The impact of hypovolemia and PEEP on recirculation in venovenous ECMO: an experimental porcine model.

BACKGROUND: Recirculation is a common problem in venovenous extracorporeal membrane oxygenation (VV ECMO) and may limit the effect of ECMO treatment due to less efficient blood oxygenation or unfavorable ECMO and ventilator settings. The impact of hypovolemia and positive end expiratory pressure (PEEP) on recirculation is unclear and poorly described in guidelines, despite clinical importance. The aim of this study was to investigate how hypovolemia, autotransfusion and PEEP affect recirculation in comparison to ECMO cannula distance and circuit flow. METHODS: In anesthetized and mechanically ventilated pigs (n = 6) on VV ECMO, we measured recirculation fraction (RF), changes in recirculation fraction (∆RF), hemodynamics and ECMO circuit pressures during alterations in PEEP (5 cmH2O vs 15 cmH2O), ECMO flow (3.5 L/min vs 5.0 L/min), cannula distance (10-14 cm vs 20-26 cm intravascular distance), hypovolemia (1000 mL blood loss) and autotransfusion (1000 mL blood transfusion). RESULTS: Recirculation increased during hypovolemia (median ∆RF 43%), high PEEP (∆RF 28% and 12% with long and short cannula distance, respectively), high ECMO flow (∆RF 49% and 28% with long and short cannula distance, respectively) and with short cannula distance (∆RF 16%). Recirculation decreased after autotransfusion (∆RF - 45%). CONCLUSIONS: In the present animal study, hypovolemia, PEEP and autotransfusion were important determinants of recirculation. The alterations were comparable to other well-known factors, such as ECMO circuit flow and intravascular cannula distance. Interestingly, hypovolemia increased recirculation without significant change in ECMO drainage pressure, whereas high PEEP increased recirculation with less negative ECMO drainage pressure. Autotransfusion decreased recirculation. The findings are interesting for clinical studies.

Extracorporeal driveline vibrations to detect left ventricular assist device thrombosis - A porcine model study.

BACKGROUND: Pump thrombosis (PT) and related adverse complications contributed to the HeartWare Ventricular Assist Device (HVAD) market withdrawal. Many patients still receive lifelong support, with deficient PT surveillance based on pump power trends. Analysis of pump vibrations is better for detecting PT. Here, we investigated the feasibility of an extracorporeal accelerometer to detect PT from pump vibrations propagated out on the driveline. METHODS: In a porcine HVAD model (n = 6), an accelerometer was attached to the pump as a reference and another to the driveline for comparisons of signals. In total, 59 thrombi were injected into the heart to induce PT, followed by intermittent thrombus washout maneuvers. Signals were compared visually in spectrograms and quantitatively in third harmonic saliences (S3H) by correlation analysis. Receiver operating characteristic curves expressed the method's outcome in sensitivity vs specificity, with the overall diagnostic performance in the area under the curve (AUC) score. RESULTS: Five experiments had good driveline signal strength, with clear spectrographic relationships between the 2 accelerometers. Third harmonic driveline vibrations were visible 20 vs 30 times in the reference. The comparison in S3H showed a strong correlation and yielded an AUC of 0.85. Notably, S3H proved robust regarding noise and false PT detections. CONCLUSIONS: An extracorporeal accelerometer on the driveline can be a readily available method for accurate HVAD PT detection before an accelerometer integration with left ventricular assist device is feasible.

Detection of inflow obstruction in left ventricular assist devices by accelerometer: A porcine model study.

