Cardiac dysfunction in hypertrophic cardiomyopathy (HCM) emerges from interacting abnormalities spanning cellular electrophysiology, calcium handling, active tension generation, and whole-heart mechanics, yet genuinely multiscale studies linking these processes remain scarce. In particular, the extent to which secondary ionic remodelling translates into organ-level dysfunction remains unclear. Here, we used a human multiscale electromechanical framework to determine how graded secondary ionic remodelling reshapes HCM disease markers across scales, from action potentials, calcium transients, and active tension to ventricular pressure–volume behaviour and electrocardiogram (ECG) morphology. By separating primary sarcomeric effects from secondary ionic remodelling within a unified biventricular framework, we show that the MYH7 mutation alone produced a hypercontractile state, while additional ionic remodelling progressively shifted the left ventricle towards a smaller-volume operating state, reducing end-diastolic volume by 4–11% and end-systolic volume by 21–24% relative to control. Peak systolic pressure remained elevated above control in all remodelled cases, by 14–21%, but declined progressively with increasing remodelling severity. Ejection fraction likewise remained above control but fell from 69.1% in the mutation-only case to 67.4%, 66.7%, and 66.0% with moderate, severe, and extreme remodelling, consistent with worsening diastolic dysfunction driven by impaired relaxation and reduced filling. Simulated ECGs showed QT prolongation of 22–53% in lead V1 and 26–56% in lead V5, together with broader and increasingly abnormal T-wave morphology. To our knowledge, these findings provide the first computational evidence linking the extent of regional cellular impairment due to secondary ionic remodelling to the degree of chamber-level diastolic dysfunction in HCM, and highlight the potential value of multiscale modelling for mechanistic phenotyping.