Ventricular Pressure Recordings Research Articles

Invasive validation of pressure-volume loops derived from cardiovascular magnetic resonance imaging and brachial blood pressure in heart failure patients

Abstract Introduction Left ventricular (LV) pressure-volume (PV) loops provide gold-standard physiological information but require invasive measurements of ventricular intracavity pressure, limiting clinical and research applications. Recent development has seen the introduction of non-invasively computed PV loops from cardiovascular magnetic resonance (CMR) volumetry and a brachial blood pressure measurement. The approach combines LV volumes with a time-varying elastance function to compute time-resolved LV pressures and was validated on invasive pressure data from a porcine model. The method is readily implemented using standard CMR sequences and provides measures of hemodynamic parameters including stroke work, myocardial efficiency, and contractile state. However, the method remains to be validated in patients using invasive left ventricular pressure recordings. Purpose To validate for the first time in human patients the performance of non-invasively computed PV loops against invasive measures. Methods Four heart failure patients underwent two subsequent sessions of CMR cine imaging and simultaneous brachial blood pressure measurement, with intravenous administration of two different vasoactive drugs, resulting in two different haemodynamic states for each patient. LV catheterization was then conducted with repeat administration of the same infusions. Pressure-volume loops were computed from CMR volumes combined with 1) a time-varying elastance function scaled to brachial blood pressure and temporally stretched to match volume data, and 2) invasive pressures averaged from multiple sampled beats. Method comparison was conducted using linear regression and Bland-Altman analysis. Results Figure 1 shows non-invasively derived PV loop parameters compared to invasive data. The non-invasive method demonstrated strong correlations and low bias for stroke work (R2=0.97, bias 4.6%, p<0.0001), potential energy (R2=0.83, bias 1.5%, p=0.001), end-systolic pressure-volume relationship (R2=0.90, bias 5.4%, p=0.0003), energy per ejected volume (R2=0.93, bias 3.5%, p=0.0001), ventricular efficiency (R2=0.99, bias 1.1%, p<0.0001), arterial elastance (R2=0.87, bias −7.8%, p=0.0006), and mean external power (R2=0.89, bias 4.6%, p=0.0005). Conclusions Pressure-volume loops can be precisely and accurately computed from cardiovascular magnetic resonance imaging and brachial cuff blood pressure in humans, and is ready for use in research applications. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Swedish Heart Lung Foundation

Novel insights into the athlete's heart: is myocardial work the new champion of systolic function?

AimsWe sought to investigate the correlation between speckle-tracking echocardiography (STE)-derived myocardial work (MW) and invasively measured contractility in a rat model of athlete's heart. We also assessed MW in elite athletes and explored its association with cardiopulmonary exercise test (CPET)-derived aerobic capacity.Methods and resultsSixteen rats underwent a 12-week swim training program and were compared to controls (n = 16). STE was performed to assess global longitudinal strain (GLS), which was followed by invasive pressure-volume analysis to measure contractility [slope of end-systolic pressure–volume relationship (ESPVR)]. Global MW index (GMWI) was calculated from GLS curves and left ventricular (LV) pressure recordings. In the human investigations, 20 elite swimmers and 20 healthy sedentary controls were enrolled. GMWI was calculated through the simultaneous evaluation of GLS and non-invasively approximated LV pressure curves at rest. All subjects underwent CPET to determine peak oxygen uptake (VO2/kg). Exercised rats exhibited higher values of GLS, GMWI, and ESPVR than controls (−20.9 ± 1.7 vs. −17.6 ± 1.9%, 2745 ± 280 vs. 2119 ± 272 mmHg·%, 3.72 ± 0.72 vs. 2.61 ± 0.40 mmHg/μL, all PExercise < 0.001). GMWI correlated robustly with ESPVR (r = 0.764, P < 0.001). In humans, regular exercise training was associated with decreased GLS (−17.6 ± 1.5 vs. −18.8 ± 0.9%, PExercise = 0.002) but increased values of GMWI at rest (1899 ± 136 vs. 1755 ± 234 mmHg·%, PExercise = 0.025). GMWI exhibited a positive correlation with VO2/kg (r = 0.527, P < 0.001).ConclusionsGMWI precisely reflected LV contractility in a rat model of exercise-induced LV hypertrophy and captured the supernormal systolic performance in human athletes even at rest. Our findings endorse the utilization of MW analysis in the evaluation of the athlete’s heart.

