What is Left Ventricular Hypertrophy (LVH)?

Left Ventricular Hypertrophy (LVH)

Left ventricular hypertrophy (LVH) is defined as an abnormal increase in left ventricular wall thickness, typically diagnosed when maximal LV wall thickness is ≥15 mm in adults (with 13-14 mm considered borderline), or when wall thickness is >2 standard deviations above the mean (z-score >2) for age, sex, or body size in children. 1

Definition and Diagnosis

• LVH is most reliably diagnosed using two-dimensional echocardiography, which demonstrates increased LV wall thickness that can be diffuse or segmental in distribution 1
• In adults, LVH is typically defined as maximal wall thickness ≥15 mm, with 13-14 mm considered borderline, particularly when other supporting evidence is present (e.g., family history) 1
• In children, LVH is defined as wall thickness >2 standard deviations above the mean (z-score >2) for age, sex, or body size 1
• Cardiovascular magnetic resonance (CMR) is increasingly used for LVH assessment, providing more precise measurements of LV wall thickness and mass 1

Prevalence and Epidemiology

• LVH is a common finding, with an estimated prevalence of approximately 0.2% (1:500) in the general population 1
• The prevalence increases with age, systolic blood pressure, and obesity 2
• LVH represents an independent risk factor for cardiovascular events and all-cause mortality 3

Pathophysiology and Classification

LVH can be classified into two major categories:

1. Primary LVH

• Not explained solely by abnormal loading conditions 4
• Often genetic in origin, as seen in hypertrophic cardiomyopathy (HCM) 1
• May be caused by:
  • Sarcomeric gene mutations (most common cause of HCM) 1
  • Storage diseases (e.g., Fabry disease, amyloidosis) 1
  • Mitochondrial disorders 1

2. Secondary LVH

• Develops in response to:
  • Pressure overload (e.g., hypertension, aortic stenosis) 1
  • Volume overload (e.g., aortic regurgitation, mitral regurgitation) 1
  • Physiologic adaptation (e.g., athlete's heart) 1

Patterns of LVH

• Concentric LVH: Increased wall thickness with normal or decreased LV cavity size, typically seen in pressure overload conditions like hypertension or aortic stenosis 1
• Eccentric LVH: Increased wall thickness with enlarged LV cavity, often seen in volume overload conditions 2
• Asymmetric LVH: Uneven distribution of hypertrophy, commonly seen in HCM 1

Clinical Significance

• LVH is a powerful independent risk factor for:
  • Coronary artery disease 5
  • Stroke 3
  • Heart failure 3
  • Sudden cardiac death 6
  • All-cause mortality 3

Differential Diagnosis

Distinguishing between different causes of LVH is important for proper management:

• Hypertrophic cardiomyopathy (HCM): Genetic disease characterized by unexplained LVH, typically with preserved or hyperdynamic LV function 1
• Hypertensive heart disease: LVH secondary to chronic pressure overload 1
• Athlete's heart: Physiologic adaptation to intensive athletic training 1
• Infiltrative/storage disorders: Fabry disease, amyloidosis, glycogen storage diseases 1

Key distinguishing features include:

• Pattern of hypertrophy (diffuse vs. segmental, symmetric vs. asymmetric) 1
• LV cavity size (dilated vs. normal/small) 1
• Presence of outflow tract obstruction 1
• Family history of HCM or sudden cardiac death 1
• Presence of genetic mutations 1
• Response to deconditioning in athletes 1

Diagnostic Approach

• Echocardiography is the first-line imaging technique for LVH assessment 4
• CMR provides added value with accurate measurement of LV volumes and mass, and tissue characterization 4
• Genetic testing may be helpful in suspected HCM cases 1
• ECG may show voltage criteria for LVH but has limited sensitivity (less than 60%) 6

Clinical Implications

• LVH represents both a manifestation of cardiovascular risk factors and an intrinsic condition causing pathologic changes in cardiovascular structure and function 3
• Even when hypertension is successfully treated, patients with LVH continue to have a poorer prognosis 6
• Regression of LVH with appropriate treatment may be associated with reduction in cardiovascular complications 5

Management Considerations

• Treatment of underlying causes (e.g., hypertension, aortic stenosis) 6
• Early intervention before electrocardiographic evidence of LVH develops 6
• Specific management approaches based on etiology (e.g., HCM-specific guidelines for those with sarcomeric mutations) 1
• Regular monitoring for disease progression and complications 4