Evaluation of Skindex-16 construct validity in routinely collected psoriasis data: a retrospective analysis of the relationship between overall physician global assessment scores and Skindex-16 and measure discordance.

Patient-reported outcome measures (PROMs) capture disease severity metrics from the patient's perspective, including health-related quality of life (HRQL). Disease-specific validation of PROMs improves their clinical utility. We evaluated construct validity (HRQL) for Skindex-16 in routinely seen psoriasis patients and characterized instances of discordance between Skindex-16 scores and clinician-reported outcome measure of disease severity. We retrospectively studied psoriasis patients seen by University of Utah Dermatology from 2016 to 2020. Cross-sectional construct validity was assessed using quantile regression and Spearman correlation between overall physician global assessment (OPGA) score and Skindex-16 scores. Longitudinal within-subject correlation was performed using linear mixed models. Discordance (10th percentile or lower OPGA and 90th percentile or higher Skindex-16 score [clear skin, poor HRQL; cspHRQL] or the reverse [severe skin, good HRQL; ssgHRQL]) was characterized descriptively. 681 first-visit patients with psoriasis were included. Median overall Skindex-16 score varied by ≥ 10 points across all levels of OPGA scores. OPGA and Skindex-16 domain scores were moderately correlated (emotions ρ = 0.54, functioning ρ = 0.47, and symptoms ρ = 53). Longitudinal correlations were similar (emotion ρxy = 0.54, functioning ρxy = 0.65, symptoms ρxy = 0.47). Visits with cspHRQL discordance occurred for each Skindex-16 domain (emotions = 7, functioning = 13, symptoms = 12). The ssgHRQL group was observed within the emotions (n = 1) and functioning (n = 23) domains. Median Skindex-16 scores are different between different levels of OPGA and show moderate cross-sectional and longitudinal correlation. This supports construct validity in patients with psoriasis. Severe discordance was rare and most often for those with clear skin but poor HRQL. These discordances can prompt further patient-clinician conversation.

Vessel Wall Enhancement on Black-Blood MRI Predicts Acute and Future Stroke in Cerebral Amyloid Angiopathy.

BACKGROUND AND PURPOSE: Cerebral amyloid angiopathy (CAA) is a known risk factor for ischemic stroke though angiographic imaging is often negative. Our goal was to determine the relationship between vessel wall enhancement (VWE) in acute and future ischemic stroke in CAA patients. MATERIALS AND METHODS: This was a retrospective study of patients with new-onset neurologic symptoms undergoing 3T vessel wall MR imaging from 2015 to 2019. Vessel wall enhancement was detected on pre- and postcontrast flow-suppressed 3D T1WI. Interrater agreement was evaluated in cerebral amyloid angiopathy-positive and age-matched negative participants using a prevalence- and bias-adjusted kappa analysis. In patients with cerebral amyloid angiopathy, multivariable Poisson and Cox regression were used to determine the association of vessel wall enhancement with acute and future ischemic stroke, respectively, using backward elimination of confounders to P < .20. RESULTS: Fifty patients with cerebral amyloid angiopathy underwent vessel wall MR imaging, including 35/50 (70.0%) with ischemic stroke and 29/50 (58.0%) with vessel wall enhancement. Prevalence- and bias-corrected kappa was 0.82 (95% CI, 0.71-0.93). The final regression model for acute ischemic stroke included vessel wall enhancement (prevalence ratio = 1.5; 95% CI, 1.1-2.2; P = .022), age (prevalence ratio = 1.02; 95% CI, 1.0-1.05; P = .036), time between symptoms and MR imaging (prevalence ratio = 0.9; 95% CI, 0.8-0.9; P < .001), and smoking (prevalence ratio = 0.7; 95% CI, 0.5-1.0; P = .042) with c-statistic = 0.92 (95% CI, 0.84-0.99). Future ischemic stroke incidence with cerebral amyloid angiopathy was 49.7% (95% CI, 34.5%-67.2%) per year over a total time at risk of 37.5 person-years. Vessel wall enhancement-positive patients with cerebral amyloid angiopathy demonstrated significantly shorter stroke-free survival with 63.9% (95% CI, 43.2%-84.0%) versus 32.2% (95% CI, 14.4%-62.3%) ischemic strokes per year, chi-square = 4.9, P = .027. The final model for future ischemic stroke had a c-statistic of 0.70 and included initial ischemic stroke (hazard ratio = 3.4; 95% CI, 1.0-12.0; P = .053) and vessel wall enhancement (hazard ratio = 2.5; 95% CI, 0.9-7.0; P = .080). CONCLUSIONS: Vessel wall enhancement is associated with both acute and future stroke in patients with cerebral amyloid angiopathy.

