Internal thoracic artery malperfusion: fast decision for an additional vein graft has impact on patient outcome

BACKGROUND: Internal thoracic artery (ITA) malperfusion has been described as a potentially devastating and lethal complication of coronary artery bypass grafting (CABG). It is our practice to perform an additional vein graft to the distal left anterior descending (LAD) artery in such cases. METHODS: From August 1999 to July 2002, 2877 CABG procedures were performed at our institution. In 65 patients (2.3%) ITA malperfusion was observed. All of them were treated with an additional vein graft to the distal LAD. All patient data were screened for the time interval between the occurrence of ITA malperfusion and the decision to perform an additional vein graft. RESULTS: Of 65 patients with ITA malperfusion, 54 patients (83%) survived (group 1), 11 patients (17%) died (group 2). There was no difference in preoperative risk status between the groups. Cross clamp time was 88 +/- 4 minutes in group 1 and 104 +/- 11 minutes in group 2 (p = 0.04). Intraoperative ITA flow to LAD was 6 +/- 1 mL/min in group 1 and 10 +/- 5 mL/min in group 2 (p = 0.2). Time between release of cross clamp and second period of cross clamping was 50 +/- 5 minutes in group 1 and 75 +/- 11 minute group 2 (p = 0.02). Time between termination of cardiopulmonary bypass (CPB) and second period of cross clamping was 23 +/- 3 minutes in group 1 and 46 +/- 7 minutes in group 2 (p = 0.003). Vein graft flow to distal LAD was 54 +/- 4 mL/min in group 1 and 52 +/- 12 mL/min in group 2 (p = 0.5). Maximum postoperative troponin I was 35 +/- 11 ng/mL in group 1 and 136 +/- 32 in group 2 (p = 0.003). CONCLUSIONS: Survivors of ITA malperfusion had shorter cross clamp times and less myocardial damage as evidenced by lower postoperative troponin I levels. Time intervals between first and second cross clamp and between termination of CPB and second cross clamp were lower in survivors, thus indicating that a fast decision for an additional vein graft may influence postoperative patient outcome.     

Stereological assessment of the blood‐air barrier and the surfactant system after mesenchymal stem cell pretreatment in a porcine non‐heart‐beating donor model for lung transplantation

More frequent utilization of non‐heart‐beating donor (NHBD) organs for lung transplantation has the potential to relieve the shortage of donor organs. In particular with respect to uncontrolled NHBD, concerns exist regarding the risk of ischaemia/reperfusion (IR) injury‐related graft damage or dysfunction. Due to their immunomodulating and tissue‐remodelling properties, bone‐marrow‐derived mesenchymal stem cells (MSCs) have been suspected of playing a beneficial role regarding short‐ and long‐term survival and function of the allograft. Thus, MSC administration might represent a promising pretreatment strategy for NHBD organs. To study the initial effects of warm ischaemia and MSC application, a large animal lung transplantation model was generated, and the structural organ composition of the transplanted lungs was analysed stereologically with particular respect to the blood–gas barrier and the surfactant system. In this study, porcine lungs (n = 5/group) were analysed. Group 1 was the sham‐operated control group. In pigs of groups 2–4, cardiac arrest was induced, followed by a period of 3 h of ventilated ischaemia at room temperature. In groups 3 and 4, 50 × 10⁶ MSCs were administered intravascularly via the pulmonary artery and endobronchially, respectively, during the last 10 min of ischaemia. The left lungs were transplanted, followed by a reperfusion period of 4 h. Then, lungs were perfusion‐fixed and processed for light and electron microscopy. Samples were analysed stereologically for IR injury‐related structural parameters, including volume densities and absolute volumes of parenchyma components, alveolar septum components, intra‐alveolar oedema, and the intracellular and intra‐alveolar surfactant pool. Additionally, the volume‐weighted mean volume of lamellar bodies (lbs) and their profile size distribution were determined. Three hours of ventilated warm ischaemia was tolerated without eliciting histological or ultrastructural signs of IR injury, as revealed by qualitative and quantitative assessment. However, warm ischaemia influenced the surfactant system. The volume‐weighted mean volume of lbs was reduced significantly (P = 0.024) in groups subjected to ischaemia (group medians of groups 2–4: 0.180–0.373 μm³) compared with the sham control group (median 0.814 μm³). This was due to a lower number of large lb profiles (size classes 5–15). In contrast, the intra‐alveolar surfactant system was not altered significantly. No significant differences were encountered comparing ischaemia alone (group 2) or ischaemia plus application of MSCs (groups 3 and 4) in this short‐term model.     

