Risk factors and differential prevention of in-hospital hemorrhagic stroke

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BACKGROUND

In-hospital mortality is a key indicator of medical care quality and reflects the overall performance of inpatient treatment. In 2020, the Russian Federation’s hospitalization rate was 169.7 ± 21.3 cases per 1,000 population. During this period, 780,900 deaths occurred in hospitals, resulting in an overall in-hospital mortality rate of 3.14% across all bed profiles [1]. Cardiovascular diseases are among the leading causes of in-hospital mortality [2].

According Unified Interdepartmental Information and Statistical System data (as of January 2025),¹ acute cerebrovascular events have the highest mortality rate among major causes of death in the Russian Federation at 15.8%, compared to 9.8% for acute myocardial infarction. In-hospital mortality associated with acute cerebrovascular events in the Russian Federation remains high, and mortality due to hemorrhagic stroke may reach 50%.²

Death from hemorrhagic stroke more often results from direct brain injury (68.9% of cases) than from extracerebral complications (31.1%) [1]. In the Russian Federation, approximately 43,000 individuals are diagnosed with hemorrhagic stroke annually, with a fatal outcome occurring in up to 50% of cases.³ Russian and international scientific data lack systematized information on the incidence and outcomes of hemorrhagic stroke developing during inpatient treatment.

Recently, increasing attention has focused on the pathogenesis, prevention, and treatment of in-hospital ischemic stroke, including the broader use of systemic thrombolytic therapy and endovascular interventions [3]. As with community-acquired strokes, most in-hospital cerebrovascular events are ischemic. Research prioritizes in-hospital ischemic stroke because of its significant prevalence and its potential for improving healthcare delivery systems.

Despite a higher case fatality rate, the low prevalence of hemorrhagic stroke leads to an underestimation of its impact on overall in-hospital mortality.

Aim

To identify the clinical characteristics and risk factors for in-patient hemorrhagic stroke to develop more effective preventive measures and decrease hospital-acquired stroke.

METHODS

This review included retrospective and prospective studies and systematic reviews describing the clinical course and risk factors of hemorrhagic stroke. Data were obtained from databases including MedLine, PubMed, Google Scholar, Scopus, and eLibrary. The search strategy was based on the following key terms: внутригоспитальный геморрагический инсульт (in-hospital hemorrhagic stroke), внутрибольничная летальность (in-hospital mortality), and внутригоспитальный ишемический инсульт (in-hospital ischemic stroke). The most-cited articles were selected, and the reference lists of all included articles and relevant systematic reviews were manually screened.

Epidemiology of in-hospital hemorrhagic stroke

Currently, there is no established definition of in-hospital hemorrhagic stroke in either Russian or international scientific data. However, based on the existing definition of hemorrhagic stroke⁴ and by analogy with in-hospital ischemic stroke, in-hospital hemorrhagic stroke is a subtype of acute cerebrovascular event encompassing all forms of nontraumatic intracranial hemorrhage (e.g., subarachnoid hemorrhage) that develop in patients undergoing inpatient diagnostic evaluation or treatment for another condition or in those hospitalized for a diagnostic or therapeutic procedure. Perioperative stroke, which is a subset of in-hospital acute cerebrovascular events, is defined as any embolic, thrombotic, or hemorrhagic cerebrovascular event occurring during surgery or within 30 days postoperatively that results in motor, sensory, or cognitive dysfunction lasting at least 24 hours. Similar to other acute cerebrovascular events, the majority of perioperative strokes are ischemic rather than hemorrhagic [4]. Thus, perioperative hemorrhagic and perioperative ischemic strokes can occur either inpatient or outpatient (i.e., occurring within 30 days of hospital discharge).

