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Introduction of laparoscopic abdominal aortic aneurysm repair
266 Abstracts
Introduction of laparoscopic abdominal aortic aneurysm repair Howard AQ, Bennett PC, Ahmad I, et al. Brit J Surg 2015;102:368-74. Conclusion: Laparoscopic abdominal aortic aneurysm (AAA) repair can be performed safely with apparently equivalent outcomes to open repair in patients unfavorable for EVAR. Summary: While previously investigated in both North America and Europe, laparoscopic abdominal aortic aneurysm (AAA) repair was only recently developed in the UK. It was approved by the National Institute for Health and Care Excellence in 2007, with special arrangements for consent and audit or research. There are no randomized clinical trials to support laparoscopic AAA repair over open AAA repair. In addition, the availability of fenestrated and branched stent-graft devices, have broadened the scope of EVAR, potentially further reducing the number of AAAs requiring an alternative method of repair. The authors postulate that laparoscopic aortic surgery may be cost-effective owing to a reduced need for higher levels of care postoperatively than open repair and that it could be a useful technique as an alternative to EVAR in patients who are medically fit, seeking definitive repair without need for lifelong surveillance. This was a single-center series to evaluate the results of a laparoscopic aortic program after it was introduced into the National Health Service in the UK. Patients were compared with those having elective open AAA repair. There were a total of 316 patients who underwent AAA repair. Laparoscopic repair was performed in 51, open repair in 53, and endovascular repair in 212 between 2007 and 2013. The median age of patients who had laparoscopic or open repair was 72 (interquartile range, 66-75) years, and 92.3% were men. There were no significant differences in sex distribution, age of V-POSSUM physiology scores between laparoscopic and open repair patients. Of the 51 laparoscopic procedures, 6 were totally laparoscopic, 43 were laparoscopically assisted, and 2 were converted to open repair. Pain scores were similar on days 1 and 3 after laparoscopic and open repair, even though epidurals were used in the open group. Pain scores were lower on day 5 and 7 after laparoscopic procedures. Patients who had laparoscopic repair had significantly fewer postoperative cardiopulmonary and renal complications (P ¼ .017) and were discharged from hospitals sooner (median, 5 [interquartile range (IQR), 3-7] vs 8 [IQR, 6-11] days; P ¼ .001). Aortic clamp times were longer with laparoscopic repair (90 [63-120] minutes) vs open repair (76 [IQR, 57-105] minutes; P ¼ .048). Operative times were also longer with laparoscopic repair (330 [IQR, 270-390] minutes vs 240 [IQR, 180-300] minutes; P < .001). There was one death in the first 30 days in both groups. There were two conversions from laparoscopic repair to open repair for uncontrollable lumbar artery bleeding. The aneurysms repaired with open repair were larger than those with laparoscopic repair (6.8 cm vs 6.0 cm; P ¼ .001). Comment: The paper is not a rousing endorsement for laparoscopic repair of AAA. It demonstrates that it can be done, but certainly does not reach the threshold of saying it should be done or should be considered equivalent or perhaps preferable to open repair of AAA. At this time the procedure is likely remain a niche procedure that may be more about the doctor than the patient.
Alcohol Consumption at Midlife and Risk of Stroke During 43 Years of Follow-Up Cohort and Twin Analyses Kadlecová P, Andel R, Mikulik R, et al. Stroke 2015;46:627-33. Conclusion: Stroke risk is associated with heavy drinking (>2 drinks/d) in midlife and seems more important than well known risk factors such as hypertension and diabetes, until the age of approximately 75 years. Summary: Alcohol is a potential risk factor for stroke with a J- or U-shaped association (Patra J, et al. BMC Public Health 2010;10:258. http://dx.doi.org/10.1186/1471-2458-10-258). The authors decided to test the hypothesis that heavy drinkers and nondrinkers would have a greater stroke risk compared to very-light drinkers. Light drinkers were chosen as the reference category as opposed to nondrinkers to avoid potential bias caused by ex-drinkers who had stopped drinking alcohol for health problems and who might therefore possess preexisting susceptibilities. Data was derived from a population -based cohort of middle aged Swedish twins with 43 years of follow-up. All 11,644 members of the population-based Swedish Twin Registry born 1886 to 1925 with alcohol data aged less than 60 years were included. Interaction of midlife alcohol consumption by age at stroke was evaluated in Cox-regression and analyses of monozygotic twins were used. Covariates were baseline age, sex, cardiovascular diseases, diabetes mellitus, stress reactivity, body mass index, smoking, depression, and exercise. Altogether, 29% of participants developed stroke. Compared with very-light drinkers (<0.5 drinks/d), heavy drinkers (>2 drinks/d) had greater risk of
