- Email: [email protected]
Stroke: cautions and promises
748
Hypertension Highlights / Journal of the American Society of Hypertension 9(10) (2015) 747–749
and benefits of endovascular compared with open repair for AAA can be difficult to determine. Recently, Schermerhorn et al3 published an observational study that examined the perioperative and long-term survival, reintervention rate, and complications after endovascular repair as compared with open procedures in propensity score–matched cohorts of Medicare beneficiaries who underwent AAA repair during the period from 2001 to 2008. Although it is an observational study, with up to 8 years of follow-up, these data likely represent our best opportunity to balance the short- and long-term outcomes of these procedures. Consistent with previous studies, the rate of survival over the first 3 years favored endovascular repair, after which time survival rates were similar—meaning that the risk of mortality was actually slightly higher with endovascular than with open repair over years 4 to 8. Not surprisingly, over 8 years of follow-up, the risk of reintervention was higher with endovascular repair. A somewhat more worrisome finding was that the risk of aneurysm rupture after repair was considerably higher with endovascular as compared with open repair (5.4% vs. 1.4%; P < .001). This relatively high rate of rupture over only 8 years of follow-up raises concerns about the durability of endovascular repair in patients who in many cases may live for decades after intervention. Although these data suggest that open repair may still be a reasonable option for many younger, healthier patients, the upfront, short-term benefit of endovascular repair on mortality, complications, and hospital stay still make endovascular repair attractive for most patients despite this relatively high risk of reintervention and rupture in longterm follow-up. Hopefully, as devices and technical expertise improve so will long-term outcomes. In the meantime, however, these data highlight the importance of long-term surveillance of patients who have undergone endovascular repair of AAA with at least annual duplex ultrasound or computerized tomographic angiography. In many cases, endoleak or other technical complications can be identified in surveillance and easily treated, potentially decreasing the risk of subsequent rupture. It is unlikely that most of these patients will continue to see their vascular interventionalist for years after their procedure. As such, in most cases, the clinician managing the patient’s hypertension (primary care provider, cardiologist, or hypertension specialist) may be the most appropriate member of the health care team to manage their vascular surveillance. Health care delivery systems also need to move aggressively toward developing robust surveillance systems of care for their patients who have undergone endovascular repair of AAA and other vascular interventions. Finally, future research needs to focus on novel means, including antihypertensive therapies, of decreasing the risk of long-term reintervention and aneurysm rupture after endovascular AAA repair.
Michael J. Bloch, MD, FACP, FASH, FSVM, FNLA Associate Professor, Medical Director, Department of Medicine, University of Nevada School of Medicine, Vascular Care, Renown Institute for Heart and Vascular Health, Reno, NV, USA [email protected] http://dx.doi.org/10.1016/j.jash.2015.07.015
References 1. Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL, et al; American Association for Vascular Surgery. ACC/AHA 2005 Practice guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006;113: e463–654. 2. Final recommendation statement: abdominal aortic aneurysm: screening. Reno, NV: U.S. Preventive Services Task Force; 2014. Available at: http://www. uspreventiveservicestaskforce.org/Page/Document/Reco mmendationStatementFinal/abdominal-aortic-aneurysmscreening. Accessed July 25, 2015. 3. Schermerhorn ML, Buck DB, O’Malley J, Curran T, McCallum JC, Darling J, et al. Long term outcomes of abdominal aortic aneurysm in the Medicare population. N Eng J Med 2015;373:328–38.
STROKE: CAUTIONS AND PROMISES According to Philip Gorelick in his American Society of Hypertension Self-Assessment Guide (JASH .2015; 9:320), about 795,000 strokes occur in the U.S. each year, 75% first strokes, the remainder recurrent, most ischemic from local occlusion or distant emboli, the remainder hemorrhagic. Prevention by effective antihypertensive therapy has been well documented, but the management of the post-stroke interval, both immediate and long-term, has been problematical. Fortunately, a new approach—revascularization by catheter removal of the clot responsible for ischemic stroke—is now rapidly being shown to be superior to the current treatment of choice, intravenous thrombolysis.
