The effect of haemorrhagic shock and resuscitation on fracture healing in a rabbit model: an animal study.

Aims: Little is known about the effect of haemorrhagic shock and resuscitation on fracture healing. This study used a rabbit model with a femoral osteotomy and fixation to examine this relationship. Materials and Methods: A total of 18 male New Zealand white rabbits underwent femoral osteotomy with intramedullary fixation with 'shock' (n = 9) and control (n = 9) groups. Shock was induced in the study group by removal of 35% of the total blood volume 45 minutes before resuscitation with blood and crystalloid. Fracture healing was monitored for eight weeks using serum markers of healing and radiographs. Results: Four animals were excluded due to postoperative complications. The serum concentration of osteocalcin was significantly elevated in the shock group postoperatively (p < 0.0001). There were otherwise no differences with regard to serum markers of bone healing. The callus index was consistently increased in the shock group on anteroposterior (p = 0.0069) and lateral (p = 0.0165) radiographs from three weeks postoperatively. The control group showed an earlier decrease of callus index. Radiographic scores were significantly greater in the control group (p = 0.0025). Conclusion: In a rabbit femoral osteotomy model with intramedullary fixation, haemorrhagic shock and resuscitation produced larger callus but with evidence of delayed remodelling. Cite this article: Bone Joint J 2018;100-B:1234-40.

Autologous bone marrow transplantation for children with AML in first remission.

In Children's cancer group (CCG) 2891, newly diagnosed patients with AML were randomized between standard and intensive timing induction therapies. Patients in first remission who lacked an HLA matched family donor were randomized between an autologous bone marrow transplantation (ABMT) where marrow was purged with 4 hydroperoxycyclophosphamide and consolidation chemotherapy. One hundred and thirty seven patients received an ABMT. Myeloid and platelet engraftment occurred at a median of 44 and 42 days, respectively. Disease-free survival (DFS), relapse-free survival and overall survival at 8 years post induction were 47% (95% confidence interval (CI): 38-55), 50% (CI: 42-59) and 55% (CI: 46-63), respectively. Multivariate analysis of DFS showed WBC <50 000/microl and having received intensively timed induction therapy were associated with improved DFS. Recipients who received intensive timed induction therapy and whose WBC was less than 50 000/microl had a DFS at 8 years of 62% (CI: 49-73). Conversely, recipients who received intensive timed induction therapy patients whose WBC was > or =50 000/microl had a DFS of 33% (CI: 17-50), P=0.003. The results confirm previous studies that ABMT is effective post remission therapy for pediatric patients with AML in first remission.

The use of power beams in surface modification.

This review of surface modification technologies focuses on the use of power beams, that is, lasers and electron beams, to modify polymer surfaces. A novel electron-beam materials processing technique is also described that offers scope for generating new types of surface functionality on metals used to construct stents and implants.

Postremission therapy for children with acute myeloid leukemia: the children's cancer group experience in the transplant era.

We reviewed consolidation therapy results and analyzed postremission outcomes for 1464 children less than 21 years old at diagnosis in five consecutive Children's Cancer Group acute myeloid leukemia trials between 1979 and 1996. Children in remission were allocated to allogeneic bone marrow transplantation (BMT) (N=373) in first remission, if a matched family donor was available. Remaining children were assigned consolidation chemotherapy (N=688) or autologous purged BMT (N=217), or withdrew from study before assignment, or with unknown data (N=186). Overall and disease-free survival were superior for children assigned allogeneic transplants. High (>50,000/microl) diagnostic white blood cell (WBC) count was prognostic for inferior outcome, but French-American-British (FAB) subtypes were not. Inv(16) is a favorable karyotypic feature for children in first remission and t(8;21) is not. Allogeneic transplantation benefit was evident in most children, including those with high or low diagnostic WBC count, each FAB subtype, and t(8;21), but was not seen in children with inv(16). Therefore, these data suggest reserving matched related donor allogeneic transplantation for children with inv(16) for second remission, but not those with t(8;21).

Prediction of long-term outcomes by signal-averaged electrocardiography in patients with unsustained ventricular tachycardia, coronary artery disease, and left ventricular dysfunction.

