From the Thoracic and Cardiovascular Institute, Sparrow Health System & Michigan State University, Lansing, Michigan. The authors report no conflicts of interest regarding the content herein. Manuscript submitted February 12, 2009, provisional acceptance given March 3, 2009, final version accepted March 11, 2009. Address for correspondence: Ranjan K. Thakur, MD, MPH, Thoracic and Cardiovascular Institute, 405 West Greenlawn, Suite 400, Lansing, MI 48910. E-mail: firstname.lastname@example.org
_______________________________________________ ABSTRACT: A patient with a dual-chamber pacemaker with dynamic atrio-ventricular delay (AVD) experienced acute substernal chest pain. The rhythm strip in the ambulance showed intermittent ST elevation in the inferior leads. An emergent cardiac catheterization revealed nonobstructive coronary artery disease. Rate-responsive dual-chamber pacing with dynamic AVD was responsible for varying degrees of ventricular fusion due to competition with the patient’s normal conduction. Intermittent ST elevation, evident only during ventricular fusion should have suggested secondary ventricular repolarization and not myocardial injury, but concomitant chest pain and inconspicuous bipolar pacing artifacts added to the confusion. Ventricular pacing may not only mask acute ST-T changes due to myocardial injury, but can also mimic acute myocardial infarction.
J INVASIVE CARDIOL 2009;21:E164–E165 Key words: Pacemaker, myocardial infarction, ST-segment elevation Diagnosis of acute myocardial infarction (AMI) can be challenging in patients with a paced rhythm because secondary ST-T-wave changes can obscure acute repolarization changes due to MI. This is the first reported case of cardiac pacing mimicking an AMI. Case Description. A 71-year-old hypertensive male with a history of smoking presented to an emergency department following an episode of syncope preceded by dizziness and feeling of numbness over the face. There was no seizure activity. He had experienced multiple episodes of syncope and underwent a tilt table test, which was normal. He also had a past history suggestive of myocardial infarction. Nine months previously, he received an Insignia 1290 dual-chamber rate-responsive pacemaker (Boston Scientific Corp., Natick, Massachusetts) for symptomatic bradycardia due to sick-sinus syndrome. Pacemaker interrogation 1 month previously had not shown any abnormalities. His pacemaker was programmed to pace at 60–120 beats per minute (bpm) with dynamic atrioventricular delay (AVD). The patient was transferred to a tertiary-care facility for further evaluation. While in the ambulance, he developed severe substernal chest pain associated with ST elevation in the inferior leads on the cardiac monitor (Figure 1). He was started on intravenous (IV) nitroglycerin infusion in the ambulance. His blood pressure was 110/69 mmHg and the remainder of the examination was normal. His cardiac biomarkers were normal: troponin 0.07 ng/mL and CPK 73 U/L. He was suspected to have transient coronary spasm and underwent an emergent cardiac catheterization, which showed nonobstructive coronary artery disease involving the left circumflex and right coronary arteries with thrombolysis in myocardial infarction (TIMI)-3 flow and normal left ventricular systolic function. His chest pain resolved spontaneously. Discussion. Analysis of the rhythm strips from the ambulance (leads I–III) revealed atrioventricular synchronous pacing at a rate of 85–90 bpm associated with intermittent and varying degrees of ST elevation in the inferior leads. ST elevation was present only intermittently, as seen in Figure 1. Careful analysis of the beats with ST elevation suggests ventricular fusion evidenced by the presence of a ventricular pacing artifact and the QRS complex being a hybrid of normal and paced beats. Rate-responsive dual-chamber pacing with dynamic AVD was responsible for generating varying degrees of fusion because of competition with the patient’s normal AV conduction. Ventricular fusion was not recognized because the bipolar pacing artifacts were inconspicuous — as they generally are — and the index of suspicion for an ischemic event was heightened by the presence of chest pain and ST elevation. The intermittent nature of the patient’s ST elevation should have suggested secondary ventricular repolarization abnormality and not myocardial injury. The electrocardiogram (ECG) is a vital source of information in diagnosing AMI. Diagnosis of AMI in a paced patient is difficult because of secondary ST-T wave changes, which can mask an ongoing infarction.1,2 This can give rise to difficulties in applying conventional methods of diagnosis of an AMI.3 Because of a similar sequence of ventricular activation in left bundle branch block (LBBB) and right ventricular (RV) apical pacing, the criteria for diagnosing MI in the setting of LBBB are also applicable to RV apical pacing. Sgarbossa et al analyzed all pacemaker patients in the GUSTO 1 trial and derived ECG signs suggestive of AMI which include: 1) ST-segment elevation ≥ 1 mm in the presence of a positive QRS complex; 2) ST-segment depression ≥ 1 mm in lead V1, V2 or V3; and 3) ST-segment elevation ≥ 5 mm in the presence of a negative QRS complex.4 But in their subgroup analysis, patients who had intrinsic and/or fusion beats were excluded. While ST-T wave changes in AMI can be concealed by a paced rhythm, this is the first reported case of a patient in whom ventricular fusion mimicked an AMI. It illustrates the difficulties of interpreting ST-T wave changes in a paced patient.
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