JOURNAL OF VASCULAR SURGERY July 2015
stroke (hazard ratio, 1.34; P ¼ .02) and the effect for nondrinkers approached significance (hazard ratio, 1.11; P ¼ .08). Age increased stroke risk for nondrinkers (P ¼ .012) and decreased it for heavy drinkers (P ¼ .04). Midlife heavy drinkers were at high risk from baseline till the age of 75 years when hypertension and diabetes mellitus grew to being the more relevant risk factors. In analyses of monozygotic twin-pairs, heavy drinking shortened the time to stroke by 5 years (P ¼ .04). Comment: The data indicate that alcohol consumption should be considered an age-varying risk factor for stroke. Heavy drinking in midlife actually has a greater risk factor for stroke than more traditional risk factors such as hypertension and diabetes up to about the age of 75 years, at which point the more traditional risk factors for stroke are then predominant. Antiplatelet Treatment Compared With Anticoagulation Treatment for Cervical Artery Dissection (CADISS): A Randomised Trial CADISS Trial Investigators. Lancet Neurol 2015;14:361-67. Conclusion: There is no difference in the efficacy of antiplatelet and anticoagulant drugs at preventing stroke and death in patients with symptomatic carotid and vertebral artery dissection. Summary: Cervical artery dissection accounts for 1 to 2% of all ischemic strokes. However, in young and middle-aged people it accounts for 10 to 25% of stroke (Debette S et al, Lancet Neurol 2009;8:668-78). Embolism from thrombus forming at the dissection site is thought to play the major role in stroke pathogenesis following dissection of cervical arteries (Kennedy F et al, Neurology 2012;79:686-9). Embolization as the mechanism of stroke with dissection is suggested by embolic pattern (Srinivasan J et al, Stroke 1996;27:1226-30) and transcranial Doppler studies (Lucas C et al, Stroke 1998;29:2646-8). There is controversy as to whether anticoagulant or antiplatelet drugs are sufficient for preventing embolism associated with cervical artery dissection (Menon RK et al, J Neurol Neurosurg Psychiatry 2008;79:612). The authors sought to determine whether antiplatelet or anticoagulant drugs were more effective as a treatment strategy in preventing stroke following cervical carotid artery dissection. Additionally, they sought to establish the true risk of recurrent stroke with cervical carotid artery dissection. This was a randomized trial in hospitals with specialized stroke or neurology services (39 in the UK and seven in Australia). Admitted patients included those with extracranial carotid and vertebral dissection with onset of symptoms within the previous 7 days. Patients were randomly assigned (1:1) by an automated telephone randomization service to receive antiplatelet drugs or anticoagulant drugs, with the specific treatment decided by the local commission. Treatment was for 3 months. Patients and clinicians were not masked to allocation, but investigators who assessed the end points were. The primary endpoint was ipsilateral stroke or death in the intention to treat population. 250 participants were enrolled in the study (118 carotid, 132 vertebral). Meantime to randomization was 3.65 days (standard deviation, 1.91). Presenting symptoms were stroke or transient ischemic attack (n ¼ 224) and local symptoms (headache, neck pain, or Horner’s syndrome; n ¼ 26). 126 participants were assigned to antiplatelet treatment vs 124 anticoagulant treatment. Overall, 4 of the 250 patients (2% had stroke recurrence and all of these were ipsilateral). Stroke or death occurred in 3 (2%) of 126 antiplatelet patients vs 1 (1%) of 124 anticoagulant patients (odds ratio, 0.335, 95% confidence interval, 0.006-4.233; P ¼ .63). There was one major bleeding (subarachnoid hemorrhage) in the anticoagulant group, but no deaths. Central review of imaging failed to confirm dissection in 52 patients. Preplanned per-protocol analysis excluding these patients showed stroke or death in three (3%) of 101 patients in the antiplatelet group vs 1 (1%) of 96 patients in the anticoagulant group (odds ratio, 0.346; 95% confidence interval, 0.006-4.390; P ¼ .66). Comment: This is the first randomized trial comparing antiplatelet treatment with anticoagulant treatment for treatment of cervical artery dissection. Interestingly, recurrent stroke risk at 3 months was rare in both groups with no significant difference between treatments. There are several limitations to the trial. Because it was relatively small and recurrences were rare, it is clearly underpowered. A definitive study examining the question of stroke recurrence following cervical artery dissection is likely to need such a large sample size as to be impractical to ever perform. Many dissections could not be confirmed by central adjudication of imaging, indicating perhaps poor imaging or actually misinterpretation of original images. It is also unclear whether the data in this population of patients was primarily spontaneous cervical artery dissections can apply to those who suffer cervical artery dissection in the course of trauma.
