80 resultados para carotid angioplasty and stenting


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AbstractBackground:Patients undergoing arterial vascular surgery are considered at increased risk for post-operative complications.Objective:To assess the incidence and predictors of complications and death, as well as the performance of two models of risk stratification, in vascular surgery.Methods:This study determined the incidence of cardiovascular complications and deaths within 30 days from surgery in adults. Univariate comparison and logistic regression assessed the risk factors associated with the outcomes, and the receiver operating characteristic (ROC) curve assessed the discriminatory capacity of the revised cardiac risk index (RCRI) and vascular study group of New England cardiac risk index (VSG-CRI).Results:141 patients (mean age, 66 years; 65% men) underwent the following surgeries: carotid (15); lower limbs (65); abdominal aorta (56); and others (5). Cardiovascular complications and death occurred within 30 days in 28 (19.9%) and 20 (14.2%) patients, respectively. The risk predictors were: age, obesity, stroke, poor functional capacity, altered scintigraphy, surgery of the aorta, and troponin change. The scores RCRI and VSG-CRI had area under the curve of 0.635 and 0.639 for early cardiovascular complications, and 0.562 and 0.610 for death in 30 days.Conclusion:In this small and selected group of patients undergoing arterial vascular surgery, the incidence of adverse events was elevated. The risk assessment indices RCRI and VSG-CRI did not perform well for complications within 30 days.

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Abstract Background: The kinetics of high-sensitivity troponin T (hscTnT) release should be studied in different situations, including functional tests with transient ischemic abnormalities. Objective: To evaluate the release of hscTnT by serial measurements after exercise testing (ET), and to correlate hscTnT elevations with abnormalities suggestive of ischemia. Methods: Patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing primary angioplasty were referred for ET 3 months after infarction. Blood samples were collected to measure basal hscTnT immediately before (TnT0h), 2 (TnT2h), 5 (TnT5h), and 8 hours (TnT8h) after ET. The outcomes were peak hscTnT, TnT5h/TnT0h ratio, and the area under the blood concentration-time curve (AUC) for hscTnT levels. Log-transformation was performed on hscTnT values, and comparisons were assessed with the geometric mean ratio, along with their 95% confidence intervals. Statistical significance was assessed by analysis of covariance with no adjustment, and then, adjusted for TnT0h, age and sex, followed by additional variables (metabolic equivalents, maximum heart rate achieved, anterior wall STEMI, and creatinine clearance). Results: This study included 95 patients. The highest geometric means were observed at 5 hours (TnT5h). After adjustments, peak hscTnT, TnT5h/TnT0h and AUC were 59% (p = 0.002), 59% (p = 0.003) and 45% (p = 0.003) higher, respectively, in patients with an abnormal ET as compared to those with normal tests. Conclusion: Higher elevations of hscTnT may occur after an abnormal ET as compared to a normal ET in patients with STEMI.

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Objective The present study evaluated the reliability of digital panoramic radiography in the diagnosis of carotid artery calcifications. Materials and Methods Thirty-five patients under high-risk for development of carotid artery calcifications who had digital panoramic radiography were referred to undergo ultrasonography. Thus, 70 arteries were assessed by both methods. The main parameters utilized to evaluate the panoramic radiography reliability in the diagnosis of carotid artery calcifications were accuracy, sensitivity, specificity and positive predictive value of this method as compared with ultrasonography. Additionally, the McNemar's test was utilized to verify whether there was a statistically significant difference between digital panoramic radiography and ultrasonography. Results Ultrasonography demonstrated carotid artery calcifications in 17 (48.57%) patients. Such individuals presented with a total of 29 (41.43%) carotid arteries affected by calcification. Radiography was accurate in 71.43% (n = 50) of cases evaluated. The degree of sensitivity of this method was 37.93%, specificity of 95.12% and positive predictive value of 84.61%. A statistically significant difference (p < 0.001) was observed between the methods evaluated in their capacity to diagnose carotid artery calcifications. Conclusion Digital panoramic radiography should not be indicated as a method of choice in the investigation of carotid artery calcifications.