BACKGROUND: An abnormal signal-averaged ECG (SAECG) is a noninvasive marker of the substrate of sustained ventricular tachycardia after myocardial infarction. We assessed its prognostic ability in patients with asymptomatic unsustained ventricular tachycardia, coronary artery disease, and left ventricular dysfunction. METHODS AND RESULTS: A blinded core laboratory analyzed SAECG tracings from 1925 patients in a multicenter trial. Cox proportional hazards modeling was used to examine individual and joint relations between SAECG variables and arrhythmic death or cardiac arrest (primary end point), cardiac death, and total mortality. We also assessed the prognostic utility of SAECG at different levels of ejection fraction (EF). A filtered QRS duration >114 ms (abnormal SAECG) independently predicted the primary end point and cardiac death, independent of clinical variables, cardioverter-defibrillator implantation, and antiarrhythmic drug therapy. With an abnormal SAECG, the 5-year rates of the primary end point (28% versus 17%, P=0.0001), cardiac death (37% versus 25%, P=0.0001), and total mortality (43% versus 35%, P=0.0001) were significantly higher. The combination of EF <30% and abnormal SAECG identified a particularly high-risk subset that constituted 21% of the total population. Thirty-six percent and 44% of patients with this combination succumbed to arrhythmic and cardiac death, respectively. CONCLUSIONS: SAECG is a powerful predictor of poor outcomes in this population. The noninvasive combination of an abnormal SAECG and reduced EF may have utility in selecting high-risk patients for intervention.

Prediction of sustained ventricular tachycardia inducible by programmed stimulation in patients with coronary artery disease. Utility of clinical variables.

BACKGROUND: Cardiologists often use clinical variables to determine the need for electrophysiological studies to stratify patients for risk of sudden death. It is not clear whether this is rational in patients with coronary artery disease, left ventricular dysfunction, and nonsustained ventricular tachycardia. METHODS AND RESULTS: We analyzed the first 1721 patients enrolled in the Multicenter UnSustained Tachycardia Trial to determine whether clinical variables could predict which patients would have inducible sustained monomorphic ventricular tachycardia. The rate of inducibility of sustained ventricular tachycardia was significantly higher in patients with a history of myocardial infarction and in men compared with women. There was a progressively increased rate of inducibility with increasing numbers of diseased coronary arteries. There was a significantly lower rate of inducibility in patients with prior coronary artery bypass surgery and in patients who also had noncoronary cardiac disease. The rate of inducibility was higher in patients of white race, patients with recent (

Polymorphic ventricular tachycardia induced by programmed stimulation: response to procainamide.

OBJECTIVES: This study was designed to evaluate the effects of procainamide on polymorphic ventricular tachycardia induced by programmed stimulation and to correlate the responses with heart disease, left ventricular endocardial activation abnormalities and the signal-averaged electrocardiogram (ECG). BACKGROUND: Polymorphic ventricular tachycardia is induced frequently during electrophysiologic studies. In many patients this response is an artifact of programmed stimulation; in others, it appears to be clinically relevant. Previous observations have suggested that in some patients type IA antiarrhythmic agents can change the response to programmed stimulation from polymorphic to uniform ventricular tachycardia. METHODS: Programmed right ventricular stimulation was performed in the absence of antiarrhythmic drugs and after procainamide. Signal-averaged ECGs and left ventricular maps were performed during sinus rhythm in the absence of antiarrhythmic drugs. RESULTS: We evaluated 79 consecutive patients undergoing clinical electrophysiologic studies, in whom polymorphic ventricular tachycardia was the only arrhythmia induced in the absence of antiarrhythmic drugs. After procainamide administration, uniform monomorphic ventricular tachycardia was induced in 24 patients (Group 1), inducible polymorphic ventricular tachycardia persisted in 30 patients (Group 2) and no ventricular tachycardia could be induced in the remaining 25 patients (Group 3). Twenty-three (96%) of 24 patients developing uniform ventricular tachycardia after procainamide administration had coronary artery disease compared with 63% of Group 2 and 48% of Group 3 patients (p = 0.003). Left ventricular aneurysms were also found more frequently (46%) in the patients developing uniform ventricular tachycardia after procainamide than in either Group 2 or Group 3 (13% and 0%, respectively, p < 0.008). Abnormalities of the signal-averaged ECG typically seen in patients with spontaneous reentrant sustained ventricular tachycardia were significantly more frequent in patients who developed inducible uniform ventricular tachycardia after procainamide than in those who did not. Similarly, patients developing uniform ventricular tachycardia after procainamide had more extensive abnormalities of left ventricular endocardial activation revealed by catheter maps during sinus rhythm. CONCLUSIONS: The conversion of inducible polymorphic ventricular tachycardia to uniform ventricular tachycardia after procainamide administration occurs almost exclusively in patients with coronary disease, previous myocardial infarction and abnormal left ventricular function. This response may permit activation mapping of tachycardias, allowing the application of surgical or catheter ablation techniques that would otherwise not be possible in such patients.

