Biomechanical characterization of the native porcine aortic root.

A thorough understanding of the well-functioning, native aortic root is pivotal in an era, where valve sparing surgical techniques are developed and used with increasing frequency. The objective of this study was to characterize the local structural stiffness of the native aortic root, to create a baseline for understanding how different surgical interventions affect the dynamics of the aortic root. In this acute porcine study (N = 10), two dedicated force transducers were implanted to quantify the forces acting on both the annular plane and on the sinotubular junction (STJ). To assess the changes in geometry, eleven sonomicrometry crystals were implanted within the aortic root. The combination of force and length measurements yields the radial structural stiffness for each segment of the aortic root. The least compliant segment at the annular plane was the right-left interleaflet triangle with a stiffness modulus of 1.1 N mm-1 (SD0.4). At the sinotubular junction the same segment (right-left) was most compliant, compared with the two other segments, however not statistically significant different. The elastic energy storage was derived from the aortic root pressure volume relationship; the mean elastic energy storage was 826 µJ (SD529). In conclusion, the aortic root has been characterized in terms of both segmental forces, segmental change in length and elastic energy storage. This study is the first to assess the radial structural stiffness of different segments of the aortic root. The presented data is reference for further studies regarding the impact of surgical interventions on the aortic root.

The giraffe kidney tolerates high arterial blood pressure by high renal interstitial pressure and low glomerular filtration rate.

BACKGROUND: The tallest animal on earth, the giraffe (Giraffa camelopardalis) is endowed with a mean arterial blood pressure (MAP) twice that of other mammals. The kidneys reside at heart level and show no sign of hypertension-related damage. We hypothesized that a species-specific evolutionary adaption in the giraffe kidney allows normal for size renal haemodynamics and glomerular filtration rate (GFR) despite a MAP double that of other mammals. METHODS: Fourteen anaesthetized giraffes were instrumented with vascular and bladder catheters to measure glomerular filtration rate (GFR) and effective renal plasma flow (ERPF). Renal interstitial hydrostatic pressure (RIHP) was assessed by inserting a needle into the medullary parenchyma. Doppler ultrasound measurements provided renal artery resistive index (RI). Hormone concentrations as well as biomechanical, structural and histological characteristics of vascular and renal tissues were determined. RESULTS: GFR averaged 342 ± 99 mL min(-1) and ERPF 1252 ± 305 mL min(-1) . RIHP varied between 45 and 140 mmHg. Renal pelvic pressure was 39 ± 2 mmHg and renal venous pressure 32 ± 4 mmHg. A valve-like structure at the junction of the renal and vena cava generated a pressure drop of 12 ± 2 mmHg. RI was 0.27. The renal capsule was durable with a calculated burst pressure of 600 mmHg. Plasma renin and AngII were 2.6 ± 0.5 mIU L(-1) and 9.1 ± 1.5 pg mL(-1) respectively. CONCLUSION: In giraffes, GFR, ERPF and RI appear much lower than expected based on body mass. A strong renal capsule supports a RIHP, which is >10-fold that of other mammals effectively reducing the net filtration pressure and protecting against the high MAP.

Serotonin markers show altered transcription levels in an experimental pig model of mitral regurgitation.

Serotonin (5-hydroxytryptamine, 5-HT) signalling is implicated in the pathogenesis of myxomatous mitral valve disease (MMVD) through 5-HT1B receptor (R), 5-HT2AR and 5-HT2BR-induced myxomatous pathology. Based on increased tryptophan hydroxylase-1 (TPH-1) and decreased serotonin re-uptake transporter (SERT) in MMVD-affected valves, increased valvular 5-HT synthesis and decreased clearance have been suggested. It remains unknown how haemodynamic changes associated with mitral regurgitation (MR) affect 5-HT markers in the mitral valve, myocardium and circulation. Twenty-eight pigs underwent surgically induced MR or sham-operation, resulting in three MR groups: control (CON, n = 12), mild MR (mMR, n = 10) and severe MR (sMR, n = 6). The gene expression levels of 5-HT1BR, 5-HT2AR, 5-HT2BR, SERT and TPH-1 were analysed using quantitative PCR (qPCR) in the mitral valve (MV), anterior papillary muscle (AP) and left ventricle (LV). MV 5-HT2BR was also analysed with immunohistochemistry (IHC) in relation to histological lesions and valvular myofibroblasts. All 5-HTR mRNAs were up-regulated in MV compared to AP and LV (P <0.01). In contrast, SERT and TPH-1 were up-regulated in AP and LV compared to MV (P <0.05). In MV, mRNA levels were increased for 5-HT2BR (P = 0.02) and decreased for SERT (P = 0.03) in sMR vs. CON. There were no group differences in 5-HT2BR staining (IHC) but co-localisation was found with α-SMA-positive cells in 91% of all valves and with 33% of histological lesions. In LV, 5-HT1BR mRNA levels were increased in sMR vs. CON (P = 0.01). In conclusion, these data suggest that MR may affect mRNA expression of valvular 5-HT2BR and SERT, and left ventricular 5-HT1BR in some pigs.

