Pacemaker-mediated angina

Abstract

Angina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back or arm. It is typically aggravated by exertion or emotional stress and relieved by nitroglycerin. Atherosclerotic coronary artery disease is the most common cause of angina. Dual-chamber pacemakers track the atrial electrical activity by pacing the ventricle. The present article reports the first case in the literature involving pacemaker-mediated angina. A 78-year-old man complained of chest pain shortly after the placement of a permanent dual-chamber pacemaker and experienced immediate relief of his pain after the pacemaker mode was switched from tracking the atrium and pacing the ventricle to sensing and pacing the ventricle. The pain was identified as angina pectoris. The comprehensive history-taking performed before pacemaker placement helped to quickly identify the cause of the patient’s pain.

Chest pain during pacemaker placement may indicate a critical complication. Obtaining a detailed history before placement is very important, particularly in patients who exhibit multiple risk factors for coronary artery atherosclerosis.

CASE PRESENTATION

A 78-year-old Caucasian man presented to hospital after experiencing a syncopal episode while walking from his bedroom to his kitchen. He also complained of experiencing worsening dizziness for several weeks before admission. On questioning, he complained of angina on moderate exertion, which he had not experienced since the decline in his functional capacity. The patient had type 2 diabetes mellitus, hypertension and hypercholesterolemia. He had a remote history of tobacco use and had ceased smoking 30 years before admission. His father had died of a heart attack late in his sixth decade of life. The patient was taking metformin, acetylsalicylic acid, simvastatin and lisinopril. His physical examination was remarkable for bradycardia, with a heart rate of 40 beats/min. The patient’s blood pressure was 160/70 mmHg and was equal in both arms. Orthostatic hypotension was not observed during the examination. An early-peaking systolic murmur was detected at the right upper sternal border, which changed the intensities of heart sounds, and intermittent cannon A waves in the jugular venous pulse. An electrocardiogram revealed a complete heart block with an escape rhythm of 40 beats/min (Figure 1). Laboratory testing revealed no electrolyte abnormalities, and test results for cardiac enzymes were negative. The patient underwent placement of a permanent pacemaker the following morning. Insertion of the leads was uneventful; however, after connecting the leads with the device, the pacemaker began tracking the atrial activity and pacing the ventricle (DDD mode), with a heart rate between 100 beats/min and 105 beats/min, and the patient began experiencing angina pectoris similar to the pain he had previously described. A focused physical examination revealed clear lung fields, S4 gallop and the previously described systolic murmur. His blood pressure was 170/80 mmHg and oxygen saturation was 98% on a 2 L nasal cannula. Several minutes later, the pacemaker mode was switched to sensing and pacing the ventricle (VVI mode) with a heart rate of 68 beats/min (Figure 2) and the patient experienced near-immediate relief of his angina pectoris. The patient underwent left heart catheterization, which revealed severe triple-vessel coronary artery disease (Figures 3, 4, 5 and 6) and no significant gradient across the aortic valve. He underwent a successful coronary artery bypass surgery.

Figure 1).

An electrocardiogram showing complete heart block with slow escape rhythm

Figure 2).

An electrocardiogram recorded after pacemaker placement

Figure 3).

Coronary angiogram. The arrow indicates the left circumflex artery stenosis

Figure 4).

Coronary angiogram. The arrows indicate the right coronary artery stenoses

Figure 5).

Coronary angiogram. The white arrow indicates the left anterior descending coronary artery being filled by collaterals (black arrow) from the right coronary artery

Figure 6).

Coronary angiogram. The arrow indicates the occluded left anterior descending artery

DISCUSSION

There is no question that ischemic heart disease remains a major public health problem. Chronic stable angina is the initial manifestation of ischemic heart disease in approximately one-half of patients (1,2). The reported annual incidence of angina among individuals older than 30 years of age is 213 per 100,000 (1). Angina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back or arm. It is typically aggravated by exertion or emotional stress and relieved by nitroglycerin. Angina usually occurs in patients with coronary artery disease (CAD) involving at least one large epicardial artery. The history and clinical examination are the most important steps in the evaluation of patients with chest pain, and allow the clinician to estimate the likelihood of clinically significant CAD with a high degree of accuracy (3). Significant CAD is defined angiographically as CAD with ≥70% stenosis of at least one major epicardial artery segment or ≥50% stenosis of the left main coronary artery. Although lesions involving a lower extent of stenosis may also cause angina, they have much less prognostic significance (4). A detailed description of the symptom complex enables the clinician to characterize the chest pain (5). Five components are typically considered: the quality, location and duration of pain, factors that provoke the pain and factors that relieve the pain. After a history of the pain is obtained, the physician makes a global assessment of the symptom complex. One classification scheme for chest pain used in many studies includes three groups: typical angina, atypical angina and noncardiac chest pain (6). Typical presentations of stable angina are chest discomfort and associated symptoms precipitated by activity (eg, running, walking) with minimal or nonexistent symptoms at rest. Symptoms typically abate several minutes following cessation of the precipitating activity and recur when the activity is resumed.

A detailed history of our patient revealed that he had complained of typical angina for a significant period of time but had not experienced angina for several weeks before admission, subsequent to complaints of a decline in his functional capacity. We believe that this decline in functional capacity was precipitated by developing bradycardia secondary to a complete heart block. The patient experiencined a decline in his exercise capacity due to the bradycardia but did not seek medical attention until he experienced a syncopal episode. After pacemaker placement with DDD mode application, the pacemaker tracking of the atrial P waves raised his ventricular rate to more than 100 beats/min from 40 beats/min. This sudden increase in heart rate led to myocardial ischemia due to the increased oxygen demand and caused the patient to experience typical angina. Given the fact that the patient’s history had been reviewed carefully before his procedure, a decision was made to change the pacemaker mode to VVI (rate of 68 beats/min) and the patient experienced near-immediate relief of his angina.

CONCLUSION

Pacemaker-mediated angina is an angina pectoris evoked by a sudden increase in heart rate in response to tracking the atrial activity by pacing the ventricle. Obtaining a detailed history is crucial before pacemaker insertion. Without obtaining a detailed history, this type of chest pain may be mistaken as a procedure-related complication, causing unnecessary tests to be ordered and leading to operator panic during pacemaker placement.