An observational time-series study on the behavioral effects of adjunctive artisanal cannabidiol use by adults with treatment resistant epilepsies.

BACKGROUND: For approximately 30% of people with epilepsy, seizures are not well-controlled by anti-seizure medication (ASM). This condition, called treatment resistant epilepsy (TRE), is associated with increased morbidity and mortality, and substantially impacts the quality of life of both the individual and their family. Non-responsiveness to ASMs leads many people with TRE to seek alternative therapies, such as cannabinoid-based medication, particularly cannabidiol (CBD), with or without medical or professional advice. This is due in part to widespread reporting in the media about the benefits of CBD for seizures in some forms of epilepsy. METHODS: Adults with TRE, opting to add CBD to their existing treatment regime, completed this prospective, observational, longitudinal, quasi-experimental, time-series study. We hypothesized that adjunctive CBD use would positively impact participants' quality of life and psychological well-being in comparison to a baseline period without CBD use. Participants were followed for a period of approximately six months - for approximately one month of baseline prior to the initiation of CBD use and approximately five months after the initiation of CBD use. Participants provided urine samples and completed behavioral questionnaires that assessed quality of life, anxiety/depression, and adverse events during baseline and at two times during CBD use. RESULTS: Complete case analyses (n = 10) showed a statistically significant improvement in quality of life, a statistically significant decrease in anxiety symptoms, and a statistically significant decrease in the experience of adverse events over time (p < 0.05). Improvements noted in the experience of depression symptoms did not reach statistical significance. Urinalysis revealed the majority of participants had no CBD/metabolites in their system at the beginning of the study, and confirmed the presence of CBD/metabolites in participants' urine after CBD was added to their treatment regime. Analysis of missing data using multiple imputation supported the findings of the complete case analysis. INTERPRETATION: For a small group of individuals with TRE of varying etiologies, adjunctive use of artisanal CBD was associated with improvements in the behavioral and psychological symptoms of TRE, as well as improved medication tolerability.

Impact of Hypoxia-Ischemia on Neurogenesis and Structural and Functional Outcomes in a Mild-Moderate Neonatal Hypoxia-Ischemia Brain Injury Model.

Hypoxic-ischemic encephalopathy (HIE) is a common type of brain injury caused by a lack of oxygen and blood flow to the brain during the perinatal period. The incidence of HIE is approximately 2−3 cases per 1000 live births in high-income settings; while in low- and middle-income countries, the incidence is 3−10-fold higher. Therapeutic hypothermia (TH) is the current standard treatment for neonates affected by moderate−severe HIE. However, more than 50% of all infants with suspected HIE have mild encephalopathy, and these infants are not treated with TH because of their lower risk of adverse outcomes. Despite this, several analyses of pooled data provide increasing evidence that infants who initially have mild encephalopathy may present signs of more significant brain injury later in life. The purpose of this study was to expand our knowledge about the effect of mild−moderate hypoxia-ischemia (HI) at the cellular, structural, and functional levels. An established rat model of mild−moderate HI was used, where postnatal day (P) 7 rats were exposed to unilateral permanent occlusion of the left carotid artery and 90 min of 8% hypoxia, followed by TH or normothermia (NT) treatment. The extent of injury was assessed using histology (P14 and P42) and MRI (P11 and P32), as well as with short-term and long-term behavioral tests. Neurogenesis was assessed by BrdU staining. We showed that mild−moderate HI leads to a progressive loss of brain tissue, pathological changes in MRI scans, as well as an impairment of long-term motor function. At P14, the median area loss assessed by histology for HI animals was 20% (p < 0.05), corresponding to mild−moderate brain injury, increasing to 55% (p < 0.05) at P42. The data assessed by MRI corroborated our results. HI led to a decrease in neurogenesis, especially in the hippocampus and the lateral ventricle at early time points, with a delayed partial recovery. TH was not neuroprotective at early time points following mild−moderate HI, but prevented the increase in brain damage over time. Additionally, rats treated with TH showed better long-term motor function. Altogether, our results bring more light to the understanding of pathophysiology following mild-moderate HI. We showed that, in the context of mild-moderate HI, TH failed to be significantly neuroprotective. However, animals treated with TH showed a significant improvement in motor, but not cognitive long-term function. These results are in line with what is observed in some cases where neonates with mild HIE are at risk of neurodevelopmental deficits in infancy or childhood. Whether TH should be used as a preventive treatment to reduce adverse outcomes in mild-HIE remains of active interest, and more research has to be carried out in order to address this question.

