Hermann Kuppe

Intraoperative radiofrequency maze ablation for atrial fibrillation: the Berlin modification

BACKGROUND The Cox-maze procedure combined with an operation for organic heart disease is highly successful in the elimination of chronic atrial fibrillation. However, it prolongs significantly the aortic cross-clamp and operating time. In this study, a simplified left atrial maze procedure, which is a short procedure performed using a surgical radiofrequency ablation probe, is added to elective open heart procedures in patients with atrial fibrillation. METHODS Forty-eight adults with atrial fibrillation (duration, 6 months to 36 years) underwent elective open heart operations (isolated valve procedures or coronary artery bypass grafting, n = 27 patients; combined procedures, n = 21 patients) combined with intraoperative radiofrequency ablation of the left atrium. The postoperative follow-up period ranged from 1 to 11 months (mean, 4 months). Possible predictors for persistent postoperative atrial fibrillation were determined among 40 variables by univariate and multivariate analyses. RESULTS Intraoperative radiofrequency ablation prolonged the aortic cross-clamp time for 6 to 14 minutes (mean, 11 minutes). Freedom from atrial fibrillation was 100% intraoperatively, 25% at 1 week after operation (12 of 48 patients), 59% at 1 month postoperatively (16 of 27 patients), 64% at 3 months postoperatively (16 of 25 patients), and 92% at 6 months postoperatively (12 of 13 patients). The only predictor of postoperative atrial fibrillation was the presence of coronary artery disease (odds ratio, 7.5; 80% confidence interval, 2.24-25.13). CONCLUSIONS Intraoperative radiofrequency ablation of the left atrium combined with an operation for organic heart disease effectively eliminates atrial fibrillation without significant prolongation of the aortic cross-clamp and operative time. The presence of coronary artery disease decreases the success rate during the first 6 postoperative months.

Right-to-left ventricular end-diastolic diameter ratio and prediction of right ventricular failure with continuous-flow left ventricular assist devices.

BACKGROUND Left ventricular assist device (LVAD) implantation is an accepted therapy for patients with end-stage heart failure. Post-operative right ventricular failure (RVF) still remains a major cause of morbidity and mortality in these patients. This study sought to identify echocardiography parameters to select patients with high risk of RVF after LVAD implantation. METHODS Prospectively collected pre-operative transesophageal echocardiography (TEE) and clinical data were evaluated in patients pre-selected for isolated LVAD or biventricular assist device (BiVAD) implantation. According to prevalence of RVF during the first post-operative 48 hours, patients were divided into those who developed RVF (isolated LVAD with RVF) and those who did not (isolated LVAD without RVF). Echocardiographic parameters for RV geometry, RV function, LV geometry, and the RV-to-LV end-diastolic diameter ratio (R/L ratio) were evaluated. For identification of the optimal cutoff of R/L ratio, receiver operating characteristics curves were constructed. RESULTS An isolated LVAD was implanted in 115 patients and BiVAD in 22 patients. RVF developed in 15 patients (13%) after isolated LVAD implantation. The R/L ratio was markedly increased in the isolated LVAD with RVF and BiVAD groups compared with the isolated LVAD without RVF group. According to the receiving operating curve, the cutoff for the R/L ratio to predict RVF was 0.72. The odds ratio that RVF will develop is 11.4 in patients with an R/L ratio >0.72 (p = 0.0001). CONCLUSIONS Increased R/L ratio successfully identifies patients with high risk of RVF after isolated LVAD implantation. Beyond standard measurements of RV function, the consideration of R/L ratio may be useful to improve risk stratification in patients before isolated LVAD implantation.

