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2. Overview of the current status of familial hypercholesterolaemia care in over 60 countries - The EAS Familial Hypercholesterolaemia Studies Collaboration (FHSC)

Author

Vallejo-Vaz, Antonio J., Marco, Martina De, Stevens, Christophe A. T., Akram, Asif, Freiberger, Tomas, Hovingh, G. Kees, Kastelein, John J. P., Mata, Pedro, Raal, Frederick J., Santos, Raul D., Soran, Handrean, Watts, Gerald F., Abifadel, Marianne, Aguilar-Salinas, Carlos A., Al-Khnifsawi, Mutaz, Alkindi, Fahad A., Alnouri, Fahad, Alonso, Rodrigo, Al-Rasadi, Khalid, Al-Sarraf, Ahmad, Ashavaid, Tester F., Binder, Christoph J., Bogsrud, Martin P., Bourbon, Mafalda, Bruckert, Eric, Chlebus, Krzysztof, Corral, Pablo, Descamps, Olivier, Durst, Ronen, Ezhov, Marat, Fras, Zlatko, Genest, Jacques, Groselj, Urh, Harada-Shiba, Mariko, Kayikcioglu, Meral, Lalic, Katarina, Lam, Carolyn S. P., Latkovskis, Gustavs, Laufs, Ulrich, Liberopoulos, Evangelos, Lin, Jie, Maher, Vincent, Majano, Nelson, Marais, A. David, März, Winfried, Mirrakhimov, Erkin, Miserez, André R., Mitchenko, Olena, Nawawi, Hapizah M., Nordestgaard, B. rge G., Paragh, György, Petrulioniene, Zaneta, Pojskic, Belma, Postadzhiyan, Arman, Reda, Ashraf, Reiner, Željko, Sadoh, Wilson E., Sahebkar, Amirhossein, Shehab, Abdullah, Shek, Aleksander B., Stoll, Mario, Su, Ta-Chen, Subramaniam, Tavintharan, Susekov, Andrey V., Symeonides, Phivos, Tilney, Myra, Tomlinson, Brian, Truong, Thanh-Huong, Tselepis, Alexandros D., Tybjærg-Hansen, Anne, Vázquez-Cárdenas, Alejandra, Viigimaa, Margus, Vohnout, Branislav, Widén, Elisabeth, Yamashita, Shizuya, Banach, Maciej, Gaita, Dan, Jiang, Lixin, Nilsson, Lennart, Santos, Lourdes E., Schunkert, Heribert, Tokgözoğlu, Lale, Car, Josip, Catapano, Alberico L., Ray, Kausik K., Schreier, Laura, Pang, Jing, Dieplinger, Hans, Hanauer-Mader, Gabriele, Desutter, Johan, Langlois, Michel, Mertens, Ann, Rietzschel, Ernst, Wallemacq, Caroline, Isakovic, Dzenana, Dzankovic, Amra M., Obralija, Jasna, Pojskic, Lamija, Sisic, Ibrahim, Stimjanin, Ena, Torlak, Vildana A., Jannes, Cinthia E., Krieger, Jose E., Pereira, Alexandre C., Ruel, Isabelle, Asenjo, Sylvia, Cuevas, Ada, Pećin, Ivan, Miltiadous, George, Panayiotou, Andrie G., Vrablik, Michal, Benn, Marianne, Heinsar, Silver, Béliard, S., Gouni-Berthold, Ioanna, Hengstenberg, Wibke, Julius, Ulrich, Kassner, Ursula, Klose, Gerald, König, Christel, König, Wolfgang, Otte, Britta, Parhofer, Klaus, Schatz, Ulrike, Schmidt, Nina, Steinhagen-Thiessen, Elisabeth, Vogt, Anja, Antza, Christina, Athyros, Vasilios, Bilianou, Eleni, Boufidou, Amalia, Chrousos, George, Elisaf, Moses, Garoufi, Anastasia, Katsiki, Niki, Kolovou, Genovefa, Kotsis, Vasilios, Rallidis, Loukianos, Rizos, Christos, Skalidis, Emmanouel, Skoumas, Ioannis, Tziomalos, Kostantinos, Shawney, J. P. S., Abbaszadegan, Mohammad