A mathematical model of the mechanical link between shortening of the cardiomyocytes and systolic deformation of the left ventricular myocardium.

BACKGROUND: Left ventricular myocytes are arranged in a complex three-dimensional mesh. Since all myocytes contract approximately to the same degree, mechanisms must exist to enable force transfer from each of these onto the framework as a whole, despite the transmural differences in deformation strain. This process has hitherto not been clarified in detail. OBJECTIVE: To present a geometrical model that establishes a mechanical link between the three-dimensional architecture and the function of the left ventricular myocardium. METHODS: The left ventricular equator was modeled as a cylindrical tube of deformable but incompressible material, composed of virtual cardiomyocytes with known diastolic helical and transmural angles. By imposing reference circumferential, longitudinal, and torsional strains onto the model, we created a three-dimensional deformation field to calculate passive shortening of the myocyte surrogates. We tested two diastolic architectures: 1) a simple model with longitudinal myocyte surrogates in the endo- and epicardium, and circular ones in the midwall, and 2) a more accurate architecture, with progressive helical angle distribution varying from -60° in the epicardium to 60° in the endocardium, with or without torsion and transmural cardiomyocyte angulation. RESULTS: The simple model caused great transmural unevenness in cardiomyocyte shortening; longitudinal surrogates shortened by 15% at all depths equal to the imposed longitudinal strain, whereas circular surrogates exhibited a maximum shortening of 23.0%. The accurate model exhibited a smooth transmural distribution of cardiomyocyte shortening, with a mean (range) of 17.0 (13.2-20.8)%. Torsion caused a shortening of 17.0 (15.2-18.9)% and transmural angulation caused a shortening of 15.2 (12.4-18.2)%. Combining the effects of transmural angulation and torsion caused a change of 15.2 (13.2-16.5)%. CONCLUSION: A continuous transmural distribution of the helical angle is obligatory for smooth shortening of the cardiomyocytes, but a combination of torsional and transmural angulation changes is necessary to execute systolic mural thickening whilst keeping shortening of the cardiomyocytes within its physiological range.

In Vitro System for Measuring Chordal Force Changes Following Mitral Valve Patch Repair.

BACKGROUND: Attention towards optimization of mitral valve repair methods is increasing. Patch augmentation is one strategy utilized to correct functional mitral regurgitation or systolic anterior motion in complex mitral valve repairs. This article describes a system for investigating the redistribution of chordae tendineae tension as a reflection of altered stress distribution of the valve leaflet following patch augmentation. METHODS AND MATERIALS: An in vitro test setup was constructed to hold native porcine mitral valves containing an annulus and papillary muscle positioning system. The alterations caused by patch augmentation should be visual from both the atrial and ventricular views. Ventricular pressure was regulated stepwise in a range of 0-150 mmHg. To test the system, the anterior mitral leaflet was extended by a pericardial patch sutured to the mid/basal part of the leaflet, and the chordae tendineae force was measured as the ventricular pressure was applied. RESULTS: The system demonstrated the capacity to hold native porcine mitral valves and introducing patch repairs according to clinical practice. The porcine mitral valve test setup indicated strong correlation between the forces in the mitral valve secondary chordae tendineae and the applied transvalvular pressure (R2 = 0.95). CONCLUSION: This test setup proved the ability to obtain normal mid-systolic mitral valve function, secondary chordae force measurements, and important preservation of the visual access: Hence, obtaining the pressure-force relationship as well as identifying any shift of the secondary chordae insertion point on the anterior leaflet relative to the coaptation zone was made possible.