Natural shear wave propagation speed is influenced by both changes in myocardial structural properties as well as loading conditions

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Research Foundation - Flanders (FWO) Background Shear wave elastography (SWE) is a promising tool for the non-invasive assessment of myocardial stiffness. It is based on the evaluation of the propagation speed of shear waves by high frame rate echocardiography. These waves can be induced by for instance mitral valve closure (MVC) and the speed at which they travel is related to the instantaneous stiffness of the myocardium. Myocardial stiffness is defined by the local slope of the stress-strain relation and can therefore be altered by both changes in structural properties of the myocardium as well as loading conditions. Purpose The aim of this study was to investigate how changes in myocardial structural properties as well as loading conditions affect shear wave speed after MVC. Methods Until now, 8 pigs (weight: 33.6 ± 5.4 kg) were included. The following interventions were performed: 1) preload was reduced by balloon occlusion of the vena cava inferior, 2) afterload was increased by balloon occlusion of descending aorta, 3) preload was increased by intravenous administration of 500 ml of saline and 4) ischemia/reperfusion injury (I/R injury) was induced in the septal wall by balloon occlusion of the LAD for 90 min. with subsequent reperfusion for 40 min. Echocardiographic and left ventricular pressure recordings were simultaneously obtained during each intervention. Left ventricular parasternal long-axis views were acquired with an experimental high frame rate ultrasound scanner (average frame rate: 1279 ± 148 Hz). Shear waves were visualized on tissue acceleration maps by drawing an M-mode line along the interventricular septum. Shear wave propagation speed after MVC was calculated by assessing the slope of the wave pattern on the tissue acceleration map (Figure A). Results The change in left ventricular end-diastolic pressure (LVEDP) and shear wave speed after MVC between baseline and each intervention are shown in Figure B and C, respectively. Preload reduction resulted in significant lower LVEDP compared to baseline (p &amp;lt; 0.01), while the other loading changes did not have a significant effect. Shear wave speed after MVC significantly increased by afterload and preload increase (p &amp;lt; 0.01). I/R injury resulted in increased shear wave speed (p &amp;lt; 0.01) without significantly altering LVEDP. There was a good positive correlation between the change in LVEDP and the change in shear wave speed induced by loading changes (r = 0.76; p &amp;lt; 0.001) (Figure D). However, the correlation became less strong if data of I/R injury was taken into account as well (r = 0.63; p &amp;lt; 0.001). Conclusion Our results suggest that SWE is capable to characterize myocardial tissue properties and besides has the potential as a novel method for the estimation of left ventricular filling pressures. However, in the presence of structural changes of the myocardium, care should be taken when estimating filling pressures based on shear wave propagation speed. Abstract Figure.

