Cryografts implantation in human circulation would ensure a physiological transition in the arterial wall energetics, damping and wave reflection.

Each artery conduces blood (conduit function, CF) and smoothes out the pulsatility (buffering function, BF), while keeping its wall protected against the high oscillations of the pulse waves (damping function, xi). These functions depend on each segment viscoelasticity and capability to store and dissipate energy. When a graft/prosthesis is implanted, the physiological gradual transition in the viscoelasticity and functionality of adjacent arterial segments is disrupted. It remains to be elucidated if the cryografts would allow keeping the physiological biomechanical transition. The aim of this study was to evaluate the cryografts capability to reproduce the functional, energetic and reflection properties of patients' arteries and fresh homografts. Common carotid's pressure, diameter and wall-thickness were recorded in vivo (15 patients) and in vitro (15 cryografts and 15 fresh homografts from donors). Calculus: elastic (Epd) and viscous (Vpd) indexes, CF, BF, dissipated (WD) and stored (WPS) energy and xi. The graft-patient's artery matching was evaluated using the reflection coefficient (Gamma) and reflected power (WGamma). Cryografts did not show differences in Epd, Vpd, BF, CF, WD, WPS, and xi, in respect to fresh homografts and patients' arteries, ensuring a reduced Gamma and WGamma. Cryografts could be considered as alternatives in arterial reconstructions since they ensure the gradual transition of patients' arteries biomechanical and functional behavior.

Detection of left ventricular regional myocardial ischaemia in dogs by intraventricular conductance catheter.

Nine adult mongrel dogs were instrumented with ultrasonic microcrystals to measure left ventricular basal anteroposterior diameter and midwall myocardial segment length near the cardiac apex. Pneumatic cuff occluders were positioned around the left circumflex coronary artery near its origin and around the left anterior descending coronary artery two thirds of the way along its length. A pressure microtransducer was implanted into the left ventricle. Ten days after instrumentation the animals were anaesthetised with morphine chlorhydrate and pentobarbital sodium. An eight electrode catheter was advanced into the left ventricle to measure ventricular apical and basal regional and total electrical conductance. Minor ischaemia caused by occlusion of the left anterior descending artery was detected only by the electrode pair located near the apex, as decreased local ejection fraction. Major ischaemia caused by left circumflex artery occlusion was detected by both apical and basal electrode pairs and by total conductance, the three conductance signals indicating reduced ejection fractions compared with control values. The basal diameter signal indicated that basal regional motility changed only during major ischaemia, thus confirming the specificity of the changes in the basal conductance signals. The apical segment length signal confirmed the altered motility indicated by the apical conductance signal. These results suggest that regional wall motion abnormalities may be detected by the use of a multielectrode conductance catheter.

Animal model of acute pulmonary thromboembolism treated by local recirculation of streptokinase through the lung.

Massive acute pulmonary thromboembolism has a high mortality within the first few hours. Surgical intervention can remove only larger thrombi. Systemic fibrinolytic administration requires many hours for adequate treatment. We describe an anesthetized dog model of acute, massive, disseminated pulmonary thromboembolism achieved by injection of 1.7 ml/kg of 1-hour-old thrombi directly into the pulmonary artery. The emboli were lysed with 50,000 IU streptokinase recirculated for 20 minutes through the isolated pulmonary vascular bed by use of a roller pump while the systemic bed was supported by conventional cardiopulmonary bypass. On reestablishing natural circulation all hemodynamic parameters returned to preembolism values. Success of lysis was histologically confirmed. Perfusion of the pulmonary vascular bed without inclusion of streptokinase in the perfusate worsened the hemodynamic state of the animals compared with an untreated nonperfused control group.

Experimental acute right ventricular failure and right ventricular assist in the dog.

We describe a technique for the production of acute progressive right ventricular failure in experimental animals that mimics the hemodynamic characteristics of right ventricular failure found in some patients being weaned from extracorporeal circulation after surgical repair of left ventricular abnormalities. The technique combines three alterations of right ventricular state: excision of the tricuspid valve, ventriculotomy, and ligation of the right coronary artery. Seven control dogs died within 3 hours after this intervention. Death was due to low cardiac output as a result of low left atrial and pulmonary arterial pressures. Right atrial pressure was high. Use of a right ventricular assist device in an additional seven dogs to pump blood from the right atrium to the pulmonary artery confirmed good preservation of left ventricular function by reestablishing adequate left ventricular filling pressure. All seven dogs survived for more than 3 hours. The validity of the technique in restricting failure principally to the right ventricle was thus demonstrated.

Chronic aortic counterpulsation with latissimus dorsi in heart failure: clinical follow-up.

