The Characteristics of Postoperative Mediastinitis During the Changing Phases of Cardiac Surgery.

BACKGROUND: Mediastinitis is a serious complication of open heart surgery associated with high mortality, considerable health care costs, and prolonged hospital stay. We examined characteristics and incidence of mediastinitis during 29 years when indications and patient material have been in a process of change. METHODS: This was a retrospective population-based study comprising all mediastinitis patients more than 16 years of age after open heart surgery between 1990 and 2018 from a population of 1.7 million. Patient records of 50 mediastinitis patients from 2004 to 2014 were reviewed and compared with 120 patients from 1990 to 1999. RESULTS: Annual mediastinitis rate varied 0% to 1.5% with a decreasing trend-from a level exceeding 1.2% to approximately 0.3%-over the study period. In 2004 to 2014 patients with mediastinitis were older, more often smokers, and more often had diabetes mellitus and renal insufficiency than in 1990 to 1999. No difference in length of hospital treatment, antibiotic prophylaxis or treatment, intensive care unit treatment, or mortality was observed between 1990 to 1999 and 2004 to 2014. Coronary artery bypass graft surgery became less common and valve replacement and hybrid operations more common among operations leading to mediastinitis. Staphylococcus aureus increased (from 25% to 56%, p = .005) whereas coagulase-negative staphylococci (46% to 23%, P < .001) and gram-negative bacteria (18% to 12%, P = .033) decreased as causative agents. Surgery for mediastinitis remained similar except introduction of vacuum-assisted closure treatment. CONCLUSIONS: The rate of mediastinitis decreased during these 29 years. No difference in 30-day mortality in mediastinitis was seen: 0.9% in 1990 to 1999 and 2% in 2004 to 2014.

Unilateral pulmonary oedema after minimally invasive and robotically assisted mitral valve surgery.

OBJECTIVES: Unilateral pulmonary oedema (UPO) is a severe complication of minimally invasive cardiac surgery. UPO rates and UPO-related mortality vary considerably between different studies. Due to lack of consistent diagnostic criteria for UPO, the aim of this study was to create a reproducible radiological classification for UPO. Also, risk factors for UPO after robotic and minimally invasive mitral valve operations were evaluated. METHODS: Two hundred and thirty-one patients who underwent elective minimally invasive mitral valve surgery between January 2009 and March 2017 were evaluated. Chest radiographs of the first postoperative morning were categorized into 3 UPO grades based on the severity of radiological signs of pulmonary oedema described in this study. The radiographs were analysed by 2 independent radiologists and interobserver agreement was evaluated. The clinical significance of the classification was evaluated by comparing postoperative PaO2/FiO2 values and total ventilation times between the different UPO grades. Also, multivariable logistic regression analysis was employed to identify risk factors for UPO. RESULTS: Interobserver agreement was substantial (Kappa = 0.780). Median total ventilation times were significantly longer with increasing severity of UPO, 15 (interquartile range 12-18) h for no UPO, 18 (interquartile range 15-24) h for grade I UPO and 25 (interquartile range 21-31) h for grade II UPO. Pulmonary hypertension [adjusted odds ratios (AOR) 2.51, 95% confidence intervals (CI) 1.43-4.40; P = 0.001], moderate or severe heart failure (AOR 2.88, 95% CI 1.27-6.53; P = 0.011), body mass index (AOR 1.14, 95% CI 1.02-1.28; P = 0.017) and cardiopulmonary bypass time (AOR 1.02, 95% CI 1.01-1.03; P < 0.001) were identified as independent risk factors for UPO and robotic approach (AOR 0.27, 95% CI 0.12-0.62; P = 0.002) as protective against UPO. CONCLUSIONS: Due to the variability of the diagnostic criteria for UPO in previous studies, a radiological classification for UPO is required to reliably assess the rates and risk factors for UPO. The radiological classification described in this study demonstrated high interobserver agreement and correlated with total ventilation times and postoperative PaO2/FiO2 values.

