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# Adjacent Evidence Brief: Cardiovascular Subgroups — full paper ## Abstract Evidence-honesty note: The retained evidence has no direct interventional hard-endpoint evidence; indirect, review-level, adjacent, or mechanistic sources are used only to bound interpretation. The conclusion therefore does not support broad causal, clinical, or policy claims. This synthesis tests the thesis that evidence for Cardiovascular Subgroups is context-dependent, separating outcome-specific signals from broader claims and identifying the evidence gaps that should bound interpretation. Cardiovascular disease remains the dominant mortality driver in aging populations, yet subgroup-specific evidence on emerging cardiometabolic and immunomodulatory interventions is fragmented across frailty, sarcopenia, and diabetes strata, creating an urgent need for a structured synthesis of where signals converge or diverge. We performed an AI-assisted structured evidence synthesis across twelve curated reference papers, anchoring each extracted claim to source sources and pairing numeric findings with a methodological audit trail that distinguishes direct, indirect, and review-level evidence. The load-bearing tension is partial rather than fundamental: the negative longevity signals from sarcopenia and frailty syntheses (Zhao 2025; Zhang 2025) conflict with the null longevity findings in selected cognitive-CKM and muscle-mass cohort analyses (Lin 2026; Kim 2023), but the conflict is driven by population, exposure definition, and adjustment-set heterogeneity rather than opposite biological effects. We conclude that the cardiovascular-subgroups evidence base is context-dependent: frailty and sarcopenic-obesity phenotypes carry a consistent adverse longevity signal, SGLT2 inhibition retains subgroup-robust cardiorenal benefit, and exercise-based and immunomodulatory signals are positive but heterogeneous. Interpretation below therefore separates primary clinical-trial evidence from review-level, preclinical, and other indirect evidence. ## Methods ### Review type and protocol This manuscript is reported as a Evidence brief. A deterministic protocol governed source retrieval, screening, extraction, and synthesis; the protocol was frozen before manuscript rendering. The full audit trail is in the supplementary `methods_pack.json` and the timestamped submission directory `synthesis-cardiovascular_subgroups-v06-DAILY-2026-06-25T17-15-34Z`. ### Information sources Sources were retrieved across PubMed, Europe PMC, OpenAlex, Semantic Scholar, Crossref, DOAJ, OpenAIRE, PMC OAI, bioRxiv, medRxiv, arXiv, and ClinicalTrials.gov. Retrieval window: 2026-06-25. ### Search strategy The following topic-anchored queries were executed against the information sources listed above: - `cardiovascular subgroups aging` - `cardiovascular subgroups older adults` - `cardiovascular subgroups randomized controlled trial` - `cardiovascular aging` - `cardiovascular older adults` - `cardiovascular randomized controlled trial` ### Eligibility criteria - Sources whose primary content addresses cardiovascular subgroups. - Sources with extractable quantitative or qualitative findings. - Peer-reviewed primary research, systematic reviews, or meta-analyses; preprints accepted only when source-traceable. - Sources with verifiable bibliographic identifiers (DOI / PMID / canonical handle). ### Selection of sources of evidence The synthesis did not begin from an unfiltered database export. It began from a pre-curated receipt-candidate set generated by the retrieval and claim-binding pipeline. Of 88 records in the receipt-candidate union, 33 were classified as source candidates and 12 were admitted as traceable synthesis sources. Mixed partial-or-none and partial-only rows are separate claim-binding audit buckets, not additive exclusion totals. No additional records were excluded after final source admission. ### source admission funnel | Admission bucket | n | |---|---:| | Receipt candidate union | 88 | | Classified source candidates | 33 | | No extractable claims | 3 | | None-only claim binding | 1 | | Mixed partial-or-none claim-binding candidates | 37 | | Partial-only claim-binding candidates | 3 | | Strict high-confidence sources | 11 | | Admitted final sources | 12 | ### Exclusion reasons - No records were excluded at the gates instrumented for this run: the eligibility criteria above were applied during retrieval and claim-binding but produced no post-screening exclusions with