What is the risk of sudden cardiac death in patients presenting with hemodynamically stable sustained ventricular tachycardia after myocardial infarction?

OBJECTIVES: This study sought to determine the long-term risk of sudden cardiac death in patients with hemodynamically stable sustained ventricular tachycardia complicating coronary artery disease. BACKGROUND: The prognosis and risk of sudden cardiac death in patients with a history of myocardial infarction and ventricular tachyarrhythmias have not been clearly defined. Prior studies are limited by a short follow-up period and by inclusion of patients with heterogeneous cardiac diseases and presenting arrhythmias. METHODS: A retrospective cohort analysis was performed on data from 124 patients, followed up for a mean of 36 +/- 30 months, who received electrophysiologically guided therapy for hemodynamically stable ventricular tachycardia after remote myocardial infarction. RESULTS: Seventy-eight patients were treated pharmacologically (medical group), and 46 patients underwent map-guided subendocardial resection (surgical group). Nine patients (7.3%) died suddenly, 5 (4.0%) died of noncardiac causes, 9 (7.3%) died of a perioperative complication, and 20 (23.4%) died of other cardiac causes. At 1, 2 and 3 years, sudden death occurred at cumulative rates of 2 +/- 1%, 3 +/- 2% and 7 +/- 3%, whereas total mortality was 20 +/- 4%, 28 +/- 4% and 32 +/- 5% (mean +/- SD). Sudden cardiac death (p = 0.047) and total mortality (p = 0.036) were higher in patients with multivessel disease and were similar for both treatment groups. CONCLUSIONS: Although the overall mortality in postinfarction patients presenting with hemodynamically stable ventricular tachycardia treated with electrophysiologically guided antiarrhythmic therapy is high, the risk of sudden death in these patients appears to be low (average 2.4%/year).

Sustained ventricular tachyarrhythmias during the early postinfarction period: electrophysiologic findings and prognosis for survival.

Forty patients with sustained tachycardia occurring 3 to 65 days after myocardial infarction underwent programmed ventricular stimulation within 3 months of the infarction. Patients were characterized clinically by a complicated initial 48 hours of hospitalization for their acute infarction (85% of study group). The development of bundle branch block in association with infarction occurred with an unusually high frequency (32%). Ventricular tachycardia similar in configuration to spontaneous arrhythmia was induced with programmed ventricular stimulation in 33 (83%) of the 40 patients. In 15 (45%) of these 33 patients, additional morphologically distinct ventricular tachycardia not seen clinically was initiated. The induction of ventricular tachycardia was not significantly related to the time after myocardial infarction at which spontaneous ventricular tachycardia was initially observed. Only 20 of the 40 patients are alive after a mean follow-up period of 20 +/- 15 months. Twelve of the 20 deaths were sudden cardiac deaths. Sixteen of the 33 patients with inducible ventricular tachycardia died; 8 of the 16 deaths were sudden. By comparison, four of the seven patients with no inducible ventricular tachycardia died (probability [p] = not significant), all suddenly. The mode of therapy did not influence subsequent survival. It appears that in patients with sustained ventricular tachycardia occurring more than 48 hours after a recent myocardial infarction, ventricular tachycardia similar to that clinically observed can usually be induced by programmed stimulation. In addition, multiple morphologically distinct ventricular tachycardias, some of which have not been previously observed, are frequently induced. Finally, the prognosis for survival is poor, regardless of inducibility or mode of therapy, and may in part be related to a changing arrhythmia substrate.

