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

Arrhythmia Clinic Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Tlalpan, México 14000 DF, Mexico.
Cardiology journal (Impact Factor: 1.15). 01/2008; 15(3):261-7.
Source: PubMed

ABSTRACT 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.
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.
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.
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.

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    ABSTRACT: During the past 50 years there have been vast improvements in the treatment of chronic heart failure (CHF). CHF was initially considered to be a cardio-renal problem - an acute disorder leading to volume expansion and oedema. Diuretics and digitalis were the only available treatments. Subsequently, CHF was considered to be the result of both myocardial dysfunction and increased tone in the pulmonary and peripheral circulations. The presence of peripheral vasoconstriction suggested that circulatory failure was an important component of the disease, and vasodilators were added to therapy. In the more recent past, experimental and clinical studies have demonstrated that CHF is also characterized by increased neurohormonal activation. This has led to the use of angiotensin-converting enzyme inhibitors, beta-blockers and spironolactone in CHF. Increased neurohormonal activity is now recognized as one of the major pathophysiological factors that contribute to the progression of CHF. Activation of neurohormonal mechanisms is only compensatory in the short term; chronic activation produces detrimental changes in the myocardirun, kidneys and peripheral vasculature. This article provides an overview of the key neurohormonal systems that are activated in CHF.