BACKGROUND: Left ventricular assist devices (LVAD) provide circulatory blood pump support for severe heart failure patients. Pump inflow obstructions may lead to stroke and pump malfunction. We aimed to verify in vivo that gradual inflow obstructions, representing prepump thrombosis, are detectable by a pump-attached accelerometer, where the routine use of pump power (PLVAD) is deficient. METHOD: In a porcine model (n = 8), balloon-tipped catheters obstructed HVAD inflow conduits by 34% to 94% in 5 levels. Afterload increases and speed alterations were conducted as controls. We computed nonharmonic amplitudes (NHA) of pump vibrations captured by the accelerometer for the analysis. Changes in NHA and PLVAD were tested by a pairwise nonparametric statistical test. Detection sensitivities and specificities were investigated by receiver operating characteristics with areas under the curves (AUC). RESULTS: NHA remained marginally affected during control interventions, unlike PLVAD. NHA elevated during obstructions within 52-83%, while mass pendulation was most pronounced. Meanwhile, PLVAD changed far less. Increased pump speeds tended to amplify the NHA elevations. The corresponding AUC was 0.85-1.00 for NHA and 0.35-0.73 for PLVAD. CONCLUSION: Elevated NHA provides a reliable indication of subclinical gradual inflow obstructions. The accelerometer can potentially supplement PLVAD for earlier warnings and localization of pump.

Detection of inflow obstruction in left ventricular assist devices by accelerometer: An in vitro study.

Inflow obstruction in left ventricular assist devices (LVAD) may lead to embolic stroke and pump malfunction. We investigated if an accelerometer detected graded LVAD inflow obstructions. Detection performances were compared to the current continuous surveillance routine based on the pump power consumption (PLVAD). In ten mock circuit experiments, four different-sized pendulating balloons obstructed HVAD™ inflow conduits cross-section areas by 14%-75%. Nonharmonic amplitudes (NHA) of continuous signals from a triaxial accelerometer attached to the LVAD were compared against single-point PLVAD values, using load and speed alterations as control interventions. We analyzed the NHA band power with a pairwise nonparametric statistical test. The detection performances were analyzed by receiver operating characteristics with areas under the curves (AUC). The NHA remained unaffected during load alterations. In contrast, NHA increased significantly from the 27% obstruction level (AUC≥0.82), an effect amplified by increased pump speed. PLVAD did not change significantly below the maximal 75% obstruction level (AUC≤0.36). In conclusion, NHA detected the inflow obstructions much better than PLVAD. The technique may provide a future monitoring modality of any pendulating obstructive inflow pathology.

Improved Detection Of Thromboembolic Complications In Left Ventricular Assist Device By Novel Accelerometer-Based Analysis.

We have previously demonstrated that accelerometer-based vibration analysis detects thromboembolism and pump thrombosis in HeartWare Left Ventricular Assist Device (HVAD) using the third harmonic frequency (pump_speedx3). Thromboembolism also affected the amplitude of the nonharmonic frequencies. The aim of this study was to determine whether nonharmonic-amplitude (NHA) analysis can improve the diagnosis of thromboembolic complications. An accelerometer was attached to HVAD in three in vitro and seven in vivo experiments. Control interventions, including load and pump speed alternations (n = 107), were followed by thromboembolic events (n = 60). A sliding fast-Fourier-transform was analyzed, and changes in NHAs were quantified in the acute phase and in a steady state. Receiver operating characteristic curves were constructed with cutoff values of NHA to detect thromboembolic events. Positive predictive values were calculated on the basis of a specificity of 1. In the acute phase, NHA change was 6.5 times higher under thromboembolism than under control interventions (p < 0.001). Most thromboembolic events lead to concomitant changes in both NHA and third-harmonic amplitude. Combining the two methods improved the PPV by 8.3%. At steady state, signal changes predominantly demonstrated either NHA or third-harmonic changes. Combined signal analysis improved the PPV by 36%. This method enhanced the detection of thromboembolism and pump thrombosis in the HVAD.

Myocardial electrophysiological and mechanical changes caused by moderate hypothermia-A clinical study.

