Şeymagül Karaca

Şeymagül Karaca

orcid

Research Focus & Metrics

Academic Career Length

1Year (2026-Present)

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

Representative Publications

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19 March 2026 in Journal of Clinical Medicine
Verified
Journal Article
Open access
PDF file
SESelen Eski
Selen Eski
HTHatice Taşkan
Hatice Taşkan
ÖEÖzkan Eravcı
Özkan Eravcı
ŞKŞeymagül Karaca
Şeymagül Karaca
AAAhmet ARSLAN
Ahmet ARSLAN
EYErkan Yildirim Yildirim
Erkan Yildirim Yildirim
Background/Objectives: Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide. The 2023 American Heart Association PREVENT equations represent a contemporary approach to cardiovascular risk estimation, yet they rely on resting clinical and biochemical parameters. This study aimed to evaluate the association between PREVENT-estimated 10-year cardiovascular risk and treadmill exercise testing (TET)-derived physiological variables. Methods: We conducted a single-center observational study of 391 participants (mean age 42.9 ± 9.0 years, 56.8% male) who underwent symptom-limited treadmill testing. Ten-year cardiovascular risk was estimated using PREVENT for total cardiovascular disease (CVD), ASCVD, and heart failure (HF). Hierarchical multivariable regression was performed using log-transformed PREVENT risk estimates to quantify the incremental association of exercise capacity (METs), hemodynamic markers (double product), autonomic recovery (heart rate recovery), and the ST/HR index beyond demographic (age, sex, BMI) and extended clinical base models incorporating available PREVENT input covariates. Results: Beyond the demographic base model, treadmill parameters were significantly associated with log-transformed PREVENT-CVD risk (ΔR2 = 0.026, p < 0.001; Cohen’s f2 = 0.154). Double product (standardized β = 0.116), HRR at 1 min (standardized β = −0.081), and maximum METs (standardized β = −0.079) were independently associated with risk estimates. However, when the full set of available PREVENT input covariates was included in the base model, the incremental association was negligible (ΔR2 = 0.0004, p = 0.386), indicating substantial overlap between exercise-derived physiology and PREVENT-embedded clinical information. The incremental association was greatest in participants with intermediate (1–5%) and higher (≥5%) estimated risk (ΔR2 = 0.052 and 0.246, respectively). Approximately 14% of participants shifted to a different quartile of estimated risk after inclusion of treadmill data. Conclusions: Treadmill-derived physiological parameters are significantly associated with PREVENT-estimated cardiovascular risk, but this association largely reflects shared pathophysiology with PREVENT input variables rather than statistically independent incremental information. Exercise testing may serve as a physiological complement to static risk estimation, particularly in intermediate-risk populations, by providing a dynamic physiological assessment that complements resting clinical measurements. Prospective studies with adjudicated cardiovascular outcomes are needed before clinical implementation.