Heart rate limitation and cardiac unloading in sevoflurane post-conditioning.

BACKGROUND: Sevoflurane post-conditioning (SePost) has been found to alleviate ischemic myocardial reperfusion injury through the activation of prosurvival kinases. Lowered myocardial oxygen demand from reduced cardiac work may also contribute to cardioprotection, and is much less well-studied. Our aim was to examine the simultaneous effects of SePost on cardiac work (here, rate-pressure product, RPP) and myocardial infarct size in a porcine model. METHODS: Anesthetized 25 kg pigs were randomly allocated to two groups and underwent 45 min regional coronary artery balloon occlusion and subsequent 2 h reperfusion. SePost (n = 10) was given as sevoflurane 1.5-3% end-tidal concentration during reperfusion while controls (n = 12) were untreated. Aortic blood pressure was measured directly, while mixed-venous oxygen saturation and cardiac output were measured in the pulmonary artery. Cardiac work was determined as RPP. Post-mortem, histologic myocardial infarct size (IS), and area at risk were determined in transverse heart slices after tetrazolium stain. RESULTS: Myocardial infarct size was reduced from (control) 55.0 (mean) ± 13.6% (standard deviation) to 32.5 ± 13.4% in group SePost (P = 0.0009). During reperfusion, SePost resulted in lower heart rate (P = 0.0003), cardiac output (P = 0.0123), mixed-venous oxygen saturation (P = 0.0103), blood pressure, and RPP (P < 0.0001). RPP was highly correlated to IS (P = 0.0055). CONCLUSION: SePost (1.5-3%) reduced infarct size after regional myocardial ischemia in vivo and reduced cardiac work was significantly correlated to myocardial salvage.

Post-conditioning with cyclosporine A fails to reduce the infarct size in an in vivo porcine model.

BACKGROUND: Cyclosporine A has generated intense interest in the field of cardioprotection due to its ability to protect the mitochondria at reperfusion by blocking the opening of the mitochondrial permeability transition pore. The aim of our study was to examine the cardioprotective effect of Sandimmun, a clinically available formulation of cyclosporine A, in an in vivo large mammal model. METHODS: Forty-eight pigs were randomly allocated to one of three groups: (i) Control group (Con, n=19), (ii) Cyclosporine group, (Cyclo, n=19) Sandimmun 10 mg/kg i.v. bolus 5 min before reperfusion and (iii) Pre-conditioning group (Precon, n=10) two cycles of 10 min ischemia interspersed with 30-min reperfusion. The study was further sub-divided into a metabolic protocol, evaluating myocardial metabolism by measuring changes in the interstitial lactate concentration, and a coronary flow protocol. All animals were subjected to 40 min of left anterior descending coronary artery occlusion, followed by 180 min of reperfusion before histochemical staining and assessment of infarct size by planimetry. RESULTS: Infarct sizes were measured as: Con 51.4 +/- 16.5%, Cyclo 47.3 +/- 15.7% and Precon 2.4 +/- 3.6%, with no significant difference between the Con and Cyclo groups but a highly significant difference between the Precon and Cyclo and Con groups (P<0.0001 for both comparisons). In the Cyclo group, the interstitial lactate concentration was significantly increased compared with the Con group at 6-min reperfusion, although significantly lower at 14 min presumably due to accelerated washout. CONCLUSION: In this large animal model, a 10 mg/kg bolus administration of Sandimmun 5 min before reperfusion did not reduce the infarct size.

Can sites prone to flow induced vascular complications in a-v fistulas be assessed using computational fluid dynamics?

