Biomedical subjects

P Foëx

Publications and source records attributed to P Foëx.

At least 55 records · Page 3Linked to original sources

PubMed1996

Effects of preload on regional nonischemic end-systolic performance.

BACKGROUND: Nonischemic segmental performance, assessed by end-systolic measures of shortening and thickening, decreases during ischemia. These changes in performance are likely to be dependent on the size, and, possibly, the site of the ischemic zone. This study was designed to examine the effect of preload, independently from ischemic zone size, on nonischemic end-systolic performance. METHODS: Twelve beagles were instrumented with sonomicrometers and micromanometer pressure gauges. End-systolic pressure length and thickness relationship data were obtained during vena caval balloon inflation. Control data were obtained both in left anterior descending and in left circumflex regions at left ventricular end-diastolic pressures of 5, 10 and 15 mmHg. The left circumflex artery was occluded for 90 s and nonischemic end-systolic pressure length and thickness data were obtained at each diastolic pressure. A 20 min recovery period was allowed between coronary occlusions. RESULTS: The isovolumic bulge in the ischemic area was more pronounced at an end-diastolic pressure of 5 mmHg than it was at an end-diastolic pressure of 15 mmHg. The slope of the nonischemic end-systolic pressure length and thickness relationships decreased at an end-diastolic pressure of 5 mmHg, whereas at 10 and 15 mmHg the slope of these relationships did not change significantly. The shift in the nonischemic end-systolic pressure-length relationship to the right was more pronounced at a low end-diastolic pressure (5 mmHg) than it was at a high end-diastolic pressure (15 mmHg). Similarly, the extent of the shift in the end-systolic pressure-thickness relationship to the left was more marked at a low end-diastolic pressure than it was at the higher end-diastolic pressure. CONCLUSION: Regional ischemia decreases the end-systolic performance of the nonischemic region. The extent of the shift and the degree to which the slopes of the nonischemic end-systolic relations decrease are influenced by loading conditions.

Animals↗

PubMed1996

Silent myocardial ischaemia in patients undergoing transurethral prostatectomy. A study to evaluate risk scoring and anaesthetic technique with outcome.

Ninety four patients undergoing transurethral resection of the prostate underwent Holter electrocardiographic monitoring pre- and postoperatively. There was no difference in silent myocardial ischaemia incidence or load between the spinal (n = 60) and the general anaesthesia (n = 34) groups. Ischaemic heart disease and a higher Detsky score both significantly increased the incidence of silent myocardial ischaemia but not the ischaemic load of those patients that actually demonstrated ischaemia. In this specific surgical population, not undergoing cardiac or vascular surgery, both ischaemic heart disease and cardiac risk scores are poor predictors of ischaemic load. Merely the presence of short duration silent myocardial ischaemia probably has little predictive value for postoperative adverse outcome.

Aged↗

PubMed1996

Hypertension, admission blood pressure and perioperative cardiovascular risk.

We performed a retrospective case-control study to investigate hypertension and admission blood pressure as risk factors for postoperative cardiovascular death. We identified records of 76 patients who had died of a cardiovascular cause within 30 days of anaesthesia and elective surgery and 76 matched controls. From the records of each patient (case and control) we recorded the admission blood pressure and details of any history of hypertension. A pre-operative history of hypertension was strongly associated with perioperative cardiovascular death (p < 0.001 with one degree of freedom: odds ratio 4.14, 95% confidence intervals 1.63-11.69). There was no association between systolic or diastolic pressure at admission for operation and perioperative cardiovascular death. The mean admission systolic pressure of the cases was 145.5 mmHg (range 90-250 mmHg) and that of the controls was 146.5 mmHg (range 100-200 mmHg). The mean admission diastolic pressure of the cases was 83.2 mmHg (range 60-130 mmHg), and that of the controls was 84.5 mmHg (range 60-110 mmHg).

Aged↗

PubMed1995

Platelet-activating factor (PAF) does not affect diastolic function in isolated rat hearts.

