute Myocardial Infarction in 2 Ambulant Subjects

ROBIN J. NORTHCOTE, MRCP DAVID BALLANTYNE, MD, FRCP (Glasg.)

The use of ambulatory electrocardiography has in- creased the possibility of monitoring a subject during myocardial infarction (MI). Case reports1,2 have docu- mented the electrocardiographic events associated with sudden cardiac death.

We report electrocardiographic events recorded by Holter ambulatory monitoring in 2 patients with out- of-hospital acute MI. Both subjects were monitored with a 2-channel recorder (Oxford Instruments Medilog 2).

From the Department of Medical Cardiology, The Victoria Infirmary, Glasgow, United Kingdom. Manuscript received April 26, 1983; revised manuscript received June 16, 1983, accepted June 21. 1983.

FIGURE 1. Case l-standard 12-lead electrocardiogram showing early features of a transmural anteroseptal myocardial infarction.

Case 1: A 44-year-old man who had an inferior wall, transmural MI 8 months previously was being monitored as part of a general assessment of his cardiac status. After 12 hours and 15 minutes of monitoring (at 22.30 hours), he de- veloped crushing central chest pain. Two hours later, he was admitted to the hospital, and his chest pain was relieved using major analgesics. In the 3 weeks before this event, he had a gradual onset of angina1 symptoms. His only therapy at this time was nifedipine, 10 mg 4 times daily. Holter monitoring was continued until 11 hours after admission to

November 1, 1983 THE AMERICAN JOURNAL OF CARDIOLOGY Volume 52 1147

t lime,hcurs Onset chest pain, 12h.15m.j

FIGURE 2. Case l-heart rate and frequency of ventricular ectopic beats throughout a 24-hour continuous electrocardiogram, with onset of chest pain after 12 hours and 15 minutes of monitoring.

hospital. A fresh anteroseptal MI was confirmed by a stan- dard 12-lead electrocardiogram (Fig. 1) and elevation of serum enzymes.

Analysis of the continuous electrocardiographic (ECG) recording revealed an increase in heart rate and frequency of ventricular ectopic beats (VEBs) before the onset of chest pain. These findings persisted for 1 hour after the onset of symptoms (Fig. 2). Thereafter, both heart rate and VEBs diminished. Throughout monitoring, ST-segment depression in the modified V5 lead (MV& persisted. In the 30 minutes before the onset of symptoms, ST-segment depression in lead MV5 and ST-segment elevation in lead MV1 became pro- nounced (Fig. 3). All VEBs recorded were long cycle beats (RRJQT > 1). Paired VEBs occurred only in the first hour after onset of symptoms.

Case 2:A 51-year-old woman, who had episodes of palpi- tations after an anterior wall MI 2 months previously un- derwent ambulatory electrocardiography. After 10 hours of monitoring (at 21.45 hours), central chest pain developed and she was admitted to the hospital, where another anterior MI was confirmed. At the time of this MI she was taking no medication. Analysis of the ambulatory ECG recording showed an increase in the mean hourly heart rate, from 82 to 98 beatslmin, in the 2 hours before the onset of chest pain. After the onset of chest pain the number of VEBs increased dramatically, reaching 193 in the first hour and diminishing thereafter. ST-segment depression in lead MVg became more pronounced in the hour before the onset of chest pain, and remained so afterwards (Fig. 4). All VEBs were unifocal, long-cycle beats (RRJQT < 1). Two episodes of ventricular bigeminy occurred in the first hour after the onset of symp- toms.

FIGURE 3. Case l-electrocardiogram recorded before the onset of chest pain (17.03 hours) and at the time of onset of symptoms (22.30 hours).

In both cases, similar ECG changes occurred in as- sociation with the acute MI. Heart rate increased before the onset of symptoms, with the greatest frequency of VEBs in the first hour thereafter. ST-segment changes indicative of myocardial ischemia occurred well before the onset of symptoms and persisted thereafter.

Sudden death complicating MI is most often a result of development of a ventricular tachyarrhythmia, which is more prevalent in the first few hours after the onset of symptoms.3 We are unaware of any documentation of ECG events preceding MI. Most cases report ECG findings at least several minutes after the onset of symptoms. Thus, the ECG antecedents of MI in am- bulant subjects are not clearly understood. In our cases, increased ventricular ectopic activity was most evident before and in the first hour after the onset of symp- toms.

Some workers4T5 have advocated the use of antiar- rhythmic drugs immediately when the patient with acute MI is seen by medical attendants. Perhaps this measure will decrease the likelihood of a ventricular tachyarrhythmia in the early stages.

1.

2.

3.

4.

5.

References

Lahiri A, Balasubramian V, Raftery EB. Sudden death during ambulatory monitoring. Br Med J 1979;1:1676-1678. Pool J, Kunsi K, Van Wermeskerken JL. Two monitored cases of sudden death outside hospital. Br Heart J 1978;40:627-629. Lawrie DM, Higgins MR, Godman MJ, Oliver MF, Jullan DG, Donald KW. Ventricular fibrillation complicating acute myocardial infarction. Lancet 1968;2:523-528. Yusuf S, Pet0 R, Bennett D, Ramsdale D, Fume L, Bray C, Sleight P. Early intravenous atenolol treatment in suspected acute myocardial infarction: preliminary report of a randomised trial. Lancet 1980;2:273-276. Norrls RM, Barnaby PF, Geary GG. Intravenous &blockers during unstable angina and threatened infarction. Br J Clin Pharm 1982;14:298-39%

H 8 8 8 n n n N I N N

FIGURE 4. Case 2-electrocardiogram before the onset of chest pain (12.20 hours), at the onset of symptoms (21.30 hours) and persistence of ST-segment changes almost 1 hour later (22.24 hours).