cme test questions: september 2012

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31. Sanya EO, Tutaj M, Brown CM, et al. Abnormal heart rate and blood pressure responses to baroreflex stimulation in multiple sclerosis pa- tients. Clin Auton Res 2005; 15:213–218. 32. Fisher JP, Fadel PJ. Therapeutic strategies for targeting excessive central sympathetic activation in human hypertension. Exp Physiol 1995; 5:572–580. 33. Dibona GF. Physiology in perspective: the wisdom of the body. Neural control of the kidney. Am J Physiol Regul Integr Comp Physiol 2005; 289:R633–R641. 34. Mahfoud F, Schlaich M, Kinderman I, et al. Effect of renal sympathetic denervation on glucose metabolism in patients with resistant hyperten- sion. Circulation 2011; 123:1940 –1946. 35. Witkowski A, Prejbisz A, Florczak E, et al. Effects of renal sympathetic denervation on blood pressure, sleep apnea course, and glycemic control in patients with resistant hypertension and sleep apnea. Hypertension 2011; 58:559 –565. 36. Matthew B, Patel SB, Reams GP, Freeman RH. Obesity-hypertension: emerging concepts in pathophysiology and treatment. Am J Med Sci 2007; 334:23–30. 37. Boer-Martins L, Figueiredo VN, Demacq C, et al. Relationship of auto- nomic imbalance and circadian disruption with obesity and type 2 diabe- tes in resistant hypertensive patients. Cardiovasc Diabetol 2011; 10:24. 38. Lambert G, Straznicky NE, Lambert EA, et al. Sympathetic nervous activation in obesity and the metabolic syndrome— causes, consequences, and therapeutic implications. Pharmacol Ther 2010; 126:159 –172. 39. Seals DR, Bell C. Chronic sympathetic activation: consequences and causes of age associated obesity? Diabetes 2004; 53:276 –284. 40. Davy KP, Orr JS. Sympathetic nervous system behavior in human obesity. Neurosci Biobehav Rev 2009; 33:116 –124. 41. Bell DSH. Treatment of diabetic hypertension. Diabetes Obes Metab 2009; 1:433– 444. 42. Frontoni S, Bracaglia D, Gigli F. Relationship between autonomic dys- function, insulin resistance and hypertension in diabetes. Nutr Metab Cardiovasc Dis 2005; 15:441– 449. 43. Nonogaki K, Iguchi A. Stress, acute hyperglycemia, and hyperlipid- emia: role of the autonomic nervous system and cytokines. Trends Endocrinol Metab 1997; 8:192–197. 44. Damon DH. Vascular-dependent effects of elevated glucose on post- ganglionic sympathetic neurons. Am J Physiol Heart Circ Physiol 2011; 300:H1386 –H1392. 45. Suzuki H, Nishizawa M, Ichikawa M, et al. Basal sympathetic nerve activity is enhanced with augmentation of baroreceptor reflex in Wistar fatty rats: a model of obesity-induced NIDDM. J Hypertens 1999; 17: 959 –964. 46. Inskip J, Plunet W, Ramer L, Ramsey JB, Yung A. Cardiometabolic risk factors in experimental spinal cord injury. J Neurotrauma 2010; 27:275–285. 47. Hamed SA, Hamed EA, Ezz Eldin AM, Mahmoud NM. Vascular risk fac- tors, endothelial function, and carotid thickness in patients with migraine: relationship to atherosclerosis. J Stroke Cerebrovasc Dis 2010; 19:92–103. 48. Horie R, Yamori Y. Neural factors and genetic disposition in cerebro- vascular atherogenesis in rats. Clin Exp Hypertens 1980; 2:1097–1115. CME TEST QUESTIONS: SEPTEMBER 2012 Examination available at http://learn.sirweb.org/. To take the online JVIR CME tests, please log into the SIR Learning Center with your SIR user name and password. Nonmembers: If you do not already have an SIR username and password, please click on “Create an Account” to gain access to the SIR Learning Center. Once in the Learning Center, click on the “Publication” activity type for a listing of all available JVIR CME Tests. Each test will be available online for three years from the month/date of publication. The CME questions in the September issue are derived from the article “Catheter-based Arterial Sympathectomy: Hypertension and Beyond” by Prince et al. 1. Regarding the medical treatment of patients with hy- pertension: a) More than half of patients are able to reach their target blood pressure. b) One criterion for adding another medication is reaching 50% of the maximum dose of the current drug. c) Most patients require two medications for control. d) Resistant hypertension is seen in only 5% of patients. 2. All of the following are true regarding the sympathetic nervous system EXCEPT: a) It causes increased vascular tone as a common underlying condition in hypertensive patients. b) It can be evaluated by radioisotope dilution spill- over analysis, which detects excess, unmetabolized epinephrine from synaptic clefts. c) It enervates the renal cortex, leading to renin secretion. d) It can be surgically denervated, resulting in lower- ing of blood pressure. 3. The described radiofrequency ablation device: a) Results in ablation of the nerve fibers in the renal arterial intima. b) Is activated with four to six 2-minute treatments delivered to the renal artery. c) Uses delivery of low energy, below 5 watts. d) Should only be used to treat one vessel per treat- ment session. 4. Human studies regarding the use of renal sympathetic denervation using radiofrequency ablation techniques: a) Demonstrated significant blood pressure improve- ment in the experimental group at 6 months. b) Have shown mild vessel narrowing at 3 months of follow-up. c) Note continued blood pressure reduction has not been seen beyond 6 months after treatment. d) Describe no ablation-related complications. 1134 Catheter-based Arterial Sympathectomy Prince et al JVIR

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Page 1: CME Test Questions: September 2012

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1134 � Catheter-based Arterial Sympathectomy Prince et al � JVIR

31. Sanya EO, Tutaj M, Brown CM, et al. Abnormal heart rate and bloodpressure responses to baroreflex stimulation in multiple sclerosis pa-tients. Clin Auton Res 2005; 15:213–218.

