Search PubMed⌕ Search

Biomedical subjects

J L Anderson

Publications and source records attributed to J L Anderson.

At least 37 records · Page 2Linked to original sources

Statin therapy, lipid levels, C-reactive protein and the survival of patients with angiographically severe coronary artery disease.

OBJECTIVES: The joint predictive value of lipid and C-reactive protein (CRP) levels, as well as a possible interaction between statin therapy and CRP, were evaluated for survival after angiographic diagnosis of coronary artery disease (CAD). BACKGROUND: Hyperlipidemia increases risk of CAD and myocardial infarction. For first myocardial infarction, the combination of lipid and CRP levels may be prognostically more powerful. Although lipid levels are often measured at angiography to guide therapy, their prognostic value is unclear. METHODS: Blood samples were collected from a prospective cohort of 985 patients diagnosed angiographically with severe CAD (stenosis > or =70%) and tested for total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and CRP levels. Key risk factors, including initiation of statin therapy, were recorded, and subjects were followed for an average of 3.0 years (range: 1.8 to 4.3 years) to assess survival. RESULTS: Mortality was confirmed for 109 subjects (11%). In multiple variable Cox regression, levels of TC, LDL, HDL and the TC:HDL ratio did not predict survival, but statin therapy was protective (adjusted hazard ratio [HR] = 0.49, p = 0.04). C-reactive protein levels, age, left ventricular ejection fraction and diabetes were also independently predictive. Statins primarily benefited subjects with elevated CRP by eliminating the increased mortality across increasing CRP tertiles (statins: HR = 0.97 per tertile, p-trend = 0.94; no statins: HR = 1.8 per tertile, p-trend < 0.0001). CONCLUSIONS: Lipid levels drawn at angiography were not predictive of survival in this population, but initiation of statin therapy was associated with improved survival regardless of the lipid levels. The benefit of statin therapy occurred primarily in patients with elevated CRP.

Aged↗

Cytomegalovirus seropositivity and C-reactive protein have independent and combined predictive value for mortality in patients with angiographically demonstrated coronary artery disease.

BACKGROUND: The role of inflammation in coronary artery disease (CAD) is being increasingly recognized. Markers of inflammation (eg, C-reactive protein [CRP]) and infection (eg, seropositivity to Chlamydia pneumoniae, cytomegalovirus [CMV], and Helicobacter pylori) have been proposed as risk factors for CAD, but these associations require further evaluation. METHODS AND RESULTS: We prospectively tested whether CRP levels and IgG seropositivity to C pneumoniae, CMV, and H pylori are predictors of subsequent mortality in 985 consecutive patients with angiographically demonstrated CAD (stenosis >/=70%). Patients were followed for an average of 2.7 years (range 1.5 to 4.0 years). Patients averaged 65 years of age; 77% were men; and 110 (11.2%) died during follow-up. CRP levels were significantly elevated in nonsurvivors compared with survivors (mean CRP 3.1 mg/dL versus 1.5 mg/dL, P:=0.003). After controlling for all known baseline variables, the 2nd and 3rd tertiles of CRP compared with the 1st produced a Cox hazard ratio (HR) for mortality of 2.4 (P:=0.001). Of the 3 infectious markers tested, only seropositivity to CMV (HR=1.9, P:<0.05) was predictive of mortality. The majority of mortality risk associated with elevated CRP or CMV seropositivity occurred when both risk factors were present (P: for trend <0.0001). Other independent predictors of increased risk of mortality were age (HR=1.07 per year, P:<0.0001), left ventricular ejection fraction (HR=0.97 per percent, P:<0.0001), and diabetes mellitus (HR=1.7, P:=0.02). CONCLUSIONS: CMV seropositivity and elevated CRP, especially when in combination, are strong, independent predictors of mortality in patients with CAD. This suggests an interesting hypothesis that a chronic, smoldering infection (CMV) might have the capacity to accelerate the atherothrombotic process.

Aged↗

Randomized secondary prevention trial of azithromycin in patients with coronary artery disease: primary clinical results of the ACADEMIC study.

