LAUSR

A 75-year-old woman with hypertension consulted our department because of an electrocardiographic abnormality. On physical examination, her blood pressure was 144/93 mmHg and pulse rate was 70 beats per minute. Her respiratory and heart sounds were normal upon auscultation. Blood sampling data showed mild anemia and high plasma brain natriuretic peptide level of 244 pg/mL. Chest radiography revealed a cardiothoracic ratio of 57%. Twelvelead electrocardiography revealed ST segment depression in leads I, II, aVF, and V3–V6. Two-dimensional transthoracic echocardiography revealed left ventricular (LV) hypertrophy at the interventricular septum (IVS; thicknesses of the IVS and LV posterior wall, 16 and 9 mm, respectively) with a LV ejection fraction of 57%. Left atrial volume index was 56.9 mL/m2. An apical 4-chamber view at end-diastole (Fig. 1a) and end-systole (Fig. 1b) revealed high trabeculations and hypokinesis at the lateral wall (arrow). The ratio of the thickness of the noncompacted layer to that of the compacted layer at end-systole was 2.7. Hypertrophy at the interventricular septum was also observed (arrowhead). Color flow imaging showed blood flow at intertrabecular recesses (Fig. 1c, arrowheads), diagnosing LV noncompaction [1]. An enhanced computed tomographic scan confirmed hypertrabeculation at the lateral wall (Fig. 1d, arrowhead). Pulsed Doppler echocardiography at the mitral inflow revealed an E wave of 39 cm/s, an A wave of 80 cm/s, and a deceleration time of an E wave of 176 ms (Fig. 1c). A pulsed tissue Doppler echocardiogram showed s′ wave of 4.4 cm/s and e′ waves of 2.9 cm/s at the septal annulus (Fig. 1f) and s′ wave of 4.5 cm/s and e′ wave of 2.9 cm/s at the lateral annulus (Fig. 1g). As these 4 values were lower than normal reference values for her age [2], lateral noncompaction and septal hypertrophy might be related to regional systolic and diastolic dysfunction. The E/e′ ratio using the mean values was 13 and was not elevated, suggesting normal LV filling pressure [3]. It is known that LV hypertrophy appears in LV noncompaction as an undulating phenotype [4]. Hamada et al. reported a rare case with LV noncompaction mimicking hypertrophic obstructive cardiomyopathy [5]. In the present case, LV hypertrophy was at the opposite side to the noncompaction and could be caused by idiopathic hypertrophic cardiomyopathy or hypertensive heart disease. In conclusion, this is a rare case with LV lateral noncompaction and septal hypertrophy showing diastolic dysfunction at both regions.