Usefulness of electrophysiologic study to determine the clinical tolerance of arrhythmia recurrences during amiodarone therapy.

The relation of clinical and electrophysiologic variables to outcome was evaluated in 121 patients treated with amiodarone for sustained ventricular tachyarrhythmias. Electrophysiologic study was performed in all patients a mean of 14 days after beginning amiodarone therapy. Forty-six patients who were given oral amiodarone therapy experienced arrhythmia recurrence. Multivariate analysis was performed using 16 clinical and electrophysiologic variables to determine which factors were associated with 1) arrhythmia recurrence and 2) a poorly tolerated arrhythmia recurrence (that is, cardiac arrest or sudden cardiac death) during oral amiodarone therapy. No variable predicted arrhythmia recurrence. Five variables correlated significantly with a poorly tolerated arrhythmia recurrence. Hemodynamic stability of the arrhythmia induced on electrophysiologic testing during amiodarone therapy had the best predictive value (p less than 0.001). Younger age, lower ejection fraction, a poorly tolerated rhythm at clinical presentation and absence of left ventricular aneurysm were also associated with a poorly tolerated arrhythmia recurrence. Only 3 of 57 patients who had a well tolerated arrhythmia induced on electrophysiologic testing during amiodarone therapy had recurrence of a poorly tolerated arrhythmia versus 19 of 47 who had hemodynamically unstable arrhythmias induced during amiodarone therapy (p less than 0.001). Thus, electrophysiologic testing during amiodarone therapy appears useful in identifying patients who are prone to have catastrophic arrhythmia recurrences and could allow for the institution of additional or alternative modes of therapy.

Differences in inducibility and prognosis of in-hospital versus out-of-hospital identified nonsustained ventricular tachycardia in patients with coronary artery disease: clinical and trial design implications.

OBJECTIVES: The goal of this study was to describe the influence of the clinical setting (in-hospital vs. out-of-hospital) in which nonsustained ventricular tachycardia (NSVT) is discovered on the rate of inducibility of sustained ventricular tachycardia (VT), arrhythmic events and survival in patients with coronary artery disease (CAD) and left ventricular (LV) dysfunction. BACKGROUND: In-hospital presentation of sustained VT is independently associated with lower long-term overall survival. The impact of the clinical setting in which NSVT is documented is unknown. METHODS: In the Multicenter Unsustained Tachycardia Trial (MUSTT), designed to assess the benefit of randomized antiarrhythmic therapy guided by electrophysiologic testing in patients with asymptomatic NSVT, CAD and LV dysfunction, eligible patients were enrolled irrespective of the setting in which the index arrhythmia was discovered. In this retrospective analysis, we compared the rate of VT inducibility and outcome of MUSTT-enrolled patients with in-hospital versus out-of-hospital presentation of NSVT. RESULTS: Monomorphic sustained VT was induced in 35% and 28% of the patients whose index NSVT occurred in-hospital and out-of-hospital, respectively (adjusted p = 0.006). Cardiac arrest or death due to arrhythmia at two- and five-year follow-ups were 14% and 28% for untreated patients with in-hospital-identified NSVT and 11% and 21% for the out-of-hospital group (adjusted p = 0.10). Overall mortality rates at two- and five-year follow-ups were 24% and 48% for inpatients and 18% and 38% for outpatients (adjusted p = 0.018). In patients randomized to antiarrhythmic therapy, there was no significant interaction between patient status (in-hospital vs. out-of-hospital) and treatment impact on the rates of total mortality (p = 0.98) and arrhythmic events (p = 0.08). CONCLUSIONS: In patients with CAD and impaired LV function, asymptomatic NSVT identified in-hospital, compared with that identified out-of-hospital, is associated with a higher rate of induction of sustained VT and overall mortality. Therefore, in similar patients, the clinical setting in which NSVT is discovered should be taken into account when formulating patient risk, treatment and clinical trial design.

Analysis of the resetting phenomenon in sustained uniform ventricular tachycardia: incidence and relation to termination.