Negative-Feedback Loop Attenuates Hydrostatic Lung Edema via a cGMP-Dependent Regulation of Transient Receptor Potential Vanilloid 4

Although the formation of hydrostatic lung edema is generally attributed to imbalanced Starling forces, recent data show that lung endothelial cells respond to increased vascular pressure and may thus regulate vascular permeability and edema formation. In combining real-time optical imaging of the endothelial Ca2+ concentration ([Ca2+]i) and NO production with filtration coefficient (Kf) measurements in the isolated perfused lung, we identified a series of endothelial responses that constitute a negative-feedback loop to protect the microvascular barrier. Elevation of lung microvascular pressure was shown to increase endothelial [Ca2+]i via activation of transient receptor potential vanilloid 4 (TRPV4) channels. The endothelial [Ca2+]i transient increased Kf via activation of myosin light-chain kinase and simultaneously stimulated NO synthesis. In TRPV4 deficient mice, pressure-induced increases in endothelial [Ca2+]i, NO synthesis, and lung wet/dry weight ratio were largely blocked. Endothelial NO formation limited the permeability increase by a cGMP-dependent attenuation of the pressure-induced [Ca2+]i response. Inactivation of TRPV4 channels by cGMP was confirmed by whole-cell patch-clamp of pulmonary microvascular endothelial cells and intravital imaging of endothelial [Ca2+]i. Hence, pressure-induced endothelial Ca2+ influx via TRPV4 channels increases lung vascular permeability yet concomitantly activates an NO-mediated negative-feedback loop that protects the vascular barrier by a cGMP-dependent attenuation of the endothelial [Ca2+]i response. The identification of this novel regulatory pathway gives rise to new treatment strategies, as demonstrated in vivo in rats with acute myocardial infarction in which inhibition of cGMP degradation by the phosphodiesterase 5 inhibitor sildenafil reduced hydrostatic lung edema.

Prophylactic Perioperative Sodium Bicarbonate to Prevent Acute Kidney Injury Following Open Heart Surgery: A Multicenter Double-Blinded Randomized Controlled Trial

In a double-blinded randomized controlled trial, Anja Haase-Fielitz and colleagues find that an infusion of sodium bicarbonate during open heart surgery did not reduce the risk for acute kidney injury, compared with saline control.

Anaphylactic reactions to aprotinin reexposure in cardiac surgery: relation to antiaprotinin immunoglobulin G and E antibodies.

BackgroundAprotinin, a serine proteinase inhibitor, reduces bleeding during cardiac surgery. As aprotinin is derived from bovine lung, it has antigenic properties. This investigation examined the incidence of anaphylactic reactions in patients reexposed to aprotinin and the relation to preformed antiaprotinin immunoglobulin (Ig)G and IgE antibodies. MethodsThis prospective observational study conducted at five centers in Germany evaluated patients undergoing repeat cardiac surgery reexposed to aprotinin between 1995 and 1996. Antiaprotinin IgG and IgE antibody measurements, using a noncommercial enzyme-linked immunosorbent assay and an immunofluorescence assay, respectively, were performed preoperatively and postoperatively. An anaphylactic reaction was defined as major changes from baseline within 10 min of aprotinin administration of systolic pressure 20% or greater, heart rate 20% or greater, inspiratory pressure greater than 5 cm H2O, or a skin reaction. ResultsIn 121 cases (71 adults, 46 children), a mean aprotinin reexposure interval of 1,654 days (range, 16–7,136 days) was observed. Preoperative antiaprotinin IgG (optical density ratio > 3) and IgE antibodies (radioallergosorbent test [RAST] score < 3) were detected in 18 and 9 patients, respectively. High concentrations of each (IgG, optical density ratio > 10; IgE, RAST score ≥ 3) were detected in five patients. Three patients (2.5%; 95% confidence interval, 0.51–7.1%) experienced an anaphylactic reaction after aprotinin exposure, followed by full recovery; these patients had reexposure intervals less than 6 months (22, 25, and 25 days) and the highest preoperative IgG concentrations of all patients (P < 0.05). Assay sensitivity was 100%, as no anaphylactic reactions occurred in IgG-negative patients (95% confidence interval, 0.0–3.1%); assay specificity was 98%. Preoperative IgE measurements were quantifiable in two of three reactive patients and in three nonreacting patients. ConclusionsQuantitative detection of antiaprotinin IgE and IgG lacks specificity for predictive purposes; however, quantitation of antiaprotinin IgG may identify patients at risk for developing an anaphylactic reaction to aprotinin reexposure.

Hypoxic pulmonary vasoconstriction requires connexin 40-mediated endothelial signal conduction.

