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Biomedical subjects

Michael Horowitz

Publications and source records attributed to Michael Horowitz.

At least 37 records · Page 2Linked to original sources

Resection of a recurrent paraganglioma via an endoscopic transnasal approach to the jugular fossa.

OBJECTIVE: To present a novel endoscopic, transnasal approach to a recurrent paraganglioma of the jugular fossa (glomus jugulare). STUDY DESIGN: Case report and review of the literature. SETTING: The study was carried out at the University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, U.S.A. PATIENT: A 64-year-old woman presented to the University of Pittsburgh Medical Center with a 9-month history of left otalgia, occasional vertigo, facial pain, and recurrent epistaxis. She had undergone two previous procedures over the past 35 years for a glomus tympanicum. Physical examination revealed a mass in the left nasopharynx originating from the eustachian tube. A computed tomographic scan revealed an expansive mass in the left jugular foramen extending into the posterior parapharyngeal space suggestive of a large jugular paraganglioma. INTERVENTION: The patient underwent preoperative embolization of the paraganglioma. An endoscopic, transnasal approach along the eustachian tube, the ascending parapharyngeal carotid artery, and into the jugular fossa was used to remove the tumor. Intraoperative image guidance assisted in the identification of key anatomic landmarks. RESULTS: Postoperative magnetic resonance imaging revealed a thin rim of enhancement at the posterior aspect of the jugular fossa consistent with residual tumor. The patient was discharged to home on postoperative Day 1 in stable condition. There have been no complications with 4 months of follow-up, and the left facial paralysis secondary to preoperative embolization has resolved. CONCLUSION: We report the successful subtotal resection of a recurrent paraganglioma via a novel endoscopic, transnasal, transclival, transpetrous approach with image guidance. This approach allowed the near-total resection of a recurrent glomus jugulare with minimal surgical morbidity. Technological advances and surgical experience with nasal endoscopy and image guidance allow minimally invasive surgical management of select extracranial lesions of the lateral cranial base.

Embolization, Therapeutic↗

Gastrointestinal motility and glycemic control in diabetes: the chicken and the egg revisited?

Upper gastrointestinal dysfunction occurs frequently in diabetes and potentially contributes to both abdominal symptoms and impaired glycemic control; conversely, variations in blood glucose concentration reversibly affect gut motility in humans. In this issue of the JCI, Anitha et al. report apoptosis of rodent enteric neurons under hyperglycemic conditions, both in vitro and in vivo, associated with impaired PI3K activity and preventable by glial cell line-derived neurotrophic factor. These observations add to recent insights gained from animal models regarding the etiology of diabetic gastrointestinal dysfunction, but investigators must strive to translate animal data to human diabetes.

Animals↗

Fasting and nutrient-stimulated plasma peptide-YY levels are elevated in critical illness and associated with feed intolerance: an observational, controlled study.

INTRODUCTION: Delayed gastric emptying and feed intolerance occur frequently in the critically ill. In these patients, gastric motor responses to nutrients are disturbed. Peptide YY (PYY) slows gastric emptying. The aim of this study was to determine fasting and nutrient-stimulated plasma PYY concentrations and their relationship to cholecystokinin (CCK) in critically ill patients. METHODS: Studies were performed in 19 unselected mechanically ventilated critically ill patients (12 males; 48 +/- 7 years old) in a randomised, single-blind fashion. Subjects received a 60-minute duodenal infusion of Ensure at either 1 or 2 kcal/minute. Blood samples were collected at baseline and at 20, 40, 60, and 180 minutes following commencement of the nutrient infusion for the measurement of plasma PYY and CCK concentrations (using radioimmunoassay). Patient data were compared to 24 healthy subjects (17 males; 43 +/- 2 years old). RESULTS: Fasting PYY concentration was higher in patients (P < 0.05), particularly in those with feed intolerance (P < 0.05). Plasma PYY concentrations were higher in patients during nutrient infusion (area under the curve [AUC] at 1 kcal/minute: 2,265 +/- 718 versus 1,125 +/- 138 pmol/l.min, P < 0.05; at 2 kcal/minute: 2,276 +/- 303 versus 1,378 +/- 210 pmol/l.min, P = 0.01) compared to healthy subjects. The magnitude of PYY elevation was greater in patients during the 1 kcal/minute infusion (AUC: 441 +/- 153 versus 186 +/- 58 pmol/l.min, P < 0.05), but not the 2 kcal/minute infusion. Fasting and nutrient-stimulated plasma CCK concentrations were higher in patients (P < 0.05). There was a relationship between plasma PYY and CCK concentrations during fasting (r = 0.52, P < 0.05) and nutrient infusion (r = 0.98, P < 0.0001). CONCLUSION: In critical illness, both fasting and nutrient-stimulated plasma PYY concentrations are elevated, particularly in patients with feed intolerance, in conjunction with increased CCK concentrations.

