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The present study aimed to investigate the impact of pulmonary hypertension (PH) on short-term survival after LVAD implantation with or without tricuspid annuloplasty valve repair (TVr) performed to treat regurgitation and avoid RV-failure post-LVAD insertion. Data of 24 patients receiving LVAD-implantation are assessed and compared. The primary outcome is in-hospital survival. Of 24 patients studied, 17 (70.8%) survived hospital stay: age (62.2 ± 12.3 vs 66.1 ± 8.5 years), preoperative LV-EF (15.9 ± 5.3% vs 13.6 ± 3.8%) vs. non-survivors, respectively. Survivors received preoperatively Impella (35.3% vs 0%, p = 0.037), had shorter intubation time (3.3 ± 3.5 vs 11.4 ± 11.1 days, p = 0.0053) and ICU stay (12.4 ± 9.8 vs 34.3 ± 34 days, p = 0.01) versus non-survivors. Non-survivors had more severe PH (37.0 ± 9.6 vs 29.8 ± 12.2 mmHg, p = 0.044) than survivors. Linear regression analysis revealed that cardiac operations performed concomitant with LVAD implantation increased mortality in patients with severe PH ( p = 0.04), whereas isolated TVr performed concomitant with LVAD implantation did not increase mortality neither in the entire patient cohort ( p = 0.569) nor in patients with severe PH ( p = 0.433). LVAD with TVr improved survival in patients suffering from severe PH (vs. moderate PH), however this difference did not reach the level of significance due to the small number of patients ( p = 0.08). LVAD-implantation alone improved survival of patients suffering from moderate PH ( p = 0.045, vs. severe PH). Surgical correction of tricuspid regurgitation concomitant or before LVAD implantation improves early survival in patients suffering from severe PH when compared to LVAD implantation alone. Patients suffering from severe PH tend to benefit more from TVr than those suffering from moderate PH.

Thoracic endovascular aortic repair (TEVAR) is the treatment option of choice for almost all pathologies of the descending thoracic aorta. The aim of the present study is to determine the impact of aortic pathology on the occurrence of post-implantation syndrome (PIS) after TEVAR.Seventy-four patients undergoing TEVAR for aortic dissection (TAD, 25), aortic aneurysm (TAA, 26), and aortic rupture or perforated ulcer (TAR/PAU, 23) were included in this retrospective study. The clinical outcome measures were persistent inflammation at hospital discharge and in-hospital mortality.PIS was assessed in 22.97% of all patients, predominantly in the TAD group (p=0.03). CRP increased after TEVAR (156.6± 94.5, p0.001; 108.1±57.7, p0.01 and 117.8±70.4, p0.05) vs. baseline (58.1±77.5, 31.94±52.1 and 31.9±52.1 mg/L, in TAD, TAA and TAR/PAU, respectively) and this increase was more accentuated in TAD group (p0.05). Stent-length was similar in all groups (p=0.226), but correlated with postoperative CRP only in TAD (R=0.576, p=0.013). Fresh parietal thrombus correlated with CRP (R=0.4507, p=0.0005) and is (OR=1.0883, p=0.0001), together with the pathology of aortic dissection (OR=6.2268, p=0.0288), a predictor of PIS after TEVAR. Whereas mortality (5.4%) did not correlate with PIS (p=0.38) either with aortic pathology (p=0.225), hospital stay after TEVAR was significantly prolonged by PIS (p=0.03).Aortic dissection is associated with more inflammation after TEVAR than aortic aneurysm, rupture or perforated ulcer, with the amount of fresh parietal thrombus playing the most significant role in the occurrence of PIS. Importantly, PIS prolongs hospital stay but not mortality after TEVAR.