BACKGROUND: Dynamic aortomyoplasty is an alternative technique to heart transplantation. The goal of our study was to evaluate the benefits of aortic counterpulsation obtained by dynamic thoracic aortomyoplasty in patients with heart failure refractory to pharmacologic treatment and contraindications to heart transplant or cardiomyoplasty. METHODS: In this study we compared preoperative and postoperative data from five out of six carefully selected patients who were treated with dynamic thoracic aortomyoplasty. This surgical technique wraps the right latissimus dorsi muscle flap around the ascending aorta. This muscle flap was electrically stimulated during diastole, following a muscle-conditioning protocol, to obtain diastolic augmentation. At the 6-month follow-up period we evaluated, invasively and noninvasively, the hemodynamic and clinical effects of aortomyoplasty. RESULTS: We observed a significant decrease in the number of hospitalizations (P = 0.01), NYHA functional class (P = 0.01), cardiothoracic ratio (P = 0.02), right ventricular diameter (P = 0.03), left atrial diameter (P = 0.04), and pulmonary artery systolic pressure (P = 0.04); and a significant increase in the 6-minute walking test (P = 0.01), cardiac index (P = 0.04), noninvasive evaluation of diastolic augmentation (P = 0.01), left ventricular shortening fraction (P = 0.01), and radioisotopic left ventricular ejection fraction (P = 0.02). We also found a nonsignificant decrease in the left ventricular diameter (P = 0.08) and wedge pressure (P = 0.19); and a nonsignificant increase in peak oxygen consumption (P = 0.13). CONCLUSIONS: Dynamic thoracic aortomyoplasty in heart failure resulted in an important improvement of hemodynamic parameters, heart functional data, and clinical functional class, when comparing preoperative data with the 6-month follow-up data.

Dynamic abdominal and thoracic aortomyoplasty in heart failure: assessment of counterpulsation.

BACKGROUND: Aortic counterpulsation, either biologic or mechanical, is a useful technique to support circulation during left ventricular dysfunction. METHODS: In this study we used an induced cardiac failure model in acute open chest sheep to compare hemodynamic improvements between thoracic and abdominal aortic counterpulsation. This was achieved with left latissimus dorsi and left hemidiaphragm muscle flaps. RESULTS: Thoracic and abdominal aortic counterpulsation in heart failure resulted in a significant improvement of hemodynamic parameters. Subendocardial viability index, defined as diastolic pressure-time index to systolic tension-time index, in thoracic and abdominal aortomyoplasty showed significant improvement (p<0.05) when cardiac assistance was performed by electrical stimulation of each muscle flap. A new counterpulsation index derived from diastolic and systolic areas beneath the aortic pressure curve was tested, obtaining a correlation coefficient with the subendocardial viability index of 0.758 (p<0.001). Values of subendocardial viability index and counterpulsation index showed minimal variability. CONCLUSIONS: Treatment of experimentally induced cardiac failure with dynamic abdominal aortic counterpulsation allows an effective hemodynamic improvement in open chest sheep. Furthermore, this diastolic arterial pressure augmentation could be evaluated through a new counterpulsation index derived from diastolic and systolic areas beneath the aortic pressure curve.

Dynamic aortomyoplasty to assist left ventricular failure.

The efficacy of skeletal muscle contractile force to augment left ventricular function has been demonstrated experimentally and clinically by the cardiomyoplasty procedure. Another approach in biomechanical cardiac assistance is the use of electrostimulated skeletal muscle in an extracardiac position. We describe an autologous counterpulsating device using the native ascending aorta as a ventricular chamber wrapped by an electrostimulated latissimus dorsi muscle flap (LDMF). This model avoids thrombotic complications observed in skeletal muscle neo-ventricles associated with prosthetic chambers. In 8 goats, a right LDMF was transferred to the thoracic cavity by removal of the second rib. In 4 goats, the diameter of the aorta was enlarged by surgical implantation (using lateral clamping) of an autologous pericardial patch. The LDMF was wrapped around the ascending aorta and electrostimulated using an external diastolic pulse generator connected to a sensing myocardial lead and to LDMF pacing electrodes. Hemodynamic studies were performed (left ventricular, aortic, and pulmonary artery pressures and rate of rise of left ventricular pressure). The LDMF diastolic counterpulsation was performed using a burst of 30 Hz, with a delay from the R wave adjusted to provide optimal diastolic augmentation. Percent increase in the subendocardial viability index was calculated during unassisted and assisted cardiac cycles (1:2) at baseline and after acute heart failure induced by the administration of high doses of propranolol hydrochloride (3 mg/kg intravenously). Diastolic aortic counterpulsation by the stimulated LDMF resulted in a significant improvement in the subendocardial viability index both at baseline and after induced cardiac failure in both groups, though the increase was greater in the group with aortic enlargement.

