Association between infarct location and haemorrhagic transformation of acute ischaemic stroke after intravenous thrombolysis.

AIM: To evaluate the association between computed tomography (CT)-based imaging variables at the time of admission and haemorrhagic transformation (HT) after intravenous thrombolysis (IVT). MATERIALS AND METHODS: One hundred and eight patients who were treated with IVT for acute ischaemic stroke (AIS) during January 2021 to July 2023 were analysed retrospectively. The infarct location was classified as cortical or subcortical in accordance with the Alberta Stroke Program Early CT Score (ASPECTS) system. Logistic regression and receiver operating characteristic curve analyses were performed to determine the relationship between ischaemic variables and HT. RESULTS: Of the total, 18 (16.7%) patients had HT and seven (6.5%) had symptomatic intracerebral haemorrhage (sICH). Multivariate analysis revealed that cortical ASPECTS was independently associated with HT (odds ratio [OR], 0.197; 95% confidence interval [CI], 0.076-0.511; p=0.001) and cortical ASPECTS was independently associated with sICH (OR, 0.066; 95% CI, 0.009-0.510; p=0.009). To predict HT and sICH, cortical ASPECTS (HT area under the curve [AUC] = 0.881, sICH AUC = 0.971) provided a higher AUC compared with ASPECTS (HT AUC = 0.850, sICH AUC = 0.918). CONCLUSION: Cortical ASPECTS seen on CT at the time of admission is associated with HT and sICH after IVT.

A rare case of renal infarction due to heroin and amphetamine abuse: case report.

BACKGROUND: Renal infarctions as a result of recreational drug use are rare and are commonly associated with cocaine use. Although amphetamines have a similar mechanism of action as cocaine, there are few reports linking them to ischemic events, and only one to renal infarction. Similarly, few reports link heroin use with infarcts, but never in the kidney. Although uncommon, several mechanisms have been implicated in heroin and amphetamine-induced infarction, including vasculopathy, vasculitis and the activation of the coagulation cascade. CASE PRESENTATION: 47-year-old female with a past medical history of non-intravenous heroin and amphetamine abuse, chronic obstructive pulmonary disease, hypertension, hyperlipidemia presented with right lower extremity swelling and rash, which was diagnosed as cellulitis and treated appropriately. Incidentally, the patient was found to have an acute kidney injury and further workup identified multiple renal infarcts in the right kidney. The patient had no past medical history of clotting disorders. Blood culture and urine cultures were sterile; autoimmune and hypercoagulable workup were negative. Urinalysis was unremarkable. Urine toxicology was only positive for opiates and amphetamines, which were thought to be the most likely cause of the renal infarct. Patient was lost to outpatient follow up due to noncompliance, but returned to the hospital for re-emergence of her cellulitis, during which no new infarcts were discovered, and the previous renal infarct had scarred over. CONCLUSION: There are very few reports of heroin and amphetamine-induced infarctions. This case report describes a rare but important complication of heroin/amphetamine abuse that could be easily overlooked.

Renal infarction associated with low dose intravenous immunoglobulin in a kidney transplant recipient with sepsis: a case report and literature review.

BACKGROUND: The use of human intravenous immunoglobulin gamma (IVIG) is associated with thromboembolic events as a complication. There are few reported cases of renal infarction during IVIG use in the general population, but transplant kidney may be more susceptible to thromboembolic events following IVIG use. CASE PRESENTATION: A 41-year-old woman visited with fever and pain at the transplant kidney. Six years ago, she underwent kidney transplantation from a deceased donor. Laboratory and radiologic findings were compatible to septic condition, secondary to acute pyelonephritis. We started antibiotics, inotropics, and IVIG. The patient abruptly developed gross hematuria and urine output decreased to 100 cc/day during IVIG administration. Renal doppler and pathologic findings revealed renal infarction. Oliguria and azotemia persisted and she is undergoing maintenance hemodialysis. CONCLUSION: Our case shows that infarction of transplant kidney can be caused by IVIG use in a patient with severe infection. Thus, when using IVIG for kidney transplant patients with high risk of thromboembolic events, we may be careful to prevent the thromboembolic events.

Bilateral macular infarction after gemcitabine and carboplatin chemotherapy.