Adult↗

Intra/extra-aneurysmal stent placement for management of complex and wide-necked- bifurcation aneurysms: eight cases using the waffle cone technique.

OBJECTIVE: To describe a novel application of the Neuroform stent (Boston Scientific-Target, Fremont, CA) for the management of eight wide-necked aneurysms. METHODS: All patients were treated using a single Neuroform stent placed partially into the aneurysm and into the afferent artery. The portion of the stent protruding into the aneurysm fundus provided neck support for the subsequent successful coiling. CONCLUSION: The Neuroform stent is a versatile device that can be used in a variety of ways to assist in the coiling of wide-necked aneurysms. The technique described here may be used for bifurcation aneurysms in lieu of using two stents in a Y configuration.

Aged↗

Intracranial head and neck tumors: endovascular considerations, present and future.

To review the literature on endovascular therapies available to clinicians to aid in the management of head, neck, and intracranial tumors. Hypervascular tumors of the head and neck region, as well as the intracranial region, are associated with large amounts of blood loss intraoperatively. Preoperative embolization of selected hypervascular tumors has been proposed in the literature as a method of reducing blood loss intraoperatively. This technique involves superselective catheterization of the feeding arteries to the tumor bed and then by infusion of embolic particles to saturate the tumor bed in the hopes of inducing necrosis. For less vascular tumors, selective infusion of chemotherapeutic agents has been reported as a method of reducing the systemic toxic effects of these medications. Endovascular therapies for hypervascular and less vascular tumors hold promise, although multicenter randomized controlled trials are required to help identify the patients that will benefit the most.

Antineoplastic Agents↗

Outcome and complications of gastric bypass in super-super obesity versus morbid obesity.

BACKGROUND: Roux-en-Y gastric bypass (RYGBP) reduces the co-morbidities of obesity. Patients with super-super obesity (BMI>or=60) present additional technical and medical challenges. This study compares the results in super-super-obese patients with patients with a BMI of <60 over a 5.5-year period. METHODS: Retrospective analysis was performed of the 504 patients who underwent open RYGBP from January 1999 through June 2004. Patients were divided into 2 groups: Group A (444 patients) had a BMI <60, and Group B (60 patients) had a BMI>or=60, and also had a greater percentage of males. The groups were otherwise similar in demographics and co-morbidities. RESULTS: Concomitant ventral herniorrhaphy was performed in 23 patients (5%) in Group A and in 3 patients (5%) in Group B. Concomitant cholecystectomy was done in 11.2% in Group A and 10% in Group B. Group A patients had an incidence of leaks of 1.3%, and there were no leaks in Group B. Wound infection rate for Group A was 5% vs 1.7 % in Group B (NS). Mortality for both groups was similar. The stricture rate for Group A was 0.9% compared with 1.7 % for Group B. After 1 year, excess weight lost was 41.7% in Group A and 38.3% in Group B. The development of anemia was not statistically different (8.3% vs 11.0 %). Incidence of postoperative gallbladder disease and incisional hernia was similar. CONCLUSIONS: Super-super-obese patients should not be excluded from RYGBP because of a perceived increased risk based upon BMI.

Adolescent↗

Is routine cholecystectomy necessary at the time of Roux-en-Y gastric bypass?