Temporary mechanical circulatory support for severe cardiac failure: experimental study.

We describe a technique for mechanical cardiac assistance in an acute model of severe cardiac failure. Cardiac dysfunction was induced by a high dose of halothane in 13 dogs. Seven served as controls. Following median sternotomy, a pneumatically driven device was implanted in the other six dogs in a para-aortic position, using a simple surgical technique without cardiopulmonary bypass. The aorta was cross-clamped during cardiac assistance. During hemodynamic studies, the seven control animals with induced cardiac failure showed high end-diastolic left ventricular and right atrial pressures with low cardiac index and systolic left ventricular and aortic pressures. All dogs in this group died within 30 minutes. Use of a monovalvular cardiac assist device in the experimental group of six dogs to pump blood from the aortic root to the descending aorta in a counterpulsation manner, confirmed good preservation of systemic hemodynamic parameters after induction of heart failure. All animals in this treated group survived more than 45 minutes. Hemodynamically, the device acts as a new ventricle and the impaired left ventricle functionally becomes a left atrium. This condition is clinically appropriate for recovery of left ventricular function in severe acute myocardial failure.

[Assisted circulation to the right ventricle through pulmonary counterpulsation using a biological method]. / Assistência circulatória ao coração direito através da contrapulsação pulmonar usando-se um método biológico.

PURPOSE: To study the hemodynamic effects of latissimus dorsi dynamic pulmonaroplasty in open chest animals. METHODS: Six anesthetized mongrel dogs were subjected to diastolic counterpulsation using electrically stimulated latissimus dorsi muscle flap wrapped around the aortic and pulmonary arteries roots and gated to the surface electrocardiogram. Aortic and Pulmonanary pressures as well as cardiac output and cardiac index were measured. RESULTS: Diastolic counterpulsation resulted in a significant increase in cardiac output (from 2.35 +/- 0.26 to 2.45 +/- 0.28 l/min) (p < 0.005) and cardiac index (from 0.108 +/- 0.020 to 0.113 +/- 0.020 l/min/kg) (p < 0.05). The diastolic pulmonary arterial efficiency index showed a significant increase when latissimus dorsi stimulation was on (from 8.37 +/- 0.60 to 11.65 +/- 0.83 mmHg); (p < 0.005). CONCLUSION: Latissimus dorsi dynamic pulmonaroplasty provides an effective means of arterial counter pulsation in open chest dogs.

Adventitia-dependent mechanical properties of brachiocephalic ovine arteries in in vivo and in vitro studies.

AIM: An adventitia dependent regulation of the vascular smooth muscle tone has been described. However, if the adventitia plays an active role on arterial wall biomechanical behaviour and functions remains to be established. Our aim was to characterize the influence of adventitia on arterial wall mechanical properties and the arterial conduit and buffer functions. METHODS: Ovine brachiocephalic arteries were studied in vivo (n = 8) and in vitro (with null tone) in a circulation mock (n = 8). Isobaric, isoflow and isofrequency studies were performed. In each segment, pressure and diameter waves were assessed before and after adventitia removal. From the arterial stress-strain relationship, we derived the elastic and the viscous modulus. The buffering and conduit functions were calculated using the Kelvin-Voigt's time constant and the inverse of the characteristic impedance, respectively. RESULTS: In in vivo studies arterial diameter decreased after adventitia removal (P < 0.05). Elastic and viscous modulus in in vivo studies were significantly higher in adventitia-removed arteries, compared with values in intact vessels (P < 0.05). This behaviour was not observed in in vitro experiments. An impairment of buffer and conduit functions was observed in vivo after adventitia removal (P < 0.05), while both functions remain unchanged in in vitro studies (P > 0.05). CONCLUSIONS: Arterial wall viscosity and elasticity were influenced by adventitia removal in in vivo studies, possibly by a smooth muscle-dependent mechanism, since it was not present in in vitro experiments. Adventitia would be involved in a physiological mechanism of arterial wall viscous and elastic properties regulation, that could influence arterial buffering and conduit functions.

In vivo angiotensin II receptor blockade and converting enzyme inhibition on canine aortic viscoelasticity.

