Successful reduction of a high defibrillation threshold by a combined implantation of a subcutaneous array and azygos vein lead.

A 72-year-old man with nonischemic cardiomyopathy was referred because his implantable cardioverter defibrillator had failed to terminate spontaneous ventricular fibrillation (VF). Defibrillation threshold (DFT) testing confirmed that 830-V shocks failed to defibrillate VF despite optimization of the biphasic waveform and reversal of shock polarity. The placement of a new right ventricular lead and the addition of a subcutaneous array failed to defibrillate VF at 830 V. The combination of a subcutaneous array and azygos vein coil successfully defibrillated VF. The mechanism for successful DFT reduction was likely greater current supplied to the posterior basal left ventricle by the azygos vein lead.

Increased cycle length during long-duration ventricular fibrillation is caused by decreased upstroke velocity as well as prolonged refractoriness.

BACKGROUND: Cycle length (CL) increases as ventricular fibrillation (VF) progresses. OBJECTIVE: The purpose of this study was to test the hypotheses that increased CL is due to increased diastolic interval (DI), not increased action potential duration (APD), and that the DI increase is not solely due to increased postrepolarization refractoriness. METHODS: In 10 swine, VF was recorded for 20 minutes using a floating microelectrode through a hole in a 504-electrode epicardial plaque. Mean APD, DI, action potential amplitude (APA), maximum change in voltage during the AP upstroke (V(max)), and CL were calculated from the floating microelectrode recordings each minute of VF. The refractory period was estimated from the minimum DI (DI(min)). In two animals, rapid pacing was performed to gauge refractoriness. RESULTS: As VF progressed, CL, DI, and DI(min) increased (P <.05), whereas APD, V(max), and APA decreased (P <.05). At 20 minutes, DI(min) was not different from mean DI at VF onset. Pacing captured, but 53% of paced wavefronts blocked within the plaque. CONCLUSION: Increasing CL in VF is due to increased DI and not APD, which shortens. The increase in DI(min) over time is much less than the increase in mean DI, indicating that the myocardium is excitable during much of the DI. This finding, along with the ability to pace at a CL shorter than the native VF CL and the poor paced wavefront propagation, suggests that the increase in DI is due not only to increased postrepolarization refractoriness but also to poor wavefront propagation because of decreased APA and V(max) secondary to global ischemia caused by VF.

Chemical ablation of the Purkinje system causes early termination and activation rate slowing of long-duration ventricular fibrillation in dogs.

Endocardial mapping has suggested that Purkinje fibers may play a role in the maintenance of long-duration ventricular fibrillation (LDVF). To determine the influence of Purkinje fibers on LDVF, we chemically ablated the Purkinje system with Lugol solution and recorded endocardial and transmural activation during LDVF. Dog hearts were isolated and perfused, and the ventricular endocardium was exposed and treated with Lugol solution (n = 6) or normal Tyrode solution as a control (n = 6). The left anterior papillary muscle endocardium was mapped with a 504-electrode (21 x 24) plaque with electrodes spaced 1 mm apart. Transmural activation was recorded with a six-electrode plunge needle on each side of the plaque. Ventricular fibrillation (VF) was induced, and perfusion was halted. LDVF spontaneously terminated sooner in Lugol-ablated hearts than in control hearts (4.9 +/- 1.5 vs. 9.2 +/- 3.2 min, P = 0.01). After termination of VF, both the control and Lugol hearts were typically excitable, but only short episodes of VF could be reinduced. Endocardial activation rates were similar during the first 2 min of LDVF for Lugol-ablated and control hearts but were significantly slower in Lugol hearts by 3 min. In control hearts, the endocardium activated more rapidly than the epicardium after 4 min of LDVF with wave fronts propagating most often from the endocardium to epicardium. No difference in transmural activation rate or wave front direction was observed in Lugol hearts. Ablation of the subendocardium hastens VF spontaneous termination and alters VF activation sequences, suggesting that Purkinje fibers are important in the maintenance of LDVF.

Perioperative medical comorbidities in the orthopaedic patient.

Evaluation and management of medical comorbidities in the perioperative period can help improve surgical morbidity and mortality. Perioperative evaluation essentially is risk assessment and minimization. Patients undergoing orthopaedic treatment may benefit from temporizing measures to reduce systemic complications associated with some procedures. Patients at increased risk of cardiac ischemia should undergo risk stratification to determine possible perioperative interventions. Use of perioperative medications and/or consultation with specialists can help to address heart murmurs, bacterial endocarditis, prior stenting, heart failure, and hypertension. Patients with severe or unstable chronic obstructive pulmonary disease require the involvement of pulmonary care specialists. Renal failure can require nephrology consultation, particularly in cases of worsening renal function or urinary outflow obstruction. Hematologic considerations include bleeding and clotting. Prophylaxis should be used in patients with risk factors for peptic ulcer, as well as respiratory failure and hypotension. Nutritional status and liver disease also must be monitored and treated preoperatively. Orthopaedic diabetic patients should be placed on modified oral hypoglycemic or insulin regimens; recalcitrant cases merit consultation. Effective communication among all members of the patient's caregiving team is paramount.

