Safety and efficacy of elective carotid artery stenting in high-risk patients.

OBJECTIVES: We sought to evaluate the safety and efficacy of carotid artery stenting (CAS) in high risk patients. BACKGROUND: Carotid endarterectomy (CE) has been shown to be more effective than medical therapy, but it has limitations. Carotid artery stenting may be a reasonable alternative, particularly in high-risk patients. METHODS: We prospectively evaluated the safety and efficacy of CAS in 170 consecutive patients who underwent the procedure in 192 carotid arteries. Of the patients enrolled, 129 (76%) would have been excluded from the major trials of CE and 54 (32%) were referred by vascular surgeons. This series represents a very high-risk group that included patients with unstable angina, previous ipsilateral CE, contralateral carotid artery occlusion and other severe comorbid illnesses. Only 25 (24%) of 104 symptomatic patients would have met the North American Symptomatic Carotid Endarterectomy Trial (NASCET) entry criteria. The patients' mean age was 73 +/- 8 years (95 confidence interval [CI] 57 to 89), and 42 patients (25%) were > or = 80 years old. Patients had an independent neurologic examination before and after the procedure. RESULTS: The procedural success rate was 99%, including 73 patients who had a coronary intervention. Mean carotid artery stenosis was 78 +/- 10% before (95 CI 58 to 98) and 2 +/- 3% after the procedure (95 CI -4 to 8). During the initial hospital period and 30 days after CAS, there was one major and two category 2 minor strokes, as well as two category 1 minor strokes (total 30-day stroke rate was 2.9% for treated patients or 2.6% for treated arteries). There were no myocardial infarctions or deaths during or within 30 days of CAS. None of the NASCET-eligible patients had a stroke. At a mean follow-up of 19 +/- 11 months, three patients (2%) had asymptomatic restenosis. No other major strokes or neurologic deaths occurred. CONCLUSIONS: Carotid artery stenting is feasible, can be performed even in high-risk patients and is associated with a low restenosis rate.

The current status of chemodectomas.

An analysis of the current status of chemodectomas including the report of two additional cases is presented. One patient with a rare malignant intrathoracic tumor failed to survive palliative pneumonectomy. To our knowledge, this represents the seventeenth histologically proved case. The other patient had the more common carotid body tumor which was managed satisfactorily by subadventitial carotid excision. Comments are made regarding the clinical recognition and treatment of chemodectomas in general. Historical, anatomic, physiologic, and pathologic features are emphasized.

Demonstration of macromolecular inhibitors of calcification and nucleational factors in fluid from calcifying sites in cartilage.

An extracellular fluid phase (C(f1)), aspirated by micropuncture techniques from the hypertrophic cell zone of calcifying epiphyseal certilage, has been characterized in a calcifying system in vitro in respect to the behavior of sedimenting and supernatant fractions after high speed ultracentrifugation. To perform these tests on the starting samples of 20 nl of C(f1), macroscopic analytical methods were scaled down for the identification of relevant organic components, including hexuronic acid and proteinpolysaccharides (PPL). The mineral accretion system was designed to simulate physiologic conditions in the calcifying cartilage septa of normal rats, and the mineral used for seeding was an immature calcium phosphate similar to native cartilage mineral. Normal C(f1) or its dilutions in synthetic lymph up to 1:4 completely prevented mineral accretion in vitro. The inhibitory action was localized to the sedimented fractions after ultracentrifugation and could be destroyed by incubation with trypsin or hyaluronidase. The sediment of C(f1) contained 2 mg of hexuronic acid per ml of C(f1) and gave a strong reaction of identification for a light fraction of PPL by fluorescent antibodies to rat PPL. PPL fractions were tested in the same mineral accretion systems as C(f1) and exhibited responses similar to those of C(f1). Also, there was evidence of a mineral phase in C(f1) of normal rats, in C(f1) of rats with healing rickets, but not in C(f1) of untreated rachitic rats. These results are interpreted to indicate that certain PPLs function as an inhibitor of crystal growth at extracellular sites premonitory to calcification. Evidence for a low density inhibitor of mineral accretion was found in normal serum but not in C(f1).

Partition of calcium, phosphate, and protein in the fluid phase aspirated at calcifying sites in epiphyseal cartilage.

A reproducible method, adapted from renal micropuncture techniques, was developed for sampling 10-40 mmul of a clear fluid from epiphyseal cartilage of normal or rachitic rats in vivo, either from the hypertrophic cell zone (C(f1)) or surface resting cell cartilage (L(f1)). Characterization of this fluid depended upon quantitation of protein, total inorganic phosphate (P(it)), total calcium (Ca(t)), nucleotide, and hemoglobin in volumes of 20 mmul. Established methods for macroscale measurements of each of these parameters have been modified to permit direct spectrophotometric readings on samples of 10(-10)-10(-11) g. The fluid from hypertrophic and peripheral resting cell cartilage was of an extracellular nature as evidenced by a high chloride and sodium, as well as low potassium, protein, and nucleotide content. The pH of fluid isolated from endochrondral plates in vivo was measured under oil as a function of P(CO2) and the computed bicarbonate was elevated above concurrent serum levels. After ultracentrifugation of C(f1) of normal, rachitic, and healing rachitic animals, nonprotein-bound calcium (Ca(f)) and phosphate (P(if)) were determined on supernatant fluids. The hypertrophic cell cartilage fluid of rachitic rats was distinguished by a high ratio C(f1)/serum of P(if). This ratio returned to normal during treatment of rickets. The upper limit for ionic activity A(1) Ca(++) x A HPO(4) (=) was too low to initiate precipitation of brushite or dicalcium phosphate but was in a range of supersaturation in respect to crystalline apatites. Thus these data are consistent with initiation of calcification by heterogeneous nucleation of mineral in the septal matrix but can be reconciled alternately with a precipitation mechanism only if the site of initial mineral phase separation is outside the septal matrix.