Background
Adolescents with Down syndrome (DS) are two to three times more likely to be obese than their typically developing peers. When preventing or treating obesity, it is useful for clinicians ...to understand an individual's energy intake needs. Predictive resting energy expenditure (REE) equations are often recommended for general use in energy intake recommendations; however, these predictive equations have not been validated in youth with DS. The aim of this study was to compare the accuracy of seven commonly used predictive equations for estimating REE in adolescents who are typically developing to REE measured by indirect calorimetry in adolescents with DS.
Methods
Adolescents with DS participated in a 90‐min laboratory visit before 10:00 a.m. after a 12‐h overnight fast and a 48‐h abstention from aerobic exercise. REE was measured via indirect calorimetry, and estimated REE was derived using the Institute of Medicine, Molnar, Muller and World Health Organization equations. Mean differences between the measured and predicted REE for each equation were evaluated with equivalency testing, and P‐values were adjusted for multiple comparisons using the Holm method.
Results
Forty‐six adolescents with DS (age: 15.5 ± 1.7 years, 47.8% female, 73.9% non‐Hispanic White) completed the REE assessment. Average measured REE was 1459.5 ± 267.8 kcal/day, and the Institute of Medicine equations provided the most accurate prediction of REE with a 1.7 ± 11.2% (13.9 ± 170.3 kcal/day) overestimation. This prediction was not statistically different from the measured REE P‐value = 0.582; 95% confidence interval (CI): −64.5, 36.7, and the difference between the measured and predicted REE was statistically equivalent to zero (P‐value = 0.024; 90% CI: −56.1, 28.3).
Conclusions
The results suggest that the Institute of Medicine equation may be useful in predicting REE in adolescents with DS. Future research should confirm these results in a larger sample and determine the utility of the Institute of Medicine equation for energy intake recommendations during a weight management intervention.
The use of bivariable selection (BVS) for selecting variables to be used in multivariable analysis is inappropriate despite its common usage in medical sciences. In BVS, if the statistical p value of ...a risk factor in bivariable analysis is greater than an arbitrary value (often
p = 0.05), then this factor will not be allowed to compete for inclusion in multivariable analysis. This type of variable selection is inappropriate because the BVS method wrongly rejects potentially important variables when the relationship between an outcome and a risk factor is confounded by any confounder and when this confounder is not properly controlled. This article uses both hypothetical and actual data to show how a nonsignificant risk factor in bivariable analysis may actually be a significant risk factor in multivariable analysis if confounding is properly controlled. Furthermore, problems resulting from the automated forward and stepwise modeling with or without the presence of confounding are also addressed. To avoid these improper procedures and deficiencies, alternatives in performing multivariable analysis, including advantages and disadvantages of the BVS method and automated stepwise modeling, are reviewed and discussed.
Acetylcholine is believed to dilate normal blood vessels by promoting the release of a vasorelaxant substance from the endothelium (endothelium-derived relaxing factor). By contrast, if the ...endothelium is removed experimentally, acetylcholine constricts blood vessels. We tested the hypothesis that muscarinic cholinergic vasodilation is impaired in coronary atherosclerosis. Graded concentrations of acetylcholine and, for comparison, the nonendothelial-dependent vasodilator nitroglycerin were infused into the left anterior descending artery of eight patients with advanced coronary stenoses (greater than 50 percent narrowing), four subjects with angiographically normal coronary arteries, and six patients with mild coronary atherosclerosis (less than 20 percent narrowing). Vascular responses were evaluated by quantitative angiography. In several segments each of four normal coronary arteries, acetylcholine caused a dose-dependent dilation from a control diameter of 1.94 +/- 0.16 mm to 2.16 +/- 0.15 mm with the maximal acetylcholine dose (P less than 0.01). In contrast, all eight of the arteries with advanced stenoses showed dose-dependent constriction, from 1.05 +/- 0.05 to 0.32 +/- 0.16 mm at the highest concentration of acetylcholine (P less than 0.01), with temporary occlusion in five. Five of six vessels with minimal disease also constricted in response to acetylcholine. All vessels dilated in response to nitroglycerin, however. We conclude that paradoxical vasoconstriction induced by acetylcholine occurs early as well as late in the course of coronary atherosclerosis. Our preliminary findings suggest that the abnormal vascular response to acetylcholine may represent a defect in endothelial vasodilator function, and may be important in the pathogenesis of coronary vasospasm.
In postmenopausal women with coronary artery disease, conjugated equine estrogen with or without continuous administration of medroxyprogesterone acetate has failed to slow the progression of ...atherosclerosis. Whether 17beta-estradiol (the endogenous estrogen molecule) alone or administered sequentially with medroxyprogesterone acetate can slow the progression of atherosclerosis is unknown.