The behaviour of natural shear waves under different loading conditions

Abstract Background Shear wave imaging (SWI) is a novel ultrasound technique based on the detection of transverse waves traveling through the myocardium using high frame rate echocardiography. These waves can be naturally induced e.g. by mitral valve closure (MVC). Their propagation velocity is dependent on the stiffness of the myocardium. Previous studies have shown the potential of SWI for the non-invasive assessment of myocardial stiffness. So far, the influence of loading on shear wave propagation velocities has not been extensively investigated. Purpose The aim of this study was to explore how loading changes affect shear wave propagation velocities after MVC. Methods Until now, 5 pigs (weight: 33.5±6.9 kg) were included. Echocardiographic images and left ventricular pressure recordings were simultaneously acquired during acute loading alterations: 1) preload was reduced by balloon occlusion of the vena cava inferior, 2) afterload was increased by balloon occlusion of the descending aorta and 3) preload was increased by intra-venous administration of 500 ml of saline. Left ventricular parasternal long-axis views were acquired with an experimental high frame rate ultrasound scanner (average frame rate: 1247±179 Hz). Shear waves were visualized on tissue acceleration maps by drawing an M-mode line along the interventricular septum. Shear wave propagation velocities after MVC were calculated by measuring the slope of the wave front on the acceleration maps (Figure A). Results The changes in left ventricular end-diastolic pressures (LV EDP) between baseline and each intervention are shown in Figure B. Preload reduction resulted in significantly reduced LV EDP (p&amp;lt;0.01). The shear wave propagation velocities after MVC dropped with preload reduction and increased significantly by increasing afterload as well as preload (both p&amp;lt;0.05) (Figure C). There was a good positive correlation between the change in LV EDP and the change in shear wave velocities (r=0.83; p&amp;lt;0.001) (Figure D). Conclusion The shear wave propagation velocity after MVC was significantly influenced by alterations in left ventricular loading conditions and changes in these velocities were related to changes in LV EDP. These results indicate that shear wave measurements at MVC might be a potential novel parameter for the estimation of left ventricular filling pressures. More pigs will be included in the future to further confirm these findings. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Fonds Wetenschappelijk Onderzoek - Vlaanderen

Lack of scarring is not always a sign of cardiac health: Functional and molecular characterization of the rat heart's following chronic reperfusion.

Even though the coronary reperfusion process is the most important tool to preserve cardiac function, after myocardial infarction, reperfusion of acutely ischemic myocardium can induce injury. We aimed to evaluate the functional and molecular aspects 4 weeks after myocardial ischemia-reperfusion (IR) in rats. Male Wistar rats (N = 47) were subjected to myocardial IR by short-term (30 min) ligation and subsequent reperfusion of the left descending coronary artery. Control rats (N = 7) underwent the same surgical maneuver without coronary ligation. After 4 weeks, rats had their cardiac function examined by ventricular pressure recording under basal condition or pharmacological stress. Myocardial fibrosis and molecular mediators of IR injury (reactive oxygen species, tumor necrosis factor-alpha and matrix-metalloproteinase-2) were assessed as well. Most of the rats subjected to IR did not show macroscopic signs of infarct, while only 17% of these animals showed large myocardial infarction scars. Of note, all animals submitted to IR presented the functional and molecular parameters altered when compared with the control subjects. Cardiac function was attenuated in all animals submitted to IR, regardless the presence or size of macroscopic cardiac scars. Interstitial fibrosis, matrix-metalloproteinase-2 activity and the expression of tumor necrosis factor-alpha were higher in the myocardium of all IR rats as compared to the control subjects (p<0.05). Myocardium superoxide anion and hydrogen peroxide were increased in rats without or with mild cardiac scars. These results show that IR leads to myocardial injury in rats. Besides, even the animals with an apparent healthy myocardium (without infarct scar) presented cardiac dysfunction and molecular changes that may contribute to the development of heart failure over time.

O14-5 - Constrictive Pericarditis after Repeated Accumulation of Pericardial Effusion due to Long-term Chylopericardium

Primary chylopericardium is a rare disease characterized by the accumulation of chylous fluid containing high triglyceride in the pericardial cavity without a specific cause. We report a case of severe constrictive pericarditis due to 9-year history of primary chylopericardium and surgical ligation of the thoracic duct and pericardial window creation. A 24-year old woman diagnosed as primary chyropericardium, was admitted to our hospital for further treatment of heart failure. She had undergone ligation of the thoracic duct and the creation of a pericardial window. She complained of exertional dyspnea and physical examination revealed elevated jugular venous pressure. Chest X-ray showed a normal cardiac silhouette with extensive transudative pleural effusion. Echocardiogram showed severe mitral regurgitation which was slightly observed before surgery, a few pericardial effusion. Left and right ventricular simultaneous pressure recordings revealed equilibration of both ventricular diastolic pressures and a dip-and-plateau configuration. A CT scan demonstrated the thickened pericardium. Based on these findings, she was diagnosed as constrictive pericarditis and severe mitral regurgitation probably due to worsening mitral annular disjunction caused by the tight pericardium adhesion to the myocardium. During surgery, extensive tissue adhesions were observed from pericardium to epicardium. Histological examination revealed fibro-adipose pericardium with chronic inflammation and myxoid degeneration. She successfully underwent pericardiectomy and mitral valve plasty, and discharged home with greatly improved symptoms.

