Heart rate reserve during dipyridamole stress test applied to potential heart donors in brain death.
Aged
Brain Death
Coronary Artery Disease
/ diagnosis
Dipyridamole
/ pharmacology
Echocardiography, Stress
Electrocardiography
Exercise Test
/ methods
Female
Heart Rate
/ drug effects
Heart Transplantation
Humans
Male
Middle Aged
Tissue Donors
Vasodilator Agents
/ pharmacology
Ventricular Dysfunction, Left
/ diagnosis
Journal
Minerva cardioangiologica
ISSN: 1827-1618
Titre abrégé: Minerva Cardioangiol
Pays: Italy
ID NLM: 0400725
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
pubmed:
27
2
2020
medline:
29
4
2021
entrez:
27
2
2020
Statut:
ppublish
Résumé
A blunted heart rate reserve (HRR) during dipyridamole stress echocardiography (DSE) is a prognostically unfavorable sign of cardiac autonomic dysfunction. Short-term adjustments of heart rate (HR) are thought to rise from changes in neural input to the heart. DSE is applied in potential heart donors to rule out underlying coronary artery disease and left ventricular dysfunction. The aim of this study is to assess HRR during DSE in brain death. We enrolled two groups: group 1 (N.=49, 22 men, 54.6±8.8 years) with patients in brain death enrolled in the nationwide marginal donor heart recruiting program; group 2 (N.=49, 18 men, 66.4±12.0 years) referred to DSE for suspected or known coronary artery disease. All underwent DSE (0.84 mg/kg in 6') by quality-controlled readers certified via web-based training (1487/CE Lazio-1). We assessed left ventricular contractile reserve (LVCR) as stress/rest ratio of force (systolic blood pressure/end-systolic volume). HRR was calculated as the peak/rest HR ratio from 12-lead EKG. The two study groups were similar for prevalence of inducible ischemia (4/49 vs. 9/49, P=NS). Group 1 showed higher resting HR (group 1: 88.1±15.5 bpm vs. group 2: 66.5±11.5 bpm, P<0.01) and similar peak HR (group 1: 94.7±15.3 bpm vs. group 2: 89.5±19.3 bpm, P=0.144), with blunted HRR (group 1: 1.08±0.10 bpm vs. group 2: 1.36±0.31 bpm, P<0.01). HRR was unrelated to LVCR. HRR is almost abolished and unrelated to LVCR in brain-dead patients during DSE. The modulation of neural input to the heart is essential to determine HRR, and plays no significant role in determining the inotropic response during DSE.
Sections du résumé
BACKGROUND
BACKGROUND
A blunted heart rate reserve (HRR) during dipyridamole stress echocardiography (DSE) is a prognostically unfavorable sign of cardiac autonomic dysfunction. Short-term adjustments of heart rate (HR) are thought to rise from changes in neural input to the heart. DSE is applied in potential heart donors to rule out underlying coronary artery disease and left ventricular dysfunction. The aim of this study is to assess HRR during DSE in brain death.
METHODS
METHODS
We enrolled two groups: group 1 (N.=49, 22 men, 54.6±8.8 years) with patients in brain death enrolled in the nationwide marginal donor heart recruiting program; group 2 (N.=49, 18 men, 66.4±12.0 years) referred to DSE for suspected or known coronary artery disease. All underwent DSE (0.84 mg/kg in 6') by quality-controlled readers certified via web-based training (1487/CE Lazio-1). We assessed left ventricular contractile reserve (LVCR) as stress/rest ratio of force (systolic blood pressure/end-systolic volume). HRR was calculated as the peak/rest HR ratio from 12-lead EKG.
RESULTS
RESULTS
The two study groups were similar for prevalence of inducible ischemia (4/49 vs. 9/49, P=NS). Group 1 showed higher resting HR (group 1: 88.1±15.5 bpm vs. group 2: 66.5±11.5 bpm, P<0.01) and similar peak HR (group 1: 94.7±15.3 bpm vs. group 2: 89.5±19.3 bpm, P=0.144), with blunted HRR (group 1: 1.08±0.10 bpm vs. group 2: 1.36±0.31 bpm, P<0.01). HRR was unrelated to LVCR.
CONCLUSIONS
CONCLUSIONS
HRR is almost abolished and unrelated to LVCR in brain-dead patients during DSE. The modulation of neural input to the heart is essential to determine HRR, and plays no significant role in determining the inotropic response during DSE.
Identifiants
pubmed: 32100982
pii: S0026-4725.20.05093-8
doi: 10.23736/S0026-4725.20.05093-8
doi:
Substances chimiques
Vasodilator Agents
0
Dipyridamole
64ALC7F90C
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
249-257Commentaires et corrections
Type : CommentIn