Objective: Long-term outcomes of mitral valve (MV) repair versus MV replacement for ischemic mitral regurgitation (IMR) in patients undergoing either prior (PCR) or concomitant coronary revascularization (CCR) by surgery (CABG) or intervention (PCI) are uncertain. Methods and Results: Of 446 patients receiving MV surgery for IMR between July 2006 and December 2010, 125 patients—87 CCR (69.1%) and 38 PCR (30.9%)—were eligible for inclusion in the study. Survival was higher in CCR versus PCR at long-term follow-up (78.83% vs. 57.9%, p = 0.016). The incidence of MACCE was lower in the CCR compared to PCR at both hospital discharge (34.11% vs. 63.57%, p = 0.003) and at follow-up (34.11% vs. 65.79%, p = 0.0008). Patients receiving CABG or CABG with PCI in PCR had higher mortality risks after MV surgery than CCR patients (X2 = 6.029, p = 0.014 and X2 = 6.466, p = 0.011, respectively). Whereas in the PCR group, MV repair and MV replacement achieved similar survival probability (X2 = 1.551, p = 0.213), MV repair in the CCR group led to improved survival compared to MV replacement (X2 = 3.921, p = 0.048). In MV replacement, LAD-CABG improved survival compared to LAD-PCI (U = 15,000.00, Z = −2.373 p = 0.018), and a substantial impact of arterial IMA-LAD grafting was revealed in the Cox-regression analysis (HR 0.334, CI: 0.113–0.989, p = 0.048) as opposed to venous-LAD grafting (HR 0.588, CI: 0.166–2.078, p = 0.410). Conclusion: Early treatment of IMR concomitant to coronary revascularization enhances long-term survival compared to delayed MV surgery after PCR. MV repair is not superior to MV replacement when performed late after coronary revascularization; however, MV repair leads to better survival than MV replacement when performed concomitantly with CABG with arterial LAD revascularization.

OBJECTIVES The pathophysiology of delirium after cardiac surgery is complex. The present study aims to determine perioperative risk factors and construct a scoring system for postoperative delirium based on the type of surgery. METHODS Three hundred patients undergoing coronary artery bypass grafting (CABG; n = 150) or valve and/or aortic surgery ± CABG (n = 150) were retrospectively evaluated. RESULTS The incidence of delirium (32%) was similar in subgroups (28.7% and 33.33%, P = 0.384). Delirium patients were older [71.3 (standard deviation: 8.5) vs 66.6 (standard deviation: 9.5), P < 0.001; 70.0 (standard deviation: 9.6) vs 62.5 (standard deviation: 12.6), P < 0.001] and required more packed red blood cell units [2.1 (standard deviation: 2.1) vs 4.2 (standard deviation: 4.0), P < 0.001; 2.4 (standard deviation: 3.3) vs 5.4 (standard deviation: 5.9), P < 0.001] and fresh frozen plasma units [6.1 (standard deviation: 2.9) vs. 8.0 (standard deviation: 4.2), P < 0.001; 6.3 (standard deviation: 3.4) vs 10.8 (standard deviation: 7.2), P < 0.001] in CABG and valve/aortic subgroups, respectively. Delirium was associated with longer operation time [298.3 (standard deviation: 98.4) vs 250.6 (standard deviation: 67.8) min, P < 0.001], cardiopulmonary bypass (CPB) time [171.5 (standard deviation: 54.9) vs 140.98 (standard deviation: 45.8) min, P < 0.001] and cardiac arrest time [112 (standard deviation: 35.9) vs 91.9 (standard deviation: 28.6), P < 0.001] only in the valve/aortic group (versus non-delirium). Multivariate regression analysis identified an association between delirium and age [odds ratio: 1.056 (95% confidence interval: 1.002–1.113), P = 0.041], CPB time [odds ratio: 1.1014 (95% confidence interval: 1.004–1.025), P = 0.007], fresh frozen plasma transfusion [odds ratio: 1.127 (95% confidence interval: 1.006–1.262), P = 0.039] and atrial fibrillation [odds ratio: 4.801 (95% confidence interval: 1.844–12.502), P < 0.001] after valve/aortic surgery (area under the curve 0.835, P < 0.001) and between delirium and age [odds ratio: 1.089 (95% confidence interval: 1.023–1.160), P = 0.007] and ventilation time [odds ratio: 1.068 (95% confidence interval: 1.026–1.113), P = 0.001] after isolated CABG (area under the curve 0.798, P < 0.001). The cross-validation of the results by k-fold logistic regression revealed for the entire patient cohort an overall average accuracy of the prediction model of 0.764, with a false-positive rate of 0.052 and a false-negative rate of 0.18. CONCLUSIONS Age, CPB time, ventilation, transfusion and atrial fibrillation are differently associated with delirium depending on the operative characteristics. Optimization of intraoperative parameters and use of risk calculators may enable early institution of pharmacotherapy and improve overall outcome after cardiac surgery.

