Acute Myocardial Infarction Mimicking Apical Hypertrophic Cardiomyopathy

Graphical abstract

Highlights

• •Myocardial edema mimics apical hypertrophy in myocardial infarction.
• •Contrast echocardiography enhances evaluation of the cardiac apex.
• •Serial echocardiography is useful in monitoring myocardial edema.

Introduction

Myocardial edema is a common feature in various cardiovascular conditions, including myocarditis, takotsubo syndrome, and myocardial infarction. It typically presents as increased myocardial wall thickness, often observed on imaging, and can mimic other pathologies such as hypertrophic cardiomyopathy (HCM). The identification of myocardial edema is crucial, as it can significantly affect management and outcomes, especially when distinguishing it from other conditions that may require different therapeutic approaches.

We present the case of an octogenarian patient with a distal left anterior descending coronary artery (LAD) infarction, initially diagnosed with apical HCM. Transthoracic echocardiography (TTE) with ultrasound enhancing agents (UEAs) improved visualization of the left ventricle, while serial imaging helped distinguish myocardial edema from true hypertrophy. This case underscores the importance of recognizing myocardial edema as a reversible condition, which resolved during follow-up, confirming the initial diagnosis of myocardial infarction rather than apical HCM.

Case Presentation

An 87-year-old patient presented to the emergency department with a 3-day history of central chest heaviness radiating to the neck, associated with dyspnea, diaphoresis, and nausea. The medical history included atrial fibrillation (AF), congestive heart failure, stroke, and hypercholesterolemia.

Medications on index admission included digoxin 125 μg/d, rivaroxaban 15 mg/d, simvastatin 20 mg/d, allopurinol 100 mg in the morning, carbimazole 5 mg/d, magnesium 1,000 mg/d, and denosumab every 6 months. Physical examination revealed a blood pressure of 155/60 mm Hg, with otherwise unremarkable vital signs, bibasilar crackles, dual heart sounds with no murmurs, and no other significant findings. Blood tests were significant for serum creatinine 107 μmol/L (normal range, <73 μmol/L), estimated glomerular filtration rate 40 mL/min/1.73 m² (normal range, >90 mL/min/1.73 m²), and cardiac troponin I 278 ng/L (normal range, <34 ng/L), with a peak value of 11,269 ng/L 24 hours later.

Electrocardiography showed widespread ST-segment elevation, maximal in leads V₂ to V₄, meeting criteria for ST-segment elevation myocardial infarction and prompting activation of the coronary catheterization laboratory (Figure 1A). The patient was loaded with aspirin and clopidogrel and received an intravenous nitroglycerin infusion. Invasive coronary angiography revealed normal left main, circumflex, and right coronary arteries, with a distal occlusion in the LAD with Thrombolysis In Myocardial Infarction grade 1 flow (Figure 2A) wrapping the apex. Balloon angioplasty was performed on the distal occlusion, restoring flow with slight residual narrowing at the site of the occlusion (Figure 2B and C, Videos 1-3). The differential diagnosis included thrombosis secondary to plaque rupture or embolism secondary to AF.

Figure 1.

Twelve-lead electrocardiography demonstrates AF and extensive ST-segment elevation in precordial leads V₂ through V₆ on admission (A), deep, symmetric T-wave inversions in the anterior precordial and inferolateral limb leads during the second admission (B), and resolution of the ST-segment and T-wave changes on follow-up (C).

Figure 2.

Invasive coronary angiography, right anterior oblique cranial view after selective left coronary artery contrast injection, demonstrates distal LAD total occlusion (A, arrow) and reperfusion with mild residual luminal narrowing after percutaneous transluminal balloon coronary angioplasty (B, arrow).

After angiography, acute pulmonary edema developed, and TTE revealed a left ventricular (LV) size at the upper end of normal with moderately impaired systolic function (LV ejection fraction 32%, Simpson biplane) and regional wall motion abnormalities, including akinesia of the mid to apical segments and basal hyperkinesis (Figure 3A-D). The right ventricle also showed apical dyskinesia. A sclerotic aortic valve with mild aortic regurgitation, mild mitral regurgitation, and moderate tricuspid regurgitation was noted (Figure 3G and H). An LV thrombus was not seen using TTE with a UEA (small bolus injection). A UEA was administered to improve endocardial visualization in difficult-to-image regions (Figure 3E and F, Video 4). Euvolemia was achieved with diuresis, and the patient was discharged with bisoprolol 1.25 mg/d, rosuvastatin 20 mg at night, apixaban 2.5 mg twice daily, clopidogrel 75 mg/d, and ramipril 5 mg, with a diagnosis of infarction in the distal LAD territory.

Figure 3.