Localizing the L5 Vertebra Using Nerve Morphology on MRI: An Accurate and Reliable Technique.

BACKGROUND AND PURPOSE: Multiple methods have been used to determine the lumbar vertebral level on MR imaging, particularly when full spine imaging is unavailable. Because postmortem studies show 95% accuracy of numbering the lumbar vertebral bodies by counting the lumbar nerve roots, attention to lumbar nerve morphology on axial MR imaging can provide numbering clues. We sought to determine whether the L5 vertebra could be accurately localized by using nerve morphology on MR imaging. MATERIALS AND METHODS: One hundred eight cases with full spine MR imaging were numbered from the C2 vertebral body to the sacrum with note of thoracolumbar and lumbosacral transitional states. The origin level of the L5 nerve and iliolumbar ligament were documented in all cases. The reference standard of numbering by full spine imaging was compared with the nerve morphology numbering method. Five blinded raters evaluated all lumbar MRIs with nerve morphology technique twice. Prevalence and bias-adjusted κ were used to measure interrater and intrarater reliability. RESULTS: The L5 nerve arose from the 24th presacral vertebra (L5) in 106/108 cases. The percentage of perfect agreement with the reference standard was 98.1% (95% CI, 93.5%-99.8%), which was preserved in transitional and numeric variation states. The iliolumbar ligament localization method showed 83.3% (95% CI, 74.9%-89.8%) perfect agreement with the reference standard. Inter- and intrarater reliability when using the nerve morphology method was strong. CONCLUSIONS: The exiting L5 nerve can allow accurate localization of the corresponding vertebrae, which is essential for preprocedure planning in cases where full spine imaging is not available. This neuroanatomic method displays higher agreement with the reference standard compared with previously described methods, with strong inter- and intrarater reliability.

Vitamin D and Vulnerable Carotid Plaque.

BACKGROUND AND PURPOSE: MR imaging-detected carotid intraplaque hemorrhage indicates vulnerable plaque with high stroke risk. Angiotensin II stimulates intraplaque hemorrhage in animal models, and the angiotensin system is highly regulated by vitamin D. Our purpose was to determine whether low vitamin D levels predict carotid intraplaque hemorrhage in humans. MATERIALS AND METHODS: In this cross-sectional study, 65 patients with carotid disease underwent carotid MR imaging and blood draw. Systemic clinical confounders and local lumen imaging markers were recorded. To determine the association of low vitamin D levels with MR imaging detected intraplaque hemorrhage, we performed multivariable Poisson regression by using generalized estimating equations to account for up to 2 carotid arteries per patient and backward elimination of confounders. MR imaging detected intraplaque hemorrhage volume was also correlated with vitamin D levels and maximum plaque thickness. Thirty-five patients underwent carotid endarterectomy, and histology-detected intraplaque hemorrhage was correlated with vitamin D levels and total plaque area. RESULTS: Low vitamin D levels (<30 ng/mL, prevalence ratio = 2.05, P = .03) were a significant predictor of MR imaging detected intraplaque hemorrhage, along with plaque thickness (prevalence ratio = 1.40, P < .001). MR imaging detected intraplaque hemorrhage volume linearly correlated with plaque thickness (partial r = 0.45, P < .001) and low vitamin D levels (partial r = 0.26, P = .003). Additionally, histology-detected intraplaque hemorrhage area linearly correlated with plaque area (partial r = 0.46, P < .001) and low vitamin D levels (partial r = 0.22, P = .03). The association of intraplaque hemorrhage volume with low vitamin D levels was also higher with ischemic stroke. CONCLUSIONS: Low vitamin D levels and plaque thickness predict carotid intraplaque hemorrhage and outperform lumen markers of vulnerable plaque. This research demonstrates a significant link between low vitamin D levels and carotid intraplaque hemorrhage.

Prediction of Carotid Intraplaque Hemorrhage Using Adventitial Calcification and Plaque Thickness on CTA.

