Display Settings:

Items per page

Results: 1 to 20 of 2094

1.
Figure 1

Figure 1. Sudden cardiac death rate per year. From: Cystatin C and Sudden Cardiac Death Risk in the Elderly.

x-axis: cystatin C and creatinine-based estimated GFR tertiles
y-axis: sudden cardiac death rates per year (% per year)

Rajat Deo, et al. Circ Cardiovasc Qual Outcomes. ;3(2):159-164.
2.
Fig. 3

Fig. 3. From: Sudden death prevention in heart failure: The case of CIBIS III.

Sudden death during the first year. At one year, in the bisoprolol-first group 16 patients had a sudden death versus 29 in the enalapril-first group: HR for sudden death, bisoprolol-first versus enalapril-first 0.54; 95% CI 0.29–1.00: P=0.049.

EMILIO VANOLI, et al. Heart Int. 2006;2(2):73.
3.
Figure 1

Figure 1. Time to sudden cardiac death in medically-treated arm by QRSd < or ≥ 140 milliseconds (ms). From: Association of prolonged QRS duration with ventricular tachyarrhythmias and sudden cardiac death in the Multicenter Automatic Defibrillator Implantation Trial II (MADIT-II).

Kaplan-Meier curve of freedom from sudden cardiac death in medically-treated arm in patients with QRSd ≥ 140 milliseconds (ms) compared to patients with QRSd < 140 ms.

Ritesh Dhar, et al. Heart Rhythm. ;5(6):807-813.
4.
<b>Figure 2</b>

Figure 2. From: Do risk factors differ between explained sudden unexpected death in infancy and sudden infant death syndrome?.

 Distribution by season of death for sudden infant death syndrome (SIDS) and explained sudden unexpected death in infancy (SUDI).

M Vennemann, et al. Arch Dis Child. 2007 February;92(2):133-136.
5.
Figure 1

Figure 1. From: F-MARC: the FIFA Sudden Death Registry (FIFA-SDR).

Starting internet-page of the FIFA Sudden Death Registry (FIFA-SDR) at http://www.sudden-death-in-football.com. By clicking the field ‘REPORT A CASE’ persons can report cases on a sudden death or successfully resuscitated sudden death of a football player via a confidential online access leading to the questionnaire.

Jürgen Scharhag, et al. Br J Sports Med. 2015 May;49(9):563-565.
6.
Figure 3

Figure 3. From: MODE AND MECHANISMS OF DEATH FOLLOWING ORTHOTOPIC HEART TRANSPLANTATION.

(A) Mechanism of death in sudden death patients with documented rhythm at the time of death (n=26); (B) Mechanism of death in non-sudden death patients with documented rhythm at the time of death (n=65); (C) Mechanism of death in sudden death patients due to acute ischemia with documented rhythm at the time of death (n=18). SD= sudden death, NSD=non-sudden death, PEA=pulseless electrical activity, VF=ventricular fibrillation. The mechanism of death was not known in 37% of SD (16 of 41) and 13% (10 of 75) of NSD patients.

Marmar Vaseghi, et al. Heart Rhythm. 2009 April;6(4):503-509.
7.
Figure 1

Figure 1 . From: Comparative epidemiology of sudden infant death syndrome and sudden intrauterine unexplained death.

Definitions of sudden infant death syndrome (SIDS) and sudden intrauterine unexplained death (SIUD).

J Froen, et al. Arch Dis Child Fetal Neonatal Ed. 2002 September;87(2):F118-F121.
8.
Figure 1

Figure 1. From: Late gadolinium enhancement cardiovascular magnetic resonance for sudden cardiac death risk stratification in hypertrophic cardiomyopathy.

Kaplan-Meier survival estimates for A) sudden cardiac death or aborted sudden cardiac death; and B) cardiovascular mortality of aborted sudden cardiac death stratified by left ventricular ejection fraction.

Tevfik F Ismail, et al. J Cardiovasc Magn Reson. 2013;15(Suppl 1):O67-O67.
9.
Figure 4

Figure 4. From: Postmortem computed tomography is an informative approach for prevention of sudden unexpected natural death in the elderly.

Reliability levels of causes of sudden death inferred from PMCT findings and supporting information. The level A group, wherein the causes of sudden death can be established from PMCT findings, comprised 27.1% of all cases examined by PMCT, whereas the level B group, wherein the causes of sudden death are inferable with considerable reliability, accounted for 4.9% of the total cases. The level C group, wherein the causes of sudden death are inferable with low reliability, and the level D group with no significant PMCT findings represented 11.1% and 56.9% of the total cases, respectively. Abbreviation: PMCT, postmortem computed tomography.

Toshihiro Kaneko, et al. Risk Manag Healthc Policy. 2010;3:13-20.
10.
Figure 1

Figure 1. From: SUDDEN DEATH AFTER PEDIATRIC HEART TRANSPLANTATION.

Kaplan-Meier freedom from sudden death and hazard of sudden death post-transplant.

Kevin P. Daly, et al. J Heart Lung Transplant. ;30(12):1395-1402.
11.
Fig. 1

Fig. 1. From: Dentate gyrus abnormalities in sudden unexplained death in infants: morphological marker of underlying brain vulnerability.

