The relationship between multiple concussions and multidimensional sleep quality in collegiate-aged, active athletes.

OBJECTIVES: Determine the association of cumulative concussion and repetitive head impacts with self-reported sleep quality in healthy collegiate-aged athletes. METHODS: Collegiate-aged athletes (N = 212; mean age 21.00, 62.7% male) completed semistructured interviews for sport and concussion history and the Pittsburgh Sleep Quality Index (PSQI). Number of concussions was retrospectively determined based on the 1993 American Congress of Rehabilitation Medicine (ACRM) criteria; repetitive head impact was measured based on the cumulative years of contact sport exposure. Associations of number of concussions and repetitive head impact exposure with global PSQI score, overall poor (PSQI >5) vs. good sleep, and binarized subscale scores were tested. Secondary analyses were conducted using alternative concussion criteria and metrics of repetitive head impact. RESULTS: The number of prior concussions was associated with higher PSQI global scores (B(SE)= 0.50(0.13), p < .001). Participants with more concussions were more likely to be poor sleepers (OR=1.52, p < .001), report poorer sleep quality (OR=1.29, p = .037), longer sleep latency (OR=1.34, p = .005), more sleep disturbances (OR=1.56, p = .001), increased use of sleep medications or sleep aids (OR=1.35, p = .008), and more sleep-related daily dysfunction (OR=1.38, p = .002). Similar results were observed for alternative definitions of concussion. No metric of repetitive head impact was associated with any sleep quality metric. CONCLUSIONS: More prior concussions, but not repetitive head impact exposure, are associated with worse self-reported sleep, with subscale analyses showing concussion history associated with multiple aspects of subjective sleep quality rather than sleep quantity. Sleep represents an important factor to consider for future research aimed at characterizing and ultimately preventing adverse long-term health outcomes associated with concussion history.

Extent and severity of coronary disease and mortality in patients with end-stage renal failure evaluated for renal transplantation.

The purpose of this study is to explore the relationship between coronary artery disease (CAD), transplantation status and subsequent mortality in end-stage renal disease (ESRD) patients undergoing evaluation for renal transplantation. Two hundred fifty-three ESRD patients at high risk for CAD underwent coronary angiography as part of a renal transplant evaluation. The cohort was divided into three groups: Group 1 (n = 127) had no vessels with >or=50% stenosis, Group 2 (n = 56) had one vessel with >or=50% stenosis and Group 3 (n = 70) had two or more vessels with >or=50% stenosis. Long-term survival was determined; median follow-up was 3.3 years. The baseline characteristics were similar except for older age and higher proportion of diabetes mellitus, dyslipidemia and peripheral vascular disease in Groups 2 and 3 patients as compared to Group 1. Survival was worse in Group 3 compared to Group 1 (p < 0.0001). Each of the three subgroups had better survival with renal transplantation than those who did not undergo transplantation (p < 0.0001). Although the degree of CAD is related to subsequent mortality, transplantation is associated with better survival regardless of the extent and severity of CAD. Thus, the presence of CAD should not exclude ESRD patients from consideration for this therapy.

The ultrastructural basis of alveolar-capillary membrane permeability to peroxidase used as a tracer.

The permeability of the alveolar-capillary membrane to a small molecular weight protein, horseradish peroxidase (HRP), was investigated by means of ultrastructural cytochemistry. Mice were injected intravenously with HRP and sacrificed at varying intervals. Experiments with intranasally instilled HRP were also carried out. The tissue was fixed in formaldehyde-glutaraldehyde fixative. Frozen sections were cut, incubated in Graham and Karnovsky's medium for demonstrating HRP activity, postfixed in OsO4, and processed for electron microscopy. 90 sec after injection, HRP had passed through endothelial junctions into underlying basement membranes, but was stopped from entering the alveolar space by zonulae occludentes between epithelial cells. HRP was demonstrated in pinocytotic vesicles of both endothelial and epithelial cells, but the role of these vesicles in net protein transport appeared to be minimal. Intranasally instilled HRP was similarly prevented from permeating the underlying basement membrane by epithelial zonulae occludentes. Pulmonary endothelial intercellular clefts stained with uranyl acetate appeared to contain maculae occludentes rather than zonulae occludentes. HRP did not alter the ultrastructure of these junctions.

Scraping of aortic debris by coronary guiding catheters: a prospective evaluation of 1,000 cases.

