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Published on: October 28, 2020
Tip of the iceberg: a tertiary care centre retrospective study of left ventricular hypertrophy aetiologies
Maxime Beneyto1,2, Eve Cariou3,2, Jérémy Brunel3,2
1Cardiology, CHU Toulouse Pôle Cardiovasculaire et Métabolique, Toulouse, France beneyto.maxime@gmail.com.
Insights
Mild left ventricular hypertrophy (LVH) often involves cardiac amyloidosis and sarcomeric hypertrophic cardiomyopathy. Early identification of these causes in LVH patients is crucial for targeted treatment and family screening.
Area of Science:
- Cardiology
- Cardiovascular Diseases
- Medical Diagnostics
Background:
- Left ventricular hypertrophy (LVH) is a common cardiovascular condition.
- Accurate phenotyping of LVH is essential for guiding patient management.
- Tertiary centers manage a diverse range of LVH aetiologies.
Purpose of the Study:
- To characterize the aetiologies of left ventricular hypertrophy (LVH) in patients referred to a tertiary center.
- To investigate the prevalence of different LVH causes, particularly in cases with mild LVH (12-14 mm LVWT).
- To understand the distribution of LVH aetiologies based on left ventricular wall thickness.
Main Methods:
- Retrospective observational study of consecutive patients referred for LVH aetiological workup (LVWT ≥ 12 mm).
- Exclusion of patients with severe aortic stenosis.
- Expert consensus adjudication of LVH aetiologies after reviewing diagnostic workup.
Main Results:
- 41% of referred patients had mild LVH (maximal LVWT < 15 mm).
- Cardiac amyloidosis (34.3%) and sarcomeric hypertrophic cardiomyopathy (32.1%) were the leading causes of LVH.
- Cardiac amyloidosis and sarcomeric hypertrophic cardiomyopathy were prevalent in mild LVH and increased with LVH severity.
Conclusions:
- Mild LVH encompasses various aetiologies requiring specific treatments and follow-up.
- Cardiac amyloidosis is currently the predominant cause of LVH in tertiary care settings.
- Early diagnosis of underlying LVH aetiologies facilitates timely interventions and cascade screening.
Aims:
To phenotype patients referred to a tertiary centre for the exploration of a left ventricular hypertrophy (LVH) starting from 12 mm of left ventricular wall thickness (LVWT).
Methods And Results:
Consecutive patients referred for aetiological workup of LVH, beginning at 12 mm of LVWT were retrospectively included in this tertiary single-centred observational study. Patients presenting with severe aortic stenosis were excluded. Aetiological workup was reviewed for each subject and aetiologies were adjudicated by expert consensus.Among 591 patients referred for LVH aetiological workup, 41% had a maximal LVWT below 15 mm. LVH aetiologies were led by cardiac amyloidosis (CA, 34.3%), followed by sarcomeric hypertrophic cardiomyopathy (S-HCM, 32.1%), hypertensive cardiomyopathy (21.7%), unknown aetiology (7.6%) and other (4.2%), including Anderson-Fabry's disease (1.7%). CA and S-HCM affected over 50% of patients with mild LVH (12-14 mm); the prevalence of these aetiologies rose with LVH severity. Among patients with Anderson-Fabry's disease, 4 (40%) had a maximal LVWT <15 mm.
Conclusions:
Mild LVH (ie, 12-14 mm) conceals multiple aetiologies that can lead to specific treatment, cascade family screening and specific follow-up. Overall, CA is nowadays the leading cause of LVH in tertiary centers.
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