StrokeNCT07299994
Efficacy and Safety of Intravenous Thrombolysis in Branch Atheromatous Disease
An observational study of Stroke and Thrombolysis, run by Sigmund Freud PrivatUniversitat at 8 sites in 3 countries.
Trial summary
Rationale and Relevance: Branch Atheromatous Disease (BAD) describes an atherosclerotic occlusion of one of the deep penetrating cerebral arteries, including the lenticulostriate artery (LSA), paramedian pontine artery (PPA), and anterior choroidal artery (ACHA). Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Stroke, Thrombolysis, DAPT(Dual Antiplatelet Therapy)
- Type of treatment
- Injection or infusion
- How many people
- 462 participants
- Where
- 8 sitesin 3 countries
- Study dates
- 1 Jan 2026to 31 Dec 2026
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: All patients with a BAD-related stroke, aged over 18 years, with symptom onset no more than 24 hours before admission, who were treated in one of the stroke units of the participating institutions.
Who may be able to join
- aged over 18 years, with acute ischemic stroke and symptom onset no more than 24 hours before admission, who were treated in one of the stroke units of the participating institutions.
- All enrolled patients must have undergone a cerebral MRI for inclusion:
- DWI lesion: single isolated deep subcortical stroke AND
- The affected vessel involves the LSA, PPA, or ACHA, and the infarct lesion on DWI conforms to one of the following characteristics (A, B, OR C):
- LSA: "Comma-like" infarct lesions with "fan-shaped" extension from bottom to top in the coronary position OR ≥ 3 layers (layer thickness 5 mm) on axial DWI.
- PPA: Infarct lesion extending from the deep pons to the ventral pons on axial DWI.
- ACHA: Infarct within the anterior choroidal artery territory.
Who cannot join
- Typical recent small subcortical infarction (RSSI) (oval, <20mm in all axes)
- ≥ 50% stenosis on the parent artery (i.e., BA, MCA, or ICA)
- Stroke due to other clearly identified causes or possible cardioembolic etiology.
Trial locations and contacts
8 sites in 3 countries. Contact the study team or a site near you to ask about taking part.
8 sites in 3 countries
Austria4 sites, 4 recruiting
- Recruiting
Clinic Favoriten
Vienna, State of Vienna, 1100
Christoph Kirchstetter, Dr., +431601912008, christoph.kirchstetter@gesundheitsverbund.at
- Recruiting
Clinic Hietzing
Vienna, State of Vienna, 1130
Vera Kopfer, Dr., vera.kopfer@gesundheitsverbund.at
- Recruiting
Department of Neurology, St. John's Hospital, Vienna, Austria
Vienna, 1020
Julian Frederic Hotz, DDr., +43 1 211210, julian.hotz@meduniwien.ac.at
Marek Sykora, Prof. Dr., +43 1 211210, marek.sykora@bbwien.at
- Recruiting
Department of Neurology, Medical University of Vienna
Vienna, 1090
Stefan Greisenegger, Prof. Dr., +43 1 404000, stefan.greisenegger@meduniwien.ac.at
Germany3 sites, 3 recruiting
- Not yet recruiting
Department of Neurology, Berlin Institute of Health, Charité-Universitätsmedizin Berlin
Berlin, 12200
Christian Nolte, Prof. Dr., +49 30 450 560 676, christian.nolte@charite.de
- Recruiting
Department of Neurology, Heidelberg University Hospital
Heidelberg, 69120
Jan Purrucker, Prof. Dr., 00496221560, jan.purrucker@med.uni-heidelberg.de
- Recruiting
Department of Neurology & Stroke, University of Tübingen
Tübingen, 72076
Sven Poli, Prof. Dr., 00497071290, sven.poli@uni-tuebingen.de
Switzerland1 site, 1 recruiting
- Not yet recruiting
Department of Neurology, Universityhospital of Bern
Bern, 3010
Julian Frederic Hotz, DDr., 0041316320648, julian.hotz@insel.ch
About this study
Official title: Efficacy and Safety of Intravenous Thrombolysis in Branch Atheromatous Disease - a Retrospective Data Analysis
Rationale and Relevance:
Branch Atheromatous Disease (BAD) describes an atherosclerotic occlusion of one of the deep penetrating cerebral arteries, including the lenticulostriate artery (LSA), paramedian pontine artery (PPA), and anterior choroidal artery (ACHA). BAD is frequently associated with early neurological deterioration (END), particularly progressive motor deficits that contribute to increased disability. Despite its clinical relevance, BAD remains underrepresented in major radiomorphological classification systems such as TOAST, which has led to limited evidence and unclear treatment strategies. Previous studies suggest that the efficacy of intravenous thrombolysis (IVT) may be reduced in BAD compared to other stroke etiologies.