R., Aminzadeh, Majid, Hosseini, Sousan, Mobini, Moein, Vakili, Rahim, Zaeri, Hossein, Agar, Ruth, Boran, Gerard, Colwell, Nial, Crowley, Vivion, Durkin, Maeve, Griffin, Damian, Kelly, Michael, Rakovac-Tisdall, Ana, Bitzur, Rafael, Cohen, Hofit, Eliav, Osnat, Ellis, Avishay, Gavish, Dov, Harats, Dror, Henkin, Yaacov, Knobler, Hila, Leavit, Leah, Leitersdorf, Eran, Rubinstein, Ardon, Schurr, Daniel, Shpitzen, Shoshi, Szalat, Auryan, Arca, Marcello, Averna, Maurizio, Bertolini, Stefano, Calandra, Sebastiano, Tarugi, Patrizia, Erglis, Andrejs, Gilis, Dainus, Nesterovics, Georgijs, Saripo, Vita, Upena-Roze, Arta, Elbitar, Sandy, Jambart, S. lim, Khoury, Petra El, Gargalskaite, Urte, Kutkiene, Sandra, Al-Khateeb, Alyaa, An, Chua Y., Ismail, Zaliha, Kasim, Sazzli, Ibrahim, Khairul S., Radzi, Ahmad B. M., Kasim, Noor A., Nor, Noor S. M., Ramli, Anis S., Razak, Suraya A., Muid, Suhaila, Rosman, Azhari, Sanusi, Abd R., Razman, Aimi Z., Nazli, Sukma A., Kek, Teh L., Azzopardi, Conrad, Aguilar Salinas, Carlos A., Vázquez-Cárdenas, N. Alejandra, Galán, Gabriela, Magaña-Torres, M. T., Martagon, Alexandro, Mehta, Roopa, Wittekoek, M. E., Isara, Alphonsus R., Obaseki, Darlington E., Ohenhen, Oluwatoyin A., Holven, Kirsten B., Gruchała, Marcin, Baranowska, Marlena, Borowiec-Wolny, Justyna, Gilis-Malinowska, Natasza, Michalska-Grzonkowska, Aleksandra, Pajkowski, Marcin, Parczewska, Aleksandra, Romanowska-Kocejko, Marzena, Stróżyk, Aneta, Żarczyńska-Buchowiecka, Marta, Kleinschmidt, Mariola, Alves, Ana C., Medeiros, Ana M., Ershova, Alexandra, Korneva, Victoria, Kuznetsova, Tatiana, Malyshev, Pavel, Meshkov, Alexey, Rozhkova, Tatiana, Rajkovic, Natasa, Popovic, Ljiljana, Lukac, Sandra S., Stosic, Ljubica, Rasulic, Iva, Lalic, Nebojsa M., Chua, Terrance S. J., Ting, Sharon P. L., Raslova, Katarina, Battelino, Tadej, Cevc, Matija, Jug, Borut, Kovac, Jernej, Podkrajsek, Katarina T., Sustar, Ursa, Trontelj, Katja J., Marais, David, Isla, Leopoldo Perez de, Martin, François J., Charng, Ming-Ji, Chen, Pei-Lung, Kayikçioglu, Meral, Dell’oca, Nicolás, Fernández, Graciela, Ressia, Andrés, Reyes, Ximena, Zelarayan, Mario, Alieva, Rano B., Hoshimov, Shavkat U., Kurbanov, Ravshanbek D., Nizamov, Ulugbek I., Lima-Martínez, Marcos M., Nguyen, Mai-Ngoc Thi, Do, Doan-Loi, Kim, Ngoc-Thanh, le, Hong-An, le, Thanh-Tung, Centre of Excellence in Complex Disease Genetics, Elisabeth Ingrid Maria Widen / Principal Investigator, Institute for Molecular Medicine Finland, University of Helsinki, Genomic Discoveries and Clinical Translation, Kardiyoloji, Lee Kong Chian School of Medicine (LKCMedicine), Pfizer Incorporated, European Atherosclerosis Society, ACS - Atherosclerosis & ischemic syndromes, Vascular Medicine, ACS - Pulmonary hypertension & thrombosis, and Ege Üniversitesi