PURPOSE: To report a case of macular infarction after doublet chemotherapy with gemcitabine and carboplatin. METHODS: A middle-aged lady presenting with bilateral macular infarction post-chemotherapy for metastatic cervical malignancy was investigated for thromboembolic risks and treated. RESULTS: The macular perfusion and edema improved with control of hypertension and treatment with pentoxifylline. Visual improvement was satisfactory, and the possible associated risk such as hypertension was noted. CONCLUSION: This case underscores the need for active screening of patients on chemotherapy with gemcitabine and carboplatin for retinal vascular occlusive changes when hypertension is associated.

Taking varenicline for smoking cessation: A rare cause of pulmonary thromboembolism with infarction.

Varenicline (Champix®, Chantix®) is a partial agonist of the α4ß2 nicotinic acetylcholine receptor (nAChR) and a full agonist of the α7 nAChR. It has been used for smoking cessation since 2006. Varenicline has been associated with adverse cardiovascular (CV) events, including myocardial infarction, which may be caused by activation of the α7 nAChR receptor that in turn stimulates parasympathetic output from the brainstem to the heart, release of catecholamines, and has a prothrombotic effect. However, among the adverse CV events, the issue related to the varenicline-induced pulmonary thromboembolism (PTE) has not being addressed. We report a case of PTE with pulmonary infarction presenting as right flank pain that resulted from the use of varenicline (the total score of adverse drug reaction probability scale, 6; probable association between varenicline and pulmonary PTE) in a patient without underlying CV disease and in whom low probability of PTE (Wells score was zero) was identified.

Unilateral hemorrhagic macular infarction associated with marijuana, alcohol and antiepileptic drug intake.

A 55-year-old male presented with a complaint of a painless and sudden loss of vision in the right eye. Fundus photography revealed loss of transparency and edema in the central macular region. Optical coherence tomography showed increased reflectivity and diffused swelling in the inner retinal layers. Fluorescein angiography revealed a large area of capillary non-perfusion with a pronounced hypofluorescent area with distinct borders. To our knowledge, this is the first report of a hemorrhagic macular infarction associated with marijuana and pregabalin misuse.

RISK-FACTORS, PATHOGENESIS, AND PHARMACEUTICAL APPROACHES FOR TREATMENT OF STEROID-INDUCED BONE INFARCTION OF FEMORAL HEAD.

During first year of steroid usage, osteocyte necrosis and blood vessel blockage may occur, which subsequently may produce steroid-induced bone infarction (SIBI) resulting in painful movement of patient. For treatment of SIBI, pharmaceutical strategy is the basic approach. It involves the use of various pharmacologically active compounds including bisphosphonates, hyperbaric oxygen (HBO), coenzyme Q10, erythropoietin, antihyperlipidemics, anticoagulants, antioxidants, and tissue repair protein. Out of these, there is no pharmaceutical agent that may completely treat this disease because many factors are found to be responsible for SIBI development; therefore, there are multiple biomarkers of this disease. This situation argues for need of new therapeutic agents for SIEB1.

Prothrombin complex concentrate (Beriplex P/N)-related renal and cerebral infarctions in a patient with warfarin-associated intracerebral hemorrhage.

A 45-year-old man receiving warfarin treatment suffered from an intracerebral hemorrhage. Four-factor prothrombin complex concentrate (PCC) was administered to correct coagulopathy. However, bilateral renal infarcts and a cerebral infarct developed on day 5 and 7, respectively after PCC administration. Although the occurrence of PCC-related thromboembolism is low, health care practitioners should closely follow-up the symptoms and signs of thrombosis after PCC administration.

Non-invasive monitoring of tumor-vessel infarction by retargeted truncated tissue factor tTF-NGR using multi-modal imaging.

