What is Concentric Left Ventricular Hypertrophy (LVH)?

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Concentric Left Ventricular Hypertrophy (LVH)

Concentric LVH is characterized by normal left ventricular cavity size with uniformly increased wall thickness and increased left ventricular mass, typically developing as an adaptive response to pressure overload conditions such as hypertension or aortic stenosis. 1

Definition and Pathophysiology

Concentric LVH represents a specific geometric pattern of cardiac remodeling where:

  • The left ventricle adapts to systolic pressure overload through a hypertrophic process
  • Wall thickness increases while chamber volume remains normal or decreases
  • Left ventricular mass increases
  • Relative wall thickness is increased
  • Myocytes add sarcomeres in parallel, increasing cell width rather than length 1

This adaptation develops gradually, usually over decades in conditions like aortic stenosis, allowing the left ventricle to generate higher systolic pressures while maintaining normal wall stress (afterload). The increased wall thickness helps counter high intracavitary systolic pressure, preserving ejection fraction in the early stages. 1

Diagnostic Criteria

Concentric LVH is diagnosed echocardiographically using several parameters:

  • Increased left ventricular mass index (LVMI)
  • Normal cavity size
  • Increased relative wall thickness (RWT)
  • RWT is calculated as (posterior wall thickness × 2)/LV diastolic diameter 1

Various cutoff values are used based on:

  • Overall LV mass (g)
  • LV mass/body surface area (g/m²)
  • LV mass/height (g/m)
  • LV mass/height^2.7 (g/m^2.7) 1

Causes and Associated Conditions

Concentric LVH most commonly develops in response to:

  1. Hypertension (most common cause)
  2. Aortic stenosis
  3. Other conditions causing pressure overload

The pattern is characterized by high systemic pressure coupled with high peripheral resistance. 1

Functional and Clinical Implications

Concentric LVH has several important functional consequences:

  • Diastolic dysfunction: Increased wall thickness and diminished chamber compliance lead to elevated end-diastolic pressure without chamber dilation
  • Coronary perfusion abnormalities: Reduced coronary blood flow per gram of muscle and limited coronary vasodilator reserve
  • Increased sensitivity to ischemic injury: Higher risk of larger infarcts and mortality
  • Atrial contribution: Forceful atrial contraction becomes critical for ventricular filling; loss of atrial contraction (e.g., atrial fibrillation) can cause clinical deterioration 1

Progression and Prognosis

While initially compensatory, concentric LVH carries significant risks:

  • Increased morbidity and mortality
  • Risk of progression to heart failure (both with preserved and reduced ejection fraction)
  • Transition from compensated hypertrophy to heart failure, often with an increase in LV end-diastolic and end-systolic volumes and decreased ejection fraction 1
  • Associated with changes in diastolic function, longitudinal and radial myocardial function, and atrial size 1

Distinction from Other Forms of LVH

Concentric LVH differs from eccentric LVH in several important ways:

  • Eccentric LVH: Associated with volume rather than pressure overload, typically due to valvular regurgitation or high cardiac output states. Shows increased LV cavity size, normal wall thickness, and increased LV mass. 1

  • Concentric remodeling: Increased relative wall thickness but normal LV mass, often seen in early hypertensive heart disease. 1

Advanced Imaging Findings

Newer imaging techniques have revealed that concentric LVH, while traditionally considered symmetrical, may actually demonstrate significant regional heterogeneity:

  • MRI tissue tagging shows substantial regional intramyocardial strain heterogeneity
  • The septum often shows more severely depressed strain patterns compared to the posterior wall 2

This regional heterogeneity may have important implications for understanding the pathophysiology and progression of concentric LVH.

Professional Medical Disclaimer

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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