Impact of competitive flow on wall shear stress in coronary surgery: computational fluid dynamics of a LIMA-LAD model

Competitive flow from native coronary vessels is considered a major factor in the failure of coronary bypass grafts. However, the pathophysiological effects are not fully understood. Low and oscillatory wall shear stress (WSS) is known to induce endothelial dysfunction and vascular disease, like atherosclerosis and intimal hyperplasia. The aim was to investigate the impact of competitive flow on WSS in mammary artery bypass grafts. Using computational fluid dynamics, WSS was calculated in a left internal mammary artery (LIMA) graft to the left anterior descending artery in a three-dimensional in vivo porcine coronary artery bypass graft model. The following conditions were investigated: high competitive flow (non-significant coronary lesion), partial competitive flow (significant coronary lesion), and no competitive flow (totally occluded coronary vessel). Time-averaged WSS of LIMA at high, partial, and no competitive flow were 0.3-0.6, 0.6-3.0, and 0.9-3.0 Pa, respectively. Further, oscillatory WSS quantified as the oscillatory shear index (OSI) ranged from (maximum OSI = 0.5 equals zero net WSS) 0.15 to 0.35, < 0.05, and < 0.05, respectively. Thus, high competitive flow resulted in substantial oscillatory and low WSS. Moderate competitive flow resulted in WSS and OSI similar to the no competitive flow condition. Graft flow is highly dependent on the degree of competitive flow. High competitive flow was found to produce unfavourable WSS consistent with endothelial dysfunction and subsequent graft narrowing and failure. Partial competitive flow, however, may be better tolerated as it was found to be similar to the ideal condition of no competitive flow

Human cardiomyocyte calcium handling and transverse tubules in mid-stage of post-myocardial-infarction heart failure

Aims: Cellular processes in the heart rely mainly on studies from experimental animal models or explanted hearts from patients with terminal end-stage heart failure (HF). To address this limitation, we provide data on excitation contraction coupling, cardiomyocyte contraction and relaxation, and Ca2+ handling in post-myocardial-infarction (MI) patients at mid-stage of HF. Methods and results: Nine MI patients and eight control patients without MI (non-MI) were included. Biopsies were taken from the left ventricular myocardium and processed for further measurements with epifluorescence and confocal microscopy. Cardiomyocyte function was progressively impaired in MI cardiomyocytes compared with non-MI cardiomyocytes when increasing electrical stimulation towards frequencies that simulate heart rates during physical activity (2 Hz); at 3 Hz, we observed almost total breakdown of function in MI. Concurrently, we observed impaired Ca2+ handling with more spontaneous Ca2+ release events, increased diastolic Ca2+, lower Ca2+ amplitude, and prolonged time to diastolic Ca2+ removal in MI (P &lt; 0.01). Significantly reduced transverse-tubule density (−35%, P &lt; 0.01) and sarcoplasmic reticulum Ca2+ adenosine triphosphatase 2a (SERCA2a) function (−26%, P &lt; 0.01) in MI cardiomyocytes may explain the findings. Reduced protein phosphorylation of phospholamban (PLB) serine-16 and threonine-17 in MI provides further mechanisms to the reduced function. Conclusions: Depressed cardiomyocyte contraction and relaxation were associated with impaired intracellular Ca2+ handling due to impaired SERCA2a activity caused by a combination of alteration in the PLB/SERCA2a ratio and chronic dephosphorylation of PLB as well as loss of transverse tubules, which disrupts normal intracellular Ca2+ homeostasis and handling. This is the first study that presents these mechanisms from viable and intact cardiomyocytes isolated from the left ventricle of human hearts at mid-stage of post-MI HF

Reduced reactive hyperemia may explain impaired flow-mediated dilation after on-pump cardiac surgery

In previous studies, Flow Mediated Dilation (FMD) was used to study the effect of cardiac surgery on endothelial function. This study investigated the effect of on‐pump cardiac surgery on FMD and reactive hyperemia. The FMD‐response and reactive hyperemia were measured in 25 patients the morning before‐ and the first morning after cardiac surgery. Brachial artery diameter and blood flow were measured with ultrasound at baseline before 5 min occlusion of the blood flow to the forearm, and continuously for 3 min after release of the occlusion. An exponential wash‐out model was fitted to the blood flow over time. Nineteen patients remained for final data analysis. Data are mean ± SEM. The FMD response was reduced after surgery from 3.3 ± 0.5% to 1.4 ± 0.6% (P = 0.02). Max blood flow after cuff release was reduced from 342 ± 30 mL preoperatively to 305 ± 30 mL postoperatively (P < 0.00) and fell toward baseline significantly quicker; preoperative half‐life was 36 ± 2.4 sec. versus 29 ± 1.9 sec postoperatively (P < 0.00). Resting blood flow was reduced from 84 ± 9 mL/min to 66 ± 9 mL/min, (P < 0.00). Brachial artery baseline diameter was unaffected by coronary artery bypass surgery (P = 0.3). The observed reduction in brachial artery FMD after surgery, by previous authors taken to represent endothelial dysfunction, may at least partly be due to reduced hyperemic flow postoperatively. In studies where FMD is measured on multiple occasions, flow data should also be included. Reduced postoperative blood flow to the arm may indicate regional differences in vascular resistance after cardiac surgery