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Objective: To study the stenosis of the carotid arteries in patients with symptomatic peripheral arterial disease.Methods: we assessed 100 consecutive patients with symptomatic peripheral arterial disease in stages of intermittent claudication, rest pain or ulceration. Carotid stenosis was studied by echo-color-doppler, and considered significant when greater than or equal to 50%. We used univariate analysis to select potential predictors of carotid stenosis, later taken to multivariate analysis.Results: The prevalence of carotid stenosis was 84%, being significant in 40% and severe in 17%. The age range was 43-89 years (mean 69.78). Regarding gender, 61% were male and 39% female. Half of the patients had claudication and half had critical ischemia. Regarding risk factors, 86% of patients had hypertension, 66% exposure to smoke, 47% diabetes, 65% dyslipidemia, 24% coronary artery disease, 16% renal failure and 60% had family history of cardiovascular disease. In seven patients, there was a history of ischemic cerebrovascular symptoms in the carotid territory. The presence of cerebrovascular symptoms was statistically significant in influencing the degree of stenosis in the carotid arteries (p = 0.02 at overall assessment and p = 0.05 in the subgroups of significant and non-significant stenoses).Conclusion: the study of the carotid arteries by duplex scan examination is of paramount importance in the evaluation of patients with symptomatic peripheral arterial disease, and should be systematically conducted in the study of such patients.

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Objective: to investigate the effect of administration of supraphysiological âcaroteno on biological parameters (ectoscopy and blood pressure), laboratory (malondialdehyde) and histological (liver and carotid arteries) of spontaneously hypertensive rats prone to stroke (SHR-sp).Methods: we used 36 male rats were divided into three groups, each containing 12 rats Wistar, SHR and SHR-sp, subdivided into six control animals and six animals treated with supraphysiological doses of âcaroteno for two periods of ten weeks interspersed with one week interruption. In the experiment were assessed daily physical examination and blood pressure (plethysmography). At sacrifice, blood was collected for measurement of serum malondialdehyde, liver and carotid arteries for histological examination.Results: temporary change in color of the fur, decreased significantly (p<0.0001) blood pressure (20mg supplementation âcaroteno) and serum levels of malondialdehyde (p<0.05) and increased amount of elastic fibers in the carotid wall of SHR and SHR-sp.Conclusion: supplementation of supraphysiological âcaroteno caused no toxic effects, showed positive response in the modulation of blood pressure and lower serum malondialdehyde. No significant morphological changes were found in both groups, except an increase in the number of elastic fibers in the muscle layer carotid suggesting elastosis in SHR and SHR-sp.

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Objective: The paper analyzes the supply and the utilization of hemodynamic services in Rio de Janeiro, Brazil.Methods: It's an exploratory study that uses data obtained from Brazilian official databases. The period of supply analysis was from 1999 to 2009, and of utilization was from 2008 to October 2012.Results: Since 1999 there is a growth of hemodynamic equipment purchase. The private sector concentrates most of the supply, but it has been reducing its availability to SUS. The rate between population and equipment in Brazil exceeds the ones of some rich countries. In the sense of supply, there are in 2009, a supply rate of 1,4 equipments for 1 million inhabitants in RJ state, larger than brazilian rate, of 3,4 but the rates are similar for public customers.Conclusion: Interventional cardiology procedures have improved in the state, but in a different way. And this is because the public hospitals at Rio de Janeiro have mostly reduced their production, while the private ones have increased their production. The observed result is the SUS users performing their procedures at great distances.