UNLABELLED: Although the phenomenon of resetting has been studied in several experimental and clinical rhythms, it has not been systematically analyzed in ventricular tachycardia. To define the incidence and determinants of resetting as well as its relation to ventricular tachycardia termination, the response to programmed stimulation was prospectively studied during 78 electrically induced episodes of sustained, uniform ventricular tachycardia (mean cycle length 365 +/- 59 ms) in 53 patients. Single and double ventricular extrastimuli were introduced during 78 and 39 episodes of ventricular tachycardia, respectively. Rapid ventricular pacing was performed during 27 episodes. Resetting occurred in response to single ventricular extrastimuli in 43 (55%) of 78 ventricular tachycardias, to double extrastimuli in 31 (79%) of 39 ventricular tachycardias and to rapid pacing in 23 (85%) of 27 ventricular tachycardias. No ventricular tachycardia characteristic distinguished those tachycardias that were reset from those not reset. Termination of ventricular tachycardia occurred in 7 (9%) of 78 episodes with single ventricular extrastimuli, 14 (36%) of 39 episodes with double ventricular extrastimuli and 13 (48%) of 27 episodes with rapid pacing. Termination was less frequent than resetting with both single (9 versus 55%) and double (36 versus 79%) extrastimuli, as well as rapid pacing (48 versus 85%). Resetting preceded termination in 7 of 7 ventricular tachycardias terminated with single ventricular extrastimuli, 12 of 14 terminated with double ventricular extrastimuli and 9 of 13 terminated by rapid pacing. Ventricular tachycardias that were terminated could not be differentiated from those that were reset without termination. IN CONCLUSION: Resetting with programmed extrastimuli is common in hemodynamically stable sustained ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular endocardial activation during right ventricular pacing: effect of underlying heart disease.

Endocardial catheter mapping of the left ventricle was performed in 40 patients during right ventricular pacing to determine the effect of underlying myocardial infarction on endocardial activation. Group I comprised 18 patients without infarction, Group II 12 patients with inferior infarction and Group III 10 patients with anteroseptal infarction. Thirty-nine of the 40 patients had only a single left ventricular breakthrough site located on the midseptum in 33 cases, apical septum in 4 cases and basal septum in 2 cases. The earliest left ventricular local activation time during right ventricular pacing was earlier in Group III (40 +/- 11 ms) than in Group I (55 +/- 17 ms) and Group II (60 +/- 15 ms) (p less than 0.01). Total endocardial activation time was significantly longer in Group III (118 +/- 30 ms) than in Group I (76 +/- 14 ms) and Group II (72 +/- 20 ms) (p less than 0.001). The latest left ventricular site of activation during right ventricular pacing was the inferoposterior base in 14 (77%) of the 18 Group I patients, and 10 (83%) of the 12 Group II patients. The latest site of activation in Group III patients was variable. It is concluded that: left ventricular endocardial activation patterns and conduction times are influenced by the site of previous infarction. Longer total endocardial activation in Group III suggests that specialized conducting tissue in the septal and anterior walls may play an important role in left ventricular activation during right ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Cycle length-dependent effects on normal and abnormal intraventricular electrograms: effect of procainamide.

The effect of procainamide (mean concentration 9.1 +/- 2.0 micrograms/ml) on cycle length-dependent changes in electrographic characteristics was determined in 10 patients with prior myocardial infarction. Intracardiac bipolar electrograms were recorded from an abnormal left ventricular site in the distribution of prior (greater than 6 month) myocardial infarction and from a normal right ventricular site. Pacing was performed for 15 beats from the right ventricular apex at cycle lengths of 600 (or 500), 400 and 300 ms. In the control state, the QRS width, the normal electrogram and in 9 of the 10 patients the abnormal electrogram did not change with decreasing cycle lengths. After procainamide the mean QRS width increased from 203 +/- 32 to 240 +/- 50 ms (+18%, p less than 0.01) at a paced cycle length of 600 (or 500) ms, from 198 +/- 34 to 245 +/- 59 ms (+24%, p less than 0.01) at a paced cycle length of 400 ms and from 197 +/- 36 to 258 +/- 67 ms (+31%, p less than 0.01) at a paced cycle length of 300 ms.(ABSTRACT TRUNCATED AT 250 WORDS)

Limited role of intravenous propafenone hydrochloride in the treatment of sustained ventricular tachycardia: electrophysiologic effects and results of programmed ventricular stimulation.