Arterio-venous fistulas (shunts between arteries and veins) are the preferred vascular access for hemodialysis. Despite their superior patency, compared with synthetic tubes and grafts, functional problems and inadequate flow rates are the common complications. Local flow conditions, in particular low and oscillating wall shear stresses (WSS), are central to vascular problems and a robust framework for analyzing flow conditions in vascular structures could provide an understanding of the mechanisms leading to vascular complications, such as stenoses, aneurisms, and thromboses. We hypothesize that a validated computational fluid dynamics (CFD) framework can be used to identify critical fistula configurations with elevated risk of complications. Therefore, the aim of the present study was to develop a CFD framework for analyzing fluid flow in complex vascular structures, such as arterio-venous fistulas validated by comparisons of in vitro volume flows with CFD results and flow fields from ultrasound scans with CFD simulations. Volume flows measured in vitro and CFD data differed quantitatively. However, good relative correlations exist between the data using logarithmic scales. Qualitatively, visual comparisons between ultrasound and CFD images showed good agreement between the two methods. In addition, WSS levels and the oscillatory shear index (OSI) were calculated and visualized on the model surface. The method was successfully validated and the method is deemed suitable for more thorough investigations into the field of vascular complications in a-v fistulas.

Jugular venous pooling during lowering of the head affects blood pressure of the anesthetized giraffe.

How blood flow and pressure to the giraffe's brain are regulated when drinking remains debated. We measured simultaneous blood flow, pressure, and cross-sectional area in the carotid artery and jugular vein of five anesthetized and spontaneously breathing giraffes. The giraffes were suspended in the upright position so that we could lower the head. In the upright position, mean arterial pressure (MAP) was 193 +/- 11 mmHg (mean +/- SE), carotid flow was 0.7 +/- 0.2 l/min, and carotid cross-sectional area was 0.85 +/- 0.04 cm(2). Central venous pressure (CVP) was 4 +/- 2 mmHg, jugular flow was 0.7 +/- 0.2 l/min, and jugular cross-sectional area was 0.14 +/- 0.04 cm(2) (n = 4). Carotid arterial and jugular venous pressures at head level were 118 +/- 9 and -7 +/- 4 mmHg, respectively. When the head was lowered, MAP decreased to 131 +/- 13 mmHg, while carotid cross-sectional area and flow remained unchanged. Cardiac output was reduced by 30%, CVP decreased to -1 +/- 2 mmHg (P < 0.01), and jugular flow ceased as the jugular cross-sectional area increased to 3.2 +/- 0.6 cm(2) (P < 0.01), corresponding to accumulation of approximately 1.2 l of blood in the veins. When the head was raised, the jugular veins collapsed and blood was returned to the central circulation, and CVP and cardiac output were restored. The results demonstrate that in the upright-positioned, anesthetized giraffe cerebral blood flow is governed by arterial pressure without support of a siphon mechanism and that when the head is lowered, blood accumulates in the vein, affecting MAP.

Hypertrophied hearts: what of sevoflurane cardioprotection?

BACKGROUND: Recent studies have demonstrated that inhalation anaesthetics, like sevoflurane, confer cardioprotection both experimentally and clinically. However, coexisting cardiac disease might diminish anaesthetic cardioprotection and could partly explain why the clinical results of cardioprotection with anaesthetics remain controversial--in contrast to solid experimental evidence. Concomitant left ventricular hypertrophy is found in some cardiac surgery patients and could change cardioprotection efficacy. Hypertrophy could potentially render the heart less susceptible to sevoflurane cardioprotection and more susceptible to ischaemic injury. We investigated whether hypertrophy blocks sevoflurane cardioprotection, and whether tolerance to ischaemia is altered by left ventricular hypertrophy, in an established experimental animal model of ischaemia-reperfusion. METHODS: Anaesthetized juvenile pigs (n=7-12/group) were subjected to 45 min distal coronary artery balloon occlusion, followed by 120 min of reperfusion. Controls were given pentobarbital, while sevoflurane cardioprotection was achieved by 3.2% inhalation throughout the experiment. Chronic banding of the ascending aorta resulted in left ventricular hypertrophy development in two further groups and these animals underwent identical ischaemia-reperfusion protocols, with or without sevoflurane cardioprotection. Myocardial infarct sizes were compared post-mortem. RESULTS: The mean myocardial infarct size (% of area-at-risk) was reduced from mean 55.0 (13.6%) (+/-SD) in controls to 17.5 (13.2%) by sevoflurane (P=0.001). Sevoflurane reduced the infarct size in hypertrophied hearts to 14.6 (10.4%) (P=0.001); however, in hypertrophic controls, infarcts were reduced to 34.2 (10.2%) (P=0.001). CONCLUSION: Sevoflurane abrogated ischaemic injury to similar levels in both normal and left ventricular hypertrophied hearts.