Platelet-activating factor might be responsible for the alterations of diastolic function observed in different disease states and these potential effects have not been studied. The effect of incremental concentrations of platelet-activating factor (to a maximum of 200 nM) was therefore examined in isolated perfused rat heart. Platelet-activating factor decreased coronary flow rate and contractility in a dose-dependent manner. Although high-dose platelet-activating factor decreased peak -dP/dt compared to baseline, this was not significant when compared to vehicle-administered control. There were no changes in the time constant of left ventricular relaxation and the chamber stiffness constant. These results do not support a major direct role of platelet-activating factor in diastolic dysfunction.

Animals↗

PubMed1995

[Myocardial ischemia and anesthesia].

Patients with coronary artery disease are particularly at risk perioperatively, as myocardial infarction, unstable angina, severe arrhythmia and cardiac death may occur. These events are often preceded by prolonged silent myocardial ischaemia (MI). Moreover, perioperative MI predicts long-term adverse cardiac outcome. Therefore, it is logical to prevent and treat MI. However, the detection of perioperative MI is difficult because of low sensitivity of ST-segment monitoring, low specificity of echocardiography and insufficient availability of equipment for its monitoring. A pragmatic approach is described, including preoperative consideration of myocardial revascularization prior to non-cardiac surgery and perioperative administration of antianginal agents; the effects of clonidine are discussed as well. The role of anaesthetic techniques and normovolaemic haemodilution is considered. MI episodes may be prevented or their duration may be shortened by treating tachycardia, hypotension and, possibly, hypertension. The risks of MI are particularly high during the postoperative period because increased global oxygen consumption associated with recovery, ventilator weaning, shivering and pain may lead to tachycardia and increased ventricular load. These factors must be taken into account in order to prevent MI and improve postoperative cardiac outcome.

Anesthesia↗

PubMed1995

The influence of preload on post-systolic shortening in ischaemic myocardium.

Post-systolic shortening is a wall motion abnormality defined as shortening of cardiac muscle after the end of ejection and usually regarded as a manifestation of ischaemia. This study was designed to determine whether changes in preload may alter the magnitude of ischaemia-induced post-systolic shortening. Eleven beagles were anaesthetized (halothane 0.8%) and instrumented for measurement of pressures, flows and dimensions in the apical subendocardium supplied by the left anterior descending coronary artery. Myocardial ischaemia was obtained by tightening a micrometer-controlled snare around the left anterior descending coronary artery. Post-systolic shortening, calculated as end-systolic length minus minimum length divided by end-systolic length, was measured at different levels of preload. Increasing the preload from 4 to 17 mmHg caused a significant reduction in post-systolic shortening (8.9% vs. 12.9%, P < 0.05, Student's paired t-test); post-systolic shortening was negatively correlated with coronary perfusion pressure (r = 0.35, P < 0.01) and positively correlated with systolic bulging. This study demonstrates that the amount of post-systolic shortening depends on the volume status, which therefore has to be taken into account in interpreting regional wall motion abnormalities, such as those detected by echocardiography.

Animals↗

PubMed1994

Regional nonischemic performance as assessed by end-systolic measures of shortening and thickening.

OBJECTIVES: Nonischemic contractile segmental performance was characterized by the end-systolic pressure-length and pressure-thickness relations during regional ischemia induced by proximal left anterior descending and left circumflex coronary artery occlusions. BACKGROUND: The increases in shortening and thickening of the nonischemic myocardium during acute ischemia have been attributed to alterations in the regional loading conditions. However, it is uncertain to what extent ischemia affects the contractile performance of the nonischemic zone. METHODS: Twenty-seven beagle dogs were instrumented with sonomicrometers and micromanometer pressure gauges. End-systolic pressure-length and pressure-thickness relation data were obtained during vena cava balloon inflation. Control data were obtained in both left anterior descending and left circumflex regions. Then, in random order, either the left anterior descending or left circumflex coronary artery was occluded for 90 s, and hemodynamic and nonischemic end-systolic pressure-length and pressure-thickness data were obtained. After a 45-min recovery period, the other artery was occluded, and the same recordings were obtained. RESULTS: The end-systolic pressure-length relation exhibited variable degrees of rightward and downward shifts and the end-systolic pressure-thickness relation variable degrees of leftward and downward shifts. Left circumflex coronary artery occlusion was associated with a greater downward displacement (decreased slope) of the nonischemic end-systolic pressure-length relation than left anterior descending coronary artery occlusion. The baseline slope was the best predictor of the change in slope of the end-systolic pressure-length and pressure-thickness relations. The left circumflex coronary artery supplied a larger proportion of left ventricular myocardial mass than the left anterior descending coronary artery. CONCLUSION: Acute ischemia profoundly affects the end-systolic performance of the nonischemic segment. Furthermore, the site, and probably size, of the ischemic zone may be important determinants of nonischemic contractile performance.