Epicardial bridge via the coronary sinus musculatures revealed by ultra-high-definition mapping.

Mapping and ablation of perimitral flutter, a macro-reentrant tachycardia, can be sometimes challenging. We describe a case of perimitral atrial flutter following the pulmonary vein isolation in which mitral isthmus ablation failed to terminate the arrhythmia due to epicardial-endocardial breakthrough via the muscle fibers of coronary sinus. Ultra-high-definition mapping system was utilized to locate the epicardial bridge, and spot ablation of the lesion subsequently terminated the arrhythmia.

Substrate Targeted Ablation of Atrial Fibrillation Guided by High Density Voltage Mapping: Long-Term Results.

BACKGROUND: Long-term ablation results for atrial fibrillation (AF) have been disappointing, particularly for non-paroxysmal AF (NPAF). We hypothesize fibrosis in paroxysmal AF (PAF) and NPAF would be reflected in voltage fragmentation and visualized by high density mapping. Targeted ablation of discrete low voltage bridges (LVB) would eliminate endocardial fragmentation and should have a positive effect on long-term sinus rhythm (SR) survival. OBJECTIVE: To assess the efficacy of LVB ablation on SR survival in patients with PAF and NPAF, as well as, determine its impact on P wave duration (PWD) and LA volume (LAV). METHODS: 56 patients (29PAF/26NPAF) had a voltage gradient map (VGM) created, high and low voltage limits were adjusted to image LVB. Ablation was performed until no LVB were observed. Baseline PWD and LAV were obtained and reassessed 6 months' post ablation. Patients were followed for 5 years with intermittent monitors. RESULTS: Termination of AF in NPAF was 88%. PWD normalized in PAF and were normal in NPAF post ablation. LAV decreased significantly in NPAF. At 5 years, SR was observed in 89% of PAF and 67% of NPAF. CONCLUSIONS: 1. LVB ablation terminates AF in NPAF 88%; 2. Both PWD and LAV were improved; 3. Maintenance of SR was observed in 89% and 67% (PAF vs NPAF); 4. The present study demonstrates efficacy of a simplified, individualized, and unified methodology for AF ablation.

Discovery of an Experimental Model of Unicuspid Aortic Valve.

BACKGROUND: The epithelial growth factor receptor family of tyrosine kinases modulates embryonic formation of semilunar valves. We hypothesized that mice heterozygous for a dominant loss-of-function mutation in epithelial growth factor receptor, which are EgfrVel/+ mice, would develop anomalous aortic valves, valve dysfunction, and valvular cardiomyopathy. METHODS AND RESULTS: Aortic valves from EgfrVel/+ mice and control mice were examined by light microscopy at 2.5 to 4 months of age. Additional EgfrVel/+ and control mice underwent echocardiography at 2.5, 4.5, 8, and 12 months of age, followed by histologic examination. In young mice, microscopy revealed anatomic anomalies in 79% of EgfrVel/+ aortic valves, which resembled human unicuspid aortic valves. Anomalies were not observed in control mice. At 12 months of age, histologic architecture was grossly distorted in EgfrVel/+ aortic valves. Echocardiography detected moderate or severe aortic regurgitation, or aortic stenosis was present in 38% of EgfrVel/+ mice at 2.5 months of age (N=24) and in 74% by 8 months of age. Left ventricular enlargement, hypertrophy, and reversion to a fetal myocardial gene expression program occurred in EgfrVel/+ mice with aortic valve dysfunction, but not in EgfrVel/+ mice with near-normal aortic valve function. Myocardial fibrosis was minimal or absent in all groups. CONCLUSIONS: A new mouse model uniquely recapitulates salient functional, structural, and histologic features of human unicuspid aortic valve disease, which are phenotypically distinct from other forms of congenital aortic valve disease. The new model may be useful for elucidating mechanisms by which congenitally anomalous aortic valves become critically dysfunctional.

Fibrotic Aortic Valve Stenosis in Hypercholesterolemic/Hypertensive Mice.