Objectives We aimed to develop a simple, reliable, and timesaving technique for the therapy of thoracoabdominal aortic (TAA) aneurysms that are not suitable for endovascular repair. Methods In this pilot study, we sought to combine the advantages of classic open vascular procedure with the use of endoscopic surgical tools and small skin incisions to develop a minimally invasive approach for TAA replacement. The following procedures were used: endoscopic exposure and closure of the lower intercostal arteries; small posterolateral thoracotomy and left retroperitoneal incisions to expose the anastomotic regions of the aorta; partial anticoagulation; passive bypass and sequential aortic clamping; tunnelling of the graft through the native aortic lumen (endoaneurysmorrhaphy) and open performance of vascular anastomosis. Results Five mixed-breed dogs (25-35 kg) underwent minimally invasive TAA replacement. All animals survived the operation without blood transfusion (lowest Hb = 5.5 mg/dl). Total operation time was 364 ± 46.3 min. Clamping times were 17.6 ± 3.2 min for proximal anastomosis, 33.2 ± 2.48 min for visceral patch and 11 ± 2.3 min for distal anastomosis. The pull-through procedure of graft through the native aorta was performed during the visceral clamp time. Conclusions Surgical replacement of the TAA through small transverse incisions of the thoracic and abdominal wall is feasible and allows open performance of all vascular anastomosis with no leakage at any anastomotic site. Further experimental studies and clinical implementation are needed to establish the safety and long-term outcome of minimally invasive TAA replacement as a possible primary therapeutic tool for complex aneurysms that are not suitable for endovascular treatment and require open surgical repair.

Introduction: Acknowledging the superior long term patency of infrainguinal saphenous bypass to distal popliteal artery, debate continues regarding the choice of alternative conduits and possible surgical adjuncts to improve inflow and graft salvage. The objective of this retrospective study was to determine the effectiveness of proximal anastomotic patch as adjunct to open surgical below the knee popliteal revascularization.

Transapical transcatheter aortic valve implantation over mini left anterior thoracotomy (TA-TAVI) and sutureless aortic valve implantation over mini right anterior thoracotomy (RAMT-AVR) are considered indicated in a narrow range of high-risk patients not eligible for mini-sternotomy or for transfemoral endovascular procedures.