Three-Dimensional Echocardiography-Derived Non-Invasive Right Ventricular Pressure-Volume Analysis

In patients with pulmonary hypertension, repeated evaluations of right ventricular (RV) function are still required for clinical decision making, but the invasive nature of current pressure-volume analysis makes conducting regular follow-ups in a clinical setting infeasible. We enrolled 12 patients with pulmonary arterial hypertension (PAH) and 10 with pulmonary venous hypertension (PVH) May 2016–October 2016. All patients underwent a clinically indicated right heart catheterization (RHC), from which the yielded right ventricular pressure recordings were conjugated with RV volume by 3-D echocardiography to generate a pressure-volume loop. A continuous-wave Doppler envelope of tricuspid regurgitation was transformed into a pressure gradient recording by the simplified Bernoulli equation, and then a systolic pressure gradient-volume (PG-V) diagram was generated from similar methods. The area enclosed by the pressure-volume loop was calculated to represent semi-invasive right ventricular stroke work (RVSWRHC). The area between the PG-V diagram and x-axis was calculated to estimate non-invasive RVSW (RVSWecho). Patients with PAH have higher RV pressure, lower pulmonary arterial wedge pressure and larger RV volume that was contributed by the dilation of RV mid-cavity minor dimension. We found no significant difference of traditional parameters between these two groups, but RVSW values were significantly higher in PAH patients. The RVSW values of these two methods were significantly correlated by the equation RVSWecho = 0.8447 RVSWRHC + 129.38 (R2 = 0.9151, p < 0.001). The linearity remained satisfactory in both groups. We conclude that a PG-V diagram is a reliable method to estimate RVSW and to depict pathophysiological status.

Three-Dimensional Echocardiography-Derived Non-Invasive Right Ventricular Pressure-Volume Analysis

In patients with pulmonary hypertension, repeated evaluations of right ventricular (RV) function are still required for clinical decision making, but the invasive nature of current pressure-volume analysis makes conducting regular follow-ups in a clinical setting infeasible. We enrolled 12 patients with pulmonary arterial hypertension (PAH) and 10 with pulmonary venous hypertension (PVH) May 2016–October 2016. All patients underwent a clinically indicated right heart catheterization (RHC), from which the yielded right ventricular pressure recordings were conjugated with RV volume by 3-D echocardiography to generate a pressure-volume loop. A continuous-wave Doppler envelope of tricuspid regurgitation was transformed into a pressure gradient recording by the simplified Bernoulli equation, and then a systolic pressure gradient-volume (PG-V) diagram was generated from similar methods. The area enclosed by the pressure-volume loop was calculated to represent semi-invasive right ventricular stroke work (RVSWRHC). The area between the PG-V diagram and x-axis was calculated to estimate non-invasive RVSW (RVSWecho). Patients with PAH have higher RV pressure, lower pulmonary arterial wedge pressure and larger RV volume that was contributed by the dilation of RV mid-cavity minor dimension. We found no significant difference of traditional parameters between these two groups, but RVSW values were significantly higher in PAH patients. The RVSW values of these two methods were significantly correlated by the equation RVSWecho = 0.8447 RVSWRHC + 129.38 (R2 = 0.9151, p < 0.001). The linearity remained satisfactory in both groups. We conclude that a PG-V diagram is a reliable method to estimate RVSW and to depict pathophysiological status.

A Physiological Controller for Turbodynamic Ventricular Assist Devices Based on Left Ventricular Systolic Pressure.

