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655 results on '"Priori, SG"'

1. A common polymorphism associated with antibiotic-induced cardiac arrhythmia.

Author

Sesti, F, Abbott, GW, Wei, J, Murray, KT, Saksena, S, Schwartz, PJ, Priori, SG, Roden, DM, George, AL, and Goldstein, SA

Subjects
CHO Cells, Animals, Humans, Long QT Syndrome, Sulfamethoxazole, Potassium Channels, Potassium Channels, Voltage-Gated, DNA Primers, Mutagenesis, Amino Acid Sequence, Base Sequence, Mutation, Missense, Polymorphism, Single Nucleotide, Molecular Sequence Data, Middle Aged, Female, Cricetinae, Male, MIRP1, LQTS, SNP, Bactrim, sulfamethoxazole, Voltage-Gated, Mutation, Missense, Polymorphism, Single Nucleotide, Heart Disease, Cardiovascular, Clinical Research, Genetics, Prevention, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals
Abstract

Drug-induced long QT syndrome (LQTS) is a prevalent disorder of uncertain etiology that predisposes to sudden death. KCNE2 encodes MinK-related peptide 1 (MiRP1), a subunit of the cardiac potassium channel I(Kr) that has been associated previously with inherited LQTS. Here, we examine KCNE2 in 98 patients with drug-induced LQTS, identifying three individuals with sporadic mutations and a patient with sulfamethoxazole-associated LQTS who carried a single-nucleotide polymorphism (SNP) found in approximately 1.6% of the general population. While mutant channels showed diminished potassium flux at baseline and wild-type drug sensitivity, channels with the SNP were normal at baseline but inhibited by sulfamethoxazole at therapeutic levels that did not affect wild-type channels. We conclude that allelic variants of MiRP1 contribute to a significant fraction of cases of drug-induced LQTS through multiple mechanisms and that common sequence variations that increase the risk of life-threatening drug reactions can be clinically silent before drug exposure.

Published
2000

3. Enhancing rare variant interpretation in inherited arrhythmias through quantitative analysis of consortium disease cohorts and population controls

Author

Walsh R, Lahrouchi N, Tadros R, Kyndt F, Glinge C, Postema PG, Amin AS, Nannenberg EA, Ware JS, Whiffin N, Mazzarotto F, Škoric-Milosavljevic D, Krijger C, Arbelo E, Babuty D, Barajas-Martinez H, Beckmann BM, Bézieau S, Bos JM, Breckpot J, Campuzano O, Castelletti S, Celen C, Clauss S, Corveleyn A, Crotti L, Dagradi F, de Asmundis C, Denjoy I, Dittmann S, Ellinor PT, Ortuño CG, Giustetto C, Gourraud JB, Hazeki D, Horie M, Ishikawa T, Itoh H, Kaneko Y, Kanters JK, Kimoto H, Kotta MC, Krapels IPC, Kurabayashi M, Lazarte J, Leenhardt A, Loeys BL, Lundin C, Makiyama T, Mansourati J, Martins RP, Mazzanti A, Mörner S, Napolitano C, Ohkubo K, Papadakis M, Rudic B, Molina MS, Sacher F, Sahin H, Sarquella-Brugada G, Sebastiano R, Sharma S, Sheppard MN, Shimamoto K, Shoemaker MB, Stallmeyer B, Steinfurt J, Tanaka Y, Tester DJ, Usuda K, van der Zwaag PA, Van Dooren S, Van Laer L, Winbo A, Winkel BG, Yamagata K, Zumhagen S, Volders PGA, Lubitz SA, Antzelevitch C, Platonov PG, Odening KE, Roden DM, Roberts JD, Skinner JR, Tfelt-Hansen J, van den Berg MP, Olesen MS, Lambiase PD, Borggrefe M, Hayashi K, Rydberg A, Nakajima T, Yoshinaga M, Saenen JB, Kääb S, Brugada P, Robyns T, Giachino DF, Ackerman MJ, Brugada R, Brugada-Terradellas J, Gimeno JR, Hasdemir C, Guicheney P, Priori SG, Schulze-Bahr E, Makita N, Schwartz PJ, Shimizu W, Aiba T, Schott JJ, Redon R, Ohno S, Probst V, Behr ER, Barc J, Bezzina CR, and Nantes Referral Center for inherited cardiac arrhythmia

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, LQTS, variant interpretation, cardiovascular diseases, Brugada, ACMG/AMP guidelines
Abstract

PURPOSE: Stringent variant interpretation guidelines can lead to high rates of variants of uncertain significance (VUS) for genetically heterogeneous disease like long QT syndrome (LQTS) and Brugada syndrome (BrS). Quantitative and disease-specific customization of American College of Medical Genetics and Genomics/Association for Molecular Pathology (ACMG/AMP) guidelines can address this false negative rate. METHODS: We compared rare variant frequencies from 1847 LQTS (KCNQ1/KCNH2/SCN5A) and 3335 BrS (SCN5A) cases from the International LQTS/BrS Genetics Consortia to population-specific gnomAD data and developed disease-specific criteria for ACMG/AMP evidence classes-rarity (PM2/BS1 rules) and case enrichment of individual (PS4) and domain-specific (PM1) variants. RESULTS: Rare SCN5A variant prevalence differed between European (20.8%) and Japanese (8.9%) BrS patients (p = 5.7 × 10(-18)) and diagnosis with spontaneous (28.7%) versus induced (15.8%) Brugada type 1 electrocardiogram (ECG) (p = 1.3 × 10(-13)). Ion channel transmembrane regions and specific N-terminus (KCNH2) and C-terminus (KCNQ1/KCNH2) domains were characterized by high enrichment of case variants and >95% probability of pathogenicity. Applying the customized rules, 17.4% of European BrS and 74.8% of European LQTS cases had (likely) pathogenic variants, compared with estimated diagnostic yields (case excess over gnomAD) of 19.2%/82.1%, reducing VUS prevalence to close to background rare variant frequency. CONCLUSION: Large case-control data sets enable quantitative implementation of ACMG/AMP guidelines and increased sensitivity for inherited arrhythmia genetic testing.

Published
2021

4. Arrhythmic Mitral Valve Prolapse: Introducing an Era of Multimodality Imaging-Based Diagnosis and Risk Stratification

Author

Kukavica, D, Guglielmo, M, Baggiano, A, Muscogiuri, G, Fusini, L, Muratori, M, Tamborini, G, Mantegazza, V, Trancuccio, A, Arnò, C, Mazzanti, A, Pepi, M, Priori, S, Pontone, G, Kukavica D, Guglielmo M, Baggiano A, Muscogiuri G, Fusini L, Muratori M, Tamborini G, Mantegazza V, Trancuccio A, Arnò C, Mazzanti A, Pepi M, Priori SG, Pontone G, Kukavica, D, Guglielmo, M, Baggiano, A, Muscogiuri, G, Fusini, L, Muratori, M, Tamborini, G, Mantegazza, V, Trancuccio, A, Arnò, C, Mazzanti, A, Pepi, M, Priori, S, Pontone, G, Kukavica D, Guglielmo M, Baggiano A, Muscogiuri G, Fusini L, Muratori M, Tamborini G, Mantegazza V, Trancuccio A, Arnò C, Mazzanti A, Pepi M, Priori SG, and Pontone G

Abstract

Mitral valve prolapse is a common cardiac condition, with an estimated prevalence between 1% and 3%. Most patients have a benign course, but ever since its initial description mitral valve prolapse has been associated to sudden cardiac death. Although the causal relationship between mitral valve prolapse and sudden cardiac death has never been clearly demonstrated, different factors have been implicated in arrhythmogenesis in patients with mitral valve prolapse. In this work, we offer a comprehensive overview of the etiology and the genetic background, epidemiology, pathophysiology, and we focus on the state-of-the-art imaging-based diagnosis of mitral valve prolapse. Going beyond the classical, well-described clinical factors, such as young age, female gender and auscultatory findings, we investigate multimodality imaging features, such as alterations of anatomy and function of the mitral valve and its leaflets, the structural and contractile anomalies of the myocardium, all of which have been associated to sudden cardiac death.

Published
2021

6. Ranolazine as an Alternative Therapy to Flecainide for SCN5A V411M Long QT Syndrome Type 3 Patients

Author

Cano J, Zorio E, Mazzanti A, Arnau MÁ, Trenor B, Priori SG, Saiz J, and Romero L

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, Long QT Syndrome, V411M, flecainide, in-silico model, ranolazine, sodium current channelopathy, cardiovascular diseases
Abstract

The prolongation of the QT interval represents the main feature of the long QT syndrome (LQTS), a life-threatening genetic disease. The heterozygous SCN5A V411M mutation of the human sodium channel leads to a LQTS type 3 with severe proarrhythmic effects due to an increase in the late component of the sodium current (INaL). The two sodium blockers flecainide and ranolazine are equally recommended by the current 2015 ESC guidelines to treat patients with LQTS type 3 and persistently prolonged QT intervals. However, awareness of pro-arrhythmic effects of flecainide in LQTS type 3 patients arose upon the study of the SCN5A E1784K mutation. Regarding SCN5A V411M individuals, flecainide showed good results albeit in a reduced number of patients and no evidence supporting the use of ranolazine has ever been released. Therefore, we ought to compare the effect of ranolazine and flecainide in a SCN5A V411M model using an in-silico modeling and simulation approach. We collected clinical data of four patients. Then, we fitted four Markovian models of the human sodium current (INa) to experimental and clinical data. Two of them correspond to the wild type and the heterozygous SCN5A V411M scenarios, and the other two mimic the effects of flecainide and ranolazine on INa. Next, we inserted them into three isolated cell action potential (AP) models for endocardial, midmyocardial and epicardial cells and in a one-dimensional tissue model. The SCN5A V411M mutation produced a 15.9% APD90 prolongation in the isolated endocardial cell model, which corresponded to a 14.3% of the QT interval prolongation in a one-dimensional strand model, in keeping with clinical observations. Although with different underlying mechanisms, flecainide and ranolazine partially countered this prolongation at the isolated endocardial model by reducing the APD90 by 8.7 and 4.3%, and the QT interval by 7.2 and 3.2%, respectively. While flecainide specifically targeted the mutation-induced increase in peak INaL, ranolazine reduced it during the entire AP. Our simulations also suggest that ranolazine could prevent early afterdepolarizations triggered by the SCN5A V411M mutation during bradycardia, as flecainide. We conclude that ranolazine could be used to treat SCN5A V411M patients, specifically when flecainide is contraindicated.