Read more
Objectives:
The primary objective of this study is to evaluate the efficacy and safety of IVT compared with single antiplatelet therapy (SAPT) and dual antiplatelet therapy (DAPT) in patients with BAD-related stroke. A secondary objective is to examine the impact of acute-phase blood pressure fluctuations on END and functional neurological outcomes.
Design and Methods:
This international multicenter study will be conducted retrospectively according to the STROBE guidelines. Eligible patients include those with BAD-related stroke treated at one of the participating centers between 2010 and 2025. Inclusion criteria comprise characteristic diffusion-weighted MRI patterns in predefined vascular territories (LSA, PPA, ACHA) and a symptom onset ≤24 hours before admission. Patients with typical lacunar infarcts or with other identified stroke etiologies will be excluded.
Endpoints:
Primary endpoints include functional outcome at three months, defined as a favorable outcome with a modified Rankin Scale score of 0-1; occurrence of END, defined as a ≥4-point worsening on the NIHSS within 24-48 hours; and symptomatic intracerebral hemorrhage. Collected data include clinical, imaging, and therapeutic variables, as well as blood pressure trajectories and pre-stroke treatments (as detailed in the study protocol).
Statistical Analysis:
Analyses will be performed using SPSS and R. Descriptive statistics, univariate analyses, and multivariable models (IPTW and Poisson regression) will be applied. Results will be reported as adjusted relative risks with 95% confidence intervals.
Significance:
This study will provide the first comprehensive evaluation of IVT versus SAPT/DAPT in BAD-related stroke, and will investigate the clinical impact of blood pressure changes in this specific stroke subtype. The findings aim to support evidence-based treatment recommendations for a currently underrecognized and poorly understood stroke etiology.
Read the detailed description
Intracranial branch atheromatous disease (BAD )describes an occlusion of deep penetrating intracranial arteries, leading to subcortical infarction. These perforators include the lenticulostriate arteries (LSA), paramedian pontine arteries (PPA), anterior choroidal artery (ACHA), thalamoperforating arteries, and Heubner's artery. This study specifically focuses on BAD affecting the LSA, PPA, and ACHA territories.
Unlike classical lacunar infarction, which is typically attributed to lipohyalinotic degeneration or fibrinoid necrosis of small distal perforators (<200 µm), BAD involves more proximal and larger perforating arteries (approximately 700-800 µm in diameter). The underlying pathophysiology is thought to be predominantly atherosclerotic plaque involvement at or near the origin of the perforating artery from a parent vessel, resulting in progressive luminal narrowing, branch occlusion, or flow impairment. This distinguishes BAD from traditional small vessel disease and places it within a spectrum of intracranial atherosclerotic disease.
Despite its distinct vascular mechanism, BAD is not formally classified as a separate etiological subtype in major stroke classification systems such as TOAST or NINDS criteria. As a result, cases are often categorized under "small vessel occlusion" or "stroke of undetermined etiology," contributing to under-recognition and limited systematic evidence regarding optimal management strategies.
