Genetic Predisposition to Ventricular Arrhythmias and. Sudden Death in Hypertrophic Cardiomyopathy
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1 Dott.ssa Daria Santini Dottorato di Ricerca in Medicina Sperimentale Genetic Predisposition to Ventricular Arrhythmias and Sudden Death in Hypertrophic Cardiomyopathy Background Hypertrophic cardiomyopathy (HCM) is the most common inherited form of heart disease and a leading cause of sudden death (SD) in the young. Mechanisms and substrates triggering ventricular arrhythmia are still poorly understood, and it has been speculated that specific sets of gene mutations/variants may predispose to SD. However, it is not known whether variants of genes encoding ion channels and proteins involved in cardiac remodelling may be candidate to define individual susceptibility to SD or act as riskmodifiers. Study aim Address the question whether gene variants of proteins involved in electrical homeostasis and/or myocardial remodelling can be regarded as predictors of SD or correlate with myocardial fibrosis and/or arrhythmia burden in HCM. Preliminary results Study Population In the first part of the study we provided clinical and genetic characterization of 290 patients with hypertrophic cardiomyopathy, including a subgroup of 60 recipients of an implantable defibrillator (implantable cardioverter defibrillator, ICD). Mean age was 40±19 years and the majority were men (n=190; 66%). 83 patients (29%) had obstructive HCM. Common risk factors for SD in this population were unexplained syncope (n= 32; 11%), massive LV hypertrophy (n= 34; 12%), family history of SD (n= 63; 22%), non-sustained ventricular tachycardia (n= 101; 35%) and abnormal exercise blood pressure (n= 23; 8%). Nineteen patients (22%) had end-stage disease (table 1). 1
2 Table 1. Characteristics of the study population. 24 (8%) 17 (6%) 2
3 All study patients have been assessed for gene variants of the following systems: - Natriuretic peptides o ProANP o HPaII o Scal o NPRC o BNP - Renin-angiotensin system o AGT 174 o AGT 235 o Aldesterone o AT1-receptor - Cytokines/inflammatory molecules o TNF o IGF-1 receptor o COX-2 o e-nos o CRP o Fibrinogen o TGF-beta1 o IL-6 IL-10 - Calcium handling proteins o Casq2 o Ryr2 o NCX1 o FKBP o SERCA 2 In the second part of the study project, we sought to determine whether the allelic variants of these genes have a role in the expression of certain phenotypes associated with a high risk of SD as massive hypertrophy, late Gadolinium enhancement (LGE) at MRI and endstage evolution. 3
4 Table 2. Massive LVH Massive LVH - Massive LVH + P N=266 N=24 ANP 15 (6%) 2 (8%) Hpall 10 (4%) 1 (4%) Scall 79 (30%) 8 (33%) NPRC 120 (45%) 11 (46%) BNP 173 (65%) 17 (71%) AGT (25%) 1 (4%) AGT (72%) 19 (79%) Aldosterone 195 (73%) 19 (79%) AT1 Receptor 98 (37%) 10 (42) UCP (53%) 14 (58%) UCP2-exon (54%) 12 (50%) TNF 50 (19%) 4 (17%) IGF Receptor 165 (63%) 14 (58%) IGF1 124 (47%) 3 (12%) IGF2 121 (46%) 10 (46%) COX2 113 (43%) 9 (37%) E NOS 139 (52%) 14 (58%) CRP 147 (56%) 14 (58%) Fibrinogen 124 (47%) 8 (33%) TGF-beta (69%) 17 (74%) IL6 111 (42%) 11 (46%) IL (58%) 15 (63%) CASQ2 149 (56%) 17 (71%) RYR2 intron (73%) 15 (63%) RYR2 exon 32 8 (3%) 2 (8%) Ncx1 166 (63%) 13 (54%) FKBP1-B 124 (47%) 10 (42%) SERCA2 intron (26%) 6 (25%) SERCA2 exon (7%) 3 (13%) PLN 215 (81%) 19 (79%)
