Concentric left ventricular hypertrophy (LVH) is characterized by adaptive thickening of the myocardium in response to pressure overload from chronic hypertension or aortic valve stenosis. LVH can also be seen in genetic conditions like Fabry disease or hypertrophic cardiomyopathy with chaotic sarcomeric disarray at the cellular level.
LVH leads to a loss of compliance and impaired diastolic filling. The increased resting LV pressure leads to an increase in end-systolic wall stress and the parallel replication of sarcomeres with concentric LVH. The thickened myocardium also requires much more oxygen (risk of ischemia) and alters the conduction system increasing the risk for arrhythmias.
This transgastric, mid-papillary transesophageal echocardiography (TEE) view shows severe, concentric LVH. Note that at end-systole, the LV cavity is completely obliterated, suggesting a preserved ejection fraction. These “kissing papillary muscles” do not universally translate to: “give fluids.” Chamber size must be assessed at end-diastole. If the LV end-diastolic volume is still low, one must consider underfilling related to right heart dysfunction.