- Email: [email protected]
Patient Selection for Interventional Therapy
angiotensin-converting enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. N Eng1 J Med 2000; 342:145-153.
• 1 of the 90 who received lA therapy was thought to have smali vessel disease as the cause of the stroke.
21. PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood pressure-lowering regimen among 6,105 individuals with previous strake or transient ischemic attack. Lancet 2001; 358:10331041.
Who Gets What? tPA Options Blood pressure, time windowand CT exclusions are strictly adhered to in aj[ of the following protocols. Specific consent forms are signed for off-labe1 use of tPA and when the stroke is severe, statistics regarding increased risk of hemorrhage are discussed with the family and patient (when possible). • lf the patient presents with a mild stroke (NIHSS 4-10) within the 3 hour window, we might elect to use IV tPA alone according to the FOA approved protoc01 of 0.9 mgm/kgm 10% bolus, the rest over one hour. (No special consent is required). • lf the patient with an NlHSS of 4 -1 Ohas aphasia or severe hemiparesis, we may e1ect to use the combined lV/lA pratocol usually reserved for more severe strokes (see next bul1et). • lf the patient has a moderate to severe stroke (NIHSS >10) within 3 hours, we administer IV tPA at 0.6mgm/kgm 15% bolus, the rest over 30 minutes and prepare to go to angiography. If the patient improves significantly, we may cancel the angiogram. lf, on angiography, we find a clot (usually lCA, T-lesion, MI, M2, or basi1ar) we use intraarterial tPA usual1y to a maximum dose of 20-25 mgm so that the total dose is approximately 0.9 mgm/kgm. • lf the patient has a moderate to severe stroke (NlHSS > 10) and presents after 3 hours but before 6 hours, we consider intra-arterial tPA a10ne, particularly if the CT head scan is negative. The dose of lA tPA will depend on a more sophisticated evaluation of how the col1aterals look on the angiogram. • Other situations in which lA alone is general1y se1ected include: post procedure (cardiac catheterization) cases, post-operative cases, patients on coumadin, very e1derly patients or patients with a remote history if intracranial hemorrhage. • If the patient is rapidly improving at 3 hours, we will hold the IV tPA and closely monitor the patient. lf deterioration occurs, the patient is taken to the angiography suite and given lA therapy if a clot is located. • If there is atotal lCA occlusion, we may push the catheter through the clot and search for a distal embolus which is often present at MI. We can then come back and angioplasty and stent the carotid Jesion. • For basilar attery occlusions and retinal artery occlusions, we may extend the 6-hour time windowo
2:50 p.m. Patient Se1ection for Interventiona1 Therapy Marilyn Reimel~ MD Mid-America Brain and Stroke Institute Saint Luke's Hospital Kansas City, MO Background The Stroke Center at Saint Luke's Hospital in Kansas City opened in 1993 with the goal of standardizing care for the large patient volume and coordinating communication among the many practitioners who are important in the management of stroke. No one had imagined routine acute intervention, and a neur010gist in the emergency roor~ was a reportable siting. Two peop1e changed the landscape. Graham Lee, MOa neurointerventional radiologist came to Kansas City from NYC because Kansas resembled the plains of Rhodesia where he grew up. Having trained with Dr. Berenstein in NYC, he had used intra-arteria1 urokinase to 1yse clots in acute stroke. His early successes in reversing strokes at Saint Luke's changed our mindset permanently. We viewed every case as a possible "save" unless proven othelwise by time or circumstance. When Tom Brott, MO al10wed the Saint Luke's team to be one of Cincinnati's contributing hospitals in the NlNOS tPA trial, we discovered "ful1 speed ahead." We became friends with EMS, bonded
with the nurses and physicians in the emergency department, and neurologists became as at home in the EO as the cardi010gists. Current Practice Since 1999, we have used tPA for intra-arterial (IA) as wel1 as intravenous (IV) 1ysis. A recent review of our interventional cases from January of 2000 tllrough June 2002 revea1ed the fol1owing data: • 142/781 08.2%) of ischemic strakes were treated with tPA • 52/142 (36%) IV; 55/142 (39%) lA; 35/142 (25%) IV folIowed by lA • Overall hospital mortality rate was 12.7% with the lowest rate in the IV group at 5.8%. • Symptomatic hemorrhage rate was 9.2% (IV = 1.9%, lA=14.6%, IV/lA=11.4%) • Patients who received lA therapy were statistical1y 01der and presented with a higher NIHSS score. • 57% (51/90) of patients who received lA therapy a10ne or in combination with IV therapy were found to have a cardiac source for the stroke.