Clinically, BAD may initially present similarly to lacunar stroke syndromes, particularly pure motor or sensorimotor deficits. However, a main feature is early neurological deterioration (END), typically occurring within the first 24-48 hours after onset. END is characterized by stepwise or progressive worsening of neurological deficits, most commonly motor impairment, which is thought to reflect ongoing ischemia due to dynamic thrombo-atherosclerotic processes, hemodynamic instability, or progressive perforator occlusion. This clinical course is associated with worse functional outcomes and higher rates of long-term disability compared with stable lacunar infarcts.
From a therapeutic perspective, optimal acute management of BAD remains uncertain. Intravenous thrombolysis (IVT), while standard for acute ischemic stroke within the therapeutic window, appears to yield less consistent benefit in BAD compared to other stroke subtypes.
Given these uncertainties, this study aims to evaluate real-world treatment effectiveness of IVT compared with antiplatelet-based strategies in patients with imaging-confirmed BAD. In addition, the study investigates the potential role of early hemodynamic variability, particularly blood pressure fluctuations, as a modifiable factor influencing END and functional outcome.
This is an international, multicenter, retrospective observational cohort study conducted according to STROBE guidelines. Participating stroke centers contribute consecutively treated patients meeting predefined radiological and clinical criteria over a 15-year period. All included patients underwent standardized neuroimaging with MRI, allowing for consistent identification of infarct topography and exclusion of alternative stroke mechanisms.
Clinical data, imaging findings, acute treatment strategies, blood pressure profiles, and outcome measures are extracted from institutional stroke databases and anonymized prior to central analysis. Comparative effectiveness analyses will be performed to assess differences between treatment groups, with adjustment for baseline imbalances using appropriate statistical methods, including propensity score-based approaches.
Overall, this study seeks to address a gap in stroke literature by providing multicenter evidence on the comparative effectiveness of intravenous thrombolysis versus antiplatelet strategies in BAD, while simultaneously clarifying the prognostic significance of early hemodynamic changes in this under-recognized stroke subtype.
- Conditions
- Stroke, Thrombolysis, DAPT(Dual Antiplatelet Therapy), SAPT(Single Antiplatelet Therapy), Acute Ischemic Stroke
- Keywords
- Acute ischemic Stroke, Branch Atheromatous Disease, Thrombolysis, DAPT, SAPT
- Medical subject headings
- Stroke, Ischemic Stroke
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| IVT group | Patients who received intravenous thrombolysis as part of acute stroke treatment, if eligible. | |
| Antiplatelet group | Patients who received SAPT or DAPT as part of acute stroke treatment. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Favorable outcome (mRS 0-1) at three months.
Modified Rankin Scale (mRS) score at three months, with a favorable outcome defined as mRS 0-1 at three months.
Measured: Three months after acute ischemic stroke treatment
Early neurological deterioration within 24-48 hours after symptom onset
Early neurological deterioration (END), defined as a worsening of the NIHSS score by ≥4 points within 24-48 hours after symptom onset.
Measured: within 24-48 hours after acute ischemic stroke onset
Occurrence of symptomatic intracerebral hemorrhage.
Occurrence of symptomatic intracerebral hemorrhage within three months after acute ischemic stroke treatment.
Measured: within three months after acute ischemic stroke treatment.
Secondary outcomes (1)
Good functional outcome (mRS 0-2)
Modified Rankin Scale (mRS) score at three months, with a good outcome defined as mRS 0-2 at three months.
Measured: three months after acute ischemic stroke treatment.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted23 Dec 2025
- Study start1 Jan 2026
- Primary completion31 Dec 2026 (estimated)
- Study completion31 Dec 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (16)Papers the sponsor has linked to this study.
