HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Ruggero De Paulis Luigi Chiariello Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Penta de Peppo, A. Articles by Chiariello, L. Search for Related Content PubMed PubMed Citation Articles by Penta de Peppo, A. Articles by Chiariello, L.

Ann Thorac Surg 1999;68:112-118
© 1999 The Society of Thoracic Surgeons

---

Original Articles

Recovery of LV contractility in man is enhanced by preischemic administration of enflurane

^a Department of Cardiac Surgery, Tor Vergata University of Rome, European Hospital, Rome, Italy
^b Department of Anesthesiology, Tor Vergata University of Rome, European Hospital, and Department of Biostatistics, Ospedale Fatebenefratelli Rome, Italy

Address reprint requests to Dr Penta de Peppo, Department of Cardiac Surgery, Tor Vergata University of Rome, European Hospital, Via Portuense 700, 00149 Rome, Italy

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
Background. Volatile anesthetics enhance postischemic functional recovery in animal models; this effect has not been investigated in man.

Methods. Twenty-two patients undergoing coronary surgery were randomized to enflurane administration (0.5% to 2%) for 5 minutes to reduce systolic blood pressure by 20% to 25% immediately before cardioplegic arrest. Left ventricular contractility was assessed by pressure-area relations using echocardiographic automated border detection during inflow occlusion before and after cardiopulmonary bypass. Linear regression analysis in 16 patients with paired data sets assessed changes in contractility.

Results. The relation was highly linear (r = 0.95 ± 0.02). A change of slope versus the change in x intercept was detected in controls (mean difference, 16.1 mm Hg/cm², 95% confidence limits, 5.9 to 26.3; 2.2 cm², 95% confidence limits, -1.1 to 5.5; p = 0.007), which was different from those of treated patients (mean difference, 0.7 mm Hg/cm², 95% confidence limits, -2.2 to 3.7; -0.06 cm², 95% confidence limits, -1.6 to 1.5; p > 0.2). Analysis of covariance in the overall group confirmed a significant effect of treatment (p = 0.002).

Conclusions. Enflurane enhances postischemic functional recovery, possibly through pharmacologic preconditioning of myocardium.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
Several experimental studies have shown that volatile anesthetics, when administered immediately before an ischemic interval, enhance postischemic left ventricular (LV) functional recovery [1–3]. Freedman and associates [1] demonstrated that enflurane administration in the isolated rat heart decreases high-energy phosphate utilization during ischemia and improves functional recovery, and they hypothesized energy saving related to the myocardial depression effect. Also, halothane and isoflurane, when administered before ischemia, preserve ultrastructure and improve recovery of myocardial contractility in animal experiments [2, 3]. Investigations with isoflurane suggest that this protective effect may be caused by pharmacologic preconditioning of myocardium [4], probably through activation of adenosine triphosphate-sensitive K⁺ channels.

To verify the hypothesis that the preischemic administration of volatile anesthetics might exert protection against prolonged ischemia in the human myocardium, we tested the effect of enflurane on the recovery of contractility after cardiopulmonary bypass during coronary artery bypass grafting. Enflurane was selected because it was routinely used in the anesthetic management during cardiac operations in our institution. Moreover, clinical investigations have shown that enflurane [5] and halothane [6] control autonomic reflexes and maintain myocardial oxygen balance in cardiac anesthesia. In particular, fentanyl-enflurane anesthesia can preserve myocardial oxygenation with mild hemodynamic depression in coronary artery bypass grafting [7], whereas myocardial oxygen balance might not be optimal with isoflurane anesthesia [8] owing to coronary vasodilation. Left ventricular function was assessed by pressure-area relations, a load-independent estimation of contractility [9–12], using transesophageal echocardiographic automated border detection and hemodynamic monitoring.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
Twenty-two consecutive patients with stable anginal symptoms and multivessel disease undergoing isolated elective coronary artery bypass grafting in a 4-month period were selected for the study after informed consent and institutional review board approval. Criteria for exclusion are:

