Sustained sympathoinhibitory effects of cardiac resynchronization therapy in severe heart failure

Guido Grassi, Antonio Vincenti, Roberta Brambilla, Fosca Quarti Trevano, Raffaella Dell'Oro, Antonio Cirò, Giuseppe Trocino, Antonella Vincenzi, Giuseppe Mancia

Research output: Contribution to journalArticle

29 Citations (Scopus)

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 (mean±SEM age, 68.4±1.5 years) in New York Heart Association (NYHA) class III and IV under medical treatment with an intraventricular conduction delay (QRS duration ≥130 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 ≈10 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 (44.1±3.6 vs 30.7±3.0 bs/min, -30.5%, P<0.02) and as burst frequency corrected for heart rate (68.3±5.9 vs 47.3±4.3 bs/100 beats, -32.1%, P<0.02). 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.

Original languageEnglish
Pages (from-to)727-731
Number of pages5
JournalHypertension
Volume44
Issue number5
DOIs
StatePublished - Nov 1 2004
Externally publishedYes

Fingerprint

Cardiac Resynchronization Therapy
Heart Failure
Blood Pressure
Exercise
Therapeutics
Oxygen Consumption
Stroke Volume
Heart Rate
Muscles
Control Groups

Keywords

  • Autonomic nervous system
  • Electrical stimulation
  • Heart failure
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Sustained sympathoinhibitory effects of cardiac resynchronization therapy in severe heart failure. / Grassi, Guido; Vincenti, Antonio; Brambilla, Roberta; Trevano, Fosca Quarti; Dell'Oro, Raffaella; Cirò, Antonio; Trocino, Giuseppe; Vincenzi, Antonella; Mancia, Giuseppe.

In: Hypertension, Vol. 44, No. 5, 01.11.2004, p. 727-731.

Research output: Contribution to journalArticle

Grassi, G, Vincenti, A, Brambilla, R, Trevano, FQ, Dell'Oro, R, Cirò, A, Trocino, G, Vincenzi, A & Mancia, G 2004, 'Sustained sympathoinhibitory effects of cardiac resynchronization therapy in severe heart failure', Hypertension, vol. 44, no. 5, pp. 727-731. https://doi.org/10.1161/01.HYP.0000144271.59333.a7
Grassi, Guido ; Vincenti, Antonio ; Brambilla, Roberta ; Trevano, Fosca Quarti ; Dell'Oro, Raffaella ; Cirò, Antonio ; Trocino, Giuseppe ; Vincenzi, Antonella ; Mancia, Giuseppe. / Sustained sympathoinhibitory effects of cardiac resynchronization therapy in severe heart failure. In: Hypertension. 2004 ; Vol. 44, No. 5. pp. 727-731.
@article{b0e7b81d30294358a58331e09e004b8d,
title = "Sustained sympathoinhibitory effects of cardiac resynchronization therapy in severe heart failure",
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 (mean±SEM age, 68.4±1.5 years) in New York Heart Association (NYHA) class III and IV under medical treatment with an intraventricular conduction delay (QRS duration ≥130 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 ≈10 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 (44.1±3.6 vs 30.7±3.0 bs/min, -30.5{\%}, P<0.02) and as burst frequency corrected for heart rate (68.3±5.9 vs 47.3±4.3 bs/100 beats, -32.1{\%}, P<0.02). 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.",
keywords = "Autonomic nervous system, Electrical stimulation, Heart failure, Sympathetic nervous system",
author = "Guido Grassi and Antonio Vincenti and Roberta Brambilla and Trevano, {Fosca Quarti} and Raffaella Dell'Oro and Antonio Cir{\`o} and Giuseppe Trocino and Antonella Vincenzi and Giuseppe Mancia",
year = "2004",
month = "11",
day = "1",
doi = "10.1161/01.HYP.0000144271.59333.a7",
language = "English",
volume = "44",
pages = "727--731",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Sustained sympathoinhibitory effects of cardiac resynchronization therapy in severe heart failure

AU - Grassi, Guido

AU - Vincenti, Antonio

AU - Brambilla, Roberta

AU - Trevano, Fosca Quarti

AU - Dell'Oro, Raffaella

AU - Cirò, Antonio

AU - Trocino, Giuseppe

AU - Vincenzi, Antonella

AU - Mancia, Giuseppe

PY - 2004/11/1

Y1 - 2004/11/1

N2 - 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 (mean±SEM age, 68.4±1.5 years) in New York Heart Association (NYHA) class III and IV under medical treatment with an intraventricular conduction delay (QRS duration ≥130 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 ≈10 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 (44.1±3.6 vs 30.7±3.0 bs/min, -30.5%, P<0.02) and as burst frequency corrected for heart rate (68.3±5.9 vs 47.3±4.3 bs/100 beats, -32.1%, P<0.02). 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.

AB - 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 (mean±SEM age, 68.4±1.5 years) in New York Heart Association (NYHA) class III and IV under medical treatment with an intraventricular conduction delay (QRS duration ≥130 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 ≈10 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 (44.1±3.6 vs 30.7±3.0 bs/min, -30.5%, P<0.02) and as burst frequency corrected for heart rate (68.3±5.9 vs 47.3±4.3 bs/100 beats, -32.1%, P<0.02). 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.

KW - Autonomic nervous system

KW - Electrical stimulation

KW - Heart failure

KW - Sympathetic nervous system

UR - http://www.scopus.com/inward/record.url?scp=7244239085&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=7244239085&partnerID=8YFLogxK

U2 - 10.1161/01.HYP.0000144271.59333.a7

DO - 10.1161/01.HYP.0000144271.59333.a7

M3 - Article

VL - 44

SP - 727

EP - 731

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 5

ER -