OBJECTIVE: Hypercholesterolemia and hypertension are associated with aortic valve stenosis (AVS) in humans. We have examined aortic valve function, structure, and gene expression in hypercholesterolemic/hypertensive mice. APPROACH AND RESULTS: Control, hypertensive, hypercholesterolemic (Apoe(-/-)), and hypercholesterolemic/hypertensive mice were studied. Severe aortic stenosis (echocardiography) occurred only in hypercholesterolemic/hypertensive mice. There was minimal calcification of the aortic valve. Several structural changes were identified at the base of the valve. The intercusp raphe (or seam between leaflets) was longer in hypercholesterolemic/hypertensive mice than in other mice, and collagen fibers at the base of the leaflets were reoriented to form a mesh. In hypercholesterolemic/hypertensive mice, the cusps were asymmetrical, which may contribute to changes that produce AVS. RNA sequencing was used to identify molecular targets during the developmental phase of stenosis. Genes related to the structure of the valve were identified, which differentially expressed before fibrotic AVS developed. Both RNA and protein of a profibrotic molecule, plasminogen activator inhibitor 1, were increased greatly in hypercholesterolemic/hypertensive mice. CONCLUSIONS: Hypercholesterolemic/hypertensive mice are the first model of fibrotic AVS. Hypercholesterolemic/hypertensive mice develop severe AVS in the absence of significant calcification, a feature that resembles AVS in children and some adults. Structural changes at the base of the valve leaflets include lengthening of the raphe, remodeling of collagen, and asymmetry of the leaflets. Genes were identified that may contribute to the development of fibrotic AVS.

Spontaneous Aortic Regurgitation and Valvular Cardiomyopathy in Mice.

OBJECTIVE: We studied the mechanistic links between fibrocalcific changes in the aortic valve and aortic valve function in mice homozygous for a hypomorphic epidermal growth factor receptor mutation (Wave mice). We also studied myocardial responses to aortic valve dysfunction in Wave mice. APPROACH AND RESULTS: At 1.5 months of age, before development of valve fibrosis and calcification, aortic regurgitation, but not aortic stenosis, was common in Wave mice. Aortic valve fibrosis, profibrotic signaling, calcification, osteogenic markers, lipid deposition, and apoptosis increased dramatically by 6 and 12 months of age in Wave mice. Aortic regurgitation remained prevalent, however, and aortic stenosis was rare, at all ages. Proteoglycan content was abnormally increased in aortic valves of Wave mice at all ages. Treatment with pioglitazone prevented abnormal valve calcification, but did not protect valve function. There was significant left ventricular volume overload, hypertrophy, and fetal gene expression, at all ages in Wave mice with aortic regurgitation. Left ventricular systolic function was normal until 6 months of age in Wave mice, but became impaired by 12 months of age. Myocardial transverse tubules were normal in the presence of left ventricular hypertrophy at 1.5 and 3 months of age, but became disrupted by 12 months of age. CONCLUSIONS: We present the first comprehensive phenotypic and molecular characterization of spontaneous aortic regurgitation and volume-overload cardiomyopathy in an experimental model. In Wave mice, fibrocalcific changes are not linked to valve dysfunction and are epiphenomena arising from structurally incompetent myxomatous valves.

Cerebral hemodynamic changes of mild traumatic brain injury at the acute stage.

Mild traumatic brain injury (mTBI) is a significant public health care burden in the United States. However, we lack a detailed understanding of the pathophysiology following mTBI and its relation to symptoms and recovery. With advanced magnetic resonance imaging (MRI), we can investigate brain perfusion and oxygenation in regions known to be implicated in symptoms, including cortical gray matter and subcortical structures. In this study, we assessed 14 mTBI patients and 18 controls with susceptibility weighted imaging and mapping (SWIM) for blood oxygenation quantification. In addition to SWIM, 7 patients and 12 controls had cerebral perfusion measured with arterial spin labeling (ASL). We found increases in regional cerebral blood flow (CBF) in the left striatum, and in frontal and occipital lobes in patients as compared to controls (p = 0.01, 0.03, 0.03 respectively). We also found decreases in venous susceptibility, indicating increases in venous oxygenation, in the left thalamostriate vein and right basal vein of Rosenthal (p = 0.04 in both). mTBI patients had significantly lower delayed recall scores on the standardized assessment of concussion, but neither susceptibility nor CBF measures were found to correlate with symptoms as assessed by neuropsychological testing. The increased CBF combined with increased venous oxygenation suggests an increase in cerebral blood flow that exceeds the oxygen demand of the tissue, in contrast to the regional hypoxia seen in more severe TBI. This may represent a neuroprotective response following mTBI, which warrants further investigation.

The EKG in hypothermia and hyperthermia.

