A young patient with left ventricular hypertrophy and accidentally discovered aortic dissection: hypertensive heart or hypertrophic cardiomyopathy?

Abstract

171 LV outflow tract gradient (10 mm Hg at rest and 14 mm Hg after the Valsalva test). There was moderate LA enlargement (LA volume index, 37.2 ml/m2), impaired LV relaxation (E/A, 0.88; E/e’, 6.6; E ‐wave deceleration time, 297 ms), and a normal ascending aorta diameter (FIGURE 1B). Cardiovascular magnetic resonance imaging confirmed concentric LV hypertrophy (maxi‐ mally 18 mm) and increased myocardial mass (LV mass index, 124 ml/m2; normal range, 59– 92 ml/m2) (FIGURE 1C). Due to vascular murmur in the abdomen, ul‐ trasound imaging was performed and revealed abdominal aortic dissection (FIGURE 1D). A com‐ puted tomography scan confirmed aortic dis‐ section originating below renal arteries and involving common iliac arteries (Stanford B; FIGURE 1E and 1F). The presence of thrombi formed at the site of the aortic dissection suggested a chronic presentation. The patient was managed conservatively with strict BP control, intensified antihypertensive treatment (metoprolol, telmisartan, torasemide, spironolactone, amlodipine, clonidine), and close follow ‐up.1 Secondary causes of hypertension, in‐ cluding renal artery stenosis, abnormal kidney and adrenal glands, hyperaldosteronism, hyper‐ and hypothyroidism, were excluded. Genetic analysis did not reveal any potential‐ ly disease ‐causing mutation. Next ‐generation sequencing was conducted with the TruSight A 36‐year ‐old man with a family history of hy‐ pertension and sudden cardiac death, who was admitted a month earlier to a local hospital due to acute cardiogenic pulmonary edema and new‐ ly diagnosed hypertension, was referred to our institution with suspicion of hypertrophic car‐ diomyopathy (HCM). On admission, the patient was asymptom‐ atic and did not complain of fatigue, chest pain, or syncope. On physical examination, his blood pressure (BP) was significantly elevated (180/100 mm Hg). The lungs were clear on aus‐ cultation. Pulse in the radial and femoral arter‐ ies was preserved. Neither edema of lower ex‐ tremities nor heart murmur were detected. Ab‐ dominal auscultation revealed vascular murmur in the umbilical region. The baseline level of N‐terminal pro–B‐type natriuretic peptide was 811.4 pg/ml (normal range, 0–125 pg/ml), high ‐sensitivity troponin T, 20.2 ng/l (normal range, 0–14 ng/l), and cre‐ atinine, 1.4 mg/dl (normal range, 0.7–1.2 mg/dl). The standard 12‐lead electrocardiogram showed sinus rhythm, left atrial (LA) enlargement, and left ventricular (LV) hypertrophy (FIGURE 1A). No significant pathology was present on chest X ‐ray. Transthoracic echocardiography revealed con‐ centric LV hypertrophy (maximally 19 mm at the interventricular septum) with preserved LV ejec‐ tion fraction (70%), moderately decreased global longitudinal strain (–13.7%), and nonsignificant Correspondence to: Monika Gawor, PhD, Department of Cardiomyopathy, Institute of Cardiology, ul. Alpejska 42, 04-628 Warszawa, Poland, phone: +48 22 343 46 71, email: [email protected] Received: November 18, 2019. Revision accepted: December 17, 2019. Published online: December 17, 2019. Kardiol Pol. 2020; 78 (2): 171-173 doi:10.33963/KP.15159 Copyright by the Author(s), 2020 C L I N I C A L V I G N E T T E