Vagal neurostimulation in patients with coronary artery disease
Identifieur interne : 001950 ( Main/Exploration ); précédent : 001949; suivant : 001951Vagal neurostimulation in patients with coronary artery disease
Auteurs : A. V Zamotrinsky [Russie] ; B. Kondratiev [Russie] ; J. W De Jong [Pays-Bas]Source :
- Autonomic Neuroscience: Basic and Clinical [ 1566-0702 ] ; 2001.
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 central sympatholytic 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 of noradrenergic 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 μm) had the following densities: 2.7±0.2%, 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 (Ei) to late (Ai) 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.
Url:
DOI: 10.1016/S1566-0702(01)00227-2
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W De Jong</name><affiliation wicri:level="3"><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Thoraxcenter, Erasmus University, Rotterdam</wicri:regionArea><placeName><settlement type="city">Rotterdam</settlement><region nuts="2" type="province">Hollande-Méridionale</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Autonomic Neuroscience: Basic and Clinical</title><title level="j" type="abbrev">AUTNEU</title><idno type="ISSN">1566-0702</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001">2001</date><biblScope unit="volume">88</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="109">109</biblScope><biblScope unit="page" to="116">116</biblScope></imprint><idno type="ISSN">1566-0702</idno></series><idno type="istex">D69F27741357BFF2ABB9CDFF8AC22A6C6F8149B2</idno><idno type="DOI">10.1016/S1566-0702(01)00227-2</idno><idno type="PII">S1566-0702(01)00227-2</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1566-0702</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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 central sympatholytic 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 of noradrenergic 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 μm) had the following densities: 2.7±0.2%, 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 (Ei) to late (Ai) 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.</div></front></TEI><affiliations><list><country><li>Pays-Bas</li><li>Russie</li></country><region><li>Hollande-Méridionale</li></region><settlement><li>Rotterdam</li></settlement></list><tree><country name="Russie"><noRegion><name sortKey="Zamotrinsky, A V" sort="Zamotrinsky, A V" uniqKey="Zamotrinsky A" first="A. V" last="Zamotrinsky">A. V Zamotrinsky</name></noRegion><name sortKey="Kondratiev, B" sort="Kondratiev, B" uniqKey="Kondratiev B" first="B" last="Kondratiev">B. Kondratiev</name><name sortKey="Zamotrinsky, A V" sort="Zamotrinsky, A V" uniqKey="Zamotrinsky A" first="A. V" last="Zamotrinsky">A. V Zamotrinsky</name></country><country name="Pays-Bas"><region name="Hollande-Méridionale"><name sortKey="De Jong, J W" sort="De Jong, J W" uniqKey="De Jong J" first="J. W" last="De Jong">J. 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