Hypothermia and hyperthermia are relatively common clinical conditions that are associated with significant morbidity and mortality, especially if not promptly recognized and treated. Both of these conditions associated with extreme alterations in core body temperatures can be accompanied by alteration in cardiac function, often with manifest EKG changes. However, some of the EKG changes associated with hypothermia and heat stroke are non-specific and lead to diagnostic dilemmas. We here present 2 clinical cases, one each for hypothermia and hyperthermia to describe the EKG changes associated with these clinical conditions. We also present a review of available literature on these subjects.

Risk factors and outcomes for patients with bloodstream infection due to Acinetobacter baumannii-calcoaceticus complex.

Identifying patients at risk for bloodstream infection (BSI) due to Acinetobacter baumannii-Acinetobacter calcoaceticus complex (ABC) and providing early appropriate therapy are critical for improving patient outcomes. A retrospective matched case-control study was conducted to investigate the risk factors for BSI due to ABC in patients admitted to the Detroit Medical Center (DMC) between January 2006 and April 2009. The cases were patients with BSI due to ABC; the controls were patients not infected with ABC. Potential risk factors were collected 30 days prior to the ABC-positive culture date for the cases and 30 days prior to admission for the controls. A total of 245 case patients were matched with 245 control patients. Independent risk factors associated with BSI due to ABC included a Charlson's comorbidity score of ≥ 3 (odds ratio [OR], 2.34; P = 0.001), a direct admission from another health care facility (OR, 4.63; P < 0.0001), a prior hospitalization (OR, 3.11; P < 0.0001), the presence of an indwelling central venous line (OR, 2.75; P = 0.011), the receipt of total parenteral nutrition (OR, 21.2; P < 0.0001), the prior receipt of ß-lactams (OR, 3.58; P < 0.0001), the prior receipt of carbapenems (OR, 3.18; P = 0.006), and the prior receipt of chemotherapy (OR, 15.42; P < 0.0001). The median time from the ABC-positive culture date to the initiation of the appropriate antimicrobial therapy was 2 days (interquartile range [IQR], 1 to 3 days). The in-hospital mortality rate was significantly higher among case patients than among control patients (OR, 3.40; P < 0.0001). BSIs due to ABC are more common among critically ill and debilitated institutionalized patients, who are heavily exposed to health care settings and invasive devices.

Aortic valve sclerosis in mice deficient in endothelial nitric oxide synthase.

Risk factors for fibrocalcific aortic valve disease (FCAVD) are associated with systemic decreases in bioavailability of endothelium-derived nitric oxide (EDNO). In patients with bicuspid aortic valve (BAV), vascular expression of endothelial nitric oxide synthase (eNOS) is decreased, and eNOS(-/-) mice have increased prevalence of BAV. The goal of this study was to test the hypotheses that EDNO attenuates profibrotic actions of valve interstitial cells (VICs) in vitro and that EDNO deficiency accelerates development of FCAVD in vivo. As a result of the study, coculture of VICs with aortic valve endothelial cells (vlvECs) significantly decreased VIC activation, a critical early phase of FCAVD. Inhibition of VIC activation by vlvECs was attenuated by N(G)-nitro-l-arginine methyl ester or indomethacin. Coculture with vlvECs attenuated VIC expression of matrix metalloproteinase-9, which depended on stiffness of the culture matrix. Coculture with vlvECs preferentially inhibited collagen-3, compared with collagen-1, gene expression. BAV occurred in 30% of eNOS(-/-) mice. At age 6 mo, collagen was increased in both bicuspid and trileaflet eNOS(-/-) aortic valves, compared with wild-type valves. At 18 mo, total collagen was similar in eNOS(-/-) and wild-type mice, but collagen-3 was preferentially increased in eNOS(-/-) mice. Calcification and apoptosis were significantly increased in BAV of eNOS(-/-) mice at ages 6 and 18 mo. Remarkably, these histological changes were not accompanied by physiologically significant valve stenosis or regurgitation. In conclusion, coculture with vlvECs inhibits specific profibrotic VIC processes. In vivo, eNOS deficiency produces fibrosis in both trileaflet and BAVs but produces calcification only in BAVs.

Pioglitazone attenuates valvular calcification induced by hypercholesterolemia.

