Abstract

Scenario: An 87-year-old woman with a history of atrial fibrillation, hypertension, and hyperlipidemia came to the emergency department with substernal chest pain that was not relieved with nitroglycerin. She was found to be in atrial fibrillation with rapid ventricular response and had dynamic troponin levels that were concerning for myocardial infarction. Left-sided cardiac catheterization revealed severe coronary disease with about 80% occlusion of the left main and left anterior descending coronary arteries; however, percutaneous coronary intervention (PCI) was not done because of the patient’s hemodynamic instability. After the catheterization, she continued to have substernal chest pain for 2 days and was taken back for emergent PCI with temporary mechanical ventricular support. Two drug-eluting stents were placed. Her bedside electrocardiography (ECG) strip after the emergent PCI is shown here.Atrial bigeminy with a sinus rate of 35 beats per minute and right bundle branch block (RBBB).This patient exhibited multiple deficits in conduction due to acute occlusion of the left main and left anterior descending (LAD) coronary arteries leading to infarction of the surrounding myocardium. The left main coronary artery arises from the aorta, passes between the pulmonary trunk and the left atrial appendage, and bifurcates into the LAD and the left circumflex coronary artery. The LAD, of interest in this example, supplies oxygenated blood to the interventricular septum and left ventricle. Occlusion of both the left main and LAD coronary arteries likely led to the atrial bigeminy and RBBB seen here.Occlusion of the left main coronary artery can induce ischemia in the left atrium and left atrial appendage, propogating atrial bigeminy, a regularly irregular rhythm where a premature atrial contraction (PAC) follows each normal sinus beat (N). Ischemia propagates spontaneous electrical activity such as PACs and disrupts normal conduction. When another region of the atria depolarizes before the sinoatrial node, PACs occur; the PACs may be sporadic or patterned (eg, bigeminy, trigeminy). On an ECG, PACs may show a P wave morphology different from the sinus beat or no P wave preceding the QRS complex. If the P wave preceding the QRS complex is not visible, the P wave is most likely embedded in the preceding T wave. Both PACs and sinus beats travel down the same conduction pathway to the ventricle, producing a morphologically similar QRS complex; this feature differentiates PACs from premature ventricular contractions, which have grossly different morphologies, unless there is an existing BBB (as here), which makes distinguishing PACs from premature ventricular contractions challenging.The wide QRS complexes with slurred qRs morphology in lead V1 and the discordant T waves are due to RBBB, most likely caused by the occlusion of the LAD. In about 90% of patients, the proximal LAD septal perforators perfuse the right bundle branch and the anterior fascicle of the left bundle branch. Thus, occlusion of the LAD may have caused subsequent ischemia in the intraventricular septum, slowing conduction through the bundle branches and inducing an RBBB in this patient. Importantly, an RBBB does not preclude assessment of ST-segment elevation indicative of transmural ischemia due to coronary occlusion, but since it is unknown if the RBBB was preexisting, it is best to review a previous ECG tracing.After emergent PCI, the patient developed atrial bigeminy and remained in the irregular rhythm for 6 hours. She did not develop new ischemic symptoms and did not require more interventions. She remained clinically unstable with a bradycardic sinus rate in atrial bigeminy, but no signs or symptoms of hypoperfusion were noted. The bedside nurse closely monitored the patient and the ECG because atrial bigeminy can progress to atrial fibrillation. Optimal guideline-based therapies for acute coronary syndrome, including dual antiplatelet therapy, are indicated to maintain stent patency. Careful monitoring of the ST segments for ischemia is indicated.

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