The purpose of this report is to determine the feasibility of short transverse skin incision (STI4 cm) for eversion (EEA) and patch (PEA) endarterectomy with or without shunt by comparing it with the outcomes after long transverse skin incision (LTI 4-8 cm).Of 164 elective consecutive patients (71 ± 2.73% symptomatic) operated at one institution over 24 months, 81 were treated with STI, while 83 patients received LTI. The LTI and STI groups did not differ in terms of age, symptoms, or risk factors. EEA or PEA under locoregional (LRA) or general (GA) anesthesia were performed.STI was associated with shorter operation times (75.19 ± 15.33 vs. 94.87 ± 41 and 99.4 ± 27.36 vs. 132.66 ± 51.32, respectively, P0.01) and similar clamping times (26.05 ± 5.71 vs. 26.07 ± 7.14 and 34.04 ± 9.49 vs. 42.5 ± 20.8, respectively) in the EEA and PEA groups that did not receive shunts compared with the corresponding LTI groups, and the operating room stays of the STI patients operated on GA were shorter than that of the corresponding LTI patients (181.11 ± 39.16 vs. 212.5 ± 64, P0.001). Nonsignificant differences were found between the corresponding STI and LTI shunt groups. No perioperative deaths occurred. STI was associated with less perioperative complications than LTI. Macroscopically nondistinguishable scar was present in 85% in the STI and 52% in the LTI groups (P0.001). Postoperative local irritation and paresthesia occurred similarly in the STI (11%) and LTI (14%) groups.STIs are feasible for PEA and EEA. STIs produce significantly better cosmetic outcomes and shorter operation times than LTI and have similar rates of complication and similar incidences of local discomfort. Although no neurological consequences of using STIs for PEAs with shunts were revealed, STI should be applied with caution until sufficient patch length and long-term patency of this procedure are demonstrated.

Intestinal injury is thought to play a central role in the occurrence of multiorgan dysfunction after on-pump coronary surgery. Clinical benefits of off-pump revascularisation remain, however, controversial.Hepatic enzymes and plasmatic IL-6, IL-8 and intestinal-type fatty acid binding protein (I-FABP) were determined in 20 patients (age 65-75) undergoing either on-pump (n = 10) or off-pump (n = 10) coronary surgery. Haemodynamic and biochemical parameters, catecholamine and volume therapy were monitored.Central venous pressure (CVP) was significantly higher in the off-pump group during and 12h after operation (9.5 ± 1.35 vs. 6.21 ± 0.63 mmH2O, p = 0.012). Higher GGT and GLDH levels occurred in the off-pump group and correlated with the elevated I-FABP levels at 24h (935.8 ± 83.7 vs. 370.4 ± 67.7 pg/mL, p0.001). CVP correlated with I-FABP peak values (Pearson's coefficient 0.852). IL-6 and IL-8 were released to a lower extent in the off-pump group compared to on pump (p0.05) at 24h (139.3 ± 27.7 vs. 279.4 ± 56.2 and 15.3 ± 7.4 vs. 38.5 ± 13.8 pg/mL) and at 72 h post-operatively (4.5 ± 2.1 vs. 30.1 ± 12.1 and 7.8 ± 1.2 vs. 17.1 ± 5.2 pg/mL).While inflammatory activation is reduced with CPB avoidance, elevated CVP during off-pump surgery is followed by temporary postoperative enterocyte damage that may threaten the normal function of the gastrointestinal system and lead - in certain groups of high risk patients--to irrecoverable injury.

Eversion endarterectomy (EEA) of the internal carotid artery requires less distal surgical exposure than conventional patch reconstruction endarterectomy. However, the technical success after EEA was tremendously contradictive especially with respect to the external carotid artery (ECA) patency rate. The purpose of this study was to determine the effect of elliptical EEA on the quality and outcome of external carotid artery desobliteration.Clinical outcome and carotid disease progression at one year were evaluated in thirty patients receiving EEA through short transverse skin incision either in general anesthesia (GA, 22 patients) or locoregional anesthesia (LRA, 8 patients).One patient (GA group) required early revision for bleeding. There was no postoperative stroke, nerve damage or death. At one year, ipsilateral systolic peak velocity (SPV) measurements showed no disease progression in the internal (75.30±19.31; 62.88±28.51 cm/s) or in the external carotid artery (118.92±58.30; 79.00±27.15 cm/s, GA; RLA, respectively). The incidence of ipsilateral ECA stenosis50% decreased from 64% preoperatively to 16 % at one year (P0.001). On the contralateral side, incidence of ECA stenosis50% increased from 27% preoperatively to 56% after one year (p=0.018). On the ipsilateral side, all patients in the RLA group had less than 50% stenosis of ECA at one year after the operation (P=0.021 vs. pre-OP), while in the GA group four patients developed 50-74% stenosis and one patient75% stenosis of ECA (P0.001 vs. pre-OP). These results were not significantly different between the two groups and demonstrated a total of 96.7% ECA patency at one year.Elliptical transsection for EEA enables outstanding ECA revascularization with good patency at one year. Type of anesthesia does not affect the quality of the eversion technique.

