One of the leading causes of death and permanent disability in the globe is acute ischemic stroke. Reperfusion therapy with intravenous thrombolysis and endovascular thrombectomy has dramatically improved results in suitably selected patients[1]. However, hemorrhagic transition may occur if blood supply is restored to severely ischemic and structurally damaged tissue. HT encompasses a range of conditions, from little petechial hemorrhages to massive parenchymal hematomas.

HT's clinical significance varies. While PH1 and especially PH2 reflect more clinically important forms of hemorrhage, hemorrhagic infarction types HI1 and HI2 typically consist of petechial bleeding without major mass effect. According to the ECASS classification, small petechial hemorrhages are classified as HI1, confluent petechial hemorrhages without mass effect as HI2, hematomas involving less than 30% of the infarct with mild mass effect as PH1, and hematomas involving more than 30% of the infarct with substantial mass effect as PH2 [2-3].

Because PH2 has been linked to neurological decline and death, it is very significant. While HI1, HI2, and PH1 did not show the same negative predictive effect, PH2 was significantly linked to early neurological impairment and three-month death in the ECASS-I cohort.

Advanced age, significant neurological impairment, hypertension, hyperglycemia, atrial fibrillation, big infarct size, and reperfusion therapy are among the clinical factors that have been linked to HT. However, the anatomical and physiological state of the ischemic brain cannot be fully assessed by clinical features alone [4].

Additional details on the biological state and degree of ischemia tissue can be obtained by MRI. DWI enables quick infarct volume calculation and shows cytotoxic edema. Quantitative information about the degree of diffusion restriction is provided by ADC maps. Tissue damage and a higher chance of future hemorrhagic transformation have been linked to extremely low ADC levels. According to studies, ADC values ≤550 ×10^-6 mm²/s may be a predictor of HT [5–6].

Perfusion-weighted imaging offers further data on transit time, cerebral blood volume, and cerebral blood flow. Tissue with reduced vascular integrity may be indicated by severe or persistent hypoperfusion. Similarly, more severe tissue damage and disruption of the blood-brain barrier may be indicated by FLAIR hyperintensity. Pre-existing microbleeds and susceptibility anomalies that could increase the risk of bleeding can be shown by SWI [7-8].

This prospective observational study was designed to include 100 consecutive adult patients presenting with acute ischemic stroke at a tertiary-care hospital. Patients were recruited over the defined study period after institutional ethical approval and informed consent from the patient or legally authorized representative. Inclusion criteria Patients were eligible if they: 1. Were aged ≥18 years. 2. Presented with a clinical diagnosis of acute ischemic stroke. 3. Had symptom onset or last-known-well time within 24 hours. 4. Demonstrated acute ischemic lesions on DWI. 5. Underwent MRI within 24 hours of presentation. 6. Had adequate clinical and radiological follow-up for assessment of HT. Exclusion criteria Patients were excluded if they had: 1. Primary intracerebral hemorrhage on initial imaging. 2. Previous large territorial infarction affecting interpretation. 3. Intracranial tumor or vascular malformation. 4. Major traumatic intracranial hemorrhage. 5. Severe MRI contraindication. 6. Inadequate imaging quality. 7. Incomplete follow-up imaging. Clinical assessment At admission, demographic characteristics, vascular risk factors, time from symptom onset to imaging, blood pressure, blood glucose, history of hypertension, diabetes mellitus, atrial fibrillation and antithrombotic medication use were recorded. Neurological severity was assessed using the National Institutes of Health Stroke Scale (NIHSS). MRI protocol MRI was performed using a standardized stroke protocol. Sequences included: • Axial T1-weighted imaging • T2-weighted imaging • FLAIR • DWI • ADC maps • SWI • MR angiography • Perfusion-weighted imaging when available Assessment of hemorrhagic transformation Follow-up imaging was performed within 24–48 hours and subsequently as clinically indicated, with final HT assessment through day 7. Statistical analysis Continuous variables were expressed as mean ± standard deviation and categorical variables as frequency and percentage. Continuous variables were compared using the independent-samples t-test or Mann–Whitney U test according to data distribution. Categorical variables were compared using the chi-square test or Fisher's exact test. Variables showing significant association with HT on univariate analysis were entered into multivariable logistic regression. Odds ratios (OR) with 95% confidence intervals (CI) were calculated. A p-value <0.05 was considered statistically significant.

A total of 100 patients with acute ischemic stroke were included. The mean age was 61.8 ± 11.7 years, with 63% males and 37% females. Hypertension was present in 67%, diabetes mellitus in 42%, atrial fibrillation in 18% and previous antiplatelet/anticoagulant use in 21%.

Hemorrhagic transformation occurred in 24 patients (24%). Among patients with HT, HI1 was observed in 7 (29.2%), HI2 in 6 (25.0%), PH1 in 7 (29.2%) and PH2 in 4 (16.7%).

Patients developing HT had significantly higher baseline NIHSS scores and larger DWI lesion volumes than those without HT. The mean NIHSS was 15.4 ± 5.1 in the HT group compared with 9.6 ± 4.4 in the non-HT group (p<0.001). Mean DWI lesion volume was 68.2 ± 31.6 mL in the HT group versus 31.7 ± 19.8 mL among patients without HT (p<0.001).

Table 1: Baseline clinical characteristics according to occurrence of hemorrhagic transformation

HT = hemorrhagic transformation; NIHSS = National Institutes of Health Stroke Scale; BP = blood pressure.

