Progress in cardiovascular diseases · 2026
Hypertension and clinical outcomes following thoracic radiotherapy.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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McCrohan Megan, Patel Prem, Busby Tyren, Ghazi Sanam, Holtman Adia, Siefker Anna, Wade Elizabeth, Goyal Akash, McLaughlin Eric, Jin Ning, Merritt Robert E, Diaz Dayssy, Ferdousi Mussammat, Ruz Patrick, Reddy Sohil, Wu Trudy, DiCostanzo Dominic, Faught Austin M, Brammer Jonathan, Osuji Evans, Kola-Kehinde Onaopepo, Williams Terence M, Welliver Meng, Miller Eric D, Addison Daniel
Аннотация
BACKGROUND: Radiation therapy (RT) is highly efficacious in treating thoracic malignancies. However, RT has been linked to potential cardiotoxicity. Yet, the long-term incidence, severity, and implications of HTN-development post-RT are unknown.
METHODS: Leveraging a large US-based Comprehensive-Cancer-Center-cohort of patients treated with thoracic-RT from 2007 to 2019, we included patients ≥18 years old with histologically confirmed esophageal or lung cancers. The primary outcome was incidence of incident/new or worsened HTN [systolic-blood-pressure-(SBP) ≥130 mmHg] after RT-initiation. The secondary outcomes were major-adverse-cardiac-events (MACE- heart-failure, myocardial-infarction, arrhythmia, stroke, and sudden-death), disease-progression, and overall-survival, by HTN-status. Differences in outcomes by HTN-status were also evaluated via landmark-analysis, excluding those with undiagnosed HTN. Observed new HTN rates were compared to Framingham-predicted-rates, and absolute-excess-risks were estimated. Multivariate regression was used to define the relation between clinical and RT measures and both new or worsened HTN-development and survival-outcomes.
RESULTS: Overall, 439 RT-treated patients (238 esophageal; 201 lung; 66.7% male; mean age 63.6 years; 65% baseline HTN) were identified. Over a median follow-up of 23 months, 255 (58.1%) developed new or worsened HTN; median SBP increase of 7 mmHg. In landmark-analysis, the cumulative incidence of new or worsened HTN by 1-year was 48.0% and 63.4%, respectively. Using the JNC-8 cutoff of ≥140/90 mmHg, the new HTN rate was 21.6% at 1-year, translating to a 3.4-fold higher rate than the Framingham-predicted-rate (RR 3.37, P < 0.001). In multivariate regression, RT-dose was consistently associated with new or worsened HTN-development (P < 0.05); those with RT-induced-HTN saw improved progression-free-survival and overall-survival (HR 0.67 and 0.54, P < 0.01, respectively). Beyond traditional factors, only RT-dose is consistently associated with MACE (P < 0.05). No specific antihypertensive class prevented RT-related HTN.
CONCLUSIONS: These data suggest that thoracic-RT increases early HTN risk.
METHODS: Leveraging a large US-based Comprehensive-Cancer-Center-cohort of patients treated with thoracic-RT from 2007 to 2019, we included patients ≥18 years old with histologically confirmed esophageal or lung cancers. The primary outcome was incidence of incident/new or worsened HTN [systolic-blood-pressure-(SBP) ≥130 mmHg] after RT-initiation. The secondary outcomes were major-adverse-cardiac-events (MACE- heart-failure, myocardial-infarction, arrhythmia, stroke, and sudden-death), disease-progression, and overall-survival, by HTN-status. Differences in outcomes by HTN-status were also evaluated via landmark-analysis, excluding those with undiagnosed HTN. Observed new HTN rates were compared to Framingham-predicted-rates, and absolute-excess-risks were estimated. Multivariate regression was used to define the relation between clinical and RT measures and both new or worsened HTN-development and survival-outcomes.
RESULTS: Overall, 439 RT-treated patients (238 esophageal; 201 lung; 66.7% male; mean age 63.6 years; 65% baseline HTN) were identified. Over a median follow-up of 23 months, 255 (58.1%) developed new or worsened HTN; median SBP increase of 7 mmHg. In landmark-analysis, the cumulative incidence of new or worsened HTN by 1-year was 48.0% and 63.4%, respectively. Using the JNC-8 cutoff of ≥140/90 mmHg, the new HTN rate was 21.6% at 1-year, translating to a 3.4-fold higher rate than the Framingham-predicted-rate (RR 3.37, P < 0.001). In multivariate regression, RT-dose was consistently associated with new or worsened HTN-development (P < 0.05); those with RT-induced-HTN saw improved progression-free-survival and overall-survival (HR 0.67 and 0.54, P < 0.01, respectively). Beyond traditional factors, only RT-dose is consistently associated with MACE (P < 0.05). No specific antihypertensive class prevented RT-related HTN.
CONCLUSIONS: These data suggest that thoracic-RT increases early HTN risk.