RESUMEN

AIM: Low-density lipoprotein cholesterol (LDL-C) level reduction is highly effective in preventing the occurrence of a cardiovascular event. Contrariwise, an inverse association exists between LDL-C levels and prognosis in some patients with cardiovascular diseases-the so-called "cholesterol paradox." This study aimed to investigate whether the LDL-C level on admission affects the long-term prognosis in patients who develop acute coronary syndrome (ACS) and to examine factors associated with poor prognosis in patients with low LDL-C levels. METHODS: We enrolled 410 statin-naïve patients with ACS, whom we divided into low- and high-LDL-C groups based on an admission LDL-C cut-off (obtained from the Youden index) of 122 mg/dL. Endothelial function was assessed using the reactive hyperemia index 1 week after statin initiation. The primary composite endpoint included all-cause death, as well as myocardial infarction and ischemic stroke occurrences. RESULTS: During a median follow-up period of 6.1 years, 76 patients experienced the primary endpoint. Multivariate Cox regression analysis revealed that patients in the low LDL-C group had a 2.3-fold higher risk of experiencing the primary endpoint than those in the high LDL-C group (hazard ratio, 2.34; 95% confidence interval, 1.29-4.27; p=0.005). In the low LDL-C group, slow gait speed (frailty), elevated chronic-phase high-sensitivity C-reactive protein levels (chronic inflammation), and endothelial dysfunction were significantly associated with the primary endpoint. CONCLUSIONS: Patients with low LDL-C levels at admission due to ACS had a significantly worse long-term prognosis than those with high LDL-C levels; frailty, chronic inflammation, and endothelial dysfunction were poor prognostic factors.

Asunto(s)

RESUMEN

Background: In patients with established heart failure (HF) low total cholesterol levels associate with worse prognosis. Evidence concerning the impact of Low-density lipoprotein cholesterol (LDL-c) in HF is scarce. We aimed to evaluate the prognostic impact of LDL-c in patients with HF, both with and without diabetes mellitus (DM). Methods: We retrospectively analyzed outpatients with chronic HF with systolic dysfunction followed in our HF clinic from January/2012 to May/2018. LDL-c was calculated using the Friedewald's formula. Patients without a complete lipid profile were excluded. The endpoint under analysis was all-cause mortality. Patients were followed until January/2021. A Cox-regression analysis was used to study the prognostic impact of LDL-c. The LDL-c cut-off used was 100 mg/dL (mean value). Analysis was stratified according to the coexistence of DM. Multivariate models were built adjusting for age, sex, coronary artery disease, atherosclerotic non-coronary artery disease, arterial hypertension, smoking status, statin use, severity of systolic dysfunction, creatinine clearance and evidence-based therapy. Results: We studied 522 chronic HF patients, mean age was 70 years, 66.5% males. Severe systolic dysfunction was present in 42.7%, 30.5% had coronary heart disease, 60.5% had arterial hypertension, 41.6% had DM. A total of 92.0% were treated with beta blocker, 87.5% with an ACEi/ARB and 29.1% with a MRA. During a median follow-up of 53 (interquartile range 33-73) months, 235 (45%) patients died. Patients with LDL-c ≤100 mg/dL presented increased multivariate-adjusted risk of all-cause mortality: HR = 1.58 (95% CI: 1.08-2.30), p = 0.02. When patients were stratified according to DM, LDL-c ≤100 mg/dL was independently associated with increased death risk - HR = 1.55 (95% CI:1.05-2.30), p = 0.03 in patients without DM; in patients with DM no association was detected - multivariate-adjusted HR = 1.18 (95% CI: 0.77-1.80), p = 0.44. Conclusion: Non-DM HF patients with LDL-c>100 mg/dL have a 35% reduction in the mortality risk when compared with those with lower values. The "cholesterol paradox" in HF also applies to LDL-c in non-DM patients.

RESUMEN

Lipid-lowering drugs (LLDs) have protective effects against coronary artery disease (CAD) and cerebrovascular disease (CVD); however, a paradoxical association with cholesterol has been identified in several diseases, such as diabetes, dementia, and atrial fibrillation. We aimed to analyze the association between LLDs and cholesterol levels in older adults with type 2 diabetes mellitus (T2DM). This cross-sectional study enrolled consecutive patients aged ≥50 years from three centers in Taiwan. A multiple logistic regression model was used, and odds ratios (ORs) for different levels of total cholesterol (TC) or low-density-lipoprotein cholesterol (LDL-C) compared with the highest level were adjusted for age, triglyceride level, sex, comorbidities, and medications. Among the 3688 participants, 572 with and 676 without T2DM used LLDs. After adjusting for age and sex, the non-T2DM group demonstrated better medical conditions, cognition, and daily function than the T2DM group, regardless of LLD use. Compared to the highest TC level (≥240 mg/dL), ORs were significantly increased as TC levels decreased. A similar pattern of T2DM prevalence was observed in LDL-C levels. Older people with T2DM demonstrated low cognitive and daily functions. Significantly reduced TC and LDL levels were associated with a higher T2DM prevalence in older adults regardless of LLD use. T2DM was associated with impaired cognitive and daily functioning. A higher prevalence of T2DM in older people with low cholesterol levels raises doubt surrounding cognition and daily function being jeopardized when the "lower is better" strategy is applied for the secondary prevention of CAD or CVD.

