P1507Substantial cardiovascular risks in heterozygous familial hypercholesterolemia patients with acute myocardial infraction who exhibited multi-vessel disease

Abstract

Background: Heterozygous Familial hypercholesterolemia (HeFH) is associated with a marked elevation of low-density lipoprotein cholesterol (LDL-C) level and premature coronary artery disease including acute myocardial infarction (AMI). While HeFH subjects have been shown to harbor extensive atherosclerosis, clinical and angiographic characteristics and cardiovascular outcomes in HeFH patients with AMI has not been fully characterized yet. Purpose: The current study sought to elucidate clinical presentation, angiographical characteristics and cardiovascular outcomes in HeFH subjects with AMI. Methods: Between 2007 and 2014, 958 consecutive patients with De novo AMI receiving percutaneous coronary intervention were analyzed. HeFH was diagnosed according to Dutch Lipid Clinic Network criteria. The occurrence of cardiovascular events (cardiac death, acute coronary syndrome and revascularization) was evaluated during the observational period Results: The prevalence of definite/ probable and possible HeFH was 1.7% (16/958) and 7.3% (70/958), respectively. HeFH patients with AMI were more likely to be younger (53±11 vs. 70±12 years, p<0.001), and less likely to have a history of hypertension (52.0% vs. 69.0%, p=0.004) and type 2 diabetes mellitus (23% vs. 34%, p=0.04). Severer myocardial damage (peak CPK level: 4063±3481 vs. 2914±3153U/l, p=0.002) and a higher frequency of culprit lesion at the proximal segment of left anterior descending artery (34.0% vs. 25.0%) were observed in HeFH subjects although the latter comparison did not meet statistical significance (p=0.09). Furthermore, the presence of multi-vessel coronary artery disease and chronic total occlusion of non-culprit vessel was observed in 50.0% and 24.0% of HeFH cases, respectively. Of note, HeFH subjects with multi-vessel disease were more likely to exhibit higher Killip class compared to those with single vessel disease (Killip class ≥2: 21.0% vs. 5.0%, p=0.04). Following the commencement of a statin, HeFH subjects with multi-vessel coronary artery disease achieved a significantly lower level of LDL-C (2.4±0.6 vs. 2.7±0.6 mmol/l, p=0.04). However, during the 4-year observational period, the occurrence of cardiovascular events was still substantially higher in HeFH patients with multi-vessel coronary artery disease (23.0% vs. 5.0%, p=0.02). (Figure). Conclusions: HeFH was associated with severer presentation of AMI reflected by a larger size of myocardial infraction and a higher Killip class especially in those with multi-vessel disease. Despite favourable control of LDL-C with a statin in HeFH patients with AMI and multi-vessel disease, their cardiovascular events continued to considerably occur. Our findings indicate HeFH patients with AMI and multi-vessel disease as a high-risk category who potentially require further intensification of lipid lowering therapy.