Accuracy of a Novel Approach to Measuring Arterial Thermodilution Cardiac Output During Intra-Aortic Counterpulsation

Objective: To assess the agreement between a novel approach of arterial and the pulmonary artery bolus thermodilution for measuring cardiac output in critically ill patients during aortic counterpulsation. Methods: Eighteen male patients aged 37-80years, undergoing preoperative insertion of an intra-aortic balloon pump (IABP) and elective coronary artery bypass grafting. A thin 1.3FG thermistor was introduced through the pressure lumen to the tip of an 8FG IABP catheter, and the pump rate was set at 1:1. After arrival in the intensive care unit cardiac output (CO) was measured under haemodynamic steady-state conditions hourly for 8-11h, and arterial bolus thermodilution (BCOiabp) and pulmonary artery bolus thermodilution (BCOpulm) were determined after the patients' admission to the intensive care unit. Results: A total of 198 data pairs were obtained: 177 with aortic counterpulsation and 21 without. During aortic counterpulsation, median CO was 6.8l/min for BCOiabp and 6.1l/min for BCOpulm, without aortic counterpulsation; corresponding values were 7.1l/min for BCOiabp and 6.5l/min for BCOpulm with aortic counterpulsation. Mean bias was +0.77l/min, limits of agreement ( ± 2SD) were -1.27/+2.81l/min, and mean error (2SD/[(BCOiabp+BCOpulm)/2] was 31.4%. Without aortic counterpulsation, corresponding values were +0.43l/min, -1.03/+1.87l/min, and 22.4%. Conclusions: Agreement between BCOiabp and BCOpulm was satisfactory for CO values between 2.0 and 10l/min only without aortic counterpulsation. BCOiabp CO measurements during aortic counterpulsation after coronary artery bypass grafting cannot be recommended at the present tim

Acute perioperative-stress-induced increase of atherosclerotic plaque volume and vulnerability to rupture in apolipoprotein-E-deficient mice is amenable to statin treatment and IL-6 inhibition

Myocardial infarction and stroke are frequent after surgical procedures and consume a considerable amount of benefit of surgical therapy. Perioperative stress, induced by surgery, is composed of hemodynamic and inflammatory reactions. The effects of perioperative stress on atherosclerotic plaques are ill-defined. Murine models to investigate the influence of perioperative stress on plaque stability and rupture are not available. We developed a model to investigate the influence of perioperative stress on plaque growth and stability by exposing apolipoprotein-E-deficient mice, fed a high cholesterol diet for 7 weeks, to a double hit consisting of 30 min of laparotomy combined with a substantial blood loss (approximately 20% of total blood volume; 400 µl). The innominate artery was harvested 72 h after the intervention. Control groups were sham and baseline controls. Interleukin-6 (IL-6) and serum amyloid A (SAA) plasma levels were determined. Plaque load, vascular smooth muscle cell (VSMC) and macrophage content were quantified. Plaque stability was assessed using the Stary score and frequency of signs of plaque rupture were assessed. High-dose atorvastatin (80 mg/kg body weight/day) was administered for 6 days starting 3 days prior to the double hit. A single dose of an IL-6-neutralizing antibody or the fusion protein gp130-Fc selectively targeting IL-6 trans-signaling was subcutaneously injected. IL-6 plasma levels increased, peaking at 6 h after the intervention. SAA levels peaked at 24 h (n=4, P<0.01). Plaque volume increased significantly with the double hit compared to sham (n=8, P<0.01). More plaques were scored as complex or bearing signs of rupture after the double hit compared to sham (n=5-8, P<0.05). Relative VSMC and macrophage content remained unchanged. IL-6-inhibition or atorvastatin, but not blocking of IL-6 trans-signaling, significantly decreased plaque volume and complexity (n=8, P<0.01). Using this model, researchers will be able to further investigate the pathophysiology of perioperative plaque stability, which can result in myocardial infarction, and, additionally, to test potential protective strategies

