An evaluation of cardiac output by five arterial pulse contour techniques during cardiac surgery.

The bias, precision and tracking ability of five different pulse contour methods were evaluated by simultaneous comparison of cardiac output values from the conventional thermodilution technique (COtd). The five different pulse contour methods included in this study were: Wesseling's method (cZ); the Modelflow method; the LiDCO system; the PiCCO system and a recently developed Hemac method. We studied 24 cardiac surgery patients undergoing uncomplicated coronary artery bypass grafting. In each patient, the first series of COtd was used to calibrate the five pulse contour methods. In all, 199 series of measurements were accepted by all methods and included in the study. COtd ranged from 2.14 to 7.55 l.min(-1), with a mean of 4.81 l.min(-1). Bland-Altman analysis showed the following bias and limits of agreement: cZ, 0.23 and - 0.80 to 1.26 l.min(-1); Modelflow, 0.00 and - 0.74 to 0.74 l.min(-1); LiDCO, - 0.17 and - 1.55 to 1.20 l.min(-1); PiCCO, 0.14 and - 1.60 to 1.89 l.min(-1); and Hemac, 0.06 and - 0.81 to 0.93 l.min(-1). Changes in cardiac output larger than 0.5 l.min(-1) (10%) were correctly followed by the Modelflow and the Hemac method in 96% of cases. In this group of subjects, without congestive heart failure, with normal heart rhythm and reasonable peripheral circulation, the best results in absolute values as well as in tracking changes in cardiac output were measured using the Modelflow and Hemac pulse contour methods, based on non-linear three-element Windkessel models.

Less invasive determination of cardiac output from the arterial pressure by aortic diameter-calibrated pulse contour.

BACKGROUND: Cardiac output by modelflow pulse contour method can be monitored quantitatively and continuously only after an initial calibration, to adapt the model to an individual patient. The modelflow method computes beat-to-beat cardiac output (COmf) from the radial artery pressure, by simulating a three-element model of aortic impedance with post-mortem data from human aortas. METHODS: In our improved version of modelflow (COmfc) we adapted this model to a real time measure of the aortic cross-sectional area (CSA) of the descending aorta just above the diaphragm, measured by a new transoesophageal echo device (HemoSonic 100). COmf and COmfc were compared with thermodilution cardiac output (COtd) in 24 patients in the intensive care unit. Each thermodilution value was the mean of four measurements equally spread over the ventilatory cycle. RESULTS: Least squares regression of COtd vs COmf gave y=1.09x[95% confidence interval (CI) 0.96-1.22], R2=0.15, and of COtd vs COmfc resulted in y=1.02x(95% CI 0.96-1.08), R2=0.69. The limits of agreement of the un-calibrated COmf were -3.53 to 2.79, bias=0.37 litre min(-1) and of the diameter-calibrated method COmfc, -1.48 to 1.32, bias=-0.08 litre min(-1). The coefficient of variation for the difference between methods decreased from 28 (un-calibrated) to 12% after diameter-calibration. CONCLUSIONS: After diameter-calibration, the improved modelflow pulse contour method reliably estimates cardiac output without the need of a calibration with thermodilution, leading to a less invasive cardiac output monitoring method.

Mean cardiac output by thermodilution with a single controlled injection.