OBJECTIVES: This study was designed to determine the incidence and to quantitate aortic debris retrieved during placement of guiding catheters in patients undergoing percutaneous interventions. BACKGROUND: Studies have shown that atherosclerotic aortic debris predisposes patients to spontaneous or procedurally related ischemic events. METHODS: In 1,000 consecutive percutaneous interventions, the amount of visible atheromatous material from large-lumen-guiding catheters was recorded. Clinical characteristics and in-hospital complications were prospectively collected and associated with debris production. RESULTS: Visible aortic debris (1+ to 3+) occurred more frequently with the Judkins left (JL) catheter, followed by the multipurpose (Multi) catheter compared to any other type of guiding catheter (65%, p = 0.001 and 60%, p = 0.01, respectively). Large debris (2+ and 3+) was observed most frequently with the Multi (odds ratio 3.79, C.I. = 2.32 to 6.21, p = 0.001), JL (odds ratio 2.83, C.I. = 1.98 to 4.05, p = 0.001) and voda left (VL) (odds ratio 2.73, C.I. = 1.51 to 4.95, p = 0.001) catheters. The Judkins right (JR) catheter type was least likely to produce any debris (24%, p = 0.001). A history of unstable angina (p = 0.05) or myocardial infarction (p = 0.003) was associated with a decreased incidence of debris production. The presence of debris was not found to be associated with in-hospital ischemic complications. CONCLUSIONS: Studies have shown that atherosclerosis of the aorta is a potential source of systemic embolism in patients undergoing cardiac catheterization. Our study shows that in more than 50% of percutaneous revascularization procedures, guiding catheter placement is associated with scraping debris from the aorta. Design characteristics of the JL, Multi and VL guiding catheters make them most likely to produce such debris. Meticulous attention to allow the debris to exit the back of the catheter is essential to prevent injecting atheromatous debris into the vascular bed.

Long-term clinical outcome and predictors of major adverse cardiac events after percutaneous interventions on saphenous vein grafts.

OBJECTIVES: The purpose of this study was to examine the long-term clinical outcome after percutaneous intervention of saphenous vein grafts (SVG) and to identify the predictors of major adverse cardiac events (MACE). BACKGROUND: Percutaneous interventions of SVGs have been associated with more procedural complications and higher restenosis rates compared with interventions on native vessels. METHODS: From 1993 to 1997, 1,062 patients underwent percutaneous intervention on 1,142 SVG lesions. Procedural, in-hospital and long-term clinical outcomes were recorded in a database and analyzed. RESULTS: In-hospital MACE occurred in 137 patients (13%) including death (8%), Q-wave myocardial infarction (MI) (2%) and coronary artery bypass surgery (3%). Late MACE occurred in 565 patients (54%) including death (9%), Q-wave MI (9%) and target vessel revascularization (36%). Any MACE occurred in 457 (43%) patients. Follow-up was available in 1,056 (99%) patients at 3 +/- 1 year. Univariate predictors were restenotic lesion (odds ratio [OR]: 2.47, confidence interval [CI]: 1.13 to 3.85, p = 0.0003), unstable angina (OR: 1.99, CI: 1.27 to 2.91, p = 0.04) and congestive heart failure (CHF) (OR: 1.97, CI: 1.14 to 3.24, p = 0.02) for in-hospital MACE, and peripheral vascular disease (PVD) (OR: 2.18, CI: 1.34 to 3.44, p = 0.002), intra-aortic balloon pump placement (OR: 2.08, CI: 1.13 to 3.85, p = 0.02) and previous MI (OR: 1.97, CI: 1.14 to 3.25, p = 0.007) for late MACE. Independent multivariate predictors for late MACE were restenotic lesion (relative risk [RR] 1.33, p = 0.02), PVD (RR: 1.31, p = 0.01), CHF (RR: 1.42, p = 0.01) and multiple stents (RR: 1.47, p = 0.004). Angiographic follow-up was available for 422 patients. Angiographic restenosis occurred in 122 (29%) of stented SVGs and 181 (43%) of nonstented SVGs (p = 0.04). Stent implantation did not confer a survival benefit. CONCLUSIONS: Despite the use of new interventional devices, SVG interventions are associated with significant morbidity and mortality; SVG stenting is not associated with better three-year event-free survival. This may be due to progressive disease at nonstented sites.

Intranasal nicotine spray does not augment the adverse effects of cigarette smoking on myocardial oxygen demand or coronary arterial dimensions.