Introduction of laparoscopic abdominal aortic aneurysm repair Howard AQ, Bennett PC, Ahmad I, et al. Brit J Surg 2015;102:368-74. Conclusion: Laparoscopic abdominal aortic aneurysm (AAA) repair can be performed safely with apparently equivalent outcomes to open repair in patients unfavorable for EVAR. Summary: While previously investigated in both North America and Europe, laparoscopic abdominal aortic aneurysm (AAA) repair was only recently developed in the UK. It was approved by the National Institute for Health and Care Excellence in 2007, with special arrangements for consent and audit or research. There are no randomized clinical trials to support laparoscopic AAA repair over open AAA repair. In addition, the availability of fenestrated and branched stent-graft devices, have broadened the scope of EVAR, potentially further reducing the number of AAAs requiring an alternative method of repair. The authors postulate that laparoscopic aortic surgery may be cost-effective owing to a reduced need for higher levels of care postoperatively than open repair and that it could be a useful technique as an alternative to EVAR in patients who are medically fit, seeking definitive repair without need for lifelong surveillance. This was a single-center series to evaluate the results of a laparoscopic aortic program after it was introduced into the National Health Service in the UK. Patients were compared with those having elective open AAA repair. There were a total of 316 patients who underwent AAA repair. Laparoscopic repair was performed in 51, open repair in 53, and endovascular repair in 212 between 2007 and 2013. The median age of patients who had laparoscopic or open repair was 72 (interquartile range, 66-75) years, and 92.3% were men. There were no significant differences in sex distribution, age of V-POSSUM physiology scores between laparoscopic and open repair patients. Of the 51 laparoscopic procedures, 6 were totally laparoscopic, 43 were laparoscopically assisted, and 2 were converted to open repair. Pain scores were similar on days 1 and 3 after laparoscopic and open repair, even though epidurals were used in the open group. Pain scores were lower on day 5 and 7 after laparoscopic procedures. Patients who had laparoscopic repair had significantly fewer postoperative cardiopulmonary and renal complications (P ¼ .017) and were discharged from hospitals sooner (median, 5 [interquartile range (IQR), 3-7] vs 8 [IQR, 6-11] days; P ¼ .001). Aortic clamp times were longer with laparoscopic repair (90 [63-120] minutes) vs open repair (76 [IQR, 57-105] minutes; P ¼ .048). Operative times were also longer with laparoscopic repair (330 [IQR, 270-390] minutes vs 240 [IQR, 180-300] minutes; P < .001). There was one death in the first 30 days in both groups. There were two conversions from laparoscopic repair to open repair for uncontrollable lumbar artery bleeding. The aneurysms repaired with open repair were larger than those with laparoscopic repair (6.8 cm vs 6.0 cm; P ¼ .001). Comment: The paper is not a rousing endorsement for laparoscopic repair of AAA. It demonstrates that it can be done, but certainly does not reach the threshold of saying it should be done or should be considered equivalent or perhaps preferable to open repair of AAA. At this time the procedure is likely remain a niche procedure that may be more about the doctor than the patient.
Alcohol Consumption at Midlife and Risk of Stroke During 43 Years of Follow-Up Cohort and Twin Analyses Kadlecová P, Andel R, Mikulik R, et al. Stroke 2015;46:627-33. Conclusion: Stroke risk is associated with heavy drinking (>2 drinks/d) in midlife and seems more important than well known risk factors such as hypertension and diabetes, until the age of approximately 75 years. Summary: Alcohol is a potential risk factor for stroke with a J- or U-shaped association (Patra J, et al. BMC Public Health 2010;10:258. http://dx.doi.org/10.1186/1471-2458-10-258). The authors decided to test the hypothesis that heavy drinkers and nondrinkers would have a greater stroke risk compared to very-light drinkers. Light drinkers were chosen as the reference category as opposed to nondrinkers to avoid potential bias caused by ex-drinkers who had stopped drinking alcohol for health problems and who might therefore possess preexisting susceptibilities. Data was derived from a population -based cohort of middle aged Swedish twins with 43 years of follow-up. All 11,644 members of the population-based Swedish Twin Registry born 1886 to 1925 with alcohol data aged less than 60 years were included. Interaction of midlife alcohol consumption by age at stroke was evaluated in Cox-regression and analyses of monozygotic twins were used. Covariates were baseline age, sex, cardiovascular diseases, diabetes mellitus, stress reactivity, body mass index, smoking, depression, and exercise. Altogether, 29% of participants developed stroke. Compared with very-light drinkers (<0.5 drinks/d), heavy drinkers (>2 drinks/d) had greater risk of
JOURNAL OF VASCULAR SURGERY July 2015