The statistical surveillance of in-hospital stroke remains challenging. For the purposes of simplifying statistical reporting, strokes developing more than 24 hours after hospital admission are commonly classified as in-hospital events [5]. In estimating in-hospital ischemic stroke incidence, inaccuracies may occur, leading to under- or overestimation of the actual figures. This is attributable to several factors:

• Underestimation: Ischemic strokes that develop outside the hospital may be diagnosed with delay and erroneously classified as in-hospital.
• Overestimation: Clinicians may overdiagnose ischemic stroke in the absence of sufficient evidence.
• Overestimation: Incorrect interpretation of neuroimaging findings (e.g., CT or MRI) may result in an erroneous diagnosis of ischemic stroke.

That is, the registration of in-hospital ischemic stroke is prone to distortion due to difficulties in differentiating between community-acquired and in-hospital cases and potential diagnostic and interpretative errors. In addition, ischemic stroke is often recorded as the presumed cause of death. However, definitive confirmation or exclusion of acute ischemic brain changes is possible only with postmortem pathological examination [5].

Statistical accounting of in-hospital hemorrhagic stroke is more straightforward, owing to its overt clinical presentation, severe neurological deficits, and the high sensitivity of non-contrast CT for detecting hyperacute intracranial hemorrhage. Although errors in estimating in-hospital hemorrhagic stroke incidence are also possible, their likelihood is substantially lower than that observed for in-hospital ischemic stroke.

Russian stroke registries generally include cases identified in hospitals, whether admitted by emergency services or self-referred; however, differentiation between community-acquired and in-hospital stroke is often not performed, which may affect the morbidity pattern [6]. Although the incidence of in-hospital ischemic strokes in the Russian Federation can be estimated using data from international registries and modeling approaches, the epidemiology of in-hospital hemorrhagic stroke remains largely unexplored [7].

Risk factors. The 2022 Russian clinical guidelines for hemorrhagic stroke⁵ describe its primary and secondary forms and outline common and specific risk factors contributing to its development. In contrast to out-of-hospital hemorrhagic stroke, in-hospital hemorrhagic stroke is influenced by unique risk factors: high-technology medical care, new or modified pharmacotherapy, and the decompensation of concomitant somatic diseases (Table 1).

 

Table 1. Risk factors for in-hospital hemorrhagic stroke

I. General	II. Specific	III. Unique
Long-standing hypertension, often accompanied by intracranial atherosclerosis	1) Cerebrovascular conditions: aneurysms, arteriovenous malformations, and dural arteriovenous fistulas 2) Cerebral venous sinus and cortical vein thrombosis 3) Vasculopathies 4) Moyamoya disease 5) Hemorrhage into a tumor 6) Hemorrhagic transformation of cerebral infarction 7) Infectious diseases involving the brain 8) Eclampsia	Associated with medical interventions and/ or pharmacotherapy 1) Endovascular surgical interventions on the head and neck vessels 2) Systemic thrombolytic therapy 3) Antithrombotic therapy Associated with somatic condition 1) Hypertension: drug-induced and/or surgery-induced 2) Drug-induced thrombocytopenia or thrombocytopenia (hereditary or acquired) pharmacologically compromised by antithrombotic agents

 

Common risk factors most frequently lead to out-of-hospital hemorrhagic stroke, primarily due to poor patient adherence, physiological adaptation to persistently increased arterial blood pressure, and delayed medical care. Although hypertensive (primary) in-hospital hemorrhagic stroke is the most common variant, it is more amenable to primary prevention than other forms. The Russian healthcare system has successfully implemented prevention strategies for patients with these vascular risk factors.^6,7 Moreover, hemodynamic parameter correction in patients with hypertension during hospitalization is more rapid and effective.

Specific risk factors for hemorrhagic stroke are associated with the condition of the brain and/or cerebral vessels. The prevalence of conditions leading to secondary hemorrhagic stroke is comparable between hospitalized and nonhospitalized patients. These specific risk factors are well studied and largely preventable (Table 1). The findings were based on expanded screening and assessment of the impact of diseases and their complications on the risk of hemorrhagic stroke. In-hospital hemorrhagic stroke may be caused by previously undiagnosed or uncorrected specific risk factors; in these cases, additional risk factors contribute minimally.