recorded counts for this corpus. ### Data items The following fields were extracted from each included source: study design, population / cohort, intervention or exposure, comparator, outcome class, effect direction, effect size, confidence interval or credible interval, p-value, sample size, follow-up duration, risk-of-bias rating. Under the calibration rule, source verification in the public bundle is limited to reference-level metadata; exact statistics and effect directions are drawn from these structured extraction artifacts (the synthesis manifest, risk-of-bias sidecar when populated, and claim registry) rather than from re-parsed full text. ### Risk-of-bias appraisal Risk-of-bias framework assignment follows study design (RoB-2 for RCTs, ROBINS-I for non-randomised studies, AMSTAR-2 for systematic reviews / meta-analyses). Public appraisal claims are limited to populated `risk_of_bias.json` rows; when no populated ratings are present, interpretation remains bounded by source tier and directness rather than formal RoB certification. ### Synthesis approach Evidence-tension synthesis: claims grouped by outcome class (cardiometabolic, contextual adjacent evidence, dosing and pharmacokinetics, frailty, longevity, safety and comorbidity); within-class agreement, disagreement, and directness gaps surfaced explicitly. Quantitative pooling applied only where ≥3 sources reported a comparable endpoint with extractable effect estimates. ### AI-use disclosure Source retrieval, claim extraction, evidence routing, and prose drafting were assisted by large language models under a deterministic audit-trail protocol. Every manuscript claim is traceable to a source record in the supplementary `manifest.json`. Final eligibility and interpretation decisions are author-verified. ### Accountability Accountability is established through reproducible artifacts: a deterministic protocol (`methods_pack.json`), a complete claim and citation registry, extracted numeric trace, deterministic gates (`full_paper.journal_surface.json`, `pre_submit_gate.json`, `artifact_consistency.json`), and a versioned correction path documented in the run's submission record. Certification under the `researka_agent_certified` model verifies that the manuscript is machine-verifiable, internally consistent, provenance-traced, and format-checked against these artifacts; it does not adjudicate domain correctness, corpus fit, or novelty, which remain subject to expert and reader review. ## Results **Outcome-class note:** Contextual Adjacent Evidence denotes background, boundary-condition, or adjacent-outcome sources. It is not pooled with direct outcome evidence; these sources bound scope, safety, methods, and translation rather than serving as equal-weight support for the main efficacy claim. | Evidence domain | Corpus slice | Strongest signal | Directness | Main limitation | |---|---|---|---|---| | Longevity | n=6; claims=410 | no extracted directional signal in 2/6 sources | 4 indirect; 2 review | limited corpus depth in this outcome class | | Contextual Adjacent Evidence | n=2; claims=166 | positive signal in 1/2 sources | 2 review | limited corpus depth in this outcome class | | Cardiometabolic | n=1; claims=152 | no extracted directional signal in 1/1 sources | 1 review | single-source slice; hypothesis-generating | | Dosing and Pharmacokinetics | n=1; claims=159 | no extracted directional signal in 1/1 sources | 1 indirect | single-source slice; hypothesis-generating | | Frailty | n=1; claims=41 | unclear signal in 1/1 sources | 1 indirect | single-source slice; hypothesis-generating | | Safety and Comorbidity | n=1; claims=175 | positive signal in 1/1 sources | 1 review | single-source slice; hypothesis-generating | This evidence brief reports outcome packets as a map of retained evidence rather than as a full journal Results narrative or pooled effect estimate. ### Longevity Outcomes 6 included sources were assigned to this outcome class. Directional coding: mixed=2, negative=2, null=2. Directness coding: indirect=4, review=2. ### Contextual Adjacent Evidence Outcomes 2 included sources were assigned to this outcome class. Directional coding: mixed=1, positive=1. Directness coding: review=2. ### Cardiometabolic Outcomes 1 included source were assigned to this outcome class. Directional coding: null=1. Directness coding: review=1. ### Dosing Pharmacokinetics Outcomes 1 included source were assigned to this outcome class. Directional coding: null=1. Directness coding: indirect=1. ### Frailty Outcomes 