Published
2020

7. Novel insights on Andersen-Tawil syndrome type 1

Author

Mazzanti, A, Guz, D, Trancuccio, A, Pagan, E, Chargeishvili, T, Biernacka, EK, Sacilotto, L, Zorio, E, Sarquella-Brugada G, Nof, E, Anastasakis, A, Sansone, V, Jimenez-Jaimez, J, Cruz, F, Priori, SG, and ATS1 Int Res Grp

Published
2020

8. Transethnic genome-wide association study provides insights in the genetic architecture and heritability of long QT syndrome

Author

Lahrouchi, N, Tadros, R, Crotti, L, Mizusawa, Y, Postema, P, Beekman, L, Walsh, R, Hasegawa, K, Barc, J, Ernsting, M, Turkowski, K, Mazzanti, A, Beckmann, B, Shimamoto, K, Diamant, U, Wijeyeratne, Y, Kucho, Y, Robyns, T, Ishikawa, T, Arbelo, E, Christiansen, M, Winbo, A, Jabbari, R, Lubitz, S, Steinfurt, J, Rudic, B, Loeys, B, Shoemaker, M, Weeke, P, Pfeiffer, R, Davies, B, Andorin, A, Hofman, N, Dagradi, F, Pedrazzini, M, Tester, D, Bos, J, Sarquella-Brugada, G, Campuzano, Ó, Platonov, P, Stallmeyer, B, Zumhagen, S, Nannenberg, E, Veldink, J, van den Berg, L, Al-Chalabi, A, Shaw, C, Shaw, P, Morrison, K, Andersen, P, Müller-Nurasyid, M, Cusi, D, Barlassina, C, Galan, P, Lathrop, M, Munter, M, Werge, T, Ribasés, M, Aung, T, Khor, C, Ozaki, M, Lichtner, P, Meitinger, T, van Tintelen, J, Hoedemaekers, Y, Denjoy, I, Leenhardt, A, Napolitano, C, Shimizu, W, Schott, J, Gourraud, J, Makiyama, T, Ohno, S, Itoh, H, Krahn, A, Antzelevitch, C, Roden, D, Saenen, J, Borggrefe, M, Odening, K, Ellinor, P, Tfelt-Hansen, J, Skinner, J, van den Berg, M, Olesen, M, Brugada, J, Brugada, R, Makita, N, Breckpot, J, Yoshinaga, M, Behr, E, Rydberg, A, Aiba, T, Kääb, S, Priori, S, Guicheney, P, Tan, H, Newton-Cheh, C, Ackerman, M, Schwartz, P, Schulze-Bahr, E, Probst, V, Horie, M, Wilde, A, Tanck, M, Bezzina, C, Lahrouchi N, Tadros R, Crotti L, Mizusawa Y, Postema PG, Beekman L, Walsh R, Hasegawa K, Barc J, Ernsting M, Turkowski KL, Mazzanti A, Beckmann BM, Shimamoto K, Diamant UB, Wijeyeratne YD, Kucho Y, Robyns T, Ishikawa T, Arbelo E, Christiansen M, Winbo A, Jabbari R, Lubitz SA, Steinfurt J, Rudic B, Loeys B, Shoemaker MB, Weeke PE, Pfeiffer R, Davies B, Andorin A, Hofman N, Dagradi F, Pedrazzini M, Tester DJ, Bos JM, Sarquella-Brugada G, Campuzano Ó, Platonov PG, Stallmeyer B, Zumhagen S, Nannenberg EA, Veldink JH, van den Berg LH, Al-Chalabi A, Shaw CE, Shaw PJ, Morrison KE, Andersen PM, Müller-Nurasyid M, Cusi D, Barlassina C, Galan P, Lathrop M, Munter M, Werge T, Ribasés M, Aung T, Khor CC, Ozaki M, Lichtner P, Meitinger T, van Tintelen JP, Hoedemaekers Y, Denjoy I, Leenhardt A, Napolitano C, Shimizu W, Schott JJ, Gourraud JB, Makiyama T, Ohno S, Itoh H, Krahn AD, Antzelevitch C, Roden DM, Saenen J, Borggrefe M, Odening KE, Ellinor PT, Tfelt-Hansen J, Skinner JR, van den Berg MP, Olesen MS, Brugada J, Brugada R, Makita N, Breckpot J, Yoshinaga M, Behr ER, Rydberg A, Aiba T, Kääb S, Priori SG, Guicheney P, Tan HL, Newton-Cheh C, Ackerman MJ, Schwartz PJ, Schulze-Bahr E, Probst V, Horie M, Wilde AA, Tanck MWT, Bezzina CR., Lahrouchi, N, Tadros, R, Crotti, L, Mizusawa, Y, Postema, P, Beekman, L, Walsh, R, Hasegawa, K, Barc, J, Ernsting, M, Turkowski, K, Mazzanti, A, Beckmann, B, Shimamoto, K, Diamant, U, Wijeyeratne, Y, Kucho, Y, Robyns, T, Ishikawa, T, Arbelo, E, Christiansen, M, Winbo, A, Jabbari, R, Lubitz, S, Steinfurt, J, Rudic, B, Loeys, B, Shoemaker, M, Weeke, P, Pfeiffer, R, Davies, B, Andorin, A, Hofman, N, Dagradi, F, Pedrazzini, M, Tester, D, Bos, J, Sarquella-Brugada, G, Campuzano, Ó, Platonov, P, Stallmeyer, B, Zumhagen, S, Nannenberg, E, Veldink, J, van den Berg, L, Al-Chalabi, A, Shaw, C, Shaw, P, Morrison, K, Andersen, P, Müller-Nurasyid, M, Cusi, D, Barlassina, C, Galan, P, Lathrop, M, Munter, M, Werge, T, Ribasés, M, Aung, T, Khor, C, Ozaki, M, Lichtner, P, Meitinger, T, van Tintelen, J, Hoedemaekers, Y, Denjoy, I, Leenhardt, A, Napolitano, C, Shimizu, W, Schott, J, Gourraud, J, Makiyama, T, Ohno, S, Itoh, H, Krahn, A, Antzelevitch, C, Roden, D, Saenen, J, Borggrefe, M, Odening, K, Ellinor, P, Tfelt-Hansen, J, Skinner, J, van den Berg, M, Olesen, M, Brugada, J, Brugada, R, Makita, N, Breckpot, J, Yoshinaga, M, Behr, E, Rydberg, A, Aiba, T, Kääb, S, Priori, S, Guicheney, P, Tan, H, Newton-Cheh, C, Ackerman, M, Schwartz, P, Schulze-Bahr, E, Probst, V, Horie, M, Wilde, A, Tanck, M, Bezzina, C, Lahrouchi N, Tadros R, Crotti L, Mizusawa Y, Postema PG, Beekman L, Walsh R, Hasegawa K, Barc J, Ernsting M, Turkowski KL, Mazzanti A, Beckmann BM, Shimamoto K, Diamant UB, Wijeyeratne YD, Kucho Y, Robyns T, Ishikawa T, Arbelo E, Christiansen M, Winbo A, Jabbari R, Lubitz SA, Steinfurt J, Rudic B, Loeys B, Shoemaker MB, Weeke PE, Pfeiffer R, Davies B, Andorin A, Hofman N, Dagradi F, Pedrazzini M, Tester DJ, Bos JM, Sarquella-Brugada G, Campuzano Ó, Platonov PG, Stallmeyer B, Zumhagen S, Nannenberg EA, Veldink JH, van den Berg LH, Al-Chalabi A, Shaw CE, Shaw PJ, Morrison KE, Andersen PM, Müller-Nurasyid M, Cusi D, Barlassina C, Galan P, Lathrop M, Munter M, Werge T, Ribasés M, Aung T, Khor CC, Ozaki M, Lichtner P, Meitinger T, van Tintelen JP, Hoedemaekers Y, Denjoy I, Leenhardt A, Napolitano C, Shimizu W, Schott JJ, Gourraud JB, Makiyama T, Ohno S, Itoh H, Krahn AD, Antzelevitch C, Roden DM, Saenen J, Borggrefe M, Odening KE, Ellinor PT, Tfelt-Hansen J, Skinner JR, van den Berg MP, Olesen MS, Brugada J, Brugada R, Makita N, Breckpot J, Yoshinaga M, Behr ER, Rydberg A, Aiba T, Kääb S, Priori SG, Guicheney P, Tan HL, Newton-Cheh C, Ackerman MJ, Schwartz PJ, Schulze-Bahr E, Probst V, Horie M, Wilde AA, Tanck MWT, and Bezzina CR.

