A 27-year-old man is brought to the emergency department due to a syncopal episode. He passed out while unloading heavy packages from his truck during a hot summer day. According to a witness, the episode lasted 30 seconds, and he regained consciousness quickly. The patient has had no chest pain or palpitations. Over the past year, he has had brief episodes of lightheadedness related to intense exercise. Medical history is otherwise insignificant. He works for a landscaping company. Blood pressure is 130/75 mm Hg while supine and 125/75 mm Hg while standing and pulse is 78/min and regular. Oxygen saturation is 98% on room air. On examination, the patient has no murmur. The lungs are clear to auscultation. ECG shows T-wave inversion in leads V₄-V₆. Complete blood count, serum electrolytes, and cardiac enzymes are within normal limits. Which of the following is the most appropriate next step in management?

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Explanation: 11ec25c8_d352_fa1e_bc81_178ac9ea2e7e_MD0003_00 This young patient's exertional syncope and ECG demonstrating T-wave inversions in the lateral leads (V₄-V₆) raise suspicion for hypertrophic cardiomyopathy (HCM). The systolic murmur characteristic of HCM is sometimes absent because left ventricular outflow tract (LVOT) obstruction may be absent or only present with exertion. ECG is usually abnormal and may show left axis deviation or disruptions in depolarization (eg, prominent Q waves) or repolarization (eg, T-wave inversions). ₄ ₆ systolic murmur Syncope due to HCM is usually exertional and typically results from one of the following: Reduced cardiac output due to dynamic LVOT obstruction: Exertion-related factors (eg, dehydration, reduced LV filling time) lead to low LV blood volume, which can exacerbate the obstruction and markedly reduce cardiac output. This mechanism likely explains this patient's episodes of exertional lightheadedness. Ischemia-induced ventricular tachycardia: HCM causes increased myocardial O₂ demand (increased muscle mass) and reduced myocardial O₂ supply (myocardial disarray with microvascular dysfunction), even at rest. Intense exertion amplifies this O₂ supply-demand mismatch and can trigger ventricular arrhythmias; LVOT obstruction (causing reduced O₂ supply) can further exacerbate this mechanism. Ventricular arrhythmia that does not terminate (as it does with syncope) is the typical cause of sudden cardiac death in HCM. HCM is diagnosed with echocardiography, which can demonstrate asymmetric LV hypertrophy primarily affecting the interventricular septum, dynamic LVOT obstruction, LV diastolic dysfunction, and left atrial dilation. (Choice A) Ambulatory ECG monitoring is helpful in diagnosing intermittent arrhythmias and could detect paroxysmal atrial fibrillation or ventricular tachycardia in patients with HCM. However, echocardiography is needed to confirm the diagnosis. (Choice C) Coronary angiography is used to diagnose atherosclerotic coronary artery disease, which is unlikely in this young patient. In patients with HCM, the epicardial coronary arteries are normal; microvascular disease that is often present is not detectable by coronary angiography. (Choice D) Syncope due to acute pulmonary embolism (PE) is not typically exertional. In addition, PE is unlikely in this patient with normal heart rate and oxygen saturation. (Choice E) Reassurance and routine follow-up is not appropriate because unmanaged HCM puts this patient at increased risk for sudden cardiac death. Educational objective: Physical examination is frequently normal in hypertrophic cardiomyopathy (HCM). Patients with suspected HCM (eg, exertional syncope and abnormal ECG) should undergo echocardiography to confirm the diagnosis. References: Misconceptions and facts about hypertrophic cardiomyopathy. (http://www.ncbi.nlm.nih.gov/pubmed/26299316) New perspectives on the prevalence of hypertrophic cardiomyopathy. (http://www.ncbi.nlm.nih.gov/pubmed/25814232)

A 27-Year-Old Man Is Brought to the Emergency Department Due