BACKGROUND: Chlamydia pneumoniae is associated with coronary artery disease (CAD), although its causal role is uncertain. A small preliminary study reported a >50% reduction in ischemic events by azithromycin, an antibiotic effective against C pneumoniae, in seropositive CAD patients. We tested this prospectively in a larger, randomized, double-blind study. METHODS AND RESULTS: CAD patients (n=302) seropositive to C pneumoniae (IgG titers >/=1:16) were randomized to placebo or azithromycin 500 mg/d for 3 days and then 500 mg/wk for 3 months. The primary clinical end point included cardiovascular death, resuscitated cardiac arrest, nonfatal myocardial infarction (MI), stroke, unstable angina, and unplanned coronary revascularization at 2 years. Treatment groups were balanced, and azithromycin was generally well tolerated. During the trial, 47 first primary events occurred (cardiovascular death, 9; resuscitated cardiac arrest, 1; MI, 11; stroke, 3; unstable angina, 4; and unplanned coronary revascularization, 19), with 22 events in the azithromycin group and 25 in the placebo group. There was no significant difference in the 1 primary end point between the 2 groups (hazard ratio for azithromycin, 0.89; 95% CI, 0.51 to 1.61; P:=0.74). Events included 9 versus 7 occurring within 6 months and 13 versus 18 between 6 and 24 months in the azithromycin and placebo groups, respectively. CONCLUSIONS: This study suggests that antibiotic therapy with azithromycin is not associated with marked early reductions (>/=50%) in ischemic events as suggested by an initial published report. However, a clinically worthwhile benefit (ie, 20% to 30%) is still possible, although it may be delayed. Larger (several thousand patient), longer-term (>/=3 to 5 years) antibiotic studies are therefore indicated.

Adult↗

Plasma homocysteine predicts mortality independently of traditional risk factors and C-reactive protein in patients with angiographically defined coronary artery disease.

BACKGROUND: Plasma homocysteine (tHCY) has been associated with coronary artery disease (CAD). We tested whether tHCY also increases secondary risk, after initial CAD diagnosis, and whether it is independent of traditional risk factors, C-reactive protein (CRP), and methylenetetrahydrofolate reductase (MTHFR) genotype. METHODS AND RESULTS: Blood samples were collected from 1412 patients with severe angiographically defined CAD (stenosis >/=70%). Plasma tHCY was measured by fluorescence polarization immunoassay. The study cohort was evaluated for survival after a mean of 3.0+/-1.0 years of follow-up (minimum 1.5 years, maximum 5.0 years). The average age of the patients was 65+/-11 years, 77% were males, and 166 died during follow-up. Mortality was greater in patients with tHCY in tertile 3 than in tertiles 1 and 2 (mortality 15.7% versus 9.6%, P:=0.001 [log-rank test], hazard ratio [HR] 1.63). The relative hazard increased 16% for each 5-micromol/L increase in tHCY (P:<0.001). In multivariate Cox regression analysis, controlling for univariate clinical and laboratory predictors, elevated tHCY remained predictive of mortality (HR 1.64, P:=0.009), together with age (HR 1. 72 per 10-year increment, P:<0.0001), ejection fraction (HR 0.84 per 10% increment, P:=0.0001), diabetes (HR 1.98, P:=0.001), CRP (HR 1. 42 per tertile, P:=0.004), and hyperlipidemia. Homozygosity for the MTHFR variant was weakly predictive of tHCY levels but not mortality. CONCLUSIONS: In patients with angiographically defined CAD, tHCY is a significant predictor of mortality, independent of traditional risk factors, CRP, and MTHFR genotype. These findings increase interest in tHCY as a secondary risk marker and in secondary prevention trials (ie, with folate/B vitamins) to determine whether reduction in tHCY will reduce risk.

Aged↗

Risk factors for congenital hypothyroidism: an investigation of infant's birth weight, ethnicity, and gender in California, 1990-1998.

