Really I appreciate your logical queries.. But it's difficult to answer exactly but Science is totally based on logic.

I don't know a definite answer to this but I would postulate that it is down to evolutionary pressures. For a variant associated with a disease to become prevalent, individuals with the condition need to survive to an age where they can reproduce. The more prevalent the variant the more likely the mutation initially occurred earlier within the population. You suggest that it could be because of the size of the proteins which does place them at a higher risk of variation but if you look at titin which is also a protein in which variants may underlie HCM it is larger than both of these yet it is a less frequent cause so although size may matter it is not the major determinant.

Joseph Westaby True, the relative contribution of a gene to disease has been attributed to gene size, evolutionary conservation and mutational rate (Petrovski et al., 2013). Alfares et al., 2015, examined the frequency of variants per kilobase of DNA coding sequence (CDS) across 18 HCM-associated genes revealed a non-linear relationship between gene size and gene contribution. The MYBPC3 gene was found to be the largest source of P/LP variants with an average of 34 variants per kilobase among HCM cases despite having a shorter CDS length of 4548 bps compared to MYH7 that had a larger CDS length of 6576 bps and an average of 16 variants per kilobase. This only shows that maybe MYH7 is less tolerant to functional mutations than MYBPC3, yet does not explain the preponderance of MYBPC3 and MYH7 in HCM.

MYBPC3 is the most common mutated gene in hypertrophic cardiomyopathy.I am totally agreed but Why so Might be the genetic predisposition or environmental predisposition