OBJECTIVE: A new method to estimate mean cardiac output by thermodilution with a single duration-controlled injection was evaluated in patients. DESIGN: Prospective criterion standard study. SETTING: University hospital cardiac surgical intensive care unit and cardiac operation room. PATIENTS: Of 33 patients, 24 underwent coronary bypass graft surgery, four had a valve replacement, and five were treated in the intensive care unit. INTERVENTIONS: Interventions consisted of thermodilution cardiac output measurements. One single duration-controlled injection of cold fluid was used to calculate cardiac output. This controlled injection was performed with a duration equal to one whole ventilation cycle of the ventilator. An algorithm adapted to this duration-controlled injection calculated cardiac output. Moreover, this algorithm has properties to reduce errors caused by artificial ventilation and thermal noise. MEASUREMENTS AND MAIN RESULTS: In 33 patients, the averaged values of four measurements equally spread over the ventilatory cycle (phase-controlled) were compared with the values of two single duration-controlled measurements. The measurements were performed during periods of stable respiration and circulation. No significant difference was observed between the mean of four phase-controlled measurements and the mean of the two duration-controlled measurements. The cardiac output values in the intensive care patients were significantly higher compared with the two other patient groups (p <.05). The difference between the two methods could not be subdivided for the three patient groups (p >.05). The coefficient of variation of the single duration-controlled thermodilution measurements was significantly lower than the single phase-controlled measurements, 3% vs. 6% (p <.01). CONCLUSIONS: One single duration-controlled injection thermodilution measurement is as accurate and repeatable as the mean of four phase-controlled measurements and is clinically feasible.

The volume-dependency of parallel conductance throughout the cardiac cycle and its consequence for volume estimation of the left ventricle in patients.

OBJECTIVE: To study the hypothesis that the electrical conductance of tissues and fluids (parallel conductance (G(p))) around the ventricle depends on left ventricular volume throughout the cardiac cycle. METHODS: We extended a recently developed method to determine G(p) throughout the cardiac cycle. First, we compared the estimates of parallel conductances obtained with the new method (G(a)(p)) with those of the conventional one (G(1)(p)), both averaged over the cardiac cycles. Secondly, G(a)(p) was determined throughout the cardiac cycle and its volume dependency was assessed. Thirdly, the factor alpha was calculated as the ratio between stroke volume, obtained by the conductance method using G(1)(p), and that obtained by a thermodilution method. Because the non-homogeneous field was indicated to be the reason for the dependency of G(p) on left ventricular volume as well as for the need for alpha, we tested whether the hypothesis implies that a correction with alpha is not needed if G(p) is determined throughout the cardiac cycle. RESULTS: We found a negative linear relation between G(p) and left ventricular volume. This relation appeared to be reproducible within each patient. Furthermore, we found that alpha deviates from 1 primarily due to the dependency of G(p) on left ventricular volume. CONCLUSION: To obtain stroke volume or to determine absolute left ventricular volume continuously within a cardiac cycle, G(p) should be determined throughout each cardiac cycle and if a constant G(p) throughout the cardiac cycle is used a correction with the factor alpha should be made to correct for a possible influence of electrical field heterogeneity.

A comparison of cardiac output derived from the arterial pressure wave against thermodilution in cardiac surgery patients.

In three clinical centres, we compared a new method for measuring cardiac output with conventional thermodilution. The new method computes beat-to-beat cardiac output from radial artery pressure by simulating a three-element model of aortic input impedance, and includes non-linear aortic mechanical properties and a self-adapting systemic vascular resistance. We compared cardiac output by continuous model simulation (MF) with thermodilution cardiac output (TD) in 54 patients (18 female, 36 male) undergoing coronary artery bypass surgery. We made three or four conventional thermodilution estimates spread equally over the ventilatory cycle. In 490 series of measurements, thermodilution cardiac output ranged from 2.1 to 9.3, mean 5.0 litre min(-1). MF differed +0.32 (1.0) litre min(-1) on average with limits of agreement of -1.68 and +2.32 litre min(-1). Differences decreased when the first series of measurements in a patient was used to calibrate the model. In 436 remaining series, the mean difference became -0.13 (0.47) litre min(-1) with limits of agreement of -1.05 and +0.79 litre min(-1). When consecutive measurements were made, the change was greater than 0.5 litre min(-1), on 204 occasions. The direction of change was the same with both methods in 199. The difference between the methods remained near zero during surgery suggesting that a single calibration per patient was adequate. Aortic model simulation with radial artery pressure as input reliably monitors changes in cardiac output in cardiac surgery patients. Before calibration, the model cannot replace thermodilution, but after calibration the model method can quantitatively replace further thermodilution estimates.