- Other trials for StrokeStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Retrospective
- Enrolment
- 462 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Sigmund Freud PrivatUniversitat
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Julian Frederic Hotz, DDr., Principal investigator, 1. Department of Neurology, St. John's Hospital, Vienna, Austria, 2. Department of Neurology, University Hospital, Bern, Switzerland, 3. Department of Medicine I, Division of Infectious Diseases and Tropical Medicine, Medical University of Vienna, ViennaMarek Sykora, Prof. Dr., Principal investigator, 1. Sigmund Freud University Vienna, Austria, 2. Department of Neurology, St. John's Hospital, Vienna, Austria
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07299994
- Sponsor's protocol ID
- 17823177
- Status last verified
- Dec 2025
- First submitted
- 10 Dec 2025
- Last updated
- 16 Jul 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Yes: Individual participant data that underlie the results after deidentification
Publications
Naimi AI, Whitcomb BW. Estimating Risk Ratios and Risk Differences Using Regression. Am J Epidemiol. 2020 Jun 1;189(6):508-510. doi: 10.1093/aje/kwaa044. No abstract available.
PubMed 32219364Barow E, Boutitie F, Cheng B, Cho TH, Ebinger M, Endres M, Fiebach JB, Fiehler J, Ford I, Galinovic I, Nickel A, Puig J, Roy P, Wouters A, Magnus T, Thijs V, Lemmens R, Muir KW, Nighoghossian N, Pedraza S, Simonsen CZ, Gerloff C, Thomalla G; WAKE-UP Investigators. Functional Outcome of Intravenous Thrombolysis in Patients With Lacunar Infarcts in the WAKE-UP Trial. JAMA Neurol. 2019 Jun 1;76(6):641-649. doi: 10.1001/jamaneurol.2019.0351.
PubMed 30907934Xu J, Xu X, Wang H, He L, Liu Q, Du Y, Wang J. Dual Antiplatelet Therapy Plus Argatroban Prevents Early Neurological Deterioration in Branch Atherosclerosis Disease. Stroke. 2022 Jan;53(1):e19-e20. doi: 10.1161/STROKEAHA.121.036356. Epub 2021 Nov 17.
PubMed 34784740Liu B, Zhang H, Wang R, Qu H, Sun Y, Zhang W, Zhang S. Early administration of tirofiban after urokinase-mediated intravenous thrombolysis reduces early neurological deterioration in patients with branch atheromatous disease. J Int Med Res. 2020 May;48(5):300060520926298. doi: 10.1177/0300060520926298.
PubMed 32459110Wu X, Liu Y, Nie C, Kang Z, Wang Q, Sun D, Li H, Liu Y, Mei B. Efficacy and Safety of Intravenous Thrombolysis on Acute Branch Atheromatous Disease: A Retrospective Case-Control Study. Front Neurol. 2020 Jul 7;11:581. doi: 10.3389/fneur.2020.00581. eCollection 2020.
PubMed 32733357Kobayashi Y, Kondo Y, Yamamoto K, Hirayama S, Kuasano Y, Tazawa KI, Shimizu Y, Sato A, Sekijima Y. Tissue plasminogen activator for acute branch atheromatous disease exhibits transient improvement and worsening. J Neurol Sci. 2024 Oct 15;465:123201. doi: 10.1016/j.jns.2024.123201. Epub 2024 Aug 30.
PubMed 39217764Yamamoto Y, Ohara T, Hamanaka M, Hosomi A, Tamura A, Akiguchi I. Characteristics of intracranial branch atheromatous disease and its association with progressive motor deficits. J Neurol Sci. 2011 May 15;304(1-2):78-82. doi: 10.1016/j.jns.2011.02.006. Epub 2011 Mar 13.
PubMed 21402390Duan Z, Fu C, Chen B, Xu G, Tao L, Tang T, Hou H, Fu X, Yang M, Liu Z, Zhang X. Lesion patterns of single small subcortical infarct and its association with early neurological deterioration. Neurol Sci. 2015 Oct;36(10):1851-7. doi: 10.1007/s10072-015-2267-1. Epub 2015 Jun 2.
