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• W3123868278 abstract "Familial hypercholesterolaemia (FH) is an inherited disease caused by a mutation in the low density lipoprotein (LDL) receptor gene.1Schmidt E.B. Hedegaard B.S. Retterstøl K. Familial hypercholesterolaemia: history, diagnosis, screening, management and challenges.Heart. 2020; 106: 1940-1946Crossref PubMed Scopus (2) Google Scholar FH leads to high levels of plasma LDL cholesterol (LDL-C) from birth and increased risk of early atherosclerosis and premature cardiovascular disease (CVD).1Schmidt E.B. Hedegaard B.S. Retterstøl K. Familial hypercholesterolaemia: history, diagnosis, screening, management and challenges.Heart. 2020; 106: 1940-1946Crossref PubMed Scopus (2) Google Scholar The prevalence of heterozygous FH is about 1:250 persons in Norway.1Schmidt E.B. Hedegaard B.S. Retterstøl K. Familial hypercholesterolaemia: history, diagnosis, screening, management and challenges.Heart. 2020; 106: 1940-1946Crossref PubMed Scopus (2) Google Scholar It has been shown previously that 15% of deceased FH patients had an aortic aneurysm (AA) at the time of death, in whom no sex differences were found.2Krogh H.W. Mundal L. Holven K.B. Retterstol K. Patients with familial hypercholesterolaemia are characterized by presence of cardiovascular disease at the time of death.Eur Heart J. 2015; 37: 1398-1405Crossref PubMed Scopus (54) Google Scholar The mean age of death was 60 years, and mean age of first CVD event was 44 years in FH patients.2Krogh H.W. Mundal L. Holven K.B. Retterstol K. Patients with familial hypercholesterolaemia are characterized by presence of cardiovascular disease at the time of death.Eur Heart J. 2015; 37: 1398-1405Crossref PubMed Scopus (54) Google Scholar At the time of death, 93% of the FH patients had established CVD.2Krogh H.W. Mundal L. Holven K.B. Retterstol K. Patients with familial hypercholesterolaemia are characterized by presence of cardiovascular disease at the time of death.Eur Heart J. 2015; 37: 1398-1405Crossref PubMed Scopus (54) Google Scholar The primary aim of this study was to compare the incidence of hospitalisation for aortic pathology (AP) in patients with a genetically verified FH mutation with the incidence in the Norwegian population of about five million people, adjusted for age, sex, and calendar years. This study was approved by the Regional Committee of Medical and Health Research Ethics Southeastern Norway (reference 2011/1343 REK). The study design and methods have been described previously.3Mundal L.J. Igland J. Veierød M.B. Holven K.B. Ose L. Selmer R.M. et al.Impact of age on excess risk of coronary heart disease in patients with familial hypercholesterolaemia.Heart. 2018; 104: 1600-1607Crossref PubMed Scopus (28) Google Scholar Briefly, this is a registry based prospective cohort study including 4 489 persons ≥ 25 years of age with genetically verified FH during 1992–2009. AP was defined according to the International Classification of Diseases, version 9 (ICD9: 441) or version 10 (ICD10: I71.0 – I71.9). Data on all hospitalisations due to AP were obtained from the Cardiovascular Disease in Norway Project (CVDNOR; https://cvdnor.w.uib.no) and on death (date and cause) were obtained from the Norwegian Cause of Death Registry. Data on hospitalisations were obtained for the period 1994–2009, but in order to make sure that the study population was free of AP at the start of follow-up we used 1994–2000 as a washout period to search for previous events and estimated incidence rates and standardised incidence ratios (SIRs) for the period 2001–2009. Patients with AP or death before 2001 were excluded. After exclusion, the cohort contained 3 174 persons who were followed from 1 January 2001 or time of FH diagnosis (if FH diagnosis after 1 January 2001) until first hospitalisation with AP as primary or secondary diagnosis, death from other causes, or 31 December 2009, whichever occurred first. SIRs were calculated for AP as the ratio of observed to expected number of cases using indirect standardisation with incidence rates for the total Norwegian population in one year age groups (obtained from the CVDNOR project) as reference rates. A total of 17 FH patients were hospitalised due to AP (Table 1). Data on the specific diagnostic codes in the FH patients and number of incident cases by sex are given in Table 1. Most of the FH patients (82.4%) were hospitalised due to abdominal aortic aneurysm (AAA); ICD-10 codes: I71.3 and I71.4. Risk of AP was 3.8 fold higher in FH men 50–69 years of age (SIR 3.8, 95% CI 2.1–6.9) and 1.9 fold higher in FH men 70+ years of age (SIR 1.9, 95% CI 2.1–6.9) than the general population. No significantly increased risk of AP was found in FH women.Table 1Incidence rates and standardised incidence ratios for aortic pathology during 2001–2009 among 3 174 persons with familial hypercholesterolaemia in NorwaySex and age group – yIncident cases – nPerson years in 1 000Crude incidence rate per 1 000 person years (95% CI)Expected number of casesSIR (95% CI)Women 25–4906.000.1– 50–6923.30.6 (0.2–2.4)0.92.3 (0.6–9.2) ≥7010.61.6 (0.2–11.1)1.01.0 (0.1–6.9) Total3∗The specific ICD-10 diagnostic code and number of individuals (n): I71.4 (2), I71.6 (1).9.90.3 (0.1–0.9)2.01.5 (0.5–4.6)Men 25–4905.500.4– 50–69112.74.1 (2.3–7.4)2.93.8 (2.1–6.9) ≥7030.39.0 (2.9–27.8)1.51.9 (2.1–6.9) Total14†The specific ICD-10 diagnostic code and number of individuals (n): I71.2 (1), I71.3 (2), I71.4 (10), I71.9 (1).8.61.6 (1.0–2.8)4.82.9 (1.7–5.0)CI = confidence interval; ICD = International Classification of Diseases; SIR = standardised incidence rate.