Computer control versus manual control of systemic hypertension during cardiac surgery.

BACKGROUND: We recently demonstrated the feasibility of computer controlled infusion of vasoactive drugs for the control of systemic hypertension during cardiac surgery. The objective of the current study was to investigate the effects of computer controlled blood pressures on hemodynamic stability when compared to conventional manual control. METHOD: Systemic artery blood pressures were managed either by computer (80 patients) or by a well-trained anesthesiologist (80 patients). The vasodilator drugs sodium nitroprusside and nitroglycerin were used. Hemodynamic stability was determined from the standard deviation of the mean arterial pressure samples and from the percentages of time that arterial pressure was hypertensive or hypotensive. RESULTS: The average standard deviation of the mean arterial pressure samples was smaller for the computer controlled than for the manually controlled group: 7.5+/-2.2 (mean+/-SD) versus 8.9+/-2.3 mmHg (P<0.0001). The systemic artery pressure was less hypertensive and less hypotensive in the computer controlled than in the manually controlled group: 9.4+/-5.7 versus 13.1+/-6.0% (P<0.0001) and 8.0+/-5.9 versus 11.8+/-7.4% (P<0.0001), respectively. CONCLUSION: We conclude that, compared with manual control, computer control of systemic hypertension significantly improved hemodynamic stability during cardiac surgery.

Acute and short-term effects of partial left ventriculectomy in dilated cardiomyopathy: assessment by pressure-volume loops.

OBJECTIVES: The aim of this study was to evaluate the short-term effects of partial left ventriculectomy (PLV) on left ventricular (LV) pressure-volume (P-V) loops, wall stress, and the synchrony of LV segmental volume motions in patients with dilated cardiomyopathy. BACKGROUND: Surgical LV volume reduction is under investigation as an alternative for, or bridge to, heart transplantation for patients with end-stage dilated cardiomyopathy. METHODS: We measured P-V loops in eight patients with dilated cardiomyopathy before, during and two to five days after PLV. The conductance catheter technique was used to measure LV volume instantaneously. RESULTS: The PLV reduced end-diastolic volume (EDV) acutely from 141+/-27 to 68+/-16 ml/m2 (p < 0.001) and to 65+/-6 ml/m2 (p < 0.001) at two to five days postoperation (post-op). Cardiac index (CI) increased from 1.5+/-0.5 to 2.6+/-0.6 l/min/m2 (p < 0.002) and was 1.8+/-0.3 l/min/m2 (NS) at two to five days post-op. The LV ejection fraction (EF) increased from 15+/-8% to 35+/-6% (p < 0.001) and to 26+/-3% (p < 0.003) at two to five days post-op. Tau decreased from 54+/-8 to 38+/-6 ms (p < 0.05) and was 38+/-5 ms (NS) at two to five days post-op. Peak wall stress decreased from 254+/-85 to 157+/-49 mm Hg (p < 0.001) and to 184+/-40 mm Hg (p < 0.003) two to five days post-op. The synchrony of LV segmental volume changes increased from 68+/-6% before PLV to 80+/-7% after surgery (p < 0.01) and was 73+/-4% (NS) at two to five days post-op. The LV synchrony index and CI showed a significant (p < 0.0001) correlation. CONCLUSIONS: The acute decrease in LV volume in heart-failure patients following PLV resulted at short-term in unchanged SV, increases in LVEF, and decreases in peak wall stress. The increase in LV synchrony with PLV suggests that the transition to a more uniform LV contraction and relaxation pattern might be a rationale of the working mechanism of PLV.

A new approach to determine parallel conductance for left ventricular volume measurements.