The influence of the renin-angiotensin system (RAS) on the aortic wall mechanical properties under angiotensin I converting enzyme inhibition (enalaprilat, 0.3 mg/kg iv) or angiotensin II receptor (AT1) blockade (E-3174, 1 mg/kg iv) was examined in eight normotensive and eight renovascular hypertensive conscious dogs. Aortic diameter (D; sonomicrometry)-pressure (P; microtransducer) hysteresis loops during steady state and during rapid distal aortic occlusion allowed (after hysteresis elimination) calculation of the aortic wall viscosity index, the purely elastic P-D relationship, and derivation into compliance-pressure curves. At the early stage ofrenovascular hypertension when activation of RAS is more pronounced, aortic wall stiffness and wall viscosity were increased as compared with normotensive states. Blood pressure remained unchanged in normotensive animals and was reduced during hypertension after antihypertensive treatments. In hypertensive animals, enalaprilat and E-3174 decreased viscosity index and shifted the compliance-pressure curve upward with respect to pretreatment conditions. In normotensive dogs, whereas E-3174 did not change the compliance-pressure curve and viscosity index, enalaprilat increased compliance and reduced viscosity index. We concluded that in normotensive dogs converting enzyme inhibition modifies arterial viscoelastic parameters by angiotensin-independent mechanisms that contribute to the modulation of the buffering function of large arteries.

Inconsistency of the slope and the volume intercept of the end-systolic pressure-volume relationship as individual indexes of inotropic state in conscious dogs: presentation of an index combining both variables.

We tested the ability of the slope (Emax) and the volume intercept (Vo) of the end-systolic pressure-volume relationship (ESPVR) to indicate contractility changes in conscious dogs instrumented with sonomicrometers measuring left ventricular diameter in three orthogonal axes and a left ventricular pressure microtransducer. ESPVRs were generated by inferior vena caval occlusion under control conditions (C1 and C2) and during enhanced (I+) and depressed (I-) inotropic states achieved by infusion of dobutamine and injection of propranolol, respectively. No significant difference between the first control (C1) and I+ or between the second control (C2) and I- were found for either Emax (C1, 5.31 +/- 1.68 mm Hg/ml, mean +/- SD; I+, 5.37 +/- 1.44; C2, 5.20 +/- 1.62; I-, 4.18 +/- 1.32) or Vo (C1, 10.3 +/- 9.6 ml; I+, 7.3 +/- 9.1; C2, 9.9 +/- 9.0; I-, 12.7 +/- 12.5), despite significant changes in other indexes of contractility. Comparison of changes in Emax in individual animals in response to I+ and I- revealed that 63% were nonsignificant, 28% were significant and expected, and 9% were significant and paradoxical. Within defined volume limits and irrespective of individual changes in Emax and Vo, in all animals I+ shifted the ESPVR above and to the left of C1 and I- shifted the ESPVR below and to the right of C2. We thus integrated the changes in Emax and Vo by measuring the area beneath each ESPVR between defined limits of end-systolic volume. The values for area were: C1, 612 +/- 150 mm Hg.ml; I+, 745 +/- 191 (p less than .001); C2, 520 +/- 198; I-, 420 +/- 139 (p less than .001). We conclude that (1) neither Emax nor Vo are individually reliable indexes of changed contractility, and (2) the area beneath the ESPVR between defined end-systolic volume limits is a consistent indicator of variations in inotropic state.

Hemodynamic effects of cardiomyoplasty in an experimental model of acute heart failure and atrial fibrillation.

The aim of our work was to study the hemodynamic effects of dynamic cardiomyoplasty on an acute animal model of atrial fibrillated heart failure. Eight anesthetized open chest dogs suffering from atrial fibrillation and heart failure, obtained by topic acetylcholine and propranolol, were treated by a cardiomyoplasty procedure performed with an electrostimulated latissimus dorsi muscle flap (LDMF). Values considered for analysis during LDMF stimulation were selected from cardiac cycles with R-R intervals similar to those when the LDMF was not stimulated (+/- 20 ms). Atrial fibrillated heart failure showed a significant increase of systemic vascular resistance, end diastolic left ventricular pressure (EDLVP) and right atrial pressure (p < 0.05), and a significant decrease in cardiac output, systolic left ventricular pressure (SLVP), and mean aortic pressure (p < 0.05) compared with control values. LDMF stimulation in atrial fibrillated heart failure resulted in a significant increase of SLVP, cardiac output, and mean aortic pressure (p < 0.05) and a significant decrease of systemic vascular resistance, EDLVP, and right atrial pressure (p < 0.05) compared with nonstimulated values. The highest LVP values were obtained with R-R intervals long enough to allow an adequate LV filling. We conclude that dynamic cardiomyoplasty provides an appropriate recovery in this animal model of atrial fibrillated heart failure. Cardiomyoplasty is an appropriate procedure for cardiac assist when R-R intervals allow an adequate LV filling.