PubMed 26032577Park MG, Oh EH, Kim BK, Park KP. Intravenous tissue plasminogen activator in acute branch atheromatous disease: Does it prevent early neurological deterioration? J Clin Neurosci. 2016 Nov;33:194-197. doi: 10.1016/j.jocn.2016.04.011. Epub 2016 Jul 21.
PubMed 27452127Nakase T, Yoshioka S, Sasaki M, Suzuki A. Clinical evaluation of lacunar infarction and branch atheromatous disease. J Stroke Cerebrovasc Dis. 2013 May;22(4):406-12. doi: 10.1016/j.jstrokecerebrovasdis.2011.10.005. Epub 2011 Nov 30.
PubMed 22133744Uchiyama S, Toyoda K, Kitagawa K, Okada Y, Ameriso S, Mundl H, Berkowitz S, Yamada T, Liu YY, Hart RG; NAVIGATE ESUS Investigators. Branch atheromatous disease diagnosed as embolic stroke of undetermined source: A sub-analysis of NAVIGATE ESUS. Int J Stroke. 2019 Dec;14(9):915-922. doi: 10.1177/1747493019852177. Epub 2019 May 27.
PubMed 31132967Adams HP Jr, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh EE 3rd. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke. 1993 Jan;24(1):35-41. doi: 10.1161/01.str.24.1.35.
PubMed 7678184Zhou L, Yao M, Peng B, Zhu Y, Ni J, Cui L. Atherosclerosis Might Be Responsible for Branch Artery Disease: Evidence From White Matter Hyperintensity Burden in Acute Isolated Pontine Infarction. Front Neurol. 2018 Oct 9;9:840. doi: 10.3389/fneur.2018.00840. eCollection 2018.
PubMed 30356780Kwan MW, Mak W, Cheung RT, Ho SL. Ischemic stroke related to intracranial branch atheromatous disease and comparison with large and small artery diseases. J Neurol Sci. 2011 Apr 15;303(1-2):80-4. doi: 10.1016/j.jns.2011.01.008. Epub 2011 Feb 1.
PubMed 21277587Petrone L, Nannoni S, Del Bene A, Palumbo V, Inzitari D. Branch Atheromatous Disease: A Clinically Meaningful, Yet Unproven Concept. Cerebrovasc Dis. 2016;41(1-2):87-95. doi: 10.1159/000442577. Epub 2015 Dec 16.
PubMed 26671513
Study at a glance
From the registry record, last updated by the sponsor on 16 Jul 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Efficacy and Safety of Intravenous Thrombolysis in Branch Atheromatous Disease - a Retrospective Data Analysis
- ClinicalTrials.gov ID
- NCT07299994
- Acronym / sponsor ID
- 17823177
- Conditions
- Stroke, Thrombolysis, DAPT(Dual Antiplatelet Therapy), SAPT(Single Antiplatelet Therapy), Acute Ischemic Stroke
- Keywords
- Acute ischemic Stroke, Branch Atheromatous Disease, Thrombolysis, DAPT, SAPT
- Study type
- Observational
- Recruitment status
- Recruiting
- Enrolment
- 462 participants (estimated)
- Lead sponsor
- Sigmund Freud PrivatUniversitatUniversity, hospital or other
- Study start
- 1 Jan 2026 (actual)
- Primary completion
- 31 Dec 2026 (estimated)
- Study completion
- 31 Dec 2026 (estimated)
- First posted
- 23 Dec 2025 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Rationale and Relevance:
Branch Atheromatous Disease (BAD) describes an atherosclerotic occlusion of one of the deep penetrating cerebral arteries, including the lenticulostriate artery (LSA), paramedian pontine artery (PPA), and anterior choroidal artery (ACHA). BAD is frequently associated with early neurological deterioration (END), particularly progressive motor deficits that contribute to increased disability. Despite its clinical relevance, BAD remains underrepresented in major radiomorphological classification systems such as TOAST, which has led to limited evidence and unclear treatment strategies. Previous studies suggest that the efficacy of intravenous thrombolysis (IVT) may be reduced in BAD compared to other stroke etiologies.