OBJECTIVES: To determine absolute ventricular volume with the conductance catheter technique, the electrical conductance of tissues and fluids (parallel conductance) around the ventricle should be determined precisely. METHODS: A new objective method to estimate parallel conductance based on analysis of the dilution curve of hypertonic saline was investigated. The parallel conductances obtained with the new method (G(a)(p)) were compared to those obtained with the conventional method (G(l)(p)). The study was performed in the left ventricle of 12 patients. RESULTS: G(a)(p) was not significantly different from G(l)(p). For the G(l)(p) method the average percentage difference between duplicate values, both taken as absolute values, was 15.06% and for the G(a)(p) method it was 4. 01%. Thus the reproducibility of the method is a factor four better than that of the method. This difference appeared to be significant. CONCLUSION: We conclude that a smaller number of injections will be required to obtain the same precision using our method.

Left ventricular wall stress normalization in chronic pressure-overloaded heart: a mathematical model study.

It is generally accepted that the left ventricle (LV) hypertrophies (LVH) to normalize systolic wall stress (sigma(s)) in chronic pressure overload. However, LV filling pressure (P(v)) may be elevated as well, supporting the alternative hypothesis of end-diastolic wall stress (sigma(d)) normalization in LVH. We used an LV time-varying elastance model coupled to an arterial four-element lumped-parameter model to study ventricular-arterial interaction in hypertension-induced LVH. We assessed model parameters for normotensive controls and applied arterial changes as observed in hypertensive patients with LVH (resistance +40%, compliance -25%) and assumed 1) no cardiac adaptation, 2) normalization of sigma(s) by LVH, and 3) normalization of sigma(s) by LVH and increase in P(v), such that sigma(d) is normalized as well. In patients, systolic and diastolic blood pressures increase by approximately 40%, cardiac output (CO) is constant, and wall thickness increases by 30-55%. In scenarios 1 and 2, blood pressure increased by only 10% while CO dropped by 20%. In scenario 2, LV wall thickness increased by only 10%. The predictions of scenario 3 were in qualitative and quantitative agreement with in vivo human data. LVH thus contributes to the elevated blood pressure in hypertension, and cardiac adaptations include an increase in P(v), normalization of sigma(s), and preservation of CO in the presence of an impaired diastolic function.

Ventricular motion during the ejection phase: a computational analysis.

In the present paper, the study of the ventricular motion during systole was addressed by means of a computational model of ventricular ejection. In particular, the implications of ventricular motion on blood acceleration and velocity measurements at the valvular plane (VP) were evaluated. An algorithm was developed to assess the force exchange between the ventricle and the surrounding tissue, i.e., the inflow and outflow vessels of the heart. The algorithm, based on the momentum equation for a transitory flowing system, was used in a fluid-structure model of the ventricle that includes the contractile behavior of the fibers and the viscous and inertial forces of the intraventricular fluid. The model calculates the ventricular center of mass motion, the VP motion, and intraventricular pressure gradients. Results indicate that the motion of the ventricle affects the noninvasive estimation of the transvalvular pressure gradient using Doppler ultrasound. The VP motion can lead to an underestimation equal to 12.4 +/- 6.6%.

The double-orifice technique as a standardized approach to treat mitral regurgitation due to severe myxomatous disease: surgical technique.

OBJECTIVES: Mitral-valve repair in Barlow's disease is challenging; conventional techniques are difficult to perform, and there is a high risk of a postoperative suboptimal result. Double-orifice repair has been applied in a standardized approach to treat patients with severe mitral regurgitation and bileaflet prolapse due to Barlow's disease. METHODS: Since 1993, 82 patients with severe mitral regurgitation due to Barlow's disease underwent correction applying the edge-to-edge concept. They were submitted to double-orifice repair in a standardized fashion, suturing the middle portions of both leaflets. RESULTS: There were no hospital deaths. The repair was unsatisfactory in one patient who underwent valve replacement soon after the repair. The mean postoperative valve area was 3.7+/-0.79 cm(2) against a mean preoperative value of 9.2+/-2.1 cm(2). No or mild regurgitation was found in all but three patients who showed moderate residual regurgitation. There were no late deaths. Freedom from reoperation was 86+/-14% at 5 years. At the latest follow-up, all patient but one were New York Heart Association (NYHA) functional class I, and echo-Doppler assessment of valve reconstruction showed stable valve function in all patients. CONCLUSIONS: The double-orifice repair can be used as a standardized approach to treat valve regurgitation due to Barlow disease with low risk and good early and mid-term results.