2. Fisher JP, Fadel PJ. Therapeutic strategies for targeting excessivecentral sympathetic activation in human hypertension. Exp Physiol 1995;5:572–580.

3. Dibona GF. Physiology in perspective: the wisdom of the body. Neuralcontrol of the kidney. Am J Physiol Regul Integr Comp Physiol 2005;289:R633–R641.

4. Mahfoud F, Schlaich M, Kinderman I, et al. Effect of renal sympatheticdenervation on glucose metabolism in patients with resistant hyperten-sion. Circulation 2011; 123:1940–1946.

5. Witkowski A, Prejbisz A, Florczak E, et al. Effects of renal sympatheticdenervation on blood pressure, sleep apnea course, and glycemic controlin patients with resistant hypertension and sleep apnea. Hypertension2011; 58:559–565.

6. Matthew B, Patel SB, Reams GP, Freeman RH. Obesity-hypertension:emerging concepts in pathophysiology and treatment. Am J Med Sci2007; 334:23–30.

7. Boer-Martins L, Figueiredo VN, Demacq C, et al. Relationship of auto-nomic imbalance and circadian disruption with obesity and type 2 diabe-tes in resistant hypertensive patients. Cardiovasc Diabetol 2011; 10:24.

8. Lambert G, Straznicky NE, Lambert EA, et al. Sympathetic nervousactivation in obesity and the metabolic syndrome—causes, consequences,

9. Seals DR, Bell C. Chronic sympathetic activation: consequences andcauses of age associated obesity? Diabetes 2004; 53:276–284.

0. Davy KP, Orr JS. Sympathetic nervous system behavior in humanobesity. Neurosci Biobehav Rev 2009; 33:116–124.

1. Bell DSH. Treatment of diabetic hypertension. Diabetes Obes Metab2009; 1:433–444.

2. Frontoni S, Bracaglia D, Gigli F. Relationship between autonomic dys-function, insulin resistance and hypertension in diabetes. Nutr MetabCardiovasc Dis 2005; 15:441–449.

3. Nonogaki K, Iguchi A. Stress, acute hyperglycemia, and hyperlipid-emia: role of the autonomic nervous system and cytokines. TrendsEndocrinol Metab 1997; 8:192–197.

4. Damon DH. Vascular-dependent effects of elevated glucose on post-ganglionic sympathetic neurons. Am J Physiol Heart Circ Physiol 2011;300:H1386–H1392.

5. Suzuki H, Nishizawa M, Ichikawa M, et al. Basal sympathetic nerveactivity is enhanced with augmentation of baroreceptor reflex in Wistarfatty rats: a model of obesity-induced NIDDM. J Hypertens 1999; 17:959–964.

6. Inskip J, Plunet W, Ramer L, Ramsey JB, Yung A. Cardiometabolic riskfactors in experimental spinal cord injury. J Neurotrauma 2010; 27:275–285.

7. Hamed SA, Hamed EA, Ezz Eldin AM, Mahmoud NM. Vascular risk fac-tors, endothelial function, and carotid thickness in patients with migraine:relationship to atherosclerosis. J Stroke Cerebrovasc Dis 2010; 19:92–103.

8. Horie R, Yamori Y. Neural factors and genetic disposition in cerebro-

and therapeutic implications. Pharmacol Ther 2010; 126:159–172. vascular atherogenesis in rats. Clin Exp Hypertens 1980; 2:1097–1115.

CME TEST QUESTIONS: SEPTEMBER 2012

Examination available at http://learn.sirweb.org/. To take the online JVIR CME tests, please log into the SIRLearning Center with your SIR user name and password. Nonmembers: If you do not already have an SIR username andpassword, please click on “Create an Account” to gain access to the SIR Learning Center. Once in the Learning Center,click on the “Publication” activity type for a listing of all available JVIR CME Tests. Each test will be available onlinefor three years from the month/date of publication.

The CME questions in the September issue are derived from the article “Catheter-based Arterial Sympathectomy:Hypertension and Beyond” by Prince et al.

1. Regarding the medical treatment of patients with hy-pertension:a) More than half of patients are able to reach their

target blood pressure.b) One criterion for adding another medication is

reaching 50% of the maximum dose of the currentdrug.

c) Most patients require two medications for control.d) Resistant hypertension is seen in only 5% of

patients.

2. All of the following are true regarding the sympatheticnervous system EXCEPT:a) It causes increased vascular tone as a common

underlying condition in hypertensive patients.b) It can be evaluated by radioisotope dilution spill-

over analysis, which detects excess, unmetabolizedepinephrine from synaptic clefts.

c) It enervates the renal cortex, leading to reninsecretion.

d) It can be surgically denervated, resulting in lower-ing of blood pressure.

3. The described radiofrequency ablation device:a) Results in ablation of the nerve fibers in the renal

arterial intima.b) Is activated with four to six 2-minute treatments

delivered to the renal artery.c) Uses delivery of low energy, below 5 watts.d) Should only be used to treat one vessel per treat-

ment session.

4. Human studies regarding the use of renal sympatheticdenervation using radiofrequency ablation techniques:a) Demonstrated significant blood pressure improve-

ment in the experimental group at 6 months.b) Have shown mild vessel narrowing at 3 months of

follow-up.c) Note continued blood pressure reduction has not

been seen beyond 6 months after treatment.d) Describe no ablation-related complications.