Hypertension Highlights / Journal of the American Society of Hypertension 9(10) (2015) 747–749
Before thrombolysis became available, the presence of often very high blood pressure during the immediate poststroke period prompted the use of various antihypertensive drugs, despite the known potential of spread of the ischemic area by lowering of systemic BP. Likely the best trial of such therapy was done with the angiotensin receptor blocker candesartan but no beneficial effects on activities of daily living and level of needed care was seen 6 months later (Hornslien AG et al. J Hypertens. 2015; 33:1487). Moreover, after a mean 2-year follow-up of 541 hypertensives with left ventricular hypertrophy after a stroke, those who had achieved a systolic BP below 144 mm Hg had a significantly increased risk of cardiovascular and all-cause mortality than did those with higher BPs. (Okin PM et al. Stroke. 2015; 46:2113). Clearly, antihypertensive drug therapy is not the solution for acute ischemic stroke. Thrombolysis within 4.5 hours of the initial stroke symptoms did much better and became the treatment of choice (Emberson J et al. Lancet. 2015; 385:1366). However, over the past year, a number of series of patients with a proximal intracranial occlusion in the anterior circulation have been reported to obtain revascularization and functional improvement by catheter-based thrombectomy (Goyal M et al. NEJM. 2015; 372:1019; Htyte N et al. Catheter. Cardiovasc Interv. 2015; 85:1043, only 2 of many more). Better selection of those patients with still viable brain tissue has been predicted to increase success to 80%–90% of patients who have thrombectomy (Al-Ali F et al. Front Neurol. 2015; 6:117). Not surprisingly, the call has gone out to interventional cardiologists to enlarge the small pool of neurologists who are trained to do the procedure (Apps A et al. BMJ. 2015; 351:h3969). Thus, while more cautions over drug therapy have been sounded, the promises of a new approach to the therapy of acute ischemic strokes seem ever so achievable. Norman M. Kaplan, MD Clinical Professor of Medicine U.Texas Southwestern Medical School Dallas, TX, USA [email protected] http://dx.doi.org/10.1016/j.jash.2015.08.004
HIGHLY VARIABLE SEEMS BAD
BLOOD
PRESSURE
Blood pressure is constantly variable and those with no variability are likely dead. The presence of variability has been recognized ever since multiple blood pressures could be measured but not until Peter Rothwell et al clearly describe (Lancet. 2010; 375:895) the prognostic significance of short-term visit-to-visit variability to cardiovascular disease did the inherent danger of variability become
749
widely recognized. At the same time, these investigators showed a progressively increased rate of stroke with increasing BP variability (Webb AJ et al. Lancet. 2010; 375:906) and a reduced risk of stroke with less variability as provided by calcium-channel blockers (Rothwell PM et al. Lancet Neurol. 2010; 9:469). Although not universally accepted as an independent risk factor, the evidence keeps growing, the latest from a retrospective analysis of data from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial, which corroborated an increased risk for cardiovascular disease mortality and morbidity with increased visit-to-visit BP variability measured once a month at seven visits (Muntner P et al. Ann Intern Med. 2015, published online on 28 July 2015). Others have shown an association between long-term variability, measured once a year for four visits and new onset of chronic renal disease in a large Japanese population, an association that was independent of the level of BP (Yano Y, et al. Hypertension. 2015; 66:30), unlike most data that do show an association with the level of BP (Asayama K, et al. Hypertension. 2015; 65:1170). Which brings us to 2 important questions about variability for which definite answers are not now available: first, what is the mechanism(s) for variability? and second, of greater clinical importance, is how best to ascertain it? Should it be beat-to-beat, minute-to-minute, interval-tointerval (as with ambulatory BP monitoring), visit-to-visit at clinician’s offices at variable intervals, or even less frequently. And a third, perhaps most important question remains: does reducing variability reduce cardiovascular events?, a question that may take many years of clinical observation to settle. Meanwhile, the advice of Asayama et al (Hypertension. 2015; 65:1170) seems worth following ‘‘Clinicians might reduce stroke incidence more by targeting systolic blood pressure variability along with BP level, preferentially using calcium-channel blockers, which might result in less blood pressure variability than other antihypertensive drug classes.’’ However, these authors go on to write ‘‘Blood pressure level, not variability, remains centerfold in the primary and secondary prevention of blood pressure-related complications.’’ Although we await certainty as to the value of reducing BP variability, it seems worth following my mother’s advice about taking a shower after every ball game: ‘‘It wouldn’t hurt.’’ Norman M. Kaplan, MD Clinical Professor of Medicine U.Texas Southwestern Medical School Dallas, TX, USA [email protected] http://dx.doi.org/10.1016/j.jash.2015.08.008