OBJECTIVE: Development of calcific aortic valve stenosis involves multiple signaling pathways, which may be modulated by peroxisome proliferator-activated receptor-γ). This study tested the hypothesis that pioglitazone (Pio), a ligand for peroxisome proliferator-activated receptor-γ, inhibits calcification of the aortic valve in hypercholesteremic mice. METHODS AND RESULTS: Low density lipoprotein receptor(-/-)/apolipoprotein B(100/100) mice were fed a Western-type diet with or without Pio (20 mg/kg per day) for 6 months. Pio attenuated lipid deposition and calcification in the aortic valve, but not aorta. In the aortic valve, Pio reduced levels of active caspase-3 and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Valve function (echocardiography) was significantly improved by Pio. To determine whether changes in gene expression are associated with differential effects of Pio on aortic valves versus aorta, Reversa mice were fed Western diet with or without Pio for 2 months. Several procalcific genes were increased by Western diet, and the increase was attenuated by Pio, in aortic valve, but not aorta. CONCLUSIONS: Pio attenuates lipid deposition, calcification, and apoptosis in aortic valves of hypercholesterolemic mice, improves aortic valve function, and exhibits preferential effects on aortic valves versus aorta. We suggest that Pio protects against calcific aortic valve stenosis, and Pio or other peroxisome proliferator-activated receptor-γ ligands may be useful for early intervention to prevent or slow stenosis of aortic valves.

The effect of different dialysate magnesium concentrations on QTc dispersion in hemodialysis patients.

BACKGROUND: Electrolyte changes during dialysis affect corrected QT (QTc) and QTc dispersion (QTcd), a surrogate marker of arrhythmogenicity. The impact of magnesium on QTcd is not clear. METHODS: Twenty-two stable patients on maintenance hemodialysis were enrolled in this study. Each underwent two consecutive hemodialysis sessions at least 2 days apart, the first against normal magnesium dialysate (with magnesium at 1.8 mg/dL) followed by a low magnesium dialysate (with magnesium at 0.6 mg/dL). Pre- and post-dialysis weights, blood pressure, electrolytes, and 12-lead surface EKG were recorded. The QT interval and the QTcd were calculated before and after dialysis in both sessions. RESULTS: Of 22 patients, 16 were female. The mean age ± SD was 53.7 ± 18.0 years. The mean change of QTcd (pre- vs. post-dialysis) was 9.5 ms (p = 0.120) and 9.3 ms (p = 0.145) in low and normal magnesium groups, respectively. Using univariate analysis, there was a statistically significant decrease in the mean blood pressure, weight, potassium, magnesium, and QTc interval post-dialysis (compared to pre-dialysis) in both groups (p ≤ 0.049). Post-dialysis concentrations of sodium and calcium were unchanged (compared to pre-dialysis) but bicarbonate increased with both dialysate groups (p < 0.001). The mean change of QTcd was not significant pre- versus post-dialysis by univariate analysis in either group. Multiple linear regression analysis adjusting for pertinent factors did not change the results in either of the two groups. CONCLUSION: Using a low magnesium dialysate bath in hemodynamically stable hemodialysis patients without preexisting advanced cardiac disease does not significantly impact QTcd.

Age-related tonsillar regrowth in children undergoing powered intracapsular tonsillectomy.

OBJECTIVES: To review our experience with intracapsular tonsillectomy using powered instrumentation (PIT) in the management of tonsillar hypertrophy. DESIGN: Retrospective database review of pediatric patients undergoing PIT. METHODS: The medical records of 636 patients under 11 years of age who underwent PIT performed by the senior author (RFW), predominantly for obstructive sleep disturbance, were reviewed. Data were subsequently analyzed from 559 of these patients for clinical evidence of tonsillar regrowth, post-operative tonsillar hemorrhage, and post-operative dehydration due to pain. Specific information for possible correlation of age at the time of surgery and any increased rate of regrowth was primarily examined. RESULTS: There were a total of 33 patients who had clinical evidence of regrowth. Children less than 5 years of age had 5 times the incidence of regrowth (p<0.001). Out of the group that exhibited regrowth, 5 patients exhibited evidence of recurrent upper airway obstruction and underwent a complete tonsillectomy. The age of this complete tonsillectomy group ranged from 1.1 to 2.7 years. Out of all patients undergoing PIT, there was 1 incident of delayed post-operative dehydration due to emesis but not due to pain. There were 2 incidents of delayed post-operative tonsillar bleeds. All three complications were self-limited and did not require re-hospitalization. CONCLUSIONS: PIT is a safe procedure with a small risk of tonsillar regrowth being age related. The incidence of postoperative complications following PIT is relatively low (0.54%).