Automated infusion of vasoactive and inotropic drugs to control arterial and pulmonary pressures during cardiac surgery.

OBJECTIVE: To evaluate the feasibility of a closed-loop system for simultaneous control of systemic arterial and pulmonary artery blood pressures during cardiac surgery. DESIGN: Feasibility study. SETTING: The cardiac surgery operating room. PATIENTS: The performance of the multiple-drug closed-loop system was evaluated during cardiac surgery in 30 patients who required treatment with more than one vasoactive or inotropic drug. INTERVENTIONS: A multiple-drug closed-loop system integrated five single-drug blood pressure controllers. Arterial hypertension was controlled using sodium nitroprusside or nitroglycerin, arterial hypotension was controlled using noradrenaline or dobutamine, and pulmonary hypertension was controlled using nitroglycerin. The anesthesiologist selected target pressures and single-drug blood pressure controllers. The multiple-drug closed-loop system had a set of priority rules that automatically activated from the selected single-drug controllers the optimum single-drug controller for each hemodynamic state. Drug infusion rates of the nonactive controllers were kept constant. The initial knowledge that was used to construct the priority rules was obtained from standard anesthetic protocols on perioperative management of cardiac surgical patients. A supervisory computer program defined the actions to be taken in cases of infusion pump problems, invalid pressure measurements, and during unexpected increases and decreases in systemic arterial pressure. MEASUREMENTS AND MAIN RESULTS: The activation of single-drug controllers by the priority rules was accurate and fast. On average, a different single-drug controller was activated once every 7.2 mins. As a measure of variability, the average deviation of mean arterial pressure and mean pulmonary artery pressure from their target values was evaluated and was 8.6+/-4.0 and 4.4+/-4.0 mm Hg, respectively, before cardiopulmonary bypass and 8.0+/-3.6 and 2.4+/-0.9 mm Hg, respectively, after cardiopulmonary bypass. None of the single-drug controllers showed any signs of unstable response. CONCLUSION: Closed-loop control of both arterial and pulmonary pressures using multiple drugs is feasible during cardiac surgery.

Tracing best PEEP by applying PEEP as a RAMP.

OBJECTIVE: The aim of this study was to show the feasibility of a slow, continuously increasing level of positive end-expiratory pressure (PEEP) (ramp manoeuvre) in selecting best PEEP and to evaluate whether best PEEP, as defined by maximal oxygen transport, coincides with best systemic arterial oxygenation or best compliance. DESIGN: In 11 anaesthetized piglets, PEEP was increased between 0 cmH2O (zero end-expiratory pressure; ZEEP) and 15 cmH2O (PEEP15) with a constant rate of 0.67 cmH2O x min(-1). This ramp manoeuvre was performed both under normal conditions and after induction of an experimental lung oedema. During the ramp manoeuvre, haemodynamic and pulmonary variables were monitored almost continuously. RESULTS: During the rise in PEEP, cardiac output declined in a non-linear way. In the series with normal conditions, best PEEP was always found at ZEEP. In the series with experimental lung oedema, best PEEP, as defined by maximum oxygen transport, was found at PEEP1-6, as defined by maximal compliance, at PEEP7.5 and by maximal arterial oxygen tension (PaO2) at PEEP10-14. CONCLUSIONS: Best PEEP according to oxygen transport is lower than best PEEP according to compliance and PaO2; the use of PEEP as a ramp might prevent unnecessarily high levels of PEEP.