The aim of this study was to investigate effects of poly(ADP-ribose) polymerase (PARP) inhibition on mesenteric vascular function and metabolism in an experimental model of cardiopulmonary bypass (CPB) with cardiac arrest. Twelve anesthetized dogs underwent 90-min hypothermic CPB. After 60 min of cardiac arrest, reperfusion was started for 40 min following application of either saline vehicle (control, n = 6) or a potent PARP inhibitor, PJ-34 (10 mg/kg iv bolus and 0.5 mg·kg−1·min−1 infusion for 20 min, n = 6). PJ-34 led to better recovery of cardiac output (2.2 ± 0.1 vs. 1.8 ± 0.2 l/min in control) and mesenteric blood flow (175 ± 38 vs. 83 ± 4 ml/min, P < 0.05 vs. control) after reperfusion. The impaired vasodilator response of the superior mesenteric artery to acetylcholine, assessed in the control group after CPB (−32.8 ± 3.3 vs. −57.6 ± 6.6% at baseline, P < 0.05), was improved by PJ-34 (−50.3 ± 3.6 vs. −54.3 ± 4.1% at baseline, P < 0.05 vs. control). Although plasma nitrate/nitrite concentrations were not significantly different between groups, mesenteric nitric oxide synthase activity was increased in the PJ-34 group ( P < 0.05). Moreover, the treated group showed a marked attenuation of mesenteric venous plasma myeloperoxidase levels after CPB compared with the control group (75 ± 1 vs. 135 ± 9 ng/ml, P < 0.05). Pharmacological PARP inhibition protects against development of post-CPB mesenteric vascular dysfunction by improving hemodynamics, restoring nitric oxide production, and reducing neutrophil adhesion.

Objective: Free radical production and related cytotoxicity during ischemia and reperfusion might lead to DNA strand breakage, which activates the nuclear enzyme poly-ADP-ribose synthetase and initiates an energy-consuming and inefficient cellular metabolic cycle with transfer of the adenosine diphosphate-ribosyl moiety of nicotinamide adenine dinucleotide (NAD+) to protein acceptors. We investigated the effects of poly-ADP-ribose synthetase inhibition on myocardial and endothelial function during reperfusion in an experimental model of cardiopulmonary bypass. Methods: Twelve anesthetized dogs underwent hypothermic cardiopulmonary bypass. After 60 minutes of hypothermic cardiac arrest, reperfusion was started after application of either saline vehicle (control, n = 6) or PJ34 (10 mg/kg), a potent poly-ADP-ribose synthetase inhibitor (n = 6). Biventricular hemodynamic variables were measured by means of a combined pressure-volume conductance catheter, and the slope of the end-systolic pressure-volume relationships was calculated at baseline and after 60 minutes of reperfusion. Left anterior descending coronary blood flow, endothelium-dependent vasodilatation to acetylcholine, and endothelium-independent vasodilatation to sodium nitroprusside were also determined. Results: The administration of PJ34 led to a significantly better recovery of left and right ventricular systolic function (P < .05) after 60 minutes of reperfusion. In addition, the inotropic adaptation potential of the right ventricle to an increased afterload was better preserved in the PJ34 group. Coronary blood flow was also significantly higher in the PJ34 group (P < .05). Although the vasodilatory response to sodium nitroprusside was similar in both groups, acetylcholine resulted in a significantly higher increase in coronary blood flow in the PJ34 group (P Conclusions: Poly-ADP-ribose synthetase inhibition improves the recovery of myocardial and endothelial function after cardiopulmonary bypass with hypothermic cardiac arrest.

