HYPERTROPHY: A COMPARATIVE CASE SERIES

Anakhanım  Safarova; Shafa Shahbazova

doi:10.28942/acj.v28i2y2026.145

Abstract

Left ventricular hypertrophy (LVH) represents a common imaging phenotype with diverse etiologies. Differentiating hypertrophic cardiomyopathy, infiltrative disease, metabolic disorders and pressure-overload remodeling remains challenging using echocardiography alone. This comparative case series demonstrates how multiparametric cardiac magnetic resonance (CMR), integrating ventricular morphology, native T1 mapping and late gadolinium enhancement (LGE), improves etiological diagnosis. Four representative patients with unexplained LVH underwent standardized 3.0-T CMR. Distinct imaging signatures enabled differentiation between cardiac amyloidosis, genetically confirmed mitochondrial cardiomyopathy, pressure-overload hypertrophy secondary to aortic valve disease and hypertrophic cardiomyopathy. These cases emphasize that LVH is a phenotype rather than a diagnosis and illustrate the incremental diagnostic value of comprehensive tissue characterization.

Full article

Introduction

Left ventricular hypertrophy is encountered in a broad spectrum of cardiovascular diseases. Although increased wall thickness is easily recognized on echocardiography, substantial overlap exists among different disease entities. CMR has emerged as the reference imaging modality because it combines accurate assessment of ventricular morphology and function with myocardial tissue characterization. Native T1 mapping and LGE provide disease-specific biomarkers that frequently establish the correct diagnosis and influence subsequent management. The purpose of this case series is to compare four clinically distinct causes of LVH using a uniform multiparametric CMR approach.

Aim

To demonstrate how multiparametric CMR differentiates various causes of left ventricular hypertrophy using representative comparative clinical cases.

Methods

The present retrospective educational case series included four representative patients referred for evaluation of unexplained LVH. Clinical presentation, electrocardiography, echocardiography and standardized 3.0-T CMR findings were reviewed. Final diagnoses were established through integration of clinical and imaging findings, with genetic confirmation in the mitochondrial cardiomyopathy case. Representative images were selected to highlight distinguishing CMR features.

Results – Representative Cases

Representative Case A – Cardiac Amyloidosis

Age/Sex: 60-year-old male

Presentation: Fatigue, dyspnea, complete AV block, ventricular tachycardia.

Echocardiography: LV wall thickness 20 mm, LVEF 60%; suspected HCM.

CMR Findings:

Concentric LV hypertrophy (maximum wall thickness 25 mm)

Native T1: 1355–1614 ms

Diffuse circumferential subendocardial LGE

Final Diagnosis: Cardiac amyloidosis.

Representative Case B – Genetically Confirmed Mitochondrial Cardiomyopathy

Age/Sex: 20-year-old male

Presentation: Recurrent exertional syncope and progressive exertional dyspnea.

Echocardiography: Mild LV hypertrophy (15 mm); suspected HCM.

CMR Findings:

Maximum wall thickness 15–17 mm

Low native T1: 1079–1125 ms

Focal basal inferolateral mid-wall LGE

Diagnostic confirmation: Genetic testing confirmed mitochondrial cardiomyopathy.

Final Diagnosis: Genetically confirmed mitochondrial cardiomyopathy.

Representative Case C – Pressure-Overload LVH Secondary to Aortic Valve Disease

Age/Sex: 55-year-old male

Presentation: Progressive exertional dyspnea.

Echocardiography: Severe aortic valve disease (AS/AR), IVS 19 mm; suspected HCM.

CMR Findings:

LV remodeling with maximum wall thickness 15 mm

Native T1: 1263–1308 ms

No LGE

Final Diagnosis: Pressure-overload LV hypertrophy secondary to aortic valve disease

Representative Case D – Hypertrophic Cardiomyopathy

Age/Sex: 58-year-old male

Presentation: Exertional dyspnea and chest pain

Echocardiography: Asymmetric septal hypertrophy (24–26 mm), systolic anterior motion (SAM), LVOT gradient 75 mmHg.

CMR Findings:

Asymmetric hypertrophy

Native T1: 1357–1451 ms

Patchy non-ischemic LGE at the RV insertion points with additional ischemic enhancement related to coexisting coronary artery disease

Final Diagnosis: Hypertrophic cardiomyopathy with coexisting obstructive coronary artery disease.

Discussion

Although all patients initially presented with LVH, multiparametric CMR demonstrated unique disease-specific imaging signatures. Diffuse subendocardial LGE with markedly elevated native T1 supported cardiac amyloidosis, whereas low native T1 and focal inferolateral fibrosis suggested mitochondrial cardiomyopathy. Absence of LGE and near-normal tissue characterization favored pressure-overload remodeling, while asymmetric hypertrophy with RV insertion-point fibrosis was characteristic of hypertrophic cardiomyopathy. These findings illustrate the importance of integrating morphology with tissue characterization rather than relying solely on wall thickness.

Conclusion

Multiparametric CMR is a comprehensive noninvasive imaging technique for the etiological evaluation of left ventricular hypertrophy. By combining ventricular morphology with myocardial tissue characterization, it enables accurate differentiation of diverse LVH phenotypes and facilitates