stroke (hazard ratio, 1.34; P ¼ .02) and the effect for nondrinkers approached significance (hazard ratio, 1.11; P ¼ .08). Age increased stroke risk for nondrinkers (P ¼ .012) and decreased it for heavy drinkers (P ¼ .04). Midlife heavy drinkers were at high risk from baseline till the age of 75 years when hypertension and diabetes mellitus grew to being the more relevant risk factors. In analyses of monozygotic twin-pairs, heavy drinking shortened the time to stroke by 5 years (P ¼ .04). Comment: The data indicate that alcohol consumption should be considered an age-varying risk factor for stroke. Heavy drinking in midlife actually has a greater risk factor for stroke than more traditional risk factors such as hypertension and diabetes up to about the age of 75 years, at which point the more traditional risk factors for stroke are then predominant. Antiplatelet Treatment Compared With Anticoagulation Treatment for Cervical Artery Dissection (CADISS): A Randomised Trial CADISS Trial Investigators. Lancet Neurol 2015;14:361-67. Conclusion: There is no difference in the efficacy of antiplatelet and anticoagulant drugs at preventing stroke and death in patients with symptomatic carotid and vertebral artery dissection. Summary: Cervical artery dissection accounts for 1 to 2% of all ischemic strokes. However, in young and middle-aged people it accounts for 10 to 25% of stroke (Debette S et al, Lancet Neurol 2009;8:668-78). Embolism from thrombus forming at the dissection site is thought to play the major role in stroke pathogenesis following dissection of cervical arteries (Kennedy F et al, Neurology 2012;79:686-9). Embolization as the mechanism of stroke with dissection is suggested by embolic pattern (Srinivasan J et al, Stroke 1996;27:1226-30) and transcranial Doppler studies (Lucas C et al, Stroke 1998;29:2646-8). There is controversy as to whether anticoagulant or antiplatelet drugs are sufficient for preventing embolism associated with cervical artery dissection (Menon RK et al, J Neurol Neurosurg Psychiatry 2008;79:612). The authors sought to determine whether antiplatelet or anticoagulant drugs were more effective as a treatment strategy in preventing stroke following cervical carotid artery dissection. Additionally, they sought to establish the true risk of recurrent stroke with cervical carotid artery dissection. This was a randomized trial in hospitals with specialized stroke or neurology services (39 in the UK and seven in Australia). Admitted patients included those with extracranial carotid and vertebral dissection with onset of symptoms within the previous 7 days. Patients were randomly assigned (1:1) by an automated telephone randomization service to receive antiplatelet drugs or anticoagulant drugs, with the specific treatment decided by the local commission. Treatment was for 3 months. Patients and clinicians were not masked to allocation, but investigators who assessed the end points were. The primary endpoint was ipsilateral stroke or death in the intention to treat population. 250 participants were enrolled in the study (118 carotid, 132 vertebral). Meantime to randomization was 3.65 days (standard deviation, 1.91). Presenting symptoms were stroke or transient ischemic attack (n ¼ 224) and local symptoms (headache, neck pain, or Horner’s syndrome; n ¼ 26). 126 participants were assigned to antiplatelet treatment vs 124 anticoagulant treatment. Overall, 4 of the 250 patients (2% had stroke recurrence and all of these were ipsilateral). Stroke or death occurred in 3 (2%) of 126 antiplatelet patients vs 1 (1%) of 124 anticoagulant patients (odds ratio, 0.335, 95% confidence interval, 0.006-4.233; P ¼ .63). There was one major bleeding (subarachnoid hemorrhage) in the anticoagulant group, but no deaths. Central review of imaging failed to confirm dissection in 52 patients. Preplanned per-protocol analysis excluding these patients showed stroke or death in three (3%) of 101 patients in the antiplatelet group vs 1 (1%) of 96 patients in the anticoagulant group (odds ratio, 0.346; 95% confidence interval, 0.006-4.390; P ¼ .66). Comment: This is the first randomized trial comparing antiplatelet treatment with anticoagulant treatment for treatment of cervical artery dissection. Interestingly, recurrent stroke risk at 3 months was rare in both groups with no significant difference between treatments. There are several limitations to the trial. Because it was relatively small and recurrences were rare, it is clearly underpowered. A definitive study examining the question of stroke recurrence following cervical artery dissection is likely to need such a large sample size as to be impractical to ever perform. Many dissections could not be confirmed by central adjudication of imaging, indicating perhaps poor imaging or actually misinterpretation of original images. It is also unclear whether the data in this population of patients was primarily spontaneous cervical artery dissections can apply to those who suffer cervical artery dissection in the course of trauma.