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

Hermann Yao,Frédéric Chague,Yves Cottin,Philippe Brunel,Florence Bichat,Laura Tribouillard,Michel Farnier,Damien Brunet,Maud Maza,Marianne Zeller,Luc Rochette

doi:10.1186/s12944-021-01467-z

Abstract

BackgroundAlthough patients with familial heterozygous hypercholesterolemia (FH) have a high risk of early myocardial infarction (MI), the coronary artery disease (CAD) burden in FH patients with acute MI remains to be investigated.MethodsThe data for all consecutive patients hospitalized in 2012–2019 for an acute MI and who underwent coronary angiography were collected from a multicenter database (RICO database). FH (n = 120) was diagnosed using Dutch Lipid Clinic Network criteria (score ≥ 6). We compared the angiographic features of MI patients with and without FH (score 0–2) (n = 234) after matching for age, sex, and diabetes (1:2).ResultsAlthough LDL-cholesterol was high (208 [174–239] mg/dl), less than half of FH patients had chronic statin treatment. When compared with non-FH patients, FH increased the extent of CAD (as assessed by SYNTAX score; P = 0.005), and was associated with more frequent multivessel disease (P = 0.004), multiple complex lesions (P = 0.022) and significant stenosis location on left circumflex and right coronary arteries. Moreover, FH patients had more multiple lesions, with an increased rate of bifurcation lesions or calcifications (P = 0.021 and P = 0.036, respectively). In multivariate analysis, LDL-cholesterol levels (OR 1.948; 95% CI 1.090–3.480, P = 0.024) remained an independent estimator of anatomical complexity of coronary lesions, in addition to age (OR 1.035; 95% CI 1.014–1.057, P = 0.001).ConclusionsFH patients with acute MI had more severe CAD, characterized by complex anatomical features that are mainly dependent on the LDL-cholesterol burden. Our findings reinforce the need for more aggressive preventive strategies in these high-risk patients, and for intensive lipid-lowering therapy as secondary prevention.

Highlights

Heterozygous familial hypercholesterolemia (FH) is one of the most common autosomal dominant genetic diseases [1], with an estimated prevalence of 1/250 in Western countries. It is characterized by high levels of LDL cholesterol (LDL-C) [2, 3], resulting in most cases from a mutation of the LDL receptor (LDL-R), apolipoprotein B, or proprotein convertase subtilisin/kexin type 9 (PCSK9)
familial heterozygous hypercholesterolemia (FH) patients had a higher incidence of hypertension (P = 0.002) and, as expected, a higher incidence of personal or family history of coronary artery disease (CAD) (p < 0.001)
LDL-cholesterol was high (208 [174–239] mg/dL), less than half of FH patients had a prescription for chronic statin treatment

Summary

Introduction

Heterozygous familial hypercholesterolemia (FH) is one of the most common autosomal dominant genetic diseases [1], with an estimated prevalence of 1/250 in Western countries. It is characterized by high levels of LDL cholesterol (LDL-C) [2, 3], resulting in most cases from a mutation of the LDL receptor (LDL-R), apolipoprotein B (apoB), or proprotein convertase subtilisin/kexin type 9 (PCSK9). Patients with familial heterozygous hypercholesterolemia (FH) have a high risk of early myocardial infarction (MI), the coronary artery disease (CAD) burden in FH patients with acute MI remains to be investigated

Objectives

Methods

Results

Conclusion