The fusion protein tTF-NGR consists of the extracellular domain of the thrombogenic human tissue factor (truncated tissue factor, tTF) and the peptide GNGRAHA (NGR), a ligand of the surface protein CD13 (aminopeptidase N), upregulated on endothelial cells of tumor vessels. tTF-NGR preferentially activates blood coagulation within tumor vasculature, resulting in tumor vessel infarction and subsequent tumor growth retardation/regression. The anti-vascular mechanism of the tTF-NGR therapy approach was verified by quantifying the reduced tumor blood-perfusion with contrast-enhanced ultrasound, the reduced relative tumor blood volume by ultrasmall superparamagnetic iron oxide-enhanced magnetic resonance imaging, and by in vivo-evaluation of hemorrhagic bleeding with fluorescent biomarkers (AngioSense(680)) in fluorescence reflectance imaging. The accumulation of tTF-NGR within the tumor was proven by visualizing the distribution of the iodine-123-labelled protein by single-photon emission computed tomography. Use of these multi-modal vascular and molecular imaging tools helped to assess the therapeutic effect even at real time and to detect non-responding tumors directly after the first tTF-NGR treatment. This emphasizes the importance of imaging within clinical studies with tTF-NGR. The imaging techniques as used here have applicability within a wider scope of therapeutic regimes interfering with tumor vasculature. Some even are useful to obtain predictive biosignals in personalized cancer treatment.

Clinical study of tirofiban compared to low molecular weight heparin in the antithrombotic treatment of progressive pontine infarction.

OBJECTIVE: To investigate the efficacy and safety of tirofiban and low molecular weight heparin (LMWH) in the treatment of patients undergoing acute progressive pontine infarction. PATIENTS AND METHODS: Patients with acute progressive pontine infarction who were hospitalized in the Neurology Department from June 2021 to June 2023 were included in the study and randomly divided into two groups, namely the experimental group (tirofiban group) and the control group (LMWH group). All patients in both groups were required to receive conventional comprehensive treatment and dual antiplatelet therapy with aspirin + clopidogrel at the beginning of admission. The National Institutes of Health Stroke Scale (NIHSS) score and Barthel Index (BI) were used to evaluate the neurological deficits on the first day of admission, the next day with stroke progression, and at discharge after treatment with tirofiban and LMWH, respectively in the two groups. The modified Rankin Scale was employed to assess prognosis on the 90th day after treatment. Clinical adverse events were followed up for 90 days, comparing the clinical efficacy and safety of the two treatment methods. RESULTS: There was no statistical significance in NIHSS score and Barthel Index between the tirofiban group and the LMWH group on the first day of admission and the next day with stroke progression (p > 0.05). After stroke progression, tirofiban and LMWH were separately used for treatment in the two groups. We found that the NIHSS score of the tirofiban group was lower than that of the LMWH group, and the Barthel Index score was higher than that of the LMWH group at discharge (p < 0.05). After three months of follow-up, the mRS score of the tirofiban group was dramatically higher than that of the LMWH group (p < 0.05). No significant harmful or adverse reactions, such as bleeding events, were found in the two groups (p > 0.05). CONCLUSIONS: Tirofiban may be more effective and safer than LMWH in controlling the progression of acute pontine infarction, but further and large-sample studies are still needed to confirm this finding.

Subtyping treatment response of tirofiban in acute ischemic stroke based on neuroimaging features.

In a previously published clinical trial, we demonstrated that tirofiban was effective and safe in acute ischemic stroke (AIS) patients who did not undergo early recanalization treatments. We aimed to evaluate neuroimaging characteristics and their clinical significance to guide tirofiban treatment. In this post hoc analysis, location of infarcts (anterior circulation stroke [ACS] vs. posterior circulation stroke [PCS]), degree of cerebral artery stenosis (≤69% vs. ≥70% or occlusion), total infarct volume, and ASPECTS were used to predict the treatment effects of tirofiban, defined as the proportions of excellent and favorable functional outcome (modified Rankin Scale [mRS] score of 0-1, 0-2) at 90 days. ACS patients were more likely to achieve excellent (OR 2.08; 95% CI 1.25-3.45; p = 0.004) and favorable functional outcome (OR 2.28; 95% CI 1.24-4.22; p = 0.008) when treated with tirofiban. However, there was no significant difference in PCS patients between tirofiban and the control group. For patients with severe stenosis (≥70% or occlusion), tirofiban treatment improved the proportion of good outcomes (OR 2.84; 95% CI 1.44-5.60; p = 0.002 for mRS 0-1; OR 2.42; 95% CI 1.22-4.77; p = 0.011 for mRS 0-2). Meanwhile, we found that tirofiban improved outcome in patients with ASPECTS 8-10 and was independent of total infarct volume. These findings support the hypothesis that patients with ACS and severe stenosis may be recommended for tirofiban treatment, which can be predicted independent of total infarct volume.