Hypertension, atrial fibrillation, higher admission glucose, higher systolic blood pressure and greater neurological deficit were more frequent among patients who developed HT.

MRI findings demonstrated strong associations with HT. Mean DWI lesion volume was significantly greater in the HT group. Minimum ADC was substantially lower among patients with HT. FLAIR hyperintensity within the DWI lesion and substantial perfusion deficit were also significantly more common.

Table 2: MRI characteristics in patients with and without hemorrhagic transformation

DWI = diffusion-weighted imaging; ADC = apparent diffusion coefficient; FLAIR = fluid-attenuated inversion recovery; SWI = susceptibility-weighted imaging.

The frequency of HT increased progressively with larger DWI lesion volume and lower ADC. Patients with DWI lesion volume ≥50 mL had approximately fourfold higher odds of developing HT compared with patients with smaller lesions.

Table 3: MRI thresholds and association with hemorrhagic transformation

OR = odds ratio; CI = confidence interval.

On multivariable logistic regression, three MRI parameters remained independently associated with HT: DWI lesion volume ≥50 mL, ADC ≤550 ×10^-6 mm²/s and significant perfusion deficit.

Table 4: Multivariable logistic regression for independent MRI predictors of hemorrhagic transformation

DWI = diffusion-weighted imaging; ADC = apparent diffusion coefficient; FLAIR = fluid-attenuated inversion recovery; SWI = susceptibility-weighted imaging; NIHSS = National Institutes of Health Stroke Scale.

In this study, 100 patients with acute ischemic stroke had their MRI-derived hemorrhagic transformation predictions assessed. 24% of patients experienced HT. The main conclusions were that HT was substantially correlated with greater DWI lesion volume, significantly lower ADC, severe perfusion deficit, and early FLAIR hyperintensity [9]. DWI lesion volume ≥50 mL, ADC ≤550 ×10^-6 mm²/s, and substantial perfusion deficit remained independent predictors after controlling for clinical and imaging factors. The current study's incidence of HT is in line with the wide range documented in cohorts of acute ischemic stroke. The radiological subtype of HT has a significant impact on its clinical importance. While PH2 can cause severe neurological decline, small petechial hemorrhages may have few clinical effects [10]. PH2 was linked to a significantly higher risk of early neurological decline and mortality, according to earlier ECASS findings. DWI lesion volume In the current investigation, DWI lesion volume was one of the best indicators of HT. The mean lesion volume was 68.2 mL in patients with HT and 31.7 mL in those without. A more than four-fold increase in the likelihood of HT was independently linked to a DWI volume of at least 50 mL [11]. Similar findings from earlier imaging investigations have shown a correlation between baseline DWI lesion volume and later HT [12]. Diffusion lesion volume and very low ADC can also indicate hemorrhagic consequences, according to evidence-based analyzes, while ADC may still be predictive on its own if lesion size is taken into account. Perfusion abnormalities Significant perfusion abnormalities were seen in 75% of HT patients. After correction, perfusion impairments continued to be independently linked to HT. Tissue exposed to protracted ischemia, compromised autoregulation, and vascular endothelial injury may be identified by severe hypoperfusion. Reperfusion of severely damaged tissue can further raise the chance of blood-brain barrier collapse [13]. Hypoperfusion and HT are linked, according to published research, with perfusion anomalies offering information in addition to DWI. FLAIR abnormalities Patients who later had HT were substantially more likely to have early FLAIR hyperintensity. Nevertheless, in the fully corrected model, its correlation was no longer statistically significant [14]. FLAIR hyperintensity may be a sign of changed water content and more severe ischemic tissue damage. FLAIR hyperintensity was found to be one of the MRI characteristics linked to HT in earlier systematic review data. SWI findings Patients with HT were more likely to have aberrant SWI susceptibility. After correction, the correlation lost its independent significance even though it was significant in univariate analysis. This implies that while SWI anomalies may play a role in risk classification, they may also be a reflection of other factors like the severity of the infarct, vascular pathology, and prior microvascular injury. However, SWI is still useful for acute stroke MRI because it can detect early hemorrhagic products and pre-existing cerebral microbleeds that would not be visible on traditional sequences [15]. Clinical implications The findings may have applications. A patient may be more vulnerable if they have an acute ischemic stroke and exhibit a significant DWI lesion, very low ADC, and severe perfusion abnormalities. Identification of this imaging pattern may facilitate repeat imaging following reperfusion and more intensive neurological surveillance [16]. The results also support the idea that advanced MRI measures and traditional clinical factors should be interpreted jointly rather than separately. While an MRI can reveal details on the degree and biological severity of the underlying tissue damage, a high NIHSS score may indicate serious stroke.

MRI is a useful tool for predicting hemorrhagic change after acute ischemic stroke. Larger DWI lesion volumes, significantly lower ADC, a substantial perfusion deficit, and early FLAIR abnormalities were linked to a higher risk of HT in this investigation. After multivariable adjustment, DWI lesion volume ≥50 mL, ADC ≤550 ×10^-6 mm²/s, and significant perfusion deficit continued to be independent predictors.

Therefore, patients at higher risk of hemorrhagic transformation may be identified and closer post-reperfusion monitoring made possible by an integrated MRI-based assessment that includes DWI, ADC, FLAIR, SWI, and perfusion imaging. To develop uniform MRI thresholds and predictive models, more prospective multicenter trials with bigger sample sizes are necessary.

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