Abstract

Background: Long QT syndrome (LQTS) is a rare genetic disorder and a major preventable cause of sudden cardiac death in the young. A causal rare genetic variant with large effect size is identified in up to 80% of probands (genotype positive) and cascade family screening shows incomplete penetrance of genetic variants. Furthermore, a proportion of cases meeting diagnostic criteria for LQTS remain genetically elusive despite genetic testing of established genes (genotype negative). These observations raise the possibility that common genetic variants with small effect size contribute to the clinical picture of LQTS. This study aimed to characterize and quantify the contribution of common genetic variation to LQTS disease susceptibility. Methods: We conducted genome-wide association studies followed by transethnic meta-analysis in 1656 unrelated patients with LQTS of European or Japanese ancestry and 9890 controls to identify susceptibility single nucleotide polymorphisms. We estimated the common variant heritability of LQTS and tested the genetic correlation between LQTS susceptibility and other cardiac traits. Furthermore, we tested the aggregate effect of the 68 single nucleotide polymorphisms previously associated with the QT-interval in the general population using a polygenic risk score. Results: Genome-wide association analysis identified 3 loci associated with LQTS at genome-wide statistical significance (P5×10-8) near NOS1AP, KCNQ1, and KLF12, and 1 missense variant in KCNE1(p.Asp85Asn) at the suggestive threshold (P10-6). Heritability analyses showed that ≈15% of variance in overall LQTS susceptibility was attributable to common genetic variation (h2SNP 0.148; standard error 0.019). LQTS susceptibility showed a strong genome-wide genetic correlation with the QT-interval in the general population (rg=0.40; P=3.2×10-3). The polygenic risk score comprising common variants previously associated with the QT-interval in the general population was greater in LQTS c

Published
2020

9. An International Multicenter Evaluation of Type 5 Long QT Syndrome: A Low Penetrant Primary Arrhythmic Condition

Author

Roberts, J, Asaki, S, Mazzanti, A, Bos, J, Tuleta, I, Muir, A, Crotti, L, Krahn, A, Kutyifa, V, Shoemaker, M, Johnsrude, C, Aiba, T, Marcondes, L, Baban, A, Udupa, S, Dechert, B, Fischbach, P, Knight, L, Vittinghoff, E, Kukavica, D, Stallmeyer, B, Giudicessi, J, Spazzolini, C, Shimamoto, K, Tadros, R, Cadrin-Tourigny, J, Duff, H, Simpson, C, Roston, T, Wijeyeratne, Y, El Hajjaji, I, Yousif, M, Gula, L, Leong-Sit, P, Chavali, N, Landstrom, A, Marcus, G, Dittmann, S, Wilde, A, Behr, E, Tfelt-Hansen, J, Scheinman, M, Perez, M, Kaski, J, Gow, R, Drago, F, Aziz, P, Abrams, D, Gollob, M, Skinner, J, Shimizu, W, Kaufman, E, Roden, D, Zareba, W, Schwartz, P, Schulze-Bahr, E, Etheridge, S, Priori, S, Ackerman, M, Roberts JD, Asaki SY, Mazzanti A, Bos JM, Tuleta I, Muir AR, Crotti L, Krahn AD, Kutyifa V, Shoemaker MB, Johnsrude CL, Aiba T, Marcondes L, Baban A, Udupa S, Dechert B, Fischbach P, Knight LM, Vittinghoff E, Kukavica D, Stallmeyer B, Giudicessi JR, Spazzolini C, Shimamoto K, Tadros R, Cadrin-Tourigny J, Duff HJ, Simpson CS, Roston TM, Wijeyeratne YD, El Hajjaji I, Yousif MD, Gula LJ, Leong-Sit P, Chavali N, Landstrom AP, Marcus GM, Dittmann S, Wilde AAM, Behr ER, Tfelt-Hansen J, Scheinman MM, Perez MV, Kaski JP, Gow RM, Drago F, Aziz PF, Abrams DJ, Gollob MH, Skinner JR, Shimizu W, Kaufman ES, Roden DM, Zareba W, Schwartz PJ, Schulze-Bahr E, Etheridge SP, Priori SG, Ackerman MJ., Roberts, J, Asaki, S, Mazzanti, A, Bos, J, Tuleta, I, Muir, A, Crotti, L, Krahn, A, Kutyifa, V, Shoemaker, M, Johnsrude, C, Aiba, T, Marcondes, L, Baban, A, Udupa, S, Dechert, B, Fischbach, P, Knight, L, Vittinghoff, E, Kukavica, D, Stallmeyer, B, Giudicessi, J, Spazzolini, C, Shimamoto, K, Tadros, R, Cadrin-Tourigny, J, Duff, H, Simpson, C, Roston, T, Wijeyeratne, Y, El Hajjaji, I, Yousif, M, Gula, L, Leong-Sit, P, Chavali, N, Landstrom, A, Marcus, G, Dittmann, S, Wilde, A, Behr, E, Tfelt-Hansen, J, Scheinman, M, Perez, M, Kaski, J, Gow, R, Drago, F, Aziz, P, Abrams, D, Gollob, M, Skinner, J, Shimizu, W, Kaufman, E, Roden, D, Zareba, W, Schwartz, P, Schulze-Bahr, E, Etheridge, S, Priori, S, Ackerman, M, Roberts JD, Asaki SY, Mazzanti A, Bos JM, Tuleta I, Muir AR, Crotti L, Krahn AD, Kutyifa V, Shoemaker MB, Johnsrude CL, Aiba T, Marcondes L, Baban A, Udupa S, Dechert B, Fischbach P, Knight LM, Vittinghoff E, Kukavica D, Stallmeyer B, Giudicessi JR, Spazzolini C, Shimamoto K, Tadros R, Cadrin-Tourigny J, Duff HJ, Simpson CS, Roston TM, Wijeyeratne YD, El Hajjaji I, Yousif MD, Gula LJ, Leong-Sit P, Chavali N, Landstrom AP, Marcus GM, Dittmann S, Wilde AAM, Behr ER, Tfelt-Hansen J, Scheinman MM, Perez MV, Kaski JP, Gow RM, Drago F, Aziz PF, Abrams DJ, Gollob MH, Skinner JR, Shimizu W, Kaufman ES, Roden DM, Zareba W, Schwartz PJ, Schulze-Bahr E, Etheridge SP, Priori SG, and Ackerman MJ.

Abstract

Background: Insight into type 5 long QT syndrome (LQT5) has been limited to case reports and small family series. Improved understanding of the clinical phenotype and genetic features associated with rare KCNE1 variants implicated in LQT5 was sought through an international multicenter collaboration. Methods: Patients with either presumed autosomal dominant LQT5 (N = 229) or the recessive Type 2 Jervell and Lange-Nielsen syndrome (N = 19) were enrolled from 22 genetic arrhythmia clinics and 4 registries from 9 countries. KCNE1 variants were evaluated for ECG penetrance (defined as QTc >460 ms on presenting ECG) and genotype-phenotype segregation. Multivariable Cox regression was used to compare the associations between clinical and genetic variables with a composite primary outcome of definite arrhythmic events, including appropriate implantable cardioverter-defibrillator shocks, aborted cardiac arrest, and sudden cardiac death. Results: A total of 32 distinct KCNE1 rare variants were identified in 89 probands and 140 genotype positive family members with presumed LQT5 and an additional 19 Type 2 Jervell and Lange-Nielsen syndrome patients. Among presumed LQT5 patients, the mean QTc on presenting ECG was significantly longer in probands (476.9±38.6 ms) compared with genotype positive family members (441.8±30.9 ms, P<0.001). ECG penetrance for heterozygous genotype positive family members was 20.7% (29/140). A definite arrhythmic event was experienced in 16.9% (15/89) of heterozygous probands in comparison with 1.4% (2/140) of family members (adjusted hazard ratio [HR] 11.6 [95% CI, 2.6-52.2]; P=0.001). Event incidence did not differ significantly for Type 2 Jervell and Lange-Nielsen syndrome patients relative to the overall heterozygous cohort (10.5% [2/19]; HR 1.7 [95% CI, 0.3-10.8], P=0.590). The cumulative prevalence of the 32 KCNE1 variants in the Genome Aggregation Database, which is a human database of exome and genome sequencing data from now over 140 0

Published
2020

11. International Triadin Knockout Syndrome Registry: The Clinical Phenotype and Treatment Outcomes of Patients with Triadin Knockout Syndrome

Author

Clemens, D, Tester, D, Giudicessi, J, Bos, J, Rohatgi, R, Abrams, D, Balaji, S, Crotti, L, Faure, J, Napolitano, C, Priori, S, Probst, V, Rooryck-Thambo, C, Roux-Buisson, N, Sacher, F, Schwartz, P, Silka, M, Walsh, M, Ackerman, M, Clemens, DJ, Tester, DJ, Giudicessi, JR, Bos, JM, Rohatgi, RK, Abrams, DJ, Priori, SG, Schwartz, PJ, Silka, MJ, Walsh, MA, Ackerman, MJ, Clemens, D, Tester, D, Giudicessi, J, Bos, J, Rohatgi, R, Abrams, D, Balaji, S, Crotti, L, Faure, J, Napolitano, C, Priori, S, Probst, V, Rooryck-Thambo, C, Roux-Buisson, N, Sacher, F, Schwartz, P, Silka, M, Walsh, M, Ackerman, M, Clemens, DJ, Tester, DJ, Giudicessi, JR, Bos, JM, Rohatgi, RK, Abrams, DJ, Priori, SG, Schwartz, PJ, Silka, MJ, Walsh, MA, and Ackerman, MJ

Abstract

Background: Triadin knockout syndrome (TKOS) is a rare, inherited arrhythmia syndrome caused by recessive null mutations in TRDN-encoded cardiac triadin. Based previously on 5 triadin null patients, TKOS has been characterized by extensive T-wave inversions, transient QT prolongation, and severe disease expression of exercise-induced cardiac arrest in early childhood refractory to conventional therapy. Methods: We have established the International Triadin Knockout Syndrome Registry to include patients who have genetically proven homozygous/compound heterozygous TRDN null mutations. Clinical/genetic data were collected using an online survey generated through REDCap. Results: Currently, the International Triadin Knockout Syndrome Registry includes 21 patients (11 males, average age of 18 years) from 16 families. Twenty patients (95%) presented with either cardiac arrest (15, 71%) or syncope (5, 24%) at an average age of 3 years. Mild skeletal myopathy/proximal muscle weakness was noted in 6 (29%) patients. Of the 19 surviving patients, 16 (84%) exhibit T-wave inversions, and 10 (53%) have transient QT prolongation > 480 ms. Eight of 9 patients had ventricular ectopy on exercise stress testing. Thirteen (68%) patients have received implantable defibrillators. Despite various treatment strategies, 14 (74%) patients have had recurrent breakthrough cardiac events. Conclusion: TKOS is a potentially lethal disease characterized by T-wave inversions in the precordial leads, transient QT prolongation in some, and recurrent ventricular arrhythmias at a young age despite aggressive treatment. Patients displaying this phenotype should undergo TRDN genetic testing as TKOS may be a cause for otherwise unexplained cardiac arrest in young children. As gene therapy advances, enrollment into the International Triadin Knockout Syndrome Registry is encouraged to better understand TKOS and to ready a well-characterized cohort for future TRDN gene therapy trials.