Hypertension Highlights / Journal of the American Society of Hypertension 9(10) (2015) 747–749
and benefits of endovascular compared with open repair for AAA can be difficult to determine. Recently, Schermerhorn et al3 published an observational study that examined the perioperative and long-term survival, reintervention rate, and complications after endovascular repair as compared with open procedures in propensity score–matched cohorts of Medicare beneficiaries who underwent AAA repair during the period from 2001 to 2008. Although it is an observational study, with up to 8 years of follow-up, these data likely represent our best opportunity to balance the short- and long-term outcomes of these procedures. Consistent with previous studies, the rate of survival over the first 3 years favored endovascular repair, after which time survival rates were similar—meaning that the risk of mortality was actually slightly higher with endovascular than with open repair over years 4 to 8. Not surprisingly, over 8 years of follow-up, the risk of reintervention was higher with endovascular repair. A somewhat more worrisome finding was that the risk of aneurysm rupture after repair was considerably higher with endovascular as compared with open repair (5.4% vs. 1.4%; P < .001). This relatively high rate of rupture over only 8 years of follow-up raises concerns about the durability of endovascular repair in patients who in many cases may live for decades after intervention. Although these data suggest that open repair may still be a reasonable option for many younger, healthier patients, the upfront, short-term benefit of endovascular repair on mortality, complications, and hospital stay still make endovascular repair attractive for most patients despite this relatively high risk of reintervention and rupture in longterm follow-up. Hopefully, as devices and technical expertise improve so will long-term outcomes. In the meantime, however, these data highlight the importance of long-term surveillance of patients who have undergone endovascular repair of AAA with at least annual duplex ultrasound or computerized tomographic angiography. In many cases, endoleak or other technical complications can be identified in surveillance and easily treated, potentially decreasing the risk of subsequent rupture. It is unlikely that most of these patients will continue to see their vascular interventionalist for years after their procedure. As such, in most cases, the clinician managing the patient’s hypertension (primary care provider, cardiologist, or hypertension specialist) may be the most appropriate member of the health care team to manage their vascular surveillance. Health care delivery systems also need to move aggressively toward developing robust surveillance systems of care for their patients who have undergone endovascular repair of AAA and other vascular interventions. Finally, future research needs to focus on novel means, including antihypertensive therapies, of decreasing the risk of long-term reintervention and aneurysm rupture after endovascular AAA repair.
Michael J. Bloch, MD, FACP, FASH, FSVM, FNLA Associate Professor, Medical Director, Department of Medicine, University of Nevada School of Medicine, Vascular Care, Renown Institute for Heart and Vascular Health, Reno, NV, USA [email protected] http://dx.doi.org/10.1016/j.jash.2015.07.015
References 1. Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL, et al; American Association for Vascular Surgery. ACC/AHA 2005 Practice guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006;113: e463–654. 2. Final recommendation statement: abdominal aortic aneurysm: screening. Reno, NV: U.S. Preventive Services Task Force; 2014. Available at: http://www. uspreventiveservicestaskforce.org/Page/Document/Reco mmendationStatementFinal/abdominal-aortic-aneurysmscreening. Accessed July 25, 2015. 3. Schermerhorn ML, Buck DB, O’Malley J, Curran T, McCallum JC, Darling J, et al. Long term outcomes of abdominal aortic aneurysm in the Medicare population. N Eng J Med 2015;373:328–38.
STROKE: CAUTIONS AND PROMISES According to Philip Gorelick in his American Society of Hypertension Self-Assessment Guide (JASH .2015; 9:320), about 795,000 strokes occur in the U.S. each year, 75% first strokes, the remainder recurrent, most ischemic from local occlusion or distant emboli, the remainder hemorrhagic. Prevention by effective antihypertensive therapy has been well documented, but the management of the post-stroke interval, both immediate and long-term, has been problematical. Fortunately, a new approach—revascularization by catheter removal of the clot responsible for ischemic stroke—is now rapidly being shown to be superior to the current treatment of choice, intravenous thrombolysis.