BACKGROUND: Morbid obesity is associated with an increased incidence of gallstones. Rapid weight loss, as occurs after Roux-en-Y gastric bypass (RYGBP) may also increase gallstone development. Standard surgical treatments for gallbladder disease and its complications might be more difficult following RYGBP. Controversy still exists whether prophylactic cholecystectomy is indicated at the time of RYGBP. METHODS: Retrospective analysis was performed on a database of 535 patients who underwent RYGBP for morbid obesity during a 5.5-year period. Patients were followed and medical records were reviewed. Ursodeoxycholic acid was not prescribed following surgery. RESULTS: 8% of patients had had cholecystectomy before the RYGBP. 75 of 492 patients (15%) were found to have gallstones at RYGBP, and cholecystectomy was performed at the same time. 3 of these patients had bile leaks but only 1 required further intervention (percutaneous transhepatic drainage for 3 weeks). Following RYGBP, 14 patients (3%) have required cholecystectomy for symptomatic cholelithiasis in the postoperative period. All were performed laparoscopically and without complication. CONCLUSIONS: Symptomatic gallbladder disease after RYGBP has not been frequent. Prophylactic cholecystectomy for a normal gallbladder is not necessary at the time of RYGBP. Patients without biliary tract symptoms may not require routine preoperative sonogram. If an abnormal gallbladder or gallstones are found at the time of an RYGBP operation, concomitant cholecystectomy should be considered.

Cholecystectomy↗

Postprandial hypotension - novel insights into pathophysiology and therapeutic implications.

Postprandial hypotension is a frequent disorder, occurring in approximately 40% of nursing-home residents, and represents a major cause of morbidity and mortality. Current approaches to management are suboptimal. While it has been generally assumed that ingestion of carbohydrate has the greatest effect, the fall in blood pressure (BP) does not appear to be mediated by the consequent elevations in blood glucose and insulin. Moreover, there is evidence that fat may decrease BP to a comparable extent to carbohydrate, although onset of the response may be slower, and that the response is affected by the type of carbohydrate. It has recently been established that the rate of nutrient delivery from the stomach into the small intestine is an important determinant of the hypotensive response to carbohydrate, so that the magnitude of the fall in BP and rise in heart rate is greater when gastric emptying is relatively more rapid. In both healthy elderly subjects and patients with type 2 diabetes, the fall in BP is attenuated when gastric emptying and small intestinal carbohydrate absorption are slowed by dietary (e.g. guar) or pharmacological (e.g. acarbose) means. Conversely, gastric distension attenuates the postprandial fall in BP. Strategies for the treatment of postprandial hypotension should, therefore, potentially be directed at (i) meal composition, particularly carbohydrate type and content, (ii) slowing gastric emptying and/or small intestinal carbohydrate absorption and/or (iii) increasing postprandial gastric distension.

Animals↗

Effects of load, and duration, of duodenal lipid on antropyloroduodenal motility, plasma CCK and PYY, and energy intake in healthy men.

Enterally administered lipid modulates antropyloroduodenal motility, gut hormone release, appetite, and energy intake. We hypothesized that these effects would be dependent on both the load, and duration, of small intestinal exposure to lipid. Eleven healthy men were studied on four occasions in a double-blind, randomized, fashion. Antropyloroduodenal motility, plasma CCK and peptide YY (PYY) concentrations, and appetite perceptions were measured during intraduodenal infusion of lipid (Intralipid) at 1) 1.33 kcal/min for 50 min, 2) 4 kcal/min for 50 min, and 3) 1.33 kcal/min for 150 min, or 4) saline for 150 min. Immediately after the infusions, energy intake was quantified. Pressure wave sequences (PWSs) were suppressed, and basal pyloric pressure, isolated pyloric pressure waves (IPPWs), plasma CCK and PYY stimulated (all P < 0.05), during the first 50 min of lipid infusion, in a load-dependent fashion. The effect of the 4 kcal/min infusion was sustained so that the suppression of antral pressure waves (PWs) and PWSs and increase in PYY remained evident after cessation of the infusion (all P < 0.05). The prolonged lipid infusion (1.33 kcal/min for 150 min) suppressed antral PWs, stimulated CCK and PYY and basal pyloric pressure (all P < 0.05), and tended to stimulate IPPWs when compared with saline throughout the entire infusion period. There was no significant effect of any of the lipid infusions on appetite or energy intake, although nausea was slightly higher (P < 0.05) with the 4 kcal/min infusion. In conclusion, both the load, and duration, of small intestinal lipid influence antropyloroduodenal motility and patterns of CCK and PYY release.

Adult↗

Fat digestion is required for suppression of ghrelin and stimulation of peptide YY and pancreatic polypeptide secretion by intraduodenal lipid.