The pathogenesis of in-hospital hemorrhagic stroke involves unique risk factors associated with endovascular surgical interventions on head and neck vessels, systemic thrombolytic and antithrombotic therapy, and somatic conditions that increase the risk of hemorrhagic complications during in-hospital procedures and pharmacotherapy. These risk factors are uncommon in out-of-hospital hemorrhagic stroke and are often underestimated in clinical practice. Moreover, the risk of in-hospital hemorrhagic stroke related to medical interventions can be minimized. In-hospital hemorrhagic stroke prevention includes correcting general and specific risk factors and managing unique risk factors through expanded diagnostic screening. Prevention strategies for in-hospital hemorrhagic stroke is classified into standard prevention (based on existing standards of medical care and clinical guidelines) and differentiated prevention (initiated in specific clinical situations). Notably, standard preventive measures for in-hospital hemorrhagic stroke may be insufficient in patients with unique risk factors. Thus, differentiated prevention is a promising approach for reducing disability and in-hospital mortality.

1. In-hospital hemorrhagic stroke as a complication of systemic thrombolytic therapy and endovascular interventions on the head and neck vessels: In acute vascular emergencies such as ischemic stroke, acute coronary syndrome, and pulmonary embolism, systemic thrombolytic therapy and endovascular procedures on the head and neck vessels are crucial in emergency care. Systemic thrombolytic therapy for myocardial infarction is associated with hemorrhagic complications, including hemorrhagic stroke in 0.4%–0.7% of cases [8]. Systemic thrombolytic therapy for ischemic stroke involves an approximately 6% risk of symptomatic hemorrhagic transformation of cerebral infarction [9]. Additionally, endovascular interventions on the head and neck vessels are associated with a high risk of hemorrhagic stroke. In the SWIFT and TREVO2 stent retriever trials, the reported incidence of hemorrhagic stroke was 2% and 7%, respectively [10, 11]. In studies evaluating bridging therapy for ischemic stroke (systemic thrombolysis followed by endovascular intervention), the incidence of hemorrhagic stroke ranged from 3% to 7% [12–14].
2. In-hospital hemorrhagic stroke as a complication of antithrombotic therapy: The expanding use of anticoagulants to prevent thromboembolic complications related to atrial fibrillation substantially contributes to the increasing incidence of drug-associated hemorrhagic stroke. In addition, the use of dual antithrombotic therapy is a crucial factor.

Long-term outpatient antithrombotic therapy is less likely to cause complications due to the establishment of a stable balance between physiological systems and the pharmacological effects of the drug. This contrasts with clinical situations wherein antithrombotic therapy is initiated for a newly diagnosed condition or when an existing antithrombotic regimen is modified. These factors disrupt the established balance, requiring the physician to carefully weigh the pros and cons of antithrombotic therapy in terms of efficacy and safety.

Pharmacotherapy may be a risk factor for hemorrhagic stroke in 14%–27% of cases [15]. Thus, the risk of hemorrhagic stroke is 11–16-fold higher in patients receiving antithrombotic therapy than in those not receiving antithrombotic agents [16–18]. Anticoagulant therapy, in turn, accounts for approximately 15% of hemorrhagic stroke cases [15].