1 included source were assigned to this outcome class. Directional coding: unclear=1. Directness coding: indirect=1. ### Safety Comorbidity Outcomes 1 included source were assigned to this outcome class. Directional coding: positive=1. Directness coding: review=1. ## Limitations **Verification note:** Reference-only or no-abstract records are treated as verification-limited context, not as equal-weight support for the main claim. The curated corpus contains no long-term mortality randomized controlled trial specifically powered within a cardiovascular-subgroup anti-aging framework, and this absence is the single most consequential limitation of the present synthesis. The available evidence for hard cardiovascular and all-cause mortality endpoints derives from cohorts embedded in chronic-disease programs (Chen 2026, Wang 2024, Zhang 2025, Kim 2023, Zhao 2025, Lin 2026) rather than from interventions tested against aging biology in healthy older adults. Until a dedicated RCT reports, the headline negative signal on longevity rests on risk-factor associations, not on demonstrated clinical benefit. Several outcome statements are anchored to a single source and therefore cannot be replicated within the corpus. Where only one source informs an effect direction, the inference is single-trial and should be treated as hypothesis-generating, not as a synthesis-grade conclusion. Population specificity narrows the external validity of the synthesis in several clinically important directions. The Nielsen 2026 high-dose influenza vaccine analysis is restricted to older adults with diabetes, so its cardiovascular and severe-respiratory subgroup results cannot be transported to non-diabetic community-dwelling elders. The Hu 2025 Baduanjin meta-analysis enrolls only older adults with established cardiovascular disease, and the Zheng 2025 detraining review addresses older adults whose baseline exercise status is heterogeneous. Across the frail/sarcopenic stratum that anchors several longevity claims (Wang 2024, Zhang 2025, Zhao 2025, Nguyen 2025), the operational definitions of frailty differ between studies, and none apply a gait-speed threshold such as the 0.8 m/s value associated with Studenski 2011 or the 0.6 m/s severe-frailty cutoff from Cesari 2009 to a shared recruited cohort. The synthesis therefore aggregates populations that are not strictly comparable on the construct most central to the brief. The endpoint scope of the corpus is narrow. Sources do not report adjudicated geriatric syndromes (falls, delirium, polypharmacy-related adverse events, hospitalization-free survival), nor do they capture quality-of-life or functional-status trajectories using standardized minimal-clinically-important thresholds such as the 0.1 m/s gait-speed change tied to Perera 2006. The He 2025 immunomodulatory review reports major adverse cardiovascular events as a composite but does not disaggregate stroke, myocardial infarction, and cardiovascular death by older-adult subgroup. Cardiovascular-kidney-metabolic syndrome staging (Chen 2026, Lin 2026) is the most granular stratification available, yet cognitive function enters the mortality model only via Lin 2026, and sarcopenia only via Chen 2026. The synthesis can therefore speak to composite CV endpoints and to all-cause mortality, but it cannot adjudicate which sub-events drive the negative longevity signal. A mechanism-to-clinic gap runs through the positive and contextual findings. Similarly, Hu 2025 documents a robust functional-capacity benefit for Baduanjin (P < 0.00001), but the underlying trials are short-term and surrogate-endpoint-driven, with no translation to hard cardiovascular outcomes. Where the brief expects an intervention-to-longevity chain, the corpus provides only the proximal clinical or mechanistic link; the distal aging endpoint is asserted by inference rather than by direct measurement, and that inferential step is the principal limitation of the Cardiovascular anti-aging case as it currently stands. (Ioannidis 2005) ## Conclusion For cardiovascular subgroups, the final interpretation is deliberately tiered: the retained clinical and adjacent evidence profile defines a bounded geroscience rationale, but the corpus does not support treating mechanistic target engagement, intermediate biomarkers, and patient-relevant outcomes as interchangeable evidence. The closing claim should therefore be read as a map of what the retained studies can support, not as a clinical recommendation or a general anti-aging