In inferior myocardial infarction, neither ST elevation in lead V1 nor ST depression in lead I are reliable findings for the diagnosis of right ventricular infarction.

OBJECTIVE: In the presence of inferior myocardial infarction (MI), ST depression (STD) in lead I has been claimed to be accurate for diagnosis of right ventricular (RV) MI. We sought to evaluate this claim and also whether ST Elevation (STE) in lead V1 would be helpful, with or without STD in V2. METHODS: Retrospective study of consecutive inferior STEMI, comparing ECGs of patients with, to those without, RVMI, as determined by angiographic coronary occlusion proximal to the RV marginal branch. STE and STD were measured at the J-point, relative to the PQ junction. The primary outcomes were sensitivity/specificity of 1) STD in lead I ≥ 0.5 mm and 2) STE in lead V1 ≥ 0.5 mm, stratified by presence or absence of posterior (inferobasal) MI, as determined by ≥0.5 mm STD in lead V2, for differentiating RVMI from non-RVMI. RESULTS: Of 149 patients with inferior STEMI, 43 (29%) had RVMI and 106 (71%) did not. There was no difference in the presence or absence of at least 0.5 mm STD in Lead I between patients with (37/43, 86%) vs. without RVMI (85/106, 80%, p = 0.56). In those with, vs. without, RVMI, (15/43, 35%) had STE in V1, versus (17/106, 16%) (p = 0.015). Specificity of STE in V1 for RVMI was 84%; sensitivity was 35%. Sensitivity was higher without (69%), than with (35%), STD in V2. CONCLUSION: Among inferior STEMI, the presence of any ST depression in lead I does not help to diagnose RVMI. ST elevation ≥0.5 mm in lead V1 is specific for RVMI, and moderately sensitive only if concomitant STD ≥ 0.5 mm in V2 is not present. Although STE in V1 is quite specific, overall the diagnostic characteristics of the standard 12­lead ECG are inadequate to definitively diagnose, or exclude, RVMI, as defined angiographically.

Discharge Glucose Is Not Associated With Short-Term Adverse Outcomes in Emergency Department Patients With Moderate to Severe Hyperglycemia.

STUDY OBJECTIVE: Hyperglycemia is frequently encountered in the emergency department (ED), and there is no consensus on optimal care before discharge. The importance of glucose reduction in the ED is unknown. We seek to determine whether an association exists between discharge glucose and 7-day adverse outcomes. METHODS: A cohort design with retrospective chart review was conducted at a high-volume urban ED. Patients were included if any glucose level was greater than or equal to 400 mg/dL and they were discharged from the ED. Generalized estimating equation models were created for the 7-day outcomes with a primary predictor of discharge glucose. RESULTS: The cohort consisted of 422 patients with 566 ED encounters. Mean arrival and discharge glucose were 491 mg/dL (SD 82 mg/dL) and 334 mg/dL (SD 101 mg/dL), respectively. In the 7-day follow-up period, 62 (13%) and 36 (7%) patients had a repeat ED visit for hyperglycemia and were hospitalized, respectively. Two patients had diabetic ketoacidosis. After adjustment for arrival glucose, whether a chemistry panel was obtained, amount of intravenous fluids administered, and amount of subcutaneous insulin administered, discharge glucose was not associated with repeat ED visit for hyperglycemia (adjusted odds ratio 0.997; 95% confidence interval 0.993 to 1.001) or hospitalization for any reason (adjusted odds ratio 0.998; 95% confidence interval 0.995 to 1.002). CONCLUSION: ED discharge glucose in patients with moderate to severe hyperglycemia was not associated with 7-day outcomes of repeat ED visit for hyperglycemia or hospitalization. Attaining a specific glucose goal before discharge in patients with hyperglycemia may be less important than traditionally thought.

ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis.