Subjects
International Cooperation, MÉTODOS EPIDEMIOLÓGICOS, 030204 cardiovascular system & hematology, Nationwide survey, Global Health, Health Services Accessibility, Doenças Cardio e Cérebro-vasculares, MOLECULAR-GENETICS, 0302 clinical medicine, Risk Factors, Prevalence, CARDIOVASCULAR RISK-FACTORS, 030212 general & internal medicine, Cooperative Behavior, DEFECTIVE APOLIPOPROTEIN B-100, GENERAL-POPULATION, education.field_of_study, medicine.diagnostic_test, Anticholesteremic Agents, Familial hypercholesterolaemia, FHSC, Primary dyslipidaemia, Biomarkers, Cholesterol, LDL, Genetic Predisposition to Disease, Health Care Surveys, Healthcare Disparities, Humans, Hyperlipoproteinemia Type II, Phenotype, Predictive Value of Tests, Treatment Outcome, Blood Component Removal, EAS Familial Hypercholesterolaemia Studies Collaboration, 3. Good health, PREVALENCE, Cholesterol, CORONARY-ARTERY-DISEASE, NATIONWIDE SURVEY, Cardiology and Cardiovascular Medicine, medicine.medical_specialty, Cardiovascular risk factors, Population, LDL-RECEPTOR, 1102 Cardiovascular Medicine And Haematology, LDL, 03 medical and health sciences, medicine, Medicine [Science], fhsc, familial hypercholesterolaemia, primary dyslipidaemia, education, Genetic testing, Government, Public health, EAS Familial Hypercholesterolaemia Studies Collaboration (FHSC) Investigators, SAFEHEART REGISTRY, 1103 Clinical Sciences, Cardiovascular System & Hematology, Family medicine, 3121 General medicine, internal medicine and other clinical medicine, Cardiovascular System & Cardiology, Business, FOLLOW-UP
Abstract

