BackgroundGenetic, observational, and clinical intervention studies indicate that circulating levels of remnant cholesterol (RC) are associated with cardiovascular diseases. However, the predictive value of RC for cardiovascular mortality in the general population remains unclear.MethodsOur study population comprised 19,650 adults in the United States from the National Health and Nutrition Examination Survey (NHANES) (1999–2014). RC was calculated from non-high-density lipoprotein cholesterol (non-HDL-C) minus low-density lipoprotein cholesterol (LDL-C) determined by the Sampson formula. Multivariate Cox regression, restricted cubic spline analysis, and subgroup analysis were applied to explore the relationship of RC with cardiovascular mortality.ResultsThe mean age of the study cohort was 46.4 ± 19.2 years, and 48.7% of participants were male. During a median follow-up of 93 months, 382 (1.9%) cardiovascular deaths occurred. In a fully adjusted Cox regression model, log RC was significantly associated with cardiovascular mortality [hazard ratio (HR) 2.82; 95% confidence interval (CI) 1.17–6.81]. The restricted cubic spline curve indicated that log RC had a linear association with cardiovascular mortality (p for non-linearity = 0.899). People with higher LDL-C (≥130 mg/dL), higher RC [≥25.7/23.7 mg/dL in males/females corresponding to the LDL-C clinical cutoff point (130 mg/dL)] and abnormal HDL-C (<40/50 mg/dL in males/females) levels had a higher risk of cardiovascular mortality (HR 2.18; 95% CI 1.13–4.21 in males and HR 2.19; 95% CI 1.24–3.88 in females) than the reference group (lower LDL-C, lower RC and normal HDL-C levels).ConclusionsElevated RC levels were associated with cardiovascular mortality independent of traditional risk factors.

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Pathological myocardial hypertrophy can be caused by a variety of diseases, mainly accompanied by myocardial interstitial fibrosis (MIF), which is a diffuse and patchy process, appearing as a combination of interstitial micro-scars and perivascular collagen fiber deposition. Different stimuli may trigger MIF without cell death by activating a variety of fibrotic signaling pathways in mesenchymal cells. This manuscript summarizes the current knowledge about the mechanism and harmful outcomes of MIF in pathological myocardial hypertrophy, discusses the circulating and imaging biomarkers that can be used to identify this lesion, and reviews the currently available and potential future treatments that allow the individualized management of patients with pathological myocardial hypertrophy.