Arterial pressure fractality is highly dependent on wave reflection.

UNLABELLED: Wave reflection is an important factor that influences pressure wave morphology and becomes more significant with aging, when cardiovascular risk increases. A pressure wave, measured at any location in the arterial tree, can be decomposed into its forward and backward components and depends on the corresponding amplitude and shifting time delays. Fractal dimension (FD) quantifies the time series complexity defined by its geometrical representation. OBJECTIVE: The aim of this study was to evaluate the arterial pressure and diameter time series in order to assess the relationship between wave reflection and arterial pressure fractal dimension (FD). METHODS: Simultaneous aortic pressure and diameter were measured in 14 conscious dogs. A pair of ultrasonic crystals, a pressure microtransducer and a pneumatic cuff occluder were positioned in the upper third of the descending aorta. RESULTS: Total reflection induced by the occlusion maneuver decreased FD concomitant to the aortic stiffening. CONCLUSION: Arterial pressure fractality is highly dependent on wave reflection.

Long-term effects of growth hormone on infarct size and left ventricular function in sheep with coronary artery occlusion.

The effects of growth hormone (GH) on infarct size and left ventricular (LV) function in experimental acute myocardial infarction (AMI) have been controversial. Moreover, little, if any, information exists regarding long-term evaluation of therapeutic doses of GH in large mammalian models of AMI. We therefore aimed to assess the effect of therapeutic doses of GH over 3.5 months on infarct size and heart function in sheep with AMI. After coronary artery ligation, sheep received subcutaneous human GH 8 IU/d (n = 8) or vehicle (n = 8) over 100 days. Infarct area was similar in GH (16.9% +/- 3% of LV area) and placebo (16.5% +/- 3.7%, P = not significant) sheep. At 3 days of treatment onset, but not at later times, GH sheep had higher LV shortening fraction (30.7% +/- 3.5% vs. 24.8% +/- 6.1%, P < 0.04), systolic anterior wall thickness (10.1 +/- 0.8 vs. 8.6 +/- 1.2 mm, P < 0.02), and cardiac index (3.8 +/- 0.6 vs. 2.8 +/- 0.7 L x min x m, P < 0.01). This evolution of function parameters paralleled that of serum insulin-like growth factor 1 levels, which differed significantly only during the first week, suggesting a direct effect of GH on LV contractility. These results may suggest the usefulness of therapeutic doses of GH at the early phases of AMI but do not support maintaining the treatment for longer time.

Assessment of pulsatile wall shear stress in compliant arteries: numerical model, validation and experimental data.

There is evidence that wall shear stress (WSS) is associated with vascular disease. In particular, it is widely accepted that vascular segments with low or oscillatory values of WSS are more probable to develop vascular disease. It is then necessary to establish a realistic model of the blood flow in blood vessels in order to determine precisely WSS. We proposed a numerical 1D model which takes into account the pulsatile nature of blood flow, the elasticity of the vessel, and its geometry. The model allows the calculation of shear stress. It was validated for stationary situations. Then, we computed the time-dependent WSS distribution from experimental data in the sheep thoracic aorta. Results showed that mean WSS calculated through steady flow and rigid walls models is overestimated. Peak WSS values for pulsatile flow must be considered since they resulted to be at least one order higher than mean values. Oscillations in shear stress in a period showed to be approximately of 40%. These findings show that the proposed model is suitable for estimating time-dependent WSS distributions, and confirm the need of using this kind of model when trying to evaluate realistic WSS in blood vessels.

Valor del BNP y de la proteína C reactiva en el diagnóstico diferencial entre angina primaria y secundaria por hipertensión arterial / Value of BNP and C reactive protein testing in the differential diagnosis between primary angina and hypertension-related angina

Introducción: A los episodios de inestabilidad anginosa precipitados por causas secundarias que, no infrecuentemente, no pueden discernirse de razones primarias se les concede poca atención. El presente trabajo intenta responder si algunos biomarcadores pueden contribuir a identificar a aquellos individuos con angina IIIb de los conocidos como anginosos IIIa de la clasificación de Braunwald. Material y métodos: En total, participaron del ensayo 64 pacientes seleccionados. De éstos, 33 tuvieron diagnóstico final de angina inestable secundaria a hipertensión arterial y 21 de angina primaria, en tanto que 10 enfermos anginosos estables, referidos para la práctica de un estudio angiográfico diagnóstico, sirvieron de control. En todos ellos, en el momento de la admisión se obtuvieron alícuotas de sangre venosa para la determinación del péptido natriurético auricular tipo B (BNP) y de proteína C reactiva ultrasensible (hs-CRP), y luego se realizó un estudio angiográfico invasivo a fin de analizar la carga aterosclerótica con puntajes (scores)angiográficos. Resultados: Los pacientes con angina primaria tuvieron una extensión aterosclerótica mayor en la angiografía (p < 0,025), más vasos comprometidos (p = 0,029) y un porcentaje mayor de estenosis (p < 0,001) que los anginosos secundarios. Los pacientes controles presentaron valores de BNP de 133 pg/mL (41; 224) [mediana (percentiles 25 y 75] y de 1,6 mg/L (0,4; 3,6) de hs-CRP. Los anginosos primarios no difirieron de los controles: 129 (95; 231) y 4,0(2,0; 5,6) para BNP y hs-CRP, respectivamente. Los anginosos secundarios tuvieron valores de 73 (19; 325) y de 4,5 (2,2; 9,0), respectivamente. No hubo diferencias significativas entre ambos cuadros anginosos: p = 0,458 para BNP y p = 0,552 para hs-CRP. Conclusiones: Independientemente de la carga aterosclerótica elevada en los anginosos primarios, el BNP y la hs-CRP no reconocieron con precisión la inestabilidad clínica inducida por un accidente de placa de la inducida...

Smart damping modulation of carotid wall energetics in human hypertension: effects of angiotensin-converting enzyme inhibition.

Damping is the conversion of mechanical energy of a structure into thermal energy, and it is related to the material viscous behavior. To evaluate the role of damping in the common carotid artery (CCA) wall in human hypertension and the possible improvement of angiotensin-converting enzyme (ACE) inhibition, we used noninvasive CCA pressure (tonometry) and diameter (B-mode echography) waveforms in normotensive subjects (NT group; n=12) and in hypertensive patients (HT group; n=22) single-blind randomized into HT-placebo (n=10) or HT-treated (ramipril, 5 to 10 mg/d during 3 months; n=12). Vascular smooth muscle (VSM) null tonus condition was achieved from in vitro pressure and diameter waveforms (Konigsberg microtransducer and sonomicrometry) measured in explanted human CCA (n=14). Arterial wall dynamics was described by viscous (eta), inertial (M), and compliance (C) parameters, mean circumferential wall stress, viscous energy dissipation (WD), peak strain energy (WSt), damping ratio (xi=WD/WSt), and modeling isobaric indexes CIso and WSt(Iso). The lack of VSM tonus isobarically increased wall stress and reduced eta, CIso, and damping (P<0.01). Wall stress, eta, and WD were greater in HT than in NT (P<0.015) and arrived near normal in HT-treated (P<0.032 respect to HT), with no changes in HT-placebo. Whereas CIso increased in HT-treated (P<0.01) approaching the NT level, xi did not vary among groups. During hypertension, because of the WSt increase, the arterial wall reacts increasing WD to maintain xi. ACE inhibition modulates VSM activation and vessel wall remodeling, significantly improving wall energetics and wall stress. This protective vascular action reduces extra load to the heart and maintains enhanced arterial wall damping.