Edmundo Cabrera Fischer

Regional Differences in Viscosity, Elasticity and Wall Buffering Function in Systemic Arteries: Pulse Wave Analysis of the Arterial Pressure-Diameter Relationship

INTRODUCTION AND OBJECTIVES Regional variations in the incidence of vascular diseases have been related to regional differences in arterial viscoelasticity. The aim of this study was to characterize the differences in the elastic and viscous modulus and in wall buffering function between central and peripheral systemic arteries, through a time-series analysis of the pressure-diameter relationship. MATERIAL AND METHOD Pressure and diameter were measured in seven arterial segments (carotid, brachiocephalic trunk, ascending aorta, proximal, middle and distal descending thoracic aorta, and femoral artery) from six sheep. Each segment was mounted on an in vitro mock circulatory system and perfused with Tyrode solution, with a pulse frequency of 1.8 Hz and systemic pressure levels. We used the Kelvin-Voigt model to calculate the pressure-diameter elastic (Epd, mmHg/mm) and viscous (Vpd, mmHg.s/mm) modulus, and to quantify the local wall buffering function (Vpd/Epd). We also calculated the incremental Youngs and pressure-strain elastic modulus and pulse wave velocity for each segment. RESULTS The elastic and viscous modulus increased from proximal to distal segments. The wall buffering function did not differ significantly between arteries. The lower rigidity of the central arteries compared to the distal ones may indicate that the systolic arterial compliance function is concentrated in the central arterial segments. On the other hand, the greater viscosity in the distal segments may indicate that viscous energy loss is concentrated in these segments. CONCLUSIONS Arterial elasticity and viscosity can be interpreted as properties that are dependent on the region of the vessel, whereas wall buffering function can be considered region-independent.

Diferencias regionales en viscosidad, elasticidad y amortiguamiento parietal de arterias sistémicas: análisis isopulsátil de la relación presión-diámetro arterial

Introduccion y objetivos Variaciones regionales en la incidencia de diversas afecciones vasculares se han relacionado con diferencias regionales en la viscoelasticidad arterial. El objetivo de este trabajo fue caracterizar las diferencias regionales en el modulo elastico, viscoso y en el amortiguamiento parietal de arterias sistemicas, centrales y perifericas, mediante el analisis de la relacion instantanea presion-diametro arterial en el dominio temporal. Material y metodo Se midieron la presion y el diametro en 7 segmentos arteriales extraidos de 6 ovejas: carotida, tronco braquiocefalico, aorta ascendente, aorta toracica descendente proximal, media y distal, y arteria femoral. Cada segmento fue montado en un sistema circulatorio in vitro y perfundido con solucion Tyrode, con frecuencia de estimulacion de 1,8 Hz y valores de presion sistemica. Utilizando un modelo Kelvin-Voigt, se obtuvieron el modulo presion-diametro elastico (Epd, mmHg/mm) y viscoso (Vpd, mmHg×s/mm), y se cuantifico la funcion de amortiguamiento parietal (FAP) como Vpd/Epd. Adicionalmente, se calculo el modulo de Young incremental y elastico presion-deformacion y la velocidad de onda del pulso de cada segmento. Resultados Los modulos elasticos y viscoso aumentaron hacia los segmentos perifericos, mientras que la FAP no mostro diferencias entre segmentos. La menor rigidez en las arterias centrales y la mayor viscosidad en las arterias perifericas podrian indicar que la funcion de reservorio arterial sistolico se concentra en las primeras y la disipacion viscosa de energia en las segundas. Conclusiones La respuesta elastica y viscosa arterial podrian considerarse dependientes de la region arterial, mientras que la constante de FAP seria un indicador independiente de la region arterial.