Recent (< 4 wk) myocardial infarction

Unstable angina

Left main or single-vessel disease

Ejection fraction 45%

Associated valvular malfunction

Peripheral atherosclerotic occlusive disease

Diabetes on oral medication or insulin treatment

Hypertension

Renal or pulmonary disease

Two patients were excluded from further analysis because poor-quality transesophageal echocardiographic images were obtained, because of incomplete endocardium visualization in one and probe failure in the other. The remaining 20 patients were randomized to receive enflurane or to serve as controls. Measurements of contractility were not completed in 4 patients, because of occurrence of supraventricular arrhythmia in 2 (1 treatment, 1 control), transient ST-segment elevation in 1 (treatment), and bleeding requiring an additional period of cardiac arrest in 1 (control). Complete preoperative and postoperative data were therefore available in 16 patients. Preoperative medications in control patients (n = 8) were nitrates in 7, Ca²⁺ antagonists in 6, and ß-blockers in 1 patient; in patients treated with enflurane (n = 8) nitrates were administered in 7, Ca²⁺ antagonists in 7, and ß-blockers in 2 patients (not significant). There were no significant differences in the clinical and operative data between groups (Table 1). Of note, the long bypass times were related to the low temperature (26°C) reached during the procedure and time required to rewarm the patients.

A 5-MHz omniplane transesophageal transducer was positioned to obtain LV short-axis plane images at the midpapillary level. This was connected to an ultrasound system with automated border detection capabilities (Sonos 2500, Hewlett-Packard, Andover, MA); controls were adjusted for optimal visualization of the endocardial border, and the region of interest was manually drawn beyond the LV area. The LV area was computed by the border detection system and continuously displayed on the screen in wave format. A 14-gauge cardioplegia-type cannula was positioned in the ascending aorta and connected to the ultrasound system for measurement of aortic pressure, using a pressure system with fluid-filled tubing and strain-gauge transducers (Abbott Labs): after calibration, pressure was displayed on the screen as a waveform, simultaneously with the LV area waveform and electrocardiogram signals.

Study protocol
Cardiac output was measured in triplicate by the thermodilution method before cannulation. A vascular ligature was positioned around the inferior vena cava to alter preload conditions by intermittent occlusion: with respiration suspended at end-expiration, the vena cava was occluded until the minimum LV area was registered; then it was released and ventilation was restored. Two to three intermittent occlusions were performed. Echocardiographic images and acquired data were recorded continuously on videotape shortly before and during caval occlusions. Before starting cardiopulmonary bypass, enflurane was added to the inspired oxygen in selected patients for 5 minutes to reduce systolic arterial pressure 20% to 25% during this period, using an end-expiratory concentration averaging 1.3% (range, 0.5% to 2%). This reduction in blood pressure reflects the depressant effect of the anesthetic agent on myocardial performance [7] and was usually achieved within 2 to 3 minutes. The protocol was completed in all selected patients. End-expiratory concentrations of enflurane were measured at the tip of the endotracheal tube by an infrared gas analyzer (Capnomac Ultima, Datex, Helsinki, Finland) that was calibrated with known standards. Cardiopulmonary bypass with core cooling (26°C) was then started, ventilation was suspended, and the ascending aorta was clamped at occurrence of ventricular fibrillation, after 1.5 ± 0.4 minutes in the control group and 1.8 ± 0.3 minutes in the enflurane group (not significant); this period between exposure to enflurane and the period of arrest is similar to the 2-minute reperfusion time used in studies on ischemic preconditioning during cardiopulmonary bypass operations [13]. The LV was decompressed through the aortic vent, and cardiac asystole was immediately induced by antegrade cold hyperkalemic blood cardioplegia. Triplicate measurements of cardiac output, again followed by two to three caval occlusions and acquisition of the related pressure and area data, were repeated 20 minutes after discontinuation of cardiopulmonary bypass. Levels of troponin I and enzymes creatine kinase (CK) and CK-MB were determined preoperatively before induction of anesthesia, and then on arrival in the intensive care unit, 12, 24, and 96 hours postoperatively.

Conduct of the operation
The conduct of the operation was similar in all patients, by using antegrade cold (4°C) blood (4:1) cardioplegia (10 mL/kg) with warm glutamate/aspartate-enriched reperfusion (500 mL) [14]; distal anastomoses were performed during a single period of aortic cross-clamping, and 50 mL of cold blood cardioplegic solution was manually injected into each vein graft after completion of the corresponding distal anastomosis. The proximal anastomoses were performed during side-clamping. Hemodynamic stability after discontinuation of cardiopulmonary bypass was achieved by colloid infusions; inotropic drugs were not used.