BACKGROUND AND PURPOSE: Carotid intraplaque hemorrhage is associated with stroke, plaque thickness, stenosis, ulceration, and adventitial inflammation. Conflicting data exist on whether calcification is a marker of plaque instability, and no data exist on adventitial calcification. Our goal was to determine whether adventitial calcification and soft plaque (a rim sign) help predict carotid intraplaque hemorrhage. MATERIALS AND METHODS: This was a retrospective cohort study of 96 patients who underwent carotid MRA and CTA within 1 month, from 2009 to 2016. We excluded occlusions (n = 4) and near occlusions (n = 0), leaving 188 carotid arteries. Intraplaque hemorrhage was detected by using MPRAGE. Calcification, adventitial pattern, stenosis, maximum plaque thickness (total, soft, and hard), ulceration, and intraluminal thrombus on CTA were recorded. Atherosclerosis risk factors and medications were recorded. We used mixed-effects multivariable Poisson regression, accounting for 2 vessels per patient. For the final model, backward elimination was used with a threshold of P < .10. Receiver operating characteristic analysis determined intraplaque hemorrhage by using the area under the curve. RESULTS: Our final model included the rim sign (prevalence ratio = 11.9, P < .001) and maximum soft-plaque thickness (prevalence ratio = 1.2, P = .06). This model had excellent intraplaque hemorrhage prediction (area under the curve = 0.94), outperforming the rim sign, maximum soft-plaque thickness, NASCET stenosis, and ulceration (area under the curve = 0.88, 0.86, 0.77, and 0.63, respectively; P < .001). Addition of the rim sign performed better than each marker alone, including maximum soft-plaque thickness (area under the curve = 0.94 versus 0.86, P < .001), NASCET stenosis (area under the curve = 0.90 versus 0.77, P < .001), and ulceration (area under the curve = 0.90 versus 0.63, P < .001). CONCLUSIONS: The CTA rim sign of adventitial calcification with internal soft plaque is highly predictive of carotid intraplaque hemorrhage.

Magnesium sulfate, chorioamnionitis, and neurodevelopment after preterm birth.

OBJECTIVE: To assess the neuroprotective effect of magnesium sulfate (MgSO4 ) in preterm children exposed to chorioamnionitis. DESIGN: A secondary analysis of a multicentre randomised controlled trial of antenatal MgSO4 administered to women at risk of preterm birth for the prevention of cerebral palsy (CP). Singleton, non-anomalous pregnancies with clinical chorioamnionitis, delivering at ≥24 weeks of gestation, were selected. Cases were exposed to antepartum MgSO4 ; controls received placebo. SETTING: Multicentre randomised controlled trial. POPULATION: Singleton, non-anomalous pregnancies with clinical chorioamnionitis, delivering at ≥24 weeks of gestation. METHODS: All data were analysed by intention to treat. Univariate and multivariate analyses were performed. MAIN OUTCOME MEASURES: Primary outcome was a composite of stillbirth, death by the age of 1 year, or moderate or severe CP by the age of 2 years. Secondary outcomes included a composite neonatal outcome as well as neurodevelopmental delay, defined as Bayley II mental and psychomotor developmental indices <70 at the age of 2 years. Subgroup analysis assessed these outcomes in children born at <28 weeks of gestation. RESULTS: A total of 396 children were included, with 192 (48.5%) randomised to MgSO4 . Maternal and delivery characteristics were similar between the groups. The primary outcome occurred in 14.1% of children exposed to MgSO4 and 12.7% of children exposed to placebo (relative risk, RR 1.29; 95% CI 0.70-2.38). Rates of stillbirth, death, moderate-severe CP, and neurodevelopmental delay did not differ between groups. In the subgroup analysis of children born at <28 weeks of gestation, there was no difference in the rates of the primary outcome, nor in the secondary outcomes assessed. [Correction added on 02 March 2016 after online publication: There were errors in statistical data analysis and these have been corrected throughout the article.] CONCLUSIONS: Among children at risk for early preterm delivery exposed to chorioamnionitis, antenatal administration of MgSO4 was not associated with improved neurodevelopmental outcome. We do not recommend any change in the guidelines on the administration of MgSO4 for neuroprotection based on this study. TWEETABLE ABSTRACT: MgSO4 was not associated with improved neurodevelopmental outcome in setting of chorioamnionitis.

Optimal Prediction of Carotid Intraplaque Hemorrhage Using Clinical and Lumen Imaging Markers.

