ReviewHeart failure reviews2008
Pathways involved in the transition from hypertension to hypertrophy to heart failure. Treatment strategies.
Review in Heart failure reviews, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 3 of them syntheses that pooled 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.
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.
Who cites it
23 citing papers in PubMed, 3 syntheses or guidelines pooled it, 105 citations in OpenAlex.
- Potential preventive effects of selected traditional Chinese medicine as adjuvant therapy on hypertensive heart disease progression by replenishing qi and activating blood circulation: a systematic review and meta-analysis of clinical trials.Frontiers in pharmacology · 2025Pooled it
- Effect of renin-angiotensin system inhibition on cardiac structure and function and exercise capacity in heart failure with preserved ejection fraction: a meta-analysis of randomized controlled trials.Heart failure reviews · 2021Pooled it
- Pooled it
- Sodium-glucose exchanger 2 inhibitor canagliflozin promotes mitochondrial metabolism and alleviates salt-induced cardiac hypertrophy via preserving SIRT3 expression.Journal of advanced research · 2025Article
- Review
- Mildly Increased Renin Expression in the Absence of Kidney Injury in the Murine Transverse Aortic Constriction Model.Frontiers in pharmacology · 2021Article
- The Vasoactive Mas Receptor in Essential Hypertension.Journal of clinical medicine · 2020Review
- Testosterone plays a permissive role in angiotensin II-induced hypertension and cardiac hypertrophy in male rats.Biology of reproduction · 2019Article
- Therapy for heart failure with preserved ejection fraction: current status, unique challenges, and future directions.Heart failure reviews · 2018Review
- Ectopic expression of S28A-mutated Histone H3 modulates longevity, stress resistance and cardiac function in Drosophila.Scientific reports · 2018Article
- Management of Heart Failure with Preserved Ejection Fraction: Current Challenges and Future Directions.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2017Review
- Heart Failure with Preserved Ejection Fraction in Older Adults.Heart failure clinics · 2017Review
- Targeting heart failure with preserved ejection fraction: current status and future prospects.Vascular health and risk management · 2016Review
- Vitamin D receptor genetics on extracellular matrix biomarkers and hemodynamics in systolic heart failure.Journal of cardiovascular pharmacology and therapeutics · 2014Article
- Hypoglycemic and hypotensive activity of a root extract of Smilax aristolochiifolia, standardized on N-trans-feruloyl-tyramine.Molecules (Basel, Switzerland) · 2014Article
- ROCK inhibition as a therapy for spinal muscular atrophy: understanding the repercussions on multiple cellular targets.Frontiers in neuroscience · 2014Review
- Heart failure with a normal ejection fraction: treatments for a complex syndrome?Current treatment options in cardiovascular medicine · 2012Article
- Review
- Primary prevention of heart failure.ISRN cardiology · 2012Article
- Preventing progression of cardiac hypertrophy and development of heart failure by paricalcitol therapy in rats.Cardiovascular research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The renin-angiotensin-aldosterone system (RAAS) is critical in regulating systemic blood pressure, water and electrolyte balance, and pituitary gland hormones. These physiologies appear to be primarily mediated by the angiotensin II/AT(1) receptor subtype system. Overstimulation of this system can predispose cardiovascular disease (CVD) characterized by excessive vasoconstriction, fibrosis, and cardiac remodeling. If untreated, the patient typically displays a continuum of pathophysiologic conditions progressing from atherosclerosis to left ventricle hypertrophy (LVH), coronary thrombosis, myocardial infarcts, with heart failure as an endpoint. Intervention with antihypertensive therapy is necessary to inhibit this progression. RAAS blocking drugs appear to be the most effective approach. Diastolic heart failure patients benefit from treatment with angiotensin converting enzyme (ACE) inhibitors and angiotensin AT(1) receptor blockers (ARBs). Elderly CVD patients evidence age-related changes in body composition that alter the distribution and half-life of medications, thus presenting special challenges to treatment. The presence of comorbidities such as diabetes, renal dysfunction, liver insufficiency further complicates any therapeutic strategy. In addition, noncompliance because of cognitive impairment, depression, confusion due to the complexity of dose regimens, and lack of an appropriate social support system can disrupt positive outcome. The present review discusses the roles of an overactive RAAS and sympathetic nervous system as primary contributors to CVD. In addition, treatment strategies are discussed, focusing on middle aged and elderly hypertensive and heart failure patients.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.