Outcome of aortic valve replacement with bioprostheses in the elderly.

BACKGROUND AND AIM OF THE STUDY: Today, the elderly population continues to increase worldwide, and rates of aortic stenosis (AS) climb with age. Since aortic valve replacement (AVR) is the current treatment for elderly patients with symptomatic AS, the number of patients undergoing AVR is expected to grow. METHODS: Among patients operated on at Helsinki University Hospital between 1992 and 1997, a cohort (n = 145) was followed after AVR with a bioprosthesis. The patients were allocated to three groups, based on their age at the time of surgery: > or = 80 years (n = 30), < 80 to > or = 70 years (n = 94), and < or = 70 years (n = 21). All data relating to preoperative risk factors were collected. A control examination, which included echocardiography, was performed at least five years after surgery, and the follow up was continued until July 2006. The number of deaths and causes of death, as well as valve-related complications, were noted. RESULTS: The 30-day mortality rates were 3.3% in the oldest (> or = 80-year) group, 6.4% in the middle (< 80 to > or = 70-year) group, and zero in the youngest (< or = 70-year) group. The mean age at death was 88 and 81 years in the oldest and middle groups, respectively. In the oldest and youngest groups, there were no reoperations, but five valve-related reoperations were performed during follow up in the middle group. At the control visit, the left ventricular ejection fraction was > 60% in all groups. In the oldest and middle groups the aortic valve gradient was lower than the preoperative level, while the left ventricular diameters and wall dimensions were smaller (p < 0.05). Valve calcification was observed in one patient in the youngest group. CONCLUSION: Elderly patients who had undergone AVR with a bioprosthesis had a good outcome after more than 10 years of follow up, with an improved cardiac function being preserved for at least seven years after surgery. Despite a severely impaired preoperative aortic valve function, octogenarians especially had a good life expectancy, possibly due to their low comorbidity rates. Hence, AVR with a bioprosthesis proved to be an excellent treatment in this patient group.

Recombinant hirudin enhances cardiac output and decreases systemic vascular resistance during reperfusion after cardiopulmonary bypass in a porcine model.

OBJECTIVE: Cardiopulmonary bypass and surgical stress are accompanied by a systemic inflammatory response and activation of coagulation. Thrombin forms fibrin and activates platelets and neutrophils. Consequently, disseminated microthrombosis might increase capillary vascular resistance and thus impair reperfusion. We hypothesized that recombinant hirudin, a direct inhibitor of thrombin, could attenuate coagulation and enhance microvascular flow during reperfusion. METHODS: Twenty pigs undergoing 60 minutes of aortic clamping and 75 minutes of normothermic perfusion were randomized in a blinded setting to receive an intravenous bolus of recombinant hirudin (10 mg, 0.4 mg/kg; n = 10) or placebo (n = 10) 15 minutes before aortic declamping and then continued with an intravenous 135-minute infusion of recombinant hirudin (3.75 mg/h, 0.15 mg/kg) or placebo. Thrombin-antithrombin complexes, activated clotting times, and several hemodynamic parameters were measured before cardiopulmonary bypass, after weaning from cardiopulmonary bypass, and at 30, 60, 90, and 120 minutes after aortic declamping. Intramucosal pH and Pco(2) were measured from the luminal surface of ileum simultaneously with arterial gas analysis at 30-minute intervals. RESULTS: Recombinant hirudin inhibited thrombin formation after aortic declamping; at 120 minutes, thrombin-antithrombin complexes levels (microg/L, mean +/- SD) were 75 +/- 21 and 29 +/- 44 (P <.001) for placebo and pigs receiving recombinant hirudin, respectively. When compared with the placebo group, pigs receiving recombinant hirudin showed significantly higher stroke volume, cardiac output, and lower systemic vascular resistance at 60 and 90 minutes after aortic declamping (P <.05). Based on arteriomucosal Pco(2) and pH differences, progressive worsening of intestinal microcirculatory perfusion occurred in the placebo group but not in the recombinant hirudin group. CONCLUSION: Infusion of thrombin inhibitor recombinant hirudin during reperfusion was associated with attenuated postischemia left ventricular dysfunction and decreased vascular resistance. Consequently microvascular flow was improved during ischemia-reperfusion injury. Control of thrombin formation during reperfusion may be a feasible approach to improve oxygen delivery to reperfused vascular beds.

