## 4 Discussion  
HCM is a complex disease that is commonly responsible for SCD, especially in young people, even though it is considered a morbidity potentially affecting any age. HCM shows marked heterogeneity in clinical features and prognosis, which creates a dilemma for physicians in setting up both diagnosis and treatment [54]. HCM is, also, a challenge for pathologists because of the great variability of phenotype, making the post-mortem diagnosis difficult, particularly in cases without anamnestic/clinical data. The macroscopic heart examination can offer findings that support the diagnosis of HCM. Asymmetrical or symmetrical hypertrophy is characteristic evidence [18; 19; 20; 21; 22; 23; 24; 25; 26; 27]. The most observed hypertrophy is the asymmetric one, with a greater thickening of the ventricular septum compared to the left ventricular free walls, with a ratio of increase equal to 30% or more [55]. Regarding the asymmetric HCM, [PERSON] [56] described the classical anatomic form, in which the septal thickening is at the basal anterior septum bulging beneath the aortic valve; thus, it determines the narrowing of the left ventricular outflow tract (LVOT) and anterior displacement of the papillary muscle (PM) and mitral leaflets [18; 20; 24; 25]. This causes the systolic anterior motion of the mitral (SAM) valve during systolic contraction, as well as the mitral leaflet-septal contact, contributing to subaortic obstruction and, gradually, mitral regurgitation [57]. Moreover, the fibrosis at the septum subjacent to the aortic valve and subaortic mitral valve lesion can be observed [16; 18; 19; 21; 23]. However, some authors highlight that the hypertrophy of the basal anterior septum and the subaortic mitral valve lesion can be occasionally observed in other conditions, such as systemic hypertension, aortic valve stenosis, or \"sigmoid septum\" [58; 59]; thus, the histological analysis is necessary to support the co-relation to HCM. Less common abnormalities of MV apparatus can be observed in the size, shape, and annulus angulation. Moreover, calcification may be found at the annulus and leaflets, as well as prolapse and clefts of the leaflets [60]. Chordae tendinae often appear fibrinous, with abnormal attachments to the leaflets and ventricular walls, and can undergo rupture [61]. Regarding papillary muscle, various abnormalities can occur, such as shortening, elongation, or thickening; abnormal attachments on the ventricular walls, or even directly to the mitral leaflets; additional heads or accessory PMs [60; 62]. In some asymmetrical cases, the left ventricular hypertrophy can show morphologic variants, which are observed to be more prominent in other regions, such as the mid-ventricle, apex, anterior-lateral and posterior-basal free walls [63]. The prevalence of the symmetrical form varied from 10% to 42% [16; 55], and it is characterized by the left ventricle concentric thickening with the reduction in the cavity size [19; 20; 22; 23; 24; 25]. A recent study performed on a large sample (\(n\). 2628) reported a prevalence of the main HCM morphological variances, as evaluated by cardiac MR, as follows: isolated basal septal hypertrophy in 46% of the subjects; reverse septal curvature in 38%; apical hypertrophy in 8% of the cases; mid-cavity obstruction with apical aneurysm in 3%; concentric HCM in 1%; and hypertrophy classified as other in 1% [64]. The apical aneurysm of the left ventricle (LVAA) represents a particular morphological variant that falls within the broad phenotypic spectrum of HCM. Its prevalence in subjects affected by hypertrophic cardiomyopathy is relatively low and is estimated to be between 2 and 5%; despite this, LVAA is probably underdiagnosed due to the intrinsic limitations of conventional echocardiography without contrast, which is commonly used for the follow-up [65].