Background. The aim of our study was to determine whether addition of the nitric oxide donor l-arginine at reperfusion may prevent the cardiopulmonary bypass (CPB)-induced vascular alterations in the intestine. Methods. Twelve dogs underwent 90-minute hypothermic CPB. After 60 minutes, the cardiac arrest-treated group (n = 6) received 40 mg/kg intravenous bolus l-arginine, followed by 3 mg/kg/min infusion for 20 minutes. Hemodynamic parameters, blood gases, lactate, and glucose were monitored. Reactive hyperemia (RH) in response to superior mesenteric artery ischemia and vasorelaxation to systemically administered vasoactive drugs (acetylcholine [ACH] and sodium nitroprusside) were assessed before and after CPB and defined as percent change of vascular resistance. Results. In the control group, CPB reduced reactive hyperemia (RH) (−26 ± 15% vs −53 ± 5%), and the response to ACH (−30 ± 3% vs −42 ± 7%). In the treated group, the post-CPB endothelial dysfunction was reversed (−37 ± 1%, P

The aim of this study was to determine the pathophysiological mechanisms of postcardiopulmonary bypass (CPB) intestinal dysfunction using an in vivo canine model of extracorporeal circulation. Six dogs underwent a 90 min hypothermic CPB with continuous monitoring of mean arterial blood pressure (MAP) and mesenteric blood flow (MBF). Reactive hyperemia and vasodilator responses of the superior mesenteric artery to acetylcholine and sodium nitroprusside were determined before and after CPB. Mesenteric lactate production, glucose consumption, creatine kinase (CK) release and venous free radicals were determined. CPB induced a significant fall (p < 0.05) in MAP and MBF. After CPB, reactive hyperemia (-26 +/- 15% versus -53 +/- 2%, p < 0.05) and the response to acetylcholine (-42 +/- 9 versus -55 +/- 6%, p < 0.05) were significantly decreased. Reperfusion increased lactate production (0.8 +/- 0.09 mmol/L versus 0.4 +/- 0.18, p < 0.05) and the CK release (446 +/- 98 U/L versus 5 +/- 19 U/L, p < 0.01). Endothelial dysfunction, conversion from aerobic to anaerobic metabolism, and intestinal cell necrosis seem to be responsible for intestinal complications associated with CPB.

The aim of the present study was to determine whether the ETA receptor antagonist LU135252 can protect the mesenterium against ischaemia/reperfusion (I/R) damage. Direct occlusion of the superior mesenteric artery was performed for 30min in two groups of dogs. Declamping was followed by 90min of reperfusion. Mesenteric release of ET-1 was studied in series 1 (n = 6). In series 2, 5min before cross-clamping, the treated group (n = 7) received an intravenous bolus of LU135252 (5mg/kg), whereas the control group (n = 6) was given vehicle. Mean arterial blood pressure and mesenteric blood flow were recorded. Mesenteric venous and systemic arterial serum lactate and glucose, plasma creatine kinase and free radical concentrations were determined at 15min intervals. Ischaemia for 30min induced a significant increase (P