BACKGROUND: Approximately 85% of primary congenital hypothyroidism (CH) is sporadic and due to malformations of the thyroid gland. Past studies have reported an increased birth weight among infants with CH. We have attempted to replicate and expand these observations, examining the association between different birth weight categories and CH stratified by infant's sex. We have also examined the prevalence of CH by mother's age and infant's ethnicity, gender, and year of birth. METHODS: A cross-sectional study was conducted on 5, 049,185 infants screened by the statewide California Newborn Screening Program between 1990 and 1998, an estimated 98.6% of all newborns in the state. Dried blood spots from a heel stick were assayed for thyroxine (T4), and presumptive positives had follow-up assays of thyroid-stimulating hormone (TSH) to determine definite positives. RESULTS: A total of 1,806 cases of CH were identified. The following findings are unlikely to be due to chance. Compared with infants with birth weights of 3,000-3,499 g, infants weighing <2,000 g and those weighing >/=4,500 g had a twofold or greater increase in the prevalence of CH. This was not explained as a result of confounding by the infant's ethnicity or gender. Compared with whites, elevated prevalence rates were found in most ethnic groups, which include the following: Hispanics, Chinese, Vietnamese, Asian Indians, Filipinos, Middle Easterners, and Hawaiians. As reported previously, black infants had about one-third the prevalence rate of whites. We also observed the frequently described female preponderance of CH. The female excess was maintained at all birth weights, however it varied by infant's ethnicity. Trends in the prevalence of CH were not associated with mother's age or with the time interval between 1990 and 1998. CONCLUSIONS: We observed an increased risk of CH in both low-birth-weight (<2,000-g) and macrosomic (>/=4,500-g) infants. This U-shaped association has not been described in past studies. We have also expanded the previously described ethnic differences in CH risk to include ethnic groups not previously studied. The unique pattern of CH occurrence suggests that further studies to define modifiable risk factors may be useful.

Birth Weight↗

A common variant of the AMPD1 gene predicts improved cardiovascular survival in patients with coronary artery disease.

OBJECTIVE: We tested whether a common AMPD1 gene variant is associated with improved cardiovascular (CV) survival in patients with coronary artery disease (CAD). BACKGROUND: Reduced activity of adenosine monophosphate deaminase (AMPD) may increase production of adenosine, a cardioprotective agent. A common, nonsense, point variant of the AMPD1 gene (C34T) results in enzymatic inactivity and has been associated with prolonged survival in heart failure. METHODS: Blood was collected from 367 patients undergoing coronary angiography. Genotyping was done by polymerase chain reaction amplification and restriction enzyme digestion, resulting in allele-specific fragments. Coronary artery disease was defined as > or =70% stenosis of > or =1 coronary artery. Patients were followed prospectively for up to 4.8 years. Survival statistics compared hetero- (+/-) or homozygotic (-/-) carriers with noncarriers. RESULTS: Patients were 66 +/- 10 years old; 79% were men; 22.6% were heterozygous and 1.9% homozygous for the variant AMPD1(-) allele. During a mean of 3.5 +/- 1.0 years, 52 patients (14.2%) died, 37 (10.1%) of CV causes. Cardiovascular mortality was 4.4% (4/90) in AMPD1(-) allele carriers compared with 11.9% (33/277) in noncarriers (p = 0.046). In multiple variable regression analysis, only age (hazard ratio, 1.11/year, p < 0.001) and AMPD1(-) carriage (hazard ratio, 0.36, p = 0.053) were independent predictors of CV mortality. CONCLUSIONS: Carriage of a common variant of the AMPD1 gene was associated with improved CV survival in patients with angiographically documented CAD. The dysfunctional AMPD1(-) allele may lead to increased cardiac adenosine and increased cardioprotection during ischemic events. Adenosine monophosphate deaminase-1 genotyping should be further explored in CAD for prognostic, mechanistic and therapeutic insights.

AMP Deaminase↗

Factors associated with assault-related firearm injuries in male adolescents.

PURPOSE: To identify factors associated with an increased prevalence of assault-related firearm injuries in male adolescents. METHODS: This study is a retrospective comparison of two samples of adolescent males from the same geographic localities regarding their involvement in the juvenile justice system (court involvement) and injury status (current or prior firearm injury at the time of the study). The subjects included adolescent male patients admitted to an urban, Level I trauma center for assault-related firearm injuries (court-involved and noncourt- involved, n = 65); and incarcerated juvenile offenders (prior firearm injury and no known firearm injury, n = 267). RESULTS: Two-thirds of the male assault-related pediatric firearm injury victims treated over a two-year period were involved in the juvenile justice system (court involved). Court-involved adolescents were almost 22 times more likely to have sustained an assault-related firearm injury, when compared to noncourt-involved patients with firearm injuries. Additional analysis documented recent substance use and/or involvement in criminal offenses in 82% of the victims. For most of the juvenile offenders (88%), court involvement preceded their injuries. Analysis of the injury patterns revealed an increased prevalence of truncal injuries (injuries to thorax or abdomen) in the court-involved victims, when compared to their noncourt-involved peers (40% and 14% for the court-involved and noncourt-involved samples, respectively; p <.05). Incarceration was associated with a 17-fold increase in the firearm injury prevalence over the court-involved, but not incarcerated, sample. CONCLUSIONS: These results suggest that involvement in substance use and/or the criminal justice system is associated with an increased risk of firearm injuries in male adolescents, and that an increased level of involvement in the juvenile justice system is associated with a concomitant increase in firearm injuries.