The electrophysiologic effects and response to programmed ventricular stimulation of intravenous propafenone, an experimental antiarrhythmic agent, were studied in a group of 14 patients with both clinical and induced sustained ventricular tachycardia. Twelve of the 14 patients had not responded to conventional antiarrhythmic drug therapy. Propafenone had no significant effect on sinus cycle length (836 +/- 170 ms before and 750 +/- 124 ms after propafenone), P wave duration (108 +/- 24 ms before and 106 +/- 23 ms after propafenone) or PR interval (181 +/- 45 ms before and 194 +/- 53 ms after propafenone). QRS duration and ventricular effective refractory periods increased significantly (109 +/- 20 to 130 +/- 21 ms and 235 +/- 24 to 256 +/- 19 ms, respectively). Ventricular tachycardia remained inducible or occurred spontaneously in 13 of 14 patients after propafenone administration. Neither mode of initiation nor mode of termination of ventricular tachycardia was predictably altered. Additional forms of ventricular tachycardia were seen in six patients. Cycle length of ventricular tachycardia was 303 +/- 73 ms before and 346 +/- 143 ms after propafenone (p = NS). In conclusion, intravenous propafenone does not significantly affect sinus rate, intraatrial conduction or atrioventricular conduction. Ventricular refractoriness and intraventricular conduction are prolonged. The mode of initiation, mode of termination and ventricular tachycardia cycle length are not predictably altered, but ventricular tachycardia occasionally occurs spontaneously after propafenone. Intravenous propafenone rarely prevents induction of ventricular tachycardia in patients with sustained ventricular tachycardia refractory to conventional antiarrhythmic agents.

Comparative electrophysiologic effects of intravenous and oral procainamide in patients with sustained ventricular arrhythmias.

Thirty-three patients with sustained ventricular arrhythmias underwent electrophysiologic testing after intravenous and again after oral procainamide administration. Two groups were identified: group 1 included 15 patients with concordant serum procainamide concentrations with less than a 3 micrograms/ml difference after intravenous (mean 8.6 +/- 2.7) and oral (mean 8.8 +/- 2.7) procainamide administration, with mean N-acetylprocainamide concentrations of 1.0 +/- 0.6 and 6.2 +/- 2.8 micrograms/ml, respectively. Group 2 included 18 patients with discordant serum procainamide concentrations after intravenous (mean 9.5 +/- 5.9 micrograms/ml) and oral (mean 14.1 +/- 5.2 micrograms/ml) procainamide, with mean N-acetylprocainamide concentrations of 0.9 +/- 0.5 and 10.7 +/- 5.7 micrograms/ml, respectively. In group 1, response to programmed stimulation was the same after intravenous and oral procainamide administration, with no inducible ventricular arrhythmia in 5 of 15 patients. In group 2, 3 of 18 patients had no inducible arrhythmia after intravenous compared with 7 of 18 patients after oral procainamide administration. There was a different response to programmed stimulation after oral compared with intravenous procainamide in 6 of 18 patients in group 2 but in none of 15 patients in group 1 (p = 0.02). The effective procainamide concentration was greater than the ineffective concentration in five of the six patients with a discordant response, and the effective route of administration was oral in five of the six patients. The change in ventricular refractoriness in group 1 was similar after intravenous (28 +/- 23 ms) and oral (29 +/- 19 ms) procainamide, whereas in group 2, refractoriness was increased more after oral (33 +/- 21 ms) than intravenous (20 +/- 17 ms) procainamide administration and paralleled the difference in procainamide concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Antiarrhythmic drug therapy in the Multicenter UnSustained Tachycardia Trial (MUSTT): drug testing and as-treated analysis.