Objectives:
The primary objective of this study is to evaluate the efficacy and safety of IVT compared with single antiplatelet therapy (SAPT) and dual antiplatelet therapy (DAPT) in patients with BAD-related stroke. A secondary objective is to examine the impact of acute-phase blood pressure fluctuations on END and functional neurological outcomes.
Design and Methods:
This international multicenter study will be conducted retrospectively according to the STROBE guidelines. Eligible patients include those with BAD-related stroke treated at one of the participating centers between 2010 and 2025. Inclusion criteria comprise characteristic diffusion-weighted MRI patterns in predefined vascular territories (LSA, PPA, ACHA) and a symptom onset ≤24 hours before admission. Patients with typical lacunar infarcts or with other identified stroke etiologies will be excluded.
Endpoints:
Primary endpoints include functional outcome at three months, defined as a favorable outcome with a modified Rankin Scale score of 0-1; occurrence of END, defined as a ≥4-point worsening on the NIHSS within 24-48 hours; and symptomatic intracerebral hemorrhage. Collected data include clinical, imaging, and therapeutic variables, as well as blood pressure trajectories and pre-stroke treatments (as detailed in the study protocol).
Statistical Analysis:
Analyses will be performed using SPSS and R. Descriptive statistics, univariate analyses, and multivariable models (IPTW and Poisson regression) will be applied. Results will be reported as adjusted relative risks with 95% confidence intervals.
Significance:
This study will provide the first comprehensive evaluation of IVT versus SAPT/DAPT in BAD-related stroke, and will investigate the clinical impact of blood pressure changes in this specific stroke subtype. The findings aim to support evidence-based treatment recommendations for a currently underrecognized and poorly understood stroke etiology.
Detailed description
Intracranial branch atheromatous disease (BAD )describes an occlusion of deep penetrating intracranial arteries, leading to subcortical infarction. These perforators include the lenticulostriate arteries (LSA), paramedian pontine arteries (PPA), anterior choroidal artery (ACHA), thalamoperforating arteries, and Heubner's artery. This study specifically focuses on BAD affecting the LSA, PPA, and ACHA territories.
Unlike classical lacunar infarction, which is typically attributed to lipohyalinotic degeneration or fibrinoid necrosis of small distal perforators (<200 µm), BAD involves more proximal and larger perforating arteries (approximately 700-800 µm in diameter). The underlying pathophysiology is thought to be predominantly atherosclerotic plaque involvement at or near the origin of the perforating artery from a parent vessel, resulting in progressive luminal narrowing, branch occlusion, or flow impairment. This distinguishes BAD from traditional small vessel disease and places it within a spectrum of intracranial atherosclerotic disease.
Despite its distinct vascular mechanism, BAD is not formally classified as a separate etiological subtype in major stroke classification systems such as TOAST or NINDS criteria. As a result, cases are often categorized under "small vessel occlusion" or "stroke of undetermined etiology," contributing to under-recognition and limited systematic evidence regarding optimal management strategies.
Clinically, BAD may initially present similarly to lacunar stroke syndromes, particularly pure motor or sensorimotor deficits. However, a main feature is early neurological deterioration (END), typically occurring within the first 24-48 hours after onset. END is characterized by stepwise or progressive worsening of neurological deficits, most commonly motor impairment, which is thought to reflect ongoing ischemia due to dynamic thrombo-atherosclerotic processes, hemodynamic instability, or progressive perforator occlusion. This clinical course is associated with worse functional outcomes and higher rates of long-term disability compared with stable lacunar infarcts.
From a therapeutic perspective, optimal acute management of BAD remains uncertain. Intravenous thrombolysis (IVT), while standard for acute ischemic stroke within the therapeutic window, appears to yield less consistent benefit in BAD compared to other stroke subtypes.