5 Table 3. End-stage Evolution End stage - End stage + P N=270 N=17 ANP 16 (6%) 1 (5%) Hpall 10 (4%) 1(5%) Scall 77 (29%) 8 (42%) NPRC 117 (44%) 12 (63%) BNP 175 (65%) 13 (68%) AGT (23%) 5 (25%) AGT (71%) 16 (95%) Aldosterone 200 (75%) 13 (68%) AT1 Receptor 103 (38%) 4 (21%) UCP (54%) 10 (56%) UCP2-exon (54%) 12 (67%) TNF 49 (18%) 5 (26%) IGF Receptor 168 (63%) 9 (53%) IGF1 117 (44%) 10 (53%) IGF2 124 (47%) 5 (26%) COX2 111 (42%) 9 (47%) E NOS 140 (52%) 11 (58%) CRP 149 (56%) 11 (61%) Fibrinogen 127 (47%) 4 (22%) TGF-beta (70%) 14 (74%) IL6 114 (43%) 7 (37%) IL (58%) 12 (63%) CASQ2 151 (57%) 12 (63%) RYR2 intron (72%) 15 (79%) RYR2 exon (4%) NCX1 167 (63%) 10 (53%) FKBP1-B 123 (46%) 19 (53%) SERCA2 intron (26%) 5 (28%) SERCA2 exon (8%) PLN 215 (81%) 16 (89%)
6 Table 4. Gadolinium Enhancement LGE LGE + P N=75 N=120 ANP 3 (4%) 6 (5%) Hpall 6 (8%) 4 (3%) Scall 26 (35%) 29 (24%) NPRC 29 (39%) 53(44%) BNP 53 (71%) 72 (60%) AGT (25%) 28 (23%) AGT (69%) 86 (72%) Aldosterone 59 (79%) 84 (70%) AT1 Receptor 27 (36%) 45 (38%) UCP (56%) 68 (57%) UCP2-exon 4 42 (56%) 67 (56%) TBF 10 (13%) 23 (19%) IGF Receptor 48 (64%) 65 (63%) IGF1 33 (44%) 58 (48%) IGF2 33 (45%) 57 (48%) COX2 29 (39%) 57 (48%) E NOS 35 (47%) 68 (57%) CRP 42 (56%) 68 (57%) Fibrinogen 31 (41%) 57 (47%) TGF-beta 1 53 (74%) 77 (67%) IL6 24 (32%) 55 (46%) IL10 43 (57%) 69 (58%) CASQ2 42 (56%) 69 (58%) RYR2 intron (69%) 90 (76%) RYR2 exon 32 4 (5%) 3 (3%) NCX1 49 (65%) 77 (64%) FKBP1-B 41 (55%) 53 (44%) SERCA2 intron (24%) 35 (29%) SERCA2 exon 15 4 (5%) 9 (8%) PLN 65 (87%) 99 (83%)
7 As shown in Table 2, patients with massive left ventricular hypertrophy (n= 24, 8%) showed lower prevalence of AGT174 (p=0.022) and IGF1 gene variant (p=0.001). Moreover, 17 patients with end-stage HCM (6%) displayed lower prevalence of the fibrinogen SNP (p=0.038) (Table 3). Finally, a subgroup of patients underwent also CMR to evaluate LGE as a surrogate marker of myocardial fibrosis. Positive LGE was present in the majority of patients (n=120; 62%). Genetic analysis did not show a significant association between evaluated SNP and myocardial fibrosis. Rome, October 12 th 2014 Dott.ssa Daria Santini Dott. Pietro Francia 7
8 Pubblicazioni scientifiche : 1. Francia P, Adduci C, Santini D, Musumeci B, Tocci G. New oral anticoagulants in non-valvular atrial fibrillation. High Blood Press Cardiovasc Prev Jun;20(2): Magrì D, Agostoni P, Cauti FM, Musumeci B, Egidy Assenza G, De Cecco CN,Muscogiuri G, Maruotti A, Ricotta A, Pagannone E, Marino L, Santini D, Proietti G, Serdoz A, Paneni F, Volpe M, Autore C. Determinants of peak oxygen uptake in patients with hypertrophic cardiomyopathy: a single-center study. Intern Emerg Med Apr;9(3): Francia P, Adduci C, Semprini L, Borro M, Ricotta A, Sensini I, Santini D, Caprinozzi M, Balla C, Simmaco M, Volpe M. Osteopontin and galectin-3 predict the risk of ventricular tachycardia and fibrillation in heart failure patients with implantable defibrillators. J Cardiovasc Electrophysiol Jun;25(6): Francia P, Santini D, Musumeci B, Semprini L, Adduci C, Pagannone E, Proietti G, Volpe M, Autore C. Clinical Impact of Nonsustained Ventricular Tachycardia Recorded by the Implantable Cardioverter-Defibrillator in Patients with Hypertrophic Cardiomyopathy. J Cardiovasc Electrophysiol Jul 28 8
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