Eptifibatide-Induced Profound Thrombocytopenia After Percutaneous Intervention for Acute Coronary Syndrome: A Challenging Clinical Scenario.

Eptifibatide is a glycoprotein (GP) IIb/IIIa inhibitor used mostly in the treatment of acute coronary syndrome (ACS). The GP IIb/IIIa antagonists occupy the fibrinogen binding site at the GP IIb/IIIa and block thrombocyte aggregation independent of the initial activation pathway. Severe thrombocytopenia has been reported with eptifibatide use. Thrombocytopenia after ACS can have multiple etiologies. Human immunodeficiency virus (HIV) infection has also been implicated in immune-mediated thrombocytopenia. In this manuscript, we report a case of acute severe thrombocytopenia secondary to eptifibatide use in a patient with a history of HIV infection who presented with an ST elevation myocardial infarction. We also review the differential diagnosis and suggest management strategies in this challenging clinical scenario.

Structural protein alterations to resistance and endurance cycling exercise training.

The muscle cytoskeleton is necessary for the effective transmission of forces generated by actin-myosin interactions. We have examined the impact of muscle force and exercise volume on the cytoskeleton by measuring desmin and dystrophin content in human skeletal muscle after 12 weeks of progressive resistance or endurance cycle training. Muscle biopsies of the vastus lateralis were obtained before and after training. Desmin and dystrophin content was determined using immunoblotting techniques. After resistance training, desmin content increased 82 +/- 18% (p < 0.05), whereas there was no change in desmin content with endurance cycling. Dystrophin content did not change in either group. One-repetition maximum and VO2max increased (p < 0.05) in the resistance and endurance groups, respectively. These data demonstrate that a high-tension stimulus impacts the cytoskeleton in contrast to high-volume concentric contractions. The tensile loading and eccentric components of resistance training are implicated in desmin alterations. Indeed, the functional improvements resulting from resistance training may be related in part to the mechanical integration provided by the desmin protein.

Single-fiber MHC polymorphic expression is unaffected by sprint cycle training.

PURPOSE: The present investigation examined single-fiber MHC alterations in response to high-intensity, short-duration, sprint cycle training. METHODS: Ten untrained college-age male subjects participated in 8 wk of a progressive sprint cycle training program. Training involved 15-s maximal sprints separated by 5 min of rest beginning with four sprints x 2 d in week 1 and increasing to six sprints x 3 d at week 8. Muscle samples from the vastus lateralis were obtained before and after training. A 30-s sprint cycle test was used to evaluate performance before and after training. RESULTS: For the 30-s sprint, mean power and total work increased from pre to post. Single-fiber analyses revealed a reduction in the MHC IIx isoform (2.0 +/- 1.0 to 0.2 +/- 0.1%, pre to post, P < 0.05) and an increase in MHC IIa (P = 0.08), whereas there was no change in hybrid fiber composition (total hybrids = 24%). Generally, MHC IIa content increased and MHC IIx decreased (P < 0.05) as demonstrated by homogenate analyses of tissue samples. CONCLUSIONS: We report that as little as 32 min of high-intensity sprint cycle training over 8 wk is sufficient to improve sprinting performance. This training response is accompanied by an increase in MHC IIa and reduction in MHC IIx content of the vastus lateralis. However, short-duration, high-intensity, sprint cycle training does not cause a reduction in hybrid muscle fiber content.

Prior exposure to indole-3-carbinol decreases the incidence of specific cyclophosphamide-induced developmental defects in mice.

BACKGROUND: Indole-3-carbinol (I3C) is a product of the hydrolysis of glucobrassicin that is found in cruciferous vegetables. I3C can intervene in toxic processes that are mediated by oxidative mechanisms because it possesses the chemical and pharmacokinetic properties necessary to provide a free radical trap. Cyclophosphamide (CP) is a bifunctional alkylating agent known to produce DNA damage and to cause developmental toxicity, including malformations, in laboratory animals. METHODS: Pregnant CD-1 mice were given a 100 mg/kg dose of I3C 24 or 48 hr before administration of 20 mg/kg CP on gestation day 10 (GD 10). Controls were given the vehicle (DMSO), I3C, or CP. This regimen was carried out to determine if I3C could protect against the developmental toxicity of alkylating agents, such as CP. Dams were sacrificed on GD 17 and their litters were examined for adverse effects. RESULTS: Treatment with I3C 48 hr before CP administration was associated with decreased fetal limb and tail malformations. Limb malformation incidences were reduced from 42% litters affected in the CP control to 16% in the I3C/CP 48-hr treatment group, and tail malformations were reduced from 45% in the CP control to 16% in the I3C/CP 48-hr treatment group, indicating a protective effect of prior exposure to I3C. I3C given 24 hr before CP had no significant protective effect, while having an apparently adverse consequence with regard to the incidence of talipes. CONCLUSIONS: Exposure of a developing mammal to indole-3-carbinol before exposure to cyclophosphamide during organogenesis can influence the teratogenicity of cyclophosphamide.

Single muscle fiber myosin heavy chain distribution in elite female track athletes.