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HolU This Works • The strake neurologist is the point person for these protocoJs.
• If the patient arrives in our ED, there are standing orders for stroke evaluation including the er head scan and appropriate lab. The ED physician contacts the stroke neurologist as soon as the patient arrives or before arrivaJ if we have advance notice from EMS or LifeFlighr. Stroke cases arriving by 5 hours have priority for er, ete. • If the patient presents to an out1ying ED within 3 hours, we will often work with the local physician to give 0.6 mgm/kgm IV tPA IF we have verified time of onset with the famiJy by a direct conversation over the phone. At that time we also disCllSS with the family the possibility of using IA tPA on arrival at our ED, including risks, benefits, ete. • Our ED notifies the stroke neurologist of the ETA of the ambulance/helicopter and we attempt to be present on arrival. • If the histOlY sounds as though we wili need to consider lA tPA, we page the interventional neuroradiologist and put him on alert that we may need him. He in tum notifies the angiography team. • The stroke neurologist then evaluates the patient, CT head scan, ete. and decides whether or not to activate the INR and angiography team. Concentric Catbeter Trial We are presently involved in the Phase I trial of the Concentric CIot Retrieval Catheter, which allows us to retrieve the ciot up to eight hours after symptom onset in patients ineligible for tPA. The stroke neurologist makes the decision as to which patients are recommended to this trial.
3:10 p.m. The Great Acute-Stroke Imaging Debate-Cf, CfA, MR, MRA, Perfusion: Pros and Cons jeffrey L. Sunsbine, MD University Hospitals OJ Cleveland Cleveland, OH
3:30 p.m. Future Possibilities Concerning lnterventional Stroke Therapy: Devices and Drugs Gary M. Nesbit, MD Oregon Healtb & Science University POl1land, OR
3:50 p.m. Break
4:15 p.m. Carotid Atherosclerosis: Two Different Diseases jobn j. "Buddy" Connors, Jll, MD St. josepb 's Hospital Tampa, FL
The Nature of Cervical Carotid Stenosis Brachiocephalic atherosclerotic disease encompasses \esions ranging from stenoses at the origin of the great vessels from the aorta to cervical carotid bifurcation disease to intracranial atherosclerotic stenoses. Use of a single inclusive term for all brachiocephalic atherosclerotic disease (including intracranial disease) is imprecise and misleading for discllssion of this group of conditions. Brachiocephalic atherosclerotic lesions in different locations have markedly different naturaI histories, treatment options, and therapeutic options. Among this group of diseases, cervical carotid atherosclerotic stenosis (CCAS) causes significant morbidity and monality. Cervical carotid atherosclerotic stenosis is unique in vasClIlar pathology in that the threat is of an embolic nature rather than hemodynamie. This is completely different from the threat posed by vascular disease in every other location, including the hean, legs or kidneys, for instance. Malignant versus Benign Cervical Carotid Stenosis Similar to cancerous neoplasms, there are two distinct types of cervical carotid atherosclerotic stenosis with two distinct and separate sets of symptoms and prognoses: embologenic and non-embologenie. Embologenic CCAS has distinct symptoms (recurrent episodes of neurological dysfunction, transient ischemic attacks (TIAs), Ol' reversible neurological deficits). Non-embologenic CCAS is completely asymptomatic. The prognosis for embologenic CCAS is markedly different than that for non-embologenic CCAS. Embologenic CCAS has about a 10% annual risk of major stroke, versus about 1% for non-embologenic CCAS. The radiological appearance of these two distinct conctitions, while possibly similar in many ways, can be quite differenr. Non-embologenic CCAS is most typical1y smooth in appearance on angiography, while embologenic CCAS not infrequently is ulcerated and irregular. Carotid Doppler ultrasound can differentiate types of plaque associated with ctifferent risks of distal embolization (echogenic, calcified, etc) and may be of prognostic value. Pathological examination will frequently reveal differences in appearance and quality of the two lesions. Therapeutic Options Medical Therapy Prior dogma determined that medical therapy neither significanrly affected the progression of atherosclerosis nor caused its regression. Certain environmental factors (tobacco, foods, etc.) are known to worsen atherosclerosis. Recent data indicate that certain pharmaceuticaIs can slow its progression (statins, anti-homocysteine therapies, etc). Warfarin and aspirin have been shown to have no effect on the progression of atherosclerosis. Similal' to the case of cel-rain malignant versus benign neoplasms, there are specific medical therapies that influence the prognosis of embologenic ("malignant") CCAS, but not non-embologenic ("benign") CCAS. Anti-
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• 1 of the 90 who received lA therapy was thought to have smali vessel disease as the cause of the stroke.
21. PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood pressure-lowering regimen among 6,105 individuals with previous strake or transient ischemic attack. Lancet 2001; 358:10331041.
Who Gets What? tPA Options Blood pressure, time windowand CT exclusions are strictly adhered to in aj[ of the following protocols. Specific consent forms are signed for off-labe1 use of tPA and when the stroke is severe, statistics regarding increased risk of hemorrhage are discussed with the family and patient (when possible). • lf the patient presents with a mild stroke (NIHSS 4-10) within the 3 hour window, we might elect to use IV tPA alone according to the FOA approved protoc01 of 0.9 mgm/kgm 10% bolus, the rest over one hour. (No special consent is required). • lf the patient with an NlHSS of 4 -1 Ohas aphasia or severe hemiparesis, we may e1ect to use the combined lV/lA pratocol usually reserved for more severe strokes (see next bul1et). • lf the patient has a moderate to severe stroke (NIHSS >10) within 3 hours, we administer IV tPA at 0.6mgm/kgm 15% bolus, the rest over 30 minutes and prepare to go to angiography. If the patient improves significantly, we may cancel the angiogram. lf, on angiography, we find a clot (usually lCA, T-lesion, MI, M2, or basi1ar) we use intraarterial tPA usual1y to a maximum dose of 20-25 mgm so that the total dose is approximately 0.9 mgm/kgm. • lf the patient has a moderate to severe stroke (NlHSS > 10) and presents after 3 hours but before 6 hours, we consider intra-arterial tPA a10ne, particularly if the CT head scan is negative. The dose of lA tPA will depend on a more sophisticated evaluation of how the col1aterals look on the angiogram. • Other situations in which lA alone is general1y se1ected include: post procedure (cardiac catheterization) cases, post-operative cases, patients on coumadin, very e1derly patients or patients with a remote history if intracranial hemorrhage. • If the patient is rapidly improving at 3 hours, we will hold the IV tPA and closely monitor the patient. lf deterioration occurs, the patient is taken to the angiography suite and given lA therapy if a clot is located. • If there is atotal lCA occlusion, we may push the catheter through the clot and search for a distal embolus which is often present at MI. We can then come back and angioplasty and stent the carotid Jesion. • For basilar attery occlusions and retinal artery occlusions, we may extend the 6-hour time windowo
2:50 p.m. Patient Se1ection for Interventiona1 Therapy Marilyn Reimel~ MD Mid-America Brain and Stroke Institute Saint Luke's Hospital Kansas City, MO Background The Stroke Center at Saint Luke's Hospital in Kansas City opened in 1993 with the goal of standardizing care for the large patient volume and coordinating communication among the many practitioners who are important in the management of stroke. No one had imagined routine acute intervention, and a neur010gist in the emergency roor~ was a reportable siting. Two peop1e changed the landscape. Graham Lee, MOa neurointerventional radiologist came to Kansas City from NYC because Kansas resembled the plains of Rhodesia where he grew up. Having trained with Dr. Berenstein in NYC, he had used intra-arteria1 urokinase to 1yse clots in acute stroke. His early successes in reversing strokes at Saint Luke's changed our mindset permanently. We viewed every case as a possible "save" unless proven othelwise by time or circumstance. When Tom Brott, MO al10wed the Saint Luke's team to be one of Cincinnati's contributing hospitals in the NlNOS tPA trial, we discovered "ful1 speed ahead." We became friends with EMS, bonded
with the nurses and physicians in the emergency department, and neurologists became as at home in the EO as the cardi010gists. Current Practice Since 1999, we have used tPA for intra-arterial (IA) as wel1 as intravenous (IV) 1ysis. A recent review of our interventional cases from January of 2000 tllrough June 2002 revea1ed the fol1owing data: • 142/781 08.2%) of ischemic strakes were treated with tPA • 52/142 (36%) IV; 55/142 (39%) lA; 35/142 (25%) IV folIowed by lA • Overall hospital mortality rate was 12.7% with the lowest rate in the IV group at 5.8%. • Symptomatic hemorrhage rate was 9.2% (IV = 1.9%, lA=14.6%, IV/lA=11.4%) • Patients who received lA therapy were statistical1y 01der and presented with a higher NIHSS score. • 57% (51/90) of patients who received lA therapy a10ne or in combination with IV therapy were found to have a cardiac source for the stroke.