Moderate hypothermia has been used to improve outcomes in comatose out-of-hospital cardiac arrest survivors during the past two decades, although the effects remain controversial. We have recently shown in an experimental study that myocardial electrophysiological and mechanical relationships were altered during moderate hypothermia. Electromechanical window positivity increased, and electrical dispersion of repolarization decreased, both of which are changes associated with decreased arrhythmogenicity in clinical conditions. Mechanical dispersion, a parameter also linked to arrhythmic risk, remained unaltered. Whether corresponding electrophysiological and mechanical changes occur in humans during moderate hypothermia, has not been previously explored. Twenty patients with normal left ventricular function were included. Measurements were obtained at 36 and 32°C prior to ascending aortic repair while on partial cardiopulmonary bypass and at 36°C after repair. Registrations were performed in the presence of both spontaneous and comparable paced heart rate during standardized loading conditions. The following electrical and mechanical parameters were explored: (1) Electromechanical window, measured as time difference between mechanical and electrical systole, (2) dispersion of repolarization from ECG T-wave, and (3) mechanical dispersion, measured as segmental variation in time to peak echocardiographic strain. At moderate hypothermia, mechanical systolic prolongation (425 ± 43-588 ± 67 ms, p < 0.001) exceeded electrical systolic prolongation (397 ± 49-497 ± 79 ms, p < 0.001), whereby, electromechanical window positivity increased (29 ± 30-86 ± 50 ms, p < 0.001). Dispersion of repolarization and mechanical dispersion remained unchanged. Corresponding electrophysiological and mechanical relationships were present at comparable paced heart rates. After rewarming, the increased electromechanical window was reversed in the presence of both spontaneous and paced heart rates. Moderate hypothermia increased electromechanical window positivity, while dispersion of repolarization and mechanical dispersion remained unchanged. This impact of hypothermia may be clinically relevant for selected groups of patients after cardiac arrest.

Left Ventricular Function Changes Induced by Moderate Hypothermia Are Rapidly Reversed After Rewarming-A Clinical Study.

OBJECTIVES: Targeted temperature management (32-36°C) is used for neuroprotection in cardiac arrest survivors. The isolated effects of hypothermia on myocardial function, as used in clinical practice, remain unclear. Based on experimental results, we hypothesized that hypothermia would reversibly impair diastolic function with less tolerance to increased heart rate in patients with uninsulted hearts. DESIGN: Prospective clinical study, from June 2015 to May 2018. SETTING: Cardiothoracic surgery operation room, Oslo University Hospital. PATIENTS: Twenty patients with left ventricular ejection fraction greater than 55%, undergoing ascending aorta graft-replacement connected to cardiopulmonary bypass were included. INTERVENTIONS: Left ventricular function was assessed during reduced cardiopulmonary bypass support at 36°C, 32°C prior to graft-replacement, and at 36°C postsurgery. Electrocardiogram, hemodynamic, and echocardiographic recordings were made at spontaneous heart rate and 90 beats per minute at comparable loading conditions. MEASUREMENTS AND MAIN RESULTS: Hypothermia decreased spontaneous heart rate, and R-R interval was prolonged (862 ± 170 to 1,156 ± 254 ms, p < 0.001). Although systolic and diastolic fractions of R-R interval were preserved (0.43 ± 0.07 and 0.57 ± 0.07), isovolumic relaxation time increased and diastolic filling time was shortened. Filling pattern changed from early to late filling. Systolic function was preserved with unchanged myocardial strain and stroke volume index, but cardiac index was reduced with maintained mixed venous oxygen saturation. At increased heart rate, systolic fraction exceeded diastolic fraction (0.53 ± 0.05 and 0.47 ± 0.05) with diastolic impairment. Strain and stroke volume index were reduced, the latter to 65% of stroke volume index at spontaneous heart rate. Cardiac index decreased, but mixed venous oxygen saturation was maintained. After rewarming, myocardial function was restored. CONCLUSIONS: In patients with normal left ventricular function, hypothermia impaired diastolic function. At increased heart rate, systolic function was subsequently reduced due to impeded filling. Changes in left ventricular function were rapidly reversed after rewarming.

Myocardial Strain Measured by Epicardial Transducers-Comparison Between Velocity Estimators.

