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Titolo:
Vagal neurostimulation in patients with coronary artery disease
Autore:
Zamotrinsky, AV; Kondratiev, B; de Jong, JW;
Indirizzi:
Inst Cardiol TSC RAMS, Div Neurocardiol, Tomsk 634012, Russia Inst CardiolTSC RAMS Tomsk Russia 634012 ocardiol, Tomsk 634012, Russia Erasmus Univ, Thoraxctr, NL-3000 DR Rotterdam, Netherlands Erasmus Univ Rotterdam Netherlands NL-3000 DR DR Rotterdam, Netherlands
Titolo Testata:
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
fascicolo: 1-2, volume: 88, anno: 2001,
pagine: 109 - 116
SICI:
1566-0702(20010412)88:1-2<109:VNIPWC>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYOCARDIAL-ISCHEMIA; NERVOUS-SYSTEM; ANGINA;
Keywords:
angina pectoris; atrial tissue; ejection fraction; microcirculation; nerve stimulation; norepinephrine; vagus; ventricular filling;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Zamotrinsky, AV Inst Cardiol TSC RAMS, Div Neurocardiol, Kievskaya Str 111, Tomsk 634012, Russia Inst Cardiol TSC RAMS Kievskaya Str 111 Tomsk Russia 634012
Citazione:
A.V. Zamotrinsky et al., "Vagal neurostimulation in patients with coronary artery disease", AUTON NEURO, 88(1-2), 2001, pp. 109-116

Abstract

We tested the hypotheses that (1) progression of coronary artery disease (CAD) increases sympathetic inflow to the heart. thus impairing cardiac blood supply, and (2) reduced sympathetic tone improves cardiac microcirculation and ameliorates severity of anginal symptoms. Electrical irritation of the nerve auricularis-a sensitive ramus of the vagus nerve-provides a centralsympatholytic action. Using this technique, we studied the effects of vagal neurostimulation (VNS) on hemodynamics, the content of atrial noradrenergic nerves and the microcirculatory bed of CAD patients. VNS was performed in the preoperative period of CAD patients with severe angina pectoris. The comparison groups consisted of untreated patients with CAD or Wolff-Parkinson-White syndrome. Atrial tissue of patients with this syndrome (n = 6); with effort angina (n = 14); with angina at rest (n = 10); and with severe angina treated with VNS (n = 8) contained the following volume percentages ofnoradrenergic nerves: 1.7 +/- 0.1%, 1.3 +/- 0.3%, 0.5 +/- 0.1% (p < 0.05 vs. the other groups) and 1.3 +/- 0.2%, respectively. In these groups, cardiac microcirculatory vessels (diameter, 10-20 <mu>m) had the following densities: 2.7 +/- 0.28. 3.4 +/- 0.2%. 2.0 +/- 0.4% (p < 0.05 vs. the other groups) and 3.3 +/- 0.3%, respectively. VNS treatment abolished angina at rest,decreased heart rate and blood pressure, It improved left ventricular ejection fraction from 50 +/- 1.5% to 58 +/- 1.0% (p < 0.05), also changing left ventricular diastolic filling. The ratio of time velocity integrals of the early (E-i) to late (A(l)) waves increased from 1.07 +/- 0.12 to 1.65 +/-0.17 after VNS (p < 0.05). In electrocardiograms of VNS-treated patients, QRS- and QT-duration were shortened, the PQ-interval did not change, but T-wave configuration improved. In the postoperative period. heart failure occurred in 90% of the control group, vs. 12% in patients treated with VNS (p < 0.05). We conclude that CAD is characterized by overactivity of sympathetic cardiac tone. Vagal stimulation reduced sympathetic inflow to the heart,seemingly via an inhibition of norepinephrine release from sympathetic nerves. VNS' sympatholytic/vagotonic action dilated cardiac microcirculatory vessels and improved left ventricular contractility in patients with severe CAD. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 07:43:36