{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T20:20:34Z","timestamp":1792268434471,"version":"4.4.0"},"reference-count":32,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Arrhythmia and Electrophysiology"],"published-print":{"date-parts":[[2024,12]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Among inherited cardiomyopathies involving the left ventricle, whether dilated or not, certain genotypes carry a well-established arrhythmic risk, notably manifested as sustained monomorphic ventricular tachycardia (SMVT). Nonetheless, the precise localization and electrophysiological profile of this substrate remain undisclosed across different genotypes.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>Patients diagnosed with cardiomyopathy and left ventricle involvement due to high-risk genetic variants and SMVT treated by electrophysiological study were recruited from 18 European\/US centers. Electrophysiological study, imaging, and outcomes data after ablation were assessed in relation to genotype.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              Seventy-one patients were included (49.6 Q1\u2013Q3 [40\u201360] years, 76% men). They were divided into 4 groups according to the affected protein: desmosomal (\n              <jats:italic toggle=\"yes\">DSP<\/jats:italic>\n              ,\n              <jats:italic toggle=\"yes\">PKP2<\/jats:italic>\n              ,\n              <jats:italic toggle=\"yes\">DSG2<\/jats:italic>\n              , and\n              <jats:italic toggle=\"yes\">DSC2<\/jats:italic>\n              ), nuclear membrane (\n              <jats:italic toggle=\"yes\">LMNA<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">TMEM43<\/jats:italic>\n              ), cytoskeleton (\n              <jats:italic toggle=\"yes\">FLNC<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">DES<\/jats:italic>\n              ), and sarcoplasmic reticulum (\n              <jats:italic toggle=\"yes\">PLN<\/jats:italic>\n              ). Desmosomal genes,\n              <jats:italic toggle=\"yes\">TMEM43<\/jats:italic>\n              , and\n              <jats:italic toggle=\"yes\">PLN<\/jats:italic>\n              were associated with biventricular disease, while variants in\n              <jats:italic toggle=\"yes\">LMNA<\/jats:italic>\n              and cytoskeleton genes had predominant left ventricle involvement (\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              =0.001). The location of the clinical-SMVT substrate was significantly different based on genotype (\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              =0.005).\n              <jats:italic toggle=\"yes\">DSP<\/jats:italic>\n              and cytoskeleton genes presented SMVTs with right bundle branch block morphology, which origin was identified in the inferolateral segments of the left ventricle. The other desmosomal genes (\n              <jats:italic toggle=\"yes\">PKP2<\/jats:italic>\n              and\n              <jats:italic toggle=\"yes\">DSG2<\/jats:italic>\n              ), along with\n              <jats:italic toggle=\"yes\">TMEM43<\/jats:italic>\n              , showed SMVTs with left bundle branch block morphology and predominantly right ventricular substrate. In contrast,\n              <jats:italic toggle=\"yes\">LMNA<\/jats:italic>\n              substrate was mainly observed in the interventricular septum. During a median of 26 Q1\u2013Q3 (10.6\u201365) months, 27% of patients experienced recurrences of clinical SMVT with differences between genotypes (log-rank 0.016). Nuclear membrane genes demonstrated the highest recurrence rate compared with desmosomal genes (hazard ratio, 4.56 [95% CI, 1.5\u201313.8]).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>The anatomic substrate of SMVTs shows a strong correlation with the underlying genotype, electrocardiographic morphology, and recurrence rate. Particularly, patients with nuclear membrane gene variants have a significantly higher recurrence rate compared with those with desmosomal gene variants.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circep.124.013145","type":"journal-article","created":{"date-parts":[[2024,11,29]],"date-time":"2024-11-29T10:01:03Z","timestamp":1732874463000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":10,"title":["Electrophysiological Phenotype-Genotype Study of Sustained Monomorphic Ventricular Tachycardia in Inherited, High Arrhythmic Risk, Left Ventricular Cardiomyopathy"],"prefix":"10.1161","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2997-2391","authenticated-orcid":true,"given":"Eva","family":"Cabrera-Borrego","sequence":"first","affiliation":[{"name":"Instituto de Investigaci\u00f3n Biosanitaria ibs.GRANADA and Virgen de las Nieves University Hospital, Cardiology Department, Granada, Spain (E.C.-B., F.J.B.-J., P.J.S.-M., M.M.-L., M.A.-L., R.M.-R., L.T.-S., J.J.-J.)."},{"name":"University of Granada, Spain (E.C.-B., M.A.-L., J.J.-J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0325-7349","authenticated-orcid":true,"given":"Francisco J.","family":"Berm\u00fadez-Jim\u00e9nez","sequence":"additional","affiliation":[{"name":"Instituto de Investigaci\u00f3n Biosanitaria ibs.GRANADA and Virgen de las Nieves University Hospital, Cardiology Department, Granada, Spain (E.C.-B., F.J.B.-J., P.J.S.-M., M.M.-L., M.A.-L., R.M.-R., L.T.-S., J.J.-J.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3432-070X","authenticated-orcid":true,"given":"Alessio","family":"Gasperetti","sequence":"additional","affiliation":[{"name":"Division of Cardiology, School of Medicine, Johns Hopkins University, Baltimore, MD 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