Objective Our aim was to analyze the outcomes of endovascular exclusion of the entire aortic arch (proximal landing in zone 0, distal landing in zone III or beyond, after Ishimaru) in which complete surgical debranching of the supra-aortic vessels (I), endovascular supra-aortic revascularization (chimney, fenestrated, or branched grafts) with partial surgical debranching (II), or total endovascular supra-aortic revascularization (III) was additionally performed. Methods Publications describing endovascular repair of the aortic arch (2000-2016) were systematically searched and reviewed. Results From a total of 53 relevant studies including 1853 patients, only 1021 patients undergoing 35 different total aortic arch procedures were found eligible for further evaluation and included in group I, II, or III (429, 190, and 402 patients, respectively). Overall early mortality was higher in group I vs groups II and III ( P = .001; 1 − β = 95.6%) but exceeded in group III (18.6%) and group II (14.0%) vs group I (8.0%; P = .044; 1 − β = 57.4%) for diseases involving zone 0. Mortality was higher in all subgroups treated for zone 0 disease compared with corresponding subgroups treated for zone I to zone III disease. The incidence of cerebral ischemic events was increased in groups I and II vs group III (7.5% and 11% vs 1.7%; P = .0001) and correlated with early mortality ( R 2 = .20; P = .033). The incidence of type II endoleaks and endovascular reintervention was similar between groups and correlated with each other ( R 2 = .37; P = .004). Type Ia endoleak occurred more often in groups II and III than in group I (7.1% and 12.1% vs 5.8%; P = .023) and correlated with midterm mortality ( R 2 = .53; P = .005). Retrograde type A dissection was low in all groups, whereas aneurysm growth was higher in group III (2.6%, 4.2%, 10.7%; P = .002), correlating with midterm mortality ( R 2 = .311; P = .009). Surgical revision slightly correlated with surgical complications ( R 2 = .18; P = .044) but not with mortality ( R 2 = .10; P = .214). Conclusions Because early mortality was significantly higher in patients receiving endovascular treatment for proximal aortic disease, endovascular-based approaches proved to be feasible alternatives to hybrid surgical procedures, especially when they were performed for aneurysms located in the distal aortic arch. Whereas cerebral ischemia accompanies both surgical and endovascular involvement of the supra-aortic vessels, endoleaks and aneurysm growth remain hallmarks of endovascular supra-aortic repair. Because surgical revision had no impact on mortality, complete surgical debranching may become the option of choice for patients with good life expectancy suffering from proximal aortic arch disease, whereas total endovascular procedures could be particularly advantageous in patients with short life expectancy and distal aortic arch disease.

The term ischemia-reperfusion injury describes the experimentally and clinically prevalent finding that tissue ischemia with inadequate oxygen supply followed by successful reperfusion initiates a wide and complex array of inflammatory responses that may both aggravate local injury as well as induce impairment of remote organ function. Conditions under which ischemia-reperfusion injury is encountered include the different forms of acute vascular occlusions (stroke, myocardial infarction, limb ischemia) with the respective reperfusion strategies (thrombolytic therapy, angioplasty, operative revascularization) but also routine surgical procedures (organ transplantation, free-tissue-transfer, cardiopulmonary bypass, vascular surgery) and major trauma/shock. Since the first recognition of ischemia-reperfusion injury during the 1970s, significant knowledge has accumulated and the purpose of this review is to present an overview over the current literature on the molecular and cellular basis of ischemia-reperfusion injury, to outline the clinical manifestations and to compile contemporary treatment and prevention strategies. Although the concept of reperfusion injury is still a matter of debate, it is corroborated by recent and ongoing clinical trials that demonstrated ischemic preconditioning, inhibition of sodium-hydrogen-exchange and administration of adenosine to be effective in attenuating ischemia-reperfusion injury.

The L-arginine-nitric oxide (NO) pathway plays an important role in ischemia-reperfusion injury. In the present study we investigated the role of NO-precursor L-arginine on cardiac and pulmonary function after reversible hypothermic ischemia. Twelve anesthetized dogs underwent cardiopulmonary bypass. After 60 minutes of hypothermic cardiac arrest, reperfusion was started with application of either saline vehicle (control, n = 6) or L-arginine (40 mg/kg i.v. bolus then 3 mg/kg i.v. infusion during the first 20 minutes of reperfusion, n = 6). The vasodilative response to acetylcholine was significantly higher in the L-arginine group (P < 0.05). The preload recruitable stroke work of the left ventricle decreased significantly after reperfusion, however remained unchanged in the L-arginine group. Arterial blood gas analysis did not show any difference between the two groups. Plasma L-arginine concentration reached peak level at 20 minutes of administration (675.0 +/- 66.6 versus 207.7 +/- 14.5 in the L-arginine group, P < 0.05) and returned to baseline at 40 minutes, while in the control group remained unchanged during ischemia and reperfusion (276.2 +/- 71.6 versus 283.8 +/- 38.5, P < 0.05). Plasma nitrite concentration followed L-arginine changes parallel, however nitrate levels increased slower. Supplementation with L-arginine during reperfusion prevents myocardial and endothelial dysfunction, however does not have any overriding effect on pulmonary function. Considerably rapid elimination of plasma L-arginine was demonstrated during early reperfusion.

