## 1 Introduction  
Sudden cardiac death (SCD) is defined as an unexpected natural death due to a cardiac cause that occurs within a short period of time, generally within the first hour from the onset of symptoms, or in subjects without any symptoms 24 h previously [1, 2].  
The annual incidence of SCD in Europe and North America is 50-100/100,000 persons [3, 4, 5]; Asia has an estimated value of 40/100,000 persons [6].  
The main cause of sudden cardiac death is coronary artery disease (CAD), with an accepted proportion of all SCDs due to CAD of \(\approx\)80%, and SCD accounts for \(\approx\)50% of all CAD-related deaths [7]. The other causes of SCD are cardiomyopathyopathies, myocarditis, valvular disease, and channelopathies. Specifically, the distribution of the SCD causes varies with age, resulting in the fact that in young people SCD is mostly due to diseases that are categorizable into those which are structural or those which are purely arrhythmogenic [8]. The structural causes include the inherited cardiomyopathies, among which hypertrophic cardiomyopathy (HCM) is reported to be the most common cause of SCD in young adults, but it is also a major cause of morbidity and mortality in the elderly [8; 9; 10].  
Hypertrophic cardiomyopathy (HCM) is defined as the presence of increased LV wall thickness (with or without RV hypertrophy) or mass that is not solely explained by abnormal loading conditions [11]. The estimated prevalence of HCM is 1:500 in a healthy young population. The penetrance is incomplete and age-related; thus, HCM can present at any age [12; 13; 14]. Some authors report that HCM is the second most frequent cause of sudden cardiac death, after atherosclerotic coronary artery disease [15].  
HCM is an autosomal dominant disease, showing a familial pattern of inheritance in approximately one-half of cases, while in the other cases, sporadic or de novo mutations are found [10]. The main genes involved in the onset of the pathology genes encode for different cardiac sarcomere proteins. These proteins can be associated with a specific macroscopic and microscopic phenotype, including asymmetrical hypertrophy, which is mostly observed in the interventricular septum, the left ventricular cavity reduction, and/or the myocyte disarray with interstitial fibrosis [11; 12]. However, HCM shows a relevant heterogeneity in both phenotype and genotype; in fact, different cardiac morphologies and different levels of severity in disease and prognosis can arise from different genes or different mutations in the same gene. This variety is confirmed by cases showing identical genetic mutations in which diverse phenotypic patterns are described between unrelated families or even among affected individuals from the same family [16].  
Clinical and judicial autopsy can provide an important contribution in the characterization of the genetic and phenotypic features of HCM. In fact, the post-mortem analysis can be a source of evidence for the genotype-phenotype correlation, especially since the so-called molecular autopsy assumed a strong role in the assessment of cardiovascular diseases with a genetic background that were causes of SCD. This should be stressed even more because some cases reveal normal cardiac macroscopic and microscopic findings. Furthermore, the European Society of Cardiology (ESC) guidelines recommend the performance of post-mortem genetic analysis in suspected SCD cases which can be related to a specific inheritable channelopathy or cardiomyopathyopathy [17].  
Therefore, the aim of this paper is to conduct a systematic review of the forensic/post-mortem literature describing HCM cases and to provide an overview of the macroscopic, microscopic, radiological, and molecular data that are useful for a confident post-mortem diagnosis. Focused attention is paid to the genetic aspects and to the analysis of any correlation between the morphological variant and the genotype patterns.