Two-dimensional TTE, first admission, parasternal long-axis (A and B), apical four-chamber without (C and D) and with (E and F) the administration of a UEA, diastolic (left, A, C and E) and systolic (right, B, D and F) views, demonstrates a borderline dilated LV cavity with normal myocardial wall thickness, globally reduced LV systolic function, apical akinesis (arrows) with compensatory basal hyperkinesis, and no apical thrombus. Two-dimensional TTE, right ventricle–focused apical four-chamber systolic view with color flow Doppler (G) and continuous-wave spectral Doppler (H), demonstrates right atrial dilation, moderate central tricuspid regurgitation, and a maximal tricuspid regurgitation transvalvular gradient of 30 mm Hg.

Two weeks later, the patient was readmitted with intermittent mild chest pain, worsening orthopnea, and paroxysmal nocturnal dyspnea. There was no fever, cough, or viral illness. Follow-up TTE showed increased apical wall thickness, with characteristics similar to apical HCM (Figure 4, Video 5). Electrocardiography revealed T-wave inversion in the anterior leads (Figure 1B). After stabilization and heart failure treatment, the patient was discharged with outpatient follow-up in 2 months. Subsequent TTE with UEAs 3 months later showed no increased LV wall thickening at the apex (Figure 5, Video 6) and mild LV dysfunction. New electrocardiography showed normalization of the T-wave inversions (Figure 1C).

Figure 4.

Two-dimensional TTE, second admission, parasternal long-axis (A and B), apical four-chamber without (C and D), apical four-chamber (E and F), and apical two-chamber (G and H) with the administration of a UEA, diastolic (left, A, C, E and G) and systolic (right, B, D, F and H) views, demonstrates regional LV wall thickening (arrows) with apical, systolic obliteration and spade-shaped appearance.

Figure 5.

two-dimensional TTE at follow-up visit, parasternal long-axis (A and B) and short-axis (C and D) without, zoomed apical four-chamber (E and F) and apical two-chamber (G and H) with the administration of a UEA, diastolic (left, A, C, E and G) and systolic (right, B, D, F and H) views, demonstrates normal regional myocardial wall thickness and function.

Discussion

This report illustrates how myocardial edema can mimic an apical HCM pattern and highlights the critical role of serial TTE in monitoring dynamic changes in LV morphology and function, particularly following an acute myocardial infarction (AMI) due to a distal LAD occlusion.

The initial presentation with a distal LAD occlusion triggered consideration of a broad differential diagnosis, including embolism and plaque rupture. Despite the absence of significant coronary atherosclerosis in other vessels and the patient’s history of AF, which initially suggested an embolic etiology, the lack of intracoronary imaging, such as intravascular ultrasound or optical coherence tomography, prevented definitive conclusions regarding the underlying cause.

In octogenarians, clinical presentations are often complicated by multiple coexisting pathologies, which can obscure the interpretation of diagnostic findings and the potential diagnostic methods to be used. In these complex cases, TTE remains the primary imaging modality, although its utility can be limited by suboptimal acoustic windows. Administration of a UEA is crucial in visualizing challenging regions, particularly the apex, for which standard imaging techniques may fall short. In this case, TTE with a UEA was used because of suboptimal image quality, primarily to rule out an apical thrombus during the initial hospitalization.^1,2 The UEA improved the resolution of the apical endocardial segments, offering a practical and noninvasive method to assess regions that are typically difficult to visualize.³

During the patient’s second hospitalization, increased apical myocardial wall thickness seen during TTE prompted the administration of a UEA. This study was essential to delineate the apex and was particularly useful because of the lack of immediate availability of cardiovascular magnetic resonance (CMR).⁴ TTE with a UEA is a safe and repeatable modality for evaluating apical hypertrophy, providing an alternative to CMR, although with certain limitations, for assessing LV wall thickness and function.³

After 12 weeks, complete regression of the hypertrophy was observed, leading us to reconsider the diagnosis of apical-variant HCM (Figure 6). Myocardial edema, a phenomenon resulting from ischemia, inflammation, or volume overload, leads to microvascular barrier disruption and fluid accumulation, causing myocardial wall thickening.⁵ Such changes are not unique to acute ischemia and infarction but are also observed in conditions such as takotsubo syndrome and myocarditis, in which myocardial edema can mimic HCM. To further investigate this, we conducted a comprehensive literature search (Table 1) that identified 10 reported cases of myocardial edema mimicking HCM.6, 7, 8, 9, 10, 11, 12, 13, 14, 15 The majority of these cases were related to takotsubo syndrome, with a few linked to myocarditis and one associated with ST-segment elevation myocardial infarction.

Figure 6.

Two-dimensional TTE, parasternal long-axis diastolic (left) and systolic (right) views from initial clinical presentation (A), second admission (B), and follow-up visit (C), demonstrates the serial changes in regional LV wall thickening, revealing a marked increase in septal thickness in (B) and normalization in (C). Note that interstudy comparison views are not strictly comparable, and apical foreshortening or misalignment may be observed, but the degree of visualized difference in wall thickness indicates that this is not related entirely to technical issues.