This study describes results from an experimental ultrasound system with miniature transducers sutured directly onto the epicardial surface and used to measure heart contractions continuously. This system was used to find velocity distributions through the myocardium. The resulting velocities were used to track the motion of four layers at different depths through the myocardium and to find the regional strain in each of the four layers. Velocities inside the myocardium vary from the epicardial to the endocardial borders. Conventional velocity estimators based on Doppler and on time delay estimation were modified to better handle these variations. Results from four different velocity estimators were tested against a simulation model for ultrasound echoes from moving tissue and on ultrasound recordings from five animals. We observed that the tested velocity estimators were able to reproduce the myocardial velocity distributions, track the myocardial layer motion and estimate strain at different positions inside the myocardium for both simulated and real ultrasound recordings. The most accurate results were obtained when the digitized ultrasound scanlines were upsampled by a factor of 10 before applying cross-correlation to estimate time delays. A modified Doppler algorithm allowing the velocity to vary linearly with time throughout the duration of the pulse packet (constant acceleration Doppler) was found to be better at capturing rapidly changing velocities compared with conventional Doppler processing. The best results were obtained using upsamling and time delay estimation, but the long computation time required by this method may make it best suited in a laboratory setting. In a real-time system, the computationally quicker constant acceleration Doppler may be preferred.

Left Ventricular Function During Epinephrine Stimulation and Hypothermia: Effects at Spontaneous and Paced Heart Rates in a Porcine Model.

Postcardiac arrest patients treated with hypothermia, frequently require vasopressors and inotropic medication. The aim of this experimental study was to investigate the effect of epinephrine on left ventricular (LV) function during hypothermia. In an open-chest porcine model, seven animals were equipped with LV micromanometer and epicardial ultrasound transducers to provide LV pressure, Tau, and wall thickness and thickening velocities in systole (S') and early diastole (e'). Arterial, central venous, and pulmonal artery pressures were recorded. Cardiac output (CO) was measured by transit-time flow probe on the ascending aorta. Hypothermia was induced using a cooling catheter through the femoral vein. Pacemaker leads were attached to the right atrium for pacing. LV volumes were obtained by two-dimensional echocardiography. Measurements were made at normothermia (38°C) and hypothermia (33°C), without and with epinephrine infusion (0.03 µg/kg/min), at spontaneous and paced heart rates (HRs) 120 and 140 beats/min. Hypothermia reduced LV stroke volume (SV). Epinephrine during hypothermia increased the SV with reduced end-systolic volumes. LV dP/dtmax and wall-thickening velocity increased. During normothermia, epinephrine increased CO mainly due to accelerated HR, but during hypothermia, the increased CO resulted from augmented SV and, to a lesser degree, elevated HR. The incomplete relaxation and shortened diastolic filling time and the following reduction in SV seen in hypothermic animals, was repealed by epinephrine. The CO remained elevated also due to a shortened systolic duration, which gave time for complete relaxation during higher HRs. Epinephrine infusion improved systolic and diastolic function during hypothermia, and thereby reversed the effects induced by hypothermia considerably. Epinephrine augmented CO at hypothermia through increases in both SV and HR, in contrast to a mainly HR-dependent effect during normothermia. Systolic duration was shortened, which gave sufficient diastolic duration for complete relaxation. This allowed diastolic filling and maintained CO at elevated HRs.

Changes in left ventricular electromechanical relations during targeted hypothermia.