P54
HolU This Works • The strake neurologist is the point person for these protocoJs.
• If the patient arrives in our ED, there are standing orders for stroke evaluation including the er head scan and appropriate lab. The ED physician contacts the stroke neurologist as soon as the patient arrives or before arrivaJ if we have advance notice from EMS or LifeFlighr. Stroke cases arriving by 5 hours have priority for er, ete. • If the patient presents to an out1ying ED within 3 hours, we will often work with the local physician to give 0.6 mgm/kgm IV tPA IF we have verified time of onset with the famiJy by a direct conversation over the phone. At that time we also disCllSS with the family the possibility of using IA tPA on arrival at our ED, including risks, benefits, ete. • Our ED notifies the stroke neurologist of the ETA of the ambulance/helicopter and we attempt to be present on arrival. • If the histOlY sounds as though we wili need to consider lA tPA, we page the interventional neuroradiologist and put him on alert that we may need him. He in tum notifies the angiography team. • The stroke neurologist then evaluates the patient, CT head scan, ete. and decides whether or not to activate the INR and angiography team. Concentric Catbeter Trial We are presently involved in the Phase I trial of the Concentric CIot Retrieval Catheter, which allows us to retrieve the ciot up to eight hours after symptom onset in patients ineligible for tPA. The stroke neurologist makes the decision as to which patients are recommended to this trial.
3:10 p.m. The Great Acute-Stroke Imaging Debate-Cf, CfA, MR, MRA, Perfusion: Pros and Cons jeffrey L. Sunsbine, MD University Hospitals OJ Cleveland Cleveland, OH
3:30 p.m. Future Possibilities Concerning lnterventional Stroke Therapy: Devices and Drugs Gary M. Nesbit, MD Oregon Healtb & Science University POl1land, OR
3:50 p.m. Break
4:15 p.m. Carotid Atherosclerosis: Two Different Diseases jobn j. "Buddy" Connors, Jll, MD St. josepb 's Hospital Tampa, FL
The Nature of Cervical Carotid Stenosis Brachiocephalic atherosclerotic disease encompasses \esions ranging from stenoses at the origin of the great vessels from the aorta to cervical carotid bifurcation disease to intracranial atherosclerotic stenoses. Use of a single inclusive term for all brachiocephalic atherosclerotic disease (including intracranial disease) is imprecise and misleading for discllssion of this group of conditions. Brachiocephalic atherosclerotic lesions in different locations have markedly different naturaI histories, treatment options, and therapeutic options. Among this group of diseases, cervical carotid atherosclerotic stenosis (CCAS) causes significant morbidity and monality. Cervical carotid atherosclerotic stenosis is unique in vasClIlar pathology in that the threat is of an embolic nature rather than hemodynamie. This is completely different from the threat posed by vascular disease in every other location, including the hean, legs or kidneys, for instance. Malignant versus Benign Cervical Carotid Stenosis Similar to cancerous neoplasms, there are two distinct types of cervical carotid atherosclerotic stenosis with two distinct and separate sets of symptoms and prognoses: embologenic and non-embologenie. Embologenic CCAS has distinct symptoms (recurrent episodes of neurological dysfunction, transient ischemic attacks (TIAs), Ol' reversible neurological deficits). Non-embologenic CCAS is completely asymptomatic. The prognosis for embologenic CCAS is markedly different than that for non-embologenic CCAS. Embologenic CCAS has about a 10% annual risk of major stroke, versus about 1% for non-embologenic CCAS. The radiological appearance of these two distinct conctitions, while possibly similar in many ways, can be quite differenr. Non-embologenic CCAS is most typical1y smooth in appearance on angiography, while embologenic CCAS not infrequently is ulcerated and irregular. Carotid Doppler ultrasound can differentiate types of plaque associated with ctifferent risks of distal embolization (echogenic, calcified, etc) and may be of prognostic value. Pathological examination will frequently reveal differences in appearance and quality of the two lesions. Therapeutic Options Medical Therapy Prior dogma determined that medical therapy neither significanrly affected the progression of atherosclerosis nor caused its regression. Certain environmental factors (tobacco, foods, etc.) are known to worsen atherosclerosis. Recent data indicate that certain pharmaceuticaIs can slow its progression (statins, anti-homocysteine therapies, etc). Warfarin and aspirin have been shown to have no effect on the progression of atherosclerosis. Similal' to the case of cel-rain malignant versus benign neoplasms, there are specific medical therapies that influence the prognosis of embologenic ("malignant") CCAS, but not non-embologenic ("benign") CCAS. Anti-
P55