Concentric Hypertrophy vs Eccentric Hypertrophy

Pathophysiologic Differences

Concentric left ventricular hypertrophy develops from chronic pressure overload with sarcomeres added in parallel, causing increased wall thickness without chamber enlargement, as noted by the European Society of Cardiology 1, 2
Eccentric hypertrophy develops from volume overload with sarcomeres added in series, lengthening myocytes, resulting in increased LV cavity size with normal wall thickness but elevated total LV mass, as reported by the European Society of Cardiology 1, 2
Concentric hypertrophy is characterized by normal or small LV cavity size with uniformly increased wall thickness, according to the European Society of Cardiology 1, 2
Eccentric hypertrophy generally presents with low-normal or mildly impaired systolic function due to chronic volume overload, as observed by the European Society of Cardiology 1, 2

Inappropriate or excessive hypertrophy leads to low systolic wall stress and high ejection fraction but is associated with high perioperative morbidity and mortality, as noted by the American Heart Association 3
The hypertrophied heart exhibits reduced coronary blood flow per gram of muscle and limited coronary vasodilator reserve even without epicardial coronary disease, according to the American Heart Association 3
Concentric hypertrophy is associated with increased sensitivity to ischemic injury with larger infarcts and higher mortality rates than non-hypertrophied hearts, as reported by the American Heart Association 3
Hemodynamic stress from exercise or tachycardia produces maldistribution of coronary blood flow and subendocardial ischemia, as observed by the American Heart Association 3

Concentric left‑ventricular hypertrophy arises from chronic pressure overload and is characterized by a relative wall thickness (RWT) ≥ 0.42 with no cavity dilation, whereas eccentric hypertrophy results from chronic volume overload, shows cavity dilation and a normal or reduced RWT < 0.42; both patterns exhibit an increased indexed left‑ventricular (LV) mass【4】【5】.

An indexed LV mass > 115 g/m² in men or > 95 g/m² in women supports the diagnosis of LV hypertrophy, irrespective of the geometric pattern【4】.

Both concentric and eccentric hypertrophy are associated with severe diastolic dysfunction, manifested by impaired relaxation and elevated filling pressures; concentric hypertrophy typically exhibits greater ventricular stiffness than eccentric hypertrophy【4】.

Myocytes elongate by adding sarcomeres in series without a significant increase in cross‑sectional area, so wall thickness remains normal or only slightly increased despite a rise in total myocardial mass. 6
The extracellular matrix loses pericellular collagen fibrils, rendering the left ventricle highly compliant. 6

The hemodynamic pattern is characterized by a supranormal ejection fraction with stroke volume divided between retrograde flow into the left atrium and forward flow across the aortic valve. 6
This condition produces marked dilation of the left ventricle and left atrium with an elevated end‑diastolic volume. 6
Progressive contractile dysfunction occurs at both the chamber and myocyte levels, distinguishing it from pressure‑overload states. 6

Diastolic retrograde flow from the aorta into the left ventricle generates chronic volume overload and progressive ventricular dilation. 6
Eccentric hypertrophy develops over weeks to months, accompanied by rising ventricular filling pressures and the emergence of heart‑failure symptoms. 6

Large arteriovenous shunts, such as aortocaval communications, create chronic volume overload and serve as experimental models of ventricular remodeling. 6
Surgical creation of abdominal aorta–inferior vena cava shunts in animal studies has provided fundamental insights into the mechanisms of volume‑overload‑induced remodeling. 6

Eccentric hypertrophy displays lower ventricular stiffness compared with concentric hypertrophy, attributable to disruption of the collagen matrix. 6