Differential Diagnoses in a Patient With Palpitations and Global Electrocardiographic Changes

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Scenario: A 39-year-old man with no prior medical history came to the emergency department with new-onset palpitations that had started earlier in the day. He described the sensation as an intermittent “fluttering” in his chest without associated chest pain, dyspnea, syncope, or presyncope. He denied prior similar episodes, recent illness, stimulant use, or family history of heart disease. A 12-lead electrocardiogram (ECG) obtained in triage was interpreted by automated software as showing “abnormal” findings, prompting urgent evaluation. He was asymptomatic, with stable vital signs and normal oxygen saturation on room air. Findings on physical examination were largely unremarkable, except for a soft systolic murmur best appreciated along the left sternal border that did not change with Valsalva maneuver or standing.Normal sinus rhythm at 75/min and left ventricular hypertrophy (LVH) with strain pattern. The observed ST-T abnormalities are most likely secondary repolarization changes due to LVH.The ECG demonstrates voltage criteria for LVH accompanied by repolarization abnormalities, including ST-segment depression and T-wave inversion in the lateral precordial leads, which are characteristic of an LVH “strain” pattern. This pattern refers to down-sloping ST-segment depression followed by asymmetric T-wave inversion, most prominently in leads reflecting the left ventricle (eg, leads I, aVL, V5, and V6). Importantly, these ST-T changes are characteristically not symmetric, which helps distinguish secondary repolarization abnormalities (as seen in LVH) from primary repolarization changes. These findings arise from a hypertrophied myocardium, where increased myocardial mass and altered cellular architecture lead to prolonged depolarization and delayed repolarization, reflecting electrical remodeling and increased wall stress.ST-T abnormalities in LVH with strain pattern can mimic acute coronary syndrome (ACS), but several features help differentiate them. Unlike LVH, ACS more commonly produces dynamic, territorial ST-T changes with reciprocal findings and T-wave inversions that are symmetric and often disproportionate to the QRS complex. Because overlap can occur, clinical context, serial ECGs, and cardiac biomarkers remain essential to distinguish LVH from acute ischemia.Left ventricular hypertrophy can be classified into several patterns based on ventricular geometry and underlying origin, including concentric hypertrophy from chronic pressure overload, eccentric hypertrophy associated with volume overload, and asymmetric or focal hypertrophy as seen in hypertrophic cardiomyopathy (HCM).In the emergency department, the initial priority is triage of the patient based on acuity by distinguishing between ACS and nonischemic causes such as structural heart disease. Evaluation of serial 12-lead ECGs, high-sensitivity troponin measurements at 0 and 1 hours, and continuous cardiac monitoring should be used to assess for ischemia. Patients with LVH are at risk for atrial fibrillation, which can be associated with palpitations, as experienced by this patient; thus, continuous ECG monitoring for this arrhythmia is warranted. In the absence of ischemia, empiric ACS therapies (eg, anticoagulation or urgent catheterization) can be deferred while maintaining close observation and serial reassessment.When ECG findings show LVH accompanied by marked repolarization abnormalities, particularly in a younger patient, the clinical focus should shift toward identifying an underlying pathologic LVH versus a benign cause or a physiologic variant. In this context, cardiology consultation is warranted, and definitive evaluation should include transthoracic echocardiography, with consideration of cardiac magnetic resonance imaging to further characterize wall thickness distribution, myocardial structure, and fibrosis.In this case, the ECG findings raised suspicion for an apical variant of HCM, but were insufficient for diagnosis. Definitive differentiation among potential causes of LVH requires advanced cardiac imaging. In this patient, findings on serial ECGs remained stable and troponin levels showed no evidence of myocardial injury, and subsequent imaging confirmed a diagnosis of apical HCM, explaining the observed ECG abnormalities. The patient was discharged home and scheduled for an outpatient cardiology consultation.

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