Treatment with acetylsalicylic acid (ASA) is associated with a relative risk of hemorrhagic stroke of 1.84, with an absolute risk of 0.1–0.4 cases per 1,000 patient-years [19]. Higher doses of ASA may further increase hemorrhagic stroke risk [20]. The use of ASA during a hemorrhagic stroke may increase the risk of death and disability [21]. When comparing combination therapy with ASA plus dipyridamole and ASA monotherapy, no substantial difference in major hemorrhagic events was observed between the two groups [19, 22, 23]. In a comparison of clopidogrel (75 mg daily) and ASA (325 mg daily), hemorrhagic complications were more frequent with ASA (intracranial hemorrhage: 0.47% vs 0.33%; other bleeding events: 0.72% vs 0.52%) [20]. Nevertheless, in a retrospective comparison of patients with intracranial hemorrhage receiving either ASA or clopidogrel, Campbell et al. reported larger hematoma volumes, a lower likelihood of discharge home, and a higher mortality in the clopidogrel group than in the ASA group [21]. Comparing prasugrel directly with clopidogrel demonstrated a higher bleeding risk for patients treated with prasugrel [24]. Compared with clopidogrel, ticagrelor was associated with a higher hemorrhagic stroke incidence, although the rates of major bleeding and fatal bleeding were comparable between the two groups [25]. In patients receiving a combination of ASA (81–162 mg/day) and clopidogrel (75 mg/day) or clopidogrel monotherapy (75 mg/day), no increase in hemorrhagic complications was observed during the first month of treatment. However, an increased bleeding risk became evident in the ASA plus clopidogrel group after 3 months of therapy. Overall, ASA and clopidogrel combination therapy increased hemorrhagic stroke incidence by 61% compared with clopidogrel monotherapy [26]. Compared with other antiplatelet agents, cilostazol demonstrated the lowest risk of bleeding and hemorrhagic stroke [27].

During vitamin K antagonist treatment, the incidence of hemorrhagic stroke was 2–9 per 100,000 persons annually, which is 7–10 times higher than the incidence of hemorrhagic stroke in patients not receiving oral anticoagulants [28, 29]. Direct oral anticoagulants have enhanced the safety of anticoagulant therapy, resulting in a considerable decrease in the risk of bleeding and hemorrhagic stroke [30]. Large randomized controlled trials on stroke prevention in patients with atrial fibrillation revealed absolute annual risks of hemorrhagic stroke ranging from 0.2% to 0.5% [31–38]. For comparison, the incidence of hemorrhagic stroke associated with unfractionated heparin therapy was 0.3% [39]. Notably, the individual cumulative risk of bleeding decreases with increasing duration of oral anticoagulant therapy [16, 40, 41]. These data confirm a higher risk of hemorrhagic stroke in patients starting oral anticoagulants during hospitalization. Combination therapy with warfarin and an antiplatelet agent increases hemorrhagic stroke incidence threefold [42, 43].

3. In-hospital hemorrhagic stroke associated with somatic condition: Clinicians should consider the effects of a patient’s somatic condition at the time of hospitalization, surgical interventions, diagnostic and therapeutic procedures, and pharmacotherapy modifications on preexisting pathophysiological mechanisms.

Several nosological entities should be considered separately due to their increased risk of hemorrhagic stroke, which may be exacerbated or induced by diagnostic and therapeutic interventions during inpatient treatment.

Drug-induced hypertension is a potential cause of increased blood pressure among hospitalized patients. Various medications can increase blood pressure through different mechanisms of action. In individuals with initially normal blood pressure, this may result in secondary hypertension. In patients diagnosed with essential hypertension, medications may represent an underrecognized cause of ineffective antihypertensive therapy, failure to achieve target blood pressure levels, refractory hypertension, and episodes of uncontrolled blood pressure increase [44].

Many medications can cause an increase in blood pressure (drug-induced hypertension). The most common contributors include:

• Hormonal agents: glucocorticoids, thyroid hormones, and growth hormone
• Anti-inflammatory agents: nonsteroidal anti-inflammatory drugs (NSAIDs)
• Stimulants: sympathomimetics and central nervous system stimulants (alcohol and amphetamines)
• Psychotropic drugs: antidepressants
• Immunosuppressive agents
• Antiangiogenic agents
• Other medications: sibutramine, antiemetic agents, physostigmine, levodopa, leflunomide, recombinant human erythropoietin, anesthetics, heavy metals, toxins, and certain dietary supplements (ginseng and licorice)

When prescribing new medications to patients already receiving antihypertensive therapy, drug-induced hypertension should be considered. Whenever possible, the use of medications that increase blood pressure should be avoided. If avoidance is not feasible, blood pressure monitoring and adjustment of antihypertensive therapy are required [44].