BACKGROUND: ST-segment elevation (STE) due to inferior STE myocardial infarction (STEMI) may be misdiagnosed as pericarditis. Conversely, this less life-threatening etiology of ST elevation may be confused for inferior STEMI. We sought to determine if the presence of any ST-segment depression in lead aVL would differentiate inferior STEMI from pericarditis. METHODS: Retrospective study of 3 populations. Cohort 1 included patients coded as inferior STEMI, cohort 2 included patients with a discharge diagnosis of pericarditis who presented with chest pain and at least 0.5 mm of ST elevation in at least 1 inferior lead. We analyzed the presenting electrocardiogram in both populations, with careful assessment of leads II, III, aVF, and aVL. In addition, we retrospectively studied a third cohort of patients with subtle inferior STEMI (<1-mm STE with occluded artery on catheterization) and assessed the sensitivity of ST depression in lead aVL for this group. RESULTS: Of 154 inferior STEMI patients, 154 had some amount of ST depression in lead aVL (100%; confidence interval, 98%-100%). Of the 49 electrocardiograms in the pericarditis group, all 49 had some inferior STE but none had any ST-segment depression in lead aVL (specificity, 100%; confidence interval, 91%-100%). In the third cohort, there were 272 inferior MIs with coronary occlusion, of which 54 were "subtle." Of these, 49 had some ST depression in lead aVL. CONCLUSION: When there is inferior ST-segment elevation, the presence of any ST depression in lead aVL is highly sensitive for coronary occlusion in inferior myocardial infarction and very specific for differentiating inferior myocardial infarction from pericarditis.

In vivo cartilage contact strains in patients with lateral ankle instability.

Damage to the anterior talofibular ligament (ATFL) and cacaneofibular ligament (CFL) during an ankle sprain may be linked to the development of osteoarthritis. Although altered tibiotalar kinematics have been demonstrated, the effects of lateral ankle instability (LAI) on in vivo cartilage strains have not been described. We hypothesized that peak cartilage strains increase, and the location is shifted in patients with ATFL injuries. We used 3-D MRI models and biplanar fluoroscopy to evaluate in vivo cartilage contact strains in seven patients with unilateral LAI. Subjects had chronic unilateral ATFL injury or combined ATFL and CFL injury, and were evaluated with increasing load while stepping onto a force plate. Peak cartilage strain and the location of the peak strain were measured using the contralateral normal ankle as a control. Ankles with LAI demonstrated significantly increased peak strain when compared with ATFL-intact controls. For example, at 100% body weight, peak strain was 29+/-8% on the injured side compared to 21+/-5% on the intact side. The position of peak strain on the injured ankle also showed significant anterior translation and medial translation. At 100% body weight, the location of peak strain in the injured ankle translated anteriorly by 15.5+/-7.1mm and medially by 12.9+/-4.3mm relative to the intact ankle. These changes correspond to the region of clinically observed osteoarthritis. Chronic LAI, therefore, may contribute to the development of tibiotalar cartilage degeneration due to altered cartilage strains.

Three-dimensional ankle kinematics and kinetics during running in women.

Stress fractures are common in athletics and are more prevalent in women. The current literature has not identified a reason for this gender difference. We hypothesized that females with a history of a second/third metatarsal stress fracture will demonstrate differences in ankle kinematics, kinetics and ground reaction forces when compared with a group of age-matched females with no stress fracture history. A total of 15 control females and nine females with a history of a second/third metatarsal stress fracture were asked to run at 3.3m/s+/-5% along a 10-m runway. Kinematics and kinetics were obtained using an 8-camera motion analysis system (240Hz) and two force plates (1200Hz). Significant differences existed in height and weight between the groups. No other statistically significant differences existed between the fracture group and the control group. Kinematic measurements do not differ significantly between women with a history of second/third metatarsal stress fracture and female control subjects. The reported kinematic and kinetic measurements do not appear to be influenced in subjects with metatarsal stress fractures, which likely result from the complex relationships between the joints in the foot and ankle. The development of second/third metatarsal stress fractures could result more from over training or changes in plantar loading instead of changes in lower extremity joint kinematics while running.