Stimulation of cholecystokinin and glucagon-like peptide-1 secretion by fat is mediated by the products of fat digestion. Ghrelin, peptide YY (PYY), and pancreatic polypeptide (PP) appear to play an important role in appetite regulation, and their release is modulated by food ingestion, including fat. It is unknown whether fat digestion is a prerequisite for their suppression (ghrelin) or release (PYY, PP). Moreover, it is not known whether small intestinal exposure to fat is sufficient to suppress ghrelin secretion. Our study aimed to resolve these issues. Sixteen healthy young males received, on two separate occasions, 120-min intraduodenal infusions of a long-chain triglyceride emulsion (2.8 kcal/min) 1) without (condition FAT) or 2) with (FAT-THL) 120 mg of tetrahydrolipstatin (THL, lipase inhibitor), followed by a standard buffet-style meal. Blood samples for ghrelin, PYY, and PP were taken throughout. FAT infusion was associated with a marked, and progressive, suppression of plasma ghrelin from t = 60 min (P < 0.001) and stimulation of PYY from t = 30 min (P < 0.01). FAT infusion also stimulated plasma PP (P < or = 0.01), and the release was immediate. FAT-THL completely abolished the FAT-induced changes in ghrelin, PYY, and PP. In response to the meal, plasma ghrelin was further suppressed, and PYY and PP stimulated, during both FAT and FAT-THL infusions. In conclusion, in healthy humans, 1) the presence of fat in the small intestine suppresses ghrelin secretion, and 2) fat-induced suppression of ghrelin and stimulation of PYY and PP is dependent on fat digestion.

Adult↗

Dose-related effects of lauric acid on antropyloroduodenal motility, gastrointestinal hormone release, appetite, and energy intake in healthy men.

We recently reported that intraduodenal infusion of lauric acid (C12) (0.375 kcal/min, 106 mM) stimulates isolated pyloric pressure waves (IPPWs), inhibits antral and duodenal pressure waves (PWs), stimulates release of cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1), and suppresses energy intake and that these effects are much greater than those seen in response to isocaloric decanoic acid (C10) infusion. Administration of C12 was, however, associated with nausea, confounding interpretation of the results. The aim of this study was to evaluate the effects of different intraduodenal doses of C12 on antropyloroduodenal (APD) motility, plasma CCK and GLP-1 concentrations, appetite, and energy intake. Thirteen healthy males were studied on 4 days in double-blind, randomized fashion. APD pressures, plasma CCK and GLP-1 concentrations, and appetite perceptions were measured during 90-min ID infusion of C12 at 0.1 (14 mM), 0.2 (28 mM), or 0.4 (56 mM) kcal/min or saline (control; rate 4 ml/min). Energy intake was determined at a buffet meal immediately following infusion. C12 dose-dependently stimulated IPPWs, decreased antral and duodenal motility, and stimulated secretion of CCK and GLP-1 (r > 0.4, P < 0.05 for all). C12 (0.4 kcal/min) suppressed energy intake compared with control, C12 (0.1 kcal/min), and C12 (0.2 kcal/min) (P < 0.05). These effects were observed in the absence of nausea. In conclusion, intraduodenal C12 dose-dependently modulated APD motility and gastrointestinal hormone release in healthy male subjects, whereas effects on energy intake were only apparent with the highest dose infused (0.4 kcal/min), possibly because only at this dose was modulation of APD motility and gastrointestinal hormone secretion sufficient for a suppressant effect on energy intake.

Adult↗

Insulin-induced hypoglycemia accelerates gastric emptying of solids and liquids in long-standing type 1 diabetes.

CONTEXT: The rate of gastric emptying of carbohydrate is a major determinant of postprandial glycemia. In healthy subjects and patients with uncomplicated type 1 diabetes, there is evidence that gastric emptying may be accelerated by insulin-induced hypoglycemia. OBJECTIVE: The objective was to determine the effects of acute hypoglycemia on gastric emptying in long-standing type 1 diabetes and evaluate whether the response to hypoglycemia is influenced by the rate of gastric emptying during euglycemia and/or autonomic dysfunction. DESIGN: Gastric emptying of a solid/liquid meal (100 g (99m)Tc-minced beef and 150 ml 67Ga-EDTA-labeled water) was measured by scintigraphy on 2 separate days, during hypoglycemia and euglycemia. SETTING: These studies took place at the Department of Nuclear Medicine, Positron Emission Tomography, and Bone Densitometry at the Royal Adelaide Hospital. PATIENTS: Twenty type 1 patients (4 female, 16 male; age, 45.9 +/- 2.3 yr; duration of known diabetes, 18.0 +/- 2.7 yr) were recruited from outpatient clinics and the Diabetes Centre at the Royal Adelaide Hospital. INTERVENTION: Hypoglycemia (approximately 2.6 mmol/liter) was established 15 min before and maintained for 45 min after meal consumption. On one of the days, autonomic nerve function was evaluated using cardiovascular reflex tests. MAIN OUTCOME MEASURE: The main outcome measure was gastric emptying during hypoglycemia when compared with euglycemia. RESULTS: Twelve of the 20 subjects had autonomic neuropathy. Gastric emptying of both solid (P < 0.001) and liquid (P < 0.05) was faster during hypoglycemia. The magnitude of this acceleration was greater when the rate of gastric emptying during euglycemia was slower (solid, percentage retention at 100 min, r = -0.52, P < 0.05; liquid, 50% emptying time, r = -0.82, P < 0.0001, but not influenced by autonomic nerve function). CONCLUSIONS: Insulin-induced hypoglycemia accelerates gastric emptying of solids and liquids in long-standing type 1 diabetes, even in those patients with delayed emptying, and is likely to be an important mechanism in the counter-regulation of hypoglycemia.