BACKGROUND: Targeted hypothermia, as used after cardiac arrest, increases electrical and mechanical systolic duration. Differences in duration of electrical and mechanical systole are correlated to ventricular arrhythmias. The electromechanical window (EMW) becomes negative when the electrical systole outlasts the mechanical systole. Prolonged electrical systole corresponds to prolonged QT interval, and is associated with increased dispersion of repolarization and mechanical dispersion. These three factors predispose for arrhythmias. The electromechanical relations during targeted hypothermia are unknown. We wanted to explore the electromechanical relations during hypothermia at 33 °C. We hypothesized that targeted hypothermia would increase electrical and mechanical systolic duration without more profound EMW negativity, nor an increase in dispersion of repolarization and mechanical dispersion. METHODS: In a porcine model (n = 14), we registered electrocardiogram (ECG) and echocardiographic recordings during 38 °C and 33 °C, at spontaneous and atrial paced heart rate 100 beats/min. EMW was calculated by subtracting electrical systole; QT interval, from the corresponding mechanical systole; QRS onset to aortic valve closure. Dispersion of repolarization was measured as time from peak to end of the ECG T wave. Mechanical dispersion was calculated by strain echocardiography as standard deviation of time to peak strain. RESULTS: Electrical systole increased during hypothermia at spontaneous heart rate (p < 0.001) and heart rate 100 beats/min (p = 0.005). Mechanical systolic duration was prolonged and outlasted electrical systole independently of heart rate (p < 0.001). EMW changed from negative to positive value (- 20 ± 19 to 27 ± 34 ms, p = 0.001). The positivity was even more pronounced at heart rate 100 beats/min (- 25 ± 26 to 41 ± 18 ms, p < 0.001). Dispersion of repolarization decreased (p = 0.027 and p = 0.003), while mechanical dispersion did not differ (p = 0.078 and p = 0.297). CONCLUSION: Targeted hypothermia increased electrical and mechanical systolic duration, the electromechanical window became positive, dispersion of repolarization was slightly reduced and mechanical dispersion was unchanged. These alterations may have clinical importance. Further clinical studies are required to clarify whether corresponding electromechanical alterations are accommodating in humans.

Detection of Thromboembolic Events and Pump Thrombosis in HeartWare HVAD Using Accelerometer in a Porcine Model.

We have recently demonstrated that accelerometer-based pump thrombosis and thromboembolic events detection is feasible in vitro. This article focuses on detection of these conditions in vivo. In an open-chest porcine model (n = 7), an accelerometer was attached to the pump casing of an implanted HeartWare HVAD. Pump vibration was analyzed by Fast Fourier Transform of the accelerometer signals, and the spectrogram third harmonic amplitude quantified and compared with pump power. Interventions included injection of thrombi into the left atrium (sized 0.3-0.4 ml, total n = 35) and control interventions; pump speed change, graft obstruction, and saline bolus injections (total n = 47). Graft flow to cardiac output ratio was used to estimate the expected number of thrombi passing through the pump. Sensitivity/specificity was assessed by receiver operating characteristic curve. Graft flow to cardiac output ratio averaged 66%. Twenty-six of 35 (74%) thrombi caused notable accelerometer signal change. Accelerometer third harmonic amplitude was significantly increased in thromboembolic interventions compared with control interventions, 64.5 (interquartile range [IQR]: 18.8-107.1) and 5.45 (IQR: 4.2-6.6), respectively (p < 0.01). The corresponding difference in pump power was 3 W (IQR: 2.9-3.3) and 2.8 W (IQR: 2.4-2.9), respectively (p < 0.01). Sensitivity/specificity of the accelerometer and pump power to detect thromboembolic events was 0.74/1.00 (area under the curve [AUC]: 0.956) and 0.40/1.00 (AUC: 0.759), respectively. Persistent high third harmonic amplitude was evident at end of all experiments, and pump thrombosis was confirmed by visual inspection. The findings demonstrate that accelerometer-based detection of thromboembolic events and pump thrombosis is feasible in vivo and that the method is superior to detection based on pump power.

Estimating Regional Myocardial Contraction Using Miniature Transducers on the Epicardium.

