Open AccessCoronary hemodynamic data in ischemic heart disease according to ischemic behavior during pacing
Author(s) -
Cribier A.,
Berland J.,
Cazor J. L.,
Letac B.
Publication year - 1983
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960060103
Subject(s) - medicine , cardiology , coronary sinus , hemodynamics , heart rate , blood pressure , arteriovenous oxygen difference , coronary perfusion pressure , blood flow , coronary circulation , anesthesia , stroke volume , resuscitation , cardiopulmonary resuscitation
In order to study the circulatory changes induced by maximal atrial pacing in coronary patients, coronary sinus blood flow (CBF) measured by continuous thermodilution, lactate extraction coefficient (K), arteriovenous difference in oxygen (AVO 2 diff), and aortic blood pressure (BP) were measured at basal state and at maximal heart rate (HR max ) in 11 patients without coronary disease (group I) and in 28 patients with severe coronary lesions, divided into two groups according to the absence (group IIa) or the presence (group IIb) of chest pain and ST‐segment depression at HR max . K was inverted in group IIb (24±17% vs −23±39%, p < 0.001), but remained unchanged in group I and group IIa. Despite similar HR max , percent increase in CBF was significantly lower in group IIb (54±34%), than in group I (113±54%, p < 0.01). This contrasts with the higher values of the product of heart rate times systolic blood pressure (HR × SBP) as well as of diastolic blood pressure (DBP) in group IIb. The decrease in coronary resistances was lower in group IIb than in group I (p < 0.001), and also lower than in group IIa (p < 0.05). The ratio MO 2 × CBF/systolic BP × HR max was significantly lowered only in group IIb (p < 0.001) confirming the imbalance between myocardial oxygen supply and oxygen demand. In coronary patients, myocardial ischemia induced by atrial pacing is related to an insufficient increase in CBF, well evidenced by continuous thermodilution.