Enhanced susceptibility for acquired torsade de pointes arrhythmias in the dog with chronic, complete AV block is related to cardiac hypertrophy and electrical remodeling.

BACKGROUND: Chronic, complete AV block (CAVB) in the dog leads to ventricular hypertrophy, which has been described as an independent risk factor for arrhythmias. In this model, we examined (1) whether the short- and long-term electrical adaptations predispose to acquired torsade de pointes arrhythmias (TdP) and (2) the nature of the structural and functional adaptations involved. METHODS AND RESULTS: We determined (1) endocardial right (RV) and left (LV) ventricular APD, DeltaAPD (LV APD-RV APD), presence of EADs at 0 weeks (acute: AAVB), and CAVB (6 weeks) and inducibility of TdP by pacing and d-sotalol (n=10); (2) steady-state and dynamic LV hemodynamics at 0 and 6 weeks (n=6); (3) plasma neurohumoral levels in time (n=7); (4) structural parameters of the LV and RV of CAVB dogs (n=6) compared with sinus rhythm (SR) dogs (n=6); and (5) expression of ventricular mRNA atrial natriuretic factor (ANF) in CAVB (n=4) and SR (n=4) dogs. Compared with AAVB, CAVB led to nonhomogeneous prolongation of LV and RV APD and different sensitivity for d-sotalol, leading to EADs (4 of 14 versus 9 of 18, P<0.05), increased DeltaAPD (45+/-30 versus 125+/-60 ms, P<0.05), and induction of TdP in most dogs (0% versus 60%, P<0.05). CAVB led to biventricular hypertrophy, whereas LV function was similar in AAVB and CAVB. The neurohumoral levels were transiently elevated. The LV and RV collagen and the capillary/fiber ratio remained normal, whereas ventricular ANF mRNA was not detectable. CONCLUSIONS: The electrical remodeling occurring after CAVB predisposes the heart to acquired TdP, whereas the structural changes (hypertrophy) are successfully aimed at maintaining cardiac function.

Asynchronous electrical activation induces asymmetrical hypertrophy of the left ventricular wall.

BACKGROUND: Asynchronous electrical activation, induced by ventricular pacing, causes regional differences in workload, which is lower in early- than in late-activated regions. Because the myocardium usually adapts its mass and structure to altered workload, we investigated whether ventricular pacing leads to inhomogeneous hypertrophy and whether such adaptation, if any, affects global left ventricular (LV) pump function. METHODS AND RESULTS: Eight dogs were paced at physiological heart rate for 6 months (AV sequential, AV interval 25 ms, ventricular electrode at the base of the LV free wall). Five dogs were sham operated and served as controls. Ventricular pacing increased QRS duration from 47.2+/-10.6 to 113+/-16.5 ms acutely and to 133.8+/-25.2 ms after 6 months. Two-dimensional echocardiographic measurements showed that LV cavity and wall volume increased significantly by 27+/-15% and 15+/-17%, respectively. The early-activated LV free wall became significantly (17+/-17%) thinner, whereas the late-activated septum thickened significantly (23+/-12%). Calculated sector volume did not change in the LV free wall but increased significantly in the septum by 39+/-13%. In paced animals, cardiomyocyte diameter was significantly (18+/-7%) larger in septum than in LV free wall, whereas myocardial collagen fraction was unchanged in both areas. LV pressure-volume analysis showed that ventricular pacing reduced LV function to a similar extent after 15 minutes and 6 months of pacing. CONCLUSIONS: Asynchronous activation induces asymmetrical hypertrophy and LV dilatation. Cardiac pump function is not affected by the adaptational processes. These data indicate that local cardiac load regulates local cardiac mass of both myocytes and collagen.

Preserved skeletal muscle structure with modified electrical stimulation protocol in a cardiomyoplasty patient: a clinico-pathological report.