Drug-induced hypertension may develop from pharmacokinetic or pharmacodynamic interactions between medications. Clinically, drug-induced hypertension should be suspected at the onset of hypertension or in cases of destabilization of previously compensated hypertension, manifested by episodes of unprovoked blood pressure increase not associated with physical or psychoemotional stress. Patients with chronic kidney disease, coronary artery disease, chronic heart failure, and prehypertension constitute a high-risk group [45].

The pathogenesis of hypertension in hospitalized patients is often related to surgical intervention and the withdrawal or failure to prescribe antihypertensive therapy in the preoperative period. The development of postoperative hypertension may be triggered by factors associated with the body’s response to surgical stress and the intervention itself, including the following:

Vascular spasm: Stress hormones released in response to surgery may cause vasoconstriction and an increase in systemic vascular resistance.

Hormonal imbalance: The activation of the renin–angiotensin–aldosterone system, which regulates blood pressure, may lead to its increase.

Impaired blood pressure regulation: Certain surgical procedures may temporarily disrupt baroreceptor function responsible for maintaining normal blood pressure.

Respiratory disturbances: Hypoxemia and hypercapnia, frequently occurring in the postoperative period, may contribute to blood pressure increase.

Physiological responses: Shivering due to intraoperative hypothermia, pain, agitation, anxiety, fluid overload (hypervolemia), nausea, and urinary bladder distension may provoke increases in blood pressure.

Drug interactions: Combinations of medications used intraoperatively and postoperatively may influence arterial blood pressure.

The highest risk of postoperative complications, including arterial hypertension, is observed following major cardiac surgery [46].

4. Drug-induced thrombocytopenia or thrombocytopenia (hereditary or acquired) compromised by medications with rheopositive and other agents: Thrombocytopenia is a hematological disorder defined as a platelet count below 150 × 10⁹/L or a decrease of more than 50% from an individual’s baseline. Thrombocytopenia is classified according to severity based on platelet count: mild, platelet count between 100 and 150 × 10⁹/L; moderate, platelet count between 50 and 100 × 10⁹/L; and severe, platelet count below 50 × 10⁹/L. In patients with severe thrombocytopenia, the risk of hemorrhagic complications, including hemorrhagic stroke, substantially increases and may be potentially fatal. This is reflected in the 2020 clinical guidelines for the management of patients with atrial fibrillation. Thrombocytopenia identified by blood tests is most commonly observed in patients treated in the infectious disease, oncology, gastroenterology, hematology, and cardiology departments. In adults, the leading cause of thrombocytopenia is acute and chronic liver disease, particularly of infectious origin. Antineoplastic agents may cause thrombocytopenia either directly, by damaging platelets or their precursors, or indirectly, through the formation of antibodies that target platelets (as observed with oxaliplatin, which can induce acute and severe thrombocytopenia). Moreover, low platelet count (thrombocytopenia) is observed in myelofibrosis and other hematologic disorders. Following myocardial infarction, thrombocytopenia develops in approximately 5% of patients and is a serious complication, as it increases the risk of hemorrhagic events more than threefold and the risk of thrombotic events nearly threefold. Over 300 medications have been identified as potential inducers of thrombocytopenia. Drugs with a confirmed or probable causal association with thrombocytopenia include quinidine, combined trimethoprim and sulfamethoxazole, furosemide, NSAIDs, and glycoprotein IIb/IIIa inhibitors. Among these, heparin remains the most common drug associated with the development of this complication [47].

DISCUSSION

To decrease in-hospital mortality, it is crucial to systematically improve the quality of medical care at all stages, from early diagnosis and effective inpatient treatment to timely hospitalization and providing qualified medical care prior to hospital admission. Improving health literacy and fostering personal responsibility for health among the population also play a critical role [2].

In conducting an in-depth analysis of the causes of in-hospital mortality, each case is classified as a preventable, potentially preventable, or non-preventable death. A substantial proportion (46.4%–57.1%) of fatal outcomes were categorized as non-preventable deaths. Nevertheless, to improve the quality of medical care, careful analysis of cases classified as potentially preventable (23.9%–39.2%) and preventable (10%–19%) is required. The evaluation of these groups represents a key approach to improving treatment outcomes [2].

