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Ann Thorac Surg 2000;70:206-211
© 2000 The Society of Thoracic Surgeons

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Original articles: Cardiovascular

Myocardial outflow of prostacyclin in relation to metabolic stress during off-pump coronary artery bypass grafting

^a Department of Thoracic Surgery, Karolinska Hospital, Stockholm, Sweden
^b Department of Cardiothoracic Anesthesia, Karolinska Hospital, Stockholm, Sweden

Address reprint requests to Dr Lockowandt, Department of Thoracic Surgery, Karolinska Hospital, S-171 76 Stockholm, Sweden
e-mail: ulflockowandt{at}yahoo.com

	Abstract

Top Abstract Introduction Patients and methods Results Comment References

 
Background. The metabolic changes, possible myocardial damage, and influence on the vascular endothelium during off-pump coronary artery bypass grafting have been investigated.

Methods. Coronary sinus and arterial blood samples were obtained before coronary arterial occlusion, after 10 minutes of ischemia, and after 1 and 10 minutes of reperfusion in 9 patients who had an anastomosis performed to the left anterior descending coronary artery off-pump bypass

Results. The mean ischemic time was 14 ± 1 minutes. The arteriovenous difference in lactate decreased during ischemia to reach a minimum at 1 minute of reperfusion (-0.15 ± 0.06 µmol/L compared to 0.21 ± 10 µmol/L before ischemia; p < 0.01). Myocardial lactate extraction decreased from 14.2 ± 6.8 µmol/min before ischemia to -10.9 ± 6.5 µmol/min after 1 minute of reperfusion (p < 0.01). Simultaneously, the arteriovenous difference in 6-keto-PGF₁, the stable metabolite of prostacyclin, decreased from -30 ± 26 pg/mL to -258 ± 80 pg/mL at 1 minute of reperfusion (p < 0.05), and the 6-keto-PGF₁ extraction over the heart decreased -556 ± 466 pg/min to -18,560 ± 5,683 pg/min (p < 0.01).

Conclusions. The localized myocardial ischemia associated with these procedures causes changes in the myocardium and endothelial influence. Coronary bypass surgery performed on the beating heart may not be superior in preventing cardiac ischemia and endothelial disturbance, compared with conventional bypass surgery.

	Introduction

Top Abstract Introduction Patients and methods Results Comment References

 
Coronary artery bypass grafting (CABG) is usually performed with cardiopulmonary bypass (CPB). However, CPB has been associated with several adverse effects [1, 2] and CABG without CPB has recently gained increased attention [3]. The short- to mid-term clinical outcome in these operations in terms of morbidity and mortality has been characterized [4, 5]. In these operations, coronary flow in the vessels being bypassed is usually interrupted while the distal anastomosis is constructed, frequently for 10 to 20 minutes. The metabolic influence and possible endothelial disturbance that result from this intraoperative, temporary interruption of coronary blood flow has not been thoroughly investigated in human subjects. In experimental ischemia in pigs, it has been demonstrated that already a 15-minute period of ischemia is associated with a 300% increase in tissue lactate [6], and lactate production is widely used as an indicator of anaerobic metabolism [7]. Furthermore, short-term ischemia and reperfusion is well known from experimental studies to induce a long-lasting impairment of endothelial function with important clinical implications in terms of development of stenosis and coronary vasospasm [8].

The aim of the present study was therefore to evaluate the myocardial metabolic disturbance during CABG without CPB, and to assess to what extent this local cardiac ischemia influences the outflow of endothelially derived vasoactive substances, ie, endothelin (ET-1), nitric oxide (NO), and prostacyclin (by determination of the stable metabolite 6-keto-PGF₁).

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment References

 
Patients
This study was approved by the Karolinska Hospital human research committee. Patients requiring grafts in the left anterior artery (LAD) system only, or in the LAD system and right coronary artery system or circumflex artery, were offered surgery without CPB. Exclusion criteria for surgery off bypass were significant left main stenosis and severely depressed left ventricular function. All patients who underwent elective coronary surgery without CPB were included after informed consent. Our study group consisted of 9 patients, all male. Three patients had had one or more myocardial infarctions. Two patients had an occluded LAD; the remaining 7 patients had significant LAD stenosis. Left ventricular function was classified as normal, mildly depressed, or moderately depressed, as evaluated from the angiogram or the perioperative transesophageal echocardiography. The preoperative and intraoperative data are shown in Table 1.