Table 1.

Summary of reported cases mimicking HCM

Case report	Patient presentation	Localization	Modality used
Iga et al. (1992)6	Vasospastic angina mimicking apical hypertrophy	Apical	TTE
Hwang et al. (2014)7	Takotsubo syndrome mimicking apical hypertrophy	Apical	TTE and CMR
Izgi et al. (2015)8	Takotsubo syndrome mimicking apical hypertrophy	Apical	TTE and CMR
Madias (2016)9	Takotsubo syndrome mimicking apical hypertrophy	Apical	TTE and CMR
Dimarco et al. (2016)10	Acute myocarditis mimicking HCM	Global	TTE and CMR
Awaya et al. (2016)11	Coronary vasospasm mimicking apical hypertrophy	Apical	TTE and CMR
Sharrack et al. (2022)12	Acute myocarditis mimicking HCM	Septal	TTE and CMR
Kuzmiakova et al. (2023)13	Blunt chest trauma resulting in apical hypertrophy	Apical	TTE and CMR
Maurizi et al. (2024)14	Takotsubo syndrome mimicking apical hypertrophy	Apical	CMR
Carvalho et al. (2024)15	Inferior ST-segment elevation myocardial infarction	Inferoseptal and inferolateral	TTE

The transient nature of apical wall thickening and its eventual resolution in our patient is consistent with studies indicating that myocardial edema following acute ischemia or infarction can cause temporary regional wall thickening. Although CMR remains the reference standard for evaluating myocardial edema, the sequence of events detected by TTE strongly suggests that this phenomenon was caused by myocardial edema. These imaging findings emphasize the importance of recognizing myocardial edema as a reversible contributor to dynamic changes in LV morphology and function, not only in myocarditis and takotsubo syndrome but also after AMI.

There is potential for misinterpretation of transient postinfarct imaging findings, particularly in the absence of prior knowledge of an AMI. Had this patient been assessed at another institution during the transient stage of postinfarct recovery, without knowing the recent AMI history or without the benefit of serial imaging, the apical wall thickening and electrocardiographic changes could have been misdiagnosed as an apical variant HCM.

Conclusion

This case demonstrates how myocardial edema following AMI can present with imaging findings resembling apical HCM. The transient nature of these changes, including regional wall thickening, emphasizes the importance of serial TTE in monitoring LV morphology and function during recovery. Recognizing this pattern is essential to prevent misdiagnosis and ensure appropriate clinical management.

Authorship contribution

Conception and design: M.G.M., M.E.S., I.A. Acquisition of data and images: C.S., E.D., M.E.S. Drafting the article: M.G.M., M.E.S., E.D. Final draft: M.G.M., M.E.S., E.D., C.S., I.A., R.S. All authors have approved the final article.

Ethics Statement

The authors declare that the work described has been carried out in accordance with The Code of Ethics of the World Medical Association (Declaration of Helsinki) for experiments involving humans.

Consent Statement

Complete written informed consent was obtained from the patient (or appropriate parent, guardian, or power of attorney) for the publication of this study and accompanying images.

Funding Statement

The authors declare that this report did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Disclosure Statement

The authors report no conflict of interest.

Supplementary Data

Video 1

Invasive coronary angiography, selective left coronary injection, demonstrates the distal LAD occlusion with Thrombolysis In Myocardial Infarction grade 1 flow.

Video 2

Invasive coronary angiography, selective left coronary injection, demonstrates a guidewire advanced through the distal LAD occlusion.

Video 3

Invasive coronary angiography, selective left coronary injection, demonstrates Thrombolysis In Myocardial Infarction grade 3 flow in the LAD after percutaneous coronary intervention (balloon angioplasty).

Video 4

Two-dimensional TTE, first admission, parasternal long-axis (A), apical four-chamber without (B) and with (C) the administration of a UEA, and zoomed apical four-chamber, right ventricle–focused tricuspid valve with color flow Doppler (D) views, demonstrates a borderline dilated LV cavity with normal myocardial wall thickness, globally reduced LV systolic function, apical akinesis with compensatory basal hyperkinesis, and moderate tricuspid regurgitation.

Video 5

Two-dimensional TTE, second admission, parasternal long-axis (A), apical four-chamber without (B) and apical four-chamber (C), apical two-chamber (D) views with the administration of a UEA, demonstrates regional LV wall thickening with apical, systolic obliteration and spade-shaped appearance.

Video 6

Two-dimensional TTE at follow-up visit, parasternal long-axis (A), short-aixs (B) without, zoomed apical four-chamber (C) and apical two-chamber (D) views with the administration of a UEA, demonstrates normal regional myocardial wall thickness and function.