Asunto(s)

RESUMEN

BACKGROUND: The level of blood lipid is closely related to prognosis in cardiovascular diseases. This study aims to analyze the effect of serum low-density lipoprotein cholesterol (LDL-C) levels on the long-term mortality in acute aortic dissection (AAD). A lower admission LDL-C level is associated with an increased risk of long-term mortality in AAD. METHODS: We analyzed the data of 284 patients with AAD admitted to the First Affiliated Hospital of Shantou University Medical College from February 2016 to September 2019. Patients were followed up post-discharge. All patients were divided into either an LDL-C low-level group or an LDL-C high-level group according to the optimal cut-off point obtained by the receiver operating characteristic (ROC) curve. The endpoint outcome was long-term mortality in AAD. A survival analysis and Cox proportional hazards model were used. RESULTS: According to the Youden index, the optimal cut-off point for LDL-C was 2.755 mmol/L. The Kaplan-Meier survival analysis curves showed that the long-term mortality of the LDL-C low-level group (<2.755 mmol/L) was significantly higher than that of the LDL-C high-level group (≥2.755 mmol/L) (log-rank χ2=13.912, P<0.001). After multivariate Cox regression analysis, LDL-C <2.755 mmol/L was still significantly associated with long-term mortality in AAD (HR=3.287, 95% CI: 1.637-6.600, P=0.001). In addition, cystatin C was also an independent risk factor for the long-term prognosis of AAD (HR=1.253, 95% CI: 1.057-1.486, P=0.009). CONCLUSIONS: A lower admission LDL-C level may be associated with an increased risk of long-term mortality in AAD.

RESUMEN

INTRODUCTION: There is evidence of positive relationships between cholesterol concentration and risk of cardiovascular diseases. However, higher mortality in patients with a low cholesterol level has been reported (the "cholesterol paradox"). MATERIAL AND METHODS: Medical records of 34 191 inpatients between 2014 and 2016 were reviewed and the relationships between total (TC), low-density lipoprotein (LDL-C) and high-density lipoprotein (HDL-C) cholesterol and triglyceride blood concentrations and all-cause in-hospital death and readmission within 14 and 30 days and 1 year were determined in univariate and multivariate analyses. RESULTS: Patients with TC in the lower quartile and LDL-C < 70 mg/dl had greater risk of the outcomes measured than individuals with a TC level in the remaining quartiles and LDL-C ≥ 70 mg/dl. Moreover, patients with TC in the highest quartile, OR (95% CI): 0.36 (0.13-0.99), p < 0.05, and LDL-C ≥ 115 mg/dl, OR (95% CI): 0.53 (0.37-0.77), p < 0.05, had the lowest all-cause in-hospital mortality. However, multivariate analysis using logistic regression and a Cox proportional hazard model showed no significant influence of blood lipid levels on the occurrence of the outcomes measured. CONCLUSIONS: A significant effect of a "cholesterol paradox" linking better prognosis with higher blood lipid concentration was found only in univariate analysis but, after adjustment for clinical characteristics in multivariate analysis, the plasma lipid level had a neutral influence on the occurrence of the measured outcomes. This suggests that a low cholesterol level should be interpreted as a biomarker of illness severity.

RESUMEN

BACKGROUND: Apolipoprotein A1 (ApoA1), a major constituent of high-density lipoprotein (HDL), has antiinflammatory and antioxidative properties and plays a prognostic role in chronic heart failure (CHF). Despite increased tumor necrosis factor α (TNFα) levels being linked to worse outcome of HF, the results are ambiguous about the association of functionally active 308 promoter polymorphism of the TNFα gene. The aims of our study were to investigate the association of ApoA1 and TNFα levels with mortality and to evaluate potential interaction between these factors and TNFα -308 polymorphism. METHODS: Together with several parameters ApoA1, TNFα levels and TNFα-308 polymorphism were determined in a cohort of 195 patients with CHF who were followed for 5 years. RESULTS: Low ApoA1 and high TNFα levels were associated with more severe disease, and ApoA1 showed the strongest relationship with HDL, total cholesterol, C-reactive protein, and N-terminal pro-B-type natriuretic peptide (NT-proBNP). TNFα -308 A carriers had significantly higher ApoA1 levels than wild-type (GG) patients (1.41 ± 0.268 vs 1.29 ± 0.324 g/L; P = .007), whereas levels of TNFα were the same in these groups. Decreased ApoA1 levels were significant predictors of 5-year mortality (NT-proBNP-adjusted HR for 1 decile decrease in ApoA1 level was 1.10 (P = .011). Interaction was found between the ApoA1 level and TNFα -308 polymorphism, because in patients with GG haplotype the adverse effect of low ApoA1 level on survival was more prevalent. CONCLUSIONS: Lower ApoA1 levels were strongly associated with adverse outcome in CHF patients in a TNFα -308 polymorphism dependent manner. These observations support the complex involvement of malnutrition and inflammation in the pathogenesis of CHF.

Asunto(s)