We conducted a double-blind, placebo-controlled trial in 226 postmenopausal women (mean age, 63.5 years) who had at least one coronary-artery lesion. Participants were randomly assigned to usual care (control group), estrogen therapy with micronized 17beta-estradiol alone (estrogen group), or 17beta-estradiol plus sequentially administered medroxyprogesterone acetate (estrogen-progestin group). In all patients the low-density lipoprotein (LDL) cholesterol level was reduced to a target of less than 130 mg per deciliter. The primary outcome was the average per-participant change between base-line and follow-up coronary angiograms in the percent stenosis measured by quantitative coronary angiography.
After a median of 3.3 years of follow-up, the mean (+/-SE) change in the percent stenosis in the 169 participants who had a pair of matched angiograms was 1.89+/-0.78 percentage points in the control group, 2.18+/-0.76 in the estrogen group, and 1.24+/-0.80 in the estrogen-progestin group (P=0.66 for the comparison among the three groups). The mean difference in the percent stenosis between the estrogen group and the control group was 0.29 percentage point (95 percent confidence interval, -1.88 to 2.46), and the mean difference between the estrogen-progestin group and the control group was -0.65 (95 percent confidence interval, -2.87 to 1.57).
In older postmenopausal women with established coronary-artery atherosclerosis, 17beta-estradiol either alone or with sequentially administered medroxyprogesterone acetate had no significant effect on the progression of atherosclerosis.
Whether higher operator case volume is associated with improved percutaneous transluminal coronary angioplasty (PTCA) clinical and cost outcomes is the subject of this study. Hospital volume-related ...improvement in clinical outcomes has been shown for coronary artery bypass grafting (CABG) and PTCA. Physician case volume-related differences in clinical outcomes have not been clearly demonstrated, and differences in hospital costs have not been examined. For clinical and cost outcomes, risk-adjusted analysis of differences in PTCA outcomes has not been reported. In addition, controversy exists about the appropriate annual case volume considered adequate to maintain skills and achieve optimal clinical outcomes in performing PTCA procedures. We studied 2,350 PTCAs performed between March 1, 1991, and February 28, 1994. Physicians were divided into 2 volume groups: high (≥50 cases/year) and low (<50 cases/year). The rate of emergency CABG after PTCA was 2.1% for high- and 3.9% for low-volume operators (p = 0.009). Hospital morbidity associated with PTCA was lower in high- than in low-volume operators (6.46% vs 10.73%, p < 0.001). The risk-adjusted ratios for emergency CABG and morbidity were 2.05 (p = 0.005) and 1.79 (p < 0.001), respectively. The length of stay averaged 4.07 ± 4.54 days for high- and 4.49 ± 4.33 days for low-volume operators (p = 0.003). Hospital costs averaged $7,977 ± $7,269 for high- and $8,278 ± $6,289 for low-volume operators (p = 0.065). The risk-adjusted ratio was 1.091 (p = 0.004) for length of stay and 1.050 (p = 0.029) for cost. Thus, PTCA performed by high-volume operators is significantly less likely to require emergency CABG and is also significantly associated with lower hospital morbidity, shorter hospital length of stay, and lower hospital costs.
To enhance detection of ischemia during percutaneous transluminal coronary angioplasty (PTCA), unipolar intracoronary electrocardiograms (ECGs) were recorded during PTCA in 25 patients from the tips ...of guidewires positioned distal to stenoses being dilated. Surface electrocardiographic leads chosen to reflect likely areas of reversible ischemia during PTCA were recorded simultaneously. In 21 of 29 stenoses dilated (72%), ST segment elevation and/or T wave peaking in intracoronary ECG appeared during balloon inflation and disappeared after deflation, accompanied by transient angina on 19 occasions. Two patients had transient ST segment elevation in intracoronary ECGs during PTCA without associated angina. ST changes in the surface ECG during PTCA were seen on only nine occasions (31%), always accompanied by ST segment elevation in the intracoronary ECG that appeared earlier and was of much greater magnitude. Five patients with prior myocardial infarction and aneurysm formation had fixed ST segment elevation in the intracoronary ECG unrelated to balloon inflation. Myocardial ischemia during PTCA can be detected easily with intracoronary ECGs and with greater sensitivity than that of the surface ECG. Furthermore, intracoronary ECGs may help to clarify the nature of chest pain during balloon inflation or during suspected complications.
