Substrate mapping of the left atrium in persistent atrial fibrillation: spatial correlation of localized complex conduction patterns in global charge-density maps to low-voltage areas in 3D contact bipolar voltage maps.

PURPOSE: This study aimed to investigate the spatial relationship between low-voltage areas (LVAs) in bipolar voltage mapping (BVM) and localized complex conduction (LCC)-cores in a global, non-contact, charge-density-based imaging, and mapping system (AcM). METHODS: Patients with history of index PVI for PsAF and scheduled for a repeat ablation procedure for recurrence of the same arrhythmia were enrolled between August 2018 and February 2020. All patients underwent both substrate mappings of the left atrium (LA) with the CARTO 3D map-ping system and with AcM. RESULTS: Ten patients where included in our analysis. All presented with persistency of PVI in all veins at the moment of repeat procedure. There was no linear relationship in BVM maps between SR and CSd (correlation coefficient 0.31 ± 0.15), SR and CSp (0.36 ± 0.12) and CSd and CSp (0.43 ± 0.10). The % overlap of localized irregular activation (LIA), localized rotational activation (LRA) and Focal (F) regions with LVA was lower at 0.2 mV compared to 0.5 mV (4.97 ± 7.39%, 3.27 ± 5.25%, 1.09 ± 1.92% and 12.59 ± 11.81%, 7.8 ± 9.20%, 4.62 ± 5.27%). Sensitivity and specificity are not significantly different when comparing composite maps with different LVA cut-offs. AURC was 0.46, 0.48, and 0.39 for LIA, LRA, and Focal, respectively. CONCLUSION: Due to wave front direction dependency, LVAs mapped with BVM in sinus rhythm and during coronary sinus pacing only partially overlap in patients with PsAF. LCC-cores mapped during PsAF partially co-localize with LVAs.

Dyslipidaemia in type II diabetic mice does not aggravate contractile impairment but increases ventricular stiffness.

AIMS: Type II diabetes, often associated with abdominal obesity, frequently leads to heart failure. Clinical and epidemiological evidence suggests that supplemental dyslipidaemia and hypertension, as clustered in the metabolic syndrome, aggravate the cardiovascular outcome. The differential impact of type II diabetes and the metabolic syndrome on left ventricular function, however, remains incompletely defined. METHODS AND RESULTS: We studied left ventricular function in vivo using pressure-volume analysis in obese diabetic mice with leptin deficiency (ob/ob) and obese diabetic dyslipidemic mice with combined leptin and low-density lipoprotein-receptor deficiency (DKO). ob/ob and DKO mice developed a diabetic cardiomyopathy, characterized by impaired contractility and relaxation, from the age of 24 weeks onwards. This was-at least partially-explained by increased apoptosis and disturbed Ca(2+) reuptake in the sarcoplasmic reticulum (SR) in both mouse models. DKO, but not ob/ob, developed increased end-diastolic ventricular stiffness, paralleled by increased left ventricular myocardial fibrosis. Cardiac output was preserved in ob/ob mice by favourable loading conditions, whereas it decreased in DKO mice. CONCLUSIONS: Type II diabetes in mice leads to impaired contractility and relaxation due to disturbed Ca(2+) reuptake in the SR, but only when dyslipidaemia and hypertension are superimposed does vascular-ventricular stiffening increase and left ventricular myocardial fibrosis develop.