Published
2019

12. Interplay Between Genetic Substrate, QTc Duration, and Arrhythmia Risk in Patients With Long QT Syndrome

Author

Mazzanti, A, Maragna, R, Vacanti, G, Monteforte, N, Bloise, R, Marino, M, Braghieri, L, Gambelli, P, Memmi, M, Pagan, E, Morini, M, Malovini, A, Ortiz, M, Sacilotto, L, Bellazzi, R, Monserrat, L, Napolitano, C, Bagnardi, V, Priori, S, Priori, SG, Mazzanti, A, Maragna, R, Vacanti, G, Monteforte, N, Bloise, R, Marino, M, Braghieri, L, Gambelli, P, Memmi, M, Pagan, E, Morini, M, Malovini, A, Ortiz, M, Sacilotto, L, Bellazzi, R, Monserrat, L, Napolitano, C, Bagnardi, V, Priori, S, and Priori, SG

Abstract

Background: Long QT syndrome (LQTS) is a common inheritable arrhythmogenic disorder, often secondary to mutations in the KCNQ1, KCNH2, and SCN5A genes. The disease is characterized by a prolonged ventricular repolarization (QTc interval) that confers susceptibility to life-threatening arrhythmic events (LAEs). Objectives: This study sought to create an evidence-based risk stratification scheme to personalize the quantification of the arrhythmic risk in patients with LQTS. Methods: Data from 1,710 patients with LQTS followed up for a median of 7.1 years (interquartile range [IQR]: 2.7 to 13.4 years) were analyzed to estimate the 5-year risk of LAEs based on QTc duration and genotype and to assess the antiarrhythmic efficacy of beta-blockers. Results: The relationship between QTc duration and risk of events was investigated by comparison of linear and cubic spline models, and the linear model provided the best fit. The 5-year risk of LAEs while patients were off therapy was then calculated in a multivariable Cox model with QTc and genotype considered as independent factors. The estimated risk of LAEs increased by 15% for every 10-ms increment of QTc duration for all genotypes. Intergenotype comparison showed that the risk for patients with LQT2 and LTQ3 increased by 130% and 157% at any QTc duration versus patients with LQT1. Analysis of response to beta-blockers showed that only nadolol reduced the arrhythmic risk in all genotypes significantly compared with no therapy (hazard ratio: 0.38; 95% confidence interval: 0.15 to 0.93; p = 0.03). Conclusions: The study provides an estimator of risk of LAEs in LQTS that allows a granular estimate of 5-year arrhythmic risk and demonstrate the superiority of nadolol in reducing the risk of LAEs in LQTS

Published
2018

14. Allele-specific silencing of mutant mRNA rescues ultrastructural and arrhythmic phenotype in mice carriers of the R4496C mutation in the ryanodine receptor gene (RYR2)

Author

Bongianino, R, Denegri, M, Mazzanti, A, Lodola, F, Vollero, A, Boncompagni, S, Fasciano, S, Rizzo, G, Mangione, D, Barbaro, S, Di Fonso, A, Napolitano, C, Auricchio, A, Protasi, F, Priori, S, Bongianino R, Denegri M, Mazzanti A, Lodola F, Vollero A, Boncompagni S, Fasciano S, Rizzo G, Mangione D, Barbaro S, Di Fonso A, Napolitano C, Auricchio A, Protasi F, Priori SG, Bongianino, R, Denegri, M, Mazzanti, A, Lodola, F, Vollero, A, Boncompagni, S, Fasciano, S, Rizzo, G, Mangione, D, Barbaro, S, Di Fonso, A, Napolitano, C, Auricchio, A, Protasi, F, Priori, S, Bongianino R, Denegri M, Mazzanti A, Lodola F, Vollero A, Boncompagni S, Fasciano S, Rizzo G, Mangione D, Barbaro S, Di Fonso A, Napolitano C, Auricchio A, Protasi F, and Priori SG

Abstract

Rationale: Mutations in the cardiac Ryanodine Receptor gene (RYR2) cause dominant catecholaminergic polymorphic ventricular tachycardia (CPVT), a leading cause of sudden death in apparently healthy individuals exposed to emotions or physical exercise. Objective: We investigated the efficacy of allele-specific silencing by RNA interference to prevent CPVT phenotypic manifestations in our dominant CPVT mice model carriers of the heterozygous mutation R4496C in RYR2. Methods and Results: We developed an in vitro mRNA and protein-based assays to screen multiple siRNAs for their ability to selectively silence mutant RYR2-R4496C mRNA over the corresponding wild-type allele. For the most performant of these siRNAs (siRYR2-U10), we evaluated the efficacy of an adeno-associated serotype 9 viral vector (AAV9) expressing miRYR2-U10 in correcting RyR2 (Ryanodine Receptor type 2 protein) function after in vivo delivery by intraperitoneal injection in neonatal and adult RyR2R4496C/+ (mice heterozygous for the R4496C mutation in the RyR2) heterozygous CPVT mice. Transcriptional analysis showed that after treatment with miRYR2-U10, the ratio between wild-type and mutant RYR2 mRNA was doubled (from 1:1 to 2:1) confirming the ability of miRYR2-U10 to selectively inhibit RYR2-R4496C mRNA, whereas protein quantification showed that total RyR2 was reduced by 15% in the heart of treated mice. Furthermore, AAV9-miRYR2-U10 effectively (1) reduced isoproterenol-induced delayed afterdepolarizations and triggered activity in infected cells, (2) reduced adrenergically mediated ventricular tachycardia in treated mice, (3) reverted ultrastructural abnormalities of junctional sarcoplasmic reticulum and transverse tubules, and (4) attenuated mitochondrial abnormalities. Conclusions: The study demonstrates that allele-specific silencing with miRYR2-U10 prevents life-threatening arrhythmias in CPVT mice, suggesting that the reduction of mutant RyR2 may be a novel therapeutic approach for CPVT.

Published
2017

16. Hydroquinidine Prevents Life-Threatening Arrhythmic Events in Patients With Short QT Syndrome

Author

Mazzanti, A, Maragna, R, Vacanti, G, Kostopoulou, A, Marino, M, Monteforte, N, Bloise, R, Underwood, K, Tibollo, V, Pagan, E, Napolitano, C, Bellazzi, R, Bagnardi, V, Priori, S, Priori, SG, Mazzanti, A, Maragna, R, Vacanti, G, Kostopoulou, A, Marino, M, Monteforte, N, Bloise, R, Underwood, K, Tibollo, V, Pagan, E, Napolitano, C, Bellazzi, R, Bagnardi, V, Priori, S, and Priori, SG

Abstract

Background Short QT syndrome (SQTS) is a rare and life-threatening arrhythmogenic syndrome characterized by abbreviated repolarization. Hydroquinidine (HQ) prolongs the QT interval in SQTS patients, although whether it reduces cardiac events is currently unknown. Objectives This study investigated whether long-term treatment with HQ reduces the occurrence of life-threatening arrhythmic events (LAE) (cardiac arrest or sudden cardiac death) in SQTS patients. Methods In this cohort study on consecutive SQTS patients, 2 analyses were performed: 1) a matched-period analysis for the occurrence of LAE in 17 SQTS patients who received long-term HQ; and 2) a comparison of the annual incidence of LAE off- and on-HQ in 16 SQTS patients who survived a cardiac arrest. Results A total of 17 patients (82% male, age 29 ± 3 years, QTc before treatment 331 ± 3 ms) received HQ therapy (584 ± 53 mg/day). Therapy was stopped in 2 cases (12%) due to gastrointestinal intolerance, and 15 patients continued treatment for 6 ± 1 year. QTc prolongation was observed in all patients (by 60 ± 6 ms; p < 0.001). We compared the occurrence of LAE during 6 ± 1 years before and after HQ, observing that patients on HQ experienced a reduction in both the rate of LAE from 40% to 0% (p = 0.03) and the number of LAE per patient from 0.73 ± 0.3 to 0 (p = 0.026). Furthermore, the annual rate of LAE in the 16 patients with a previous cardiac arrest dropped from 12% before HQ to 0 on therapy (p = 0.028). Conclusions We demonstrated for the first time that treatment with HQ was associated with a lower incidence of LAE in SQTS patients. These data point to the importance that quinidine, that in several countries has been removed from the market, remains available worldwide for patients with SQTS. In the present study, therapy with HQ has been proven to be safe, with a relatively low rate of side effects.