Analysis of left ventricular performance
Left ventricular performance before and after cardiopulmonary bypass was estimated from pressure-area data. Pressure-area relations were determined using the arterial pressure acquired with a fluid-filled catheter system (natural frequency of approximately 40 Hz) and the end-systolic LV area acquired by automated border detection. It has been shown that changes in femoral arterial pressure acquired with a fluid-filled pressure system with a resonant frequency of 40 Hz well represent LV pressure changes recorded by high-fidelity LV catheters with superior characteristics; this is a less-invasive method to serially assess LV contractility in individual patients, particularly useful in the clinical setting [9]. Instead of femoral arterial pressure, we used ascending aortic pressure, which should more precisely represent LV pressure, and the peak systolic instead for end-systolic LV area [10, 15], further reducing the need for additional instrumentation for fine alignment of the pressure-area tracings during cardiac operations. To determine pressure-area relationship, multiple data points were generated by off-line analysis of the recorded measurements on the ultrasound system. Measurements were taken for a mean of 10 beats (range, 8 to 16 beats) simultaneously reading the end-systolic areas, defined as the smallest endocardial cavity areas, and the corresponding peak systolic pressures in the ascending aorta; these beats were selected from an optimally recorded run. Data were picked up on a computer, and systolic pressure-area data were fitted with a linear regression. As an example, the curves obtained in one patient are shown in Figure 1. Slopes and x intercepts of these relations were used to characterize LV performance, and their perioperative variations were assessed to identify any individual shift of slope as an index of changing LV performance.

View larger version (23K): [in this window] [in a new window]   Fig 1. Example of the curves obtained with the pressure and area data points of the peak systolic pressure–end-systolic area relation, taken from 11 beats during the preoperative and postoperative inflow occlusions in patient 4 (control group).

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
Perioperative data
No patient exhibited myocardial ischemia intraoperatively at the automated ST-segment analysis or postoperatively on routine electrocardiograms. No new segments of altered motility were observed after cardiopulmonary bypass, and all patients presented an uneventful postoperative course. Arterial systolic blood pressure decreased by 23% (125 ± 14 to 96 ± 12 mm Hg) during administration of enflurane. Preoperative and postoperative cardiac index showed no differences within or between patients of the control and treatment groups (2.2 ± 0.5 to 2.4 ± 0.7 L · min^-1 · m^-2 and 2.1 ± 0.5 to 2.3 ± 0.3 L · min^-1 · m^-2, respectively; not significant). Postoperative peak troponin I, CK, and CK-MB levels increased from baseline in both groups, without differences between groups (Table 2).

View larger version (19K): [in this window] [in a new window]   Fig 2. Effect of treatment on perioperative difference () in slope and x intercept (Ao) of peak systolic pressure–end-systolic area relations in the overall group of patients. As shown by crowding of data points around the origin for effect of enflurane treatment, no significant change was measured by analysis of covariance in these patients, different from controls (p = 0.002).

	Comment

Top Abstract Introduction Patients and methods Results Comment References

Use of ventricular pressure-area relations is a sensitive and load-independent method for accurate estimation of LV contractility within the physiologic range of LV dimensions found in the clinical setting [11, 12]. Moreover previous data on serial intraoperative assessment of LV contractility in individual patients have shown that changes in arterial pressure acquired with fluid-filled catheters during inferior vena caval occlusion are similar to changes in LV pressure acquired with high-fidelity catheters [9]. In fact, Gorcsan and colleagues [9] showed in 21 studies on 14 patients a highly linear correlation (r = 0.96) between end-systolic elastance acquired by standard arterial pressure monitoring and simultaneous elastance by high-fidelity LV pressure monitoring, both before and after cardiopulmonary bypass. Inasmuch as arterial pressure is routinely acquired in the operating room, the possibility of using arterial pressure to reflect LV pressure facilitates the clinical application of this method for rapid estimation of ventricular contractility in selected patients. Use of arterial peak systolic instead of end-systolic pressure, with end-systolic area, for determination of pressure-area relationship has also been proposed for the excellent linear correlation between these parameters [10, 15]. This greatly simplifies measurements in the operative setting during cardiac operations, obviating both the risk of placement of LV catheters and the need of additional instrumentation to carefully calibrate and align pulse tracings to detect end-systolic values.

