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1.
Europace ; 16(12): 1752-8, 2014 Dec.
Article in English | MEDLINE | ID: mdl-25061228

ABSTRACT

AIMS: Sudden cardiac death (SCD) is among the most common causes of death in western countries including Germany. Whereas risk stratification and primary prevention is still insufficient, we also lack accurate incidence estimates. Current estimates vary widely (18.6-128/100,000/year), but data on SCD incidence in Germany are missing. Depending on SCD definitions, death needs to occur between 1 and 24 h after the onset of symptoms. METHODS AND RESULTS: In the district of Aurich (190,000 inhabitants, Lower Saxony, Germany), emergency medical service (EMS) is provided by a district government operated single carrier and two hospitals. To evaluate all EMS calls in this district from 2002 to 2009, we obtained EMS protocols, medical records, and death certificates for data analysis and adjudication of SCD. We defined SCD according to the definition of the World Health Organization, considering patients with cardiac arrest within ≤1 h after the onset of symptoms. We also required cardiopulmonary resuscitation being performed by EMS personnel. The overall mortality rate in the district of Aurich (1060/100,000/year) corresponded well with the average mortality rate in Germany (1030/100,000/year). During the observation period, we adjudicated 1212 SCD cases, equivalent to an annual rate of 151 SCD cases (81 cases/100,000/year). Rates remained remarkably stable over time, and affected a considerable number of individuals of working age (32/100,000/year). CONCLUSION: Consistent with prior reports, the SCD incidence in a district of Germany is substantial. Despite an elaborate EMS system and advanced medical care, SCD rates remain stable and necessitate improved, individualized risk stratification.


Subject(s)
Cardiopulmonary Resuscitation/mortality , Death, Sudden, Cardiac/epidemiology , Death, Sudden, Cardiac/prevention & control , Emergency Medical Services/statistics & numerical data , Registries , Adolescent , Adult , Age Distribution , Aged , Aged, 80 and over , Cardiopulmonary Resuscitation/statistics & numerical data , Child , Child, Preschool , Female , Germany/epidemiology , Humans , Incidence , Infant , Infant, Newborn , Male , Middle Aged , Risk Factors , Sex Distribution , Young Adult
2.
Crit Care Med ; 30(4): 792-5, 2002 Apr.
Article in English | MEDLINE | ID: mdl-11940747

ABSTRACT

OBJECTIVE: To determine the potential role of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in the pathogenesis of cerebral salt wasting. DESIGN: Clinical case report. SETTING: Regional pediatric intensive care unit. PATIENT: A 3-yr-old boy with a cerebral infarct secondary to traumatic carotid artery dissection who developed hyponatremia associated with weight loss and excessive renal sodium excretion on the sixth day after hospitalization. MEASUREMENTS AND MAIN RESULTS: Plasma concentrations of ANP, BNP, antidiuretic hormone, and renin were determined serially and compared with concentrations measured in a group of eight healthy children undergoing elective surgical procedures. Compared with controls, ANP and BNP plasma concentrations on the eighth day after hospitalization were increased 1.9-fold and 7.7-fold, respectively. Thereafter, the course of ANP and BNP paralleled that of sodium and H2O excretion and remained elevated until the 14th (BNP) and 16th (ANP) days after hospitalization. Serum antidiuretic hormone and renin concentrations were within normal ranges during the entire observation period. CONCLUSION: Cerebral salt wasting is associated with elevated plasma concentrations of ANP and BNP. Natriuretic peptides may play a role in the pathogenesis of this syndrome.


Subject(s)
Atrial Natriuretic Factor/physiology , Cerebral Infarction/physiopathology , Hyperpituitarism/physiopathology , Hyponatremia/etiology , Natriuretic Peptide, Brain/physiology , Atrial Natriuretic Factor/blood , Carotid Artery, Internal, Dissection/complications , Carotid Artery, Internal, Dissection/physiopathology , Cerebral Infarction/complications , Child , Child, Preschool , Humans , Male , Natriuretic Peptide, Brain/blood , Renin/blood , Vasopressins/blood
3.
Crit Care Med ; 30(1): 32-7, 2002 Jan.
Article in English | MEDLINE | ID: mdl-11902285

ABSTRACT

OBJECTIVE: A biallelic polymorphism within the human interleukin (IL)-6 gene promoter region (-174 G/C) has been shown to affect IL-6 transcription in vitro and IL-6 plasma levels in healthy adults. Because IL-6 is excessively released into the circulation during sepsis and closely correlates with the clinical course, we studied whether this promoter polymorphism has an effect on the incidence and/or outcome of sepsis. DESIGN: Population-based association study in critically ill patients and healthy controls. SETTING: Surgical intensive care unit (ICU) in a German university hospital. PATIENTS: Surgical patients (n = 326) of German Caucasian origin with an ICU stay of at least 3 days admitted between 1997 and 1999 were prospectively enrolled. In a subset of 50 patients, sepsis was diagnosed according to consensus criteria (American College of Chest Physicians 1992). Healthy sex-matched adults of the same ethnic and geographic background served as controls. INTERVENTIONS: Blood sampling. MEASUREMENTS AND MAIN RESULTS: The (-174 G/C) polymorphism was genotyped by an allele-specific polymerase chain reaction. IL-6 plasma levels were determined by enzyme-linked immunosorbent assay. Genotype distribution and allele frequencies did not differ significantly between patients with or without sepsis and healthy controls. In patients who finally succumbed to sepsis, significantly less GG homozygotes were observed compared with survivors (p = .008). Median systemic IL-6 levels in septic patients closely correlated with outcome (p < .0001) but were not associated with the IL-6 promoter genotype. CONCLUSIONS: The IL-6 promoter polymorphism (-174 G/C) does not affect the incidence of sepsis. However, the GG homozygous genotype is significantly associated with an improved survival in sepsis. Because this association is independent from the systemic IL-6 response, we suggest that other genetically linked polymorphisms may be the primary cause.


Subject(s)
Interleukin-6/genetics , Polymorphism, Genetic , Promoter Regions, Genetic/genetics , Critical Illness , Enzyme-Linked Immunosorbent Assay , Humans , Interleukin-6/blood , Polymerase Chain Reaction , Prospective Studies , Sepsis/genetics
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