Animals↗

PubMed1994

Pressure-volume loops: a dynamic approach to the assessment of ventricular function.

Analysis of ventricular function in terms of pressure-volume or pressure-dimension relationships allows global and regional ventricular dynamics to be fully analyzed. In addition, this approach allows the relationships between muscle function (contractility, stiffness, potential energy) and pump function (stroke volume, stroke work) to be determined and predicted. Alterations in ventricular loading conditions can also be examined in terms of muscle and pump function. However, this analysis is more complex than initially thought and considerable care must be taken especially when regional ischemia is concerned. Moreover, some of the early assumptions have been disproved and conclusions can only be drawn from studies in which full assessment of changes in pressure and dimensions is available.

Humans↗

PubMed1994

Post-ischemic diastolic dysfunction.

Though a sustained post-ischemic decrease in contractile function has been clearly established, post-ischemic diastolic function has not been thoroughly investigated. Accordingly, 11 anesthetized (isoflurane 1%) open-chest beagles were instrumented to measure left ventricular pressure and dimensions (circumferential length and wall thickness) in an apicoanterior area supplied by the left anterior descending coronary artery (LAD). Pressure-dimension relations were modified by stepwise infusion and withdrawal of 200 mL of the animals' own blood during baseline, 45 minutes partial occlusion of the LAD (systolic bulging), and 60 minutes after the onset of reperfusion. Stiffness constants were derived from the end-diastolic pressure-length and stress-strain relations, respectively. Myocardial ischemia was associated with significant (P < 0.05) alterations of the following parameters of diastolic function: (1) 47% increase in end-diastolic pressure; (2) 22% decrease in peak negative dP/dt; (3) 9% increase in the time constant of isovolumic relaxation (tau); (4) postcystolic contraction; (5) 6% increase in end-diastolic length and 10% decrease in end-diastolic thickness; (6) 12% increase in unstressed length (creep) and 13% decrease in unstressed thickness; (7) 51% increase in chamber stiffness and a 63% increase in myocardial stiffness; and (8) 40% decrease in the peak lengthening rate. After 60 minutes of reperfusion, only end-diastolic pressure and tau had returned to baseline values whereas systolic shortening fraction, postsystolic contraction, and end-diastolic and unstressed dimensions had only partially recovered. No recovery occurred in peak negative dP/dt, chamber stiffness, myocardial stiffness, and peak lengthening rate. Thus, both myocardial ischemia and reperfusion are associated with complex changes in global and regional left ventricular diastolic function.

Anesthesia, Inhalation↗

PubMed1994

Does the choice of antihypertensive therapy influence haemodynamic responses to induction, laryngoscopy and intubation?

