(1) Background: Myocardial infarction was, until recently, recognized as a major coronary event, often fatal, with major implications for survivors. According to some authors, diabetes mellitus is an important atherogenic risk factor with cardiac determinations underlying the definition of the so-called “diabetic heart”. The present study aims to establish a correlation between the evolution of myocardial infarction in diabetic patients, by determining whether lactic acid levels, the activity of carbonic anhydrase isoenzymes, and the magnitude of ST-segment elevation are correlated with the subsequent evolution of myocardial infarction. (2) Methods: The study analyzed 2 groups of 30 patients each: group 1 consisted of diabetic patients with acute myocardial infarction, and group 2 consisted of non-diabetic patients with acute myocardial infarction. Patients were examined clinically and paraclinical, their heart markers, lactic acid, and the activity of carbonic anhydrase I and II isozymes were determined. All patients underwent electrocardiogram and echocardiography analyses. (3) Results: The results showed that diabetics develop acute myocardial infarction more frequently, regardless of how much time has passed since the diagnosis. The value of myocardial necrosis enzymes was higher in diabetics than in non-diabetics, and acute coronary syndrome occurs mainly in diabetics with poor metabolic balance. Lethality rates in non-diabetic patients with lactic acid values above normal are lower than in diabetics. (4) Conclusions: Lactic acid correlated with the activity of isozyme I of carbonic dioxide which could be early markers of the prognosis and evolution of diabetic patients with acute myocardial infarction.

Background and Objectives: Hypothyroidism can alter lipid metabolism, vascular resistance, body composition, and myocardial function. Yet the cardiovascular risk engines used in routine practice were developed in general populations and do not include thyroid status. This review examines what contemporary risk models capture, what they omit, and how thyroid dysfunction should influence interpretation without being treated as an unvalidated numerical correction. Materials and Methods: A focused narrative search of PubMed was performed for publications from January 2014 through 6 September 2026, supplemented by earlier landmark cohort studies, risk-model derivation papers, randomized trials, and professional guidelines. Evidence was organized around overt and subclinical hypothyroidism, traditional risk factors, observed cardiovascular events, and the design and validation of major risk equations. Results: SCORE2, SCORE2-OP, Framingham, QRISK3, and PREVENT differ in predicted outcomes, age ranges, geography, and required inputs; their percentages and categories are therefore not interchangeable. Thyroid status is absent from these engines. A prospective community cohort found that adding TSH produced little incremental discrimination beyond conventional scores, whereas cross-sectional studies sometimes found higher calculated risk in women with subclinical hypothyroidism. Individual-participant data suggest that excess coronary and heart-failure risk is concentrated at higher TSH levels, while a large 2025 pooled analysis found only small differences in conventional risk factors between subclinical thyroid dysfunction and euthyroidism. Levothyroxine improves lipids most clearly in overt hypothyroidism, but cardiovascular outcome benefit in older adults with mild subclinical disease remains unproven. Conclusions: Clinicians should use one validated, region- and age-appropriate cardiovascular model, confirm that the patient meets its intended-use criteria, and evaluate thyroid disease in parallel. Cross-model percentage comparisons should be avoided. Persistent TSH elevation, overt hormone deficiency, treatment status, frailty, and severe dyslipidemia belong in clinical judgment and follow-up, not in an improvised score multiplier.