Faculty Bibliography

BACKGROUND:Transient ischemic dilation (TID) of the left ventricle in myocardial perfusion SPECT (MPS) has been shown to be a clinically useful marker of severe coronary artery disease (CAD). However, TID has not been evaluated for 99mTc-sestamibi rest/stress protocols (Mibi-Mibi). We aimed to develop normal limits and evaluate diagnostic power of TID ratio for Mibi-Mibi scans. METHODS:TID ratios were automatically derived from static rest/stress MPS (TID) and gated rest/stress MPS from the end-diastolic phase (TID(ed)) in 547 patients who underwent Mibi-Mibi scans [215 patients with correlating coronary angiography and 332 patients with low likelihood (LLk) of CAD]. Scans were classified as severe (≥ 70% stenosis in proximal left anterior descending (pLAD) artery or left main (LM), or ≥ 90% in ≥ 2 vessels), mild to moderate (≥ 90% stenosis in 1 vessel or ≥ 70%-90% in ≥ 1 vessel except pLAD or LM), and normal (<70% stenosis or LLk group). Another classification based on the angiographic Duke prognostic CAD index (DI) was also applied: DI ≥ 50, 30 ≤ DI < 50 and DI < 30 or LLk group. RESULTS:The upper normal limits were 1.19 for TID and 1.23 for TID(ed) as established in 259 LLk patients. Both ratios increased with disease severity (P < .0001). Incidence of abnormal TID increased from 2% in normal patients to >36% in patients with severe CAD. Similarly, when DI was used to classify disease severity, the average ratios showed significant increasing trend with DI increase (P < .003); incidence of abnormal TID also increased with increasing DI. The incidence of abnormal TID in the group with high perfusion scores significantly increased compared to the group with low perfusion scores (stress total perfusion deficit, TPD < 3%) (P < .0001). The sensitivity for detecting severe CAD improved for TID when added to mild to moderate perfusion abnormality (3% ≤ TPD < 10%): 71% vs 64%, P < .05; and trended to improve for TID(ed)/TID(es): 69% vs 64%, P = .08, while the accuracy remained consistent if abnormal TID was considered as a marker in addition to stress TPD. Similar results were obtained when DI was used for the definition of severe CAD (sensitivity: 76% vs 66%, P < .05 when TID was combined with stress TPD). CONCLUSION/CONCLUSIONS:TID ratios obtained from gated or ungated Mibi-Mibi MPS and are useful markers of severe CAD.

BACKGROUND: The association between admission heart rate (AHR) and mortality after trauma can assist initial emergency department triage and resuscitation. In addition, increased AHR is often associated with sympathetic hyperactivity which may require targeted treatment. We determined whether AHR was a predictor for mortality in trauma patients. METHODS: The Los Angeles County Trauma System Database was queried for all injured patients admitted between 1998 and 2005 (n = 147,788). Traumatic brain injury (TBI) patients (head Abbreviated Injury Scale score >/= 3) were excluded. Demographics were compared at various AHR subgroups (<50, 50-59, 60-69, 70-79, 80-89, 90-99, 100-109, and >/= 110). Mortality was compared at various AHR ranges, and logistic regression was performed to determine significance. RESULTS: After exclusions, 103,799 trauma patients requiring admission were identified; overall mortality was 1.4%. AHR 80 to 89 demonstrated a statistically significant lower mortality (0.5%) compared with all other AHR ranges, except AHR 70 to 79 (0.6%). In trauma patients who required admission, AHR 70 to 79 and 80 to 89 were predictors of lower mortality. Mortality for 22,232 moderate to severely injured patients was 5.5% and AHR 80 to 89 demonstrated a statistically lower mortality (2.0%) than all other AHR ranges, except AHR 70 to 79 (1.9%). After moderate to severe trauma, AHR <60 and >/= 100 were associated with significantly higher mortality. CONCLUSION: Mortality after trauma increases outside the AHR range of 70 to 89 beats per minute. AHR ranges previously considered "normal" were associated with significantly increased mortality. Prospective research is required to evaluate if resuscitation goals should target heart rate at the 70 to 89 range.