The current article presents a novel physiological feedback controller for turbodynamic ventricular assist devices (tVADs). This controller is based on the recording of the left ventricular (LV) pressure measured at the inlet cannula of a tVAD thus requiring only one pressure sensor. The LV systolic pressure (SP) is proposed as an indicator to determine the varying perfusion requirements. The algorithm to extract the SP from the pump inlet pressure signal used for the controller to adjust the speed of the tVAD shows robust behavior. Its performance was evaluated on a hybrid mock circulation. The experiments with changing perfusion requirements were compared with a physiological circulation and a pathological one assisted with a tVAD operated at constant speed. A sensitivity analysis of the controller parameters was conducted to identify their limits and their influence on a circulation. The performance of the proposed SP controller was evaluated for various values of LV contractility, as well as for a simulated pressure sensor drift. The response of a pathological circulation assisted by a tVAD controlled by the introduced SP controller matched the physiological circulation well, while over- and underpumping events were eliminated. The controller presented a robust performance during experiments with simulated pressure sensor drift.

256 NEW EVIDENCE FOR VAGAL CONTROL OF THE LEFT HEART

The role of the parasympathetic innervation of the left ventricle remains controversial, although there is some evidence that vagus nerve stimulation decreases left ventricular contractility in vivo in the human and pig heart. The aim of this study was to identify the anatomical location of vagal preganglionic neurones that control ventricular contractility using an anaesthetised rat model. Male Sprague-Dawley rats (350–400 g, n=6) were anaesthetised with pentobarbitone sodium (induction 60 mg/kg i.p.; maintenance 15–20 mg/kg/hr i.v.) and artificially ventilated. The left femoral artery and both femoral veins were cannulated for the measurement of arterial pressure and administration of fluids and drugs. The right carotid artery was cannulated for left ventricular pressure recording using a Millar pressure probe. Lead II ECG was also monitored. The animal was placed in a stereotaxic frame and the dorsal surface of the brainstem was exposed. To activate vagal preganglionic neurones, an excitatory neurotransmitter glutamate (10 mM, 40 nl, pH 7.4) was microinjected into three discrete locations (separated by 0.5 mm) along the rostro-caudal extent of the left and right dorsal motor nuclei of the vagus nerve (DVMN). Responses were measured in a second group (n=3) with transoesophageal atrial pacing (TAP) to abolish chronotropic changes. A third group (n=2) underwent a spinal transection at C1 to remove sympathetic influences followed by gelofusine and vasopressin infusion to maintain mean arterial blood pressure at ∼100mmHg. Values are means±S.E.M., compared by paired student’s t-test. Glutamate microinjections into the most caudal part of the left DVMN caused a significant (p

Short-term ventricular restraint attenuates post-infarction remodeling in rats

Background/objectivesLeft ventricular restraint attenuates post-infarction remodeling, but may be associated with unfavorable long-term histological response. We hypothesized that beneficial effects can be obtained with short-term restraint during the early post-infarction period; for this purpose, we evaluated a biodegradable scaffold in the in vivo rat model and compared it with epicardial hydrogel application. MethodsA total of 230 Wistar rats (358±7g) were studied. Implantation was performed with and without prior myocardial infarction, induced by permanent coronary artery ligation. Diastolic filling was evaluated by left ventricular pressure recordings after scaffold implantation. Degradation rates and inflammatory/foreign body response were studied at 3, 7 and 15days post-ligation. Remodeling indices were evaluated by echocardiography 15days post-ligation. ResultsNo differences were found in diastolic pressure. Biodegradability was ~50% by 7days and 100% by 15days for both materials. Likewise, inflammatory/foreign body response peaked at 3days post-implant, with subsequent remission, but fibroblastic reaction was more pronounced after scaffold than after hydrogel implantation. Post-ligation, ejection fraction was higher in the scaffold (40.0±1.5%) or hydrogel groups (37.0±1.3%), compared to controls (30.6±1.9%). Wall tension index was lower with either biomaterial, but left ventricular end-diastolic diameter was shorter (p=0.044) and sphericity was attenuated (p=0.029) after scaffold, compared to hydrogel implantation. ConclusionsBoth biomaterials showed a favorable histological response and attenuated remodeling, but epicardial restraint produced better results compared to hydrogel alone. The latter approach merits further investigation due to the ease of implantation.

