[Laser coronary angioplasty for an intrastent stenosis].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Baptista.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Automated stenosis analysis is a common feature of commercially available quantitative coronary angiography (QCA) systems, allowing automatic detection of the boundaries of the stenosis, interpolation of the expected dimensions of the coronary vessel at the point of obstruction, and angiographically derived estimation of atheromatous plaque size. However, the ultimate meaning of this type of analysis in terms of the degree of underlying atherosclerotic disease remains unclear. We investigated the relationship between stenosis analysis performed with QCA and the underlying degree of atherosclerotic disease judged by intracoronary ultrasound (ICUS) imaging. METHODS AND RESULTS: In 40 coronary stenoses, automated identification of the sites of maximal luminal obstruction and the start of the stenosis was performed with QCA by use of curvature analysis of the obtained diameter function. Plaque size at these locations also was estimated with ICUS, with an additional ICUS measurement immediately proximal to the start of the stenosis. Crescentlike distribution of plaque, indicating an atheroma-free arc of the arterial wall, was recorded. At the site of the obstruction, total vessel area measured with ICUS was 16.65 +/- 4.04 mm2, whereas an equivalent measurement obtained from QCA-interpolated reference dimensions was 7.48 +/- 3.30 mm2 (P = .0001). Plaque area derived from QCA data was significantly less than that calculated from ICUS (6.32 +/- 3.21 and 13.29 +/- 4.22 mm2, respectively; mean difference, 6.92 +/- 4.43 mm2; P = .0001). At the start of the stenosis identified by automated analysis, ICUS plaque area was 9.38 +/- 3.17 mm2, and total vessel area was 18.77 +/- 5.19 mm2 (50 +/- 11% total vessel area stenosis). The arterial wall presented a disease-free segment in 28 proximal locations (70%) but in only 5 sites (12%) corresponding to the start of the stenosis and none at the obstruction (P = .0001). At the site of obstruction, all vessels showed a complete absence of a disease-free segment, and the atheroma presented a cufflike or all-around distribution with a variable degree of eccentricity. CONCLUSIONS: At the site of maximal obstruction, QCA underestimated plaque size as measured with ICUS. Atherosclerotic disease was consistently present at the start of the stenosis and was used as a reference site by automated stenosis analysis. At the start of the stenosis, ICUS demonstrated a mean 50 +/- 11% total vessel area stenosis, with a characteristic loss of disease-free arcs of arterial wall present in proximal locations. Thus, the site identified by automated stenosis analysis as the start of the stenosis does not represent a disease-free site but rather the place where compensatory vessel enlargement fails to preserve luminal dimensions, a phenomenon that seems related to the observed loss of a remnant arc of normal arterial wall.
Limited information is provided by angiography on plaque morphology and composition before balloon angioplasty. Identification of plaques associated with reduced lumen gain or a high complication rate may provide the rationale for using alternative revascularization devices. We studied 60 patients with quantitative angiography and intracoronary ultrasound (ICUS) before and after balloon dilation. Angiography was used to measure transient wall stretch and elastic recoil. ICUS was used to investigate the mechanisms of lumen enlargement among different plaque compositions and in the presence of a disease-free wall (minimal thickness < or = 0.6 mm). Compared with ultrasound, angiography underestimated the presence of vessel calcification (13% vs 78%), lumen eccentricity (35% vs 62%), and wall dissection (32% vs 57%). ICUS measurements showed that balloon angioplasty increased lumen area from 1.82 +/- 0.51 to 4.81 +/- 1.43 mm2. Lumen enlargement was the result of the combined effect of an increase in the total cross-sectional area of the vessel (wall stretching, 43%) and of a reduction in the area occupied by the plaque (plaque compression or redistribution, 57%). Vessels with a disease-free wall had smaller lumen gain than other types of vessels (2.13 +/- 1.26 vs 3.59 +/- mm2, respectively, p < 0.01). Wall stretching was the most important mechanism of lumen enlargement in vessels with a disease-free wall (79% vs 37% in the other vessels). Angiography revealed a direct correlation between temporary stretch and elastic recoil that was responsible for 26% of the loss of the potential lumen gain. Thus, lumen enlargement after balloon angioplasty is the combined result of wall stretch and plaque compression or redistribution. ICUS indicates that vessels with a remnant arc of disease-free wall are dilated mainly by wall stretching compared with other types of vessels and are associated with a smaller lumen gain.