Universal leukocyte reduction of transfused red cells does not provide benefit to patients undergoing cardiac surgery.

OBJECTIVE: A policy of universal leukocyte reduction of the blood supply in Finland was implemented at the beginning of 2003. The aim of the present evaluation was to determine the potential role of leukocyte-reduced red blood cells in decreasing postoperative infections. DESIGN: A retrospective cohort study. SETTING: A major university clinic. PARTICIPANTS: Consecutive patients undergoing cardiac surgery during the years 2002 and 2003. INTERVENTIONS: Transfused patients received either buffy-coat-depleted red blood cells before leukocyte reduction (n = 782) or leukocyte-reduced red blood cells after leukocyte reduction (n = 632). MEASUREMENTS AND MAIN RESULTS: The evaluated outcome parameters were culture-proven postoperative infections, 90-day mortality, and length of stay in the intensive care unit. The percentage of patients transfused with red blood cells (56% v 53%, p = 0.16) and amounts of transfused red blood cells (4.3 +/- 6.7 [3.0] units v 4.3 +/- 6.6 [2.0] units, means +/- standard deviation [median], p = 0.48) were comparable between the study groups (buffy-coat-depleted group and leukocyte-reduced group, respectively). The 90-day mortality (6.6% v 6.3%, p = 0.28), the length of intensive care stay (3.6 +/- 4.7 [2.0] days v 4.3 +/- 7.1 [2.0] days, p = 0.34), and the number of patients with culture-proven infections (8.8% v 10.9%, p = 0.19) were unchanged after universal leukocyte reduction. In multivariate comparisons, the leukocyte reduction was not associated with culture-proven postoperative infections and 90-day mortality. CONCLUSION: No beneficial effect of the universal leukocyte reduction in cardiac surgery was found for culture-positive infection rates, 90-day mortality, or length of intensive care stay.

Inhibition of thrombin during reperfusion improves immediate postischemic myocardial function and modulates apoptosis in a porcine model of cardiopulmonary bypass.

OBJECTIVE: Transient left-ventricular dysfunction because of myocardial reperfusion injury is a significant problem after cardiac surgery, but the underlying complex pathophysiology is still poorly understood. The authors studied early functional recovery of the postischemic myocardium and explored potential effects of thrombin inhibition on procoagulatory, proinflammatory, and proapoptotic features of myocardial ischemia-reperfusion injury. DESIGN: A randomized, blinded study. SETTING: University research laboratory. SUBJECTS: Porcine model. INTERVENTIONS: Twenty pigs undergoing 60 minutes of aortic clamping and 75 minutes of normothermic cardiopulmonary bypass (CPB) received an intravenous bolus of r-hirudin (10 mg, 0.4mg/kg, n = 10) or placebo (n = 10) 15 minutes before aortic declamping, followed by a 135-minute intravenous infusion of r-hirudin (3.75 mg, 0.15 mg/kg/h) or placebo. MEASUREMENTS AND MAIN RESULTS: Hemodynamic parameters were measured before CPB, after weaning from CPB, and at 30, 60, 90, and 120 minutes after aortic declamping. Blood was sampled, and myocardial biopsies were taken before CPB, just before aortic declamping, during reperfusion, and after 120 minutes of reperfusion to measure thrombin antithrombin complexes and to quantitate leukocyte infiltration (myeloperoxidase activity) for histologic evaluation and detection of apoptosis with caspase-3 and the TUNEL method. The r-hirudin group showed significantly higher stroke volume and cardiac output than the control group at 60 minutes and at 90 minutes after aortic declamping (p < 0.05). Microthrombosis was not observed in either group, indicating sufficient anticoagulation and excluding intravascular clots as explanations for LV dysfunction in the current experiment. Instead, ample myocardial activation of inflammation was present, but only a trend of r-hirudin-associated anti-inflammatory effect was observed. Compared with the controls, TUNEL-positive myocytes were detected significantly less frequently in the r-hirudin group (0.05 +/- 0.06 v 0.13 +/- 0.07 TUNEL-positive nuclei %, p = 0.042). CONCLUSIONS: The improved cardiac recovery in the r-hirudin group during reperfusion after cardioplegia-induced cardiac arrest was associated with significant differences in cardiomyocyte apoptosis and anti-inflammatory effects. Thus, in clinical cardiac surgery, inhibition of reperfusion- induced thrombin may offer beneficial effects by mechanisms other than direct anticoagulation.

