What are the most likely etiologies of ventricular septal hypertrophy (VSH)?

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From the Guidelines

Ventricular septal hypertrophy is most commonly caused by hypertrophic cardiomyopathy (HCM), a genetic heart condition characterized by abnormal thickening of the heart muscle, as well as other significant etiologies including chronic hypertension, aortic stenosis, athletic training, infiltrative disorders, glycogen storage diseases, and other systemic conditions. The etiologies of ventricular septal hypertrophy (VSH) can be diverse, and it is essential to consider various factors when determining the underlying cause.

Possible Causes of VSH

  • Hypertrophic cardiomyopathy (HCM): a genetic heart condition characterized by abnormal thickening of the heart muscle, which can lead to VSH 1
  • Chronic hypertension: leads to left ventricular hypertrophy as the heart works harder against increased blood pressure, resulting in VSH
  • Aortic stenosis: the narrowed aortic valve creates increased pressure load on the left ventricle, leading to VSH
  • Athletic training: can cause physiologic hypertrophy (athlete's heart), which is a benign adaptation to intense exercise, but can also lead to VSH
  • Infiltrative disorders: such as amyloidosis, sarcoidosis, and Fabry disease, can cause ventricular wall thickening through abnormal protein deposition, resulting in VSH
  • Glycogen storage diseases: like Pompe disease and Danon disease, may lead to septal hypertrophy due to glycogen accumulation in cardiac myocytes
  • Other systemic conditions: such as chronic kidney disease and obesity, are associated with ventricular hypertrophy through various pathophysiological mechanisms, including volume overload, neurohormonal activation, and inflammatory processes It is crucial to note that the diagnosis of VSH requires a comprehensive evaluation, including clinical history, physical examination, electrocardiography, echocardiography, and other diagnostic tests, to determine the underlying cause and develop an effective treatment plan 1.

Diagnostic Considerations

  • Clinical markers and testing strategies can be used to help differentiate between HCM and conditions of physiologic LVH, such as athletic training and hypertensive cardiomyopathy 1
  • The presence of a diagnostic sarcomere mutation or marked LV thickness ≥25 mm and/or LVOT obstruction with systolic anterior motion (SAM) and mitral-septal contact can support the diagnosis of HCM 1
  • Noninvasive markers, including sarcomeric mutations or family history of HCM, LV cavity dimension, diastolic function, pattern of LV hypertrophy, or short deconditioning periods, can help distinguish between pathologic LV hypertrophy (HCM) and physiologic LV hypertrophy (athlete's heart) 1

References

1
Guideline

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Dr.Oracle Medical Advisory Board & Editors, 2025

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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