The precise mechanism of action of volatile anesthetics is not known and cannot be elucidated by the results of our clinical study. However, several reports indicate that enflurane and the other halogenated anesthetics alter cellular Ca²⁺ fluxes, reducing intracellular Ca²⁺ content [16–18]. Lowering of excessive intracellular Ca²⁺ has therefore been proposed as a potential mechanism for the protective effect against ischemia. This effect may also be related to a pharmacologic preconditioning of myocardium through activation of adenosine triphosphate-sensitive K⁺ channels, resulting in reduction of the energy requirements during ischemia. This is suggested by the recent observation that administration of the volatile anesthetic isoflurane improved postischemic recovery of contractile function in canine hearts and that this beneficial effect was abolished by gliburide, a selective antagonist of adenosine triphosphate-sensitive K⁺ channels [3, 4]. These channels have also been shown to be activated by enflurane and halothane [19] and to play a key role in ischemic preconditioning in animals [20, 21], in isolated human atrial muscle [22], and in clinical studies [23]. Moreover, pharmacologic preconditioning of myocardium by potassium-channel opening has been recently shown to enhance cardioplegic protection [24, 25]. The improved recovery of LV function observed after enflurane administration in our study suggests that myocardial protection afforded by the halogenated anesthetics may have some clinical implications, as cardioplegic arrest of the heart in cardiac surgery still does not provide optimal protection of the ischemic myocardium and a transient LV dysfunction commonly occurs after cardiopulmonary bypass. In fact, our method of administration of enflurane for only 5 minutes before cardiopulmonary bypass was started is similar to the 6-minute time of ischemia proposed by others [13] to precondition the myocardium. This approach to pharmacologic preconditioning avoids induction of ischemia and the related reluctance to produce potential myocardial damage. Because -adrenergic drugs have been shown to mimic the preconditioning effect [26], an adrenergic reflex vasoconstriction secondary to the enflurane-induced decrease of blood pressure also could have been responsible for the cardioprotection observed in our study. However, this seems unlikely because enflurane blunts autonomic reflexes, and, actually, we did not observe reflex hypertension; indeed, the moderate lowering of blood pressure by enflurane is related to a depressant cardiovascular action and therefore differs from arterial vasodilation as would occur if a pure vasodilating agent was given. On the other hand, to avoid such a reflex adrenergic stimulation, we did not administrate a pure vasodilating agent as a control in the untreated group. It should be noted that administration of enflurane, because of the depressant effect of the drug, was graduated to lower the systolic arterial blood pressure by 20% to 25%, as our intention was to precondition the myocardium by giving only a mild hemodynamic depression. This is well tolerated in patients with coronary artery disease and good or mildly compromised ventricular function [7] and was indeed well supported in our patients, whose mean ejection fraction was 0.58. However, patients with depressed function may require a careful administration of the anesthetic agent because of their lesser tolerance.

There are several limitations of the study. The number of patients in this study is small. Each individual value of slope and intercept, however, was acquired by multiple measurements (10 ± 2) of pressure and area data during inflow occlusion, thus reflecting a series of well-correlated data in the same patient. This should enhance the significance of results. The selective criteria of inclusion and the use of a randomized study protocol should also overcome most drawbacks of the low power of the study and improve its clinical significance. Use of the automated border detection algorithm implies some additional limitations, as influenced by the gain setting of the echocardiographic system, effects of ventilation and caval occlusion on the position of the heart, and the assumption that ventricular geometry is symmetric. However, use of a vascular ligature for caval occlusions and suspension of ventilation at end-expiration during the measurements minimize the lateral translation of the heart. Moreover, selection of patients with normal ventricular function or only mild wall motion abnormalities overcomes the potential limitation of using area to reflect volume when the ventricular geometry is altered by severe regional myocardial dysfunction; in fact, data from patients with coronary artery disease who have only mild LV dysfunction still show close linear relation between changes in LV short-axis area and changes in volume [12, 27]. Absolute values of preoperative slope present some variability; this, however, does not necessarily indicate potential differences in preoperative myocardial contractility between patients. In fact, assessment of contractility by pressure-area relations is mainly validated for detection of individual perioperative changes. Another limitation of this method is the determination of pressure-area relations by using peak systolic pressure; it may be argued that this may not correlate in time with measurements of end-systolic area. Moreover, the time delay between these variables may be variable, depending on the degree of aortic compliance. However, peak systolic pressure, as well as end-systolic pressure, shows close linear correlation with end-systolic area for each contractile state [10, 15], therefore enabling a reliable use of the shift of this relationship to verify changes of contractility in the individual patient.

