Hanga Pál

Dr. Hanga Pál


Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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24 April 2024 in Journal of Clinical Medicine
Verified
Journal Article
Open access
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BLBalázs Csaba Lengyel
Balázs Csaba Lengyel
RMRita Magyar-Stang
Rita Magyar-Stang
HPHanga Pál
Hanga Pál
Róbert DebreczeniRóbert Debreczeni
Róbert Debreczeni
ÁSÁgnes Dóra dr Sándor
Ágnes Dóra dr Sándor
ZMZsuzsanna Mihály
Zsuzsanna Mihály
This review aims to explore advancements in perioperative ischemic stroke risk estimation for asymptomatic patients with significant carotid artery stenosis, focusing on Circle of Willis (CoW) morphology based on the CTA or MR diagnostic imaging in the current preoperative diagnostic algorithm. Functional transcranial Doppler (fTCD), near-infrared spectroscopy (NIRS), and optical coherence tomography angiography (OCTA) are discussed in the context of evaluating cerebrovascular reserve capacity and collateral vascular systems, particularly the CoW. These non-invasive diagnostic tools provide additional valuable insights into the cerebral perfusion status. They support biomedical modeling as the gold standard for the prediction of the potential impact of carotid artery stenosis on the hemodynamic changes of cerebral perfusion. Intraoperative risk assessment strategies, including selective shunting, are explored with a focus on CoW variations and their implications for perioperative ischemic stroke and cognitive function decline. By synthesizing these insights, this review underscores the potential of non-invasive diagnostic methods to support clinical decision making and improve asymptomatic patient outcomes by reducing the risk of perioperative ischemic neurological events and preventing further cognitive decline.

30 October 2025 in Life
Verified
Journal Article
Open access
PDF file
HPHanga Pál
Hanga Pál
RMRita Magyar-Stang
Rita Magyar-Stang
BCBorbála Csányi
Borbála Csányi
AGAnna Gaál
Anna Gaál
ZMZsuzsanna Mihály
Zsuzsanna Mihály
Róbert DebreczeniRóbert Debreczeni
Róbert Debreczeni
Background and Aims: Decreased cerebrovascular reactivity (CVR) in patients with significant internal carotid artery stenosis (ICAS ≥ 70%) is an independent risk factor for cerebral infarction. To evaluate CVR, changes in cerebral perfusion pressure and blood flow velocity (BFV) of the middle cerebral artery (MCA) can be estimated by CO2- (hyperventilation—HV and breath-holding—BH) and pressure–flow-based (Common Carotid Artery Compression—CCC and Valsalva Maneuver—VM) stimuli. We used a multimodal approach to characterize CVR in patients before carotid endarterectomy (CEA). Methods: HV, BH, CCC, and VM tests were performed on 31, 26, and 34 patients. BFV of MCAs was monitored by transcranial Doppler, and continuous arterial blood pressure was registered non-invasively. CVR was compared between the operated significantly stenotic and the contralateral sides. Results: The extent of HV- and BH-induced CVR was similar, but the time to the lowest HV-induced BFV was shorter on the side with significant ICAS. The response to CCC was sensitive to hemodynamic asymmetry in the transient hyperemic response ratio and in the cumulative change in the (mean arterial blood pressure)/(mean BFV) ratio. In VM, the slope of BFV increased in the ascending (2b) phase, and the time to overshoot correlated with the side of the stenosis. Conclusions: These results suggest that in patients with significant ICAS, in addition to CO2 reactivity measurements, a more complex estimation of CVR, by using hemodynamic tests (CCC and VM), should also be used to better quantify cerebral ischemic risk.

13 March 2026 in Life
Verified
Journal Article
Open access
PDF file
HPHanga Pál
Hanga Pál
RMRita Magyar-Stang
Rita Magyar-Stang
BCBorbála Csányi
Borbála Csányi
AGAnna Gaál
Anna Gaál
ZMZsuzsanna Mihály
Zsuzsanna Mihály
Róbert DebreczeniRóbert Debreczeni
Róbert Debreczeni
Background: In patients with severe atherosclerotic internal carotid artery stenosis (ICAS), the capacity of cerebral vasoreactivity (CVR)—an independent risk factor for cerebral ischemia—is reduced, and dysregulation of arterial blood pressure (ABP) may also be present. Thus, this study assessed the relationship between changes in cerebral blood flow velocity (BFV) in response to vasoactive stimuli (as measured by transcranial Doppler (TCD)), characterizing CVR and cardiovascular autonomic nervous system (CANS) function. Methods: Common carotid artery compression (CCC n = 26), hyperventilation (HV) and breath-holding (BH) tests (n = 31), and the Valsalva maneuver (VM n = 34) were used to assess CVR in patients with ICAS. In the middle cerebral arteries, BFV was monitored by TCD, whereas ABP was registered non-invasively. For statistical analysis, validated indices describing CANS function—namely, sympathetic index (SI), pressure recovery time (PRT), and Valsalva heart rate ratio (VHRR)—were selected based on the VM response. Several parameters were defined in order to evaluate CVR responses, including cerebral arterial resistance (CAR = ABP/BFV), which was correlated with the CVR indices using Spearman’s pairwise correlation and canonical correlation. Results: A significant correlation was found between several CVR indices of the HV-BH and VM tests and CANS indices of VM using Spearman’s pairwise correlation test. Regarding the HV-BH CVR and CANS indices of VM, a significant correlation was found between CAR values until it reached its maximum on the to-be-operated side (CARtimetomaxICAop) and VHRR (p = 0.041). A significant correlation was also found between the time elapsed until the CAR minimum value (CARtimetominICAop) and SI (p = 0.019). Concerning the CVR and CANS indices of the VM, a significant correlation was found between cerebrovascular Valsalva ratio on the to-be-operated side (CVARICAop) and PRT (p = 0.002). Canonical correlation analysis confirmed that impairments of CANS and CVR may be associated. Conclusions: In patients with severe ICAS, the potentially concomitant dysregulation of cerebrovascular reactivity and the cardiovascular autonomic nervous system can further increase cerebral ischemic risk.