Early ion-channel remodeling and arrhythmias precede hypertrophy in a mouse model of complete atrioventricular block

Complete atrioventricular block (CAVB) and related ventricular bradycardia are known to induce ventricular hypertrophy and arrhythmias. Different animal models of CAVB have been established with the most common being the dog model. Related studies were mainly focused on the consequences on the main repolarizing currents in these species, i.e. IKr and IKs, with a limited time point kinetics post-AVB. In order to explore at a genomic scale the electrical remodeling induced by AVB and its chronology, we have developed a novel model of CAVB in the mouse using a radiofrequency-mediated ablation procedure. We investigated transcriptional changes in ion channels and contractile proteins in the left ventricles as a function of time (12 h, 1, 2 and 5 days after CAVB), using high-throughput real-time RT-PCR. ECG in conscious and anesthetized mice, left ventricular pressure recordings and patch-clamp were used for characterization of this new mouse model. As expected, CAVB was associated with a lengthening of the QT interval. Moreover, polymorphic ventricular tachycardia was recorded in 6/9 freely-moving mice during the first 24 h post-ablation. Remarkably, myocardial hypertrophy was only evident 48 h post-ablation and was associated with increased heart weight and altered expression of contractile proteins. During the first 24 hours post-CAVB, genes encoding ion channel subunits were either up-regulated (such as Nav1.5, + 74%) or down-regulated (Kv4.2, −43%; KChIP2, −47%; Navβ1, −31%; Cx43, −29%). Consistent with the transient alteration of Kv4.2 expression, I to was reduced at day 1, but restored at day 5. In conclusion, CAVB induces two waves of molecular remodeling: an early one (≤ 24 h) leading to arrhythmias, a later one related to hypertrophy. These results provide new molecular basis for ventricular tachycardia induced by AV block.

Coupled pacing improves left ventricular function during simulated atrial fibrillation without mechanical dyssynchrony

Electrical stimulation [coupled pacing (CP)] applied near the end of the T-wave is able to create a retrograde activation of the atrioventricular (AV) node in turn to prevent rapid ventricular conduction during atrial fibrillation (AF). The impact of this pacing modality associated with cardiac resynchronization therapy (CRT) has been evaluated in the present experimental study. After inducing AF by rapid pacing in six dogs, we applied the following pacing modalities: rapid right ventricular (RV) pacing, rapid CRT, CRT with an additional RV paced beat (CP) at a specific delay (CRT + CP), and CRT with vagal stimulation (CRT-VS). Left ventricular (LV) pressure recordings and echocardiography for 2D strain analysis were performed. CRT + CP reduced the ventricular response rate and increased the LV systolic pressure and cardiac output compared with CRT alone (136 +/- 6 vs. 86 +/- 13 mmHg, P < 0.05 and 2.0 +/- 0.4 vs.1.2 +/- 0.1, P < 0.05 L/m, respectively). Compared with CRT-VS, CRT + CP increased the LV ejection fraction (LVEF = 51 +/- 10 vs. 28 +/- 4%, P < 0.05), peak global circumferential strain (-17 +/- 2 vs. -11 +/- 3%), and diastolic filling time (49 +/- 6 vs. 28 +/- 3%, P < 0.02) suggesting beneficial effects of CP beyond rate control. CRT + CP did not result in increased dyssynchrony [CRT (8.3 +/- 2%) vs. CRTCP (8.4 +/- 3%, P = NS)]. CRT + CP effectively reduces ventricular contractile rate and leads to an increase in systolic and diastolic performance without inducing mechanical dyssynchrony.

Brain death pathogenesis and diagnosis.

The criteria of brain death were evaluated in 42 neurosurgical patients in extremis. Repeated clinical and electroencephalographic examinations and continuous recording of ventricular pressure showed that the deterioration could occur suddenly or gradually. Cranial nerve reflexes and cortical EEG activity disappeared simultaneously or at different times. Ventricular pressure equalled arterial blood pressure in the terminal stage. Brain death may be presumed if cranial nerve reflexes and cortical EEG activity are absent. This assumption is supported when the cerebral perfusion pressure is below 10 mm Hg. In the present study the diagnosis was confirmed by total cerebral angiography. When no brain circulation could be demonstrated twice at an interval of 20 minutes, brain death was documented. In most patients spinal reflexes were present for some time afterwards.