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Thirty heads with the neck segment of Caiman latirostris were used. The animals were provided from a creation center called Mister Caiman, under the authorization of the Brazilian Institute of Environment and Renewable Natural Resources (Ibama). Animals were sacrificed according to the slaughtering routine of the abattoir, and the heads were sectioned at the level of the third cervical vertebra. The arterial system was washed with cold saline solution, with drainage through jugular veins. Subsequently, the system was filled with red colored latex injection. Pieces were than fixed in 20% formaldehyde, for seven days. The brains were removed, with a spinal cord segment, the duramater removed and the arteries dissected. At the level of the hypophysis, the internal carotid artery gave off a rostral branch, and a short caudal branch, continuing, naturally, as the caudal cerebral artery. This artery projected laterodorsalwards and, as it overpassed the optic tract, gave off its I (the first) central branch. Penetrated in the cerebral transverse fissure, emitting the diencephalic artery and next its II (second) central branch. Still inside the fissure, originated occipital hemispheric branches and a pineal branch. Emerged from the cerebral transverse fissure, over the occipital pole of the cerebral hemisphere. Projected rostralwards, sagital to the cerebral longitudinal fissure, as interhemispheric artery. This artery gave off medial and convex hemispheric branches to the respective surfaces of the cerebral hemispheres, anastomosed with its contralateral homologous, forming the common ethmoidal artery. This artery entered the fissure between the olfactory peduncles, emerging ventrally and dividing into ethmoidal arteries, right and left, which progressed towards the nasal cavities, vascularizing them. The territory of the caudal cerebral artery included the most caudal area of the base of the cerebral hemisphere, its convex surface, the olfactory peduncles and bulbs, the choroid plexuses and the diencephalus with its parietal organs.

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The aim of this study was to describe the topography of the spinal cord of the red-footed tortoise to establish a morphological basis for applied research in anesthesiology and morphology. Six tortoises from the state of Maranhão (Brazil) that had died of natural causes were used. The common carotid artery was used to perfuse the arterial system with saline solution (heated to 37ºC) and to fix the material with a 20% formaldehyde solution. The specimens were then placed in a modified decalcifying solution for 72 hours to allow dorsal opening of the carapace with a chisel and an orthopedic hammer. Dissection of the dorsal musculature and sectioning of the vertebral arches were performed to access the spinal cord. The results revealed the spinal cord of G. carbonaria to be an elongated, whitish mass that reached the articulation between the penultimate and last caudal vertebrae. The cervical intumescence (Intumescentia cervicalis) was located between vertebral segments C5 and T1, whereas the lumbosacral intumescence (Intumescentia lumbalis) was located between T6 and Ca1.

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Thirty Meleagris gallopavo heads with their neck segments were used. Animals were contained and euthanized with the association of mebezonium iodide, embutramide and tetracaine hydrochloride (T 61, Intervet ) by intravenous injection. The arterial system was rinsed with cold saline solution (15°C), with 5000IU heparin and filled with red-colored latex. The samples were fixed in 20% formaldehyde for seven days. The brains were removed with a segment of cervical spinal cord and after, the dura-mater was removed and the arteries dissected. The cerebral carotid arteries, after the intercarotid anastomosis, were projected around the hypophysis, until they reached the tuber cinereum and divided into their terminal branches, the caudal branch and the rostral branch. The rostral branch was projected rostrolateralwards and gave off, in sequence, two collateral branches, the caudal cerebral and the middle cerebral arteries and the terminal branch was as cerebroethmoidal artery. The caudal cerebral artery of one antimere formed the interhemispheric artery, which gave off dorsal hemispheric branches to the convex surface of both antimeres. Its dorsal tectal mesencephalic branch, of only one antimere, originated the dorsal cerebellar artery. In the interior of the cerebral transverse fissure, after the origin of the dorsal tectal mesencephalic artery, the caudal cerebral artery emitted occipital hemispheric branches, pineal branches and medial hemispheric branches, on both antimeres. The caudal cerebral artery's territory comprehended the entire surface of the dorsal hemioptic lobe, the rostral surface of the cerebellum, the diencephalic structures, the caudal pole and the medial surface of the cerebral hemisphere and in the convex surface, the sagittal eminence except for its most rostral third. Due to the asymmetry found in the caudal cerebral arteries' ramifications, the models were classified into three types and their respective subtypes.