Non-invasive assessment of systemic elastic behaviour in hypertensive patients: analysis of possible determinants.

Knowledge about the viscoelastic behaviour of the arterial wall has been proved to have physiological importance and clinical usage. Our purpose was to study the changes of the systemic arterial wall's elastic properties non-invasively, in patients with established essential and with borderline hypertension, and to evaluate its possible determinants. Three groups of normotensive, borderline and established essential hypertensive patients were evaluated. Arterial pulse wave velocity (PWV) was measured and arterial compliance (Cm) was derived in all patients. Pulse wave velocity was obtained from the pressure values of digitized carotid and radial arteries. Arterial compliance (Cm = dD/dP with P pressure and D diameter) was calculated using a formula derived from the Bramwell and Hill equation: Cm = (1,334 x D)/(2 rho x PWV2), where for D humeral diameter was used as measured by high resolution echograph, and rho is the blood density (rho = 1.06). Pulse wave velocity was significantly higher in established essential hypertensive patients with respect to normotensive patients (p < 0.05). Arterial compliance was significantly diminished in established and in borderline hypertensive patients with respect to normotensive patients (p < 0.05), which implies early alterations in hypertensive cardiovascular disease. Multiple regression analysis of the cofactors showed that age and diastolic pressure are independent determinants of Cm. Impairment of the arterial wall's intrinsic elastic properties was demonstrated in established essential hypertension, independent of age and diastolic pressure.

Paradoxically decreased aortic wall stiffness in response to vitamin D3-induced calcinosis. A biphasic analysis of segmental elastic properties in conscious dogs.

We studied the aortic elastic behavior in response to vitamin D3-induced accelerated calcinosis in conscious dogs chronically instrumented with a pressure microtransducer and a pair of ultrasonic diameter dimension gauges in the upper descending thoracic aorta. The two functional phases of the elastic segmental properties of the aorta in vivo were discriminated by computation on a beat-by-beat basis from the phasic pressure-diameter (P-D) hysteresis loops in basal conditions and during the transient state of a wide range of pressures obtained mechanically (aortic occlusion) or pharmacologically (angiotensin bolus). The overall P-D curve formed by all P-D hysteresis loops was comprised of two linear relations according to a model that assumes that only elastin is stretched at lower pressures, whereas both elastin and collagen are stretched at higher pressures. The slope of the first linear portion of the P-D curve was considered as the elastin P-D elastic modulus, and the slope of the curve obtained by subtraction between the P-D curve and the extrapolation of the elastin straight line was assumed to be the collagen P-D elastic modulus. After vitamin D3-induced calcinosis, the elastin elastic modulus was unaffected, whereas the collagen elastic modulus decreased significantly during occlusion maneuvers (58.6%, p less than 0.01) and during bolus injections of angiotensin (37.2%, p less than 0.05). The collagen elastic modulus correlated with the serum calcium concentration (r = -0.65, p less than 0.001) and with the aortic pulse pressure (r = 0.51, p less than 0.01), and this relation persisted at constant heart rate. Histopathologic analysis evidenced calcium-depositing elastic lamina, focal disappearance of collagen, and rupture of elastic fibers. The present study shows that accelerated, severe, experimental calcinosis-inducing calcium deposition inside the large artery walls is accompanied by a clear-cut paradoxical reduction in arterial rigidity that is mainly due to functional and structural modification of collagen elasticity.

Single beat evaluation of circumferential aortic elastin elastic modulus in conscious dogs. Potential application in non-invasive measurements.

A description of the arterial wall elastic properties comprehends both collagen and elastin, clearly shown in a biphasic stress-strain relationship. From chronically instrumented conscious dogs, aortic pressure-diameter curves can be obtained in a single beat, which is impossible to perform in human beings. In control conditions, the collagen fibers are almost not distended and the resistance to stretch is mainly supported by the elastin fibers. Therefore, the mechanical properties of the aorta are almost purely elastic in the basal beat to beat conditions. In this study we propose and test five indexes, which include as variables: systolic, diastolic and mean arterial pressure and diameter; besides, arterial compliance and pressure-strain elastic modulus as suggested to evaluate the elastic behaviour of the elastic fibers. This data can be easily obtained by non-invasive methods, such as Doppler-ultrasound techniques and auscultative esphygmomanometrical measurements, while the indexes evaluated can be retrieved from a single beat evaluation. Of three measurements performed in chronically instrumented conscious dogs on different days, one of these indexes, the ME5 = [formula: see text] x Rdias proved to be an accurate and reliable parameter to evaluate the mechanical behaviour of arteries. This kind of parameter may be useful for research and evaluation of several diseases that markedly alter the arterial wall compliance.