PURPOSE: Myosin heavy chain (MHC) characterization of tissue samples from the gastrocnemius muscle of six elite female athletes and 10 untrained females was performed using myosin ATPase histochemistry and gel electrophoresis. Athletes were of national and international caliber, whereas their untrained counterparts were healthy individuals not involved in a regular exercise program. METHODS: Muscle biopsies for the athletes were performed 14 wk into their training season and analyzed with sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and myosin ATPase techniques. RESULTS: Electrophoretic analysis of single muscle fibers from elite athletes revealed a MHC phenotype composition of 46 +/- 6% type I, 21 +/- 6% type IIa, and 0% type IIx, whereas 34% of the single fibers expressed multiple MHC isoforms. When compared with the elite women, untrained subjects demonstrated higher percentages of type I MHC and lower percentages of IIa MHC muscle fibers, 57 +/- 5 and 16 +/- 3%, respectively (P < 0.05). Similar to the female athletes, 27% of the fibers from untrained women possessed multiple myosin isoforms. Myosin ATPase staining demonstrated a greater percentage of type I fibers in untrained subjects versus the elite women (67 +/- 3 vs 41 +/- 2%, P< 0.05) (mean +/- SE), whereas the athletes had a higher percentage of type IIa fibers compared with the untrained women (49 +/- 5 vs 19 +/- 2%, P< 0.05). There were no differences in the percentage of IIb fibers between elite and untrained women (11 +/- 4 vs 14 +/- 2%, respectively). CONCLUSIONS: Whereas a preponderance of hybrid fibers is generally observed in untrained populations, the diverse MHC phenotype seen in these elite female athletes is uncommon. These unique findings are attributed to the chronic and varied nature of training in which these athletes were involved.

Effects of L-tyrosine and carbohydrate ingestion on endurance exercise performance.

To test the effects of tyrosine ingestion with or without carbohydrate supplementation on endurance performance, nine competitive cyclists cycled at 70% peak oxygen uptake for 90 min under four different feeding conditions followed immediately by a time trial. At 30-min intervals, beginning 60 min before exercise, each subject consumed either 5 ml/kg body wt of water sweetened with aspartame [placebo (Pla)], polydextrose (70 g/l) (CHO), L-tyrosine (25 mg/kg body wt) (Tyr), or polydextrose (70 g/l) and L-tyrosine (25 mg/kg body wt) (CHO+Tyr). The experimental trials were given in random order and were carried out by using a counterbalanced double-blind design. No differences were found between treatments for oxygen uptake, heart rate, or rating of perceived exertion at any time during the 90-min ride. Plasma tyrosine rose significantly from 60 min before exercise to test termination (TT) in Tyr (means +/- SE) (480 +/- 26 micromol) and CHO+Tyr (463 +/- 34 micromol) and was significantly higher in these groups from 30 min before exercise to TT vs. CHO (90 +/- 3 micromol) and Pla (111 +/- 7 micromol) (P < 0.05). Plasma free tryptophan was higher after 90 min of exercise, 15 min into the endurance time trial, and at TT in Tyr (10.1 +/- 0.9, 10.4 +/- 0.8, and 12.0 +/- 0.9 micromol, respectively) and Pla (9.7 +/- 0.5, 10.0 +/- 0.3, and 11.7 +/- 0.5 micromol, respectively) vs. CHO (7.8 +/- 0.5, 8.6 +/- 0.5, and 9.3 +/- 0.6 micromol, respectively) and CHO+Tyr (7.8 +/- 0.5, 8.5 +/- 0.5, 9.4 +/- 0.5 micromol, respectively) (P < 0.05). The plasma tyrosine-to-free tryptophan ratio was significantly higher in Tyr and CHO+Tyr vs. CHO and Pla from 30 min before exercise to TT (P < 0.05). CHO (27.1 +/- 0.9 min) and CHO+Tyr (26.1 +/- 1.1 min) treatments resulted in a reduced time to complete the endurance time trial compared with Pla (34.4 +/- 2.9 min) and Tyr (32.6 +/- 3.0 min) (P < 0.05). These findings demonstrate that tyrosine ingestion did not enhance performance during a cycling time trial after 90 min of steady-state exercise.

Minimum rest period for strength recovery during a common isokinetic testing protocol.

PURPOSE: The intent of this investigation was to determine the minimal time for a between sets rest period during a common isokinetic knee extension strength-testing protocol. Based on a review of the literature, a set was considered a group of four maximal coupled contractions at a specific velocity. METHODS: Eleven normal, healthy college-age men underwent unilateral knee extension testing to determine their individual isokinetic peak torque at 60, 120, 180, 240, and 300 degrees.s-1. Velocities were administered in ascending order. Between sets, rest periods of 15, 60, 180, and 300 s were assigned to subjects in a counterbalanced fashion. RESULTS: There were no differences in peak torque at the beginning velocity of 60 degrees.s-1 among any of the rest periods. At 120 degrees.s-1, peak torque production during the 15-s rest period trial was similar to 60 s but lower than 180 and 300 s. Peak torques at 180, 240, and 300 degrees.s-1 produced during the 15-s rest period test were significantly lower than measured torques at the same velocities during the 60, 180, and 300-s rest period tests (P < 0.05). There were no differences in peak torque production between the 60, 180, and 300-s rest period tests. CONCLUSION: These data demonstrate that during a common isokinetic strength testing protocol a between set rest period of at least 60 s is sufficient for recovery before the next test set.