OBJECTIVES: Using data from the Multicenter UnSustained Tachycardia Trial (MUSTT), we examined the factors used to select antiarrhythmic drug therapy and their impact on outcomes. BACKGROUND: The MUSTT examined the use of programmed ventricular stimulation (PVS) to guide antiarrhythmic therapy in patients with coronary arteriosclerosis, left ventricular dysfunction and asymptomatic, unsustained ventricular tachycardia (VT). Trial outcomes may reflect factors used to select antiarrhythmic drug therapy. METHODS: We compared subgroups of patients with inducible sustained VT randomized to PVS-guided antiarrhythmic therapy (n = 351), in particular those receiving PVS-guided antiarrhythmic drug therapy (n = 142) versus no antiarrhythmic therapy (controls, n = 353). RESULTS: "Effective" antiarrhythmic drug therapy (i.e., the term "effective" was used to denote therapy that resulted in noninducible VT or hemodynamically stable induced VT) was found for 142 of the 351 patients (43%), most often at the first or second PVS session (125/142, 88%). Mortality among the 142 patients did not differ from that among control patients. Of these 142 patients, the PVS end point was noninducibility in 91 patients and stable VT in 51 patients. Mortality did not differ between these two groups either, but arrhythmia was numerically more frequent in the PVS-induced stable VT group. Mortality was greatest in the few patients receiving propafenone (unadjusted p = 0.07, adjusted p = 0.14 vs. controls), but mortality with all agents did not differ from that of controls, even after adjustment. CONCLUSIONS: Even when presenting the results as favorably as possible, we found no benefit with PVS-guided drug therapy in patients with clinical unsustained VT who had inducible sustained VT. These findings are unaltered by using different end points for PVS or considering the response to individual drugs.

Prognostic variables in newly diagnosed children and adolescents with acute myeloid leukemia: Children's Cancer Group Study 213.

The objective of this study was to identify biologic parameters that were associated with either exceptionally good or poor outcome in childhood acute myeloid leukemia (AML). Among the children with AML who entered Children's Cancer Group trial 213, 498 patients without Down syndrome or acute promyelocytic leukemia (APL) comprise the basis for this report. Univariate comparisons of the proportion of patients attaining complete remission after induction (CR) indicate that, at diagnosis, male gender, low platelet count (< or =20 000/microl), hepatomegaly, myelodysplastic syndrome (MDS), French-American- British (FAB) category M5, high (>15%) bone marrow (BM) blasts on day 14 of the first course of induction, and +8 are associated with lower CR rates, while abnormal 16 is associated with a higher CR rate. Multivariate analysis suggests high platelet count at diagnosis (>20 000/microl), absence of hepatomegaly, < or =15% day 14 BM blast percentage, and abnormal 16 are independent prognostic factors associated with better CR. Univariate analysis demonstrated a significant favorable relationship between platelet count at diagnosis (>20 000/microl), absence of hepatomegaly, low percentage of BM blasts (< or =15%), and abnormal 16 with overall survival. Absence of hepatomegaly, < or =15% day 14 BM blast percentage, and abnormal 16 were determined to be independent prognostic factors associated with better survival.

Head and cervical spine posture in behaving rats: implications for modeling human conditions involving the head and cervical spine.

The aim of this study was to define the temporal and spatial (postural) characteristics of the head and cervical vertebral column (spine) of behaving rats in order to better understand their suitability as a model to study human conditions involving the head and neck. Time spent in each of four behavioral postures was determined from video tape recordings of rats (n = 10) in the absence and presence of an intruder rat. Plain film radiographic examination of a subset of these rats (n = 5) in each of these postures allowed measurement of head and cervical vertebral column positions adopted by the rats. When single they were quadruped or crouched most (∼80%) of the time and bipedal either supported or free standing for only ∼10% of the time. The introduction of an intruder significantly (P < 0.0001) reduced the proportion of time rats spent quadruped (median, from 71% to 47%) and bipedal free standing (median, from 2.9% to 0.4%). The cervical spine was orientated (median, 25-75 percentile) near vertical (18.8°, 4.2°-30.9°) when quadruped, crouched (15.4°, 7.6°-69.3°) and bipedal supported (10.5°, 4.8°-22.6°) but tended to be less vertical oriented when bipedal free standing (25.9°, 7.7°-39.3°). The range of head positions relative to the cervical spine was largest when crouched (73.4°) and smallest when erect free standing (17.7°). This study indicates that, like humans, rats have near vertical orientated cervical vertebral columns but, in contrast to humans, they displace their head in space by movements at both the cervico-thoracic junction and the cranio-cervical regions.