Adolescent↗

Herbicide movement and dissipation at four Midwestern sites.

This study was conducted to evaluate atrazine (2-chloro-4-ethylamino-6-isopropyl-1,3,5-triazine) and alachlor (2-chloro-N-(methoxymethyl)acetamide) dissipation and movement to shallow aquifers across the Northern Sand Plains region of the United States. Sites were located at Minnesota on a Zimmerman fine sand, North Dakota on Hecla sandy loam, South Dakota on a Brandt silty clay loam, and Wisconsin on a Sparta sand. Herbicide concentrations were determined in soil samples taken to 90 cm four times during the growing season and water samples taken from the top one m of aquifer at least once every three months. Herbicides were detected to a depth of 30 cm in Sparta sand and 90 cm in all other soils. Some aquifer samples from each site contained atrazine with the highest concentration in the aquifer beneath the Sparta sand (1.28 microg L(-1)). Alachlor was detected only once in the aquifer at the SD site. The time to 50% atrazine dissipation (DT50) in the top 15 cm of soil averaged about 21 d in Sparta and Zimmerman sands and more than 45 d for Brandt and Hecla soils. Atrazine DT50 was correlated positively with % clay and organic carbon (OC), and negatively with % fine sand. Alachlor DT50 ranged from 12 to 32 d for Zimmerman and Brandt soils, respectively, and was correlated negatively with % clay and OC and positively with % sand.

Acetamides↗

Nutrition and cancer education: ten years of progress.

The Nutrition Education and Research Program at the University of Nevada School of Medicine was awarded two separate NIH/NCI R25 cancer education grants over a ten-year period. With this support, a four-year longitudinal nutrition curriculum was implemented, including the required 20-hour freshman Medical Nutrition Course, junior and senior nutrition electives, and a senior assignment in nutrition and cancer during the rural rotation with faculty preceptors. Funding has also supported nutrition integration into the basic science courses, patient care courses, and specialty clerkships. A unique nutrition fellowship for medical students who specialize in nutrition during their four years of training and graduate with special Qualifications in Nutrition (SQIN) has also been instituted. The curriculum reflects a longitudinal, interdisciplinary, but flexible, integration of nutrition into an already crowded medical school education.

Curriculum↗

The ACADEMIC study in perspective (Azithromycin in coronary artery disease: elimination of myocardial infection with Chlamydia).

Chlamydia pneumoniae, a common cause of respiratory infection, is vasotropic and frequently found in human atheromas. Whether it plays a causal role in coronary artery disease (CAD) is uncertain. The effects of 3 months of azithromycin treatment or placebo were tested in 302 patients with chronic CAD seropositive to C. pneumoniae at 3-6 months. Azithromycin reduced a global rank sum score of 4 inflammatory markers (C-reactive protein [CRP], interleukin [IL]-1, IL-6, tumor necrosis factor-alpha; P=.011) and a global rank sum change score (+/-SD) (from 535+/-201 to 587+/-190; P=.027) at 6 (but not 3) months. Change scores for CRP and IL-6 and median IL-1 levels were lower. C. pneumoniae IgG and IgA antibody titers were unchanged. Clinical cardiovascular events at 6 months did not differ between groups (azithromycin, 9; placebo, 7). Infections were reduced and drug was well tolerated. Thus, azithromycin caused modest but significant reductions in markers of inflammation, but differences in clinical events were not evident at 6 months. However, power was limited and conclusions should await results of the 2-year evaluation and larger studies.

Aged↗

The effect of chronic azithromycin therapy on soluble endothelium-derived adhesion molecules in patients with coronary artery disease.