Hypertension Highlights / Journal of the American Society of Hypertension 9(10) (2015) 747–749
Before thrombolysis became available, the presence of often very high blood pressure during the immediate poststroke period prompted the use of various antihypertensive drugs, despite the known potential of spread of the ischemic area by lowering of systemic BP. Likely the best trial of such therapy was done with the angiotensin receptor blocker candesartan but no beneficial effects on activities of daily living and level of needed care was seen 6 months later (Hornslien AG et al. J Hypertens. 2015; 33:1487). Moreover, after a mean 2-year follow-up of 541 hypertensives with left ventricular hypertrophy after a stroke, those who had achieved a systolic BP below 144 mm Hg had a significantly increased risk of cardiovascular and all-cause mortality than did those with higher BPs. (Okin PM et al. Stroke. 2015; 46:2113). Clearly, antihypertensive drug therapy is not the solution for acute ischemic stroke. Thrombolysis within 4.5 hours of the initial stroke symptoms did much better and became the treatment of choice (Emberson J et al. Lancet. 2015; 385:1366). However, over the past year, a number of series of patients with a proximal intracranial occlusion in the anterior circulation have been reported to obtain revascularization and functional improvement by catheter-based thrombectomy (Goyal M et al. NEJM. 2015; 372:1019; Htyte N et al. Catheter. Cardiovasc Interv. 2015; 85:1043, only 2 of many more). Better selection of those patients with still viable brain tissue has been predicted to increase success to 80%–90% of patients who have thrombectomy (Al-Ali F et al. Front Neurol. 2015; 6:117). Not surprisingly, the call has gone out to interventional cardiologists to enlarge the small pool of neurologists who are trained to do the procedure (Apps A et al. BMJ. 2015; 351:h3969). Thus, while more cautions over drug therapy have been sounded, the promises of a new approach to the therapy of acute ischemic strokes seem ever so achievable. Norman M. Kaplan, MD Clinical Professor of Medicine U.Texas Southwestern Medical School Dallas, TX, USA [email protected] http://dx.doi.org/10.1016/j.jash.2015.08.004
HIGHLY VARIABLE SEEMS BAD
BLOOD
PRESSURE
Blood pressure is constantly variable and those with no variability are likely dead. The presence of variability has been recognized ever since multiple blood pressures could be measured but not until Peter Rothwell et al clearly describe (Lancet. 2010; 375:895) the prognostic significance of short-term visit-to-visit variability to cardiovascular disease did the inherent danger of variability become
749
widely recognized. At the same time, these investigators showed a progressively increased rate of stroke with increasing BP variability (Webb AJ et al. Lancet. 2010; 375:906) and a reduced risk of stroke with less variability as provided by calcium-channel blockers (Rothwell PM et al. Lancet Neurol. 2010; 9:469). Although not universally accepted as an independent risk factor, the evidence keeps growing, the latest from a retrospective analysis of data from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial, which corroborated an increased risk for cardiovascular disease mortality and morbidity with increased visit-to-visit BP variability measured once a month at seven visits (Muntner P et al. Ann Intern Med. 2015, published online on 28 July 2015). Others have shown an association between long-term variability, measured once a year for four visits and new onset of chronic renal disease in a large Japanese population, an association that was independent of the level of BP (Yano Y, et al. Hypertension. 2015; 66:30), unlike most data that do show an association with the level of BP (Asayama K, et al. Hypertension. 2015; 65:1170). Which brings us to 2 important questions about variability for which definite answers are not now available: first, what is the mechanism(s) for variability? and second, of greater clinical importance, is how best to ascertain it? Should it be beat-to-beat, minute-to-minute, interval-tointerval (as with ambulatory BP monitoring), visit-to-visit at clinician’s offices at variable intervals, or even less frequently. And a third, perhaps most important question remains: does reducing variability reduce cardiovascular events?, a question that may take many years of clinical observation to settle. Meanwhile, the advice of Asayama et al (Hypertension. 2015; 65:1170) seems worth following ‘‘Clinicians might reduce stroke incidence more by targeting systolic blood pressure variability along with BP level, preferentially using calcium-channel blockers, which might result in less blood pressure variability than other antihypertensive drug classes.’’ However, these authors go on to write ‘‘Blood pressure level, not variability, remains centerfold in the primary and secondary prevention of blood pressure-related complications.’’ Although we await certainty as to the value of reducing BP variability, it seems worth following my mother’s advice about taking a shower after every ball game: ‘‘It wouldn’t hurt.’’ Norman M. Kaplan, MD Clinical Professor of Medicine U.Texas Southwestern Medical School Dallas, TX, USA [email protected] http://dx.doi.org/10.1016/j.jash.2015.08.008