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The carotid bodies of rats made chronically hypoxic by breathing 12% O2 in a normobaric chamber (inspired PO2 91 mmHg) were compared with those of controls. Serial 5-µm sections of the organs were examined using an interactive image analysis system. The total volume of the carotid bodies was increased by 64%. The total vascular volume rose by 103% and was likely due to an increase in size of the large vessels (>12 µm lumen diameter) because the small vessel (5-12 µm lumen diameter) volume did not increase significantly while the small vessel density tended to decrease. The extravascular volume was increased by 57%. Expressed as a percentage of the total volume of the organ, the total vascular volume did not change, but the small vessel volume was significantly decreased from 7.83 to 6.06%. The large vessel volume must therefore have been increased. The proportion occupied by the extravascular volume was virtually unchanged (84 vs 82%). In accordance with these findings, the small vessel endothelial surface area per unit carotid body volume was diminished from 95.2 to 76.5 mm-1, while the extravascular area per small vessel was increased from 493 to 641 µm2 or by 30%. In conclusion, the enlargement of the carotid body in chronic hypoxia is most likely due to an increase in total vascular volume, mainly involving the "large" vessels, and to an increase in extravascular volume. This is in contrast to our previously published findings indicating that in the spontaneous insulin-dependent diabetic rat the enlargement of the carotid body is due solely to an increase in extravascular volume.

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Carotid bodies are chemoreceptors sensitive to a fall of partial oxygen pressure in blood (hypoxia). The morphological alterations of these organs in patients with chronic obstructive pulmonary disease (COPD) and in people living at high altitude are well known. However, it is not known whether the histological profile of human carotid bodies is changed in acute clinical conditions such as acute respiratory distress syndrome (ARDS). The objective of the present study was to perform a quantitative analysis of the histology of carotid bodies collected from patients who died of ARDS. A morphometric study of carotid bodies collected during routine autopsies was carried out on three groups: patients that died of non-respiratory diseases (controls, N = 8), patients that presented COPD and died of its complications or associated diseases (N = 7), and patients that died of ARDS (N = 7). Morphometric measurements of the volume fraction of clusters of chief cells were performed in five fields on each slide at 40X magnification. The numerical proportion of the four main histological cell types (light, dark, progenitor and sustentacular cells) was determined analyzing 10 fields on each slide at 400X magnification. The proportion of dark cells was 0.22 in ARDS patients, 0.12 in controls (P<0.001), and 0.08 in the COPD group. The proportion of light cells was 0.33 (ARDS), 0.44 (controls) (P<0.001), and 0.36 (COPD). These findings suggest that chronic and acute hypoxia have different effects on the histology of glomic tissue.

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A gravimetric method was evaluated as a simple, sensitive, reproducible, low-cost alternative to quantify the extent of brain infarct after occlusion of the medial cerebral artery in rats. In ether-anesthetized rats, the left medial cerebral artery was occluded for 1, 1.5 or 2 h by inserting a 4-0 nylon monofilament suture into the internal carotid artery. Twenty-four hours later, the brains were processed for histochemical triphenyltetrazolium chloride (TTC) staining and quantitation of the schemic infarct. In each TTC-stained brain section, the ischemic tissue was dissected with a scalpel and fixed in 10% formalin at 0ºC until its total mass could be estimated. The mass (mg) of the ischemic tissue was weighed on an analytical balance and compared to its volume (mm³), estimated either by plethysmometry using platinum electrodes or by computer-assisted image analysis. Infarct size as measured by the weighing method (mg), and reported as a percent (%) of the affected (left) hemisphere, correlated closely with volume (mm³, also reported as %) estimated by computerized image analysis (r = 0.88; P < 0.001; N = 10) or by plethysmography (r = 0.97-0.98; P < 0.0001; N = 41). This degree of correlation was maintained between different experimenters. The method was also sensitive for detecting the effect of different ischemia durations on infarct size (P < 0.005; N = 23), and the effect of drug treatments in reducing the extent of brain damage (P < 0.005; N = 24). The data suggest that, in addition to being simple and low cost, the weighing method is a reliable alternative for quantifying brain infarct in animal models of stroke.