Oxygen transport and myocardial function after the administration of albumin 5%, hydroxyethylstarch 6% and succinylated gelatine 4% to rabbits.

The effects of administering albumin 5%, hydroxyethylstarch 6% and succinylated gelatine 4% on oxygen transport and left ventricular function were prospectively investigated in different experimental conditions: baseline, fluid load, after 10 min of myocardial ischaemia and after reperfusion. Twenty-seven rabbits received at random one of three colloids in escalating boluses over 10-15 min to achieve left ventricular end-diastolic pressures (LVEDP) between 8 and 10mmHg. A branch of the left anterior descending coronary artery was then temporarily occluded by a ligature and released after 10 min. Myocardial function was assessed using left ventricular pressure recordings and dimension data obtained from ultrasound crystals inserted onto the ventricular wall. Blood was sampled for the determination of oxygen delivery and consumption, the oxygen extraction ratio, acid-base status, and glucose and lactate concentrations. Administration of the colloids similarly increased oxygen delivery and improved left ventricular function in all groups. Peak rate of pressure development (dP/dt(max)) and oxygen delivery were reduced during ischaemia and reperfusion. The decrease in dP/dt(max) was more pronounced in the hydroxyethylstarch group. Administration of albumin 5%, hydroxyethylstarch 6% and succinylated gelatine 4% had similar effects on oxygen delivery and myocardial function. After ischaemia and during reperfusion, the decrease in myocardial function was most pronounced with hydroxyethylstarch 6%.

Assessment of cardiovascular dynamics by pressure-area relations in pediatric patients with congenital heart disease

Objectives: It is particularly useful to separately quantify the ventricular contractility and loading conditions for a better understanding of the cardiovascular dynamics in congenital heart disease, where abnormalities in chamber and loading properties may coexist. Furthermore, ventricular contractility and loading conditions may alter independently or simultaneously with disease progression and therapeutic intervention. The objectives of the present study were (1) to test whether ventricular pressure-area analysis can provide such quantitation among patients with various forms of congenital heart disease, (2) to reveal basal cardiovascular interaction in congenital heart disease by means of pressure-area analysis, and (3) to test the feasibility of this method in a simplified and less invasive form to further enhance its clinical value. Methods: We constructed pressure-area loops during caval occlusion by using transthoracic echocardiographic automated border detection combined with ventricular pressure recordings in 59 pediatric patients with congenital heart disease and in 7 normal control subjects. Results: Area measurements obtained by automated border detection were highly reproducible, and area changes reflected volume changes. The pressure-area data provided load-independent measures of contractility, which were consistently increased by use of dobutamine ( P < .05). End-systolic and arterial elastance individually quantified simultaneous changes in ventricular contractility and loading with milrinone infusion and predicted net cardiac performance. The pressure-area analysis better characterized the ventricular contractile states under a variety of loading conditions in congenital heart disease, whereas predominant load dependence of conventional indices confounded them. Furthermore, pressure-area relations were reasonably estimated from a single beat and from aortic pressure data during abdominal compression. Conclusions: Pressure-area analysis should provide a useful modality with which to assess cardiovascular dynamics in pediatric patients with congenital heart disease in more detail and should thus help improve the management of patients with this disease.

Diastolische Ventrikelfunktion bei koronarchirurgischen Patienten vor und nach extrakorporaler Zirkulation: Vergleich dopplersonographisch und invasiv bestimmter Parameter der diastolischen Ventrikelfunktion

There is evidence that diastolic function is a major determinant of overall cardiac performance. Intraoperative use of transesophageal echocardiography (TEE) enables Doppler measurement of mitral inflow pattern (E/A ratio). The E/A ratio is suggested to be a reliable index of changes in myocardial relaxation. In the present study we compared the time course of the E/A ratio and the time constant of myocardial relaxation (τ) assessed by direct left ventricular pressure recordings in patients before and after cardiopulmonary bypass (CPB). After ethical approval, 12 patients undergoing CABG surgery were studied. Measurements of the E/A ratio and τ were performed after induction of anesthesia (I), immediately prior to CPB with the pericardium open (II), 5 min after CPB (III), and after sternal closure (IV). Time constant of myocardial relaxation was calculated as the reciprocal value of the slope of the left ventricular dP/dt and left ventricular pressure plot. The E/A ratio was significantly decreased at the end of surgery (IV). In contrast, τ was increased immediately after CPB, but decreased after sternal closure (IV). Cardiac index and heart rate both increased after CPB.¶ The results of the present study demonstrate that diastolic dysfunction occurred immediately after CPB, as indicated by an increase in the time constant of myocardial relaxation. However, τ improved rapidly to pre-CPB values. The E/A ratio alone failed to detect the initial post-CPB alteration in left ventricular relaxation.