We have measured haemodynamic responses to induction of anaesthesia, laryngoscopy and intubation in 103 mild-moderate hypertensive patients (83 patients (diastolic pressures < or = 110 mm Hg) currently receiving one of four monotherapies (ACE inhibitors, group A; beta adrenoceptor blocking drugs, group B; calcium channel antagonists, group C; diuretics, group D) and 24 were untreated hypertensive patients). Anaesthesia was induced with fentanyl 1.5-2.0 micrograms kg-1 and thiopentone 3-5 mg kg-1. Tracheal intubation was facilitated by vecuronium 0.1 mg kg-1 and anaesthesia maintained with enflurane and nitrous oxide in oxygen. Systolic and diastolic pressures (SAP, DAP) were measured at 1-min intervals by a non-invasive oscillometric method and cardiac output (CO) and stroke volume (SV) by thoracic bioimpedance. Induction of anaesthesia was associated with a decrease in SAP, DAP and CO in groups A-D (P < 0.05). Heart rate (HR) decreased in groups A and D (P < 0.01) and systemic vascular resistance (SVR) decreased in groups A and B (P < 0.05). SAP and HR increased in all groups after laryngoscopy and intubation (P < 0.01) as did SVR in groups A, B and D (P < 0.02). CO was unaltered. Similar changes occurred in the untreated hypertensive patients, although nine of 24 patients exhibited HR > or = 100 beat min-1 after laryngoscopy and intubation. Comparison of the changes in SAP, DAP, CO and SVR with time showed no differences in the five treatment groups; changes in HR were significantly less in group B compared with the other groups (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

PubMed1994

Resistant hypertension and preoperative silent myocardial ischaemia in surgical patients.

We studied 325 patients undergoing elective noncardiac surgery who had preoperative ambulatory ECG monitoring performed for a duration of 5130 h (range 8-24 h; mean 15.8 h). Sixty-four subjects (20%) had one or more episodes of ST segment depression consistent with myocardial ischaemia. Of all preoperative cardiovascular variables measured, the presence of elevated arterial pressure, despite patients being maintained on long term antihypertensive therapy, was the only factor associated significantly with the presence of preoperative silent myocardial ischaemia (P < 0.002). This correlation was confirmed when arterial hypertension was defined in four separate ways. The incidence of silent ischaemia in these patients was 33-55%. We suggest that admission arterial pressure may therefore be a useful screening test to identify patients at risk of preoperative myocardial ischaemia.

Adult↗

PubMed1994

[During experimental coronary occlusion dobutamine further slows down the time constant of isovolumetric relaxation].

It has been shown that the time constant (tau) of isovolumic left ventricular (LV) pressure fall is shortened by beta-adrenergic stimulation, possibly reflecting enhanced myocardial relaxation and improved uniformity within the LV wall. Conversely, acute regional ischaemia , slows tau due to mechanical nonuniformity between the nonischaemic and the ischaemic regions. In order to assess the effect of inotropic stimulation on LV pressure fall during acute regional ischaemia, 7 anaesthetized dogs (16 +/- 2 kg) were instrumented with LV and aortic micromanometers. Sonomicrometers were implanted in the areas supplied by the left circumflex and anterior descending arteries to monitor subendocardial segment length (L). After baseline recordings, acute regional ischaemia was induced by 60 s occlusion of the proximal circumflex artery. After a 30 min recovery, the same was repeated during dobutamine infusion (5 micrograms/kg/min). In order to derive tau from heart beats with comparable end-systolic pressures, a caval occlusion run was performed at each stage. The % systolic bulging of the ischaemic zone was defined as: (maximal L--end-diastolic L)/end-diastolic L x 100. The fitting of the exponential model used to derive tau was always good (r > or = 0.99). At comparable end-systolic pressures, tau was increased by acute regional ischaemia (36 +/- 2 versus 32 +/- 2 ms, p < 0.01) and reduced by dobutamine infusion (27 +/- 2 versus 32 +/- 2 ms, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Assessment of regional myocardial performance with end-systolic pressure length and thickness relationships.

