Krzysztof Myrda

Prospective, multicenter validation of a clinical risk score for left atrial arrhythmogenic substrate based on voltage analysis: DR-FLASH score

BACKGROUND Left atrial (LA) low-voltage areas (LVAs) are frequently observed in patients with atrial fibrillation (AF) and may predict AF recurrence after catheter ablation. OBJECTIVE The aim of this study was to develop and validate a clinical tool to identify LVAs that are associated with AF recurrence after pulmonary vein isolation (PVI). METHODS In a cohort of 238 patients, voltage maps were created during LA procedures. LVAs were defined as areas with electrogram amplitudes <0.5 mV. On the basis of regression analysis, predictors of LA substrate were identified. These parameters were used to establish a dedicated risk score (DR-FLASH score, based on diabetes mellitus, renal dysfunction, persistent form of AF, LA diameter >45 mm, age >65 years, female sex, and hypertension). This risk score was then prospectively validated in a multicenter cohort of 180 patients. The association of the score with long-term recurrence of atrial arrhythmias after circumferential PVI was tested in a retrospective cohort of 484 patients. RESULTS The DR-FLASH score effectively identified LVA substrate (C statistic = 0.801, P < .001). In the prospective multicenter validation cohort, the predictive value of the DR-FLASH score was confirmed (C statistic = 0.767, P < .001). The probability for the presence of LA substrate increased by a factor of 2.2 (95% confidence interval [CI] 1.6-2.9, P < .001) with each point scored. Furthermore, the risk of AF recurrence after PVI increased by a factor of 1.3 (95% CI 1.1-1.5, P < .001) with every additional point and was almost 2 times higher in patients with a DR-FLASH score >3 (odds ratio 1.7, 95% CI 1.1-2.8, P = .026). CONCLUSION The DR-FLASH score may be useful to identify patients who may require extensive substrate modification instead of PVI alone.

Functional polymorphism rs710218 in the gene coding GLUT1 protein is associated with in-stent restenosis

AIM To analyze the association between in-stent restenosis (ISR) and polymorphisms in genes coding IGF-1, IGFBP3, ITGB3 and GLUT1, which play an important role in the smooth muscle cell proliferation and extracellular matrix synthesis - the main components of neointima. MATERIALS & METHODS We analyzed 265 patients who underwent bare metal stent implantation. RESULTS The differences in the occurrence of ISR between genotypes of the analyzed polymorphisms in the IGF-1, IGFBP3 and ITGB3 were not statistically significant. The T/T genotype of the rs710218 polymorphism in the GLUT1 (SLC2A1) gene was more common in the ISR group compared with non-ISR patients (81.1 vs 64.8%; p = 0.02). In a multivariable model the A/A and A/T genotype remained correlated with lower occurrence of ISR (odds ratio: 0.45; 95% CI: 0.21-0.97; p = 0.03). CONCLUSION The rs710218 polymorphism in the gene coding GLUT1 protein is a novel risk factor for ISR.

Atrioventricular nodal re-entrant tachycardia mimicking ventricular tachycardia on the surface electrocardiogram.

Address for correspondence: Dr. Adam J. Wojtaszczyk, Third Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, ul. M. Curie-Skłodowskiej 9, 41–800 Zabrze, Poland, e-mail: adam.wojtaszczyk@gmail.com Conflict of interest: none declared Kardiologia Polska Copyright

Hybrid ablation in a patient with persistent, long-standing atrial fibrillation after left-sided pneumonectomy

13rd Department of Cardiology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Silesian Centre for Heart Diseases in Zabrze, Zabrze, Poland 2Department of Cardiac, Vascular, and Endovascular Surgery and Transplantology, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia, Katowice, Silesian Centre for Heart Diseases in Zabrze, Zabrze, Poland *Both authors contributed equally.