Adult↗

Initially more rapid small intestinal glucose delivery increases plasma insulin, GIP, and GLP-1 but does not improve overall glycemia in healthy subjects.

The rate of gastric emptying of glucose-containing liquids is a major determinant of postprandial glycemia. The latter is also dependent on stimulation of insulin secretion by glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). Although overall emptying of glucose approximates 1-3 kcal/min, the "early phase" of gastric emptying is usually more rapid. We have evaluated the hypothesis that increased stimulation of incretin hormones and insulin by a more rapid initial rate of small intestinal glucose delivery would reduce the overall glycemic response to a standardized enteral glucose load. Twelve healthy subjects were studied on two separate days in which they received an intraduodenal (id) glucose infusion for 120 min. On one day, the infusion rate was variable, being more rapid (6 kcal/min) between t = 0 and 10 min and slower (0.55 kcal/min) between t = 10 and 120 min, whereas on the other day the rate was constant (1 kcal/min) from t = 0-120 min, i.e., on both days 120 kcal were given. Between t = 0 and 75 min, plasma insulin, GIP, and GLP-1 were higher with the variable infusion. Despite the increase in insulin and incretin hormones, blood glucose levels were also higher. Between t = 75 and 180 min, blood glucose and plasma insulin were lower with the variable infusion. There was no difference in the area under the curve 0-180 min for blood glucose. We conclude that stimulation of incretin hormone and insulin release by a more rapid initial rate of id glucose delivery does not lead to an overall reduction in glycemia in healthy subjects.

Adult↗

Effects of drink volume and glucose load on gastric emptying and postprandial blood pressure in healthy older subjects.

Postprandial hypotension (PPH) occurs frequently in the elderly; the magnitude of the fall in blood pressure (BP) is related to the rate of glucose entry into the duodenum during intraduodenal glucose infusion and spontaneous gastric emptying (GE). It is unclear if glucose concentration affects the hypotensive response. Gastric distension may attenuate PPH; therefore, meal volume could influence the BP response. We aimed to determine the effects of 1) drink volume, 2) glucose concentration, and 3) glucose content on the BP and heart rate (HR) responses to oral glucose. Ten subjects (73.9 +/- 1.2 yr) had measurements of BP, GE, and blood glucose on 4 days after 1) 25 g glucose in 200 ml (12.5%), 2) 75 g glucose in 200 ml (37.5%), 3) 25 g glucose in 600 ml (4%), and 4) 75 g glucose in 600 ml (12.5%). GE, BP, HR, and blood glucose were measured for 180 min. After all drinks, duodenal glucose loads were similar in the first 60 min. Regardless of concentration, 600-ml (but not 200-ml) drinks initially increased BP, and in the first 30 min, systolic BP correlated (P < 0.01) with volume in both the proximal and total stomach. At the same concentration (12.5%), systolic BP fell more (P = 0.02) at the smaller volume; at the same volumes, there were no effects of concentration on BP. There was no difference in the glycemic response to drinks of identical glucose content. We conclude that 1) ingestion of glucose at a higher volume attenuates and 2) under constant duodenal load, glucose concentration (4-37%) does not affect the fall in BP.

Aged↗

Role of nitric oxide mechanisms in gastric emptying of, and the blood pressure and glycemic responses to, oral glucose in healthy older subjects.

