Evidence map›Paper›PMID 22199422›Full record

ArticleTexas Heart Institute journal2011

Central venous pressure and pulmonary capillary wedge pressure: fresh clinical perspectives from a new model of discordant and concordant heart failure.

Tony S Ma, Biykem Bozkurt, David Paniagua, Biswajit Kar, Kumudha Ramasubbu, Carl F Rothe

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Article in Texas Heart Institute journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Characterizing heart failure in the ventricular volume domain.Clinical Medicine Insights. Cardiology · 2015
    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

6 authors.

Tony S MaSection of Cardiology, Baylor College of Medicine and Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas 77030, USA. ma_tony@sbcglobal.net
Biykem Bozkurt
David Paniagua
Biswajit Kar
Kumudha Ramasubbu
Carl F Rothe

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart-failure phenotypes include pulmonary and systemic venous congestion. Traditional heart-failure classification systems include the Forrester hemodynamic subsets, which use 2 indices: pulmonary capillary wedge pressure (PCWP) and cardiac index. We hypothesized that changes in PCWP and central venous pressure (CVP), and in the phenotypes of heart failure, might be better evaluated by cardiovascular modeling. Therefore, we developed a lumped-parameter cardiovascular model and analyzed forms of heart failure in which the right and left ventricles failed disproportionately (discordant ventricular failure) versus equally (concordant failure). At least 10 modeling analyses were carried out to the equilibrium state. Acute discordant pump failure was characterized by a "passive" volume movement, with fluid accumulation and pressure elevation in the circuit upstream of the failed pump. In biventricular failure, less volume was mobilized. These findings negate the prevalent teaching that pulmonary congestion in left ventricular failure results primarily from the "backing up" of elevated left ventricular filling pressure. They also reveal a limitation of the Forrester classification: that PCWP and cardiac index are not independent indices of circulation. Herein, we propose a system for classifying heart-failure phenotypes on the basis of discordant or concordant heart failure. A surrogate marker, PCWP-CVP separation, in a simplified situation without complex valvular or pulmonary disease, shows that discordant left and right ventricular failures are characterized by differences of ≥ 4 and ≤ 0 mmHg, respectively. We validated the proposed model and classification system by using published data on patients with acute and chronic heart failure.

Indexed as

Central Venous PressureModels, CardiovascularPulmonary Wedge PressureAcute DiseaseAnimalsCardiac OutputChronic DiseaseHeart FailureHumansPhenotypePrognosisPulmonary CirculationReproducibility of ResultsVentricular Function, LeftVentricular Function, RightVentricular PressureBlood volumecardiac outputcardiovascular physiological phenomenacentral venous pressureheart failure/classification/physiopathologyheart ventricles/physiopathologyhemodynamics/physiologymodels, cardiovascularmyocardial infarction/physiopathologypulmonary wedge pressure/physiologyvascular resistance/physiologyventricular function

Identifiers

PMID22199422
PMCPMC3233309

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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.