Trends in door-to-balloon time and outcomes following primary percutaneous coronary intervention for ST-elevation myocardial infarction: an Australian perspective.

BACKGROUND: Guidelines for patients with ST-elevation myocardial infarction include a door-to-balloon time (DTBT) of ≤90 min for primary percutaneous coronary intervention. AIM: The aim of this study was to assess temporal trends (2006-2010) in DTBT and determine if a reduction in DTBT was associated with improved clinical outcomes. METHODS: We compared annual median DTBT in 1926 STEMI patients undergoing primary percutaneous coronary intervention from the Melbourne Interventional Group registry. ST-elevation myocardial infarction presenting >12 h and rescue percutaneous coronary intervention was excluded. Major adverse cardiac events were analysed according to DTBT (dichotomised as ≤90 min vs >90 min). A multivariable analysis for predictors of mortality (including DTBT) was performed. RESULTS: Baseline demographics, clinical and procedural characteristics were similar in the STEMI cohort across the 5 years, apart from an increase in out-of-hospital cardiac arrest (3.6% in 2006 vs 9.4% in 2010, P < 0.0001) and cardiogenic shock (7.7-9.6%, P = 0.07). The median DTBT (interquartile range) was reduced from 95 (74-130) min in 2006 to 75 (51-100) min in 2010 (P < 0.01). In this period, the proportion of patients achieving a DTBT of ≤90 min increased from 45% to 67% (P < 0.01). Lower mortality and major adverse cardiac event rates were observed with DTBT ≤90 min (all P < 0.01). Multivariable analysis showed that a DTBT of ≤90 min was associated with improved clinical outcomes at 12 months (odds ratio 0.48; 95% confidence interval 0.33-0.73, P < 0.01). CONCLUSION: There has been a decline in median DTBT in the Melbourne Interventional Group registry over 5 years. DTBT of ≤90 min is associated with improved clinical outcomes at 12 months.

Vascular injury associated with extremity trauma: initial diagnosis and management.

Vascular injury associated with extremity trauma occurs in <1% of patients with long bone fracture, although vascular injury may be seen in up to 16% of patients with knee dislocation. In the absence of obvious signs of vascular compromise, limb-threatening injuries are easily missed, with potentially devastating consequences. A thorough vascular assessment is essential; an arterial pressure index <0.90 is indicative of potential vascular compromise. Advances in CT and duplex ultrasonography are sensitive and specific in screening for vascular injury. Communication between the orthopaedic surgeon and the vascular or general trauma surgeon is essential in determining whether to address the vascular lesion or the orthopaedic injury first. Quality evidence regarding the optimal fixation method is scarce. Open vascular repair, such as direct repair with or without arteriorrhaphy, interposition replacement, and bypass graft with an autologous vein or polytetrafluoroethylene, remains the standard of care in managing vascular injury associated with extremity trauma. Although surgical technique affects outcome, results are primarily dependent on early detection of vascular injury followed by immediate treatment.

Traumatic atlantoaxial distraction injury: a case report.

STUDY DESIGN: Case report. OBJECTIVES: Description of a rarely reported variant of traumatic C1-C2 dislocation and discussion of a favorable outcome in a nonsurgical treatment approach. SUMMARY OF BACKGROUND DATA: Atlantoaxial dislocation most commonly involves an anterior movement of C1 in relation to C2. Often, the integrity of the transverse ligament or odontoid process is compromised, and the atlantodental interval changed. The described patient sustained a purely craniocaudal atlantoaxial distractive lesion secondary to injury sustained in a high-speed motor vehicle accident. RESULTS: The initial treatment plan involved surgical stabilization subsequent to healing of a C1 ring fracture. After 12 weeks of external stabilization, ligamentous damage appeared well resolved. That there was no gross instability delayed using a surgical option. At periodic checkup, the patient was without symptoms. CONCLUSION: In this case, conservative management of a ligamentous C1-C2 injury was effective. At 5 years after trauma the patient was without sequelae. This outcome is in contrast to previous management of injuries of this type, all of which involved surgical intervention.

Melatonin induction of filamentous structures in non-neuronal cells that is dependent on expression of the human mt1 melatonin receptor.

Melatonin has gained recent popularity as a treatment for insomnia and other sleep disorders; however, its cellular effects are unknown. We report the effects of melatonin on the cellular morphology of Chinese hamster ovary (CHO) cells transformed to express the human melatonin receptors, mt1 and MT2. Our results show that melatonin exerts a strong influence on cellular shape and cytoskeletal organization in a receptor-dependent and possibly subtype-selective manner. The cell shape change that we see after a 5-h treatment of these non-neuronal cells with a pharmacological concentration of melatonin consists of the formation of long filamentous outgrowths that are reminiscent of the neurite processes produced by differentiating nerve cells. This morphological change occurs exclusively in cells expressing the mt1 receptor. We find that the microtubule and microfilament organization within these outgrowths is similar to that of neurites. Microtubules are required for the shape change to occur as Colcemid added in combination with melatonin completely blocks outgrowth formation. We demonstrate that the number of cells showing the altered cell shape is dependent on melatonin concentration, constant exposure to melatonin and that outgrowth frequencies increase when protein kinase A (PKA) is inhibited. Concomitant melatonin-dependent increases in MEK 1/2 and ERK 1/2 phosphorylation are noted in mt1-CHO cells only. The production of filamentous outgrowths is dependent on the translation of new protein but not the transcription of new mRNA. Outgrowth number is not controlled by centrosomes but is instead controlled by the polymerization state of the actin cytoskeleton. The results of this work show that the organization of the cytoskeleton is affected by processes specifically mediated or regulated by the mt1 receptor and may represent a novel alternative mechanism for the stimulation of process formation.