Published
2017

17. Expert consensus document on the use of antiplatelet agents. The task force on the use of antiplatelet agents in patients with atherosclerotic cardiovascular disease of the European society of cardiology

Author

Patrono, C, Bachmann, F, Baigent, C, Bode, C, De Caterina, R, Charbonnier, B, Fitzgerald, D, Hirsh, J, Husted, S, Kvasnicka, J, Montalescot, G, García Rodríguez, LA, Verheugt, F, Vermylen, J, Wallentin, L, Priori, SG, Alonso Garcia, MA, Blanc, JJ, Budaj, A, Cowie, M, Dean, V, Deckers, J, Fernández Burgos, E, Lekakis, J, Lindahl, B, Mazzotta, G, Morais, J, Oto, A, Smiseth, OA, Ferreira, R, Steg, PG, Teixeira, F, Wilcox, R, and Cardiology

Subjects
Blood Platelets, medicine.medical_specialty, Process (engineering), media_common.quotation_subject, Alternative medicine, Coronary Artery Disease, Risk Assessment, Task (project management), SDG 3 - Good Health and Well-being, Risk Factors, Internal medicine, medicine, Humans, In patient, Quality (business), Heart, lung and circulation [UMCN 2.1], media_common, Clinical Trials as Topic, Atherosclerotic cardiovascular disease, business.industry, Patient Selection, Expert consensus, Clinical trial, Cardiology, Cardiology and Cardiovascular Medicine, business, Platelet Aggregation Inhibitors
Abstract

Guidelines and Expert Consensus Documents aim to present all the relevant evidence on a particular issue in order to help physicians to weigh the benefits and risks of a particular diagnostic or therapeutic procedure. They should be helpful in everyday clinical decision-making. A great number of Guidelines and Expert Consensus Documents have been issued in recent years by different organizations, the European Society of Cardiology (ESC) and by other related societies. By means of links to web sites of National Societies several hundred guidelines are available. This profusion can put at stake the authority and validity of guidelines, which can only be guaranteed if they have been developed by an unquestionable decision-making process. This is one of the reasons why the ESC and others have issued recommendations for formulating and issuing Guidelines and Expert Consensus Documents. In spite of the fact that standards for issuing good quality Guidelines and Expert Consensus Documents are well defined, recent surveys of Guidelines and Expert Consensus Documents published in peer-reviewed journals between 1985 and 1998 have shown that methodological standards were not complied within the vast majority of cases. It is therefore of great importance that guidelines and recommendations are presented in formats that are easily interpreted. Subsequently, their implementation programmes must also be well conducted. Attempts have been made to determine whether guidelines improve the quality of clinical practice and the utilization of health resources. The ESC Committee for Practice Guidelines ( CPG ) supervises and coordinates the preparation of new Guidelines and Expert Consensus Documents produced by Task Forces, expert groups or consensus panels. The Committee is also responsible for the endorsement of these Guidelines and Expert Consensus Documents or statements. The role of aspirin and other platelet-active drugs in the treatment and prevention of atherothrombosis has been reviewed recently by the Sixth American …

Published
2016

19. P401Clinical predictors of time-to-first appropriate implantable cardioverter-defibrillator discharge in high-risk patients with Brugada syndrome implanted prophylactically: analysis of 246 patients from

Author

Milman, A., primary, Probst, V., additional, Nam, GB., additional, Brugada, P., additional, Brugada, J., additional, Kusano, KF., additional, Takagi, M., additional, Priori, SG., additional, Delise, P., additional, Gaita, F., additional, Corrado, D., additional, Leenhardt, A., additional, Veltmann, C., additional, Hirao, K., additional, and Belhassen, B., additional

Published
2017
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20. Efficacy of a biological therapy for recessive Catecholaminergic Polymorphic Ventricular Tachycardia in human induced pluripotent stem cells-derived cardiomyocytes

Author

Lodola F, Di Pasquale E, Bongianino R, Denegri M, Rutigliano L, Buonocore M, Bloise R, Condorelli G, Napolitano C, Priori SG, Lodola, F, Di Pasquale, E, Bongianino, R, Denegri, M, Rutigliano, L, Buonocore, M, Bloise, R, Condorelli, G, Napolitano, C, and Priori, S

Subjects
Cardiac arrhythmias, gene therapy, physiology, Cardiac arrhythmias, gene therapy, CPVT, hiPS-CMs
Published
2015

23. Adeno-associated virus-mediated CASQ2 delivery rescues phenotypic alterations in a patient-specific model of recessive Catecholaminergic Polymorphic Ventricular Tachycardia

Author

Lodola, F, Morone, D, Denegri, M, Rutigliano, L, Bongianino, R, Nakahama, H, Gosetti, R, Rizzo, G, Vollero, A, Buonocore, M, Napolitano, C, Condorelli, G, Priori, S, Di Pasquale, E, Lodola F, Morone D, Denegri M, Rutigliano L, Bongianino R, Nakahama H, Gosetti R, Rizzo G, Vollero A, Buonocore M, Napolitano C, Condorelli G, Priori SG, Di Pasquale E, Lodola, F, Morone, D, Denegri, M, Rutigliano, L, Bongianino, R, Nakahama, H, Gosetti, R, Rizzo, G, Vollero, A, Buonocore, M, Napolitano, C, Condorelli, G, Priori, S, Di Pasquale, E, Lodola F, Morone D, Denegri M, Rutigliano L, Bongianino R, Nakahama H, Gosetti R, Rizzo G, Vollero A, Buonocore M, Napolitano C, Condorelli G, Priori SG, and Di Pasquale E

Abstract

Catecholaminergic Polymorphic Ventricular Tachycardia type 2 (CPVT2) is a highly lethal recessive arrhythmogenic disease caused by mutations in the calsequestrin-2 (CASQ2) gene. We have previously demonstrated that viral transfer of the wild-type (WT) CASQ2 gene prevents the development of CPVT2 in a genetically induced mouse model of the disease homozygous carrier of the R33Q mutation. In the present study, we investigated the efficacy of the virally mediated gene therapy in cardiomyocytes (CMs) differentiated from induced pluripotent stem cells (iPSCs) obtained from a patient carrying the homozygous CASQ2-G112+5X mutation. To this end, we infected cells with an Adeno-Associated Viral vector serotype 9 (AAV9) encoding the human CASQ2 gene (AAV9-hCASQ2). Administration of the human WT CASQ2 gene was capable and sufficient to restore the physiological expression of calsequestrin-2 protein and to rescue functional defects of the patient-specific iPSC-derived CMs. Indeed, after viral gene transfer, we observed a remarkable decrease in the percentage of delayed afterdepolarizations (DADs) developed by the diseased CMs upon adrenergic stimulation, the calcium transient amplitude was re-established and the density and duration of calcium sparks were normalized. We therefore demonstrate the efficacy of the AAV9-mediated gene replacement therapy for CPVT2 in a human cardiac-specific model system, supporting the view that the gene-therapy tested is curative in models with different human mutations of CPVT.

Published
2016

24. Allele Specific Silencing Prevents Malignant Arrhythmias and Ultrastructural Abnormalities in Ryanodine Receptor Mutant Mice

Author

Bongianino, R, Vollero, A, Lodola, F, Denegri, M, Boncompagni, S, Fasciano, S, Mazzanti, A, Mangione, D, Barbaro, S, Rizzo, G, Auricchio, A, Napolitano, C, Protasi, F, Priori, S, Bongianino R, Vollero A, Lodola F, Denegri M, Boncompagni S, Fasciano S, Mazzanti A, Mangione D, Barbaro S, Rizzo G, Auricchio A, Napolitano C, Protasi F, Priori SG, Bongianino, R, Vollero, A, Lodola, F, Denegri, M, Boncompagni, S, Fasciano, S, Mazzanti, A, Mangione, D, Barbaro, S, Rizzo, G, Auricchio, A, Napolitano, C, Protasi, F, Priori, S, Bongianino R, Vollero A, Lodola F, Denegri M, Boncompagni S, Fasciano S, Mazzanti A, Mangione D, Barbaro S, Rizzo G, Auricchio A, Napolitano C, Protasi F, and Priori SG

Published
2016

25. 2003 European Society of Hypertension???European Society of Cardiology guidelines for the management of arterial hypertension*

Author

MANCIA, GIUSEPPE, Rosei, EA, Cifkova, R, DeBacker, G, Erdine, S, Fagard, R, Farsang, C, Heagerty, AM, Kawecka Jaszcs, K, Kiowski, W, Kjeldsen, S, Luscher, T, McInnes, G, Mallion, JM, Brien, EO, Poulter, NR, Priori, SG, Rahn, KH, Rodicio, JL, Ruilope, LM, Safar, M, Staessen, JA, van Zwieten, P, Waeber, B, Williams, B, Zanchetti, A, Zannad, F., Mancia, G, Rosei, E, Cifkova, R, Debacker, G, Erdine, S, Fagard, R, Farsang, C, Heagerty, A, Kawecka Jaszcs, K, Kiowski, W, Kjeldsen, S, Luscher, T, Mcinnes, G, Mallion, J, Brien, E, Poulter, N, Priori, S, Rahn, K, Rodicio, J, Ruilope, L, Safar, M, Staessen, J, van Zwieten, P, Waeber, B, Williams, B, Zanchetti, A, and Zannad, F

Subjects
Physiology, optimal treatment hot, left-ventricular hypertrophy, end-point reduction, target-organ damage, Blood Pressure Determination, Guideline, Clinical practice, isolated systolic hypertension, Risk Assessment, Europe, ambulatory blood-pressure, randomized controlled trial, Hypertension, Internal Medicine, Humans, MED/09 - MEDICINA INTERNA, coronary-heart-disease, intima-media thickness, Cardiology and Cardiovascular Medicine, Risk Reduction Behavior, converting-enzyme-inhibition, Antihypertensive Agents
Abstract

ispartof: Journal of hypertension vol:21 issue:6 pages:1011-1053 ispartof: location:Netherlands status: published

Published
2003

26. Guidelines on the management of stable angina pectoris: executive summary: The Task Force on the Management of Stable Angina Pectoris of the European Society of Cardiology

Author

Fox K, Garcia MA, Ardissino D, Buszman P, CAMICI , PAOLO, Crea F, Daly C, De Backer G, Hjemdahl P, Lopez Sendon J, Marco J, Morais J, Pepper J, Sechtem U, Simoons M, Thygesen K, Priori SG, Blanc JJ, Budaj A, Camm J, Dean V, Deckers J, Dickstein K, Lekakis J, McGregor K, Metra M, Osterspey A, Tamargo J, Zamorano JL, Andreotti F, Becher H, Dietz R, Fraser A, Gray H, Antolin RA, Huber K, Kremastinos DT, Maseri A, Nesser HJ, Pasierski T, Sigwart U, Tubaro M, Weis M., Fox, K, Garcia, Ma, Ardissino, D, Buszman, P, Camici, Paolo, Crea, F, Daly, C, De Backer, G, Hjemdahl, P, Lopez Sendon, J, Marco, J, Morais, J, Pepper, J, Sechtem, U, Simoons, M, Thygesen, K, Priori, Sg, Blanc, Jj, Budaj, A, Camm, J, Dean, V, Deckers, J, Dickstein, K, Lekakis, J, Mcgregor, K, Metra, M, Osterspey, A, Tamargo, J, Zamorano, Jl, Andreotti, F, Becher, H, Dietz, R, Fraser, A, Gray, H, Antolin, Ra, Huber, K, Kremastinos, Dt, Maseri, A, Nesser, Hj, Pasierski, T, Sigwart, U, Tubaro, M, and Weis, M.