Aortomyoplasty counterpulsation: Experimental results and early clinical experience

BACKGROUND Presently the only clinical method of skeletal muscle augmentation of the heart is achieved by wrapping muscle around the cardiac ventricles and then stimulating the muscle to contract synchronously with cardiac systole. Intraaortic balloon counterpulsation provides diastolic counterpulsation in the short-term with the known benefits of increasing diastolic pressure and reducing ventricular afterload. Using protocols already in existence for dynamic cardiomyoplasty we have investigated the long-term use of extraaortic skeletal muscle-powered counterpulsation. METHODS In five alpine goats the right latissimus dorsi muscle (LDM) was used to achieve a wrap around the ascending aorta, which had been augmented with an elliptic pericardial patch. Electrostimulation protocols were commenced after 2 weeks and continued for 12 to 24 months. At this time baseline hemodynamic measurements were made with and without stimulation of the LDM. Acute cardiac depression was induced and further measurements were made, again with and without stimulation of the LDM. RESULTS Results in the basal state demonstrated improvement in all parameters with stimulation and a 23% increase of the subendocardial viability index. After induction of cardiac depression there was a 52% increase in cardiac output, 39% decrease in systemic vascular resistance, and 27% increase in subendocardial viability index. Histologic studies demonstrated tight adhesion between the aortic wall and the LDM, no dilatation of the aortic wall, and no deleterious effects in the aortic wall of the chronic intermittent constriction. Histochemical staining demonstrated transformation of the muscle fibers of the LDM flap into type 1 oxidative muscle fibers. CONCLUSIONS In conclusion, our present study demonstrates that in this animal model aortomyoplasty produces a chronic counterpulsation with preservation of aortic architecture. With induction of heart failure aortomyoplasty provided an effective means of cardiac assistance. The use of the ascending aorta to achieve diastolic counterpulsation may be an efficient use of skeletal muscle energy to augment the heart in selected clinical cases. Early clinical experience is described in this article.

Dynamic Aortomyoplasty in Treating End-stage Heart Failure

BACKGROUND Dynamic aortomyoplasty is an alternative to heart transplantation. The goal of our study was to evaluate the benefits of aortic counterpulsation obtained using dynamic aortomyoplasty in patients with heart failure refractory to pharmacologic treatment and with contraindications to heart transplant. METHODS In this study, we compared the pre-operative and post-operative data of 15 selected patients who underwent dynamic thoracic aortomyoplasty. In this surgical technique, the right latissimus dorsi muscle flap is wrapped around the ascending aorta. This muscle flap was electrically stimulated during diastole, following a muscle-conditioning protocol, to obtain diastolic augmentation. At 12-month follow-up, we evaluated invasively and non-invasively the hemodynamic, clinical, and functional effects of aortomyoplasty. RESULTS When comparing pre-operative data with 12-month follow-up data, we observed a significant decrease in the number of hospitalizations (p < 0.001) and in the New York Heart Association functional class (p < 0.001), and we observed significant improvement in the walking test (p < 0.001) and in peak oxygen consumption (p < 0.05). CONCLUSIONS Dynamic, biologic, chronic counterpulsation of the aorta using a latissimus dorsi flap (dynamic aortomyoplasty) in selected patients with severe heart failure significantly improved hemodynamic parameters, heart functional data, and clinical functional class. A larger clinical experience with a longer follow-up would be useful in evaluating this techniques clinical relevance.

Benefits of aortic and pulmonary counterpulsation using dynamic latissimus dorsi myoplasty