To determine the effect of metoprolol on silent ischemia and platelet aggregability, 10 patients with coronary artery disease were studied with a randomized, double-blind, placebo-controlled, ...crossover trial. Patients were treated with metoprolol (200 mg b.i.d.) or placebo for 1 week and then received the alternate therapy. Two days before the end of each treatment period, platelet aggregability was studied for 24 hours, and a 48-hour ambulatory electrocardiogram was obtained. Compared with placebo, metoprolol significantly decreased the total number (from 26 to 4, p less than 0.1) and duration (from 735 to 84 minutes, p less than 0.01) of silent ischemic episodes. This decrease was accompanied by a decrease in the mean blood pressure (from 127/81 to 118/71 mm Hg, p less than 0.01) and the mean heart rate (from 70 to 54 beats/min, p less than 0.01). The incidence of silent ischemic episodes in the morning was significantly higher in untreated patients than in treated patients. The few episodes observed during metoprolol treatment occurred at the same time as the peak incidence observed during placebo treatment. During placebo treatment, platelet aggregability increased from 6:00 to 9:00 AM as reflected by a decrease in the threshold concentrations of ADP and epinephrine required to induce biphasic platelet aggregation (from 4.8 +/- 0.8 to 2.6 +/- 0.4 microM, p less than 0.02; and from 7.3 +/- 2.3 to 1.8 +/- 0.9 microM, respectively, p less than 0.02). Metoprolol did not alter the basal level nor blunt the morning increase of platelet aggregability.
Rapid atrial pacing confirms myocardial ischemia in patients with coronary artery disease when angina is provoked, and is accompanied by an increase in left ventricular end-diastolic pressure. In ...such cases, abnormalities in the surface electrocardiogram (ECG) are often not apparent. To enhance detection of subendocardial ischemia during rapid atrial pacing, local unipolar electrograms were recorded from the tip of a 0.025 in. (0.064 cm) diameter guidewire positioned against the endocardial surface of potentially ischemic regions. Endocardial electrograms, left ventricular end-diastolic pressure and multiple surface ECG leads were recorded during rapid atrial pacing in 21 patients with coronary artery disease. Before pacing, endocardial etectrograms in all 21 patients were free of ST elevation. Marked ST elevation was apparent in 17 of the 21 patients after rapid atrial pacing and could be abolished by nitroglycerin. Moreover, in several patients, endocardial ST elevation after rapid atrial pacing was abolished after successful percutaneous transluminal coronary angioplasty of the critically stenosed artery supplying the ischemic region of myocardium.
It is concluded that ST elevation in the endocardial electrogram after rapid atrial pacing is a reflection of myocardial ischemia and may be a sensitive marker of pacing-induced ischemia appearing earlier than angina, postpacing increase in left ventricular end-diastolic pressure or ST depression in the surface ECG.
Identification of whether episodes of ambulatory ischemia are caused by increases in myocardial oxygen demand or to episodic coronary vasoconstriction in patients with stable coronary disease may be ...important to guide selection of optimal anti-ischemic therapy and to gain insight into mechanisms responsible for adverse cardiac events.
Mean minute heart rate activity during ambulatory ECG (AECG) monitoring was determined for 50 patients treated with propranolol, diltiazem, nifedipine, or placebo in a randomized, double-blind, crossover trial. Periods of heart rate increases of various magnitudes and durations and starting at various baseline heart rates on each therapy were identified throughout each 48-hour AECG recording, and the proportion of these periods associated with an ischemic episode was determined. The circadian variation of ischemic episodes categorized by the presence or absence of an increase in heart rate was analyzed. Eighty-one percent of ischemic episodes were preceded by an increase in heart rate > or = 5 beats per minute. The likelihood of developing ischemia associated with a heart rate increase was proportional to the magnitude and duration of the heart rate increase and the baseline heart rate before the increases in heart rate: likelihood ranged from 4% when the heart rate increased 5-9 beats per minute and lasted < 10 minutes to 60% when the heart rate increased > or = 20 beats per minute and lasted > or = 40 minutes. The likelihoods of developing ischemia based on changes in the heart rate variables were similar for each of the therapies. Propranolol therapy significantly reduced the magnitude and duration of heart rate increase and the baseline heart rate compared with therapy with placebo, diltiazem, or nifedipine (P < .001). Ischemic episodes associated with a heart rate increase displayed a daytime peak, whereas ischemia occurring without a heart rate increase occurred evenly throughout the day. Propranolol reduced the proportion of heart rate-related ischemic episodes and increased the proportion of non-heart rate-related episodes compared with placebo (P < .02), and nifedipine exerted the opposite effect (P = .005). Multivariate analysis indicated that the probability of developing ischemia was strongly associated with heart rate variables and was unaffected by time of day.
Most episodes of ambulatory ischemia are associated with a preceding period of increased heart rate. The likelihood of developing ischemia is predicted by heart rate variables and unaffected by time of day. Anti-ischemic efficacy is generally a result of the medication's efficacy in reducing heart rate variables. A minority of ischemic episodes are not associated with preceding periods of increased heart rate, may be caused by episodic coronary vasoconstriction, and are more effectively reduced by nifedipine than propranolol.
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