The presence of preoperative medications, unavoidable in clinical studies, particularly of calcium-channel blockers, might have interfered with ventricular function and the preconditioning phenomenon; however, they were equally distributed in both groups. Fentanyl anesthesia is an additional confounding factor and morphine, for example, is a known preconditioning mimetic agent, but because it was given to all patients, this should have not influenced the comparisons between enflurane-treated and control patients.

More research is necessary, but preliminary favorable results suggesting protective action of enflurane against myocardial ischemia in humans opens a stimulating field of application in clinical practice, particularly in light of the recent increase in the use of volatile anesthetics as part of the "fast-track" management of patients. This may also easily provide additional protection in selected patients.

	References

Top Abstract Introduction Patients and methods Results Comment References

 

1. Freedman B.M., Hamm D.P., Everson C.T., Wechsler A.S., Christian C.M. Enflurane enhances postischemic functional recovery in the isolated rat heart. Anesthesiology 1985;62:29-33.[Medline]
2. Lochner A., Harper I.S., Salie R., Genade S., Coetzee A.R. Halothane protects the isolated myocardium against excessive total intracellular calcium and structural damage during ischemia and reperfusion. Anesth Analg 1994;79:226-233.[Abstract/Free Full Text]
3. Kersten J.R., Lowe D., Hettrick D.A., Pagel P.S., Gross G.J., Warltier D.C. Glyburide, a K_ATP channel antagonist, attenuates the cardioprotective effects of isoflurane in stunned myocardium. Anesth Analg 1996;83:27-33.[Abstract]
4. Kersten J.R., Schmeling T.J., Hettrick D.A., Pagel P.S., Gross G.J., Warltier D.C. Mechanism of myocardial protection by isoflurane. Role of adenosine triphosphate-regulated potassium (K_ATP) channels. Anesthesiology 1996;85:794-807.[Medline]
5. Moffitt E.A., Imrie D.D., Scovil J.E., et al. Myocardial metabolism and haemodynamic responses with enflurane anaesthesia for coronary artery surgery. Can Anaesth Soc J 1984;31:604-610.[Medline]
6. Moffitt E.A., Sethna D.H., Bussell J.A., Raymond M., Matloff J.M., Gray R.J. Myocardial metabolism and hemodynamic response to halothane or morphine anesthesia for coronary artery surgery. Anesth Analg 1982;61:979-985.[Abstract/Free Full Text]
7. Moffitt E.A., McIntyre A.J., Barker R.A., et al. Myocardial metabolism and hemodynamic responses with fentanyl-enflurane anesthesia for coronary arterial surgery. Anesth Analg 1986;65:46-52.[Abstract/Free Full Text]
8. Moffitt E.A., Barker R.A., Glenn J.J., et al. Myocardial metabolism and hemodynamic responses with isoflurane anesthesia for coronary arterial surgery. Anesth Analg 1986;65:53-61.[Abstract/Free Full Text]
9. Gorcsan J., Denault A., Gasior T.A., et al. Rapid estimation of left ventricular contractility from end-systolic relations by echocardiographic automated border detection and femoral arterial pressure. Anesthesiology 1994;81:553-562.[Medline]
10. O’Kelly B.F., Tubau J.F., Knight A.A., et al. Measurements of left ventricular contractility using transesophageal echocardiography in patients undergoing coronary artery bypass grafting. Am Heart J 1991;122:1041-1049.[Medline]
11. Gorcsan J., Romand J.A., Mandarino W.A., Deneault L.G., Pinsky M.R. Assessment of left ventricular performance by on-line pressure-area relations using echocardiographic automated border detection. J Am Coll Cardiol 1994;23:242-252.[Abstract]