Although end-systolic pressure length and thickness relationships (ESPLR, ESPTR) are now widely used as substitutes for the end-systolic pressure volume relationships, there are some reservations about their use as an index of left ventricular (LV) performance. This study addressed three issues, namely: (1) which loading technique (decreasing preload by inferior vena cava (IVC) balloon occlusion or increasing systolic pressure by aortic constriction) is the most likely to yield usable data; (2) reproducibility of these relationships over a 30 min period; and (3) whether by using end-ejection (zero aortic flow) as a definition of end-systole, ESPLR and ESPTR can be used to characterize myocardial performance independent of load. Thirteen anesthetized beagles, weighing 16-25 kg, were used for this study, and were instrumented with sonomicrometers. We found that when ESPLR and ESPTR were constructed from data derived during aortic constriction, the slopes of these relationships were steeper and more curvilinear than when they were constructed from data recorded during IVC occlusion. In addition, the mean between ESPLR, ESPTR obtained 30 min apart was small, although there was a fair degree of variability between the first and second measurements. Using end-ejection to define end-systole, both ESPLR and ESPTR were relatively insensitive to loading conditions (LV end-diastolic pressure of 8-12 mmHg and 14-18 mmHg, aortic systolic pressure of 7-10 mmHg and 20-25 mmHg above baseline (in terms of the slope and shift (leftward or rightward) in these relationships, but were sensitive to inotropic interventions (dobutamine 2.5 micrograms/kg per min and 5 micrograms/kg per min). We conclude that, ESPLR and ESPTR, defined from measurements at end-ejection, can be used as adequate descriptors of regional myocardial performance if they were constructed from data over a similar pressure range during IVC balloon occlusion.

Animals↗

PubMed1993

Graded myocardial ischemia is associated with a decrease in diastolic distensibility of the remote nonischemic myocardium in the anesthetized dog.

OBJECTIVES: This study was designed to investigate the changes in regional distensibility of the ischemic segment and of a remote nonischemic segment brought about by graded myocardial ischemia. BACKGROUND: Ventricular distensibility is a major determinant of left ventricular end-diastolic pressure. The effects of graded myocardial ischemia on the regional distensibility of the ischemic area have not been studied. Moreover, there are few data on the effects of myocardial ischemia on the regional distensibility of the nonischemic myocardium. METHODS: Nine anesthetized open chest mongrel dogs were fitted with instruments to measure left ventricular pressure and circumferential length (sonomicrometry) in the ischemic segment and in a nonischemic segment. The pressure-length relation was modified by stepwise infusion and withdrawal of 200 ml of each dog's own blood over 30 min in five consecutive stages of regional ischemia. Unstressed dimensions were obtained by repeated inferior vena cava occlusions. In both segments, regional distensibility was assessed at end-diastole by means of the constants of the pressure-length (chamber stiffness), the pressure-strain and the force-strain (myocardial stiffness) relations. RESULTS: In the ischemic segment, partial and complete coronary occlusions were associated with a twofold increase in the chamber stiffness constant, the pressure-strain constant and the myocardial stiffness constant, whereas in the nonischemic segment the chamber stiffness constant, the pressure-strain constant and the myocardial stiffness constant increased by 50%. CONCLUSIONS: Regional myocardial ischemia is associated with a decrease in distensibility of both the ischemic and the remote nonischemic myocardium.

Analysis of Variance↗

PubMed1993

Diltiazem and regional left ventricular function during graded coronary constriction and propofol anesthesia in the dog.

Although calcium channel blockers may preserve function in ischemic myocardium, they may also produce myocardial depression and dysfunction in the presence of decreased coronary flow. This study was designed to examine the issue of possible protection afforded by diltiazem against ischemia-induced myocardial dysfunction during propofol anesthesia. In eight anesthetized and ventilated dogs, regional myocardial (ultrasonic crystals in both left anterior descending [LAD] and left circumflex [LC] perfusion areas) and global ventricular function were evaluated during progressively severe degrees of myocardial ischemia (LAD constriction) before and after intravenous diltiazem (150 micrograms/kg). As coronary flow decreased, heart rate increased, and arterial and coronary perfusion pressures, left ventricular dP/dt, and cardiac output decreased. Systemic vascular resistance was unaffected. Diltiazem without coronary constriction increased heart rate, and decreased diastolic arterial pressures, left ventricular (LV) end-diastolic, coronary perfusion pressures, LV dP/dt max, LAD coronary blood flow, stroke volume, and cardiac output. At all levels of coronary constriction following diltiazem, there were decreases in systolic and diastolic arterial pressures, stroke volume, cardiac output, LV dP/dt, and coronary perfusion pressure. Heart rate increased at critical coronary constriction, and then remained constant relative to the prediltiazem state. The regional muscle effects of the reductions in coronary flow in the LAD perfusion territory included decreased systolic shortening and increased postsystolic shortening before and after diltiazem. Diltiazem did not alter the magnitude of the alterations in systolic or postsystolic shortening brought about by coronary constriction. No changes occurred in the LC area.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Intravenous↗

PubMed1993

Regional distensibility, chamber stiffness, and elastic stiffness constant in halothane and propofol anesthesia.

