In this contemporary study, overall serious adverse events after AM were lower than previously reported. However, patients with left ventricular ejection fraction <50%, ventricular arrhythmias, or low cardiac output syndrome at presentation were at higher risk compared with uncomplicated cases that had a benign prognosis and low risk of subsequent left ventricular systolic dysfunction.

Abstract-In rats, an increase in heart rate by pacing is accompanied by progressive large-artery stiffening. Whether this is also the case in humans is unknown. We enrolled 20 patients who were chronically implanted with a pacemaker because of atrioventricular block or sick sinus syndrome. Arterial distensibility was measured by an echo-tracking device. In 10 patients, the evaluation was performed on the radial artery by using continuous finger blood pressure measurements, whereas in the remaining 10 patients, the common carotid artery was studied with a semiautomatic measure of brachial artery blood pressure. Diastolic diameter, systodiastolic diameter change, and distensibility were obtained at baseline (heart rate 63Ϯ2 beats/min) and after atrial and ventricular sequential pacing at a heart rate of 90 and 110 beats/min. At baseline, the diameter was 7.8Ϯ0.3 mm in the carotid artery and 2.4Ϯ0.1 mm in the radial artery; the respective systodiastolic diameter change values were 375.4Ϯ31.0 and 55.9Ϯ9.0 (m) and the distensibility values were 1.4Ϯ0.1 and 0.7Ϯ0.1 (1/mm Hg 10 Ϫ3 ). Blood pressure and diameter were not significantly modified by increasing heart rate, which markedly modified systodiastolic diameter change and distensibility. In the radial artery, distensibility was reduced by 47% (PϽ0.05) at a heart rate of 90 beats/min with no further reduction at 110 beats/min. In the carotid artery, distensibility was reduced by 20% at a heart rate of 90 beats/min (PϽ0.05) with a further reduction at 110 beats/min (45%, PϽ0.05). These data provide the first evidence in humans that acute increases in heart rate markedly affect arterial distensibility and that this occurs in both large-and middle-size muscle arteries within the range of "normal" heart rate values. Key Words: arterial stiffness Ⅲ heart rate Ⅲ risk factors Ⅲ human S tudies performed in rats have shown that when heart rate (HR) is increased by pacing, carotid and femoral artery distensibilities (Dist) are reduced. 1 This suggests that HR might be one of the factors that modulates arterial mechanical properties and thus, potentially participates in their abnormality in several conditions and diseases.Little evidence exists, however, as to whether HR plays a similar role in humans. This is because although a weak, positive correlation has been reported to exist between HR and pulse wave velocity in a cross-sectional survey of normotensive and hypertensive individuals, 2 studies measuring arterial stiffness during HR changes have given conflicting results. [3][4][5][6] The purpose of the present study was to fill this gap by measuring arterial Dist in response to pacing-induced increases in HR. Dist was measured both in a carotid (CA) and a radial (RA) artery because previous studies had shown that large elastic and middle-size arteries behave differently in a number of circumstances, 7-10 including those elicited in animals by HR changes. 1,11 Care was taken to exclude subjects with uncontrolled blood pressure (BP) values, hypercholesterolemia, diabetes, a...

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...

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