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Discrepancy was found between enhanced hypotension and attenuated relaxation of conduit arteries in response to acetylcholine (ACh) and bradykinin (BK) in nitric oxide (NO)-deficient hypertension. The question is whether a similar phenomenon occurs in spontaneously hypertensive rats (SHR) with a different pathogenesis. Wistar rats, SHR, and SHR treated with NO donors [molsidomine (50 mg/kg) or pentaerythritol tetranitrate (100 mg/kg), twice a day, by gavage] were studied. After 6 weeks of treatment systolic blood pressure (BP) was increased significantly in experimental groups. Under anesthesia, the carotid artery was cannulated for BP recording and the jugular vein for drug administration. The iliac artery was used for in vitro studies and determination of geometry. Compared to control, SHR showed a significantly enhanced (P < 0.01) hypotensive response to ACh (1 and 10 µg, 87.9 ± 6.9 and 108.1 ± 5.1 vs 35.9 ± 4.7 and 64.0 ± 3.3 mmHg), and BK (100 µg, 106.7 ± 8.3 vs 53.3 ± 5.2 mmHg). SHR receiving NO donors yielded similar results. In contrast, maximum relaxation of the iliac artery in response to ACh was attenuated in SHR (12.1 ± 3.6 vs 74.2 ± 8.6% in controls, P < 0.01). Iliac artery inner diameter also increased (680 ± 46 vs 828 ± 28 µm in controls, P < 0.01). Wall thickness, wall cross-section area, wall thickness/inner diameter ratio increased significantly (P < 0.01). No differences were found in this respect among SHR and SHR treated with NO donors. These findings demonstrated enhanced hypotension and attenuated relaxation of the conduit artery in response to NO activators in SHR and in SHR treated with NO donors, a response similar to that found in NO-deficient hypertension.

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Exercise-induced vessel changes modulate arterial pressure (AP) in male spontaneously hypertensive rats (SHR). Vascular endothelial growth factor (VEGF) is important for angiogenesis of skeletal muscle. The present study evaluated the time course of VEGF and angiogenesis after short- and long-term exercise training of female SHR and Wistar Kyoto (WKY) rats, 8-9 weeks (200-250 g). Rats were allocated to daily training or remained sedentary for 3 days (N = 23) or 13 weeks (N = 23). After training, the carotid artery was catheterized for AP measurements. Locomotor (tibialis anterior and gracilis) and non-locomotor skeletal muscles (temporalis) were harvested and prepared for histologic and protein expression analyses. Training increased treadmill performance by all groups (SHR = 28%, WKY = 64%, 3 days) and (SHR = 141%, WKY = 122%, 13 weeks). SHR had higher values of AP than WKY (174 ± 4 vs 111 ± 2 mmHg) that were not altered by training. Three days of running increased VEGF expression (SHR = 28%, WKY = 36%) simultaneously with an increase in capillary-to-fiber ratio in gracilis muscle (SHR = 19%, WKY = 15%). In contrast, 13 weeks of training increased gracilis capillary-to-fiber ratio (SHR = 18%, WKY = 19%), without simultaneous changes in VEGF expression. Training did not change VEGF expression and capillarity of temporalis muscle. We conclude that training stimulates time- and tissue-dependent VEGF protein expression, independent of pressure levels. VEGF triggers angiogenesis in locomotor skeletal muscle shortly after the exercise starts, but is not involved in the maintenance of capillarity after long-term exercise in female rats.

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Electrical stimulation of baroreceptor afferents was used in the 1960's in several species, including human beings, for the treatment of refractory hypertension. This approach bypasses the site of baroreceptor mechanosensory transduction. Chronic electrical stimulation of arterial baroreceptors, particularly of the carotid sinus nerve (Hering's nerve), was proposed as an ultimate effort to treat refractory hypertension and angina pectoris due to the limited nature of pharmacological therapy available at that time. Nevertheless, this approach was abandoned in the early 1970's due to technical limitations of implantable devices and to the development of better-tolerated antihypertensive medications. More recently, our laboratory developed the technique of electrical stimulation of the aortic depressor nerve in conscious rats, enabling access to hemodynamic responses without the undesirable effect of anesthesia. In addition, electrical stimulation of the aortic depressor nerve allows assessment of the hemodynamic responses and the sympathovagal balance of the heart in hypertensive rats, which exhibit a well-known decrease in baroreflex sensitivity, usually attributed to baroreceptor ending dysfunction. Recently, there has been renewed interest in using electrical stimulation of the carotid sinus, but not the carotid sinus nerve, to lower blood pressure in conscious hypertensive dogs as well as in hypertensive patients. Notably, previous undesirable technical outcomes associated with electrical stimulation of the carotid sinus nerve observed in the 1960's and 1970's have been overcome. Furthermore, promising data have been recently reported from clinical trials that evaluated the efficacy of carotid sinus stimulation in hypertensive patients with drug resistant hypertension.