Protection of the right ventricle from ischemia and reperfusion by preceding hypoxia

We have previously shown that 2 weeks of hypoxia protect the right ventricle of the rat heart from subsequent ischemia and reperfusion (I/R). In the present study, we examined the following: (1) Do shorter periods of hypoxia protect from subsequent I/R? (2) Does intermittent normoxia increase the cardioprotective effect? (3) Is hypoxia-inducible factor-1α (HIF-1α), erythropoietin (EPO), or vascular endothelial growth factor (VEGF) involved in the protective effects? Preischemic cardiac work was followed by global ischemia, reperfusion, and postischemic cardiac work (15 min each). External heart work was determined at the end of both work phases. Four groups of hearts were investigated: hearts from normoxic rats (n?=?8), hearts from rats after 24 h of continuous hypoxia (10.5% inspired oxygen, n?=?7), hearts from rats after 24 h hypoxia with a single intermission of 30 min normoxia (n?=?9), and hearts from rats after 24 h hypoxia and multiple intermissions of 30 min normoxia (n?=?7). Protein levels of HIF-1α and mRNA levels of EPO and VEGF were determined in right ventricular tissue of normoxic and hypoxic hearts. Postischemic right heart recovery was better in all three hypoxic groups compared with normoxic hearts (61.8?±?5.9%, 65.6?±?3.0%, and 75.7?±?2.6% vs. 46.0?±?3.9%, p?p?p?=?0.02). No differences in EPO and VEGF mRNA levels were found between normoxic and hypoxic hearts. Twenty-four hours of continuous hypoxia protect the isolated working right heart from subsequent ischemia and reperfusion. When preceding hypoxia is interrupted by multiple reoxygenation periods, there is a further significant increase in cardiac functional recovery. HIF-1α may be involved in the protective effect.     

Predictors and outcome of gastrointestinal complications in patients undergoing cardiac surgery

OBJECTIVE: To determine the incidence and independent predictors of gastrointestinal complications (GICs) following cardiac surgery. SUMMARY BACKGROUND DATA: Gastrointestinal ischemia and hemorrhage represent a rare but devastating complication following heart surgery. The profile of patients referred for cardiac surgery has changed during the last decade, questioning the validity of previously reported incidence and risk factors. METHODS: We retrospectively analyzed prospectively collected data from 4819 patients undergoing cardiac surgery between 1998 and 2004. Patients with GICs were compared with the entire patient population. Study endpoints were mortality, postoperative morbidities, and long-term survival. RESULTS: GICs occurred in 51 (1.1%) patients. Etiologies were intestinal ischemia (n = 30; 59%) and hemorrhage (n = 21; 41%). The incidence decreased during the study period (1998-2001: 1.3%, 2002-2004: 0.7%; P = 0.04). The incidence per type of procedure was as follows: coronary artery bypass grafting (CABG)/valve (2.4%), aortic surgery (1.7%), valve surgery (1.0%), and CABG (0.5%; P = 0.001). Multivariate analysis revealed age (odds ratio [OR] = 2.1), myocardial infarction (OR = 2.5), CHF (OR = 2.4), hemodynamic instability (OR = 2.8), cardiopulmonary bypass time >120 minutes (OR = 6.2), peripheral vascular disease (OR = 2.2), renal (OR = 3.2), and hepatic failure (OR = 10.8) as independent predictors of GICs. The overall hospital mortality among patients with GICs was 33%. Long-term survival was significantly decreased in patients with GICs compared with the control group. CONCLUSIONS: Gastrointestinal complications following cardiac surgery remain rare with an incidence <1% in a contemporary series. The key to a lower incidence of GICs lies in systematic application of preventive measures and new advances in intraoperative management. Identification of independent risk factors would facilitate the determination of patients who would benefit from additional perioperative monitoring. Future resources should therefore be redirected to mitigate GICs in high-risk patients.     

Acute cardiac inflammatory responses to postischemic reperfusion during cardiopulmonary bypass.

