A Second Look Matters: Stress-Induced Cardiomyopathy Mimicking Apical Hypertrophic Cardiomyopathy

Description of Clinical Presentation: A 67-year-old female patient, hypertensive, dyslipidemic, with no prior cardiac history, presented with an episode of oppressive precordial pain in functional class II, associated with dyspnea. The symptom gradually diminished and disappeared the following day. Five days later, it recurred, this time with less intensity and shorter duration, and it resolved spontaneously afterward. One week later, the patient attended a scheduled follow-up appointment with her primary care physician. An electrocardiogram showed symmetrical negative T waves in the precordial and inferior leads, prompting the patient to be referred to the emergency department.

Physical examination did not reveal any pathological findings. Laboratory results showed ultrasensitive troponin T levels of 27 pg/mL (cutoff value - 99th percentile - in healthy population: 15 pg/mL), with no other notable abnormalities.

Diagnostic Techniques and Their Most Important Findings: The echocardiogram showed preserved biventricular function, eccentric hypertrophy of the left ventricle, no regional wall motion abnormalities or valvular diseases.

The episode was interpreted as a NSTEMI, leading to hospitalization, anti-ischemic treatment, and coronary cineangiography. The latter revealed coronary arteries with no angiographically significant stenosis. In the context of Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA), a cardiac MRI was performed.

The MRI showed preserved biventricular systolic function, with increased wall thickness in the apical and basal anteroseptal segments (15 mm), with preserved motion. There was diffuse late gadolinium enhancement in the apical segments, with a non-ischemic necrotic pattern; increased T1 and T2 mapping times at the apical level. The findings were reinterpreted as possible apical hypertrophic cardiomyopathy with intramyocardial gadolinium and edema in the apical segments, suggesting an active inflammatory process. It was recommended to repeat the study in 3-6 months to assess evolution.

The patient evolved steadily, and the MRI at 6 months showed preserved biventricular function, normal wall thickness, no edema, and normal T1 and T2 mapping. Late gadolinium enhancement persisted at the basal anteroseptal and latero-apical areas, with an intramyocardial distribution and a non-ischemic-necrotic pattern. The new electrocardiogram was normal.

The initial diagnosis was then interpreted as a Takotsubo syndrome in the subacute phase. The patient had a good recovery and did not experience a recurrence of the episode.

Learning Points from this Case: Takotsubo Syndrome is one of the alternative diagnoses for MINOCA or ANOCA (angina with non-obstructive coronary artery disease). While the most commonly reported phenotype is apical ballooning, there are various phenotypes and stages throughout its evolution.

In the subacute phase of the disease, a transient apical thickening may occur, which mimics hypertrophic cardiomyopathy. There is controversy regarding whether this presentation could correspond to a higher-risk variant.

MRI - T1 mapping: 4 chamber - short axis - 2 chamber
MRI short axis - T2 - T2 mapping
MRI after 6 months - normal T1 mapping