Experimental and clinical studies have recently shown variable degrees of structural abnormalities in the transposed and chronically stimulated muscle graft after cardiomyoplasty procedure. The postoperative stimulation protocol of wrapped skeletal muscle has been claimed to be a major determinant of late structural derangement. Therefore, a modified stimulation protocol had been used after a cardiomyoplasty procedure in a 63-year-old patient. Improved postoperative hemodynamic data could be detected by pressure/volume analysis. After unexpected sudden death occurred at 15 months, autoptic examination showed preserved muscle structure, suggesting that a prudent stimulation protocol may maintain muscle viability and contribute to effective cardiac support.

Left ventricular pressure-volume relationships before and after cardiomyoplasty in patients with heart failure.

BACKGROUND: The aim of this study was to elucidate whether beneficial effects of cardiomyoplasty (CMP) in patients with dilated cardiomyopathy are the result of a decrease in existing ventricular dilatation or a prevention of further dilatation. METHODS AND RESULTS: Combined micromanometer-conductance catheters were used to evaluate left ventricular pressure-volume relationships in six patients with dilated cardiomyopathy before and at 6 and 12 months after CMP. Acute changes in preload and afterload were induced by a standardized leg-tilting intervention and a bolus infusion of nitroglycerin. After CMP, end-diastolic volume (EDV) decreased from 138+/-10 to 103+/-18 mL/m2 (P<.01) at 6 months and to 83+/-17 mL/m2 (P<.01) at 12 months. End-diastolic pressure (EDP) decreased from 20.2+/-6.4 to 13.9+/-7.7 mm Hg (P<.01) at 6 months after CMP. Peak ejection rate and ejection fraction increased at 6 months after CMP from 594+/-214 to 799+/-214 mL/s (P<.05) and from 26.6+/-4.7% to 40.1+/-8.3% (P<.05), respectively. Peak dP/dt decreased at 12 months after CMP from -842+/-142 to -712+/-168 mm Hg/s (P<.05). Leg-tilting before CMP increased EDP from 20.2+/-6.4 to 25.6+/-5.2 mm Hg (P<.01), end-systolic pressure (ESP) from 118+/-17 to 122+/-17 mm Hg (P<.05), and tau from 50.8+/-2.8 to 53.8+/-2.3 ms (P<.05). Six months after CMP, leg-tilting also increased EDV from 103+/-18 to 110+/-22 mL/m2 (P<.05) and ESV from 62+/-14 to 66+/-14 mL/m2 (P<.05). Before CMP, nitroglycerin decreased EDP from 20.2+/-6.4 to 10.4+/-3.8 mm Hg (P<.01), ESP from 118+/-17 to 96+/-11 mm Hg (P<.05), ESV from 100+/-11 to 89+/-7 mL/m2 (P<.05), and tau from 50.8+/-2.8 to 44.5+/-3.7 ms (P<.05). Six months after CMP, nitroglycerin decreased EDP, ESP, and tau to similar values. CONCLUSIONS: Our findings show that up to 1 year after CMP, marked decreases in left ventricular volume are present. Our measurements suggest that CMP actively reduced the dilated ventricle but did not prevent a higher EDV on an increased venous return. The latissimus dorsi muscle wrap contraction results in better synchronization of contraction and more rapid emptying of the left ventricle.

Detection of dicrotic notch in arterial pressure signals.