Subjects
Male, medicine.medical_specialty, Cardiotonic Agents, medicine.medical_treatment, Placebo-controlled study, Revascularization, Coronary Angiography, Risk Assessment, law.invention, Angina Pectoris, Coronary artery disease, Electrocardiography, Pharmacotherapy, Randomized controlled trial, law, Diabetes mellitus, Internal medicine, medicine, Myocardial Revascularization, Humans, Myocardial infarction, Angioplasty, Balloon, Coronary, Coronary Artery Bypass, Medical History Taking, Referral and Consultation, Aged, Executive summary, business.industry, Clinical Laboratory Techniques, Middle Aged, medicine.disease, Cardiology, Exercise Test, Female, Stents, Cardiology and Cardiovascular Medicine, business
Abstract

Under the heading ‘Hypertension, diabetes, and other disorders’ on page 1358, the guidelines1 lean on the taskforce report on CVD prevention2 suggesting ‘considering a lower threshold for institution of pharmacological therapy for hypertension (130/85) for patients with established coronary heart disease (which would include patients with …

Published
2006

27. Efficacy of a biological therapy for recessive Catecholaminergic Polymorphic Ventricular Tachycardia in human induced pluripotent stem cells-derived cardiomyocytes

Author

Lodola, F, Di Pasquale, E, Bongianino, R, Denegri, M, Rutigliano, L, Buonocore, M, Bloise, R, Condorelli, G, Napolitano, C, Priori, S, Lodola F, Di Pasquale E, Bongianino R, Denegri M, Rutigliano L, Buonocore M, Bloise R, Condorelli G, Napolitano C, Priori SG, Lodola, F, Di Pasquale, E, Bongianino, R, Denegri, M, Rutigliano, L, Buonocore, M, Bloise, R, Condorelli, G, Napolitano, C, Priori, S, Lodola F, Di Pasquale E, Bongianino R, Denegri M, Rutigliano L, Buonocore M, Bloise R, Condorelli G, Napolitano C, and Priori SG

Published
2015

28. Therapeutic Modulation Of Cardiac Function By Selective Peptidomimetic-Mediated Targeting Of The L-Type Calcium Channel Machinery

Author

Rusconi, F, Ceriotti, P, Miragoli, M, Di Pasquale, E, Carullo, P, Salvarani, N, Rocchetti, M, Rossi, S, Lodola, F, Caprari, S, Viggiani, G, Cazade, M, Kunderfranco, P, Chemin, J, Bang, M, Polticelli, F, Zaza, A, Napolitano, C, Priori, S, Condorelli, G, Catalucci, D, Rusconi F, Ceriotti P, Miragoli M, Di Pasquale E, Carullo P, Salvarani N, Rocchetti M, Rossi S, Lodola F, Caprari S, Viggiani G, Cazade M, Kunderfranco P, Chemin J, Bang ML, Polticelli F, Zaza A, Napolitano C, Priori SG, Condorelli G, Catalucci D, Rusconi, F, Ceriotti, P, Miragoli, M, Di Pasquale, E, Carullo, P, Salvarani, N, Rocchetti, M, Rossi, S, Lodola, F, Caprari, S, Viggiani, G, Cazade, M, Kunderfranco, P, Chemin, J, Bang, M, Polticelli, F, Zaza, A, Napolitano, C, Priori, S, Condorelli, G, Catalucci, D, Rusconi F, Ceriotti P, Miragoli M, Di Pasquale E, Carullo P, Salvarani N, Rocchetti M, Rossi S, Lodola F, Caprari S, Viggiani G, Cazade M, Kunderfranco P, Chemin J, Bang ML, Polticelli F, Zaza A, Napolitano C, Priori SG, Condorelli G, and Catalucci D

Published
2015

29. Mutations of cardiac calsequestrin and cardiac arrhythmias: novel insights on pathogenesis and therapy

Author

Bongianino, R, Lodola, F, Denegri, M, Boncompagni, S, Valle, G, Persampieri, S, Liu, N, Auricchio, A, Protasi, F, Volpe, P, Napolitano, C, Priori, S, Bongianino R, Lodola F, Denegri M, Boncompagni S, Valle G, Persampieri S, Liu N, Auricchio A, Protasi F, Volpe P, Napolitano C, Priori SG, Bongianino, R, Lodola, F, Denegri, M, Boncompagni, S, Valle, G, Persampieri, S, Liu, N, Auricchio, A, Protasi, F, Volpe, P, Napolitano, C, Priori, S, Bongianino R, Lodola F, Denegri M, Boncompagni S, Valle G, Persampieri S, Liu N, Auricchio A, Protasi F, Volpe P, Napolitano C, and Priori SG

Published
2015

30. Guidelines on diagnosis and treatment of pulmonary arterial hypertension. The Task Force on Diagnosis and Treatment of Pulmonary Arterial Hypertension of the European Society of Cardiology

Author

GALIE', NAZZARENO, Torbicki A, Barst R, Dartevelle P, Haworth S, Higenbottam T, Olschewski H, Peacock A, Pietra G, Rubin LJ, Simonneau G, Priori SG, Garcia MA, Blanc JJ, Budaj A, Cowie M, Dean V, Deckers J, Burgos EF, Lekakis J, Lindahl B, Mazzotta G, McGregor K, Morais J, Oto A, Smiseth OA, Barbera JA, Gibbs S, Hoeper M, Humbert M, Naeije R, Pepke Zaba J., Galie N, Torbicki A, Barst R, Dartevelle P, Haworth S, Higenbottam T, Olschewski H, Peacock A, Pietra G, Rubin LJ, Simonneau G, Priori SG, Garcia MA, Blanc JJ, Budaj A, Cowie M, Dean V, Deckers J, Burgos EF, Lekakis J, Lindahl B, Mazzotta G, McGregor K, Morais J, Oto A, Smiseth OA, Barbera JA, Gibbs S, Hoeper M, Humbert M, Naeije R, and Pepke-Zaba J

Subjects
Arterial Occlusive Disease, Hypertension, Pulmonary, Arterial Occlusive Diseases, Cardiovascular Agents, HIV Infections, Dyspnea, Cardiovascular Agent, Risk Factors, Humans, HIV Infection, Connective Tissue Diseases, Hemangioma, Connective Tissue Disease, Human
Abstract

No abstract available

Published
2004

32. Mutations of cardiac calsequestrin and cardiac arrhythmias: novel insights on pathogenesis and therapy

Author

Denegri M, Lodola F, Bongianino R, Avelino-Cruz JE, De Giusti VC, Curcio A, Villani L, Volpe P, Boncompagni S, Protasi F, Auricchio A, Valle G, Napolitano C, Priori SG, Denegri, M, Lodola, F, Bongianino, R, Avelino-Cruz, J, De Giusti, V, Curcio, A, Villani, L, Volpe, P, Boncompagni, S, Protasi, F, Auricchio, A, Valle, G, Napolitano, C, and Priori, S

Subjects
cardiac calsequestrin, cardiac arrhythmias, gene therapy
Published
2013

33. Viral gene transfer is able to revert phenotypical manifestation of recessive Catecholaminergic Polymorphic Ventricular Tachycardia in highly symptomatic adult knock-in mice

Author

Denegri M, Bongianino R, Lodola F, Boncompagni S, Liu N, Avelino-Cruz JE, De Giusti VC, Curcio A, Pietrangelo L, Villani L, Protasi F, Auricchio A, Napolitano C, Priori SG, Denegri, M, Bongianino, R, Lodola, F, Boncompagni, S, Liu, N, Avelino-Cruz, J, De Giusti, V, Curcio, A, Pietrangelo, L, Villani, L, Protasi, F, Auricchio, A, Napolitano, C, and Priori, S

Subjects
Viral gene transfer, recessive Catecholaminergic Polymorphic Ventricular Tachycardia, gene therapy
Published
2013

36. Paradoxical effect of increased diastolic Ca(2+) release and decreased sinoatrial node activity in a mouse model of catecholaminergic polymorphic ventricular tachycardia

Author

Neco P, Torrente AG, Mesirca P, Zorio E, Liu N, Priori SG, Napolitano C, Richard S, Benitah JP, Mangoni ME, and Gómez AM

Subjects
cardiovascular system, cardiovascular diseases
Abstract

Catecholaminergic polymorphic ventricular tachycardia is characterized by stress-triggered syncope and sudden death. Patients with catecholaminergic polymorphic ventricular tachycardia manifest sinoatrial node (SAN) dysfunction, the mechanisms of which remain unexplored.