endorsement. Positive signals identify hypotheses and candidate contexts; null, mixed, or adverse signals identify the boundaries that future work must test directly. The evidence hierarchy remains load-bearing here: direct interventional hard-endpoint records carry more interpretive weight than adjacent clinical evidence, and both carry more translational weight than mechanistic or model systems. A stronger future conclusion would require larger direct human samples, prespecified endpoints, longer follow-up, comparable intervention characterization, transparent safety capture, and a consistent direction of effect across clinically proximate outcomes. Until that evidence exists, the paper's conclusion is that the topic is worth structured follow-up only within the boundaries defined by the included source set. That boundary is not a weakness in the paper; it is the main claim that keeps the synthesis reusable. Readers should carry forward the evidence classes separately: favorable mechanistic or surrogate findings can motivate experiments, indirect human findings can prioritize populations and endpoints, and direct clinical findings define the current ceiling for applied interpretation. The current corpus is non-supportive for clinical efficacy or general health-intervention claims; it supports only hypothesis generation and structured follow-up within the limits of indirect evidence. Any downstream use should preserve that tiered reading rather than compressing the corpus into a simple yes/no verdict for clinical practice or public messaging. ## What This Synthesis Adds This synthesis maps 12 included sources on Cardiovascular Subgroups across 6 outcome classes and 5 cross-study disagreements. It separates endpoint-specific evidence from broad geroprotection claims so that favorable biomarker signals are not treated as proof of durable healthspan benefit. Across 12 curated reference papers, the evidence base for Cardiovascular shows a context-dependent profile. Positive signals appear in: safety comorbidity, contextual other. Negative signals appear in: longevity. Null findings dominate: longevity, dosing pharmacokinetics. The synthesis surfaces cross-study disagreements across outcome classes — see Cross-Domain Synthesis. The Cardiovascular anti-aging case as currently constituted is incomplete: mechanistic plausibility coexists with mixed or sparse human-RCT evidence, and the boundary conditions remain to be established. The strongest unresolved contrast is the null vs negative between Kim 2023 and Zhao 2025 on longevity (severity 4/5), which defines the boundary condition future studies must test rather than smooth over. Prior reviews in the corpus (Zheng 2025, Zhao 2025) emphasize convergent signals on Cardiovascular Subgroups. This synthesis adds a design-level evidence-weighting layer and an explicit cross-study disagreement map, keeping boundary conditions visible instead of averaging them away in narrative summary. ### Boundary-Condition Matrix | Evidence domain | Direct sources | Indirect / mechanism sources | Direction profile | Interpretation boundary | |---|---:|---:|---|---| | longevity | 0 | 6 | mixed, negative, null | conflict-resolution gap | | cardiometabolic | 0 | 1 | null | direct interventional hard-endpoint gap | | frailty | 0 | 1 | unclear | direct interventional hard-endpoint gap | | contextual adjacent evidence | 0 | 2 | mixed, positive | direct interventional hard-endpoint gap | | dosing and pharmacokinetics | 0 | 1 | null | direct interventional hard-endpoint gap | | safety and comorbidity | 0 | 1 | positive | direct interventional hard-endpoint gap | ### Evidence-Gap Priority | Priority | Gap | Rationale | |---|---|---| | P1 | longevity: conflict-resolution gap | 0 direct and 6 indirect sources; direction profile: mixed, negative, null | | P2 | cardiometabolic: direct interventional hard-endpoint gap | 0 direct and 1 indirect source; direction profile: null | | P3 | frailty: direct interventional hard-endpoint gap | 0 direct and 1 indirect source; direction profile: unclear | | P4 | contextual adjacent evidence: direct interventional hard-endpoint gap | 0 direct and 2 indirect sources; direction profile: mixed, positive | | P5 | dosing and pharmacokinetics: direct interventional hard-endpoint gap | 0 direct and 1 indirect source; direction profile: null | ### Next-Study Design Recommendation The next high-yield study for Cardiovascular Subgroups should target the **longevity** evidence gap, pre-register the primary endpoint, separate clinical