Post Cardiac Surgery Stunning Reduces Stroke Work, but Leaves Cardiac Power Output Unchanged in Patients with Normal Ejection Fraction

This study assesses positional changes in cardiac power output and stroke work compared to classic haemodynamic variables, measured before and after elective coronary artery bypass graft surgery. The hypothesis was that cardiac power output was altered in relation to cardiac stunning. The study is a retrospective analysis of data from two previous studies performed in a tertiary care university hospital. Thirty-six patients scheduled for elective coronary artery bypass graft surgery, with relatively preserved left ventricular function, were included. A pulmonary artery catheter and a radial artery catheter were placed preoperatively. Cardiac power output and stroke work were calculated through thermodilution both supine and standing prior to induction of anaesthesia and again day one postoperatively. Virtually all systemic haemodynamic parameters changed significantly from pre- to postoperatively, and from supine to standing. Cardiac power output was maintained at 0.9-1.0 (+/- 0.3) W both pre- and postoperatively and from supine to standing on both days. Stroke work fell from pre- to postoperatively from 1.1 to 0.8 J (p<0.001), there was a significant fall in stroke work with positional change preoperatively from 1.1 to 0.9 J (p<0.001). Postoperatively the stroke work remained at 0.8 J despite positional change. Cardiac power output was the only systemic haemodynamic variable which remained unaltered during all changes. Stroke work appears to be a more sensitive marker for temporary cardiovascular dysfunction than cardiac power output. Further studies should explore the relationship between stroke work and cardiac performance and whether cardiac power output is an autoregulated intrinsic physiological parameter

Cardiac power integral: a new method for monitoring cardiovascular performance

Cardiac power (PWR) is the continuous product of flow and pressure in the proximal aorta. Our aim was to validate the PWR integral as a marker of left ventricular energy transfer to the aorta, by comparing it to stroke work (SW) under multiple different loading and contractility conditions in subjects without obstructions in the left ventricular outflow tract. Six pigs were under general anesthesia equipped with transit time flow probes on their proximal aortas and Millar micromanometer catheters in their descending aortas to measure PWR, and Leycom conductance catheters in their left ventricles to measure SW. The PWR integral was calculated as the time integral of PWR per cardiac cycle. SW was calculated as the area encompassed by the pressure– volume loop (PV loop). The relationship between the PWR integral and SW was tested during extensive mechanical and pharmacological interventions that affected the loading conditions and myocardial contractility. The PWR integral displayed a strong correlation with SW in all pigs (R2 > 0.95, P < 0.05) under all conditions, using a linear model. Regression analysis and Bland Altman plots also demonstrated a stable relationship. A mixed linear analysis indicated that the slope of the SW-to-PWR-integral relationship was similar among all six animals, whereas loading and contractility conditions tended to affect the slope. The PWR integral followed SW and appeared to be a promising parameter for monitoring the energy transferred from the left ventricle to the aorta. This conclusion motivates further studies to determine whether the PWR integral can be evaluated using less invasive methods, such as echocardiography combined with a radial artery catheter

Cardiac power parameters during hypovolemia, induced by the lower body negative pressure technique, in healthy volunteers

Background Changes in cardiac power parameters incorporate changes in both aortic flow and blood pressure. We hypothesized that dynamic and non-dynamic cardiac power parameters would track hypovolemia better than equivalent flow- and pressure parameters, both during spontaneous breathing and non-invasive positive pressure ventilation (NPPV). Methods Fourteen healthy volunteers underwent lower body negative pressure (LBNP) of 0, −20, −40, −60 and −80 mmHg to simulate hypovolemia, both during spontaneous breathing and during NPPV. We recorded aortic flow using suprasternal ultrasound Doppler and blood pressure using Finometer, and calculated dynamic and non-dynamic parameters of cardiac power, flow and blood pressure. These were assessed on their association with LBNP-levels. Results Respiratory variation in peak aortic flow was the dynamic parameter most affected during spontaneous breathing increasing 103 % (p < 0.001) from baseline to LBNP −80 mmHg. Respiratory variation in pulse pressure was the most affected dynamic parameter during NPPV, increasing 119 % (p < 0.001) from baseline to LBNP −80 mmHg. The cardiac power integral was the most affected non-dynamic parameter falling 59 % (p < 0.001) from baseline to LBNP −80 mmHg during spontaneous breathing, and 68 % (p < 0.001) during NPPV. Conclusions Dynamic cardiac power parameters were not better than dynamic flow- and pressure parameters at tracking hypovolemia, seemingly due to previously unknown variation in peripheral vascular resistance matching respiratory changes in hemodynamics. Of non-dynamic parameters, the power parameters track hypovolemia slightly better than equivalent flow parameters, and far better than equivalent pressure parameters