Tirofiban use with clopidogrel and aspirin decreases adverse cardiovascular events after percutaneous coronary intervention for ST-elevation myocardial infarction: a meta-analysis of randomized trials.

Current guidelines deemed usefulness of routine early glycoprotein IIb/IIIa inhibitor (GPI) administration in ST-elevation myocardial infarction (STEMI) before primary percutaneous coronary intervention (PCI) with dual antiplatelet therapy as uncertain. We aimed to examine the current evidence for the use of tirofiban, a nonpeptide glycoprotein IIb/IIIa inhibitor, in STEMI patients treated with dual antiplatelet therapy. We performed systematic searches of MEDLINE, EMBASE, and CENTRAL databases for randomized controlled trials (RCTs) of tirofiban use in STEMI patients treated with aspirin and clopidogrel which reported clinical and/or angiographic outcomes after primary PCI. Data were combined using random effect and fixed effect models for heterogeneous and homogeneous outcomes respectively using Review Manager 5 (The Nordic Cochrane Centre, The Cochrane Collaboration, 2008). Six randomized controlled trials were eligible for the inclusion; involving 708 patients in tirofiban group and 721 control subjects. Routine tirofiban use decreased the major adverse cardiovascular events (odds ratio [OR] 0.50; 95% confidence interval [CI], 0.26-0.94). Corrected thrombolysis in myocardial infarction (TIMI) frame count was also reduced with tirofiban (mean difference -8.48 [95% CI, -12.62 to -4.34]). There were no significant differences in the rates of postprocedure TIMI flow grade 3 and TIMI myocardial perfusion/blush grade 3, major bleeding by TIMI criteria, or mortality in the 2 groups. Current analysis of available studies suggests that routine and early tirofiban use before primary PCI may decrease the major cardiovascular events in STEMI patients treated with aspirin and clopidogrel without any significant increase in major bleeding. An adequately powered randomized trial is urgently needed to confirm the above findings and estimate the effect size.

Does "hidden undercuffing" occur among obese patients? Effect of arm sizes and other predictors of the difference between wrist and upper arm blood pressures.

Arm size can affect the accuracy of blood pressure (BP) measurement, and "undercuffing" of large upper arms is likely to be a growing problem. Therefore, the authors investigated the relationship between upper arm and wrist readings. Upper arm and wrist circumferences and BP were measured in 261 consecutive patients. Upper arm auscultation and wrist BP was measured in triplicate, rotating measurements every 30 seconds between sites. Upper arm BP was 131.9+/-20.6/71.6+/-12.6 mm Hg in an obese population (body mass index, 30.6+/-6.6 kg/m(2)) with mean upper arm size of 30.7+/-5.1 cm. Wrist BP was higher (2.6+/-9.2 mm Hg and 4.9+/-6.6 mm Hg, respectively, P<.001); however, there was moderate concordance for the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) strata (kappa value=0.27-0.71), and the difference was >or=5 mm Hg in 72% of the patients. The authors conclude that there was poor concordance between arm and wrist BP measurement and found no evidence that "hidden undercuffing" was associated with obesity; therefore, they do not support routine use of wrist BP measurements.

Potential effect of an apoprotein B-based algorithm on management of new patients with hypertriglyceridemia referred to a specialty lipid clinic.

BACKGROUND: In patients with hypertriglyceridemia, non-high density lipoprotein cholesterol (nonHDL-C) is a targeted goal. However, apoprotein B100 (apoB) may be superior in predicting cardiovascular risk so we assessed the utility of an apoB-based. METHODS: New patients (n = 125) who had both apoB and standard lipids measured on the same day were included and we determined the concordances of having achieved goal lipid levels based upon proposed apoB versus nonHDL-C (ATP III) targets in patients with elevated TG (>or=150 mg*dl(-1)) levels. RESULTS: Although apoB was correlated with nonHDL-C (r = 0.47, p or= 150 mg*dl(-1), as specifically outlined in ATP III guidelines. In total, > 50% of all subjects would have been treated either more or less aggressively following an apoB-based therapeutic algorithm. CONCLUSIONS: Our findings confirm that the majority of patients referred with hypertriglyceridemia would be managed differently by following an apoB-based treatment algorithm compared to ATP III guidelines. Although many patients would be candidates for more intense therapy, many would be treated less aggressively.