BACKGROUND: Although avoiding hypotension is a primary focus after trauma, elevated systolic blood pressure (SBP) is frequently disregarded. The purpose of this study was to determine the association between elevated admission SBP and delayed outcomes after trauma. METHODS: The Los Angeles County Trauma System Database was queried for all patients between 2003 and 2008 with blunt injuries who survived for at least 2 days after admission. Demographics and outcomes (pneumonia and mortality) were compared at various admission SBP subgroups (>/=160 mm Hg, >/=170 mm Hg, >/=180 mm Hg, >/=190 mm Hg, >/=200 mm Hg, >/=210 mm Hg, and >/=220 mm Hg). Patients with moderate-to-severe traumatic brain injury (TBI), defined as head Abbreviated Injury Score >/=3, were then identified and compared with those without using multivariable logistic regression. RESULTS: Data accessed from 14,382 blunt trauma admissions identified 2,601 patients with moderate-to-severe TBI (TBI group) and 11,781 without moderate-to-severe TBI (non-TBI group) who were hospitalized >/=2 days. Overall mortality was 2.9%, 7.1% for TBI patients, and 1.9% for non-TBI patients. Overall pneumonia was 4.6%, 9.5% for TBI patients, and 3.6% for non-TBI patients. Regression modeling determined SBP >/=160 mm Hg was a significant predictor of mortality in TBI patients (adjusted odds ratio [AOR], 1.59; confidence interval [CI], 1.10-2.29; p = 0.03) and non-TBI patients (AOR, 1.47; CI, 1.14-1.90; p = 0.003). Similarly, SBP >/=160 mm Hg was a significant predictor for increased pneumonia in TBI patients (AOR, 1.79; CI, 1.30-2.46; p = 0.0004), compared with non-TBI patients (AOR, 1.28; CI, 0.97-1.69; p = 0.08). CONCLUSIONS: In blunt trauma patients with or without TBI, elevated admission SBP was associated with worse delayed outcomes. Prospective research is necessary to determine whether algorithms that manage elevated blood pressure after trauma, especially after TBI, affect mortality or pneumonia.

BACKGROUND: This analysis explored the association between gender and systolic blood pressure (SBP) in trauma patients and then established how gender influenced outcomes in those with elevated SBP. METHODS: Demographics and outcomes were compared using the Los Angeles County Trauma System Database and multivariable modeling determined predictors for SBP, pneumonia, and mortality. RESULTS: Age and male sex were significant predictors for increased SBP, whereas the Injury Severity Score (ISS) >/=16 was a significant predictor for decreased SBP. In both male and female TBI patients, SBP >/=160 mmHg was associated with increased pneumonia (Adjusted odds ratio [AOR] = 1.74, P = .002 and AOR = 2.37, P = .046, respectively), whereas SBP >/=160 mmHg was a predictor for mortality only among male TBI patients (AOR = 1.48, P = .03). In non-TBI patients, SBP >/=160 mmHg was not a predictor for pneumonia or mortality in either sex. CONCLUSIONS: In this retrospective review of trauma registry data, men presented with higher SBP. In patients with TBI, regardless of gender, increased SBP was associated with increased pneumonia, and in men with TBI increased SBP was associated with increased mortality. The cause and relevance of these epidemiological findings require further investigation.

The aim of this study was to assess how increasing age affects mortality in trauma patients with Glasgow Coma Scale (GCS) 3. The Los Angeles County Trauma System Database was queried for all patients aged 20 to 99 years admitted with GCS 3. Mortality was 41.8 per cent for the 3306 GCS 3 patients. Mortality in the youngest patients reviewed, those in the third decade, was 43.5 per cent. After logistic regression analysis, patients in the third decade had similar mortality rates to patients in the sixth (adjusted OR, 0.88; CI, 0.68 to 1.14; P = 0.33) and seventh decades (adjusted OR, 0.96; CI, 0.70 to 1.31; P = 0.79). A significantly lower mortality rate, however, was noted in the fifth decade (adjusted OR, 0.76; CI, 0.61 to 0.95; P = 0.02). Conversely, significantly higher mortality rates were noted in the eighth (adjusted OR, 1.93; CI, 1.38 to 2.71; P = 0.0001) and combined ninth/tenth decades (adjusted OR, 2.47; CI, 1.71 to 3.57; P < 0.0001). Given the high survival in trauma patients with GCS 3 as well as continued improvement in survival compared with historical controls, aggressive care is indicated for patients who present to the emergency department with GCS 3.