Third ventriculostomy in normal pressure hydrocephalus

Improvement in three out of four cases of normal pressure hydrocephalus after third ventriculostomy is reported. Pre- and postoperative ventricular pressure recording suggested that this improvement may be occurring in the absence of an improvement in ventricular pressures.Third ventriculostomy may relieve periventricular tissue stress and thus improve local blood flow, which is a likely mechanism in the syndrome of normal pressure hydrocephalus.

Early changes in the time course of myocardial contraction after correcting aortic regurgitation

Background. Correcting aortic regurgitation causes significant changes in left ventricular loading conditions, but few observations have been made intraoperatively of early effects on myocardial function. Methods. We studied 18 patients (mean age, 59 ± 12 years; 14 men) in whom aortic regurgitation was corrected with a stentless biologic valve. Overall left ventricular function was studied by thermodilution cardiac output, ventricular filling pressure, and systemic arterial pressure. Regional myocardial function was assessed from intraoperative transesophageal M-mode echocardiography and high fidelity ventricular pressure recordings before cardiopulmonary bypass, and 0.5, 1, 3, 6, 12, and 20 hours after operation. Time course of contraction, and magnitude of left ventricular systolic wall stress, dimensional shortening, myocardial power, and stroke work were measured. Results. Global hemodynamics: there was an immediate decrease in left ventricular stroke volume (58 ± 31 mL versus 80 ± 30 mL, p = 0.004) and stroke work index (250 ± 86 mJ/m versus 401 ± 198 mJ/m, p = 0.005), but systemic arterial pressure (79 ± 11 mm Hg versus 65 ± 10 mm Hg, p = 0.002), increased at constant heart rate and end-diastolic pressure. Regional myocardial function and timing: peak systolic wall stress, dimensional shortening rate, and myocardial power production were all unchanged with operation. However, myocardial stroke work decreased (3.0 ± 1.3 mJ/cm versus 4.8 ± 2.4 mJ/cm, p = 0.009), attributable to shortening of the duration of systole (475 ± 91 ms versus 543 ± 67 ms, p < 0.001). Diastolic time increased from 34% ± 18% to 71% ± 33% of systolic pulse duration ( p < 0.001). Conclusions. Correcting aortic regurgitation causes an early decrease in regional and global stroke work and increases diastolic time, although systolic wall stress does not decrease immediately. These beneficial effects are achieved by reducing the duration rather than altering the peak intensity (power) of myocardial contraction.

Calculation of the aortic valve gradient from the left ventricular–femoral and aortic–femoral pairs of pressure waveforms

Accurate measurement of the transaortic gradient is important in the invasive assessment of the significance of aortic stenosis. The mean gradient obtained from simultaneous left ventricular and aortic pressure recordings is the gold standard, but requires two central catheters. We hypothesized that a gradient calculated by subtracting the aortofemoral from the ventriculofemoral gradient would reproduce the ventriculoaortic gradient. In 24 patients sequential recordings of the aortofemoral, ventriculofemoral, and ventriculoaortic pressures pairs were obtained. The calculated ventriculoaortic gradient was obtained by subtracting the aortofemoral gradient from the ventriculofemoral gradient. Both of these gradients were measured by computer, using a systolic ejection period between the crossovers of the upslope and downslope of the left ventricular waveform with the femoral waveform. The ventriculoaortic gradient calculated using this technique correlated closely with the gradient measured by two central catheters (R = 0.99). This technique is accurate and does not require two central catheters.