Vol 15, No 3 (2008)
Original articles
Published online: 2008-04-14

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Changes in the arrhythmic profile of patients treated for heart failure are associated with modifications in their myocardial perfusion conditions

Enrique Asensio-Lafuente, Lilia Castillo-Martínez, Arturo Orea-Tejeda, Rubén Silva-Tinoco, Joel Dorantes-García, René Narváez-David, Verónica Rebollar-González
Cardiol J 2008;15(3):261-267.


Background: Heart failure (HF) patients can benefit from a proper RS. We had observed that they show an increase in the number of arrhythmias during the first year of pharmacological treatment.
Methods: We carried out a prospective observational study in which patients in an HF Clinic were included when they had follow-up Holter monitoring. Patients also had a baseline myocardial perfusion scan (Tc99 sestaMIBI/dypiridamole) and a control scan.
Results: We included 90 patients with follow-up Holter and 35 with scintigraphy, for analysis. Fifty-six (62.2%) were men and the average age was 60.8 ± 14.6 years. Follow-up periods were divided by six-month intervals up to 18 months or more, an increase in premature ventricular contractions (PVCs) occurred in the six-month to one-year period (1915.4 ± ± 4686.9 vs. 2959 ± 6248.1, p = 0.09). In the one-year to 18-month control, PVCs went from 781.6 ± 1082.4 to 146.9 ± 184.1, p = 0.05. The increase in PVCs correlated with a reduction in scintigraphy-detected ischemic territories, 5.64 ± 5.9 vs. 3.18 ± 3 (p = 0.1) and a gain in those showing a reverse redistribution pattern (0.18 ± 0.6 vs. 2.09 ± 4.01, p = 0.1). Necrotic territories and time domain heart rate variability did not show significant changes.
Conclusions: PVCs increase during the first year of HF treatment, and then they tend to diminish and stabilize. These changes seem to correlate with changes in the perfusion state of the patient. While ischemic territories decrease, reverse redistribution increases, showing that endothelial dysfunction could have a relevant role in arrhythmia generation, possibly because of membrane instability of recovered hibernating myocardium. (Cardiol J 2008; 15: 261-267)

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