OBJECTIVE:Interleukin-6 (IL6) is a major inflammatory mediator and one of the first cytokines produced after traumatic brain injury (TBI). This study evaluates early behavioral changes and acute inflammation after TBI in IL6 knock-out mice using electromagnetic controlled cortical impact. METHODS:IL6 knock-out (KO) and C57BL/6 (WT) male mice were subjected to TBI or sham injury (n = 6 mice per group) using electromagnetic controlled cortical impact. Behavioral deficits were tested by standard performance tests. Brain IL1β expression was measured by ELISA and HSP70 expression was measured by Western blot. RESULTS:After TBI, KO showed reduced performance on the neuroscreen compared with wild type (KO 3.2 ± 0.7 versus WT 4.7 ± 0.2 points, P = 0.007), less exploratory activity in the open field test (KO 1090.2 ± 1799.2 versus WT 5636.8 ± 1291.8 regions explored per hour, P = 0.003) less rearing behavior in the open field test (KO 36.4 ± 79.2 versus WT 346.5 ± 18.5 rearing per hour, P = 0.0006), reduced travel on the rotarod (KO 3.5 ± 4.0 versus WT 13.0 ± 4.0 cm, P = 0.0109), and reduced time balanced on the rotarod (KO 15.0 ± 11.5 versus WT 36.2 ± 5.9 s, P = 0.0109). After TBI, IL6 knock-out mice had significantly elevated IL1β (KO 58.16 ± 17.54 versus WT 14.98 ± 8.33 pg/mL, P = 0.003 and nonsignificantly increased HSP70 levels (KO 0.93 ± 0.96 versus WT 0.68 ± 0.97, P = 0.77). CONCLUSION/CONCLUSIONS:IL6 deficiency after TBI is associated with poor behavior performance, and appears to affect expression of IL1β and, possibly, HSP70.

BACKGROUND:Hyperglycemia after traumatic brain injury (TBI) is an independent predictor of mortality. Insulin deficiency, as opposed to elevated blood glucose, might be the reason for increased mortality. TBI patients with diabetes mellitus (DM) were analyzed to determine how insulin deficiency affects mortality after TBI. METHODS:NTDB version 7 was queried for patients with isolated moderate to severe TBI (head abbreviated injury score [AIS]≥3 with AIS≤3 for other body regions). Demographics and outcomes were compared between TBI patients with insulin-dependent DM (IDDM), noninsulin-dependent DM (NIDDM), and those without DM. Logistic regression analysis was used to investigate the relationship between mortality and DM. RESULTS:Overall, 51,585 patients with isolated moderate to severe TBI were analyzed. Mortality was 14.4% and 8.2% in patients with and without DM, respectively (p<0.0001). Although head AIS scores were similar, patients with DM had a statistically higher Glasgow coma scale (GCS) at presentation compared with patients without DM (GCS score 12.4 vs. GCS score 10.9; p<0.0001). After multivariable logistic regression analysis, DM was an independent predictor for mortality (odds ratio 1.5, confidence interval 1.29-1.74, p<0.0001). When comparing TBI patients with IDDM to NIDDM, mortality was 17.1% for IDDM and 13.0% for NIDDM (p=0.025). CONCLUSION/CONCLUSIONS:DM is a significant predictor for mortality after moderate to severe TBI. Insulin deficiency is a likely contributor to increased mortality after TBI as IDDM patients have higher mortality than NIDDM patients who have higher mortality than no-DM patients.

BACKGROUND:Recent evidence suggests a survival advantage in trauma patients who receive controlled or hypotensive resuscitation volumes. This study examines the threshold crystalloid volume that is an independent risk factor for mortality after trauma. METHODS:This study analyzed prospectively collected data from a Level I Trauma Center between January 2000 and December 2008. Demographics and outcomes were compared in elderly (≥70 years) and nonelderly (<70 years) trauma patients who received crystalloid fluid in the emergency department (ED) to determine a threshold volume that was an independent predictor for mortality. RESULTS:A total of 3,137 patients who received crystalloid resuscitation in the ED were compared. Overall mortality was 5.2%. Mortality among the elderly population was 17.3% (41 deaths), whereas mortality in the nonelderly population was 4% (116 deaths). After multivariate logistic regression analysis, fluid volumes of 1.5 L or more were significantly associated with mortality in both elderly (odds ratio [OR]: 2.89, confidence interval [CI] [1.13-7.41], p=0.027) and nonelderly patients (OR: 2.09, CI [1.31-3.33], p=0.002). Fluid volumes up to 1 L were not associated with significantly increased mortality. At 3 L, mortality was especially pronounced in the elderly (OR: 8.61, CI [1.55-47.75] p=0.014), when compared with the nonelderly (OR=2.69, CI [1.53-4.73], p=0.0006). CONCLUSION/CONCLUSIONS:ED volume replacement of 1.5 L or more was an independent risk factor for mortality. High-volume resuscitations were associated with high-mortality particularly in the elderly trauma patient. Our finding supports the notion that excessive fluid resuscitation should be avoided in the ED and when required, operative intervention or intensive care admission should be considered.