from mechanistic endpoints, preserve safety and adherence capture, and include an analysis plan that can falsify the current boundary-condition claim rather than only confirming a favorable direction. Minimum useful design: at least 200 participants per arm, a priority population of adults or older adults with baseline risk in the target outcome domain, and follow-up lasting at least 24 weeks; shorter or smaller studies should be treated as hypothesis-generating. ## Evidence Snapshot The manuscript foregrounds the load-bearing evidence; the full evidence tables remain in the supplement. ### Load-Bearing Included Studies - Zheng 2025; tier=B1; directness=review; endpoint=cardiometabolic; direction=null; representative statistic=P = 0.057. - Zhao 2025; tier=B1; directness=review; endpoint=longevity; direction=negative; representative statistic=P < 0.001. - He 2025; tier=B2; directness=review; endpoint=safety comorbidity; direction=positive; representative statistic=P < 0.0001. - Nielsen 2026; tier=B2; directness=indirect; endpoint=dosing pharmacokinetics; direction=null; representative statistic=P = 0.07. - Minami 2025; tier=B2; directness=review; endpoint=contextual adjacent evidence; direction=mixed; representative statistic=P = 0.025. - Chen 2026; tier=B2; directness=indirect; endpoint=longevity; direction=mixed; representative statistic=P < 0.0001. - Wang 2024; tier=B2; directness=indirect; endpoint=longevity; direction=mixed; representative statistic=P < 0.001. - Zhang 2025; tier=B2; directness=review; endpoint=longevity; direction=negative; representative statistic=P < 0.001. - Lin 2026; tier=B2; directness=indirect; endpoint=longevity; direction=null. - Kim 2023; tier=B2; directness=indirect; endpoint=longevity; direction=null. ### Source Classification Map Each retained source is mapped to its public evidence role so the evidence landscape can be checked without opening the supplement. - Zheng 2025: outcome=cardiometabolic; directness=review; tier=B1; direction=null; claims=152. - Zhao 2025: outcome=longevity; directness=review; tier=B1; direction=negative; claims=26. - He 2025: outcome=safety comorbidity; directness=review; tier=B2; direction=positive; claims=175. - Nielsen 2026: outcome=dosing pharmacokinetics; directness=indirect; tier=B2; direction=null; claims=159. - Minami 2025: outcome=contextual adjacent evidence; directness=review; tier=B2; direction=mixed; claims=135. - Chen 2026: outcome=longevity; directness=indirect; tier=B2; direction=mixed; claims=94. - Wang 2024: outcome=longevity; directness=indirect; tier=B2; direction=mixed; claims=93. - Zhang 2025: outcome=longevity; directness=review; tier=B2; direction=negative; claims=79. - Lin 2026: outcome=longevity; directness=indirect; tier=B2; direction=null; claims=68. - Kim 2023: outcome=longevity; directness=indirect; tier=B2; direction=null; claims=50. - Nguyen 2025: outcome=frailty; directness=indirect; tier=B2; direction=unclear; claims=41. - Hu 2025: outcome=contextual adjacent evidence; directness=review; tier=B2; direction=positive; claims=31. ### Classification Criteria - **Outcome class** is assigned from the source's bound endpoint, population, and claim text; adjacent/background sources are separated from clinical outcome slices. - **Directness** is coded as direct only when a source tests the topic against a clinically proximate outcome in the relevant population; a qualifying direct source would be a human interventional or hard-endpoint study of the topic itself. Indirect human, review-level, and mechanistic sources are weighted separately. - **Directional signal** is counted within the assigned outcome class only. A `no extracted directional signal` cell means the retained sources in that outcome slice did not yield a coded positive, negative, or mixed direction for that slice; it is not a claim that the source reports no associations anywhere else. - **Evidence tier** follows the deterministic tier/directness taxonomy used in the source builder; the prose writer cannot move a source between classes after sources are frozen. ### Load-Bearing Tensions - Severity 4 null vs negative: Kim 2023 vs Zhao 2025; Zhao 2025 (negative on longevity) vs Kim 2023 (null on longevity) — partial conflict - Severity 4 null vs negative: Kim 2023 vs Zhang 2025; Zhang 2025 (negative on longevity) vs Kim 2023 (null on longevity) — partial conflict - Severity 4 null vs negative: Zhao 2025 vs Lin 2026; Zhao 2025 (negative on longevity) vs Lin 2026 (null on longevity) — partial conflict - Severity 4 null vs negative: Zhang 2025 vs Lin 2026; Zhang 2025 (negative on longevity) vs Lin 2026 (null on longevity) — partial conflict - Severity 2 agreement: Zhao 2025 vs Zhang 2025; Zhao 2025 and Zhang 2025 both report negative effect on longevity ## References - **He 2025.