Comparison of long-term outcomes of young patients after a coronary event associated with familial hypercholesterolemia

Abstract

Objective Familial hypercholesterolemia (FH) is an important cause of premature coronary artery disease (CAD). Prognosis data are lacking in patients with FH and coronary artery disease particularly in the era of widespread statin use. We compared long-term prognosis between patients with and without FH after a coronary event. Methods In this retrospective study, 865 patients younger than 40 years of age with CAD were enrolled. FH was diagnosed based on the Dutch Lipid Clinic Network algorithm. Baseline characteristics, coronary angiographic findings and prognosis during median follow-up of 5 (3–8) years were compared between patients with or without FH. Results Definite or probable FH was detected in 37 patients (4.3%) and possible FH in 259 patients (29.9%). FH was associated with significantly higher prevalence of multi-vessel lesions ( p < 0.001) and higher Gensini score ( p = 0.008). In the subset of 706 patients for whom follow-up data were available, 127 (18.0%) suffered major adverse cardiovascular and cerebrovascular events (MACCE). FH was associated with increased risk of MACCE, independently of age, sex, smoking, body mass index, hypertension or diabetes mellitus (HR = 2.30, 95%CI = 1.09 to 4.84, p = 0.028). Conclusions FH is an independent risk factor for MACCE in young patients after a coronary event during long-term follow-up. It is necessary to optimize lipid treatment of patients with FH after a coronary event.

Coronary lesion complexity in patients with heterozygous familial hypercholesterolemia hospitalized for acute myocardial infarction: data from the RICO survey

“…Only few studies have assessed the characteristics of coronary lesions in FH patients hospitalized for acute MI [ 7 , 8 , 12 – 15 ]. After matching for the main factors associated with CAD, the findings of this study suggest that the FH-associated high cholesterol burden, which starts at an early age, and inflammation are associated with CAD severity.…”

“…When individuals do not respond to treatment, fatal or non-fatal coronary events occur in approximately 50% of men < 50 y and 30% of women < 60 y [ 6 ]. FH is often found after an individual has a myocardial infarction (MI), with an estimated prevalence between 1.6 and 4.3% [ 7 , 8 ]. Furthermore, FH patients have an unfavorable prognosis after MI, with a risk of recurrence of cardiovascular or coronary events that is 2 to 3 times higher than the average [ 9 , 10 ].…”

“…Although CAD is more frequently associated with multi-vessel disease in FH patients, there are significant variations in prevalence [ 12 – 14 ]. Using the Gensini angiographic score, Wang [ 8 ] and Li [ 15 ] showed that CAD was more severe in patients with FH than in those without FH (according to the DLCN criteria). Findings from a series of 104 asymptomatic age-matched patients found that coronary lesions in CAD patients with genetically confirmed heterozygous FH are more diffuse and calcified than in patients without a genetic mutation [ 16 ].…”

Cost-Effectiveness of Alirocumab for the Secondary Prevention of Cardiovascular Events after Myocardial Infarction in the Chinese Setting

“…Women in China had higher all-cause/cardiovascular mortalities vs. men at 1-year post-MI (Dreyer et al, 2019), so we explored the value of alirocumab in female population. We involved poorly controlled FH patients after MI and assumed that the risk of MACEs was 2.3 times than those without FH (Wang et al, 2019). Meanwhile, a maximal reduction in risk of MACEs was modeled by the absolute change of LDL-C (Baigent et al, 2010).…”

Targeting Platelet in Atherosclerosis Plaque Formation: Current Knowledge and Future Perspectives

“…Dyslipidemia is a major risk factor of coronary artery disease and is associated with a poor prognosis, such as the major cardiovascular adverse event (MACE) [ 23 , 24 , 25 ]. The effects of chronic hyperlipidemia are complex, which causes lipid deposition in atherosclerotic lesions, primary endothelial damage, and increased platelet reactivity.…”