Enhanced intra-operative grading of ascending aorta atheroma by epiaortic ultrasound vs echocardiography

Aims Intra-operative grading of atheromatous plaques in the ascending aorta by epiaortic ultrasound (EAU) and transesophageal echocardiography (TEE) in patients who have undergone CABG. Methods and results Sixty patients scheduled for elective CABG were prospectively enrolled to undergo intra-operative TEE and EAU ultrasound scanning of the ascending aorta. The ascending aorta was divided into three sections; proximal, middle and distal, and four segments; anterior, posterior, medial and lateral. Degree of atherosclerosis was graded according to a modified Montgomery scale. Epiaortic ultrasound was unable to provide images for a reliable assessment in 56 areas (7.7%; 56/720) vs 322 non-visualized areas by TEE (44.7%; 298/720) (p < 0.01). Out of 563 areas that scored ≥ 2, EAU visualized 379/720 areas (52.6%), whereas TEE visualized 184/720 areas (25.5%) (p < 0.01). EAU mean scores were significantly higher for the mid (p = 0.0001) and distal (p = 0.05) sections and for the posterior segment (p < 0.01) vs TEE. TEE had a higher mean score than EAU in the anterior segment. When all EAU areas were grouped the posterior segment reached a significantly higher mean score (p < 0.01), and the anterior segment was the second mostly diseased. Conclusions EAU is the intra-operative investigation of choice because it allowed a detailed grading of atheromatous lesions over the entire length of the ascending aorta. Accurate grading by TEE was restricted only to those areas that could be sufficiently visualized. TEE has a reduced power of investigation that limits its use, especially in the distal ascending aorta, a site of great surgical manipulation

Minimally invasive beat-by-beat monitoring of cardiac power in normal hearts and during acute ventricular dysfunction

Cardiac power, the product of aortic flow and blood pressure, appears to be a fundamental cardiovascular parameter. The simplified version named cardiac power output (CPO), calculated as the product of cardiac output (CO) in L/min and mean arterial pressure (MAP) in mmHg divided by 451, has shown great ability to predict outcome in a broad spectrum of cardiac disease. Beat-by-beat evaluation of cardiac power (PWR) therefore appears to be a possibly valuable addition when monitoring circulatory unstable patients, providing parameters of overall cardiovascular function. We have developed a minimally invasive system for cardiac power measurement, and aimed in this study to compare this system to an invasive method (ttPWR). Seven male anesthetized farm pigs were included. A laptop with in-house software gathered audio from Doppler signals of aortic flow and blood pressure from the patient monitor to continuously calculate and display a minimally invasive cardiac power trace (uPWR). The time integral per cardiac cycle (uPWR-integral) represents cardiac work, and was compared to the invasive counterpart (ttPWR-integral). Signals were obtained at baseline, during mechanically manipulated preload and afterload, before and after induced global ischemic left ventricular dysfunction. We found that the uPWR-integral overestimated compared to the ttPWR-integral by about 10% (P < 0.001) in both normal hearts and during ventricular dysfunction. Bland-Altman limits of agreement were at +0.060 and -0.054 J, without increasing spread over the range. In conclusion we find that the minimally invasive system follows its invasive counterpart, and is ready for clinical research of cardiac power parameters

Postoperative Pulmonary Complications After Cardiac Surgery: The VENICE International Cohort Study.

Postoperative pulmonary complications (PPC) remain a main issue after cardiac surgery. The objective was to report the incidence and identify risk factors of PPC after cardiac surgery. An international multicenter prospective study (42 international centers in 9 countries). A total of 707 adult patients who underwent cardiac surgery under cardiopulmonary bypass. None MEASUREMENTS AND MAIN RESULTS: During a study period of 2 weeks, the investigators included all patients in their respective centers and screened for PPCs. PPC was defined as the occurrence of at least 1 pulmonary complication among the following: atelectasis, pleural effusion, respiratory failure, respiratory infection, pneumothorax, bronchospasm, or aspiration pneumonitis. Among 676 analyzed patients, 373 patients presented with a PPC (55%). The presence of PPC was significantly associated with a longer intensive care length of stay and hospital length of stay. One hundred ninety (64%) patients were not intraoperatively ventilated during cardiopulmonary bypass. Ventilation settings were similar regarding tidal volume, respiratory rate, inspired oxygen. In the regression model, age, the Euroscore II, chronic obstructive pulmonary disease, preoxygenation modality, intraoperative positive end-expiratory pressure, the absence of pre- cardiopulmonary bypass ventilation, the absence of lung recruitment, and the neuromuscular blockade were associated with PPC occurrence. Both individual risk factors and ventilatory settings were shown to explain the high level of PPCs. These findings require further investigations to assess a bundle strategy for optimal ventilation strategy to decrease PPC incidence