A comparison was made of the growth responses of prepubertal naive GH-deficient children who were randomly assigned to receive 0.3 mg/kg.week recombinant human GH administered either daily (QD) or three times weekly (TIW) over 4 yr. The effects of the two regimens on annual growth velocity, change in height SD score, bone maturation, and age at onset of puberty are presented as the mean +/- SD. During each of the 4 yr, the annual growth velocity was significantly greater in the QD vs. TIW group. At 48 months, the mean total gain in height was 9.7 cm greater in the QD group (38.4 +/- 5.5) than that in the TIW group 28.7 +/- 3.2; P = 0.0002). The mean height SD score at the end of each year was significantly greater in the QD group. After 4 yr, the total gain in height SD score was 3.2 +/- 1.2 in the QD group compared to 1.5 +/- 0.5 in the TIW group (P = 0.0003). The height SD score at 4 yr was 0.2 in the QD group (pretreatment, -2.9) compared to -1.4 in the TIW group (pretreatment, -2.9). After 4 yr of rhGH treatment, the increment in bone age was similar in the QD (4.9 +/- 1.0 yr) and TIW (4.8 +/- 1.1 yr) groups. The change in height age minus the change in bone age was more favorable in the QD (1.2 +/- 0.8 yr) than in the TIW (0.0 +/- 0.9 yr) group (P = 0.003). The mean age at onset of puberty in boys was the same in the QD (13.2 yr) and TIW (13.0 yr) groups (P = 0.71), and the mean bone age at the start of puberty was also similar (11.5 in QD and 11.3 in TIW groups; P = 0.66). The advantages of QD rhGH treatment in prepubertal GH-deficient children after 4 yr were additional gains of 1.7 height SD score and 9.7 cm in height over those treated with the TIW regimen (P = 0.0002).
BACKGROUND: Postmortem-derived findings support the common beliefs that lipid-rich coronary plaques with a thin, fibrous cap are prone to rupture and that rupture and superimposed thrombosis are the primary mechanisms causing acute coronary syndromes. In vivo imaging with intracoronary techniques may disclose differences in the characterization of atherosclerotic plaques in patients with stable or unstable angina and thus may provide clues to which plaques may rupture and whether rupture and thrombosis are active. METHODS AND RESULTS: We assessed the characteristics of the ischemia-related lesions with coronary angiography and intracoronary angioscopy and determined their compositions with intracoronary ultrasound in 44 patients with unstable and 23 patients with stable angina. The angiographic images were classified as noncomplex (smooth borders) or complex (irregular borders, multiple lesions, thrombus). Angioscopic images were classified as either stable (smooth surface) or thrombotic (red thrombus). The ultrasound characteristics of the lesion were classified as poorly echo-reflective, highly echo-reflective with shadowing, or highly echo-reflective without shadowing. There was a poor correlation between clinical status and angiographic findings. An angiographic complex lesion (n = 33) was concordant with unstable angina in 55% (24 of 44); a noncomplex lesion (n = 34) was concordant with stable angina in 61% (14 of 23). There was a good correlation between clinical status and angioscopic findings. An angioscopic thrombotic lesion (n = 34) was concordant with unstable angina in 68% (30 of 44); a stable lesion (n = 33) was concordant with stable angina in 83% (19 of 23). The ultrasound-obtained composition of the plaque was similar in patients with unstable and stable angina. CONCLUSIONS: Angiography discriminates poorly between lesions in stable and unstable angina. Angioscopy demonstrated that plaque rupture and thrombosis were present in 17% of stable angina and 68% of unstable angina patients. Currently available ultrasound technology does not discriminate stable from unstable plaques.