Activated protein C in the cardioplegic solution on a porcine model of coronary ischemia-reperfusion has deleterious hemodynamic effects.

PURPOSE: In reperfusion injury activation of coagulation and inflammation contribute to organ dysfunction. Activated protein C (APC) exhibits anticoagulant and anti-inflammatory properties in models of reperfusion injury. We hypothesized that APC could be cardioprotective after ischemia and cardiopulmonary bypass (CPB). METHODS: 20 pigs, undergoing 120 min of CPB and aortic cross-clamping, were randomized to receive 1 mg of human APC or placebo to the last cardioplegic solution given 15 min before declamping to the systemic circulation. After aortic declamping the heart was supported by continuing CPB for 30 min followed by 30 min surveillance. Thrombin-antithrombin complexes, neutrophil L-selectin expression in blood and myeloperoxidase activity (MPO) of myocardial biopsies were measured. RESULTS: There was no indication of APC-induced increased bleeding. Thrombin levels were significantly lower in the APC group than in the placebo group and so were the rates of thrombin formation during the first 3 min of reperfusion and between 10 and 30 min after declamping. There were no differences in MPO or in the proportion of L-selectin (+) to L-selectin (-) neutrophils between groups. Significant systolic hypotension in the APC group was observed at 30 and 45 min compared with the placebo group which associated with the increased mortality observed in the APC group (p = 0.019). CONCLUSIONS: Human APC in cardioplegic solution during CPB in pigs, decreased reperfusion induced thrombin formation with no associated bleeding. No anti-inflammatory effects of human APC were seen. However, in this setting, APC caused hemodynamic deterioration. The observed phenomenon could be explained by systolic hypotension potentially produced by the release of vasoactive substances generated by the APC activation of PARs in the endothelium.

N-acetylcysteine as an additive to crystalloid cardioplegia increased oxidative stress capacity in CABG patients.

OBJECTIVE: This prospective, randomized study was designed to assess the effects of N-acetylcysteine (NAC) in coronary artery bypass graft (CABG) patients. DESIGN: Thirty-five consenting CABG patients with normal myocardial function were randomly divided into control (C) patients (N = 20) who received crystalloid (Plegisol) cardioplegia, and NAC patients receiving NAC in a 0.04 mol/l solution (N = 15) in Plegisol. Simultaneous coronary sinus and aortic blood samples, and myocardial biopsies were taken 1, 5 and 10 min after declamping. Hemodynamics was measured invasively for 24 h. RESULTS: There were no adverse effects observed. The myocardial glutathione content was significantly better preserved (p = 0.0001) and myeloperoxidase activity was over two times lower in the NAC group than in the C group (p = 0.03). The trap capacity gradient between the aorta and the coronary sinus increased significantly during the first minute of reperfusion in the treatment group (p = 0.001) when compared with the C group. In the first minute after reperfusion there were more leukocytes sequestered in the coronary circulation (p = 0.04) in the C group. The invasive hemodynamic data did not differ significantly between the groups. The incidence of arrhythmias was equal. CONCLUSION: NAC increased tissue capacity against oxidative stress and decreased inflammatory response in CABG patients with normal ejection fraction.