The influence of ablation power reduction associated with oesophagus location on pulmonary vein isolation results in patients with paroxysmal atrial fibrillation: six-month follow-up

BACKGROUND Catheter ablation of atrial fibrillation (AF) could be associated with a thermal oesophageal (EO) injury. To avoid this complication intraluminal EO temperature monitoring and ablation power reduction at the areas with excessive heating could be used. However, the reduced energy could limit the ablation lesion depth, without creation of lasting transmural scar and influence on long-term ablation results. AIM The primary goal was to evaluate the homogeneity of forced ablation power reduction due to excessive EO heating in different parts of the left atrium. The secondary goal was to assess the influence of power reduction in different EO locations on long-term AF recurrence. METHODS We examined retrospectively 109 consecutive patients with symptomatic, medically refractory paroxysmal AF, who underwent pulmonary vein isolation using radiofrequency ablation. In 40.4% of the patients the EO course was central (group B) left atrium posterior wall, in 31.2% it was left sided (group A), and in 28.4% it was right sided (group C). RESULTS The maximal measured temperature (41.0 ± 1.0 vs. 39.2 ± 1.5 vs. 40.6 ± 0.7°C) and forced ablation power (15.9 ± 5.6 vs. 23.5 ± 6.1 vs. 17.4 ± 5.7 W) differed significantly according to the EO course (A, B, C, respectively). In six-month follow-up 76.15% of patients were free of arrhythmias. There was no statistically significant difference between groups (A-C) regarding the AF recurrence rate: 32.4% vs. 20.5% vs. 19.4% (p = 0.37). CONCLUSIONS The maximal intraluminal EO temperatures and the necessary level of power reduction during AF ablation are inhomogeneous in different parts of the left atrium, but they are not associated with different six-month follow-up results.

Clinical and laboratory determinants of low serum level of 25-hydroxyvitamin D during escalation of pharmacotherapy in heart failure patients.

Introduction The activation of the renin-angiotensin-aldosterone (RAA) system is a main element of the pathophysiology of chronic heart failure (CHF), determining its symptoms and prognosis. Vitamin D is an RAA inhibitor, and its deficiency frequently accompanies CHF. The factors determining the concentration of 25-hydroxyvitamin D [25(OH)D] in CHF are not well understood, although an association has been suggested between the deficiency and the advancement of CHF. Also unknown is the influence of therapeutic escalation using recommended agents on the serum level of 25(OH)D. The aim of this study was to examine the incidence of abnormal 25(OH)D concentrations in CHF patients and to establish the clinical and laboratory determinants of low activity of this metabolite. Material and methods The retrospective analysis included the data of 412 CHF patients not receiving optimal pharmacological treatment who were initially in NYHA (New York Heart Association) class III or IV. Over the period of 3 months the therapy was escalated until reaching maximum tolerated doses or those recommended by the current guidelines. After optimizing the therapy, the incidence of 25(OH)D deficiency (< 30 ng/ml) and insufficiency (< 20 ng/ml) was established, and clinical and laboratory determinants for these abnormal concentrations were analyzed. Results Normal serum level, insufficiency, and deficiency of 25(OH)D were observed in, respectively, 41.5%, 26.0% and 32.5% of patients. The NYHA class improved by at least 1 class in 63.6% of patients, remained unchanged in 32.8% of patients, and deteriorated in 3.6% of patients. In multivariables analysis, low availability of natural ultraviolet B (UVB) radiation, loss of body mass during the CHF, higher concentrations of phosphates and albumins, and the presence of diabetes increased the risk of 25(OH)D deficiency, while higher concentrations of uric acid reduced this risk. In patients with a positive response to therapy, the concentration of 25(OH)D was borderline significantly higher (p = 0.055), while insufficiency and deficiency were less frequent (p = 0.02) than in patients without a treatment response, but this pertained only to patients with higher exposure to UVB. These differences were not observed in patients with low UVB exposure. Conclusions The concentration of 25(OH)D in CHF patients is not associated with the advancement of the disease, but is strongly determined by the potential availability of UVB radiation. A positive response to therapy increases the concentration of 25(OH)D only in the case of high UVB exposure; other determinants of 25(OH)D level include the patients metabolic profile and the presence of diabetes.