Published
2012

37. CaMKII inhibition in human induced pluripotent stem cells derived from Catecholaminergic polymorphic ventricular tachycardia patients

Author

Lodola F, Di Pasquale E, Novelli V, Denegri M, Avelino-Cruz JE, Curcio A, Bongianino R, Leccioli V, Buonocore M, Bloise R, Condorelli G, Napolitano C, Priori SG, Lodola, F, Di Pasquale, E, Novelli, V, Denegri, M, Avelino-Cruz, J, Curcio, A, Bongianino, R, Leccioli, V, Buonocore, M, Bloise, R, Condorelli, G, Napolitano, C, and Priori, S

Subjects
CaMKII, human induced pluripotent stem cells cardiomyocytes, Catecholaminergic polymorphic ventricular tachycardia
Published
2012

38. Adeno-Associated Viral gene delivery of calsequestrin 2 protects adult calsequestrin 2-R33Q knock-in mice from developing ventricular tachycardias

Author

Denegri M, Avelino-Cruz JE, De Giusti VC, Lodola F, Curcio A, Bongianino R, Leccioli V, Boncompagni S, Protasi F, Auricchio A, Napolitano C, Priori SG, Lodola, F, Denegri, M, Avelino-Cruz, J, De Giusti, V, Curcio, A, Bongianino, R, Leccioli, V, Boncompagni, S, Protasi, F, Auricchio, A, Napolitano, C, and Priori, S

Subjects
Cardiac arrhythmias, physiology, Adeno-Associated Viral gene delivery, calsequestrin 2, ventricular tachycardias
Published
2012

39. ESC Guidelines on the management of cardiovascular diseases during pregnancy: the Task Force on the Management of Cardiovascular Diseases during Pregnancy of the European Society of Cardiology (ESC)

Author

Regitz Zagrosek, V, Blomstrom Lundqvist, C, Borghi, C, Cifkova, R, Ferreira, R, Foidart, Jm, Gibbs, Js, Gohlke Baerwolf, C, Gorenek, B, Iung, B, Kirby, M, Maas, Ah, Morais, J, Nihoyannopoulos, P, Pieper, Pg, Presbitero, P, Roos Hesselink JW, Schaufelberger, M, Seeland, U, Torracca, L, ESC Committee for Practice Guidelines, Bax, J, Auricchio, A, Baumgartner, H, Ceconi, Claudio, Dean, V, Deaton, C, Fagard, R, Funck Brentano, C, Hasdai, D, Hoes, A, Knuuti, J, Kolh, P, Mcdonagh, T, Moulin, C, Poldermans, D, Popescu, Ba, Reiner, Z, Sechtem, U, Sirnes, Pa, Torbicki, A, Vahanian, A, Windecker, S, Document, Reviewers, Aguiar, C, Al Attar, N, Garcia, Aa, Antoniou, A, Coman, I, Elkayam, U, Gomez Sanchez MA, Gotcheva, N, Hilfiker Kleiner, D, Kiss, Rg, Kitsiou, A, Konings, Kt, Lip, Gy, Manolis, A, Mebaaza, A, Mintale, I, Morice, Mc, Mulder, Bj, Pasquet, A, Price, S, Priori, Sg, Salvador, Mj, Shotan, A, Silversides, Ck, Skouby, So, Stein, Ji, Tornos, P, Vejlstrup, N, Walker, F, Warnes, C., ACS - Amsterdam Cardiovascular Sciences, and Cardiology

Subjects
Counseling, medicine.medical_specialty, Peripartum cardiomyopathy, Heart disease, Heart Diseases, Pregnancy Complications, Cardiovascular, Aortic Diseases, Coronary artery disease, Pregnancy, Internal medicine, Prenatal Diagnosis, Medicine, Humans, cardiovascular diseases, Pregnancy Complications, Infectious, Framingham Risk Score, business.industry, Contraindications, valvular heart disease, Atrial fibrillation, Abortion, Induced, Cardiovascular Agents, Prenatal Care, Venous Thromboembolism, medicine.disease, Heart failure, Cardiovascular agent, Hypertension, Cardiology, Female, Cardiology and Cardiovascular Medicine, business
Abstract

Table 1. Classes of recommendation Table 2. Levels of evidence Table 3. Estimated fetal and maternal effective doses for various diagnostic and interventional radiology procedures Table 4. Predictors of maternal cardiovascular events and risk score from the CARPREG study Table 5. Predictors of maternal cardiovascular events identified in congential heart diseases in the ZAHARA and Khairy study Table 6. Modified WHO classification of maternal cardiovascular risk: principles Table 7. Modified WHO classification of maternal cardiovascular risk: application Table 8. Maternal predictors of neonatal events in women with heart disease Table 9. General recommendations Table 10. Recommendations for the management of congenital heart disease Table 11. Recommendations for the management of aortic disease Table 12. Recommendations for the management of valvular heart disease Table 13. Recommendations for the management of coronary artery disease Table 14. Recommendations for the management of cardiomyopathies and heart failure Table 15. Recommendations for the management of arrhythmias Table 16. Recommendations for the management of hypertension Table 17. Check list for risk factors for venous thrombo-embolism Table 18. Prevalence of congenital thrombophilia and the associated risk of venous thrombo-embolism during pregnancy Table 19. Risk groups according to risk factors: definition and preventive measures Table 20. Recommendations for the prevention and management of venous thrombo-embolism in pregnancy and puerperium Table 21. Recommendations for drug use ABPM : ambulatory blood pressure monitoring ACC : American College of Cardiology ACE : angiotensin-converting enzyme ACS : acute coronary syndrome AF : atrial fibrillation AHA : American Heart Association aPTT : activated partial thromboplastin time ARB : angiotensin receptor blocker AS : aortic stenosis ASD : atrial septal defect AV : atrioventricular AVSD : atrioventricular septal defect BMI : body mass index BNP : B-type natriuretic peptide BP : blood pressure CDC : Centers for Disease Control CHADS : congestive heart failure, hypertension, age (>75 years), diabetes, stroke CI : confidence interval CO : cardiac output CoA : coarction of the aorta CT : computed tomography CVD : cardiovascular disease DBP : diastolic blood pressure DCM : dilated cardiomyopathy DVT : deep venous thrombosis ECG : electrocardiogram EF : ejection fraction ESC : European Society of Cardiology ESH : European Society of Hypertension ESICM : European Society of Intensive Care Medicine FDA : Food and Drug Administration HCM : hypertrophic cardiomyopathy ICD : implantable cardioverter-defibrillator INR : international normalized ratio i.v. : intravenous LMWH : low molecular weight heparin LV : left ventricular LVEF : left ventricular ejection fraction LVOTO : left ventricular outflow tract obstruction MRI : magnetic resonance imaging MS : mitral stenosis NT-proBNP : N-terminal pro B-type natriuretic peptide NYHA : New York Heart Association OAC : oral anticoagulant PAH : pulmonary arterial hypertension PAP : pulmonary artery pressure PCI : percutaneous coronary intervention PPCM : peripartum cardiomyopathy PS : pulmonary valve stenosis RV : right ventricular SBP : systolic blood pressure SVT : supraventricular tachycardia TGA : complete transposition of the great arteries TR : tricuspid regurgitation UFH : unfractionated heparin VSD : ventricular septal defect VT : ventricular tachycardia VTE : venous thrombo-embolism WHO : World Health Organization Guidelines summarize and evaluate all available evidence, at the time of the writing process, on a particular issue with the aim of assisting physicians in selecting the best management strategies for an individual patient, with a given condition, taking into account the impact on outcome, as well as the risk–benefit ratio of particular diagnostic or therapeutic means. Guidelines are no substitutes but are complements for textbooks and cover the European Society of Cardiology (ESC) Core Curriculum topics. Guidelines and recommendations should help the …

Published
2011

40. Single delivery of an adeno-associated viral construct to transfer the CASQ2 gene to knock-in mice affected by catecholaminergic polymorphic ventricular tachycardia is able to cure the disease from birth to advanced age

Author

Denegri, M, Bongianino, R, Lodola, F, Boncompagni, S, De Giusti, V, Avelino-Cruz, J, Liu, N, Persampieri, S, Curcio, A, Esposito, F, Pietrangelo, L, Marty, I, Villani, L, Moyaho, A, Baiardi, P, Auricchio, A, Protasi, F, Napolitano, C, Priori, S, Denegri M, Bongianino R, Lodola F, Boncompagni S, De Giusti VC, Avelino-Cruz JE, Liu N, Persampieri S, Curcio A, Esposito F, Pietrangelo L, Marty I, Villani L, Moyaho A, Baiardi P, Auricchio A, Protasi F, Napolitano C, Priori SG, Denegri, M, Bongianino, R, Lodola, F, Boncompagni, S, De Giusti, V, Avelino-Cruz, J, Liu, N, Persampieri, S, Curcio, A, Esposito, F, Pietrangelo, L, Marty, I, Villani, L, Moyaho, A, Baiardi, P, Auricchio, A, Protasi, F, Napolitano, C, Priori, S, Denegri M, Bongianino R, Lodola F, Boncompagni S, De Giusti VC, Avelino-Cruz JE, Liu N, Persampieri S, Curcio A, Esposito F, Pietrangelo L, Marty I, Villani L, Moyaho A, Baiardi P, Auricchio A, Protasi F, Napolitano C, and Priori SG

Abstract

Background-Catecholaminergic polymorphic ventricular tachycardia is an inherited arrhythmogenic disorder characterized by sudden cardiac death in children. Drug therapy is still insufficient to provide full protection against cardiac arrest, and the use of implantable defibrillators in the pediatric population is limited by side effects. There is therefore a need to explore the curative potential of gene therapy for this disease. We investigated the efficacy and durability of viral gene transfer of the calsequestrin 2 (CASQ2) wild-type gene in a catecholaminergic polymorphic ventricular tachycardia knock-in mouse model carrying the CASQ2R33Q/R33Q (R33Q) mutation. Methods and Results-We engineered an adeno-associated viral vector serotype 9 (AAV9) containing cDNA of CASQ2 wild-type (AAV9-CASQ2) plus the green fluorescent protein (GFP) gene to infect newborn R33Q mice studied by in vivo and in vitro protocols at 6, 9, and 12 months to investigate the ability of the infection to prevent the disease and adult R33Q mice studied after 2 months to assess whether the AAV9-CASQ2 delivery could revert the catecholaminergic polymorphic ventricular tachycardia phenotype. In both protocols, we observed the restoration of physiological expression and interaction of CASQ2, junctin, and triadin; the rescue of electrophysiological and ultrastructural abnormalities in calcium release units present in R33Q mice; and the lack of life-threatening arrhythmias. Conclusions-Our data demonstrate that viral gene transfer of wild-type CASQ2 into the heart of R33Q mice prevents and reverts severe manifestations of catecholaminergic polymorphic ventricular tachycardia and that this curative effect lasts for 1 year after a single injection of the vector, thus posing the rationale for the design of a clinical trial.