12. Gorcsan J., Gasior T.A., Mandarino W.A., Deneault L.G., Hattler B.G., Pinsky M.R. Assessment of the immediate effects of cardiopulmonary bypass on left ventricular performance by on-line pressure-area relations. Circulation 1994;89:180-190.[Abstract/Free Full Text]
13. Yellon D.M., Alkhulaifi A.M., Pugsley W.B. Preconditioning the human myocardium. Lancet 1993;342:276-277.[Medline]
14. Rosenkranz E.R., Okamoto F., Buckberg G.D., Robertson J.M., Vinten-Johansen J., Bugyi H.I. Safety of prolonged aortic clamping with blood cardioplegia. III. Aspartate enrichment of glutamate-blood cardioplegia in energy-depleted hearts after ischemic and reperfusion injury. J Thorac Cardiovasc Surg 1986;91:428-435.[Abstract]
15. Dávila-Román V.G., Creswell L.L., Rosenbloom M., Pérez J.E. Myocardial contractile state in dogs with chronic mitral regurgitation. Am Heart J 1993;126:155-160.[Medline]
16. Lynch C., Vogel S., Pratila M., Sperelakis N. Enflurane depression of myocardial slow action potentials. J Pharmacol Exp Ther 1982;222:405-409.[Abstract/Free Full Text]
17. Bosnjak Z.J., Supan F.D., Rush N.J. The effects of halothane, enflurane, and isoflurane on calcium current in isolated canine ventricular cells. Anesthesiology 1991;74:340-345.[Medline]
18. Kosk-Kosicka D., Roszczynska G. Inhibition of plasma membrane Ca²⁺-ATPase activity by volatile anesthetics. Anesthesiology 1993;79:774-780.[Medline]
19. Crystal G.J., Gurevicius J., Salem R., Zhou X. Role of adenosine triphosphate-sensitive potassium channels in coronary vasodilation by halothane, isoflurane and enflurane. Anesthesiology 1997;86:448-458.[Medline]
20. Gross G.J., Auchampach J.A. Blockade of ATP-sensitive potassium channels prevents myocardial preconditioning in dogs. Circ Res 1992;70:223-233.[Abstract/Free Full Text]
21. Gross G.J., Yao Z., Pieper G.M., Auchampach J.A. The ATP-regulated potassium channel in ischemia-reperfusion injury. Ann NY Acad Sci 1994;723:71-81.[Medline]
22. Perrault L.P., Menasché P. Preconditioning during cardiac surgery. In: Marber M.S., Yellon D.M., eds. Ischaemia. Oxford: BIOS Scientific Publishers, 1996:187-205.
23. Tomai F., Crea F., Gaspardone A., et al. Ischemic preconditioning during coronary angioplasty is prevented by glibenclamide, a selective ATP-sensitive K⁺ channel blocker. Circulation 1994;90:700-705.[Abstract/Free Full Text]
24. Menasché P., Mouas C., Grousset C. Is potassium channel opening an effective form of preconditioning before cardioplegia?. Ann Thorac Surg 1996;61:1764-1768.[Abstract/Free Full Text]
25. Kirsch M., Baufreton C., Fernandez C., et al. Preconditioning with cromakalim improves long-term myocardial preservation for heart transplantation. Ann Thorac Surg 1998;66:417-424.[Abstract/Free Full Text]
26. Bankwala Z., Hale S.L., Kloner R.A. -Adrenoceptor stimulation with exogenous norepinephrine or release of endogenous catecholamines mimics ischemic preconditioning. Circulation 1994;90:1023-1028.[Abstract/Free Full Text]
27. Gorcsan J., Gasior T.A., Mandarino W.A., Deneault L.G., Hattler B.G., Pinsky M.R. On-line estimation of changes in left ventricular stroke volume by transesophageal echocardiographic automated border detection in patients undergoing coronary artery bypass grafting. Am J Cardiol 1993;72:721-727.[Medline]

This article has been cited by other articles:

				J. Frassdorf, S. De Hert, and W. Schlack Anaesthesia and myocardial ischaemia/reperfusion injury Br. J. Anaesth., July 1, 2009; 103(1): 89 - 98. [Abstract] [Full Text] [PDF]

