Dilated Cardiomyopathy and Left Ventricular Hypertrophy Are Distinct Entities
No, dilated cardiomyopathy (DCM) and left ventricular hypertrophy (LVH) are fundamentally different conditions with opposite structural changes, though they can occasionally coexist or evolve from one to the other.
Core Structural Differences
DCM is characterized by ventricular dilatation with either normal or reduced wall thickness (eccentric hypertrophy), while LVH involves thickened ventricular walls without significant chamber enlargement (concentric hypertrophy). 1
Cellular Mechanisms
Pressure overload (as in hypertension or aortic stenosis) causes sarcomeres to be added in parallel with the myocyte's long axis, increasing cell cross-sectional area disproportionately to length, resulting in wall thickening without chamber volume change—this is LVH 1
Volume overload causes sarcomeres to be added in series along the long axis, causing disproportionate increase in cell length compared to cross-sectional area, leading to chamber enlargement with proportional wall thickening—this is the pattern seen in DCM 1
Clinical Differentiation
DCM Features
- Ventricular dilatation with systolic dysfunction (reduced ejection fraction) 1
- Either normal or reduced wall thickness 1
- Loss of myocytes and increased extracellular matrix 1
- Biventricular and biatrial enlargement with elevated filling pressures 1
LVH Features (Hypertrophic Cardiomyopathy Context)
- Massive ventricular hypertrophy without obvious cause 2
- Impaired diastolic function predominantly 2
- Myofibrillar disarray 1
- Normal or reduced chamber volumes 1
Critical Clinical Overlap and Evolution
A fraction of patients with hypertrophic cardiomyopathy (10-20%) develop a DCM phenotype after several years, representing disease evolution rather than equivalence. 1
The "Burned Out" Phenomenon
Long-standing uncontrolled hypertension can initially cause concentric LVH, but as disease progresses, the left ventricle dilates and ejection fraction declines in what is termed a "burned out" left ventricle—this represents hypertensive dilated cardiomyopathy 1
Patients with the dilated phase of hypertrophic cardiomyopathy (D-HCM) have worse prognosis than those with primary DCM despite similar treatment intensity, with 5-year survival of 45.6% versus 81.6% respectively 3
Diagnostic Pitfalls to Avoid
Under experimental conditions, differentiation between hypertrophic cardiomyopathy and DCM is not trivial because the presence of dilation does not necessarily exclude the presence of myocyte hypertrophy. 1
Key Distinguishing Features
For hypertensive heart disease versus HCM: Normal ECG or isolated increased voltage without repolarization abnormality favors hypertension; marked repolarization abnormalities, conduction disease, or Q-waves favor HCM 1
Wall thickness thresholds: Maximum LV wall thickness ≥15 mm in Caucasians or ≥20 mm in Black patients suggests HCM rather than hypertensive LVH 1
Regression test: LVH from hypertension should regress over 6-12 months with tight systolic blood pressure control (<130 mmHg), while HCM will not 1
Genetic Considerations
Gene dosage affects phenotype: homozygosity for a mutation that produces HCM when heterozygous can instead cause DCM 1
Heterozygosity in two genes that individually produce HCM can result in a DCM-like phenotype rather than HCM 1
Approximately 50% of DCM cases have a genetic cause, predominantly affecting cytoskeletal, sarcolemmal, sarcomeric, and nuclear envelope proteins 1
Prognostic Implications
The distinction matters critically for prognosis and management: patients with D-HCM are more symptomatic at diagnosis despite less severe LV dilatation and have significantly worse outcomes than primary DCM patients 3. This underscores that these conditions, while potentially sharing some pathways, represent distinct disease entities with different natural histories and treatment responses.