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V Fuster

Publications and source records attributed to V Fuster.

501 records · Page 28Linked to original sources
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Platelet deposition at high shear rates is enhanced by high plasma cholesterol levels. In vivo study in the rabbit model.

We have studied the effects of high plasma cholesterol levels on platelet-vessel wall interactions under high shear rate conditions typical of the apex of stenotic arteries (2,600 sec-1). Hypercholesterolemia was induced by feeding rabbits a 0.5% cholesterol-rich diet for 60 days. Platelet deposition was studied by use of an annular perfusion chamber and de-endothelialized abdominal rabbit aortas as substrates. After ingestion of the atherogenic diet, the experimental group of animals developed severe hypercholesterolemia, platelets became more fluid as determined by steady-state fluorescence anisotropy (p less than 0.05), and red blood cell deformability was decreased (p less than 0.001) when compared with normal controls. The fatty acid composition of platelet membranes showed an increase in the percentage of the long-chain saturated fatty acids (palmitic, C16:0, and stearic, C18:0) that may account for the lower polyunsaturated/saturated fatty acid ratio observed in the hyperlipemic animals. Total platelet deposition was significantly increased (p less than 0.05) in the hyperlipemic group as compared with the control group at 5 minutes' perfusion time, becoming less evident at 20 minutes' perfusion time. Our results suggest that the presence of hyperlipidemia may contribute to acute thrombosis by enhancing platelet-vessel wall interaction.

Animals↗
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Spontaneous and diet-induced coronary atherosclerosis in normal swine and swine with von Willebrand disease.

We have observed that pigs with impaired platelet function in the form of severe von Willebrand's disease (vWd) are resistant to spontaneous and to diet-induced aortic atherosclerosis. However, it has been reported that vWd pigs are susceptible to coronary atherosclerosis produced by balloon-induced injury of coronary arteries combined with an atherogenic diet. We have evaluated the development of coronary atherosclerosis in normal control (NC) and homozygous vWd pigs in two prospective studies: 1) as a spontaneous process in five NC and vWd pigs receiving a regular diet from the age of 3 months to 4 years; and 2) in nine NC and five vWd receiving a high-fat and high-cholesterol (2%) diet from the age of 3 to 9 months. All of the coronary arteries were analyzed postmortem in 5-mm sections. None of the NC nor the vWd pigs in the spontaneous study showed coronary atherosclerosis or myocardial lesions. In the study of diet-induced atherosclerosis, only one NC and one vWd pig had discrete stenoses; the stenoses affected the three coronary arteries and were significant (50% to 80%) in the NC and mild (greater than 25%) in the vWd pigs; no pigs showed myocardial lesions. Pigs with vWd are resistant to atherosclerosis of the aorta. To assess the resistance or susceptibility to coronary disease in these pigs, a longer follow-up study would be necessary.

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Aortic atherosclerosis in pigs with heterozygous von Willebrand disease. Comparison with homozygous von Willebrand and normal pigs.

We have reported that pigs with severe homozygous von Willebrand disease (vWd) are resistant to spontaneous and high fat, high cholesterol, diet-induced atherosclerosis. In this study we report the quantitation of aortic atherosclerotic plaques in three groups of pigs fed with a high fat, high cholesterol (2%) diet from age 3 to 9 months. Nine normal pigs (normal factor VIII antigen, VIII R:AG, and ristocetin co-factor, VIII:RWF) had a mean of 21% atherosclerotic involvement of the distal aortic surface and a 4.5% mean involvement of the entire aorta. Five homozygous vWd pigs (undetected VIII R:AG and VIII:RWF) had a mean of 4.2% atherosclerotic involvement of the distal aortic surface and 1.2% involvement of the entire aorta (p less than 0.01, rank sum test). Five heterozygous vWd pigs (approximately 35% VIII R:AG and VIII:RWF) had a mean of 25% atherosclerotic involvement of the distal aortic surface and 6% involvement of the entire aorta; the results were not significantly different from those in the normal pigs. We concluded that resistance to atherosclerosis is not found in animals with moderate reduction of VIII R:AG and VIII:RWF. This may have implications for humans, since in human vWd both factors are almost always present.

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Influence of arterial damage and wall shear rate on platelet deposition. Ex vivo study in a swine model.

To study the influence of blood flow on platelet interaction with selected biological surfaces, we have developed an ex vivo perfusion chamber system. In the present experiments, deendothelialized pig aorta and collagen Type I bundles from Achilles tendon were exposed to either native or heparinized pig blood for periods of time ranging from 1 to 30 minutes, and for flow rates corresponding to wall shear rates of 106 to 3380 sec-1. On the deendothelialized vessel wall, platelet deposition increased with both exposure time and wall shear rate, reaching a maximum value between 5 and 10 minutes of perfusion. At high shear rates and long exposure time (over 10 minutes), platelet deposition decreased from maximum values, indicating that some platelets were embolized by the flow. Ultrastructure analysis of the specimens showed platelet activation, spreading, and degranulation. Collagen induced a progressive accumulation of platelets following a power type curve of aggregate growth with exposure time without reaching a saturation level, even after long perfusion times (30 minutes) and high wall shear rates (3380 sec-1). In conclusion, the reactivity of the exposed materials and the local shear rate, defined by the blood flow and the patent luminal cross section, regulate platelet deposition to injured vascular wall.

Animals↗
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Distribution of von Willebrand factor in porcine intima varies with blood vessel type and location.

The von Willebrand factor (vWF) has been generally accepted as a marker for endothelial cells. In a systematic immunolocalization study of porcine blood vessels that used indirect immunofluorescence with a monospecific polyclonal anti-vWF and two monoclonal anti-vWFs, we observed that vWF is not universally distributed in intact, fresh endothelia. vWF is consistently localized in veins, with the exception of the pulmonic vein. In arteries, vWF is generally absent except for areas of the distal abdominal aorta, the vaso vasorum of the thoracic aorta, and the pulmonic artery. We conclude that there are regional differences in the distribution of vWF in the various endothelial beds of pigs.

Animals↗
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Functional behavior of vessels from pigs with von Willebrand disease. Values of platelet deposition are identical to those obtained on normal vessels.

Vessels from normal pigs and pigs with severe von Willebrand disease were exposed for up to 30 minutes to both nonanticoagulated and heparinized blood from normal pigs in an ex vivo perfusion system. Shear rates at the vessel surface were varied over a broad physiological range, gamma w = 212 to 3380 sec-1. The deposition of 111In-labeled platelets was determined by radiometric counting. For all shear rates and exposure times investigated, the levels of platelet deposition on de-endothelialized thoracic aorta of normal and von Willebrand disease pigs were not significantly different. Thus, the functional activity of the vessels correlated with the results obtained previously by immunofluorescence. Namely, the von Willebrand factor protein in the thoracic subendothelium of normal pigs is significantly diminished or absent and is comparable to the levels observed in von Willebrand disease pigs.

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Diagnosis of pulmonary artery hypertension.

The challenge for the clinician is to detect and diagnose pulmonary artery hypertension early, when treatment can be most beneficial. This can be done only if the clinician looks for pulmonary hypertension and confirms the diagnosis through history taking, physical examination, and electrocardiographic and chest roentgenographic evaluation.

Diagnosis, Differential↗