PURPOSE: Nicotine replacement therapy has become a popular therapy for smokers attempting to stop smoking. Unfortunately, some subjects continue to smoke while receiving it. Since nicotine is believed to be the primary constituent of cigarette smoke responsible for its acute adverse effects on myocardial oxygen supply and demand, concomitant nicotine replacement therapy and smoking theoretically could provoke a marked decrease in myocardial oxygen supply and increase in demand. This study was performed to assess the effects of cigarette smoking with and without concomitant intranasal nicotine spray on: (a) myocardial oxygen demand, (b) coronary arterial dimensions, and (c) the development of acute cardiovascular tolerance. PATIENTS AND METHODS: In 19 smokers referred for cardiac catheterization for the evaluation of chest pain, we assessed the effects of cigarette smoking with and without concomitant intranasal nicotine spray on: (a) heart rate-systolic arterial pressure product (an estimate of myocardial oxygen demand), (b) coronary arterial dimensions (measured with computer-assisted quantitative arteriography), and (c) the development of acute cardiovascular tolerance. RESULTS: Smoking a first cigarette increased rate pressure product (P < 0.001) and decreased coronary arterial dimensions (P < 0.0001). Subsequently, neither variable was altered by intranasal nicotine spray or a second cigarette. Despite a substantial increase in serum nicotine concentration with nicotine spray and smoking, acute cardiovascular tolerance appears to develop. CONCLUSIONS: Cigarette smoking causes an increase in myocardial oxygen demand and concomitant coronary arterial vasoconstriction. However, further increases in the serum nicotine concentration do not cause a greater increase in demand or decrease in coronary arterial dimensions. These data suggest that humans acutely develop tolerance to an increasing nicotine concentration, thereby helping to explain the apparent lack of a potential synergistic adverse effect associated with continued smoking during nicotine replacement therapy.

Correlation between time-domain measures of heart rate variability and scatterplots in patients with healed myocardial infarcts and the influence of metoprolol.

Scatterplots (displays of each RR interval as a function of the preceding RR interval) provide a visual assessment of nonrandom variations in heart rate. In a recent study, scatterplot length, width, and area correlated with time-domain measures of heart rate variability (HRV) in survivors of recent myocardial infarction (MI) receiving a beta blocker. We performed this study to (1) assess the relation between time-domain measures of HRV and scatterplot indexes in survivors of remote MI not receiving metoprolol and (2) to determine if metoprolol influenced scatterplot indexes. In 28 survivors of remote MI, HRV time-domain variables and scatterplot indexes were measured after 2 weeks off and 2 weeks on metoprolol. Off metoprolol, scatterplot length correlated with long-term HRV variables (SD of the difference of all RR intervals [r = 0.98], SD of the average of all 5-minute intervals [r = 0.97]), and scatterplot width correlated with short-term HRV variables (root-mean-square successive differences between RR intrevals [rMSSD] [r = 0.88]). Metoprolol increased time-domain HRV variables (mean RR interval, rMSSD, and proportion of adjacent RR intervals differing by > 50 ms [pNN50 (%)]) but did not alter scatterplot indexes. Thus, scatterplot indexes correlate with time-domain measures of HRV in survivors of remote MI not receiving metoprolol. In contrast to HRV time-domain variables, scatterplot indexes are not influenced by metoprolol.

Immediate and long-term results of elective and emergent percutaneous interventions on protected and unprotected severely narrowed left main coronary arteries.

Percutaneous revascularization of protected and unprotected left main coronary arteries is associated with acceptable immediate results, but there are significant long-term consequences, including the need for repeat percutaneous intervention (10%), myocardial infarction (7.5%), coronary artery bypass surgery (7%), and death (38%), despite the elective or emergent nature of the procedure.

Influence of metoprolol on heart rate variability in survivors of remote myocardial infarction.

We assessed the influence of metoprolol on heart rate variability in survivors of remote myocardial infarction. In 43 survivors of myocardial infarction 12 to 18 months previously (26 men and 17 women, aged 38 to 69 years), two 24-hour ambulatory electrocardiograms were recorded 2 weeks apart. In patients in group A (n=28), who had taken metoprolol for the previous year, the drug was discontinued for 2 weeks, after which the first recording was done. The second recording was done 2 weeks after metoprolol was resumed. In patients in group B (n=15), who had not taken metoprolol for the previous year, it continued to be withheld, and two 24-hour recordings were done 2 weeks apart. In group A, metoprolol increased the time domain variables indicative of enhanced vagal tone; root-mean-square successive difference in normal RR (NN) intervals was 20 +/- 11 ms (mean +/- SD) without and 24 +/- 9 ms with metoprolol (p<0.05), and the proportion of NN that differ by >50 ms (pNN50%) was 3.6 +/- 6.0 without and 5.5 +/- 6.0 with metoprolol (p<0.05). In the frequency domain, the logarithms of the 24-hour very low frequency and the 24-hour high-frequency power (reflecting parasympathetic activity) were increased (5.12 +/- 1.03 and 4.48 +/- 1.51, respectively, without metoprolol; 5.32 +/- 0.99 and 4.83 +/- 1.24, respectively, with metoprolol, p <0.05 for both). Thus, in survivors of remote myocardial infarction, metoprolol enhances parasympathetic cardiac activity in the time and frequency domain measures of heart rate variability.