Sevoflurane improves myocardial ischaemic tolerance in a closed-chest porcine model.

AIMS: Volatile anaesthetics prevent experimental myocardial ischaemia-reperfusion injury (I/R) in several species, but this finding is partially inconsistent with clinical evidence. Some experimental models may not accurately represent the complex signal transduction pathways triggered by volatile anaesthetics. We therefore investigated sevoflurane I/R prevention in vivo in a porcine model with greater likeness to human physiology than models previously used and compared it with neutral anaesthetic. METHODS AND RESULTS: Myocardial infarct size [IS/AAR] was compared in three groups of pigs (N=35) randomised to Control anaesthesia (pentobarbital infusion, n=12), sevoflurane inhalation alone (end-tidal concentration 3.2%) (Sevo, n=9), or both Combined (n=14), throughout ischaemia and reperfusion. Anterior/septal myocardial infarcts resulted from distal LAD coronary artery occlusion by balloon catheter for 45 min followed by 120 min of reperfusion. [IS/AAR] was measured in tetrazolium-stained heart slices after standardised image processing with computer-assisted planimetry. Measurements included full invasive monitoring. Control animals developed infarction in 55.0 +/- 3.9% (SEM) of the area at risk, Sevo in 17.5 +/- 4.4% (P=0.0002), and Combined with pentobarbital in 24.3 +/- 3.8% (P=0.0001) of the AAR, sevoflurane reducing infarct size significantly (68% and 60%, respectively). CONCLUSIONS: Sevoflurane markedly decreased myocardial infarct size after prolonged coronary occlusion in a porcine model. In addition to novel sevoflurane cardioprotection in the closed-chest model, which is more comparable to normal human hearts than models previously used, sevoflurane cardioprotection is substantiated in the juvenile intact organism. The perspectives underline recommending volatile anaesthetics in risk patients and in cardiac surgery.

Post-conditioning reduces infarct size in an open-chest porcine acute ischemia-reperfusion model.

BACKGROUND: Timely reperfusion is a prerequisite for myocardial salvage; however, re-oxygenation of the ischemic myocardium initiates reperfusion injury. Post-conditioning diminishes the detrimental aftermath of an acute myocardial infarction through alleviation of reperfusion injury. Ischemic post-conditioning consists of a series of brief interruptions in the coronary blood supply that has to be applied within the first minutes after re-establishing the coronary flow. METHODS: Sixteen female mixed Danish Landrace and Yorkshire pigs weighing 20 kg were included. The heart was exposed through a midline sternotomy. A snare was positioned around the left anterior descending coronary artery downstream of the second diagonal branch. After randomization to either no treatment (control group) or treatment by ischemic post-conditioning (post-conditioning group), the pigs underwent 45 min of ischemia and 180 min of reperfusion. The post-conditioning group had a post-conditioning algorithm applied consisting of 15 s of reperfusion alternating with 15 s of re-occlusion repeated 10 times. RESULTS: The groups were comparable with regard to body weight, hemodynamics and the size of the area at risk. The post-conditioning group had an absolute reduction in infarct size of 18.1% [confidence interval (CI): 6.2: 30.0%] compared with the control group (P=0.0056). In the post-conditioning group, infarction developed in 39.6+/-12.0% (1 SD) of the area at risk compared with 57.8+/-10.2% (1 SD) in the control group. CONCLUSION: When ischemic post-conditioning was applied at reperfusion, we found an absolute reduction in infarct size of 18.1% presumably attributable to a diminished reperfusion injury. The model we have developed is suitable for further studies of this promising intervention.

Gaseous emboli detection based on a dual-wavelet transform analysis.

