Objective: To explore the association between hypochloremia and mortality in critically ill patients with chronic heart failure (CHF). Methods: This is a retrospective cohort study from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database of patients with CHF diagnosed according to ICD-9 or ICD-10. Patients were divided into three groups according to serum chloride values. A multivariable logistic regression analysis was used to investigate the relationship between hypochloremia and short-term mortality. Results: A total of 2103 patients with CHF were enrolled in our study. The 30-day mortality was 6.7%. After adjusting for confounders, the 30-day mortality risks of the hypochloremia group were significantly higher than that of the group with normal serum chloride (OR 2.23, 95% CI 1.27–3.92, p = 0.005). Hypochloremia was consistently associated with increased mortality in patients that were older or had sepsis. Conclusion: Hypochloremia is associated with increased mortality in intensive care patients critically ill with CHF.

Cardiovascular disease (CVD) remains a leading global cause of mortality, with metabolic and inflammatory dysregulation playing pivotal roles. The C-reactive protein-triglyceride glucose index (CTI), a novel biomarker integrating inflammation (CRP) and insulin resistance (triglyceride-glucose index), has shown promise in predicting adverse outcomes, but its associations with CVD and mortality in the general population remain unclear. The aim of this study is to explore the association of the C-reactive protein-triglyceride glucose index with cardiovascular disease and mortality. This study analyzed data from 8720 adults in the National Health and Nutrition Examination Survey (NHANES) 2001–2010. CTI was calculated as CTI 0.412 × ln(CRP [mg/L]) + [ln(TG [mg/dL] × FPG [mg/dL])]/2. Multivariable logistic regression examined the association between CTI tertiles (T1–T3) and CVD, and Cox regression assessed the relationship between CTI tertiles and cardiovascular and all-cause mortality, with adjustment for demographic, lifestyle, and clinical factors. Higher CTI tertiles were correlated with worse metabolic profiles and higher prevalence of hypertension and diabetes ( P < .001). After full adjustment, the highest CTI tertile (T3) was associated with increased CVD risk (odds ratio = 1.50, 95% confidence interval [CI]: 1.18–1.92, P = .004), cardiovascular mortality (hazard ratio = 1.54, 95% CI: 1.06–2.25, P = .024), and all-cause mortality (hazard ratio = 1.53, 95% CI: 1.29–1.89, P < .001). Restricted cubic spline analysis revealed a nonlinear relationship between CTI and cardiovascular mortality, as well as all-cause mortality . Higher CTI is associated with prevalent CVD and independently predicts increased cardiovascular and all-cause mortality.

The management of ischemic heart disease has evolved from a narrow focus on low-density lipoprotein cholesterol (LDL-C) reduction to a comprehensive strategy targeting the regression and stabilization of coronary atherosclerotic plaque. Intravascular imaging modalities, including intravascular ultrasound (IVUS), optical coherence tomography (OCT), and near-infrared spectroscopy (NIRS), have been instrumental in characterizing the temporal sequence of plaque modification in response to lipid-lowering therapy. This review synthesizes evidence demonstrating that the effects on plaque are both time-dependent and agent-specific. Statins induce rapid plaque stabilization within weeks to months via mechanisms such asanti-inflammatory effects, fibrous cap thickening, and reduction of the lipid core. With prolonged treatment (months to years), statins promote plaque volume regression and facilitate a favorable shift in plaque composition towards a more stable, calcified phenotype. Non-statin agents further augment this regression. Ezetimibe, in combination with statins, provides synergistic LDL-C lowering and enhances plaque volume reduction. PCSK9 inhibitors, recognized as one of the most potent lipid-lowering agents currently available, have been shown in several studies to promote the regression of atherosclerotic plaques and reduce plaque volume. However, their effects on plaque composition—such as calcification, fibrous tissue, fibrofatty tissue, and necrotic core—remain controversial.

Insulin resistance (IR) is a key factor in metabolic disorders. While lipid abnormalities often coexist with IR, their independent associations remain unclear. We analyzed 4698 adults from National Health and Nutrition Examination Survey (2013–2018). The Homeostasis Model Assessment (HOMA) of IR was calculated from fasting glucose and insulin. Lipid profiles (LDLC, HDLC, total cholesterol, triglycerides [TG]) were examined in relation to HOMA-IR using multivariable-adjusted regression models. HDLC showed a inverse association with HOMA-IR ( β = −0.877, P < .001), while TG had a correlation ( β = 0.679, P < .001). LDLC and total cholesterol exhibited weaker, nonlinear relationships. High TG (Q4 odds ratio = 5.53) and low HDLC (Q4 odds ratio = 0.15) were predictive of elevated HOMA-IR ( P < .001). TG and HDLC are associated with HOMA-IR, with distinct dose-response patterns. These findings emphasize the importance of lipid management in metabolic health.