Nine mongrel dogs were acutely instrumented in order to investigate cardiac stiffness at end-diastole while left ventricular circumferential lengths were measured at two different sites (near-apical region and near-basal region). Two hundred mL of autologous blood were infused and then withdrawn to create different volume loading conditions. Four different anesthetic settings were tested: two concentrations (0.7% and 1.7%) of halothane, and two infusion rates (0.2 mg/min/kg, and 0.4 mg/min/kg) of propofol. Three parameters of cardiac stiffness were calculated: distensibility, chamber stiffness (Kp), and elastic stiffness constant (k). Chamber stiffness and elastic stiffness constant were smaller in the apical region than the basal region under halothane anesthesia at both the 0.7% and 1.7% concentrations. There were no regional differences in elastic stiffness constant (k) under propofol anesthesia at either infusion rate. However, Kp was smaller in the apical region at the low propofol infusion rate. There were no significant differences in Kp and k between the anesthetic agents, or with the increase in concentration of either agent. However, when both agent and concentration were taken into consideration, an increase in stiffness was observed with deepening halothane, but not propofol anesthesia. These results show that assessment of diastolic function must take into consideration both regional differences and the anesthetic agent, because the latter may alter such differences and, thus, alter diastolic function.

Anesthesia, Inhalation↗

PubMed1993

Nitrous oxide causes myocardial ischemia when added to propofol in the compromised canine myocardium.

We sought to determine the influence of nitrous oxide on the compromised heart during propofol anesthesia. This study investigated the cardiovascular effects of the combination propofol and nitrous oxide (N2O). Seven beagles were monitored to measure global and regional left ventricular function. Recordings both before and after critical constriction (CC) of the left anterior descending coronary artery (LAD) were performed after propofol, 300 micrograms.kg-1.min-1, and 10 min after exposure to and discontinuation of 67% N2O. Data were analyzed with ANOVA for repeated measures at 95% confidence level. In the absence of CC, N2O caused moderate, reversible hemodynamic depression (LVdP/dtmax, -13.8%; cardiac output, -17.2%; LAD coronary blood flow, -10.9%) and no regional dysfunction. After CC global hemodynamic depression was of similar magnitude (LVdP/dtmax, -19.9%; cardiac output, -9.2%; stroke volume, -9.2%) but did not recover completely. Systolic shortening in the compromised area decreased (-30.3%) and postsystolic shortening developed to represent 20.3% of total shortening. Despite only moderate hemodynamic depression, 67% N2O causes substantial regional dysfunction in compromised myocardium when added to propofol.

Anesthesia, Intravenous↗

PubMed1993

Effect of isoflurane and halothane on regional cardiac stiffness.

To investigate the possibility of regional differences in cardiac stiffness which may relate to the known regional differences in systolic left ventricular function, seven mongrel dogs were acutely instrumented and regional cardiac stiffness was measured at both apical and basal region under two different concentrations of isoflurane (1.08% and 1.9%) as well as equipotent concentrations of halothane (0.9% and 1.58%). Cardiac stiffness was determined in terms of distensibility, chamber stiffness (derived from pressure-length relationships), and an elastic stiffness constant (derived from stress-strain relationships). Regional differences in cardiac stiffness were observed for all three indices and for each anaesthetic setting except for the elastic stiffness constant under 1.9% of isoflurane. The data indicate that regional differences in cardiac stiffness exist between the apex and the base of the heart. These regional differences do not depend on the anaesthetic agent or its concentration and may contribute to the differences in systolic function.

Anesthesia, Inhalation↗