This paper describes an ultrasound system to monitor cardiac motion using miniature transducers attached directly to the epicardial surface. Our aim was to develop both a research tool for detailed studies of cardiac mechanics and a continuous, real time system for peri-operative evaluation of heart function. The system was tested on a porcine model. Two 3 mm diameter, 10 MHz ultrasound transducers were sutured to the epicardial surface. As the epicardial surface was the reference for the velocity and strain estimations, this procedure compensated for the motion of the heart. The short distance allowed for the use of high frequencies and pulse repetition rates. The system was driven in pulse-echo mode, using electronics developed for the application, and radio frequency (RF) lines were recorded at a pulse repetition rate of 2500 s-1. The endocardial border was detected using an algorithm based on fuzzy logic with filtration to reduce noise and remove outliers, and the myocardium was divided into four layers. Inside the myocardium, radial tissue velocity as a function of depth was calculated from the recorded RF signals, and the velocity estimates were used to estimate radial strain rate and strain and to track the motion of the myocardial layers. The scope of this paper is technical, giving a detailed description of system design, hardware electronics and algorithms, with examples of processed velocity patterns and myocardial strain curves. The results from this study on a porcine model demonstrate the system's ability to estimate myocardial velocity and strain patterns and to track the motion of the myocardial layers, thereby obtaining detailed information of the regional function of the myocardium.

Sepsis causes right ventricular myocardial inflammation independent of pulmonary hypertension in a porcine sepsis model.

INTRODUCTION: Right ventricular (RV) myocardial dysfunction is a common feature in septic shock. It can worsen outcome, but the etiology is poorly understood. Pulmonary artery hypertension (PAH) plays a part in the pathogenesis of the right heart dysfunction in sepsis but its importance is unknown. In pigs, PAH in sepsis is substantial and the translational value of porcine sepsis models therefore questioned. We hypothesized that porcine sepsis causes a myocardial inflammatory response which leads to myocardial dysfunction independent of PAH. MATERIALS AND METHODS: Sepsis was induced by Escherichia coli-infusion in 10 pigs resulting in PAH and increased right ventricular pressure (RVP). The same degree of RVP was achieved by external pulmonary artery banding (PAB) in a consecutive series of 6 animals. RESULTS: Sepsis, but not PAB, led to increase in endothelial damage marker PAI-1 and cytokines TNF and IL-6 (all p<0.05) in plasma. In myocardium, TNF and IL-6 were significantly elevated in sepsis, TNF in both ventricles and IL-6 mostly in RV, while IL-1ß, IL-18 and C5a were significantly higher in RV compared to LV after PAB (all p<0.05). Myocardial mRNA levels of IL-1ß, IL-6, IL-18, IP-10, E-selectin and PAI-1 were significantly elevated in RV and LV during sepsis compared to PAB, while Caspase-1 was decreased in septic compared to PAB animals (all p<0.05). Cathepsin L activity was increased in RV by PAB, while sepsis inhibited this response. Escherichia coli-induced sepsis caused myocardial inflammation independent of PAH. CONCLUSION: Prominent PAH should therefore not exclude porcine sepsis models to further our understanding of human sepsis.

Single-centre first experience with transapical transcatheter mitral valve replacement with an apical tether: factors influencing screening outcomes.

OBJECTIVES: Transcatheter mitral valve replacement has recently been introduced as an alternative treatment option for severe mitral regurgitation. We present our single-centre first experience with screening and implantation outcomes. METHODS: Twenty-five patients with mitral regurgitation grades 3 and 4 were screened based on study inclusion/exclusion criteria, echocardiography and computed tomography imaging. All patients were evaluated by the centre's Heart Team, followed by the Tendyne's internal screening process. Patients who failed the screening criteria were considered for alternative treatments. RESULTS: Of the 25 patients screened for transcatheter mitral valve replacement, 14 patients failed screening and 11 patients passed. The patients who failed screening were more often older, were women and were smaller in stature than those who passed screening. The main reason for patients to fail screening changed during the study from large annular dimensions to a small predicted neo-left ventricular outflow tract. Eight of the 11 patients who passed screening were treated using the Tendyne device, and 3 patients required alternate treatments due to urgency including 1 MitraClip procedure and 2 surgical repairs. Of the 14 patients who failed the screening, 5 patients had open surgery (4 patients received mitral valve repair and 1 mitral valve replacement). All 8 patients who underwent the Tendyne procedure were successfully treated without mortality during the observation time. CONCLUSIONS: Transcatheter mitral valve replacement is an effective and safe treatment for well-selected patients with symptomatic mitral regurgitation. For patients who fail the screening process, the MitraClip procedure or open surgical valve repair are feasible.

