Background Mortality derived from ST-elevation myocardial infarction (STEMI) has decreased due to primary percutaneous coronary intervention (PCI). Paradoxically, the incidence of heart failure secondary to left ventricular remodelling (LVR) is on the rise due to the survival derived from reperfusion strategies. The aim of this study was to assess the prognostic value for LVR of biomarkers involved in several pathophysiological mechanisms activated during STEMI treated with primary PCI. Methods 112 patients with STEMI undergoing primary PCI were evaluated. LVR was defined as a ≥20% increase in the left ventricular end-diastolic volume at 6-month follow-up assessed using echocardiogram as compared with that at discharge. Blood samples were obtained for glucose, N-terminal pro-brain natriuretic peptide, troponin T (TnT), matrix metalloproteinase 9, procollagen type-I N-terminal propeptide and high-sensitivity C reactive protein (hs-CRP). Results 24 patients (21%) developed LVR. Higher levels of maximum TnT, and matrix metalloproteinase 9 and hs-CRP at discharge, were detected as independent risk factors for LVR (OR 1.310, p=0.03; OR 1001, p=0.04; OR 1.040, p=0.04, respectively). Both TnT and hs-CRP showed significant ability to distinguish patients who developed LVR from those who did not, being the values that yielded the greatest sensitivity and specificity as follows: TnT 7.0 μg/l (73%, 84%), hs-CRP 30 mg/l (59%, 85%). Conclusions Myocardial necrosis, as measured by released TnT, and inflammation state evident due to circulating levels of CRP are factors that may play a major role in the development of LVR following STEMI treated with primary PCI.

Cardiomyopathies represent a heterogeneous group of myocardial disorders, traditionally classified by phenotype into hypertrophic, dilated, and arrhythmogenic. Historically, these conditions have been attributed to high-penetrance rare variants in key structural genes, consistent with a classical Mendelian pattern of inheritance. However, emerging evidence suggests that this model does not fully capture the full spectrum and complexity of disease expression. Many patients do not harbor identifiable pathogenic variants, while others carrying well-known disease-causing variants remain unaffected. This highlights the role of incomplete penetrance, likely modulated by additional genetic modifiers. Recent advances in genomics have revealed a broader view of the genetic basis of cardiomyopathies, introducing new players such as common genetic variants identified as risk alleles, as well as intermediate-effect variants. This continuum of genetic risk, reflecting an overall genetic influence, interacts further with environmental and lifestyle factors, likely contributing together to the observed variability in clinical presentation. This model offers a more realistic framework for understanding genetic inheritance and helps provide a clearer picture of disease expression and penetrance. This review explores the evolving genetic architecture of cardiomyopathies, spanning from a monogenic foundation to intermediate-risk variants and complex polygenic contribution. Recognizing this continuum is essential for enhancing diagnostic accuracy, guiding family screening strategies, and enabling personalized patient management.