Emboli monitoring is nowadays based on the assessment of microembolic signals by Doppler ultrasound. However, the present systems have problems in detecting multiple emboli. A more dedicated algorithm for post-processing of the recorded Doppler signals was proposed. Based on the hypothesis that single and multiple gaseous emboli can be quantified by combining discrete and continuous wavelet transformation, the aim of this study was to detect gaseous emboli and to validate our method visually. A flow rig was used where gaseous emboli were generated. Doppler signals and visual validation data of gaseous emboli were acquired simultaneously. Microembolic signals were extracted and analysed using wavelet transformation. Results were validated against a visual reference. At various degrees of bubble generation, the system had 100 per cent detection during a low frequency of bubble generation but an estimation error of 7.4 per cent during a high frequency of bubble generation. The estimation error varied between -7.4 and +3 per cent. The system had a higher rate of success in detecting large gaseous emboli in small numbers than small gaseous emboli in large numbers. Single and double emboli were successfully detected and separated, whereas gaseous emboli clouds could be detected but not quantified. Being able to separate simultaneous gaseous emboli may offer new means of increasing detectability for embolism monitoring.

Does the pre-ischaemic administration of sevoflurane reduce myocardial stunning? A porcine experimental model.

BACKGROUND: In a porcine model, the cardioprotective effect of sevoflurane was studied with regard to the preservation of myocardial contractility (myocardial stunning) after a myocardial ischaemic insult. METHODS: Twenty-seven pigs were randomized to receive either a dual 4% sevoflurane inhalation period as a supplement to pentobarbital anaesthesia or pentobarbital anaesthesia only before a 15-min ischaemic insult on the left anterior descending coronary artery. The ischaemic period was followed by 180 min of reperfusion. Myocardial contractility was assessed by myocardial sonomicrometry. RESULTS: A significant difference was found between the sevoflurane group and the control group at 5 min of reperfusion. However, subsequently, there was no overall difference between the two groups. CONCLUSION: Sevoflurane administered as a pre-ischaemic bolus does not provide long-term improvement of the myocardial contractility. However, it can be speculated that sevoflurane may induce an early improvement in contractility.

Pre-occlusion ischaemia, not sevoflurane, successfully preconditions the myocardium against further damage in porcine in vivo hearts.

BACKGROUND: Sevoflurane is proposed to possess important tissue protective effects based on experimental ischaemia-reperfusion studies from models with collateral coronary flow, unlike that of the normal human or the porcine heart. The objective was to evaluate the infarct-reducing capability of pre-ischaemic sevoflurane inhalation on myocardial infarct size in a porcine model. METHODS AND MATERIALS: The study comprised 33 pigs under pentobarbital anaesthesia. Animals were divided into three groups: control (CON), sevoflurane intervention (SEVO) and ischaemic preconditioning (IP). The distal left anterior descending coronary artery was occluded for 40 min with a percutaneous coronary intervention catheter. Before occlusion, group IP underwent two 5-min ischaemia cycles, whereas SEVO received two 5-min sevoflurane 4%v/v inhalation cycles. Animals were reperfused for 150 min. We then measured risk area (AAR) and infarct size (IS) after tetrazolium staining. The [IS/AAR-ratio] was calculated. Haemodynamics and transthoracic tissue-Doppler echocardiography were monitored. RESULTS: Control animals developed a myocardial infarction in 46.4 (+/- 6.2)% (mean +/- SEM) of the AAR. Both SEVO and IP groups had infarction mitigated, to 34.4 (5.7)% and 23.1 (5.3)%, respectively; however, only in the IP group was this significant. No significant differences between groups with respect to AAR, haemodynamics or echocardiographic variables were found. CONCLUSION: Pre-ischaemic sevoflurane was found to reduce the extent of myocardial necrosis, but the change was not significant, whereas IP reduced IS by 50% (P= 0.038). Cardioprotection is species related and no previous results from porcine models have found sevoflurane to reduce IS. Anaesthetic washout, insufficient exposure or collateral coronary blood supply, dissimilar to human, may account for positive results in rodent models.

Increased expression of endothelin B receptor in static stretch exposed porcine mitral valve leaflets.

