Publications by authors named "Michał Gibiński"

3 Publications

  • Page 1 of 1

Survival of patients with pacing-induced cardiomyopathy upgraded to CRT does not depend on defibrillation therapy.

Pacing Clin Electrophysiol 2020 05 15;43(5):471-478. Epub 2020 Apr 15.

Department of Electrocardiology and Heart Failure, Medical University of Silesia, Katowice, Poland.

Background: Permanent right ventricular pacing (RVP) results in cardiac dyssynchrony that may lead to heart failure and may be an indication for the use of cardiac resynchronization therapy (CRT). The study aimed to evaluate predictors of outcomes in patients with pacing-induced cardiomyopathy (PICM) if upgraded to CRT.

Methods: One hundred fifteen patients, 75.0 years old (IQR 67.0-80.0), were upgraded to CRT due to the decline in left ventricle ejection fraction (LVEF) caused by the long-term RVP. A retrospective analysis was performed using data from hospital and outpatient clinic records and survival data from the National Health System.

Results: The prior percentage of RVP was 100.0% (IQR 97.0-100.0), with a QRS duration of 180.0 ms (IQR 160.0-200.0). LVEF at the time of the upgrade procedure was 27.0% (IQR 21.0-32.75). The mean follow-up was 980 ± 522 days. The primary endpoint, death from any cause, was met by 26 (22%) patients. Age > 82 years (HR 5.96; 95% CI 2.24-15.89; P = .0004) and pre-CRT implantation LVEF < 20% (HR 5.63; 95%CI 2.19-14.47; P = .0003), but neither the cardioverter-defibrillator (ICD) implantation (HR 1.00; 95%CI 0.45-2.22; P = 1.00), nor the presence of atrial fibrillation (HR 1.22; 95%CI 0.56-2.64; P = .62), were independently associated with all-cause mortality.

Conclusion: Advanced age and an extremely low LVEF, but neither the presence of atrial fibrillation nor implanting an additional high voltage lead, influence the all-cause mortality in patients after long-term RVP, when upgraded to CRT.
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May 2020

[How to avoid cardiovascular consequences of the obstructive sleep apnea syndrome?]

Wiad Lek 2018;71(6):1254-1261

1 Oddział Elektrokardiologii, Górnośląskie Centrum Medyczne Im. Prof. Leszka Gieca Śląskiego Uniwersytetu Medycznego W Katowicach, Katowice, Polska, Klinika Elektrokardiologii I Niewydolności Serca Śląskiego Uniwersytetu Medycznego W Katowicach, Katowice, Polska.

Obstructive sleep apnea syndrome (OSAS) is caused by periodical upper airway occlusion during sleep resulting in snoring, episodes of apnea and excessive daytime sleepiness. OSAS is a risk factor for hypertension, arrhythmias, conduction disorders as well as stroke, coronary artery disease, chronic heart failure and pulmonary hypertension. Early polygraphy and polysomnography and continuous positive airway pressure (CPAP) treatment reduce risks of cardiovascular diseases (CVD) in patients with OSAS.
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June 2019

Dyssynchrony and the risk of ventricular arrhythmias.

JACC Cardiovasc Imaging 2013 Apr;6(4):432-44

University of Rochester Medical Center, Rochester, New York, USA.

Objectives: The aim of our study was to evaluate the relationship between left ventricular (LV) dyssynchrony and the risk of ventricular tachycardia (VT) or ventricular fibrillation (VF) in patients enrolled in the MADIT-CRT (Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy) trial.

Background: Intraventricular mechanical dyssynchrony might be an important factor in ventricular arrhythmogenesis by enhancing electrical heterogeneity in heart failure patients. The effects of dyssynchrony have not yet been evaluated in a large cohort of implantable cardioverter-defibrillator (ICD) and cardiac resynchronization therapy with defibrillator (CRT-D) patients.

Methods: LV dyssynchrony was measured at baseline and at 12-months by speckle-tracking echocardiography, defined as the standard deviation of time to peak systolic strain in 12 LV myocardial segments. The endpoint was the first VT/VF/death or VT/VF. LV dyssynchrony was evaluated in 764 left bundle branch block (LBBB) patients and in 312 non-LBBB patients.

Results: Baseline LV dyssynchrony was not predictive of VT/VF/death or VT/VF in LBBB or non-LBBB patients in either treatment arm. In CRT-D patients with LBBB, improvement in LV dyssynchrony over a year was associated with significantly lower incidence of VT/VF/death (p < 0.001) and VT/VF (p < 0.001) compared to ICD patients and to CRT-D patients with unchanged or worsening dyssynchrony. Among LBBB patients, 15% decrease in LV dyssynchrony was associated with lower risk of VT/VF/death (hazard ratio: 0.49, 95% confidence interval: 0.24 to 0.99, p = 0.049) and VT/VF (hazard ratio: 0.30, 95% confidence interval: 0.12 to 0.77, p = 0.009) as compared to ICD patients. Patients without LBBB receiving CRT-D did not show reduction in VT/VF/death or in VT/VF in relation to improving dyssynchrony when evaluating cumulative event rates or risk of events.

Conclusions: Baseline LV dyssynchrony did not predict VT/VF/death or VT/VF in mild heart failure patients with or without LBBB. CRT-induced improvement of LV dyssynchrony was associated with significant reduction of ventricular arrhythmias in patients with LBBB.
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April 2013