O' surgery case log data, where art thou?

BACKGROUND: The American College of Surgeons (ACS) Case Log represents a data system that satisfies the American Board of Surgery (ABS) Maintenance of Certification (MOC) program, yet has broad data fields for surgical subspecialties. Using the ACS Case Log, we have developed a method of data capture, categorization, and reporting of acute care surgery fellows' experiences. STUDY DESIGN: In July 2010, our acute care surgery fellowship required our fellows to log their clinical experiences into the ACS Case Log. Cases were entered similar to billable documentation rules. Keywords were entered that specified institutional services and/or resuscitation types. These data were exported in comma separated value format, deidentified, structured by Current Procedural Terminology (CPT) codes relevant to acute care surgery, and substratified by fellow and/or fellow year. RESULTS: Fifteen report types were created consisting of operative experience by service, procedure by major category (cardiothoracic, vascular, solid organ, abdominal wall, hollow viscus, and soft tissue), total resuscitations, ultrasound, airway, ICU services, basic neurosurgery, and basic orthopaedics. Results are viewable via a secure Web application, accessible nationally, and exportable to many formats. CONCLUSIONS: Using the ACS Case Log satisfies the ABS MOC program requirements and provides a method for monitoring and reporting acute care surgery fellow experiences. This system is flexible to accommodate the needs of surgical subspecialties and their training programs. As documentation requirements expand, efficient clinical documentation is a must for the busy surgeon. Although, our data entry and processing method has the immediate capacity for acute care surgery fellowships nationwide, multiple larger decisions regarding national case log systems should be encouraged.

Altered myocardial thin-filament function in the failing Dahl salt-sensitive rat heart: amelioration by endothelin blockade.

BACKGROUND: Dahl salt-sensitive rats fed a high-salt diet develop compensated left ventricular hypertrophy followed by a transition to myocardial failure. We previously reported an increase in a troponin T isoform (TnT3) and a decrease in TnT phosphorylation in failing Dahl salt-sensitive rat hearts compared with low-salt controls. The present study was undertaken to determine whether the thin filament plays a role in depression of the contractile machinery in this model. METHODS AND RESULTS: Native thin filaments (NTFs) were isolated intact from rats with compensated left ventricular hypertrophy and failing hearts and compared with age-matched controls. NTF velocity was measured as a function of free calcium in the in vitro motility assay. Maximal velocity was similar in all groups. However, NTFs from failing hearts demonstrated a reduction in calcium sensitivity compared with controls, as reflected in the pCa50 (5.88+/-0.05 versus 6.22+/-0.05, respectively, P<0.001). No difference in thin-filament motility (pCa50, V(max)) was observed in rats with compensated left ventricular hypertrophy compared with controls. Protein kinase A treatment of NTFs from control and failing hearts had no effect on thin-filament calcium sensitivity. However, the endothelin receptor blocker bosentan prevented the reduction in thin-filament calcium sensitivity found in failing hearts. CONCLUSIONS: The thin filament is a key modulator of contractile performance in the transition to failure in the Dahl salt-sensitive rat model. The alteration in thin-filament function may be mediated by an endothelin-triggered pathway potentially affecting protein kinase C signaling.