Published
2014

41. CaMKII inhibition prevents ventricular and supraventricular tachyarrhythmias in a murine model of recessive CPVT

Author

Curcio, A, Denegri, M, Lodola, F, Bongianino, R, Persampieri, S, Avelino-Cruz, J, Liu, N, Napolitano, C, Indolfi, C, Priori, S, Curcio A, Denegri M, Lodola F, Bongianino R, Persampieri S, Avelino-Cruz JE, Liu N, Napolitano C, Indolfi C, Priori SG, Curcio, A, Denegri, M, Lodola, F, Bongianino, R, Persampieri, S, Avelino-Cruz, J, Liu, N, Napolitano, C, Indolfi, C, Priori, S, Curcio A, Denegri M, Lodola F, Bongianino R, Persampieri S, Avelino-Cruz JE, Liu N, Napolitano C, Indolfi C, and Priori SG

Published
2014

42. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008

Author

Dickstein, K, Cohen-Solal, A, Filippatos, G, Mcmurray, Jj, Ponikowski, P, Poole-Wilson, Pa, Stromberg, A, van Veldhuisen DJ, Atar, D, Hoes, Aw, Keren, A, Mebazaa, A, Nieminen, M, Priori, Sg, Swedberg, K, Vahanian, A, Camm, J, De Caterina, R, Dean, V, Funck-Brentano, C, Hellemans, I, Kristensen, Sd, Mcgregor, K, Sechtem, U, Silber, S, Tendera, M, Widimsky, P, Zamorano, Jl, Auricchio, A, Bax, J, Bohm, M, Corra, U, Della Bella, P, Elliott, Pm, Follath, F, Gheorghiade, M, Hasin, Y, Hernborg, A, Jaarsma, T, Komajda, M, Kornowski, R, Piepoli, M, Prendergast, B, Tavazzi, L, Vachiery, Jl, Verheugt, Fw, and Zannad, F

Published
2008

43. Guidelines on diabetes, pre-diabetes, and cardiovascular diseases: full text

Author

Ryden, L, Standl, E, Bartnik, M, Van den Berghe, G, Betteridge, J, de Boer MJ, Cosentino, F, Jonsson, B, Laakso, M, Malmberg, K, Priori, S, Ostergren, J, Tuomilehto, J, Thrainsdottir, I, Vanhorebeek, I, Stramba Badiale, M, Lindgren, P, Qiao, Q, Priori, Sg, Blanc, Jj, Budaj, A, Camm, J, Dean, V, Deckers, J, Dickstein, K, Lekakis, J, Mcgregor, K, Metra, M, Morais, J, Osterspey, A, Tamargo, J, Zamorano, Jl, Deckers, Jw, Bertrand, M, Charbonnel, B, Erdmann, E, Ferrannini, Eleuterio, Flyvbjerg, A, Gohike, H, Juanatey, Jrg, Graham, I, Monteiro, Pf, Parhofer, K, Pyorala, K, Raz, I, Schernthaner, G, Volpe, M, and Wood, D.

Published
2007

44. Universal definition of myocardial infarction

Author

Thygesen, K, Alpert, Js, White, Hd, Jaffe, As, Apple, Fs, Galvani, M, Katus, Ha, Newby, Lk, Ravkilde, J, Chaitman, B, Clemmensen, Pm, Dellborg, M, Hod, H, Porela, P, Underwood, R, Bax, Jj, Beller, Ga, Bonow, R, Van Der Wall EE, Bassand, Jp, Wijns, W, Ferguson, Tb, Steg, Pg, Uretsky, Bf, Williams, Do, Armstrong, Pw, Antman, Em, Fox, Ka, Hamm, Cw, Ohman, Em, Simoons, Ml, Poole-Wilson, Pa, Gurfinkel, Ep, Lopez-Sendon, Jl, Pais, P, Mendis, S, Zhu, Jr, Wallentin, Lc, Fernandez-Aviles, F, Fox, Km, Parkhomenko, An, Priori, Sg, Tendera, M, Voipio-Pukki, Lm, Vahanian, A, Camm, Aj, De Caterina, R, Dean, V, Dickstein, K, Filippatos, G, Funck-Brentano, C, Hellemans, I, Kristensen, Sd, Mcgregor, K, Sechtem, U, Silber, S, Widimsky, P, Zamorano, Jl, Morais, J, Brener, S, Harrington, R, Morrow, D, Lim, M, Martinez-Rios, Ma, Steinhubl, S, Levine, Gn, Gibler, Wb, Goff, D, Tubaro, M, Dudek, D, and Al-Attar, N

Published
2007

45. European guidelines on cardiovascular disease prevention in clinical practice: full text. Fourth Joint Task Force of the European Society of Cardiology and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of nine societies and by invited experts)

Author

Graham, I, Atar, D, Borch Johnsen, K, Boysen, G, Burell, G, Cifkova, R, Dallongeville, J, De Backer, G, Ebrahim, S, Gjelsvik, B, Herrmann Lingen, C, Hoes, A, Humphries, S, Knapton, M, Perk, J, Priori, Sg, Pyorala, K, Reiner, Z, Ruilope, L, Sans Menendez, S, Scholte, Op, Reimer, Ws, Weissberg, P, Wood, D, Yarnell, J, Zamorano, Jl, Walma, E, Fitzgerald, T, Cooney, Mt, Dudina, A, Vahanian, A, Camm, J, De Caterina, R, Dean, V, Dickstein, K, Funck Brentano, C, Filippatos, G, Hellemans, I, Kristensen, Sd, Mcgregor, K, Sechtem, U, Silber, S, Tendera, M, Widimsky, P, Altiner, A, Bonora, Enzo, Durrington, Pn, Fagard, R, Giampaoli, S, Hemingway, H, Hakansson, J, Kjeldsen, Se, Larsen, L, Mancia, G, Manolis, Aj, Orth Gomer, K, Pedersen, T, Rayner, M, Ryden, L, Sammut, M, Schneiderman, N, Stalenhoef, Af, Tokgözoglu, L, Wiklund, O, and Zampelas

Subjects
cardiovascular disease, CVD, prevention of cardiovascular disease
Published
2007

46. Guidelines on diabetes, pre-diabetes, and cardiovascular diseases: executive summary. The Task Force on Diabetes and Cardiovascular Diseases of the European Society of Cardiology (ESC) and of the European Association for the Study of Diabetes (EASD)

Author

Rydén, L, Standl, E, Bartnik, M, Van den Berghe, G, Betteridge, J, de Boer MJ, Cosentino, F, Jönsson, B, Laakso, M, Malmberg, K, Priori, S, Ostergren, J, Tuomilehto, J, Thrainsdottir, I, Vanhorebeek, I, Stramba Badiale, M, Lindgren, P, Qiao, Q, Priori, Sg, Blanc, Jj, Budaj, A, Camm, J, Dean, V, Deckers, J, Dickstein, K, Lekakis, J, Mcgregor, K, Metra, Marco, Morais, J, Osterspey, A, Tamargo, J, Zamorano, Jl, Deckers, Jw, Bertrand, M, Charbonnel, B, Erdmann, E, Ferrannini, E, Flyvbjerg, A, Gohlke, H, Juanatey, Jr, Graham, I, Monteiro, Pf, Parhofer, K, Pyörälä, K, Raz, I, Schernthaner, G, Volpe, M, Wood, D, Task Force on Diabetes, Cardiovascular Diseases of the European Society of Cardiology, and European Association for the Study of Diabetes

Published
2007

47. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation- excutive summary

Author

Fuster, V, Ryden, LE, Cannom, DS, Crijns, HJ, Curtis, AB, Ellenbogen, KA, Halperin, JL, Le Heuzey, JY, Kay, GN, Lowe, JE, Olsson, SB, Prystowsky, EN, Tamargo, JL, Wann, S, Priori, SG, le Blanc, J-J, Budaj, A, Camm, AJ, Dean, V, Deckers, Jaap, Despres, C, Dickstein, K, Lekakis, J, McGregor, K, Metra, M, Morais, J, Osterspey, A, Zamorano, JL, Smith, SC, Jacobs, AK, Adams, CD, Anderson, JL, Antman, EM, Hunt, SA, Nishimura, R, Ornato, JP, Page, RL, Riegel, B, and Cardiology

Published
2007

48. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death--Executive Summary. A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society

Author

Zipes, Dp, Camm, Aj, Borggrefe, M, Buxton, Ae, Chaitman, B, Fromer, M, Gregoratos, G, Klein, G, Moss, Aj, Myerburg, Rj, Priori, Sg, Quinones, Ma, Roden, Dm, Silka, Mj, Tracy, C, SMITH SC JR, Jacobs, Ak, Adams, Cd, Antman, Em, Anderson, Jl, Hunt, Sa, Halperin, Jl, Nishimura, R, Ornato, Jp, Page, Rl, Riegel, B, Blanc, Jj, Budaj, A, Dean, V, Deckers, Jw, Despres, C, Dickstein, K, Lekakis, J, Mcgregor, K, Metra, Marco, Morais, J, Osterspey, A, Tamargo, Jl, and Zamorano, Jl

Published
2006

50. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: full text: a report of the American College of Cardiology/American Heart Association Task Force on practice guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in collaboration with the European Heart Rhythm Association and theHeart Rhythm Society

Author

Fuster, V, Rydén, Le, Cannom, Ds, Crijns, Hj, Curtis, Ab, Ellenbogen, Ka, Halperin, Jl, Le Heuzey JY, Kay, Gn, Lowe, Je, Olsson, Sb, Prystowsky, En, Tamargo, Jl, Wann, S, Smith SC Jr, Jacobs, Ak, Adams, Cd, Anderson, Jl, Antman, Em, Hunt, Sa, Nishimura, R, Ornato, Jp, Page, Rl, Riegel, B, Priori, Sg, Blanc, Jj, Budaj, A, Camm, Aj, Dean, V, Deckers, Jw, Despres, C, Dickstein, K, Lekakis, J, Mcgregor, K, Metra, Marco, Morais, J, Osterspey, A, Zamorano, Jl, American College of Cardiology, American Heart Association Task Force, European Society of Cardiology Committee for Practice Guidelines, European Heart Rhythm Association, and Heart Rhythm Society

Published
2006

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