				S. Lorsomradee, S. Cromheecke, S. Lorsomradee, and S. G De Hert Cardioprotection with Volatile Anesthetics in Cardiac Surgery Asian Cardiovasc Thorac Ann, June 1, 2008; 16(3): 256 - 264. [Abstract] [Full Text] [PDF]

				L. A. Fleisher, J. A. Beckman, K. A. Brown, H. Calkins, E. L. Chaikof, K. E. Fleischmann, W. K. Freeman, J. B. Froehlich, E. K. Kasper, J. R. Kersten, et al. ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery) Developed in Collaboration With the American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, and Society for Vascular Surgery J. Am. Coll. Cardiol., October 23, 2007; 50(17): e159 - e242. [Full Text] [PDF]

				L. A. Fleisher, J. A. Beckman, K. A. Brown, H. Calkins, E. L. Chaikof, K. E. Fleischmann, W. K. Freeman, J. B. Froehlich, E. K. Kasper, J. R. Kersten, et al. ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery) Circulation, October 23, 2007; 116(17): e418 - e500. [Full Text] [PDF]

				J. A. Symons and P. S. Myles Myocardial protection with volatile anaesthetic agents during coronary artery bypass surgery: a meta-analysis Br. J. Anaesth., August 1, 2006; 97(2): 127 - 136. [Abstract] [Full Text] [PDF]

				S. Cromheecke, V. Pepermans, E. Hendrickx, S. Lorsomradee, P. W. ten Broecke, B. A. Stockman, I. E. Rodrigus, and S. G. De Hert Cardioprotective properties of sevoflurane in patients undergoing aortic valve replacement with cardiopulmonary bypass. Anesth. Analg., August 1, 2006; 103(2): 289 - 96, table of contents. [Abstract] [Full Text] [PDF]

				S. G. De Hert Volatile Anesthetics and Cardiac Function Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2006; 10(1): 33 - 42. [Abstract] [PDF]

				M. Lange, N. Roewer, and F. Kehl Anesthetic preconditioning as the alternative to ischemic preconditioning J. Thorac. Cardiovasc. Surg., January 1, 2006; 131(1): 252 - 253. [Full Text] [PDF]

				I. Malagon, K. Hogenbirk, J. van Pelt, M. G. Hazekamp, and J. G. Bovill Effect of three different anaesthetic agents on the postoperative production of cardiac troponin T in paediatric cardiac surgery Br. J. Anaesth., June 1, 2005; 94(6): 805 - 809. [Abstract] [Full Text] [PDF]

				S. G. De Hert, F. Turani, S. Mathur, and D. F. Stowe Cardioprotection with Volatile Anesthetics: Mechanisms and Clinical Implications Anesth. Analg., June 1, 2005; 100(6): 1584 - 1593. [Abstract] [Full Text] [PDF]

				Y. Shi, W. C. Hutchins, J. Su, D. Siker, N. Hogg, K. A. Pritchard Jr., A. Keszler, J. S. Tweddell, and J. E. Baker Delayed cardioprotection with isoflurane: role of reactive oxygen and nitrogen Am J Physiol Heart Circ Physiol, January 1, 2005; 288(1): H175 - H184. [Abstract] [Full Text] [PDF]

				M. Zaugg, E. Lucchinetti, C. Garcia, T. Pasch, D. R. Spahn, and M. C. Schaub Anaesthetics and cardiac preconditioning. Part II. Clinical implications Br. J. Anaesth., October 1, 2003; 91(4): 566 - 576. [Abstract] [Full Text] [PDF]

				J. G. Bovill Anesthesia for Patients with Impaired Ventricular Function Seminars in Cardiothoracic and Vascular Anesthesia, March 1, 2003; 7(1): 49 - 54. [PDF]

				M. Tonkovic-Capin, G. J. Gross, Z. J. Bosnjak, J. S. Tweddell, C. M. Fitzpatrick, and J. E. Baker Delayed cardioprotection by isoflurane: role of KATP channels Am J Physiol Heart Circ Physiol, July 1, 2002; 283(1): H61 - H68. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Ruggero De Paulis Luigi Chiariello Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Penta de Peppo, A. Articles by Chiariello, L. Search for Related Content PubMed PubMed Citation Articles by Penta de Peppo, A. Articles by Chiariello, L.