The operation was performed through a midline sternotomy, or ministernotomy. The left internal thoracic artery (LITA) was harvested for anastomosis to the LAD. Additional grafts were performed using the saphenous vein. When multiple vessels were bypassed, the anastomosis to the LAD was constructed first. A 2-0 Prolene (Ethicon, Somerville, NJ) suture was passed around the LAD proximal and just distal to the anastomotic site. The snares were tightened for a period of 2.1 ± 0.1 minutes for ischemic preconditioning. After 4 to 5 minutes of reperfusion, the snares were tightened again to ensure an operative field as bloodless as possible. The anastomotic site was stabilized using on Origin OMS-CS cardiac stabilizer (Origin USA, Menlo Park, CA). The anastomosis was then constructed using an 8-0 Prolene suture. After completion of the LITA–LAD anastomosis the snares and the occluder on the LITA were released. Additional anastomoses were not performed until at least 10 minutes had elapsed after reestablishment of LAD flow. In one patient (patient 8) the LITA was damaged at harvest and the LAD received a saphenous vein graft.

Study protocol
A thermodilution catheter (Webster Laboratories, Altadena, CA) was inserted into the coronary sinus through the right internal jugular vein under fluoroscopic guidance [9]. The catheter was advanced to the proximal part of the great cardiac vein. The correct position in coronary sinus was verified by analysis of the blood oxygen saturation. Coronary sinus blood flow was measured in duplicate by retrograde thermodilution technique, using saline [10]. This catheter was used for coronary sinus blood sampling and flow measurements at the following time points: after opening of the pericardium but before LAD ischemia; at 10 minutes of LAD ischemia; and at 1 and 10 minutes after reestablishment of LAD flow. Simultaneous samples were drawn from the radial artery. Each sample was immediately analyzed for total oxygen content using an OSM 3 Hemoximeter connected to an ABL 505 blood gas analyzer (Radiometer A/S, Copenhagen, Denmark). The samples were collected in vacuum tubes, kept in ice slush, and centrifuged (10 minutes, 4°C) at 1,620 g within 30 minutes of collection of the last sample. The plasma was then immediately frozen at -70°C and stored until analysis. Heart rate (HR), mean arterial pressure (MAP), and ST segment deviation were recorded at each sampling point with a Tram 600 SL module, connected to a Tramscope 12C (Marquette Electronics Inc, Milwaukee, WI).

On postoperative day 1, a 12-lead ECG was recorded and peripheral venous blood samples were drawn for routine analysis of creatine kinase (CK), aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Our ECG criterion for transmural infarction were new Q-waves of more than 0.03 seconds duration in at least two anatomically adjacent leads. A localized ST elevation followed by T-wave inversion in at least two adjacent leads were considered diagnostic of acute subendocardial myocardial infarction. In the absence of ECG changes, a non–Q-wave infarction was diagnosed using the following enzymatic criteria (U/L): AST greater than 180 (with ALT < 60 and CK > 1200). The upper reference limits in our laboratory are for AST and ALT 48 U/L and for CK 1,200 U/L.

Plasma determination of lactate
Lactate in plasma was determined using a "dry chemistry" kit from Vitros (Johnson & Johnson, Arlington, TX) and analyzed spectrophotometrically in a Vitros 950 analyzer. The range of the analysis is 0.50 to 12.00 mmol/L, and the reference interval is 0.7 to 2.1 mmol/L.

Plasma determination of 6-Keto-PGF₁
Plasma samples were analyzed for the content of 6-keto-prostaglandin (PGF₁), the stable breakdown product of prostacyclin, using a commercially available enzyme immunoassay (Biotrak RPN 221, Amersham, Buckinghamshire, UK). This assay combines the use of peroxidase-labeled 6-keto-PGF₁ conjugate, a specific antiserum that can be immobilized onto precoated microtiter plates and one pot stabilized substrate solution. This provides a rapid and sensitive nonisotopic method for determination of 6-ketoPGF₁. The detection limit for the kit was 0.2 pg/well.

Plasma determination of ET-1
For extraction of ET-1–like immunoreactivity, the samples were heated at 95°C in water for 10 minutes, homogenized, and centrifuged. The content of ET-1–like immunoreactivity was then determined by radioimmunoassay using an antiserum raised against ET-1 in rabbits (the cross reactivity to ET-3 was < 8%; RAS 6911, Peninsula, Belmont, CA). Human ET-1 labeled with iodine-125 (¹²⁵I) was used as tracer and synthetic ET-1 as standard. The assay samples were incubated at 4°C in 0.1 mol/L phosphate buffer, pH 7.4, containing 0.1% bovine serum albumin and 0.1% Triton-X. The detection limit of the assays was 0.40 fmol/tube.