Left Ventricle Function During Therapeutic Hypothermia with Beta1-Adrenergic Receptor Blockade.

Therapeutic hypothermia is an established treatment in patients resuscitated from cardiac arrest. It is usually well-tolerated circulatory, but hypothermia negatively effects myocardial contraction and relaxation velocities and increases diastolic filling restrictions. A significant proportion of resuscitated patients are treated with long-acting beta-receptor blocking agents' prearrest, but the combined effects of hypothermia and beta-blockade on left ventricle (LV) function are not previously investigated. We hypothesized that beta1-adrenergic receptor blockade (esmolol infusion) exacerbates the negative effects of hypothermia on active myocardial motions, affecting both systolic and diastolic LV function. A pig (n = 10) study was performed to evaluate the myocardial effects of esmolol during hypothermia (33°C) and during normothermia, at spontaneous and pacing-increased heart rates (HRs). LV function was assessed by a LV pressure transducer, an epicardial ultrasonic transducer (wall thickness, wall thickening/thinning velocity) and an aortic ultrasonic flow-probe (stroke volume, cardiac output). The data were compared using a paired two-tailed Students t-test, and also analyzed using a linear mixed model to handle dependencies introduced by repeated measurements within each subject. The significance level was p ≤ 0.05. The effects of hypothermia and beta blockade were distinct and additive. Hypothermia reduced myocardial motion velocities and increased diastolic filling restrictions, but end-systolic wall thickness increased, and stroke volume and dP/dtmax (pumping function) were maintained. In contrast, esmolol predominantly affected systolic pumping function, by a negative inotropic effect. In combination, hypothermia and esmolol reduced myocardial velocities in systole and diastole by ∼40%, compared with normothermia without esmolol, inducing in combination both systolic and diastolic LV function impairment. The cardiac dysfunction deteriorated at increased HRs during hypothermia. Beta1-adrenergic receptor blockade (esmolol) exacerbates the negative effects of hypothermia on active myocardial contraction and relaxation. The combination of hypothermia with beta-blockade induces both systolic and diastolic LV function impairment.

Accelerometer Detects Pump Thrombosis and Thromboembolic Events in an In vitro HVAD Circuit.

Pump thrombosis and stroke are serious complications of left ventricular assist device (LVAD) support. The aim of this study was to test the ability of an accelerometer to detect pump thrombosis and thromboembolic events (TEs) using real-time analysis of pump vibrations. An accelerometer sensor was attached to a HeartWare HVAD and tested in three in vitro experiments using different pumps for each experiment. Each experiment included thrombi injections sized 0.2-1.0 mL and control interventions: pump speed change, afterload increase, preload decrease, and saline bolus injections. A spectrogram was calculated from the accelerometer signal, and the third harmonic amplitude was used to test the sensitivity and specificity of the method. The third harmonic amplitude was compared with the pump energy consumption. The acceleration signals were of high quality. A significant change was identified in the accelerometer third harmonic during the thromboembolic interventions. The third harmonic detected thromboembolic events with higher sensitivity/specificity than LVAD energy consumption: 92%/94% vs. 72%/58%, respectively. A total of 60% of thromboembolic events led to a prolonged third harmonic amplitude change, which is indicative of thrombus mass residue on the impeller. We concluded that there is strong evidence to support the feasibility of real-time continuous LVAD monitoring for thromboembolic events and pump thrombosis using an accelerometer. Further in vivo studies are needed to confirm these promising findings.