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The purpose of the present study was to use the complementary information of angiography, intravascular ultrasound, and intracoronary angioscopy before and after directional atherectomy to characterize the postatherectomy appearance of vessel wall contours and the mechanism of lumen enlargement. Directional coronary atherectomy aims at debulking rather than dilating a coronary artery lesion. The selective removal of the plaque may potentially minimize the vessel wall damage and lead to subsequent better late outcome. Whether plaque removal is the main mechanism of action has only to be assessed indirectly by angiography and warrants further investigation with detailed analysis of luminal changes and vessel wall damage by ultrasound and direct visualization with angioscopy. Twenty-six patients have been investigated by quantitative angiography, intravascular ultrasound, and intracoronary angioscopy (n = 19) before and after atherectomy. In addition, all retrieved specimens were microscopically examined. Ultrasound imaging showed an increase in lumen area from 1.95 +/- 0.70 mm2 to 7.86 +/- 2.16 mm2 at atherectomy. The achieved gain mainly resulted from plaque removal because plaque plus media area decreased from 18.16 +/- 4.47 mm2 to 13.13 +/- 3.10 mm2. Vessel wall stretching (i.e., change in external elastic lamina area) accounted for only 15% of lumen area gain. Luminal gain was higher in noncalcified (6.52 +/- 2.12 mm2) lesions than in lesions containing deeply located calcium (5.19 +/- 0.99 mm2) and lowest in superficially calcified lesions (5.41 +/- 2.41 mm2). Ultrasound imaging identified an atherectomy byte in 85% of the cases, whereas angioscopy revealed such a crevice in 74%. The complementary use of the three techniques revealed an underestimation of the presence of dissection/tear and new thrombus by angiography (10% and 4%) and ultrasound imaging (12% and 0%) compared with angioscopy (26% and 21%). The combined use of angiography, ultrasound, and angioscopy reveals that the postatherectomy luminal lining is not as regular and smooth as that seen by angiography. Luminal enlargement with atherectomy is achieved by plaque excision rather than arterial expansion.
OBJECTIVES: The purpose of this study was to assess the dual action of lumen enlargement and vessel wall damage following either balloon angioplasty or directional atherectomy, using intracoronary ultrasound, and angioscopy. BACKGROUND: Differences in the mechanisms of action of balloon angioplasty and directional atherectomy may have a significant bearing on the immediate outcome and the restenosis rate at 6 months. METHODS: A total of 36 patients were studied before and after either balloon angioplasty (n = 18) or directional atherectomy (n = 18). Ultrasound measurements included changes in lumen area, external elastic membrane area and plaque burden. In addition, the presence and extent of dissections were assessed to derive a damage score. Angioscopic assessment of the dilated or atherectomized stenotic lesions was translated into semi-quantitative dissection, thrombus and haemorrhage scores. RESULTS: Atherectomy patients had a larger angiographic vessel size compared with the angioplasty group (3.55 +/- 0.46 mm vs 3.00 +/- 0.64 mm, P < 0.05); however, minimal lumen diameter (1.18 +/- 0.96 mm vs 0.85 +/- 0.49 mm) and plaque burden (17.04 +/- 3.69 vs 15.23 +/- 4.92 mm2) measurements did not differ significantly. As a result of plaque reduction, atherectomy produced a larger increase in luminal area than the angioplasty group (5.80 +/- 1.78 mm2 vs 2.44 +/- 1.36 mm2, P < 0.0001). Lumen increase after angioplasty was the result of 'plaque compression' (50%) and wall stretching (50%). Additionally, in both groups there was indirect angioscopic evidence of thrombus 'microembolization' as an adjunctive mechanism of lumen enlargement. Angioscopy identified big flaps in six and small intimal flaps in 11 of the atherectomized patients as compared with five and 12 patients in the angioplasty group. Changes in thrombus score following both coronary interventions were identical (0.72 +/- 3.42 points atherectomy vs -0.38 +/- 3.27 points balloon angioplasty, ns). CONCLUSIONS: Lumen enlargement after directional atherectomy is mainly achieved by plaque removal (87%), whereas balloon dilation is the result of vessel wall stretching (50%) and plaque reduction (50%). Despite the fact that the luminal gain achieved by directional atherectomy is twice that achieved with balloon angioplasty, the extent of trauma induced by both techniques seems to be similar.