Long-term assessment of heart rate variability in cardiac transplant recipients.

Sympathetic and parasympathetic reinnervation of the transplanted heart were evaluated by assessing time and frequency domain measurements of heart rate variability at 5 and 8 years. Continuous 24-hour ECG measurements were performed in 13 patients (57 +/- 6 months and 90 +/- 7 months) after orthotopic cardiac transplantation and in 22 healthy age and gender-matched controls, and were analyzed for heart rate variability in the time and frequency domains. Heart rate variability measures reflective of sympathetic reinnervation were sub-normal at 5 years and unchanged at 8 years: those reflective of parasympathetic reinnervation were absent.

Myocarditis and pericarditis with tamponade associated with disseminated tuberculosis.

Tuberculous involvement of the myocardium is relatively rare. Tuberculous pericarditis with tamponade and myocarditis in a young woman with no evidence of immunosuppression and disseminated tuberculosis is described. Three distinct forms of myocardial involvement are recognized: nodular tubercles (tuberculomas) of the myocardium; miliary tubercles of the myocardium; and an uncommon diffuse infiltrative type. The myocardium is involved by a hematogenous route, by lymphatic spread or contiguously from the pericardium. The diagnosis can be made by endomyocardial biopsy if clinical suspicion is strong and echocardiographic findings are suggestive. Antituberculosis drugs may be curative. With an increasing prevalence of tuberculosis, the possibility of potentially lethal myocardial tuberculosis is important to consider.

Left ventricular mural thrombus after acute myocardial infarction.

Left ventricular mural thrombus is a well-recognized complication of acute myocardial infarction. In survivors of infarction, the incidence with which mural thrombus occurs is influenced by the location and magnitude of infarction, so that it occurs commonly in those with large anterior Q-wave infarctions, particularly in the presence of a left ventricular aneurysm. Echocardiography, radionuclide imaging with indium-111 labeled platelets, computerized tomography, and magnetic resonance imaging may be used to identify a left ventricular mural thrombus. Acute and chronic anticoagulation with heparin and warfarin, respectively, is given to prevent further thrombus formation and to reduce the incidence of systemic embolization.

The origins of ecotypic variation of rainbow trout: a test of environmental vs. genetically based differences in morphology.

Although morphological plasticity has been observed in a variety of taxa, few experimental studies have compared the relative proportion of morphological variability that is accounted for by environmentally induced plasticity, and how much is because of genetically based differences among populations. We compared the morphology of six rainbow trout (Oncorhynchus mykiss) populations from different ecotypic categories that were raised under flowing vs. standing-water conditions. Our data indicate that both environmental conditions and ecotypic differences account for a significant proportion of variation in morphology. Among ecotype effects, however, accounted for a much larger proportion of morphological variability than environmental conditions. Rainbow trout from stream populations had deeper caudal peduncles, and longer fins than lake populations, and rainbow trout from a piscivorous population had larger mouth and head lengths than all other ecotypes. Environmentally induced differences in morphology were primarily related to differences in mouth and head lengths, as well as fin length. Relative to morphometric differences from natural rainbow trout populations, most characteristics deviated in the same direction in our experimental populations. Our data indicate that morphological differences across rainbow trout populations have a genetic basis and may represent locally adaptive characteristics and highlight the role of ecology in promoting phenotypic divergence.

The effect of food abundance on territory size and population density of juvenile steelhead trout (Oncorhynchus mykiss).

Optimal territory size models predict a decrease in territory size with increasing food abundance. However, most of these models may not be applicable to juvenile salmonids in streams, because they defend contiguous territories at high densities. The optimal size of a contiguous territory is predicted to (1) be independent of food abundance when food is rare and (2) decrease only when food abundance is high enough to induce a reduction in territory size below the contiguous optimum. To test these predictions, we raised equal densities of juvenile steelhead trout in outdoor stream channels over a 32-fold range of food abundance in the absence of emigration for 25 days. Increasing competition for scarce food resulted in increasing mortality, higher willingness to emigrate, higher variance in body mass, lower growth, lower population density and lower biomass. The size of territories decreased with increasing local population density, and increased with increasing body size. However, territory size did not change with food abundance, a result consistent with the prediction of a contiguous territory size model. On average, total salmonid biomass increased 5.7 times in response to the 32-fold increase in food abundance. Our data provide strong support for an earlier quantitative relationship between the abundance of stream salmonids and their food.