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Past Issue:
Volume 13, Number 2 • April 2000
 
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BUMC Proceedings 2000;13:175-176

The whole truth: artificial pacemaker malfunction precipitates unstable angina
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D. LUKE GLANCY, MD, AND FADI NADDOUR, MD

From Section of Cardiology, Department of Medicine, Louisiana State University Medical Center, New Orleans.

Corresponding author: D. Luke Glancy, MD, Section of Cardiology, Department of Medicine, Louisiana State University Medical Center, 1542 Tulane Avenue, New Orleans, Louisiana, 70112-2822.

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he computer-assisted reading of the electrocardiogram (ECG) in Figure 1 tells the truth, but not the whole truth. Crucial data are omitted: the atria are fibrillating and the firing of the ventricular pacemaker is not only rapid, but irregular.

The ECG belongs to an 85-year-old man who came to the hospital because of unstable angina. At age 66, he had undergone a coronary artery bypass operation utilizing 5 saphenous veins, and between ages 70 and 76, he had had 3 coronary angioplasty procedures for episodes of unstable angina. Paroxysms of atrial fibrillation appeared when he was 77 and 81. At age 82, a transvenous DDD pacemaker was inserted because of symptomatic sinus pauses of up to 4 seconds. In recent years his angina had always been exertional and mild. He had been able to complete his daily 2-mile walk without difficulty with the aid of nifedipine and atenolol and with prophylactic nitroglycerin taken sublingually at both the beginning and the halfway point of the walk. Beginning 2 weeks before admission, however, any exertion brought on angina, which also began occurring at rest. On the day of admission, a 2-hour episode of chest pain was unrelieved by 3 nitroglycerin tablets.

Unstable angina frequently results from instability of a coronary plaque with an increase in coronary arterial narrowing. Not infrequently, however, worsening angina is caused by a decrease in blood oxygen carrying capacity or by an increase in myocardial oxygen demand (Table). This patient forgot to take amiodarone for 2 to 3 months, allowing atrial fibrillation to reappear. His intrinsic atrioventricular nodal disease would have prevented a rapid ventricular response, but the atrial lead of the pacemaker sensed many of the fibrillatory waves, thus causing rapid pacing of the ventricles. When the patient was admitted, his pacemaker was reprogrammed to the VVI mode at a rate of 50 beats per minute (Figure 2), and he had no further angina. Cardiac enzymes remained normal, and since his discharge, the patient has reverted to his old pattern of infrequent, mild, exertional angina.

In this patient unstable angina was not precipitated by worsening of his long-standing 3-vessel coronary disease but by the onset of atrial fibrillation and malfunction of his DDD pacemaker. The ECG was the key to making this diagnosis.

Table. Some noncoronary causes of worsening angina pectoris in patients with coronary artery disease
  • Anemia
  • Tachyarrhythmia
  • Uncontrolled systemic hypertension
  • Hyperthyroidism
  • Increased physical and/or psychological stress
  • Volume overload
  • Failure to comply with treatment

General references

Clinical Practice Guideline Number 10: Diagnosing and Managing Unstable Angina. Rockville, Md: National Heart, Lung, and Blood Institute, US Department of Health and Human Services, 1994.