Activation patterns of Purkinje fibers during long-duration ventricular fibrillation in an isolated canine heart model.

BACKGROUND: The roles of Purkinje fibers (PFs) and focal wave fronts, if any, in the maintenance of ventricular fibrillation (VF) are unknown. If PFs are involved in VF maintenance, it should be possible to map wave fronts propagating from PFs into the working ventricular myocardium during VF. If wave fronts ever arise focally during VF, it should be possible to map them appearing de novo. METHODS AND RESULTS: Six canine hearts were isolated, and the left main coronary artery was cannulated and perfused. The left ventricular cavity was exposed, which allowed direct endocardial mapping of the anterior papillary muscle insertion. Nonperfused VF was induced, and 6 segments of data, each 5 seconds long, were analyzed during 10 minutes of VF. During 36 segments of data that were analyzed, 1018 PF or focal wave fronts of activation were identified. In 534 wave fronts, activation was mapped propagating from working ventricular myocardium to PF. In 142 wave fronts, activation was mapped propagating from PF to working ventricular myocardium. In 342 wave fronts, activation was mapped arising focally. More than 1 of these 3 patterns could occur in the same wave front. CONCLUSIONS: PFs are highly active throughout the first 10 minutes of VF. In addition to retrograde propagation from the working ventricular myocardium to PFs, antegrade propagation occurs from PFs to working ventricular myocardium, which suggests PFs are important in VF maintenance. Prior plunge needle recordings in dogs indicate activation propagates from the endocardium toward the epicardium after 1 minute of VF, which suggests that focal sites on the endocardium may represent foci and not breakthrough. If so, in addition to reentry, abnormal automaticity or triggered activity may also occur during VF.

Transforming growth factor-beta in calcium alginate beads for the treatment of articular cartilage defects in the rabbit.

PURPOSE: Articular cartilage has only limited capability for intrinsic repair. The use of growth factors has been suggested to improve the repair of cartilage after injury. Reliable delivery systems for these agents are needed. In this study we tested calcium alginate for the delivery of TGF-beta in the treatment of osteochondral defects in the rabbit knee. TYPE OF STUDY: Randomized trial animal study and basic science study. METHODS: In vitro, to establish the kinetics of TGF-beta release from the alginate, 125I- labeled TGF-beta was suspended in 1.2% sodium alginate at concentrations of 1 microg/mL and 10 microg/mL. Beads were formed from 50 microL aliquots and placed into standard culture medium by immersion in calcium chloride solution and incubated at 37 degrees C. A gamma counter was used to measure the amount of TGF-beta that was released into the medium at various time points. In vivo, osteochondral defects were created in the trochlear grooves of 32 New Zealand White rabbits. Defects were treated with plain alginate or with alginate containing TGF-beta at 20 ng/mL or 2,000 ng/mL. Untreated defects served as a control. Animals were killed after 6 and 12 weeks. Knee joints were evaluated grossly with a 12-point grading scale. Histologic sections of the repair tissue were stained with Safranin O and evaluated using a 24-point grading scale by 2 independent blinded observers. Mean scores and standard deviations were calculated. P values were determined using the Student t test. RESULTS: The TGF-beta was released at a surprisingly slow but steady rate. Release rates extrapolated from the gamma counter measurements were 0.25% per hour and 0.33% per hour, for the 1 microg/mL and 10 microg/mL beads, respectively. Gross analysis scores at 6 and 12 weeks resulted in higher scores for both TGF-beta groups without reaching statistical significance. The lower TGF-beta concentration reached the highest scores, whereas the higher concentration (2,000 ng/mL) resulted in increased osteophyte formation. Histologic analysis at 6 weeks resulted in average scores ranging from 14.5 for empty defects and 18.1 for alginate-treated defects, to 20.0 and 20.3 for the 2,000 ng/mL and 20 ng/mL TGF-beta groups, respectively (P <.05). At 12 weeks, histologic scores ranged from 14.9 for empty and 14.5 for alginate to 20.1 and 20.5 for the 2,000 ng/mL and 20 ng/mL TGF-beta groups, respectively (P <.05). These results indicate a significant improvement of the quality of the repair tissue at 6 and 12 weeks with TFG-beta treatment, especially at the lower concentration. CONCLUSIONS: The use of alginate allows the controlled delivery of TGF-beta selectively to the site of injury, potentially avoiding systemic side effects. Furthermore, treatment with TGF-beta appears to improve the repair of articular cartilage defects. Longer-term studies are needed to assess whether the benefits of the TGF-beta treatment can be sustained.