The anti-arrhythmic effects of ETA receptor antagonists during myocardial ischaemia and reperfusion remain controversial. Moreover, the electrophysiological mechanism has not yet been identified. The aim of this study was to investigate the potential anti-arrhythmic and electrophysiological effects of the ETA receptor antagonist LU 135252 (LU) during myocardial ischaemia and reperfusion in a canine model. A bolus of LU (1mg/kg; n = 10) or saline (control; n = 10) was injected into the left anterior descending coronary artery before ligation of this vessel for 30min, which was followed by a 90-min reperfusion period. LU bolus administration (0.5mg/kg) was repeated every 30min. There were no differences in mean arterial blood pressure or coronary blood flow between the two groups. The determined left ventricular ischaemic mass was 25.5±1.8% and 27.8±2.2% of the total left ventricular mass in the control and LU groups respectively. The total incidence of ventricular fibrillation during ischaemia and reperfusion was 40% in the control and 50% in the LU group (not significantly different). The incidence of non-sustained and sustained ventricular tachycardias during ischaemia, reperfusion and over the whole period (ischaemia plus reperfusion) in the control group was 50%, 50% and 70% respectively, and that in the LU group was 80%, 70% and 100% respectively (no significant differences between groups). The number of ventricular premature beats was not decreased by LU during either ischaemia or reperfusion [median (25th–75th percentile): ischaemia, 20 (13–37) and 56 (32–130) for LU and control groups respectively; reperfusion, 15 (2–21) and 39 (7–74) respectively; ischaemia+reperfusion, 16 (4–35) and 43 (10–82) respectively; no significant differences between groups]. During ischaemia, the monophasic action potential duration at 90% repolarization (MAPD90) decreased significantly, while during reperfusion a significant prolongation of MAPD90 was observed in the left anterior descending region that was similar in the two groups. In conclusion, LU did not affect repolarization changes and did not have anti-arrhythmic effects during either ischaemia or reperfusion in this model.

Mesenteric dysfunction is a rare but severe complication after open heart surgery, which may be aggravated by coexistent heart failure. The aim of the study was to investigate the effects of cardiopulmonary bypass (CPB) on intestinal vascular endothelial and smooth muscle function in a canine model of heart failure.

Surgical aortobifemoral bypass procedure for aortoiliac occlusive disease remains the gold standard treatment despite rapidly expanding range of indications for endovascular repair. Besides several disadvantages such as dysparaesthesias, hernias, and unpleasant outcome, transperitoneal exposure of the aorta is also associated with operative autonomic nerve injury. In five male patients, infrarenal aorta was exposed through a small (8 cm) supraumbilical midline incision. Incision of the posterior peritoneum above the infrarenal aorta was limited to 3 cm. A 1 cm infraumbilical incision allowed transperitoneal placement of the distal aortic clamp outside of the operative field. Four centimeters transverse incisions were made over the femoral bifurcations and implantation of the aortobifemoral graft followed. Extubation was performed after an operating time of 200 to 150 minutes with 30 to 20 minutes aortic clamping time. Nonopioids or nonsteroidal anti-inflammatory drugs were intermittently administered during 12 hours of intermediate care unit monitoring. Oral alimentation started 6 hours and complete mobilization at 48 hours postoperatively. Hospital discharge followed on the fourth to tenth postoperative day. This minimally invasive technique allows a precise and controlled open performance of all vascular anastomoses minimizing intraoperative and postoperative complications and significantly decreasing patient discomfort related to standard abdominal surgery.