In patients with coronary artery disease (CAD), azithromycin therapy is associated with decreased cytokine levels and overall reduction of inflammation. Chlamydia pneumoniae (C.Pn) is a common pathogen that may be an important factor in the development and progression of atherosclerosis. Cell-adhesion molecules have an important role in recruitment of inflammatory cells during plaque development and are expressed by endothelial cells on activation. We sought to define the effect of treatment with azithromycin on circulating levels of soluble vascular cell-adhesion molecule (VCAM-I), intercellular adhesion molecule (ICAM-1), and E-selectin in patients with CAD. Plasma concentrations of VCAM-1, ICAM-1, and E-selectin were measured in 40 patients with documented CAD and a positive (> or = 1:16) immunoglobulin G (IgG) titer against C.Pn, 20 subjects with normal coronary arteries, and 14 healthy volunteers. Patients were assigned randomly to receive either 500 mg/wk of azithromycin or placebo for 3 months. Serum samples were obtained at baseline, at 3 months, and during the follow-up visit at 6 months. Patients with documented CAD exhibited elevation of VCAM-1 (535 +/- 227 ng/ ml; p = 0.0001) and E-selectin (69 +/- 29 ng/ml; p = 0.006), but not ICAM-1 (321 +/- 65 ng/ml) concentrations as compared with the patients with angiographically proven normal coronary arteries (252 +/- 80; 50 +/- 22; and 311 +/- 40 ng/ml) and healthy controls (110 +/- 18; 29 +/- 2; and 238 +/- 47 ng/ml, respectively). Prolonged treatment with azithromycin did not significantly affect the plasma levels of soluble VCAM-1, ICAM-1, and E-selectin. Soluble markers of endothelial activation are markedly increased in patients with documented CAD as compared with those with normal coronary arteries and healthy controls. Despite substantial heterogeneity in plasma E-selectin, ICAM-1, and VCAM-1 levels, long-term azithromycin treatment did not affect plasma levels of these adhesion molecules, indicative of endothelial activation, over a period of 6 months.

Adult↗

Advantages and disadvantages of trial designs: a review of analysis methods for ICD studies. AVID Investigators.

General modalities of analyses that have been used for ICD studies are reviewed. Published "typical" examples are briefly described. The historical cohort method is exemplified with previously unpublished data from the Seattle Cardiac Arrest Survivor database. The AVID Study database is used to compare the results obtained from nonrandomized methodologies with randomized methodologies. Particular issues related to the use of the ICD for example, mode of death, inability to blind, selection practice, and treatment decision times make this a natural pedagogic platform.

Bias↗

Identification of distinct carboxyl-terminal domains mediating internalization and down-regulation of the hamster alpha(1B)- adrenergic receptor.

The roles of the carboxyl-terminal tail of the alpha(1B)-adrenergic receptor in its expression, function, and regulation were investigated by site-directed mutagenesis. The receptor construct truncated after residue 363 seemed not to be properly expressed. In contrast, the receptor truncated after residue 366 and all of the longer receptor constructs were properly expressed and exhibited agonist and antagonist binding and activation of phosphoinositide hydrolysis similar to the wild-type receptor. Agonist-induced sequestration of receptors within the plasma membrane, endocytosis into intracellular vesicles, and eventual down-regulation were all absent in the receptor truncated after residue 366. A series of sequential truncations and a deletion mutation identified a critical role for residues 403 to 425, which include the previously identified sites for G protein-coupled receptor kinase phosphorylation, in agonist-induced internalization of the receptor. Similar studies identified a critical role for residues 367 to 380 in agonist-induced down-regulation. Individual point mutations converting either cysteine 367 or serine 369 to alanine selectively eliminated down-regulation, thus identifying two specific amino acid residues required for down-regulation. Importantly, several of the mutated receptors that failed to show rapid agonist-induced internalization nonetheless exhibited normal agonist-induced down-regulation. In addition to identifying specific regions and individual residues of the alpha(1B)-adrenergic receptor involved in internalization and down-regulation, these studies provide mutated receptors that internalize but do not down-regulate, that down-regulate without internalization, and that are defective in both internalization and down-regulation, all of which should be useful tools for further studies of the specific cellular compartments and molecular mechanisms involved in receptor internalization and down-regulation.

Amino Acid Sequence↗

Soluble VCAM-1 and E-selectin, but not ICAM-1 discriminate endothelial injury in patients with documented coronary artery disease.

