Evidence map›Paper›PMID 16450807›Full record

ReviewClinical cardiology2005

Epidemiology and stratification of risk for sudden cardiac death.

Philip J Podrid, Robert J Myerburg

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cardiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Obesity Arrhythmias: Role of IL-6 Trans-Signaling.International journal of molecular sciences · 2024
    Review
  5. Review
  6. Article
  7. Discussing the Score of Cardioembolic Ischemic Stroke in Chagas Disease.Tropical medicine and infectious disease · 2020
    Article
  8. Article
  9. Enhancing Autophagy Diminishes Aberrant CaFrontiers in physiology · 2019
    Article
  10. Article
  11. Review
  12. Article
  13. Arrhythmias in the Heart Transplant Patient.Arrhythmia & electrophysiology review · 2014
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Synergism between arrhythmia and hyperhomo-cysteinemia in structural heart disease.International journal of physiology, pathophysiology and pharmacology · 2011
    Article
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

2 authors at 2 institutions in 1 country.

Philip J PodridBoston University School of Medicine, Attending Physician VA Boston Healthcare System, West Roxbury VA Division, 1400 VFW Parkway West Roxbury, MA 20132, USA. philip.podrid@med.va.gov
Robert J Myerburg
Boston University · USUniversity of Miami · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sudden cardiac death (SCD) is a major cause of mortality in the United States. Approximately 65% of cases of SCD occur in patients with underlying acute or chronic ischemic heart disease. The incidence of SCD increases 2- to 4-fold in the presence of coronary disease and 6- to 10-fold in the presence of structural heart disease. Ventricular fibrillation (VF) precipitated by ventricular tachycardia (VT) is a common mechanism of cardiac arrest leading to SCD. Triggers for SCD include electrolyte disturbances, heart failure, and transient ischemia. Although a large percentage of patients with out-of-hospital SCD do not survive, successful resuscitation to hospitalization has improved in recent years. One of the challenges for preventing SCD lies in identifying individuals at highest risk for SCD within a lower-risk population. The progression from conventional risk factors of coronary artery disease to arrhythmogenesis and SCD can be represented as a cascade of changes associated with levels of increasing risk. At the first level is atherogenesis, followed by changes in atherosclerotic plaque anatomy, which may be mediated by inflammatory processes. Disruption of active plaque formed during a transitional state initiates the thrombotic cascade and acute occlusion, after which acute changes in myocardial electrophysiology become the immediate trigger for arrhythmogenesis and SCD. Each level of the cascade offers different opportunities for risk prediction. Among the classes of risk predictors are clinical markers, such as ECG measures and ejection fraction. Transient risk markers, such as inflammatory markers, are potentially useful for identifying triggers for SCD. In the future, genetic profiling is expected to allow better assessment of individual risks for SCD.

Indexed as

Arrhythmias, CardiacCardiopulmonary ResuscitationCoronary DiseaseDeath, Sudden, CardiacGenetic Predisposition to DiseaseHumansRisk FactorsRisk Reduction BehaviorUnited States

Identifiers

PMID16450807
PMCPMC6653918
OpenAlexW2076373701

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.