∗ The specific ICD-10 diagnostic code and number of individuals (n): I71.4 (2), I71.6 (1).† The specific ICD-10 diagnostic code and number of individuals (n): I71.2 (1), I71.3 (2), I71.4 (10), I71.9 (1). Open table in a new tab CI = confidence interval; ICD = International Classification of Diseases; SIR = standardised incidence rate. Risk factors including smoking status, diabetes, and hypertension were not available for this cohort. However, it has previously been shown in a subgroup of deceased FH patients that 61% were previous or active smokers, and 37% were active smokers at time of death.2Krogh H.W. Mundal L. Holven K.B. Retterstol K. Patients with familial hypercholesterolaemia are characterized by presence of cardiovascular disease at the time of death.Eur Heart J. 2015; 37: 1398-1405Crossref PubMed Scopus (54) Google Scholar When divided into age groups with a cut off of 60 years, 55% of the younger patients (< 60 years) and 10% of the older patients (> 60 years) were active smokers at time of death.2Krogh H.W. Mundal L. Holven K.B. Retterstol K. Patients with familial hypercholesterolaemia are characterized by presence of cardiovascular disease at the time of death.Eur Heart J. 2015; 37: 1398-1405Crossref PubMed Scopus (54) Google Scholar Most FH patients are on statins.1Schmidt E.B. Hedegaard B.S. Retterstøl K. Familial hypercholesterolaemia: history, diagnosis, screening, management and challenges.Heart. 2020; 106: 1940-1946Crossref PubMed Scopus (2) Google Scholar Lipid lowering therapy and LDL-C levels were not available in this study, but it has been shown previously that among deceased FH patients, 91% were on statins or statin combination treatment.2Krogh H.W. Mundal L. Holven K.B. Retterstol K. Patients with familial hypercholesterolaemia are characterized by presence of cardiovascular disease at the time of death.Eur Heart J. 2015; 37: 1398-1405Crossref PubMed Scopus (54) Google Scholar The mean duration of statin treatment was eight years.2Krogh H.W. Mundal L. Holven K.B. Retterstol K. Patients with familial hypercholesterolaemia are characterized by presence of cardiovascular disease at the time of death.Eur Heart J. 2015; 37: 1398-1405Crossref PubMed Scopus (54) Google Scholar The last registered mean LDL-C prior to death was 5.0 ± 1.8 mmol/L,2Krogh H.W. Mundal L. Holven K.B. Retterstol K. Patients with familial hypercholesterolaemia are characterized by presence of cardiovascular disease at the time of death.Eur Heart J. 2015; 37: 1398-1405Crossref PubMed Scopus (54) Google Scholar far above recommended LDL-C treatment levels. A recent systematic review and meta-analysis showed the beneficial effect of statins on total mortality in AAA repair.4Risum Ø Sandven I. Sundhagen J.O. Abdelnoor M. Effect of statins on total mortality in abdominal aortic aneurysm repair: a systematic review and meta-analysis.Eur J Vasc Endovasc Surg. 2020; https://doi.org/10.1016/j.ejvs.2020.08.007Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar A 35% relative mortality risk reduction in AAA patients on statin therapy compared with non-users suggests that statin therapy should be included in the guidelines.4Risum Ø Sandven I. Sundhagen J.O. Abdelnoor M. Effect of statins on total mortality in abdominal aortic aneurysm repair: a systematic review and meta-analysis.Eur J Vasc Endovasc Surg. 2020; https://doi.org/10.1016/j.ejvs.2020.08.007Abstract Full Text Full Text PDF PubMed Scopus (8) Google Scholar In conclusion, there was a 3.8 fold increased risk of hospitalisation due to AP in FH men 50–69 years of age, and a 1.9 fold increased risk in FH men 70+ years. No significant differences were found in FH women. These results indicate that a high cholesterol burden from birth may be important in the development of early AP. The present study emphasises the severity of FH, and the urgent need for awareness among clinicians, and vascular surgeons in particular, to optimise the earliest possible detection of AP and treatment of these patients. Larger studies with separate analyses of potential relationships between FH and thoracic and abdominal AA are warranted. None." @default.
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• W3123868278 title "Excess Aortic Pathology Risk in Patients with Genetically Verified Familial Hypercholesterolaemia: A Prospective Norwegian Registry Study" @default.
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