It has been shown that endothelial cell adhesion molecules play an important role in the development of coronary atherosclerosis and inflammatory disease. We sought to test whether soluble vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and E-selectin are increased in patients with documented coronary artery disease (CAD). Plasma levels of VCAM-1, ICAM-1 and E-selectin were measured in 40 patients with documented CAD, 20 subjects with angiographically documented normal coronary arteries, and 14 healthy volunteers. Patients with documented CAD exhibited significant elevation of VCAM-1 (535 +/- 227.1 ng/ml, p = 0.0001), E-selectin (69.4 +/- 29.4 ng/ml, p = 0.006), but not ICAM-1 (320.5 +/- 65.1 ng/ml, p = 0.9) concentrations as compared to subjects with normal coronary arteries (252.3 +/- 79.8, 49.7 +/- 22.0 and 311.4 +/- 40.2 ng/ml), and healthy controls (110.0 +/- 17.7, 29.0 +/- 2.0 and 237.5 +/- 46.5 ng/ml), respectively. Soluble markers of endothelial injury are not uniformly increased in patients with documented CAD as compared to those with normal coronary arteries and healthy controls. However, VCAM-1 and E-selectin, but not ICAM-1 could identify endothelial injury in such patients.

Adult↗

Lack of association of a common polymorphism of the plasminogen activator inhibitor-1 gene with coronary artery disease and myocardial infarction.

OBJECTIVES: The study was done to assess whether the common polymorphic allele (4G) of the plasminogen activator inhibitor-1 (PAI-1) gene is associated with coronary artery disease (CAD) or myocardial infarction (MI). BACKGROUND: Impaired fibrinolytic function has been associated with CAD and MI. Plasminogen activator inhibitor-1 plays a central role in intravascular thrombosis and thrombolysis; the common insertion/deletion polymorphism (4G/5G) of PAI-1 has been correlated with altered PAI-1 levels and proposed as a coronary risk factor. METHODS: Blood was drawn and DNA extracted from 1,353 consenting patients undergoing coronary angiography. The 4G and 5G alleles of PAI-1 were amplified using specific primers. Amplified products were visualized by staining with ethidium bromide after electrophoresis in 1.5% agarose. RESULTS: Patient age averaged 63.5 (SD 11.7) years; 70% were men, 28% had a history of MI, 66% had severe CAD (>60% stenosis), and 23% had no CAD or MI. Overall, the frequency of the 4G allele was 54.2%, and 78% of patients were 4G carriers. Genotypic distributions were: 4G/4G = 30.1%, 4G/5G = 47.9%, and 5G/5G = 21.8%. Neither carriage of 4G (CAD odds ratio [OR] = 1.08 [0.80 to 1.46], MI OR = 1.11 [0.83 to 1.49]) nor 4G/4G homozygosity (CAD OR = 1.07, MI OR = 0.98) was associated with CAD or MI. In multivariate analyses, risk factors associated with CAD were (in order): gender, age, smoking, diabetes, cholesterol, and hypertension; for MI, they were gender, smoking, and cholesterol. CONCLUSIONS: A common PAI-1 polymorphism (4G) was not importantly associated with angiographic CAD or history of MI in a Caucasian population. Modest risk (i.e., OR <1.5), especially for MI, or risk in association with other factors, cannot be excluded.

Aged↗

Design and results of the antiarrhythmics vs implantable defibrillators (AVID) registry. The AVID Investigators.

BACKGROUND: The Antiarrhythmics Versus Implantable Defibrillators (AVID) Study compared treatment with implantable cardioverter-defibrillators versus antiarrhythmic drugs in patients with life-threatening ventricular arrhythmias (VAs). AVID maintained a Registry on all patients, randomized or not, with any VA or unexplained syncope who could be considered for either of the treatment strategies. Trial-eligible arrhythmias were the categories of VF cardiac arrest, Syncopal VT, and Symptomatic VT, below. METHODS AND RESULTS: Of 5989 patients screened, 4595 were registered and 1016 were randomized. Mortality follow-up through 1996 was obtained on the 4219 Registry patients enrolled before 1997 through the National Death Index. Crude mortality rates (mean+/-SD, follow-up, 16.9+/-11.5 months) were: VF cardiac arrest, 17.0% (n=1399, 238 deaths); Syncopal VT, 21.2% (n=598, 127 deaths); Symptomatic VT, 15.8% (n=1065, 168 deaths); Stable (asymptomatic) VT, 19.7% (n=497, 98 deaths); VT/VF with transient/correctable cause, 17.8% (n=270, 48 deaths); and Unexplained syncope, 12.3% (n=390, 48 deaths). CONCLUSIONS: Patients with seemingly lower-risk or unknown-risk VAs (asymptomatic VT, and VT/VF associated with a transient factor) have a (high) mortality similar to that of higher-risk, AVID-eligible VAs. The similar (and poor) prognosis of most patients with VT/VF suggests the need for reevaluation of a priori risk grouping and raises the question of the appropriate arrhythmia therapy for a broad range of patients.

Aged↗