Reversible Lateral Wall Thickening Mimicking Apical Hypertrophic Cardiomyopathy After Reperfused <scp>STEMI</scp>

A 50-year-old male presented with acute inferior ST-segment elevation myocardial infarction (STEMI) (Figure 1a). High-sensitivity cardiac troponin I was markedly elevated at 17.72 ng/mL (reference < 0.04 ng/mL) [1]. Emergency coronary angiography revealed total occlusion of the distal left circumflex artery (LCX) as the culprit lesion (Figure 1b). Successful percutaneous coronary intervention with drug-eluting stent implantation restored Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow (Figure 1c) [2]. The left anterior descending artery showed only mild distal stenosis (approximately 20%). Transthoracic echocardiography (TTE) was performed on day 4 post-intervention using a Philips EPIQ 7C system in accordance with American Society of Echocardiography recommendations [3]. The apical views demonstrated apparent thickening of the left ventricular lateral wall, most prominently involving the anterolateral and inferolateral segments, with an end-diastolic wall thickness of approximately 16–18 mm and relatively reduced myocardial echogenicity (Figure 2a). These findings raised initial suspicion of apical hypertrophic cardiomyopathy [4]. Notably, the echocardiographic images were acquired at different cardiac phases. The apical five-chamber view was obtained in diastole, whereas the apical three-chamber view was acquired during early systole, a phase in which the lateral wall contour was more completely visualised in this case. Serial follow-up echocardiography demonstrated progressive resolution of the apparent wall thickening, with partial regression at 1 month (approximately 12 mm; Figure 2b) and complete normalisation by 8 months (approximately 9 mm; Figure 2c), arguing against true myocardial hypertrophy. Cardiac magnetic resonance (CMR) imaging was performed approximately 2.5 months after the index event using a GE Voyager Air 1.5-T system following standardised acquisition protocols [5]. Tissue characterisation demonstrated signal changes consistent with myocardial oedema predominantly involving the left ventricular lateral wall, with late gadolinium enhancement in a subendocardial distribution characteristic of ischaemic injury rather than hypertrophic cardiomyopathy (Figure 3) [6, 7]. Genetic testing did not identify pathogenic or likely pathogenic variants in genes classically associated with apical hypertrophic cardiomyopathy, including MYH7 and MYBPC3 [8]. Several incidental heterozygous variants of uncertain or likely pathogenic significance were identified in RGS5, TTN and FLNC, but these were considered unrelated to the transient imaging phenotype. This case highlights reversible myocardial oedema and post-ischaemic stunning following reperfused LCX-related inferior STEMI, which may manifest as transient lateral wall thickening and mimic apical hypertrophic cardiomyopathy on early echocardiography [9]. Careful longitudinal echocardiographic follow-up using standardised imaging protocols [3], together with complementary CMR tissue characterisation [5], is essential to avoid misdiagnosis of hereditary cardiomyopathy. This case report has several limitations. First, retrospective myocardial functional assessment using speckle-tracking echocardiography was not feasible, as the original acute-phase images were not acquired with strain analysis optimisation. Therefore, quantitative regional functional changes could not be evaluated. Second, echocardiographic images were obtained at different cardiac phases, including diastole and early systole, which may influence the apparent myocardial wall thickness. In this case, early systolic acquisition allowed more complete visualisation of the lateral wall contour, but standardised end-diastolic measurements were not consistently available for all views. Finally, no repeat CMR examinations were performed, limiting assessment of the temporal evolution of myocardial oedema. Despite these limitations, the combination of serial echocardiography and tissue characterisation by CMR was sufficient to demonstrate the transient nature of the myocardial thickening and to avoid misdiagnosis of hypertrophic cardiomyopathy. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor of this journal on request. The authors declare no conflicts of interest. The data that support the findings of this study are available from the corresponding author upon reasonable request.