PubMed: 30270054, 2-s2.0-85053666909, Background and aims: Management of familial hypercholesterolaemia (FH) may vary across different settings due to factors related to population characteristics, practice, resources and/or policies. We conducted a survey among the worldwide network of EAS FHSC Lead Investigators to provide an overview of FH status in different countries. Methods: Lead Investigators from countries formally involved in the EAS FHSC by mid-May 2018 were invited to provide a brief report on FH status in their countries, including available information, programmes, initiatives, and management. Results: 63 countries provided reports. Data on FH prevalence are lacking in most countries. Where available, data tend to align with recent estimates, suggesting a higher frequency than that traditionally considered. Low rates of FH detection are reported across all regions. National registries and education programmes to improve FH awareness/knowledge are a recognised priority, but funding is often lacking. In most countries, diagnosis primarily relies on the Dutch Lipid Clinics Network criteria. Although available in many countries, genetic testing is not widely implemented (frequent cost issues). There are only a few national official government programmes for FH. Under-treatment is an issue. FH therapy is not universally reimbursed. PCSK9-inhibitors are available in ?2/3 countries. Lipoprotein-apheresis is offered in ?60% countries, although access is limited. Conclusions: FH is a recognised public health concern. Management varies widely across countries, with overall suboptimal identification and under-treatment. Efforts and initiatives to improve FH knowledge and management are underway, including development of national registries, but support, particularly from health authorities, and better funding are greatly needed. © 2018 Elsevier B.V., Universidade de São Paulo, USP European Atherosclerosis Society, EAS Amgen Merck Sharp and Dohme, MSD, The ELSA Study suggests heterozygous FH (HeFH) may affect 1:263 Brazilians (?766,000 individuals). Currently, the only active genetic cascade screening program in Brazil is Hipercol Brasil in Sao Paulo (genetic testing for adults with low-density lipoprotein cholesterol (LDL-C) ?230?mg/dL, to maximise cost-effectiveness), with 1719 heterozygotes, 25 homozygotes, 13 compound-heterozygotes and one double-heterozygote identified by March 2018. To date, 4340 individuals from 440 families were screened. Genetic testing is funded by a government tax reduction programme (PROADI-SUS), and cascade screening by partnering between Samaritano Hospital and Heart Institute (InCor) University of Sao Paulo. Most FH patients are under non-specialist care and currently under-treated., Prevalence is unknown but assumed at 1:250. There is no state programme and few patients were diagnosed before the Latvian FH Registry was established in 2015. To date, the Registry has identified 181 cases (2.3% of 7876 estimated HeFH cases; no HoFH). Cascade screening is performed in first-degree relatives of index cases with probable/definite FH. Genetic testing is not reimbursed but has been funded by research grants for a few patients/relatives. About 5% of patients had LDL-C at target before inclusion in the Registry [ 61 ]. Statins are reimbursed 50% in primary prevention; statins and ezetimibe, 75–100% in secondary prevention; PCSK9i are available, but not reimbursed., Estimated prevalence is 1:250 (based on a meta-analysis of 6 observational studies) or 136,300 adults (only 2% diagnosed) [ 69 , 70 ]. Based on LIPIDOGRAM studies (2004–2015, ?50,000 participants), prevalence might be?1:200 [ 71 , 72 ]. Five HoFH cases are described [ 73 , 74 ]. Patients with DLCN ?3 are referred for genetic testing, funded by the National Health Program. The National Centre for FH at University Clinical Hospital, Medical University of Gdansk, was established in 2017, financed by the Ministry of Health. From August 2017, 345 patients underwent genetic testing (153 positive, including 46 relatives; 1 HoFH). Since 1999, 1884 patients (562 families) have undergone genetic testing and cascade diagnosis (data from the National Polish FH Registry, Medical University of Gdansk, established in 2000). PCSK9i are not reimbursed (under discussion with the Ministry of Health)., The EAS FHSC project has received support from a Pfizer Independent Grant for Learning & Change 2014 (No: 16157823 ) and from investigator-initiated unrestricted research grants to the European Atherosclerosis Society from Amgen , MSD , and Sanofi-Aventis .

Published
2018

9. Comparative analysis of the predictive power of different endothelial progenitor cell phenotypes on cardiovascular outcome.

Author

Schwartzenberg S, Afek A, Charach G, Rubinstein A, Ben-Shoshan Y, Kissil S, Maisel-Auslender S, Keren G, and George J

Abstract

Aim: To compare the predictive power of different endothelial progenitor cell (EPC) phenotypic markers for future cardiovascular events., Methods: Peripheral blood was collected from 76 consecutive patients with acute coronary syndromes (ACS) who underwent percutaneous coronary intervention in our institute. The various EPC phenotypes of peripheral blood mononuclear cells were CD34+CD133+, CD34+KDR+, and CD 133+KDR+. The outcome endpoint included cardiovascular mortality, recurrent ACS, and hospitalization for decompensated heart failure during a 24-mo follow-up period., Results: CD34+CD133+ cells (P = 0.034), but not CD34+KDR+ (P = 0.35) or CD 133+KDR+ cells (P = 0.19), were found to predict recurrent ACS. We found no correlation between EPCs measured by any of the three phenotypic combinations of accepted CD markers and the total combination of these separate outcomes., Conclusion: The EPC CD34+CD133+ phenotype, but not the CD34+KDR+ or the CD 133+KDR+ phenotypes, is predictive of future adverse cardiovascular outcomes.

Published
2010
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10. Usefulness of serum myeloperoxidase in prediction of mortality in patients with severe heart failure.