Given these uncertainties, this study aims to evaluate real-world treatment effectiveness of IVT compared with antiplatelet-based strategies in patients with imaging-confirmed BAD. In addition, the study investigates the potential role of early hemodynamic variability, particularly blood pressure fluctuations, as a modifiable factor influencing END and functional outcome.
This is an international, multicenter, retrospective observational cohort study conducted according to STROBE guidelines. Participating stroke centers contribute consecutively treated patients meeting predefined radiological and clinical criteria over a 15-year period. All included patients underwent standardized neuroimaging with MRI, allowing for consistent identification of infarct topography and exclusion of alternative stroke mechanisms.
Clinical data, imaging findings, acute treatment strategies, blood pressure profiles, and outcome measures are extracted from institutional stroke databases and anonymized prior to central analysis. Comparative effectiveness analyses will be performed to assess differences between treatment groups, with adjustment for baseline imbalances using appropriate statistical methods, including propensity score-based approaches.
Overall, this study seeks to address a gap in stroke literature by providing multicenter evidence on the comparative effectiveness of intravenous thrombolysis versus antiplatelet strategies in BAD, while simultaneously clarifying the prognostic significance of early hemodynamic changes in this under-recognized stroke subtype.
Study design
- Observational model
- Cohort
- Time perspective
- Retrospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| IVT group | – | –Patients who received intravenous thrombolysis as part of acute stroke treatment, if eligible. |
| Antiplatelet group | – | –Patients who received SAPT or DAPT as part of acute stroke treatment. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- All patients with a BAD-related stroke, aged over 18 years, with symptom onset no more than 24 hours before admission, who were treated in one of the stroke units of the participating institutions.
Key inclusion criteria (7 listed)
- aged over 18 years, with acute ischemic stroke and symptom onset no more than 24 hours before admission, who were treated in one of the stroke units of the participating institutions.
- All enrolled patients must have undergone a cerebral MRI for inclusion:
- LSA: "Comma-like" infarct lesions with "fan-shaped" extension from bottom to top in the coronary position OR ≥ 3 layers (layer thickness 5 mm) on axial DWI.
- PPA: Infarct lesion extending from the deep pons to the ventral pons on axial DWI.
- ACHA: Infarct within the anterior choroidal artery territory.
Key exclusion criteria (3 listed)
- Typical recent small subcortical infarction (RSSI) (oval, <20mm in all axes)
- ≥ 50% stenosis on the parent artery (i.e., BA, MCA, or ICA)
- Stroke due to other clearly identified causes or possible cardioembolic etiology.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Favorable outcome (mRS 0-1) at three months.
Time frame: Three months after acute ischemic stroke treatment
Modified Rankin Scale (mRS) score at three months, with a favorable outcome defined as mRS 0-1 at three months.
Early neurological deterioration within 24-48 hours after symptom onset
Time frame: within 24-48 hours after acute ischemic stroke onset
Early neurological deterioration (END), defined as a worsening of the NIHSS score by ≥4 points within 24-48 hours after symptom onset.
Occurrence of symptomatic intracerebral hemorrhage.
Time frame: within three months after acute ischemic stroke treatment.
Occurrence of symptomatic intracerebral hemorrhage within three months after acute ischemic stroke treatment.
1 secondary outcome
Good functional outcome (mRS 0-2)
Time frame: three months after acute ischemic stroke treatment.
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 16 Jul 2026.
- Background: PubMed 32219364Naimi AI, Whitcomb BW. Estimating Risk Ratios and Risk Differences Using Regression. Am J Epidemiol. 2020 Jun 1;189(6):508-510. doi: 10.1093/aje/kwaa044. No abstract available.
