Evidence map›Paper›PMID 35614846›Full record

ArticleClinical endocrinology2022

Role of renin-angiotensin-aldosterone system activation and other metabolic variables in relation to arterial inflammation in HIV.

Grace Shen, Teressa S Thomas, Allie R Walpert, Colin M McClure, Kathleen V Fitch, Christopher deFilippi, Martin Torriani, Colleen G Buckless, Gail K Adler, Steven K Grinspoon and 1 more

Open access · greenAbstract read
In one paragraph

Article in Clinical endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 35% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 2 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Grace ShenMetabolism Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0001-6023-8764
Teressa S ThomasMetabolism Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Allie R WalpertMetabolism Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Colin M McClureMetabolism Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Kathleen V FitchMetabolism Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Christopher deFilippiINOVA Heart and Vascular Institute, Falls Church, Virginia, USA.
Martin TorrianiDivision of Musculoskeletal Imaging and Intervention, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Colleen G BucklessDivision of Musculoskeletal Imaging and Intervention, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Gail K AdlerDivision of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Steven K GrinspoonMetabolism Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Suman SrinivasaMetabolism Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0003-1950-4770
Harvard University · USAlaska Heart and Vascular Institute · USBrigham and Women's Hospital · US

Funding

Harvard Clinical and Translational Science CenterUL1TR001102 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2013 to 2017
$106.2M
HARVARD CLINICAL AND TRANSLATIONAL SCIENCE CENTER (UL1)UL1RR025758 · NCRR · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2008 to 2011
$91.4M
ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Elizabeth Austen Lawson, Takara Leah Stanley · 1994 to 2026
$31.6M
Harvard Clinical and Translational Science Center (UL1)UL1TR000170 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2012 to 2013
$31.4M
TESTOSTERONE AND GROWTH HORMONE EFFECTS IN AIDS WASTINGR01DK049302 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI ADLER, GAIL KURR, GRINSPOON, STEVEN K. · 1995 to 2020
$12.2M
Avoiding (Heart) Failure: Physiologic-Based Targeting of the RAAS to Treat Subclinical HFpEF among PWHR01HL151293 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI SRINIVASA, SUMAN · 2020 to 2024
$4.2M
Aldosterone and Diabetic Cardiovascular Disease: Research and Mentoring ProgamK24HL103845 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ADLER, GAIL KURR · 2011 to 2021
$1.6M
Physiologic Investigation of the Renin-Angiotensin-Aldosterone System to Understand Arterial Inflammation in HIVK23HL136262 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI SRINIVASA, SUMAN · 2017 to 2021
$960k
NCATS NIH HHS UL1 TR000170NCATS NIH HHS UL1 TR001102NCRR NIH HHS UL1 RR025758NHLBI NIH HHS K23 HL136262NHLBI NIH HHS K24 HL103845NHLBI NIH HHS R01 HL151293NIDDK NIH HHS P30 DK040561NIDDK NIH HHS R01 DK049302
6 · The paper itself

Abstract

backgroundArterial inflammation remains increased among persons with HIV (PWH) compared with persons without HIV (PWOH) even when controlling for traditional risk factors. We sought to understand whether increased renin-angiotensin-aldosterone system (RAAS) activation may be related to arterial inflammation in PWH and when compared with PWOH.

designTwenty PWH and 9 PWOH followed a controlled, standardized low and liberal sodium diet to simulate a RAAS-activated and RAAS-suppressed state, respectively. We measured serum lipoprotein-associated phospholipase A2 (LpPLA2) concentrations following both conditions to assess the physiologic dynamics of aldosterone in relation to arterial inflammation.

resultsLpPLA2 levels were significantly higher among PWH versus PWOH during both the RAAS-activated state[5.3(4.2, 6.1) versus 4.0(3.0, 4.8)nmol/L, median(interquartile range),p = .01]) and RAAS-suppressed state[4.4(3.9, 5.3) versus 3.8(3.4, 4.1)nmol/L,p = .01]. Among PWH, but not PWOH, LpPLA2 increased significantly with RAAS activation(p = .03). LpPLA2 levels measured during the RAAS-suppressed state among PWH remained relatively higher than LpPLA2 levels under both conditions among PWOH. Log LpPLA2 was related to log aldosterone during the RAAS-activated state(r = .39,p = .04) among all participants. Log LpPLA2 was correlated with visceral fat(r = .46,p = .04) and log systolic blood pressure(r = .57,p = .009) during a RAAS-activated state when an increase in aldosterone was stimulated in HIV.

conclusionLpPLA2 is increased during a RAAS-activated state among PWH, but not among PWOH. Further, LpPLA2 was increased in both RAAS-activated and suppressed states in PWH compared with PWOH. These data suggest a biological link between increased aldosterone and arterial inflammation in this population. Future studies should test RAAS blockade on arterial inflammation as a targeted treatment approach in HIV.

Indexed as

ArteritisHIV Infections1-Alkyl-2-acetylglycerophosphocholine EsteraseAldosteroneHumansRenin-Angiotensin SystemSodium1-Alkyl-2-acetylglycerophosphocholine EsteraseAldosteroneSodiumHIVLpPLA2renin-angiotensin-aldosterone systemvisceral fat

Identifiers

PMID35614846
PMCPMC9532371
OpenAlexW4281554810

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.