Coronary Artery Calcification in Familial Hypercholesterolemia

Association of Coronary Plaque With Low-Density Lipoprotein Cholesterol Levels and Rates of Cardiovascular Disease Events Among Symptomatic Adults

“…This information would allow for the allocation of expensive long-term therapies to those patients with severe hypercholesterolemia most likely to benefit, whereas such therapies could be avoided in patients with limited absolute benefit. 8 That being said, the median follow-up in our study was relatively short at 4.2 years. Because 22.8% of patients with LDL-C levels of at least 190 mg/dL had detectable plaque despite having CAC scores of 0, the results should not be used to withhold longterm preventive therapy with statins, especially in younger individuals.…”

“…7(p3485) This has prevented exploring the potential value of using plaque burden and CAC for risk stratification, particularly for "derisking" (ie, lowering classification of risk) purposes, and of using personalized LDL-C management in these patients. 8 Indeed, studies on the real-world prevalence and prognostic implications of noncalcified coronary atherosclerosis in persons with LDL-C levels of at least 190 mg/dL are scarce. 5 Thus, the present study had 2 goals.…”

Role of coronary artery calcium score in the primary prevention of cardiovascular disease

“…The findings from these and other studies129 highlight the multifactorial nature of atherosclerosis, which is not only heterogenous among individuals with severe hypercholesterolemia but is also the main driver of future clinical risk. While we do not advocate cessation of, or refraining from statins in those with severely elevated levels of LDL-C (indeed, a large proportion of participants in the aforementioned studies were treated with statins, including many of those with CAC=0), CAC can provide valuable insight into risk stratification strategies for a more cost effective allocation of novel, costly lipid lowering treatments 130131132. As in patients with diabetes, this may help funnel expensive therapies such as PCSK9 inhibitors to patients most likely to benefit, and away from individuals more resilient to atherosclerosis and events who are therefore less likely to benefit.…”

“…Nevertheless, this is an area of intense debate and active research, and further studies are needed 130131132133. Specifically, a better understanding of the “warranty period” of CAC=0 in patients with severe hypercholesterolemia is needed.…”

Bibliometric and Visual Analysis of Vascular Calcification Research

“…Through the potent combination of top keywords and literature, we attribute the research hotspots as follows: 1) The mechanism of VC in CKD or dialysis patients, including inflammation (Yuan et al, 2020), VSMC phenotype of osteogenic differentiation (Yang et al, 2020), overexpression of calcification-promoting factors (oxidative stress) (Watanabe et al, 2020), parathyroid hormone (Imafuku et al, 2020), fibroblast growth factor 23 (Jiang et al, 2020) as well as the suppression of calcification inhibitors (Liu et al, 2018); 2) various pathophysiological changes (atherosclerosis, arterial calcification, arterial stiffness, etc.) accompanied by CVD, and the impact of these changes on the prognosis of patients (Stabley and Towler, 2017;Mszar et al, 2020); 3) comparison of therapeutic effects between open valve replacement surgery and minimally invasive transcatheter valve replacement for aortic valve or heart valve stenosis (Ielasi et al, 2021); and 4) molecular and cellular mechanisms of VC, including various molecular signaling pathways and abnormal proliferation (Miyata et al, 2020) or apoptosis (Boraldi et al, 2021) of cells that regulate VC.…”