Continuous monitoring of cardiac function by 3-dimensional accelerometers in a closed-chest pig model.

OBJECTIVES: Cardiac wall motions reflect systolic and diastolic function. We have previously demonstrated the ability of a miniaturized three-axis (3D) accelerometer to monitor left ventricular function in experimental models and in patients. The main aim of this study was to investigate the clinical utility of the method for monitoring the left and right ventricular function during changes in global and regional cardiac function in a postoperative closed-chest situation. METHODS: In 13 closed-chest pigs, miniaturized 3D accelerometers were placed on the left ventricle in the apical and basal regions and in the basal region of the right ventricle. An epicardial 3D motion vector was calculated from the acceleration signals in each heart region. Peak systolic velocity along this 3D vector (3D V(sys)) was compared with the positive time derivative of the left and right ventricular pressure and with cardiac index during changes in global LV function (unloading, fluid loading, esmolol, dobutamine) and with ultrasound during regional left ventricular dysfunction (3-min occlusion of the left anterior descending coronary artery). RESULTS: Significant and typical changes in accelerometer 3D V(sys) were seen in all heart regions during changes in global cardiac function. 3D V(sys) reflected the left and right ventricular contractility via significant correlations with the positive time derivative of the left and right ventricular pressure, r = 0.86 and r = 0.72, and with cardiac index r = 0.82 and r = 0.73 (all P < 0.001), respectively. The miniaturized accelerometers also detected regional dysfunction, but showed reduced ability to localize ischaemia as the 3D V(sys) in all heart regions showed similar reductions during coronary artery occlusion. CONCLUSIONS: Miniaturized 3D accelerometers placed on the heart can assess global and regional function in a closed-chest model. The technique may be used for continuous postoperative monitoring after cardiac surgery.

Systolic left ventricular function is preserved during therapeutic hypothermia, also during increases in heart rate with impaired diastolic filling.

BACKGROUND: Systolic left ventricular function during therapeutic hypothermia is found both to improve and to decline. We hypothesized that this discrepancy would depend on the heart rate and the variables used to assess systolic function. METHODS: In 16 pigs, cardiac performance was assessed by measurements of invasive pressures and thermodilution cardiac output and with 2D strain echocardiography. Left ventricle (LV) volumes, ejection fraction (EF), transmitral flow, and circumferential and longitudinal systolic strain were measured. Miniaturized ultrasonic transducers were attached to the epicardium of the LV to obtain M-mode images, systolic thickening, and diastolic thinning velocities and to determine LV pressure-wall dimension relationships. Preload recruitable stroke work (PRSW) was calculated. Measurements were performed at 38 and 33°C at spontaneous and paced heart rates, successively increased in steps of 20 up to the toleration limit. Effects of temperature and heart rate were compared in a mixed model analysis. RESULTS: Hypothermia reduced heart rate from 87 ± 10 (SD) to 76 ± 11 beats/min without any changes in LV stroke volume, end-diastolic volume, EF, strain values, or PRSW. Systolic wall thickening velocity (S') and early diastolic wall thinning velocity decreased by approximately 30%, making systolic duration longer through a prolonged and slow contraction and changing the diastolic filling pattern from predominantly early towards late. Pacing reduced diastolic duration much more during hypo- than during normothermia, and combined with slow myocardial relaxation, incomplete relaxation occurred with all pacing rates. Pacing did not affect S' or PRSW at physiological heart rates, but stroke volume, end-diastolic volume, and strain were reduced as a consequence of reduced diastolic filling and much more accentuated during hypothermia. At the ultimate tolerable heart rate during hypothermia, S' decreased, probably as a consequence of myocardial hypoperfusion due to sustained ventricular contraction throughout a very short diastole. CONCLUSIONS: Systolic function was maintained at physiological heart rates during therapeutic hypothermia. Reduced tolerance to increases in heart rate was caused by lack of ventricular filling due to diastolic dysfunction and shorter diastolic duration.