The incorporation of radioactivity from [1-14C]-galactose into TCA-precipitable material was determined in skin fibroblasts derived from 11 galactosemic patients deficient in galactose 1-phosphate uridyl transferase (GALT-). "R" ratios (designated the R phenotype) were defined as the ratio between [14C]galactose incorporation and [3H]leucine incorporation. Results were expressed as a percentage of the controls. In the GALT-strains this ratio varied from strain to strain, presumably depending on the efficiency of the secondary route via the UDP-galactose pyrophosphorylase pathway. In 10 GALT-patients without late serious clinical manifestations, the R phenotype varied from 37 to 57% of the control value. In the 11th patient, the R phenotype was only 20% of the control. Thus, we obtained a significantly lower R phenotype in one patient who was distinguished from the others by having very severe delayed neurological complications, although compliance to galactose-free diet was good. We suggest that, in this patient, the development of the UDP-galactose pyrophosphorylase pathway was not sufficient to ensure the availability of enough galactose for the necessary synthesis of glycoproteins and glycolipids. Thus the R phenotype may be an indicator of the risk of late neurological complications. The determination of the R phenotype of GALT-patients may therefore be valuable. However, further investigations of galactosemic patients with neurological complications are required to confirm this relationship.
OBJECTIVES: The purpose of this study was to determine the predictive value of quantitative coronary angiography in the assessment of the functional significance of coronary stenosis as judged from the development of left ventricular wall motion abnormalities during dobutamine-atropine stress echocardiography. BACKGROUND: Coronary angiography is the reference method for assessment of the accuracy of noninvasive diagnostic imaging techniques to detect the presence of significant coronary stenosis. However, use of arbitrary cutoff criteria for the interpretation of angiographic data may considerably influence the true diagnostic accuracy of the technique investigated. METHODS: Thirty-four patients without previous myocardial infarction and with single-vessel coronary stenosis were studied with both quantitative angiography and dobutamine-atropine stress echocardiography. Two different techniques of quantitative angiographic analysis--edge detection and videodensitometry--were used for measurement of minimal lumen diameter, percent diameter stenosis and percent area stenosis. Two-dimensional echocardiographic images were collected during incremental doses of intravenous dobutamine and later analyzed using a 16-segment left ventricular model. Angiographic cutoff criteria were derived from receiver-operating curves to define the functional significance of coronary stenosis on the basis of dobutamine-atropine stress echocardiography. RESULTS: The angiographic cutoff values with the best predictive value for the development of left ventricular wall motion abnormalities during dobutamine-atropine stress echocardiography were minimal lumen diameter of 1.07 mm, percent diameter stenosis of 52% and percent area stenosis of 75%. Minimal lumen diameter was found to have the best predictive value for a positive dobutamine stress test (odds ratio 51, sensitivity 94%, specificity 75%). CONCLUSIONS: Automated quantitative angiographic measurement of minimal lumen diameter is a practical and useful index for determining both the anatomic and functional significance of coronary stenosis, and a value of 1.07 mm is the best predictor for a positive dobutamine stress test.