BACKGROUND Intraaortic and pulmonary artery counterpulsation are useful techniques to support circulation during either left or right ventricular dysfunction. Electrically stimulated skeletal muscles wrapped around the aorta, used as means of cardiac failure treatment, have proved to be an effective method of handling experimental left ventricular failure. In this article we report an induced cardiac failure model in acute open chest dogs and describe the hemodynamic improvement of simultaneous aortic and pulmonary artery counterpulsation. METHODS This was achieved with a bilateral latissimus dorsi muscle flap, stimulated with a software written in C++ for Windows. Dynamic aortomyoplasty was performed using the left latissimus dorsi muscle flap around the descending aorta, and dynamic pulmonaromyoplasty was achieved wrapping the pulmonary trunk with the right latissimus dorsi muscle flap. In all animals blood pressures and cardiac output were measured after cardiac failure induced by a high-dose of propranolol hydrochloride (3 mg/kg intravenously) before and after latissimus dorsi muscle flap stimulation. RESULTS Aortopulmonary counterpulsation resulted in a significant increase in mean aortic pressure, mean pulmonary pressure, and cardiac output. In addition, a significant decrease was observed in end-diastolic left ventricular pressure, systemic vascular resistance, and pulmonary vascular resistance. Subendocardial viability index (diastolic pressure-time index/systolic tension-time index) in aortomyoplasty and tension time index in pulmonaromyoplasty showed significant improvement when cardiac assistance was performed by electrical stimulation of both muscles (p = 0.037 and p = 0.001, respectively). CONCLUSIONS Treatment of experimentally induced cardiac failure using aortopulmonary counterpulsation allows effective hemodynamic improvement in open-chest dogs.

The effect of the new calcium antagonist nisoldipine (BAY k-5552) on myocardial infarct size limitation in conscious dogs

The effect of the new calcium antagonist nisoldipine (BAY k-5552) on myocardial infarct size was studied in four groups of conscious dogs undergoing acute left anterior descending coronary artery occlusion. Group I received placebo for 48 hours before and for 24 hours after occlusion; group II received placebo before and nisoldipine (0.3 mg/kg orally every 6 hours) after occlusion; group III received nisoldipine before and placebo after occlusion; and group IV received nisoldipine before and after occlusion. Infarct size was quantified with the tetrazolium red staining technique. Infarcted ventricular mass was 24.5 +/- 6.6% (mean +/- SD) for group I (control), 21.4 +/- 4.4% for group II (p = NS against control), 13.9 +/- 4.5% for group III (p less than 0.05), and 14.1 +/- 4.0% for group IV (p less than 0.05). Post occlusion sudden death was 30% in non-pretreated dogs and 0% in pretreated dogs (p less than 0.001). We conclude that prophylactic oral treatment with nisoldipine decreases infarct size and lowers the incidence of sudden death in conscious dogs undergoing acute coronary occlusion.

Juxtaaortic counterpulsation: comparison with intraaortic counterpulsation in an animal model of acute heart failure.

This study was designed to compare the effects of juxtaaortic balloon counterpulsation (JABC), performed in ascending aorta and the aortic arch, with those yielded by intraaortic balloon counterpulsation (IABC) in descending aorta, in experimental animals during induced cardiac failure.JABC was achieved with a manufactured Dacron prosthesis and a balloon pump placed between the prosthesis and the wrapped aorta.JABC resulted in a significant increase of cardiac output (from 2.33 ± 0.82 to 2.61 ± 1.12 L/min, p < 0.05), cardiac index (from 0.071 ± 0.025 to 0.080 ± 0.033 L/min/kg, p < 0.05) and diastolic pressure augmentation evaluated through diastolic and systolic areas beneath the aortic pressure curve (DABAC/SABAC) index (from 0.94 ± 0.21 to 1.10 ± 0.33, p < 0.01). End diastolic aortic pressure showed a significant decrease with JABC (from 31.90 ± 7.09 to 27.83 ± 9.72 mm Hg, p < 0.05). A close association between percentage of DABAC/SABAC increases obtained with IABC and JABC was observed (r2 = 0.67; p < 0.001).Counterpulsation obtained by a juxtaaortic catheter placed in the arch and the ascending wrapped aorta results in an effective hemodynamic improvement comparable with that achieved by an intraaortic catheter in open chest sheep.

Effects of intra-aortic counterpulsation on aortic wall energetics and damping: in vivo experiments.