Heart Failure Results in Inspiratory Muscle Dysfunction Irrespective of Left Ventricular Ejection Fraction

Background: Exercise intolerance in heart failure with reduced ejection fraction (HFrEF) or heart failure with preserved ejection fraction (HFpEF) results from both cardiac dysfunction and skeletal muscle weakness. Respiratory muscle dysfunction with restrictive ventilation disorder may be present irrespective of left ventricular ejection fraction and might be mediated by circulating pro-inflammatory cytokines. Objective: To determine lung and respiratory muscle function in patients with HFrEF/HFpEF and to determine its associations with exercise intolerance and markers of systemic inflammation. Methods: Adult patients with HFrEF (n = 22, 19 male, 61 +/- 14 years) and HFpEF (n = 8, 7 male, 68 +/- 8 years) and 19 matched healthy control subjects underwent spirometry, measurement of maximum mouth occlusion pressures, diaphragm ultrasound, and recording of transdiaphragmatic and gastric pressures following magnetic stimulation of the phrenic nerves and the lower thoracic nerve roots. New York Heart Association (NYHA) class and 6-min walking distance (6MWD) were used to quantify exercise intolerance. Levels of circulating interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were measured using ELISAs. Results: Compared with controls, both patient groups showed lower forced vital capacity (FVC) (p < 0.05), maximum inspiratory pressure (PImax), maximum expiratory pressure (PEmax) (p < 0.05), diaphragm thickening ratio (p = 0.01), and diaphragm strength (twitch transdiaphragmatic pressure in response to supramaximal cervical magnetic phrenic nerve stimulation) (p = 0.01). In patients with HFrEF, NYHA class and 6MWD were both inversely correlated with FVC, PImax, and PEmax. In those with HFpEF, there was an inverse correlation between amino terminal pro B-type natriuretic peptide levels and FVC (r = -0.77, p = 0.04). In all HF patients, IL-6 and TNF-alpha were statistically related to FVC. Conclusions: Irrespective of left ventricular ejection fraction, HF is associated with respiratory muscle dysfunction, which is associated with increased levels of circulating IL-6 and TNF-alpha

Accuracy of a novel approach to measuring arterial thermodilution cardiac output during intra-aortic counterpulsation

Objective: To assess the agreement between a novel approach of arterial and the pulmonary artery bolus thermodilution for measuring cardiac output in critically ill patients during aortic counterpulsation. Methods: Eighteen male patients aged 37-80years, undergoing preoperative insertion of an intra-aortic balloon pump (IABP) and elective coronary artery bypass grafting. A thin 1.3FG thermistor was introduced through the pressure lumen to the tip of an 8FG IABP catheter, and the pump rate was set at 1:1. After arrival in the intensive care unit cardiac output (CO) was measured under haemodynamic steady-state conditions hourly for 8-11h, and arterial bolus thermodilution (BCOiabp) and pulmonary artery bolus thermodilution (BCOpulm) were determined after the patients' admission to the intensive care unit. Results: A total of 198 data pairs were obtained: 177 with aortic counterpulsation and 21 without. During aortic counterpulsation, median CO was 6.8l/min for BCOiabp and 6.1l/min for BCOpulm, without aortic counterpulsation; corresponding values were 7.1l/min for BCOiabp and 6.5l/min for BCOpulm with aortic counterpulsation. Mean bias was +0.77l/min, limits of agreement ( ± 2SD) were -1.27/+2.81l/min, and mean error (2SD/[(BCOiabp+BCOpulm)/2] was 31.4%. Without aortic counterpulsation, corresponding values were +0.43l/min, -1.03/+1.87l/min, and 22.4%. Conclusions: Agreement between BCOiabp and BCOpulm was satisfactory for CO values between 2.0 and 10l/min only without aortic counterpulsation. BCOiabp CO measurements during aortic counterpulsation after coronary artery bypass grafting cannot be recommended at the present tim