Long-term changes in vasocontractility were examined in 23 coronary segments from 20 patients with variant angina using computer-based quantitative coronary angiography and ergonovine provocation tests repeated at an interval of 42 +/- 14 months. Measurements of vasospasticity at the sites of fixed stenoses were compared with values predicted by an elementary geometric theory based on the assumption that the cross-sectional area of a vessel wall is constant regardless of its state of vasoconstriction. While all patients were symptomatic initially, only 11 remained symptomatic at follow-up. At the initial provocation test, the response was correctly predicted in four segments, was lower than expected in one, and was stronger in 18. At follow-up, only one of the four segments in which the response had been initially predicted correctly again showed the predicted response and the remaining three showed a response weaker than expected; the one segment which was initially hypocontractile remained hypocontractile at follow-up; and of the 18 segments which were initially hypercontractile, 12 exhibited hypercontractility again, four had the predicted value and the remaining two showed hypocontractility. In only one of 23 segments did the geometric theory predict the behaviour of vasospasticity at the site of fixed stenosis on both tests. Vasospastic responsiveness is a dynamic process demonstrating temporal variability and is not directly predicted by geometric theory.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Short-term administration of human growth hormone to children with idiopathic short stature can improve mean growth rate and predicted adult height. It is yet unknown whether therapy would alter pubertal development or affect final height. Three-year treatment results in a group of children with idiopathic short stature are reported. For year 1 of the study, 121 prepubertal children were randomly selected to receive somatotropin, 0.3 mg/kg per week, administered subcutaneously three times weekly (n = 63), or to be nontreatment control subjects (n = 58). After 1 year, all subjects were again randomly selected to receive either three-times-weekly or daily dosing at the same total dose. For the 92 subjects who completed 36 months of treatment, mean growth rate increased from a mean of 4.6 cm/yr before treatment to a mean of 8.0 cm/yr in the first year of treatment. Daily dosing resulted in a significantly faster mean growth rate (9.0 cm/yr) than three-times-weekly dosing (7.8 cm/yr) (p = 0.0005). Mean growth rates were 7.6 and 7.2 cm/yr during years 2 and 3, respectively, and did not differ by dosing group. Mean standardized height for all subjects improved from -2.7 to -1.6 after 3 years. When the growth rate was standardized for bone age, however, subjects who remained prepubertal had a significantly greater gain in mean height SD score than subjects who became pubertal during that 3-year period (p < 0.02). Mean standardized Bayley-Pinneau predicted adult height SD score increased from -2.7 to -1.6 and was independent of the timing of pubertal onset, but for individuals this score was more variable. Year-1 growth response, expressed as growth rate or change in height SD score, was the best predictor of growth in subsequent years. Responses to therapy could not be reliably predicted from baseline anthropometric variables, plasma insulin-like growth factor I SD score, growth hormone levels. Final height assessment will be needed to determine the ultimate benefit of therapy.
Over the past five years, the authors have developed a computerized system to record and store all the data pertaining to an endoscopic examination of the upper digestive tract. The system was designed to permit the easy storage and retrieval of data by personnel who lack computer skills and who may only have limited typing ability. The system allows for the storage and rapid retrieval of patients' individual records, as well as correction and/or deletion of these records. The system prints out copies of preliminary endoscopic findings and produces a final copy which contains histological and cytological findings. The program utilizes a standardized nomenclature, which however permits the introduction of each user's code in 16 areas of classification. It is possible to analyze statistically and correlate the stored data, permitting easy use for clinical studies. The uniformity of the methods for storage of and access to patients' records and data, along with the support of a central computer, allows multi-centre studies in the field of epidemiology. As of January 1991 30 endoscopic centres in Portugal have been equipped with this system. Overall the experience in these centres has been positive, with excellent or good participation in 76.7% of centres.
A high-performance liquid chromatography (HPLC) method with pulsed amperometric detection (PAD) was used for the determination of the acid hydrolysis products of L-iduronic acid containing oligosaccharides isolated from biological sources. This HPLC-PAD method was compared with gas chromatographic (GLC) methods. Since acid hydrolysis of oligosaccharides can produce a number of products, several uronic acid derivatives were prepared by chemical synthesis. These well characterized standards in conjunction with mass spectrometry allowed for the identification of most of the products of methanolysis or hydrolysis of glycosamino-glycans, which included chondroitin sulfates A and B (dermatan sulfate), heparin, and hyaluronic acid. (4 M) HCl in methanol 100 degrees C for 24 h was found to be optimum for GLC and 1 M aqueous HCl for 4 h at 100 degrees C for HPLC-PAD. All of the monosaccharides, hexosamines, and uronic acids could be separately identified in a single chromatographic step using either technique. Good resolution, high sensitivity (low microgram samples) and rapid analysis makes these methods particularly useful for the determination of small amounts of glycosaminoglycans and other glycoconjugates found in samples isolated from biological sources. These two techniques are specifically designed to allow the qualitative determination of the carbohydrate content and composition of samples whose carbohydrate composition and content is completely unknown.