Background: This study describes the complex association between the neutrophil-to-high-density lipoprotein cholesterol ratio (NHR), 25-hydroxyvitamin D (25(OH)D) levels, and cardiovascular disease (CVD), such as stable ischemic heart disease (IHD), ST elevation myocardial infarction (STEMI), non–ST-segment elevation myocardial infarction (NSTEMI), and unstable angina (UA). Methods: The serum 25(OH)D concentration and NHR values were analyzed in groups of patients with chronic coronary syndrome (CCS) and acute coronary syndrome (ACS). The severity of coronary artery atherosclerosis was determined using the Coronary Artery Surgery Study (CASS) scale. Results: Significant differences in 25(OH)D and NHR concentrations were observed between CCS and (ACS)/STEMI patients (p < 0.01). Higher 25(OH)D concentrations were associated with the diagnosis of CCS, and higher NHR values with the diagnosis of ACS/STEMI. The NHR threshold for ACS was set at 0.10 (p < 0.001). Patients without significant coronary artery stenosis showed significantly higher 25(OH)D levels and lower NHR values (p < 0.01). Conclusions: The significant correlation between 25(OH)D, HDL, and the NHR suggests that vitamin D, through its influence on inflammatory processes and lipid metabolism, may play a role in the pathogenesis of chronic and acute coronary syndromes. The suggested bidirectional relationship between the NHR and 25(OH)D and the role of the NHR as a predictor of vitamin D levels require further well-designed studies.

Coronary artery disease (CAD) continues to be a foremost contributor to global mortality, and the quest for modifiable risk factors could improve prophylactic strategies. Recent studies suggest a significant role of zinc (Zn) and copper (Cu) deficiency in atheromatous plaque formation. Furthermore, hair was previously described as a valuable source of information on elemental burden during the 6–8 week period before sampling. The aim of this study was to investigate the possibility of correlation between the extent of CAD evaluated with the SYNergy Between PCI With TAXUS and the Cardiac Surgery (SYNTAX) score with Cu and Zn content in hair samples, as well as with the Cu/Zn ratio in a cohort of 130 patients. Our findings describe a statistically significant inverse correlation between Cu content and the Cu/Zn ratio in hair samples and the extent of CAD. In contrast, no significant correlation was found between Zn content and the extent of CAD. Considering the scarcity of existing data on the subject, the analysis of hair samples could yield a novel insight into elemental deficiencies and their potential influence on CAD extent.

About one-tenth to one-third of patients with severe aortic stenosis (AS) do not develop left ventricular hypertrophy (LVH). Intriguingly, the absence of LVH despite severe AS is associated with lower prevalence of heart failure (HF), which challenges the classical notion of LVH as a beneficial compensatory response. Notably, the few studies that have attempted to characterize AS subjects with inadequately low left ventricular (LV) mass relative to LV afterload (i-lowLVM) described better prognosis and enhanced LV performance in AS associated with i-lowLVM, but those reports were limited to severe AS. Our aim was to compare myocardial function between moderate and severe AS with i-lowLVM. We retrospectively analyzed in-hospital records of 225 clinically stable nondiabetic patients with isolated moderate or severe degenerative AS in sinus rhythm, free of coexistent diseases. Subjects with i-lowLVM were compared to those with appropriate or excessive LVM (a/e-LVM), defined on the basis of the ratio of a measured LVM to the LVM predicted from an individual hemodynamic load. Patients with i-lowLVM and a/e-LVM did not differ in aortic valve area, LV end-diastolic diameter (LVd, a measure of LV preload), and circumferential end-systolic LV wall stress (cESS), an estimate of LV afterload. Compared to a/e-LVM, patients with i-lowLVM had increased LV ejection fraction (EF) and especially higher LV midwall fractional shortening (a better index of LV myocardial function than EF in concentric LV geometry) (p < 0.001–0.01), in both moderate and severe AS. LVd and cESS were similar in the four subgroups of the study subjects, i.e., moderate AS with i-lowLVM, moderate AS with a/e-LVM, severe AS with i-lowLVM, and severe AS with a/e-LVM (p > 0.6). Among patients with i-lowLVM, LVM did not differ significantly between moderate and severe AS (p > 0.4), while in those with a/e-LVM, LVM was increased in severe versus moderate AS (p < 0.001). In conclusion, the association of the low-LVM phenotype with better myocardial contractility may already develop in moderate AS. Additionally, cESS appears to be a controlled variable, which is kept constant over AS progression irrespective of LVM category, but even when controlled (by increasing LVM), is not able to prevent deterioration of LV function. Whether improved myocardial performance contributes to favorable prognosis and the preventive effect against HF in AS without LVH, remains to be studied.