Abstract-Evidence is available that in heart failure, cardiac resynchronization therapy by biventricular pacing improves myocardial function and exercise capacity. Whether this is accompanied by a sustained inhibition of heart failure-dependent sympathoexcitation is uncertain. In 11 heart failure patients (meanϮSEM age, 68.4Ϯ1.5 years) in New York Heart Association (NYHA) class III and IV under medical treatment with an intraventricular conduction delay (QRS duration Ն130 ms), with a markedly depressed left ventricular ejection fraction, and undergoing implantation of a biventricular pacemaker, we measured beat-to-beat blood pressure and muscle sympathetic nerve traffic. Measurements, which also included echocardiographic and clinical variables, were performed before and Ϸ10 weeks after successful resynchronization therapy. Ten age-and NYHA class-matched heart failure patients who were under medical treatment for the same time period served as controls. Long-term resynchronization therapy improved cardiac function and caused a significant increase in systolic blood pressure coupled with an improvement in maximal oxygen consumption and exercise capacity. These effects were coupled with a significant and marked reduction in sympathetic nerve traffic when expressed both as burst frequency over time (44.1Ϯ3.6 vs 30.7Ϯ3.0 bs/min, Ϫ30.5%, PϽ0.02) and as burst frequency corrected for heart rate (68.3Ϯ5.9 vs 47.3Ϯ4.3 bs/100 beats, Ϫ32.1%, PϽ0.02). No significant change in the aforementioned parameters was seen in the control group. These data provide the first direct evidence that in severe heart failure, resynchronization therapy exerts a marked and sustained sympathoinhibition. Because in heart failure sympathetic overactivity adversely affects prognosis, this may have important clinical implications. Key Words: electrical stimulation Ⅲ heart failure Ⅲ sympathetic nervous system Ⅲ autonomic nervous system C ardiac resynchronization therapy (CRT) by biventricular pacing exerts favorable effects in patients with congestive heart failure (CHF) and intraventricular conduction delay in whom it improves symptoms, functional class, and quality of life with an increase in exercise tolerance. [1][2][3] Whether the favorable effects include a reduction in the enhanced sympathetic cardiovascular drive characterizing CHF 4 -6 is uncertain, however, because the studies that have addressed this issue so far had either methodological or design limitations. That is, they assessed adrenergic function only indirectly by plasma norepinephrine assay 3,7 or used direct measurement of muscle sympathetic nerve activity (MSNA) that was confined, however, to the acute phase of biventricular pacing. 8,9 The present study was designed to determine the longterm sympathetic effects of CRT in CHF patients with an intraventricular conduction delay by using a design similar to the 1 used in the MIRACLE trial, which had shown CRT to be accompanied by a sustained improvement in patient clinical status. 3 Sympathetic activity was quantified both indire...

Congestive heart failure is characterized by a reduction of Dist of large-elastic and middle-sized muscular arteries. The reduction of large-elastic artery Dist is related to the CHF severity. These alterations can be reversed by drugs, effectively interfering with the renin-angiotensin system either at the ACE or at the angiotensin receptor level.

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Abstract-Congestive heart failure (CHF) is associated with an impaired flow-mediated vasodilation that reflects an impaired endothelial function. Limited information is available, however, on whether and to what extent this impairment is improved by pharmacological or nonpharmacological treatment. We measured radial artery diameter and blood flow by an echo-tracking Doppler device both at baseline and after 4 minutes of hand ischemia, which increases diameter through NO secretion mediated by an increase in flow and shear stress. Data were collected from 44 CHF patients (New York Heart Association class I to III) under standard treatment (diuretic, digitalis, and enalapril, 20 mg/d), in whom CHF severity was assessed by a cardiopulmonary stress test, and from 16 age-and sex-matched controls. CHF patients were then randomized to maintain for (A) 2 months of standard treatment (nϭ11), (B) treatment with double the ACE inhibitor dose (nϭ11), (C) standard treatment with an angiotensin II antagonist (losartan, 50 mg/d; nϭ11), or (D) standard treatment with bicycle training for 30 minutes, 3 times a week (nϭ11). At baseline, radial artery diameter and flow were similar in CHF patients and controls; CHF patients had a modest although significant impairment in flow increase (Ϫ36%) and a striking impairment (Ϫ78%) in diameter increase following the 4 minutes of ischemia. After 2 months, baseline diameter and flow remained unaltered in the 4 groups. After the 4 minutes of ischemia, radial artery flow and diameter increased as before in the group under standard treatment (A), whereas in the other 3 groups, the increase was significantly (PϽ0.05) and, for diameter, markedly (B, 83%; C, 92%; and D, 95%) greater. The vasodilatation induced by trinitroglycerin was similar in CHF and control subjects and not affected by treatments. In CHF, radial artery shows a marked reduction in flow-mediated vasodilation, reflecting impairment of endothelial function. This impairment can be markedly improved by treatments that effectively block the renin-angiotensin system either at ACE or at ACE plus angiotensin receptor level. This is the case also with nonpharmacological treatment of

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