Intra-aortic balloon pumping (IABP) could modify the arterial biomechanics; however, its effects on arterial wall properties have not been fully explored. This dynamical study was designed to characterize the pressure-dependent and smooth muscle-dependent effects of IABP on aortic wall energetics in an in vivo animal model. Intra-aortic balloon pumping (1:2) was performed in six anesthetized sheep in which aortic pressure and diameter signals were measured in basal, augmented (during balloon inflation), and assisted (postaugmented) beats. Energy dissipation values in augmented and assisted beats were significantly higher than those observed in basal state (p < 0.05). Assisted beats showed a significant increase of wall damping with respect to basal and augmented beats (p < 0.05). Intra-aortic balloon pumping resulted in a significant increase of pulse wave velocity (p < 0.05) in augmented beats with respect to basal state (6.3 ± 0.8 vs. 5.2 ± 0.5 m·s−1); whereas values observed in assisted beats were significantly (p < 0.05) lower than those observed in augmented beats (4.9 ± 0.5 vs. 6.3 ± 0.8 m·s−1). Our findings show that IABP determined the pressure and smooth muscle-dependent changes in arterial wall energetics and damping properties in this animal model.

Hydration Status Is Associated with Aortic Stiffness, but Not with Peripheral Arterial Stiffness, in Chronically Hemodialysed Patients

Background. Adequate fluid management could be essential to minimize high arterial stiffness observed in chronically hemodialyzed patients (CHP). Aim. To determine the association between body fluid status and central and peripheral arterial stiffness levels. Methods. Arterial stiffness was assessed in 65 CHP by measuring the pulse wave velocity (PWV) in a central arterial pathway (carotid-femoral) and in a peripheral pathway (carotid-brachial). A blood pressure-independent regional arterial stiffness index was calculated using PWV. Volume status was assessed by whole-body multiple-frequency bioimpedance. Patients were first observed as an entire group and then divided into three different fluid status-related groups: normal, overhydration, and dehydration groups. Results. Only carotid-femoral stiffness was positively associated (P < 0.05) with the hydration status evaluated through extracellular/intracellular fluid, extracellular/Total Body Fluid, and absolute and relative overhydration. Conclusion. Volume status and overload are associated with central, but not peripheral, arterial stiffness levels with independence of the blood pressure level, in CHP.

PS 05-58 ARTERIAL HYPERTENSION AND PULSE PRESSURE: RELATIONSHIP WITH PULSE WAVE VELOCITY.

Objective: Pulse Pressure (PP) and pulse wave velocity (PWV) are related to cardiovascular risk (CVR). We evaluated in patients with arterial hypertension (HT), as unique risk factor, the impact of arterial hypertension on PP and PWV, the mean and age related PWV values, the relationship between PP and PWV and the rate of changes with aging. Design and Method: 1079 subjects were randomly enrolled and 299 selected as selected as asymptomatic non-smoking hypertensive patients (HT; 50 ± 14.8years old), as the only risk factor. Blood pressure was measured in the sitting position, after 10 min rest, 3 times (Omron model 705IT), elapsed by 1 min. After that, PP was calculated as: SBP-DBP. The mean value was considered as the PP value for each subject. Carotid-femoral PWV was measurements were performed continuously for at least 10 cardiac cycles and the mean value considered as PWV value for each patient. Results: In HT, mean PWV value was 8.04 ± 1.8 m/s and increased linearly with age (r = 0.49; p < 0.001) being the year growing of 0.062 ± 0.006 m/sec (p < 0.001) without. In HT, PP increases linearly with aging (r = 0.155; p < 0.01) with a progressive year related increase (0.138 ± 0.051 mmHg/year; P < 0.001). No gender differences were found (56.31 ± 12.89 mmHg versus 54.58 ± 13.62 mmHg; p = 0.338). Finally, PWV and PP in HT showed a significant positive correlation (r = 0.191, p < 0.001). Conclusions: All these data suggest that, in HT patients, PP, as PWV, could be a reliable marker of arterial dysfunction. This is supported by the fact that PP and Arterial stiffness, evaluated as PWV are age dependent without differences in gender and were significantly related.