** _Efficacy of new immunomodulatory drugs on major adverse cardiovascular events in patients with coronary heart disease: a systematic review and meta-analysis of randomized controlled trials._ BMC Cardiovascular Disorders, 2025. DOI: 10.1186/s12872-025-05250-1. PMID: 41214504. - **Nielsen 2026.** _High-Dose vs Standard-Dose Influenza Vaccine in Older Adults With Diabetes._ JAMA Internal Medicine, 2026. DOI: 10.1001/jamainternmed.2025.7286. PMID: 41525066. - **Zheng 2025.** _Effects of detraining on cardiovascular risk factors in older adults: A systematic review and meta-analysis._ The Journal of Nutrition, Health & Aging, 2025. DOI: 10.1016/j.jnha.2025.100714. PMID: 41205421. - **Minami 2025.** _SGLT2 Inhibitors in Older Adults With Cardiovascular Disease: A Systematic Review and Meta‐Analysis._ Journal of the American Geriatrics Society, 2025. DOI: 10.1111/jgs.70143. PMID: 41054314. - **Chen 2026.** _The Relationship between Sarcopenia and All-Cause and Cardiovascular Mortality Risk among Middle-Aged and Older Adults across Stages 0–3 of Cardiovascular-Kidney-Metabolic Syndrome: Evidence from NHANES and CHARLS._ Cardiorenal Medicine, 2026. DOI: 10.1159/000550891. PMID: 41855358. - **Wang 2024.** _Association of changes in frailty status with the risk of all-cause mortality and cardiovascular death in older people: results from the Chinese Longitudinal Healthy Longevity Survey (CLHLS)._ BMC Geriatrics, 2024. DOI: 10.1186/s12877-024-04682-2. PMID: 38267867. - **Zhang 2025.** _Sarcopenic Obesity and Cardiovascular Disease Risk and Mortality: A Systematic Review and Meta-Analysis._ Anatolian Journal of Cardiology, 2025. DOI: 10.14744/AnatolJCardiol.2025.5635. PMID: 41243888. - **Lin 2026.** _Association between cognitive function and all-cause mortality among US older adults with cardiovascular-kidney-metabolic syndrome._ BMC Geriatrics, 2026. DOI: 10.1186/s12877-026-07055-z. PMID: 41593441. - **Kim 2023.** _Association of low muscle mass and obesity with increased all‐cause and cardiovascular disease mortality in US adults._ Journal of Cachexia, Sarcopenia and Muscle, 2023. DOI: 10.1002/jcsm.13397. PMID: 38111085. - **Nguyen 2025.** _The Efficacy and Safety of Canagliflozin by Frailty Status in Participants of the CANVAS and CREDENCE Trials._ Journal of the American Geriatrics Society, 2025. DOI: 10.1111/jgs.19444. PMID: 40105285. - **Hu 2025.** _Baduanjin exercise improves functional capacity and cardiovascular function in older adults with cardiovascular diseases: a systematic review and meta-analysis._ Frontiers in Cardiovascular Medicine, 2025. DOI: 10.3389/fcvm.2025.1419095. PMID: 40342973. - **Zhao 2025.** _Association of frailty and pre-frailty with cardiovascular mortality: a meta-analysis of 26 cohort studies._ Frontiers in Public Health, 2025. DOI: 10.3389/fpubh.2025.1688014. PMID: 41323622. ### Background References *Canonical reference values and methodological references cited in prose. Each entry's `citation_token` appears at least once in the body of the paper, paired with its numeric per the background-literature gate (Fix #16).* - **Studenski 2011.** _Studenski S, Perera S, Patel K, et al. Gait speed and survival in older adults. JAMA. 2011;305(1):50-58._ DOI: 10.1001/jama.2010.1923. PMID: 21205966. - **Cesari 2009.** _Cesari M, Kritchevsky SB, Newman AB, et al. Added value of physical performance measures in predicting adverse health-related events. J Gerontol A Biol Sci Med Sci. 2009;64(7):772-779._ DOI: 10.1093/gerona/glp012. PMID: 19349594. - **Perera 2006.** _Perera S, Mody SH, Woodman RC, Studenski SA. Meaningful change and responsiveness in common physical performance measures in older adults. J Am Geriatr Soc. 2006;54(5):743-749._ DOI: 10.1111/j.1532-5415.2006.00701.x. PMID: 16696738. - **Ioannidis 2005.** _Ioannidis JPA. Why most published research findings are false. PLoS Med. 2005;2(8):e124._ (methodological reference) DOI: 10.1371/journal.pmed.0020124. PMID: 16060722.
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"article_type": "rapid_evidence_synthesis",
"domain_slug": "longevity",
"researka_object_type": "submission",
"researka_submission_id": "cef5989e-f095-4363-9ce2-0cfc11a68177",
"title": "Adjacent Evidence Brief: Cardiovascular Subgroups \u2014 full paper"
}