Plasma determination of nitric oxide
Plasma samples were obtained as described above. Total NO was analyzed by a commercially available assay kit (R&D DE 1600; Minneapolis, MN). Briefly, this assay involves the enzymatic conversion of all nitrate to nitrite by nitrate reductase. The detection of total nitrite is then determined as color azo dye product of the Griess reaction, which absorbs visible light at 540 nm. The sensitivity of the NO assay was 1.35 µmol/L.

Calculations and statistical evaluation
For oxygen, lactate, and 6-keto-PGF₁, the concentration in coronary venous plasma was substracted from the concentration in arterial plasma to form the arteriovenous difference. The myocardial extraction (or outflow) of substances was calculated by multiplying the arteriovenous concentration difference by the flow in the coronary sinus, corrected for hematocrit. These parameters and MAP, HR, and coronary sinus blood flow were statistically analyzed by ordinary or repeated analysis of variance (ANOVA) with Bonferroni multiple comparison test, or Student’s t test (INSTAT software, version 2.01; GraphPad, CA). A p value of less than 0.05 was considered significant. Values are given as mean plus or minus SEM.

	Results

Top Abstract Introduction Patients and methods Results Comment References

 
Clinical outcome
One patient died on postoperative day 53 from cardiac failure and empyema. Neither this patient nor any of the other patients had signs of perioperative myocardial infarction in terms of enzyme elevation or ECG changes. The other 8 patients were discharged between 5 and 10 days postoperatively (mean, 7 ± 0.5 days).

Signs of ischemia and metabolic adjustments
The MAP before ischemia, at 10 minutes ischemia, and after 1 and 10 minutes reperfusion was 67 ± 5, 69 ± 5, 68 ± 7, and 67 ± 5 mm Hg, respectively. Likewise there was no significant change in HR over time (71 ± 5, 69 ± 4, 66 ± 4, and 71 ± 7 beats/min, respectively).

There were no signs of ischemia detected in any of the patients by the automatic analysis of the ST-segment; all ST aberrations were within 0.1 mV. In addition, no patient had any postoperative enzyme elevation suggesting perioperative myocardial infarction.

The preischemic blood flow measured in the coronary sinus was 75 ± 13 mL/min. There was a trend toward elevated flow at 1 and 10 minutes reperfusion (Fig 1), although this did not reach significance.

View larger version (10K): [in this window] [in a new window]   Fig 1. Coronary sinus blood flow. Values are given as mean ± SEM (isch = ischemia; preisch = preischemia; rep = reperfusion).

View larger version (19K): [in this window] [in a new window]   Fig 2. Arterial and coronary sinus lactate levels and arteriovenous difference in lactate levels (AV diff) on the left Y-axis, and myocardial lactate extraction on the right Y-axis. Values are given as means ± SEM. **p < 0.01, analysis of variance, repeated measures of variance with Bonferroni multiple comparison, compared with preischemic values; + p < 0.05, Student’s t test comparing arterial and coronary sinus levels.

View larger version (18K): [in this window] [in a new window]   Fig 3. Total arterial and coronary sinus oxygen content (CaO2 and CvO2, respectively) and arteriovenous oxygen difference (AVO2 diff) on the left Y-axis, and myocardial oxygen consumption on the right Y-axis. Values are given as means ± SEM.

Outflow of 6-Keto-PGF₁, ET-1, and NO

1

1

1

1

View larger version (20K): [in this window] [in a new window]   Fig 4. Arterial and coronary sinus levels of 6-ketoPGF1 and arteriovenous difference in 6-ketoPGF1 levels (AVO2 diff) on the left Y-axis and 6-ketoPGF1 extraction on the right Y-axis. Data are presented as mean ± SEM. *p < 0.05; **p < 0.01, analysis of variance with repeated measures and Bonferroni multiple comparison, compared with preischemic values.