BACKGROUND AND PURPOSE: MR imaging detects intraplaque hemorrhage with high accuracy by using the magnetization-prepared rapid acquisition of gradient echo sequence. Still, MR imaging is not readily available for all patients, and many undergo CTA instead. Our goal was to determine essential clinical and lumen imaging predictors of intraplaque hemorrhage, as indicators of its presence and clues to its pathogenesis. MATERIALS AND METHODS: In this retrospective cross-sectional study, patients undergoing stroke work-up with MR imaging/MRA underwent carotid intraplaque hemorrhage imaging. We analyzed 726 carotid plaques, excluding vessels with non-carotid stroke sources (n = 420), occlusions (n = 7), or near-occlusions (n = 3). Potential carotid imaging predictors of intraplaque hemorrhage included percentage diameter and millimeter stenosis, plaque thickness, ulceration, and intraluminal thrombus. Clinical predictors were recorded, and a multivariable logistic regression model was fitted. Backward elimination was used to determine essential intraplaque hemorrhage predictors with a thresholded 2-sided P < .10. Receiver operating characteristic analysis was also performed. RESULTS: Predictors of carotid intraplaque hemorrhage included plaque thickness (OR = 2.20, P < .001), millimeter stenosis (OR = 0.46, P < .001), ulceration (OR = 4.25, P = .020), age (OR = 1.11, P = .001), and male sex (OR = 3.23, P = .077). The final model discriminatory value was excellent (area under the curve = 0.932). This was significantly higher than models using only plaque thickness (area under the curve = 0.881), millimeter stenosis (area under the curve = 0.830), or ulceration (area under the curve= 0.715, P < .001). CONCLUSIONS: Optimal discrimination of carotid intraplaque hemorrhage requires information on plaque thickness, millimeter stenosis, ulceration, age, and male sex. These factors predict intraplaque hemorrhage with high discriminatory power and may provide clues to the pathogenesis of intraplaque hemorrhage. This model could be used to predict the presence of intraplaque hemorrhage when MR imaging is contraindicated.

Opioid-induced bowel disorders and narcotic bowel syndrome in patients with chronic non-cancer pain.

BACKGROUND: Opioids are used increasingly in the management of moderate-to-severe chronic non-cancer pain (CNCP). Opioid-induced bowel disorders (OBD) markedly impact health-related quality of life (HRQoL) and frequently limit medically indicated opioid pharmacotherapy. We assessed the risk factors, and effect of OBD on HRQoL in CNCP patients. We also estimated the likely prevalence of narcotic bowel syndrome (NBS). These effects have been reported in cancer patients but not in CNCP previously. METHODS: Ambulatory CNCP patients (n = 146) taking regularly scheduled opioids were invited to complete the Bowel-Disease-Questionnaire and a pain-sensitive HRQoL instrument. The Rome-II criteria were used to define bowel disorders. Narcotic bowel syndrome was defined as presence of daily severe to very-severe abdominal pain of more than 3 months duration requiring more than 100 mg of morphine equivalent per day. KEY RESULTS: Ninety-eight patients (69%) returned the survey. Respondents had taken opioids for 10 days to 10 years (median 365 days) at a median daily dose of 127.5 mg morphine-equivalent (range 7.5-600 mg). Constipation prevalence was 46.9% (95% CI 36.8-57.3), nausea 27% (95% CI 17.2-35.3), vomiting 9% (95% CI 17.2-35.3), and gastro-esophageal reflux disease 33% (95% CI 23.5-42.9). Chronic abdominal pain was reported by 58.2% (95% CI 53.2-73.9) and 6.4%, (95% CI 2.4-13.5) fulfilled the criteria of NBS. Prevalence of constipation increased with duration of treatment. Health-related quality of life was low in patients with chronic abdominal pain. CONCLUSION & INFERENCES: Bowel disorders including chronic abdominal pain and NBS are common in patients taking opioids for CNCP. Decreased HRQoL in patients with CNCP is driven by chronic abdominal pain.

Pertussis antibodies in postpartum women and their newborns.

