Written by: Alec Feuerbach, MD
Edited by: Robby Allen, MD; Antonia Quinn, DO
A 60(ish)-year-old woman presents to the ED describing an intermittent substernal chest pain that began the night before. She last experienced it again in the morning and has felt it intermittently in the ED. The pain is sharp, doesn’t radiate, and lasts minutes. She says she’s been feeling “off” since April when she had contracted COVID. She still feels short of breath with exertion and can’t even walk three blocks. She’s otherwise pretty healthy with only a history of pre-diabetes and high cholesterol. She denied fevers, cough, abdominal pain, nausea, and vomiting.
Though she had unremarkable triage vitals and looks uncomfortable on rounds, her ECG is:
The rhythm is sinus with borderline tachycardia (97 bpm), a normal axis, normal PR and QT intervals, with a new left bundle branch block (prolonged QRS, S waves in V1 and V2, notched R waves in I, aVL, V5 and V6) is new. Remember, though, a new left bundle block is not a STEMI equivalent (a new left bundle block represents acute MI in 2-4% of cases — the same rate as an old left bundle block and chest pain) and this ECG does not meet Sgarbossa’s original or modified criteria for acute MI (1,2). Her troponin is negative, BNP is within a normal range, and her D-Dimer is negative. Cardiology believes her pain to be atypical for ACS, but recommends placing her in observation for serial troponin testing and ECGs.
This is where the case gets interesting because her repeat ECG is:
The heart rate has slowed (73 bpm) and her bundle branch block has disappeared, but now the T waves in V1-V3 look biphasic (more on that later). Three hours later, the heart rate increases slightly (87 bpm), her blood pressure rises to 206/98 mm Hg, and the bundle branch block returns. The next morning, the heart rate is 82 bpm, and the block is gone again. On the monitor, she has short “runs” of sinus rhythm with left bundle branch pattern while holding her chest in pain. Her cardiac enzymes remain negative, but the decision is made to transfer her for a possible cath. When she arrives at the PCI-capable center, her pressure is 190/100 mm Hg and the left bundle branch block is present. A nitroglycerin drip is started. A bedside echocardiogram shows no wall motion abnormalities and a formal echo, the next day, shows only a slightly thickened aortic valve. The patient is started on an ACE inhibitor and hydrochlorothiazide. Her blood pressure improves, her ECG remains without conduction abnormality, and she is discharged.
So what’s going on? And why?
. . . to be continued . . .
References:
[1] Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators [published correction appears in N Engl J Med 1996 Apr 4;334(14):931]. N Engl J Med. 1996;334(8):481-487. doi:10.1056/NEJM199602223340801 [2] Meyers HP, Limkakeng AT Jr, Jaffa EJ, et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J. 2015;170(6):1255-1264. doi:10.1016/j.ahj.2015.09.005
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