Hypoxic pulmonary vasoconstriction (HPV) is a physiological mechanism by which pulmonary arteries constrict in hypoxic lung areas in order to redirect blood flow to areas with greater oxygen supply. Both oxygen sensing and the contractile response are thought to be intrinsic to pulmonary arterial smooth muscle cells. Here we speculated that the ideal site for oxygen sensing might instead be at the alveolocapillary level, with subsequent retrograde propagation to upstream arterioles via connexin 40 (Cx40) endothelial gap junctions. HPV was largely attenuated by Cx40-specific and nonspecific gap junction uncouplers in the lungs of wild-type mice and in lungs from mice lacking Cx40 (Cx40-/-). In vivo, hypoxemia was more severe in Cx40-/- mice than in wild-type mice. Real-time fluorescence imaging revealed that hypoxia caused endothelial membrane depolarization in alveolar capillaries that propagated to upstream arterioles in wild-type, but not Cx40-/-, mice. Transformation of endothelial depolarization into vasoconstriction involved endothelial voltage-dependent α1G subtype Ca2+ channels, cytosolic phospholipase A2, and epoxyeicosatrienoic acids. Based on these data, we propose that HPV originates at the alveolocapillary level, from which the hypoxic signal is propagated as endothelial membrane depolarization to upstream arterioles in a Cx40-dependent manner.

Cannulation of the right axillary artery for surgery of acute type A aortic dissection

OBJECTIVE The optimal choice of the arterial inflow site during operations for type A aortic dissection is not clearly defined. The aim of the prospective study was to identify whether cannulation of the right axillary artery instead of the femoral artery may improve the results of surgery for acute type A aortic dissection. METHODS Seventy consecutive patients were operated on because of acute type A aortic dissection from January 2000 to February 2002. The only difference in surgical strategy was the site of arterial cannulation: the right axillary artery was used in 20 patients [axillary group] and the left femoral artery in 50 patients [femoral group]. All patients had aortic surgery with open distal anastomosis during deep hypothermic arrest and retrograde cerebral perfusion. The mean age was 58.7 +/- 12 years with a range from 28 to 88 years (axillary group, 56.6 +/- 13 years; femoral group, 59.4 +/- 12 years; P = 0.435). Preoperatively evident organ malperfusion was identified in five (25%) patients of the axillary group and in seven (14%) of the femoral group. RESULTS There was no perioperative death. The hospital mortality rate was 5.0% for the axillary group and 22% for the femoral group (all patients, 17%). Major neurological complications occurred postoperatively in 5% of patients from the axillary group (one out of 20 patients) and in 8% of patients from the femoral group (four out of 50 patients) (all patients, 7%). CONCLUSION Cannulation of the right axillary artery improved the outcome of surgery for acute type A aortic dissection. However, postoperative complications occurred after both axillary and femoral artery cannulation.

Inflammatory response after implantation of a left ventricular assist device: comparison between the axial flow MicroMed DeBakey VAD and the pulsatile Novacor device.

The implantation of a ventricular assist device (VAD) is associated with a stimulation of the inflammatory system. We compared changes in the inflammatory response after implantation of a pulsatile Novacor left (L) VAD and the axial flow MicroMed DeBakey VAD. Six consecutive patients after implantation of a Novacor LVAD (NC) and six patients after implantation of a MicroMed DeBakey VAD (MD) were included in the investigation. Patients received LVADs for medically non treatable end-stage heart failure. Tumor necrosis factor alpha (TNF), C3a, C5a, interleukin 6 (IL-6), and neutrophil elastase were measured twice a week over a period of 3 months after implantation of the device. All tests were performed with an enzyme-linked immunosorbent assay. There was no significant difference in the clinical course of the two groups. All inflammatory parameters were elevated in both groups during the entire period of the investigation. There was no difference in TNF, polynuclear leukocyte elastase, or C3a levels between the two groups; however, IL-6 (NC: 23.6 ± 37.6 pg/ml vs. MD: 63 ± 114 pg/ml, p < 0.001) and C5a (NC: 708 ± 352 &mgr;g/L vs. MD: 1,745 ± 1,305 &mgr;g/L, p < 0.001) were increased significantly more in patients following implantation of the axial flow MicroMed DeBakey VAD. Compared with the pulsatile Novacor device, the implantation of the axial flow MicroMed DeBakey LVAD seems to be associated with an increased stimulation of one part of the inflammatory system. Further investigations are necessary for evaluation of the pathophysiologic mechanism and clinical implications of these findings.