Given the high mortality rates associated with hemorrhagic stroke, retrospective analysis of fatal outcomes in hospitalized patients is critical for a multistage strategy aimed at decreasing overall in-hospital mortality.

Understanding in-hospital hemorrhagic stroke risk factors enables the decrease of its incidence and improvement of outcomes. Recently, hemorrhagic complications associated with unique risk factors have shown a progressive increase, reflecting the substantial advances in the prevention and treatment of ischemic and thromboembolic diseases, along with the widespread implementation of an increasing number of procedures and pharmacological agents for preventing ischemic events and thromboembolism of various localizations.

The unique risk factors for hemorrhagic stroke presented in this study may represent the most common causes of in-hospital hemorrhagic stroke. These risk factors underscore the importance of differentiated prevention at the prehospital and hospital stages in patients with different clinical profiles.

The main measures for differentiated prevention of in-hospital hemorrhagic stroke should include the following:

1. In patients scheduled to undergo systemic thrombolytic therapy and endovascular interventions:

Assessment of the risk of hemorrhagic complications using contemporary risk scoring systems for hemorrhagic transformation of cerebral infarction (HAT, MSS, SEDAN, iScore, SITS-SICH, GRASPS, and SPAN100) [48].

Strict adherence to systemic thrombolytic therapy protocols⁸ and clinical guidelines for the management of patients with acute coronary syndrome,^9,10 pulmonary embolism [49], and ischemic stroke.¹¹

Initiation and resumption of antithrombotic therapy according to clinical practice guidelines.

2. In patients receiving antithrombotic therapy:

Physician awareness of the pharmacological characteristics of the prescribed drug, the possibility of in-hospital hemorrhagic stroke associated with its use compared with alternative agents, and the risks related to combined antithrombotic therapy.

Prevention of in-hospital hemorrhagic stroke and active identification and correction of risk factors are required, particularly in patients at high risk of bleeding. When anticoagulants are prescribed, careful patient monitoring is warranted, including control of anticoagulation intensity, assessment of renal function, and consideration of potential drug–drug interactions. Concomitant use of anticoagulants and antiplatelet agents should be avoided, as it remarkably increases the risk of in-hospital hemorrhagic stroke. When warfarin is used, strict monitoring of the international normalized ratio with maintenance within the therapeutic range is required, and special caution should be exercised when prescribing the drug to older patients [15].

3. In patients with in-hospital hemorrhagic stroke associated with somatic condition:

The principal tenet of differentiated prevention of in-hospital hemorrhagic stroke is the physician’s awareness of medications capable of inducing hypertension and the possibility of their substitution or dose reduction depending on the clinical situation.

Mandatory screening control of arterial blood pressure in hospitalized patients, both in the form of daily manual measurements performed by nursing staff and through 24-hour ambulatory blood pressure monitoring.

Further implementation of perioperative management recommendations for patients with hypertension within the healthcare system is crucial in the differentiated prevention of in-hospital hemorrhagic stroke [46].

Physicians of various specialties should assess platelet counts before initiating or intensifying antithrombotic therapy and should consider the risk of thrombocytopenia when selecting a pharmacological treatment strategy.

Further investigation of the mechanisms of development and preventive and therapeutic approaches for in-hospital hemorrhagic stroke increases awareness among physicians of different specialties regarding this clinical entity. This is crucial when developing treatment plans for the underlying disease, taking into account general, specific, and unique risk factors for in-hospital hemorrhagic stroke.

ADDITIONAL INFO

Author contributions: E.I. Shermatyuk: conceptualization, methodology, data curation, investigation, formal analysis, writing—original draft; N.V. Tsygan: conceptualization, formal analysis, writing—review & editing; I.V. Litvinenko: conceptualization, data curation, formal analysis; A.A. Postnov, M.G. Chernenok, V.A. Medvedev, T.V. Sergeeva: data curation, formal analysis. All authors made substantial contributions to the conceptualization, investigation, and manuscript preparation, and reviewed and approved the final version prior to publication.