The aim of this study was to evaluate the effect of mechanical stretch on the expression of ET-1 and ET(A)- and ET(B)-receptors in porcine mitral valve leaflets. Leaflet segments from 10 porcine mitral valves were exposed to a static stretch load of 1.5 N for 3.5h in buffer at 37 degrees C together with matching control segments. Subsequently, the mRNA expression of ET-1, ET(A)-R and ET(B)-R was measured by real-time RT-PCR in the chordal insertion areas. The analyses showed an increased transcription of ET(B)-receptors in stretch-exposed leaflet segments compared to unstretched segments median 2.23 (quartiles 1.37 and 2.70) vs. median 1.56 (quartiles 1.38 and 2.17, P=0.03) whereas the mRNA expression of ET(A)-receptors (P=0.90) and ET-1 (P=0.51) remained unchanged. Stretch increased the expression of ET(B)-receptors in porcine mitral valve leaflets. The finding could lead to a better understanding of the pathogenesis of myxomatous mitral valve disease.

Postoperative treatment with low molecular weight heparin after right heart assist for coronary artery bypass grafting.

Right heart assist (RHA) was used for coronary artery bypass grafting (CABG). We explored the affection of the coagulation system during surgery and evaluated two different antithrombotic treatments postoperatively. The pilot study comprised 14 patients. During surgery activated clotting time (ACT) was kept > 200 sec. By random the patients were selected to different postoperative treatments. The control group received acetyl salicylic acid (ASA) 150 mg daily, the intervention group received ASA 150 mg daily and Low Molecular Weight Heparin (LMWH) 5000 IU x2 for three days. Serum levels of prothrombin fragment 1 and 2 (F 1 + 2), plasmin-antiplasmin product (PAP), anti-Xa activity and functional antithrombin (ATIII) were measured. During surgery there was no increase of F 1 + 2 or PAP. After protamin was administered there was a significant increase of F 1 + 2 but not in PAP during the next 6 hours. Postoperative antithrombotic treatment with LMWH seems to normalise F1 + 2 while ASA does not. ACT level > 200 sec. seems sufficient for RHA-CABG surgery. Fibrinolytic agents are not necessary. It seems that postoperative LMWH treatment prevents increased thrombin formation. General recommendations with respect to antithrombotic treatment beyond ASA can not be made based on study.

Evaluation of a novel method for measuring tissue blood flow and gases.

In clinical practice a method for assessment of tissue vitality is a sought-after tool. We have developed a new sensor principle, which is able to register changes in tissue concentration of O2 and tissue flow. The technique is based on diffusion of inert gases and mass spectrometer detection of gaseous metabolites. It was hypothesized that the new sensor could register changes in vital parameters after induction and release of an ischaemic insult to muscular tissue. The sensor performance was evaluated in ten anaesthetized pigs subjected to local muscular ischaemia. Preliminary data from this study indicate the validity of registered hypoxia and reduction in tissue flow as a consequence of compromised blood supply. It was concluded that although precise calibration of the technique is not yet established, it holds promise as a technique that can be used to monitor changes in tissue vitality.

Right heart assist for beating heart coronary artery bypass grafting.

OBJECTIVE: Cardiopulmonary bypass used in conventional coronary artery bypass surgery (cCABG) entails a risk of complications. Consequently, the trend is moving towards off-pump coronary artery bypass (OPCAB). This procedure, however, may lead to haemodynamic instability due to kinking of the right ventricle when the posterior aspect of the heart is exposed. The aim of the study was to establish if a right-sided circulatory assist device (RHA) was able to maintain haemodynamic stability during OPCAB procedures. METHOD: In a prospective study 50 RHA-OPCAB patients and a control group of 50 cCABG patients were examined. Before accessing the marginal arteries, an RHA was established in the RHA-OPCAB patients. RESULTS: A stable haemodynamic condition was achieved for 98% of the RHA-OPCAB patients. The study group had less postoperative chest drain bleeding (P<0.001), shorter ventilation time (P=0.001), and lower blood levels of creatine kinase (CK) and brain CK (P<0.001) compared to the control group. CONCLUSION: The results indicate that RHA-OPCAB is a realistic alternative to cCABG. The procedure can be safely performed most likely resulting in reduced postoperative bleeding, myocardial damage, and ventilation time.