The primary aims of this study were to evaluate the effects of the nitric oxide (NO) synthase inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME) on gastric emptying (GE) of, and the blood pressure (BP), glycemic, insulin, and incretin responses to, oral glucose in older subjects. Eight healthy subjects (4 males and 4 females, aged 70.9 +/- 1.3 yr) were studied on two separate days, in double-blind, randomized order. Subjects received an intravenous infusion of either l-NAME (180 mug.kg(-1).h(-1)) or saline (0.9%) at a rate of 3 ml/min for 150 min. Thirty minutes after the commencement of the infusion (0 min), subjects consumed a 300-ml drink containing 50 g glucose labeled with 20 MBq (99m)Tc-sulfur colloid, while sitting in front of a gamma camera. GE, BP (systolic and diastolic), heart rate (HR), blood glucose, plasma insulin, and incretin hormones, glucose-dependant insulinotropic-polypeptide (GIP), and glucagon-like peptide-1 (GLP-1), were measured. l-NAME had no effect on GE, GIP, and GLP-1. Between -30 and 0 min l-NAME had no effect on BP or HR. After the drink (0-60 min), systolic and diastolic BP fell (P < 0.05) and HR increased (P < 0.01) during saline; these effects were attenuated (P < 0.001) by l-NAME. Blood glucose levels between 90 and 150 min were higher (P < 0.001) and plasma insulin were between 15 and 150 min less (P < 0.001) after l-NAME. The fall in BP, increase in HR, and stimulation of insulin secretion by oral glucose in older subjects were mediated by NO mechanisms by an effect unrelated to GE or changes in incretin hormones.

Administration, Oral↗

Evaluation of interactions between CCK and GLP-1 in their effects on appetite, energy intake, and antropyloroduodenal motility in healthy men.

There is evidence that CCK and glucagon-like peptide-1 (GLP-1) mediate the effects of nutrients on appetite and gastrointestinal function and that their interaction may be synergistic. We hypothesized that intravenous CCK-8 and GLP-1 would have synergistic effects on appetite, energy intake, and antropyloroduodenal (APD) motility. Nine healthy males (age 22 +/- 1 yr) were studied on four separate days in a double-blind, randomized fashion. Appetite and APD pressures were measured during 150-min intravenous infusions of 1) isotonic saline (control), 2) CCK-8 (1.8 pmol.kg(-1).min(-1)), 3) GLP-1 (0.9 pmol.kg(-1).min(-1)), or 4) both CCK-8 (1.8 pmol.kg(-1).min(-1)) and GLP-1 (0.9 pmol.kg(-1).min(-1)). At 120 min, energy intake at a buffet meal was quantified. CCK-8, but not GLP-1, increased fullness, decreased desire to eat and subsequent energy intake, and increased the number and amplitude of isolated pyloric pressure waves and basal pyloric pressure (P < 0.05). Both CCK-8 and GLP-1 decreased the number of antral and duodenal pressure waves (PWs) (P < 0.05), and CCK-8+GLP-1 decreased the number of duodenal PWs more than either CCK-8 or GLP-1 alone (P < 0.02). This was not the case for appetite or isolated pyloric PWs. In conclusion, at the doses evaluated, exogenously administered CCK-8 and GLP-1 had discrepant effects on appetite, energy intake, and APD pressures, and the effects of CCK-8+GLP-1, in combination, did not exceed the sum of the effects of CCK-8 and GLP-1, providing no evidence of synergism.

Adolescent↗

Hemodynamic instability after carotid artery angioplasty and stent placement: a review of the literature.

In this review of the literature the goal was to determine the frequency and relevance of hemodynamic instability after carotid artery (CA) angioplasty and stent placement. Hemodynamic instability after CA angioplasty and stent placement is a well-recognized phenomenon that occurs in 29 to 51% of patients undergoing the procedure. In some patients this problem is severe enough to warrant treatment with vasopressor agents. Features observed on clinical and angiographic evaluation can help clinicians identify patients who are at risk. Hemodynamic fluctuations encountered as a result of CA angioplasty and stent placement may have adverse clinical consequences, including a higher incidence of myocardial infarction and stroke. Proposed measures to prevent this complication include prophylactic placement of transvenous pacemakers or pretreatment with atropine. Unfortunately, no randomized trials are currently available to assess the efficacy of these approaches. Hemodynamic instability is a common finding after CA angioplasty and stent placement. Clinicians can predict which patients are at risk by considering angiographic and clinical features.

Angioplasty↗