OBJECTIVES: The investigation centers on whether there is a reperfusion-induced specific cardiac inflammatory reaction after bypass surgery. BACKGROUND: Cardiopulmonary bypass (CPB) leads to systemic inflammation. Additionally, cardiac inflammation due to reperfusion could occur. Knowledge about nature and time course of this reaction might help to develop cardioprotective interventions. METHODS: In 12 patients receiving coronary bypass grafts, arterial and coronary venous blood was obtained before onset of CPB, and 1, 5, 10, 25, 35 and 75 min after cardiac reperfusion. Plasma levels of IL6 and IL8 were measured by immunoassay. CD11b, CD41, and CD62 on blood cells were quantified by flow cytometry. Measurement of CD41, a platelet marker, on neutrophils and monocytes allowed detection of leukocyte-platelet microaggregates. RESULTS: Transcardiac veno-arterial difference of IL6 rose in the 10th and 25th min of reperfusion (from 0 to 7 pg/ml; p < 0.05), and after 75 min (15 pg/ml). IL8 did not change. CD11b on neutrophils (PMN) decreased transcardially to 95, 88 and 82% of the initial level in the 5th, 10th, and 75th min, respectively, suggesting sequestration of activated neutrophils. CD62 on platelets rose about 30% in the 75th min. Initially, leukocyte-platelet microaggregates were formed during coronary passage (+31% of the arterial level for PMN, +23% for monocytes). During reperfusion, coaggregates were retained (PMN: -1% and -7% in the 5th and 10th min, monocytes: -22%, -13% and -12% in the 1st, 5th and 10th min. CONCLUSIONS: During early reperfusion after aortic declamping, the coronary bed is already a source of proinflammatory stimuli and target for activated leukocytes, partly in conjunction with platelets. Mitigation of these phenomena might help to improve cardiac function after CPB especially in patients at risk.     

Early and late outcome of cardiac surgery in patients with liver cirrhosis.

Liver cirrhosis is a major risk factor in general surgery. Few studies have reported on the outcome of cardiac surgery in these patients. Herein we report our recent experience in this high-risk patient population according to the Child-Turcotte-Pugh classification and Model for End-Stage Liver Disease (MELD) score. Between January 1998 and December 2004, 27 patients (mean age 58 +/- 10 yr, 20 male) with cirrhosis who underwent cardiac surgery were identified. Patients were in Child-Turcotte-Pugh class A (n = 10), B (n = 11), and C (n = 6) and mean MELD score was 14.2 +/- 4.2. Operative mortality was 26% (n = 7). Stratified mortality according to Child-Turcotte-Pugh class was 11%, 18%, and 67% for class A, B, and C, respectively. No mortality occurred in patients who had revascularization without the use of cardiopulmonary bypass (n = 5). The 1-yr survival was 80%, 45%, and 16% for Child-Turcotte-Pugh class A, B, and C, respectively (P = 0.02). Major postoperative complications occurred in 22%, 56%, and 100% for Child-Turcotte-Pugh class A, B, and C, respectively. Child-Turcotte-Pugh classification was a better predictor of hospital mortality (P = 0.02) compared to MELD score (P = 0.065). In conclusion, our results suggest that cardiac surgery can be performed safely in patients with Child-Turcotte-Pugh class A and selected patients with class B. Operative mortality remains high in class C patients. Careful patient selection is critical in order to improve surgical outcome in patients with cirrhosis.     

Chronic AT1-receptor blockade does not alter cerebral oxygen supply/demand ratio during cardiopulmonary bypass in hypertensive patients

Background: The angiotensin II receptor type 1 antagonist candesartan has been hypothesized to alter vasopressor requirements and brain–blood flow by changing cerebrovascular autoregulation. Therefore, we assessed the effects of a pre-anaesthetic treatment course with candesartan on cerebral arterial-jugular bulb oxygen content difference, middle cerebral artery blood velocity, and vasopressor requirements in hypertensive patients undergoing elective on-pump coronary artery bypass graft surgery.
Methods: In a randomized, double-blind, placebo-controlled study, we evaluated the effects of candesartan (8 mg po/d, given for 6–8 days before surgery) in 35 hypertensive patients. The mean arterial pressure was maintained above 60 mmHg by bolus administration of phenylephrine, if required, and dosages were recorded.
Results: Candesartan did not significantly alter oxygen content difference across the cerebral circulation, mean middle cerebral artery blood velocity during cardiopulmonary bypass, or phenylephrine requirements either before (0.0067 μg/kg/min±0.0042 vs. 0.0056 μg/kg/min±0.0049, P =0.48) or during cardiopulmonary bypass (0.0240 μg/kg/min±0.0240 vs. 0.0250 μg/kg/min±0.0190, P =0.97) compared with placebo.
Conclusion: Thus, a 6–8-day treatment course with candesartan does not alter global cerebral perfusion and oxygen supply/demand ratio during cardiopulmonary bypass, or vasopressor requirements in hypertensive patients undergoing on-pump coronary artery bypass graft surgery, and no deleterious consequences of AT1-receptor blockade were detected.