Systemic sclerosis injures the heart chiefly through its microvasculature. Recurrent vasospasm and intimal proliferation in intramyocardial vessels cause repeated focal ischaemia, and the healing response lays down dense collagen, producing the characteristic patchy myocardial fibrosis. Because this fibrosis is scattered rather than coronary-territory based, it stiffens and weakens the ventricle globally, generating a cardiomyopathy with impaired relaxation, falling ejection fraction, conduction blocks, and ventricular arrhythmias. This myocardial scarring is the defining and most lethal cardiac change in scleroderma.
The recalled answer of mitral stenosis is rejected on clinical grounds: stenotic mitral valve disease is essentially rheumatic in origin and is not part of the scleroderma spectrum. Aortic regurgitation points instead to aortic root pathology such as Marfan syndrome, while pericarditis, though it can appear in scleroderma, is usually silent and minor compared with the myocardial disease. The clinically correct deformity is therefore myocardial fibrosis leading to cardiomyopathy.
\[\boxed{\text{Myocardial fibrosis} \rightarrow \text{cardiomyopathy (DCM)}}\]