Anticoagulation during Cardiopulmonary Bypass in Patients with Heparin-induced Thrombocytopenia Type II and Renal Impairment Using Heparin and the Platelet Glycoprotein IIb-IIIa Antagonist Tirofiban

BackgroundPatients with heparin-induced thrombocytopenia type II require an alternative to standard heparin anticoagulation. However, in patients with renal impairment, anticoagulation during cardiopulmonary bypass with agents such as danaparoid sodium or r-hirudin are associated with hemorrhage. Anticoagulation with unfractionated heparins combined with prostacyclin, a potent platelet aggregation inhibitor, is associated with severe hypotension. The authors investigated a new concept using unfractionated heparins after platelet inhibition with the short-acting platelet glycoprotein IIb–IIIa antagonist tirofiban. MethodsTen patients with heparin-induced thrombocytopenia type II and renal impairment were enrolled in the investigation. All had heparin-induced thrombocytopenia type II antibodies present as proved by the heparin-induced platelet aggregation assay, the heparin–platelet factor 4 enzyme-linked immunosorbent assay, or both. In all patients, preoperative anticoagulation to an activated partial thromboplastin time of 40–60 s was performed with r-hirudin. Anticoagulation during cardiopulmonary bypass was achieved with a bolus of 400 IU/kg unfractionated heparins after a bolus of tirofiban 10 &mgr;g/kg followed by an infusion of tirofiban at a rate of 0.15 &mgr;g · kg−1 · min−1 until 1 h before conclusion of cardiopulmonary bypass. Additional unfractionated heparins were only administered if activated clotting time decreased below 480 s. Coagulation was monitored by a abciximab-modified TEG® and the adenosine diphosphate–stimulated (20 &mgr;m) platelet aggregometry. D-dimer concentrations, as a marker of venous thromboembolism, were measured before and 12, 24, and 48 h after surgery. Postoperative antithrombotic therapy was started immediately with r-hirudin to anticoagulation to an activated partial thromboplastin time of 40–60 s. ResultsThe postoperative blood loss ranged from 110 to 520 ml. No patient needed reexploration. In no patient was there clinical evidence of thrombosis or embolism in the postoperative period or of a critical increase of the D-dimer concentrations, suggesting venous thromboembolism. Transfusion of platelets was necessary in only two patients. ConclusionsThe protocol is easy to perform and no increased postoperative bleeding and no thromboembolic complications occurred. The combination of unfractionated heparins and tirofiban may be an alternative to other anticoagulation strategies in patients with heparin-induced thrombocytopenia.

Relation of cerebral tissue oxygenation index to central venous oxygen saturation in children

ObjectiveTo evaluate the relationship between the cerebral tissue oxygenation index measured by near-infrared spectroscopy and central venous oxygen saturation (SvO2) after corrective surgery of congenital heart defects in children.DesignProspective observational clinical study.SettingA tertiary neonatal and paediatric intensive care unit for paediatric cardiology.PatientsNeonates and children consecutively admitted to the paediatric cardiology intensive care unit after corrective surgery of non-cyanotic congenital heart defects.Measurements and resultsForty-three children were studied. Cerebral tissue oxygenation index, measured non-invasively by near-infrared spectroscopy, was compared to SvO2, measured by a catheter placed in the right atrium, and to haemodynamic and respiratory parameters. Pearson’s correlation coefficients and p values were calculated. Simultaneously measured values for SvO2 (62.2±9.8%, 39.8–80.4%) and cerebral tissue oxygenation index (56.7±8.8%, 35.8–71.2%) showed a significant correlation (r=0.52, p<0.001).ConclusionCerebral tissue oxygenation index and SvO2 are not interchangeable parameters, but cerebral tissue oxygenation index reflects the haemodynamic influence on cerebral oxygenation after cardiovascular surgery. Further work is necessary to confirm the clinical role of continuous non-invasive measurement of cerebral tissue oxygenation index with regard to the variations of global systemic oxygen consumption after cardiac surgery in children.