Funding sources: The study was not supported by any external sources of funding.

Competing interests: The authors declare that they have no competing interests.

Ethics approval: Ethical review was not conducted, as the article is of a review nature.

¹ fedstat.ru [Internet]. Federal State Statistics Service of the Russian Federation. Unified Interdepartmental Information and Statistical System. Available at: https://www.fedstat.ru/indicator/61889. Accessed on: January 12, 2025.

² Clinical guidelines dated December 15, 2022. Hemorrhagic Stroke. Available at: https://cr.minzdrav.gov.ru/preview-cr/523_2. Accessed on: January 12, 2025.

³ Ibid.

⁴ Ibid.

⁵ Ibid.

⁶ Clinical guidelines dated February 14, 2023. Disorders of Lipid Metabolism. Available at: https://cr.minzdrav.gov.ru/preview-cr/752_1. Accessed on: January 12, 2025.

⁷ Clinical guidelines dated October 3, 2024. Arterial Hypertension in Adults. Available at: https://cr.minzdrav.gov.ru/preview-cr/62_3. Accessed on: January 12, 2025.

⁸ Protocol for reperfusion therapy in acute ischemic stroke. Society for Evidence-Based Neurology. Available at: https://evidence-neurology.ru/evidentiary-medicine/protokoli/protokol-reperfuzionnoi-terapi/ Accessed on: April 23, 2025.

⁹ Clinical guidelines dated November 25, 2024. ST-Segment Elevation Myocardial Infarction. Available at: https://cr.minzdrav.gov.ru/preview-cr/157_5 Accessed on: April 23, 2025.

¹⁰ Clinical guidelines dated October 23, 2024. Non–ST-Segment Elevation Acute Coronary Syndrome. Available at: https://cr.minzdrav.gov.ru/preview-cr/154_4 Accessed on: April 23, 2025.

¹¹ Clinical guidelines dated November 20, 2024. Ischemic Stroke and Transient Ischemic Attack. Available at: https://cr.minzdrav.gov.ru/preview-cr/814_1 Accessed on: April 23, 2025.

About the authors

Evgeniy I. Shermatyuk

Military Medical Academy

Author for correspondence.
Email: vmeda-nio@mil.ru
ORCID iD: 0000-0002-4163-1701

MD, Senior Resident

Russian Federation, Saint Petersburg

Nikolay V. Tsygan

Military Medical Academy

Email: vmeda-nio@mil.ru
ORCID iD: 0000-0002-5881-2242
SPIN-code: 1006-2845

MD, Dr. Sci. (Medicine), Professor

Russian Federation, Saint Petersburg

Aleksandr A. Postnov

Military Medical Academy

Email: vmeda-nio@mil.ru
ORCID iD: 0009-0001-1180-4683

6th Year Cadet

Russian Federation, Saint Petersburg

Maxim G. Chernenok

Military Medical Academy

Email: vmeda-nio@mil.ru
ORCID iD: 0000-0002-7793-4544
SPIN-code: 6460-2969

2nd Year Resident

Russian Federation, Saint Petersburg

Vadim A. Medvedev

Military Medical Academy

Email: vmeda-nio@mil.ru
ORCID iD: 0009-0005-4607-1984

5th Year Cadet

Russian Federation, Saint Petersburg

Tatyana V. Sergeeva

City Hospital of the Holy Martyr Elizabeth; Saint Petersburg State Pediatric Medical University; Saint Petersburg State University

Email: sergeevatv@eliz-spb.ru
ORCID iD: 0000-0003-2949-6268

MD, Cand. Sci. (Medicine)

Russian Federation, Saint Petersburg; Saint Petersburg; Saint Petersburg

Igor V. Litvinenko

Military Medical Academy

Email: vmeda-nio@mil.ru
ORCID iD: 0000-0001-8988-3011
SPIN-code: 6112-2792

MD, Dr. Sci. (Medicine), Professor

Russian Federation, Saint Petersburg

References

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