	Comment

Top Abstract Introduction Patients and methods Results Comment References

 
This study shows that the limited ischemia associated with CABG off bypass induces changes in myocardial metabolism with production of lactate in the heart. (Theoretically the elimination of the metabolic features of ischemia could be accomplished by the placement of an endocoronary shunt, a surgical technique not studied in this investigation.) Furthermore, there was an increased outflow of 6-keto-PGF₁ immediately upon reperfusion of the ischemic myocardium, indicating activation of the vascular endothelium with synthesis and release of prostacyclin. There were, however, no changes in the cardiac outflow of NO or ET-1 from the heart during the ischemia or at reperfusion.

Myocardial lactate production is considered to be a good indicator of myocardial ischemia [7]; however, coronary sinus lactate levels only vaguely reflect the elevated lactate levels in ischemic tissue [6]. The present finding of rather moderate myocardial lactate production, during and early after ischemia, therefore most likely represents true myocardial ischemia. This also implies that the lack of ST segment changes in the ECG are of limited value, particularly because of low sensitivity [7], and that the absence of perioperative ST changes in the patients in the present study has little bearing on assessment of ischemia.

Already, under basal conditions, the heart extracts a high and relatively fixed percentage of the oxygen from the coronary arterial blood. When the oxygen demand is not met by sufficient perfusion, ischemia develops. In our study the myocardial arteriovenous oxygen difference decreased during early reperfusion, whereas oxygen extraction increased. These changes were not statistically significant, but it might be assumed that during the postischemic hyperemia shunting of blood occurs in and adjacent to the previously ischemic myocardium.

Endothelium-derived vasoactive substances, including the vasodilators prostacyclin and NO and the vasoconstrictor ET, are involved in the local regulation of coronary blood flow. In addition to direct effects on the vascular smooth muscle tone, they have all been suggested to be of importance in the regulation of cardiac function during both physiological and pathophysiological conditions. Thus, NO, prostaglandin, and ET are all among a number of endogenous substances that have been suggested to mediate ischemic preconditioning and to have a protective effect on the development of myocardial infarction.

Hypoxia and ischemia are well-known stimuli for prostaglandin synthesis [11–13]. Prostacyclin, derived primarily from the vascular endothelium, is the main prostaglandin formed in the heart [14, 15]. Prostacyclin has potent vasodilator properties and has been suggested to have myocardial and endothelium protective actions during ischemia with infarct-limiting capacity and restoration of impaired endothelium-derived NO-release [16, 17]. Furthermore, prostaglandin products seem to be of importance in the local regulation of coronary blood flow in patients with coronary artery disease [18]. The outflow of prostacyclin from the heart during ischemia is pH-dependent and can be blocked by cyclooxygenase inhibitors such as indomethacin [18], suggesting active release and not only a spillover from disrupted endothelial cells. This is supported by the present study with lack of ET-1 or NO release from the heart, which would be expected from a damaged endothelium. Interestingly, prostacyclin is well known to cause C-fiber activation [15], and peptide release from C-fiber afferents during myocardial ischemia in a similar group of patients was recently demonstrated [19].

We did not detect any postischemic increased myocardial outflow suggesting release of ET or NO in the patients. However, this could reflect difficulties with detection of possibly released substances, and the possibility exists that the sampling periods may be too short, too late, or too few to detect any released NO or ET. In accordance, reperfusion of the ischemic isolated rabbit heart causes an immediate increased outflow of prostacyclin, whereas the outflow of NO is considerably delayed [18]. With regard to ET it has been estimated that more than 90% of ET is released abluminally [20], ie, toward the smooth muscle cells, and therefore plasma levels may represent only a very small portion of released peptides.

Whether the local ischemia and influence on the endothelium causes alterations in vascular reactivity has not been addressed in this study. It is well known that short-term ischemia can cause impairment of endothelium-dependent vasodilation, with important clinical implications in terms of decreased vasodilator capacity, susceptibility to coronary vasospasm, and development of coronary stenosis [8].

In conclusion, in this study we have demonstrated that a brief period of ischemia causes significant changes in cardiac metabolism and influences the vascular endothelium. CABG without CPB eliminates the use of the heart-lung machine, but to what extent this is superior regarding cardiac protection and endothelial preservation compared to conventional bypass surgery remains to be shown.

	Acknowledgments

 
The technical assistance by certified registered nurse anesthetist (CRNA) Gunilla Barr is gratefully acknowledged. This work was supported by grants from the Wallenberg Foundation, The Swedish Heart-Lung Foundation, the Swedish Medical Research Council, and funds from the Karolinska Institute.

	References

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