Author

Michowitz Y, Kisil S, Guzner-Gur H, Rubinstein A, Wexler D, Sheps D, Keren G, and George J

Subjects
Aged, C-Reactive Protein metabolism, Female, Heart Failure classification, Humans, Male, Natriuretic Peptide, Brain blood, Oxidative Stress, Peptide Fragments blood, Predictive Value of Tests, Proportional Hazards Models, Severity of Illness Index, Surveys and Questionnaires, Heart Failure blood, Heart Failure mortality, Peroxidase blood
Abstract

Background: Myeloperoxidase levels were shown to reflect endothelial dysfunction, inflammation, atherosclerosis and oxidative stress., Objectives: To examine the role of circulating myeloperoxidase, a leukocyte-derived enzyme, as a predictor of mortality in patients with congestive heart failure., Methods: Baseline serum MPO levels were measured in 285 consecutive CHF patients and 35 healthy volunteers. N-terminal pro-brain natriuretic peptide and high sensitivity C-reactive protein concentrations were also measured. The primary outcome endpoint was overall mortality., Results: MPO levels were significantly elevated in patients with CHF compared to healthy volunteers (P = 0.01). During a mean follow-up of 40.9 +/- 11.3 months there were 106 deaths. On a univariate Cox regression analysis MPO levels were of marginal value (P = 0.07) whereas NT-proBNP was of considerable value (P < 0.0001) in predicting all-cause mortality. By dividing our cohort according to NT-proBNP levels into high, intermediate and low risk groups a clear difference in mortality was shown. By further dividing the patient cohort according to MPO levels above or below the median (122.5 ng/ml), mortality prediction improved in the patients with intermediate NT-proBNP values., Conclusions: MPO levels are elevated in CHF and correlate with disease severity. MPO has an additive predictive value on mortality in patients with intermediate NT-proBNP levels.

Published
2008

11. The association of endothelial dysfunction and cardiovascular events in healthy subjects and patients with cardiovascular disease.

Author

Shechter M, Marai I, Marai S, Sherer Y, Sela BA, Feinberg MS, Rubinstein A, and Shoenfeld Y

Subjects
Adolescent, Adult, Aged, Aged, 80 and over, Brachial Artery diagnostic imaging, Brachial Artery drug effects, Cardiovascular Diseases diagnostic imaging, Echocardiography, Electrocardiography, Endothelium, Vascular diagnostic imaging, Endothelium, Vascular drug effects, Female, Follow-Up Studies, Humans, Male, Middle Aged, Nitroglycerin, Prognosis, Prospective Studies, Risk Factors, Time Factors, Ultrasonography, Doppler, Pulsed, Vasodilation drug effects, Vasodilator Agents, Brachial Artery physiology, Cardiovascular Diseases physiopathology, Endothelium, Vascular physiology, Vasodilation physiology
Abstract

Background: Endothelial dysfunction is recognized as a major factor in the development of atherosclerosis and it has a prognostic value., Objectives: To detect the long-term association of peripheral vascular endothelial function and clinical outcome in healthy subjects and patients with cardiovascular disease., Methods: We prospectively assessed brachial artery flow-mediated dilatation in 110 consecutive subjects (46 CVD patients and 64 healthy controls), mean age 57 +/- 11 years; 68 were men. After an overnight fast and discontinuation of all medications for > or = 12 hours, percent improvement in FMD and nitroglycerin-mediated vasodilatation were assessed using high resolution ultrasound., Results: %FMD but not %NTG was significantly lower in CVD patients (9.5 +/- 8.0% vs. 13.5 +/- 8.0%, P = 0.012) compared to healthy controls (13.4 +/- 8.0% vs. 16.7 +/- 11.0%, P = 0.084; respectively). In addition, an inverse correlation between %FMD and the number of traditional CVD risk factors was found among all study participants (r = -0.23, P = 0.015) and healthy controls (r = -0.23, P = 0.036). In a mean follow-up of 15 +/- 2 months, the composite CVD endpoints (all-cause mortality, myocardial infarction, hospitalization for heart failure or angina pectoris, stroke, coronary artery bypass grafting and percutaneous coronary interventions) were significantly more common in subjects with FMD < 6% compared to subjects with FMD > 6% (33.3% vs. 12.1%, P < 0.03, respectively)., Conclusions: Thus, brachial artery %FMD provides important prognostic information in addition to that derived from traditional risk factor assessment.

Published
2007

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