Sildenafil-induced spinal cord infarction: a case report.

Spinal cord infarction is a rare condition, accounting for only a small percentage of strokes. It can be classified into cervical and thoracolumbar infarctions, with various factors contributing to its occurrence. Sildenafil, a phosphodiesterase type 5 inhibitor commonly used for erectile dysfunction, has been associated with cardiovascular side effects, including transient hypotension. In this case report, we present the unusual occurrence of spinal cord infarction in a 65-year-old man who had self-administered high doses of sildenafil without a doctor's prescription. The patient experienced severe radicular pain in the lumbar region and subsequent weakness in the lower limbs. Evaluation revealed an anterior spinal cord infarction in the thoracic region, confirmed by MRI imaging. After excluding other potential causes, it was concluded that the intake of sildenafil likely led to systemic hypotension, resulting in spinal cord infarction. This case highlights the importance of considering sildenafil as a possible contributor to spinal cord infarction, particularly when used at high doses. Further studies are needed to better understand the relationship between sildenafil and vascular complications, including spinal cord infarction.

Renal cortical infarction following treatment with sumatriptan in a kidney allograft recipient.

Renal cortical infarction is a rare cause of acute kidney injury that results from inadequate blood flow to the kidney, most commonly as a consequence of thrombotic or embolic occlusion of the renal artery or profound hypoperfusion. We report the case of a 78-year-old female kidney transplant recipient who developed a migraine headache, took sumatriptan, and soon after developed pain over the allograft and oligoanuric acute kidney injury. Kidney allograft biopsy showed renal cortical infarction. The mechanism of action of sumatriptan involves vasoconstriction, which counters the vasodilatation that is central to the pathogenesis of migraines. This case raises important questions regarding the safety of triptans with calcineurin inhibitors (which also act to vasoconstrict), particularly in elderly patients.

Spinal infarction related to the adjuvant chemotherapy for surgically resected non-small cell lung cancer: report of a case.

We report the development of spinal infarction during adjuvant chemotherapy with tegafur, gimeracil and oteracil (TS-1) after surgery for lung adenocarcinoma. A 69-year-old female had a left upper lobectomy for pulmonary adenocarcinoma, T2aN0M0. Six weeks after the surgery, tegafur, gimeracil and oteracil were administered orally as adjuvant chemotherapy for 1 year. After 10 months of adjuvant chemotherapy, the patient suddenly showed signs of numbness and weakness in both lower limbs. The patient did not have a previous medical history, and was receiving only tegafur, gimeracil and oteracil with the stomach medication. Neurological findings showed muscle weakness, numbness and a loss of tendon reflex in both lower limbs, as well as bladder and rectal disturbance. Blood tests, brain magnetic resonance imaging and chest computed tomography showed no signs of abnormalities or metastasis. Magnetic resonance imaging of the spine showed a hyperintense lesion between the Th12 and L1 spinal levels by T2-weighted image. A spinal fluid test indicated no abnormalities, and cytological diagnosis was class II. Anti-aquaporin 4, anti-ganglioside and anti-neuronal autoantibodies were all negative. These results indicated that the patient had a spinal infarction, rather than myelitis or paraneoplastic neurological syndrome. The patient was treated with heparin and steroid pulse treatment followed by rehabilitation, and recovered sufficiently to be able to walk using a cane after 2 months. The development of spinal infarction during anti-cancer chemotherapy has not been previously reported. In this case, an association of spinal infarction with the use of adjuvant chemotherapy was strongly indicated due to the lack of abnormalities in coagulability, atherosclerotic lesions and aortic disease.

Renal infarction secondary to ketamine abuse.

Renal infarction is an uncommon condition that resulted from inadequate perfusion of the kidney and is easily missed diagnosed due to its nonspecific clinical presentations. Major risk factors for renal infarction are atrial fibrillation, previous embolism, and ischemic and valvular heart disease. Progressive decrease in renal function or even death can occur if renal infarction is not diagnosed accurately and promptly. Ketamine abuse may cause variable urinary tract injury. However, renal infarction caused by ketamine abuse has never been reported. To our knowledge, this is the first documented case of renal infarction following nasal insufflation of ketamine.