OBJECTIVE: To (1) determine the proportion of mothers and infants who had levels of IgG antibody to pertussis antigens predicted to be potentially protective at delivery; (2) evaluate the efficiency of maternal-infant antibody transport; (3) extrapolate infant antibody titers at 6 weeks; and (4) identify maternal factors associated with potentially protective infant antibodies. STUDY DESIGN: Sera from mother-infant pairs from February 2006 through to April 2007 were tested for antibody to pertussis antigens by standardized ELISA (enzyme-linked immunosorbent assay). Potentially protective antibody levels were defined as >5 ELISA units (EU) for pertussis toxin (PT), and >10 EU for fimbriae (FIM) and pertactin (PRN). Serological evidence of previous maternal infection was defined from antibody to four antigens by k-means cluster analysis. RESULT: In total, 21% (17/81) of mothers and 26% (21/81) of infants had potentially protective antibody levels at delivery. Mean infant-maternal antibody ratios for PT, FIM and PRN were 1.26, 1.36 and 1.31, respectively. At 6 weeks, 11% (9/81) of infants were predicted to have potentially protective antibody levels. Using cluster analysis, 9% (7/81) of mothers had evidence of previous pertussis infection. Infants born to these mothers were predicted to be more likely to have potentially protective antibodies at 6 weeks (43%) than those born to mothers without previous infection (8%) (P=0.03). CONCLUSION: Approximately 75% of infants were born with pertussis antibody levels lower than the modest levels associated with potential protection. Despite effective antibody transfer, nearly 90% of infants were predicted to have little antibody by 6 weeks. Maternal immunization before or during pregnancy might simulate previous pertussis infection and help protect infants through the first months of life.

Continued early onset group B streptococcal infections in the era of intrapartum prophylaxis.

OBJECTIVE: The objective of the study was to determine the rate of early onset group B streptococcus (EOGBS) infection in Utah and identify potential areas of failure in EOGBS prevention. STUDY DESIGN: We queried the microbiology records of Intermountain Healthcare for infants with culture-confirmed EOGBS between 1 January 2002 and 31 May 2006 and calculated rates of EOGBS per 1000 deliveries. We reviewed the infant and maternal records of each EOGBS case to identify possible failures in EOGBS prevention. RESULT: There were 54 cases of EOGBS among the 127 205 births (0.42/1000 births). Of all, 12 were preterm. Of the 39 (93%) women prenatally screened for GBS, 31 (79%) had negative results and 7/8 (88%) women with positive prenatal GBS screens either did not receive intrapartum antibiotic prophylaxis (IAP) or received inadequate IAP. Of the 54 infants with EOGBS, 3 (6%) died. CONCLUSION: Utah's rates of EOGBS were higher than the national average. Factors associated with EOGBS include missed screening opportunities, inadequate IAP, and false-negative maternal GBS culture.

The infusion nurse and patient complication rates of peripheral-short catheters. A prospective evaluation.

The objective of this study was to compare catheter-related complication rates in patients who had infusion devices placed by infusion nurses with complication rates in patients who had devices placed by generalist nurses. The data demonstrated that peripheral infusion devices placed by infusion nurses exhibited a statistically significant lower rate of leakage, phlebitis, and infiltration complications and remained in the vein significantly longer than those placed by generalist nurses. However, significance was not achieved with pain complication rates between the two groups. The implications of these outcomes for staff development and quality of patient care are discussed.

Cardiopulmonary events during hemodialysis: effects of dialysis membranes and dialysate buffers.

Adverse cardiac and pulmonary events are frequently observed during hemodialysis and contribute to significant morbidity and mortality. The temporal relationship between these events during the intradialytic period has not been well defined. To examine the event rate and timing of silent ischemia, cardiac ectopy, and hypoxemia, we conducted a prospective, single-blind, randomized study of 10 subjects undergoing maintenance hemodialysis with four contiguous combinations of dialysis membranes (cuprammonium or polysulfone) and dialysates (acetate or bicarbonate). The frequency of oxygen desaturation events peaked during the first 2 hours, whereas silent myocardial ischemia and supraventricular ectopies occurred more often in the later hours. Ventricular ectopy occurred steadily throughout the intradialytic period. The combination of acetate dialysis and cuprammonium membrane is associated with the most frequent events. We conclude that cardiopulmonary events can occur frequently during hemodialysis, and the frequency is dependent on the type of dialysis membrane and dialysate buffer used.

ACE inhibitor effects on platelet function in stages I-II hypertension.

Angiotensin II enhances platelet aggregation through activation of the G protein-linked pathway present in platelets. Studies of several angiotensin-converting enzyme (ACE) inhibitors have demonstrated marked differences on platelets. Therefore this prospective, randomized, double-blind, crossover study compared the ex vivo effects of equivalent antihypertensive doses of captopril, enalapril, and fosinopril on platelet aggregation and thromboxane B2 (TxB2) formation in subjects with stage I-II essential hypertension. Nineteen male subjects with a baseline mean seated blood pressure of 141 +/- 3/100 +/- 1 mm Hg were enrolled. The decline in mean arterial pressure after 4 weeks of stable dosing was 10 +/- 1, 12 +/- 1, and 11 +/- 1 mm Hg for captopril, enalapril, and fosinopril, respectively (p = NS). There was no significant change in adenosine diphosphate (ADP)-, epinephrine-, or thrombin-stimulated platelet aggregation from baseline or between ACE inhibitors. Compared with baseline, fosinopril decreased TxB2 concentrations 27.5-67.6% with all stimuli after 1 and 5 min. Captopril also decreased TxB2 formation, but this effect was stimulus and time dependent. Enalapril consistently increased TxB2 concentrations, independent of stimuli or time. We conclude that different ACE inhibitors have distinct effects on platelet TxB2 formation without significant effects on platelet aggregation. Fosinopril may be a direct antagonist ofTxA2 synthase, suggesting benefit in syndromes of platelet activation or vascular occlusion.