Examples of focal granule cell dispersion in the dentate gyrus (DG) and associated abnormalities in infants with sudden unexplained in death. a Normal infant hippocampus with landmarks for reference at its mid-body [level of the lateral geniculate nucleus (not shown)]. The DG forms the shape of a “C” at this level. Hematoxylin and eosin (H&E), ×4. b Control DG in a 4-month-old infant with explained cause of death. The DG consists of densely packed granule cells in a linear structure in its straight limbs. H&E, ×20. c Hippocampus of an infant with sudden unexplained death with focal granule cell bilamination (arrow) in the DG. H&E, ×4. d Hippocampus of a second infant with sudden unexplained death with focal granule cell bilamination (arrow) in the DG. H&E, ×10. e Hippocampus of a third infant with sudden unexplained death with focal granule cell bilamination (arrow) in the DG. H&E, ×10. f Hippocampus of a fourth infant with sudden unexplained death with focal granule cell bilamination (arrow) in the DG. H&E, ×10. g Granule cell duplication at the bend (hook) of the DG (arrow), associated with FGCB along the straight limb, in an infant with sudden unexplained death. H&E, ×20. h There are single, ectopic granule cells in the molecular layer (arrowheads). In the DG, there are immature cells, suggestive of immature neurons (Fig. 2), present in the subgranular layer. H&E, ×20. i There are immature cells in the DG (arrowheads), as well as clusters of granule cells in the molecular layer (arrow). H&E, ×20. DG dentate gyrus, ML molecular layer

Hannah C. Kinney, et al. Acta Neuropathol. 2015;129:65-80.
12.
<b>Figure 1</b>

Figure 1. From: Do risk factors differ between explained sudden unexpected death in infancy and sudden infant death syndrome?.

 Age distribution of infants with sudden infant death syndrome (SIDS) and explained sudden unexpected death in infancy (SUDI).

M Vennemann, et al. Arch Dis Child. 2007 February;92(2):133-136.
13.
Figure 3

Figure 3. From: Characteristics of Sudden Arrhythmic Death in a Diverse, Urban Community.

Rates of SAD and WHO SCD by Gender and Ethnicity
RR is for SAD. RR = relative risk; SAD = Sudden arrhythmic death; SCD = Sudden cardiac death

Daniel A. Steinhaus, et al. Am Heart J. ;163(1):125-131.
14.
Figure 1

Figure 1. From: Sudden Cardiac Death After Myocardial Infarction in Type 2 Diabetic Patients With No Residual Myocardial Ischemia.

Kaplan-Meier curves of all-cause death (A), cardiac death (B), sudden cardiac death (C), and nonsudden cardiac death (D) in patients with and without DM.

Chun-Yip Yeung, et al. Diabetes Care. 2012 December;35(12):2564-2569.
15.
Figure 2

Figure 2. From: Characteristics of Sudden Arrhythmic Death in a Diverse, Urban Community.

Stratification of WHO SCDs by Autopsy Status
SAD = Sudden arrhythmic death; SD = Sudden death; CHF = Congestive heart failure; PE = Pulmonary embolism; AI = Aortic insufficiency

Daniel A. Steinhaus, et al. Am Heart J. ;163(1):125-131.
16.
Figure 3

Figure 3. From: Predictive Value of Beat-to-Beat QT Variability Index across the Continuum of Left Ventricular Dysfunction: Competing Risks of Non-cardiac or Cardiovascular Death, and Sudden or Non-Sudden Cardiac Death.

Cumulative incidence functions for the cardiovascular death (A), non-cardiac death (B), sudden cardiac death (C) and non-sudden cardiac death (D) in 4 categories of patients.

Larisa G. Tereshchenko, et al. Circ Arrhythm Electrophysiol. ;5(4):719-727.
17.
Fig. 2.

Fig. 2. From: Gene expression analysis characterizes antemortem stress and has implications for establishing cause of death.

Comparison of gene expression in the sudden death and sudden death delayed harvest. In sudden death, liver tissue is immediately harvested. In sudden death delayed harvest, liver tissue is harvested 4 h postmortem after the mouse has cooled to 21°C. The heat map shows that delayed harvest produces distinctive differences in gene expression patterns.

David Jardine, et al. Physiol Genomics. 2011 August;43(16):974-980.
18.
Figure 2

Figure 2. Survival analysis of sudden cardiac deaths in the MRC-Older Adults trial. From: Treatment of Elderly Hypertensive Patients with Epithelial Sodium Channel Inhibitors Combined with a Thiazide Diuretic Reduces Coronary Mortality and Sudden Cardiac Death.

Survival was assessed using time from randomization to sudden death. Survival curves were constructed by the Kaplan-Meier method40 with the p value calculated using the log-rank test31.

Patricia R. Hebert, et al. J Am Soc Hypertens. ;2(5):355-365.
19.
Figure 1

Figure 1. From: Etiology of Sudden Death in the Community: Results of Anatomic, Metabolic and Genetic Evaluation.

Selection of 71 sudden death victims without an initially apparent cause of death

A. Selcuk Adabag, et al. Am Heart J. ;159(1):33-39.
20.
Figure 2b

Figure 2b. From: Epidemiology of Sudden Cardiac Death in Rural South India - Insights From The Andhra Pradesh Rural Health Initiative.

Chief underlying cause of death in sudden death

Srinivas R Madhavan, et al. Indian Pacing Electrophysiol J. 2011 Jul-Aug;11(4):93-102.

Display Settings:

Items per page

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk