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Type 2 diabetes mellitus (T2DM) is a metabolic disorder that has alarmingly increased in incidence in recent decades. One of the most serious complications of T2DM is diabetic cardiomyopathy (DCM), an often underrecognized yet severe condition that is a leading cause of mortality among diabetic patients. In the early stages of DCM, patients typically show no symptoms and maintain normal systolic and diastolic left ventricle function, making early detection challenging. Currently available clinical markers are often not specific enough to detect the early stage of DCM. Conventional biomarkers of cardiac mechanical stress and injury, such as natriuretic peptides (NPs) and cardiac troponin I (cTnI), have shown limited predictive value for patients with T2DM. NPs have proven efficacy in detecting diastolic dysfunction in diabetic patients when used alongside 2D echocardiography, but their utility as biomarkers is limited to symptomatic individuals. While cTnI is a reliable indicator of general cardiac damage, it is not specific to cardiac injury caused by high glucose levels or T2DM. This underscores the need for research into biomarkers that can enable early diagnosis and management of DCM to reduce mortality rates. Promising novel biomarkers that showed good performance in detecting diastolic dysfunction or heart failure in diabetic patients include galectin-3, ST2, FGF-21, IGFBP-7, GDF-15, and TGF-β. This review summarizes the current understanding of DCM biomarkers, aiming to generate new ideas for the early recognition and treatment of DCM by exploring related pathophysiological mechanisms. [ABSTRACT FROM AUTHOR]

Objective. Patients with preexistent aortic valve disease represent approximately 5% of the total number of patients with acute coronary syndrome (ACS): they are at high cardiovascular risk with a reserved prognosis. Material and Methods. Starting with 2006, a group of 196 patients consecutively hospitalized within the cardiology ward of the Emergency County Hospital of Baia Mare, aged 56 to 94, with different grades of degenerative AS, underwent prospective assessment over a period of 5 years. Results. A number of 54 patients (27.6%) developed ACS and 67 (34.2%) had left ventricular systolic dysfunction (LV) documented by echocardiography: Eleven (11) had LV severe systolic dysfunction, defined by EF under 30% (7 from the ACS group), 28 had moderate systolic dysfunction, defined by EF between 30-40% (13 from the ACS group) and 28 had mild systolic dysfuntion, defined by EF between 40-50% (8 from the ACS group). The ACS risk was 5.14 times higher in patients with severe systolic dysfunction (OR 5.14, 95% CI 1.43-18.34, p=0.0117), 2.68 times higher in patients with moderate systolic dysfunction (OR 2.68, 95% CI 1.18-6.11, p=0.0185) and 1.06 times higher in patients with mild systolic dysfunction (OR 1.06, 95% CI 0.44-2.57, p=0.8961) The cumulative risk for developing ACS was OR=2.84, 95% CI 1.48-5.44, p=0.0016 in patients with AS and LV dysfunction, while the cumulative incidence of ACS was 41.8%. Conclusion. Patients with degenerative AS and LV systolic dysfunction have an increased risk of developing ACS. It is of top priority to identify these patients and to establish an optimal medical/surgical therapeutical regimen in order to achieve a better prognosis, aggravated by the increased incidence of ACS. [ABSTRACT FROM AUTHOR]