- Background: PubMed 30907934Barow E, Boutitie F, Cheng B, Cho TH, Ebinger M, Endres M, Fiebach JB, Fiehler J, Ford I, Galinovic I, Nickel A, Puig J, Roy P, Wouters A, Magnus T, Thijs V, Lemmens R, Muir KW, Nighoghossian N, Pedraza S, Simonsen CZ, Gerloff C, Thomalla G; WAKE-UP Investigators. Functional Outcome of Intravenous Thrombolysis in Patients With Lacunar Infarcts in the WAKE-UP Trial. JAMA Neurol. 2019 Jun 1;76(6):641-649. doi: 10.1001/jamaneurol.2019.0351.
- Background: PubMed 34784740Xu J, Xu X, Wang H, He L, Liu Q, Du Y, Wang J. Dual Antiplatelet Therapy Plus Argatroban Prevents Early Neurological Deterioration in Branch Atherosclerosis Disease. Stroke. 2022 Jan;53(1):e19-e20. doi: 10.1161/STROKEAHA.121.036356. Epub 2021 Nov 17.
- Background: PubMed 32459110Liu B, Zhang H, Wang R, Qu H, Sun Y, Zhang W, Zhang S. Early administration of tirofiban after urokinase-mediated intravenous thrombolysis reduces early neurological deterioration in patients with branch atheromatous disease. J Int Med Res. 2020 May;48(5):300060520926298. doi: 10.1177/0300060520926298.
- Background: PubMed 32733357Wu X, Liu Y, Nie C, Kang Z, Wang Q, Sun D, Li H, Liu Y, Mei B. Efficacy and Safety of Intravenous Thrombolysis on Acute Branch Atheromatous Disease: A Retrospective Case-Control Study. Front Neurol. 2020 Jul 7;11:581. doi: 10.3389/fneur.2020.00581. eCollection 2020.
- Background: PubMed 39217764Kobayashi Y, Kondo Y, Yamamoto K, Hirayama S, Kuasano Y, Tazawa KI, Shimizu Y, Sato A, Sekijima Y. Tissue plasminogen activator for acute branch atheromatous disease exhibits transient improvement and worsening. J Neurol Sci. 2024 Oct 15;465:123201. doi: 10.1016/j.jns.2024.123201. Epub 2024 Aug 30.
- Background: PubMed 21402390Yamamoto Y, Ohara T, Hamanaka M, Hosomi A, Tamura A, Akiguchi I. Characteristics of intracranial branch atheromatous disease and its association with progressive motor deficits. J Neurol Sci. 2011 May 15;304(1-2):78-82. doi: 10.1016/j.jns.2011.02.006. Epub 2011 Mar 13.
- Background: PubMed 26032577Duan Z, Fu C, Chen B, Xu G, Tao L, Tang T, Hou H, Fu X, Yang M, Liu Z, Zhang X. Lesion patterns of single small subcortical infarct and its association with early neurological deterioration. Neurol Sci. 2015 Oct;36(10):1851-7. doi: 10.1007/s10072-015-2267-1. Epub 2015 Jun 2.
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- Individual participant dataSharing planned: Yes. Individual participant data that underlie the results after deidentification
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Julian Frederic Hotz, DDr. principal investigator
1. Department of Neurology, St. John's Hospital, Vienna, Austria, 2. Department of Neurology, University Hospital, Bern, Switzerland, 3. Department of Medicine I, Division of Infectious Diseases and Tropical Medicine, Medical University of Vienna, Vienna
Marek Sykora, Prof. Dr. principal investigator
1. Sigmund Freud University Vienna, Austria, 2. Department of Neurology, St. John's Hospital, Vienna, Austria
8 sites in 3 countries: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Stroke and Thrombolysis, run by Sigmund Freud PrivatUniversitat at 8 sites in 3 countries.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 7 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: looking for participants now, as of the sponsor's last update on 16 Jul 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 8 sites in Austria, Germany, Switzerland. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Julian Frederic Hotz, DDr. (+43 1 211210, julian.hotz@meduniwien.ac.at), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Favorable outcome (mRS 0-1) at three months. (time frame: Three months after acute ischemic stroke treatment). The study lists 3 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT07299994, which also lists 16 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 16 Jul 2026.