Subcutaneous, catheter-related inflammation in a rabbit model correlates with peripheral vein phlebitis in human volunteers.

In the development of a polyurethane vascular catheter with anti-infective properties, it became desirable to develop a measure of tissue inflammation. This was investigated in a rabbit model by implanting uncoated catheters and catheters coated with heparin (HEP), chlorhexidine (CH), or CH/HEP in the subcutaneous space with or without 10(4) Staphylococcus aureus. At intervals of 2, 4, and 7 days after implantation, animals were sacrificed; tissue blocks containing catheters were removed and preserved with formaldehyde; and sections were stained with hematoxylin and eosin. Using a histologic index, 240 sections (10 for each experimental condition) were evaluated by two investigators blinded to experimental conditions. Uncoated catheters or catheters coated with CH alone had a lower histologic index (less inflammation) than catheters coated with HEP alone or CH/HEP (P < .05). When catheters were inoculated with S. aureus, those coated with CH, with or without HEP, had a lower histologic index than uncoated catheters (P < .05). Next, 30 volunteers had a control catheter inserted in a vein in one forearm and a catheter coated with either CH alone or CH/HEP in a vein in the other forearm. After 96 h of observation there was a greater risk of phlebitis associated with CH/HEP catheters than control catheters (P < .05), and no difference in the risk of phlebitis between CH catheters and control catheters (P = 0.43). Thus, the amount of inflammation around the catheter in the subcutaneous space of rabbit correlated with the risk of peripheral vein phlebitis.

Invasive pharmacodynamic characterization of combined ibopamine and calcium blocker therapy for heart failure.

STUDY OBJECTIVE: To determine the acute hemodynamic response of single-dose coadministration of ibopamine plus nifedipine or diltiazem in patients with New York Heart Association functional class (NYHA FC) II-III congestive heart failure. DESIGN: A single-blind, placebo-controlled, two-paired, crossover study. SETTING: Cardiology clinics at two large teaching hospitals. PATIENTS: Eight patients with NYHA FC II-III congestive heart failure who met the inclusion criteria were selected randomly. INTERVENTIONS: All patients underwent right heart catheterization. Day 1 consisted of concomitant calcium channel blocker plus placebo, with cardiac and peripheral hemodynamic recordings from 30 minutes-24 hours. The design was equivalent on day 2, with single-dose administration of ibopamine plus calcium channel blocker. MEASUREMENTS AND MAIN RESULTS: Single-dose nifedipine-diltiazem augmented cardiac output and stroke volume secondary to decreasing systemic vascular resistance. The nifedipine-ibopamine and diltiazem-ibopamine subgroups demonstrated relatively equal hemodynamics, augmenting cardiac index (nifedipine 43%, p < 0.05; diltiazem 40%, p < 0.05 vs baseline) while decreasing systemic vascular resistance (nifedipine 41%, p < 0.05; diltiazem 28%, p NS vs baseline) 30 minutes after the dose. In contrast to single-dose diltiazem, the diltiazem-ibopamine subgroup exhibited an increased left ventricular filling pressure (122%, p < 0.05 vs baseline) and mean pulmonary artery pressure (43%, p < 0.05 vs baseline) at 30 minutes after the dose. One patient experienced a transient episode of chest pain associated with increased heart rate and blood pressure with diltiazem-ibopamine. CONCLUSION: Diltiazem and ibopamine should be coadministered with caution in patients with coronary artery disease and left ventricular dysfunction.

How to evaluate study methodology in published clinical research.

When reading a clinical research article, the clinician must judge if the reported findings and conclusions are valid before applying them to patient care. This concern is legitimate given the wide range of study validity in the clinical literature. In this article, the authors present many validity markers that signify the quality of the information reported from a study, such as authorship, bias, confounding, statistics, randomization, controls, blinding, and the logical framework of scientific investigations.