To the Editor:

Weidemann et al ’s review “The Different Faces of Echocardiographic Left Ventricular Hypertrophy: Clues to the Etiology” raises several important issues that need clarification. The authors do not clarify the meaning of left ventricular (LV) hypertrophy (LVH). In the cardiology community, “LVH” conveys an increase in the mass of the left ventricle. LVH reflects an increase in LV wall thickness and/or an increase in the size of the LV cavity. The pathophysiology of LVH is a pressure or volume overload or an infiltrative disease process that increases the wall thickness of the myocardium. Pressure and volume overload result in different patterns and mechanisms of cell growth. Pressure overload results in the parallel addition of sarcomeres, causing an increase in myocyte width, which in turn increases wall thickness. Alternatively, volume overload conditions yield myocyte lengthening by sarcomere replication in series.

In contemporary clinical research practice and population studies, the diagnosis of LVH is based on echocardiographic measurements of LV dimensions and the calculation of LV mass (LVM = 1.04 [(LV end-diastolic diameter in diastole + posterior wall thickness in diastole + interventricular septal thickness in diastole) – LV end-diastolic diameter in diastole ] × 0.8 + 0.6), requiring adjustments for sex, height, and body mass. However, there are a number of methodologic difficulties in the interpretation of LV mass in echocardiographic practice. The difficulties include feasibility, accuracy, and reproducibility (the standard deviation of differences in LVM between examinations is about 30 g). Additionally, LVM is uncommonly reported, and most physicians do not conceptualize ventricular hypertrophy to reflect increased LVM but rather increased thickness of the left ventricle, using the two terms synonymously. The image portrayed in the mind of the clinician when LVH is reported is that of hypertrophied walls (thick) with a normal LV cavity size. Thus, reporting a ventricle with thick walls and elucidating the broad differential of disease states that make a ventricle thick becomes imperative for the interpreting physician.

Weidemann et al. did not address this daily practice dilemma in their review of LVH, which we believe represents an issue with the syntax of LVH as echoed in the paper. Disease states with increased LVM without a thick ventricle (dilated cardiomyopathy, hemochromatosis, Wegener’s disease, and sarcoidosis) and disease entities with both increased LVM and a thick ventricle (Danon disease, cardiac oxalosis and mucopolysaccharidosis) are not addressed in the review. Thus, the authors have essentially described some disease states with a thick ventricle and increased LVM (and, therefore, LVH), leaving others unmentioned, and made no attempt to specify to the reader what they actually mean by “LVH.” Additionally, it is important to point out that amyloidosis and hypertrophic cardiomyopathy that mimic each other echocardiographically can and do frequently lead to a wall thickness > 14 mm with evidence of dynamic outflow tract obstruction, a fact ignored by the authors.

Weidemann et al. indicate that their review focuses on nonvalvular physiologic and pathologic conditions that exhibit LVH as a key cardiac finding. Implicit in the use of their term “LVH” is a thick-walled ventricle, rather than increased LVM as caused by, for example, a dilated left ventricle. Also implicit in the term “LVH” is myocyte hypertrophy. However, “LVH” does not accurately describe hearts affected by infiltrative processes, such as amyloidosis with myocyte necrosis and atrophy rather than hypertrophy; yet these hearts have thick walls with increased LVM and, therefore, LVH.

In summary, it may be important to remind the reader that all disease states that cause a thick-walled ventricle will eventually increase LVM (and therefore cause LVH), but not all LVH is a thick ventricle. The syntax of a “thick ventricle” may better serve the practicing sonographer and cardiologist as they attempt to define the disease processes that alter the myocardial mass.