OBJECTIVE: A novel algorithm to detect the dicrotic notch in arterial pressure signals is proposed. Its performance is evaluated using both aortic and radial artery pressure signals, and its robustness to variations in design parameters is investigated. METHODS: Most previously published dicrotic notch detection algorithms scan the arterial pressure waveform for the characteristic pressure change that is associated with the dicrotic notch. Aortic valves, however, are closed by the backwards motion of aortic blood volume. We developed an algorithm that uses arterial flow to detect the dicrotic notch in arterial pressure waveforms. Arterial flow is calculated from arterial pressure using simulation results with a three-element windkessel model. Aortic valve closure is detected after the systolic upstroke and at the minimum of the first negative dip in the calculated flow signal. RESULTS: In 7 dogs ejection times were derived from a calculated aortic flow signal and from simultaneously measured aortic flow probe data. A total of 86 beats was analyzed; the difference in ejection times was -0.6 +/- 5.4 ms (means +/- SD). The algorithm was further evaluated using 6 second epochs of radial artery pressure data measured in 50 patients. Model simulations were carried out using both a linear windkessel model and a pressure and age dependent nonlinear windkessel model. Visual inspection by an experienced clinician confirmed that the algorithm correctly identified the dicrotic notch in 98% (49 of 50) of the patients using the linear model, and 96% (48 of 50) of the patients using the nonlinear model. The position of the dicrotic notch appeared to be less sensitive to variations in algorithm's design parameters when a nonlinear windkessel model was used. CONCLUSIONS: The detection of the dicrotic notch in arterial pressure signals is facilitated by first calculating the arterial flow waveform from arterial pressure and a model of arterial afterload. The method is robust and reduces the problem of detecting a dubious point in a decreasing pressure signal to the detection of a well-defined minimum in a derived signal.

Cardiomyoplasty as an isolated procedure to treat refractory heart failure.

OBJECTIVE: Cardiomyoplasty represents a controversial therapy for chronic heart failure. The aim of this study is to review our experience of such a surgical procedure as an isolate approach to treat refractory left ventricular dysfunction. METHODS: Twenty-two patients were considered candidates for cardiomyoplasty because of chronic heart failure. Mean age was 58.7 +/- 5.3 (range 48-71 years), 19 patients were male and 3 were female. Ischemic or idiopathic etiology was present in 11 cases, respectively. Traditional as well as innovative techniques were used to assess hemodynamic function. Pre-operative hemodynamic profile included mean left ventricular ejection fraction of 20 +/- 5.8% (9-28%), absence of severe right ventricular failure, and mean left ventricular end-diastolic diameter of 75.5 +/- 7.4 mm (range 61-92 m). All patients were in New York Heart Association Class III or Intermittent IV despite conventional medical therapy. RESULTS: There was no intra-operative death. No additional surgery was performed. Left latissimus dorsi (LD) muscle was used in 20 cases, and right LD in two patients. Early mortality occurred in one patient (low cardiac output syndrome), whereas late mortality in five patients (three sudden deaths, one lung cancer, one heart failure). Mean follow-up is 20.7 +/- 16.7 months (3-51 months). Actuarial survival at 4 years is 70%. Cardiac index increased at 6 months (3.08 +/- 0.5 l/min per m2, P = 0.04), but no other significant changes were observed in the long term (3.03 +/- 0.7 l/min per m2, 3 +/- 0.7 l/min per m2, and 2.85 +/- 0.7 l/min per m2, at 12, 24 and 36 months, respectively). Ejection fraction improved at 6 and 12 months (29.1 +/- 1.03%, P = 0.0017; and 27.3 +/- 5.6%, P = 0.0091, respectively), while no substantial augmentation was documented at 2 and 3 years (25.6 +/- 2.5% and 25.1 +/- 4.0%, respectively). Left ventricular end-diastolic diameter was markedly reduced at 6 (73.2 +/- 8.0 mm, P = 0.0176), 12 (69.4 +/- 8.5 mm, P = 0.002) and 24 months (71.1 +/- 7.0 mm, P = 0.011), and was then stable (74.0 +/- 9.1 mm, P = 0.47) at 36 months. Postoperative pressure/volume loop evaluation showed some improvement of hemodynamic function from skeletal muscle assistance. Acute pulmonary edema episodes, as well as number of hospitalizations, were considerably reduced following cardiomyoplasty. CONCLUSIONS: In our experience, cardiomyoplasty was shown to exert moderate beneficial influence on left ventricular performance, to significantly reduce cardiac dilatation and to promote the stabilization of the disease course.