Transport time after combat-related injury and patient-reported outcomes among US service members.

INTRODUCTION: The 'golden hour' is a universal paradigm that suggests trauma patients have lower morbidity and mortality when provided with medical care within 1 hour after injury. The objective of this study was to examine whether transport time from point of injury to a military treatment facility (MTF) in-theatre was associated with patient-reported outcomes, such as post-traumatic stress disorder (PTSD), depression and quality of life (QOL), among US service members with combat-related injury. METHODS: Participants were injured between March 2003 and March 2016 and completed standardised assessments of PTSD, depression and QOL for theWounded Warrior Recovery Project (WWRP) between January 2013 and November 2017. Multivariable regressions were used to assess the relationship between transport time (≤1 hour or >1 hour from injury to MTF) and positive screens for PTSD and depression, and QOL, respectively.Overall, 45.6% of participants (n=879) arrived at an MTF within 1 hour postinjury. About 8 years passed between when participants were injured on deployment and when they completed their first WWRP assessment. Approximately 48% of participants screened positive for PTSD and 51.3% for depression, with a mean QOL score of 0.513 (SD=0.150). After adjusting for covariates, transport time was not significantly associated with PTSD (OR 1.04, 95% CI 0.79 to 1.38; p=0.77), depression (OR 0.92, 95% CI 0.69 to 1.21; p=0.55) or QOL (ß=0.009; p=0.38). CONCLUSION: Transport time was not associated with patient-reported outcomes among US service members with combat-related injury. These findings are important as we seek to understand how combat casualties may be affected by extended medical evacuation or transport times anticipated in future expeditionary operations.

Medical correlates of first-term attrition in US Navy personnel.

INTRODUCTION: First-term attrition (FTA), or failure of a military service member to complete their initial service contract, is a major financial burden and source of lost manpower in the US Navy. The objective of the present study was to examine medical correlates of FTA using healthcare and disability rating data. METHODS: In this retrospective cohort study, all US Navy-enlisted personnel between the years 2003 and 2018 with FTA (n=58 777) and regular discharge (n=203 084) were identified for analysis from accession dates in the Career History Archival Medical and Personnel System. Medical diagnoses from outpatient and inpatient records were abstracted from the Military Health System Data Repository. For a subgroup of the study population discharged with a disability rating (n=12 880), diagnoses were identified from the Integrated Disability Evaluation System. The FTA and regular discharge groups were compared using relative risks (RRs) and 95% CIs, and per cent differences for the disability subgroup analysis. RESULTS: Compared with regular discharges, those with FTA were more likely to have outpatient and inpatient diagnoses for mental health disorders. Personality disorder yielded the strongest association with FTA in both outpatient (RR=10.45, 95% CI 9.79 to 11.16) and inpatient settings (RR=18.97, 95% CI 14.16 to 25.42). Other disorders associated with FTA included schizophrenia, substance-related disorders, poisoning by psychotropic agents and adjustment disorders. In the disability analysis, the FTA group relative to regular discharges had the largest per cent differences for 'arthritis, degenerative (hypertrophic or osteoarthritis)' (10.8% vs 2.5%) and 'tibia and fibula, impairment' (3.0% vs 0.4%). CONCLUSIONS: This study provides evidence that FTA is associated with both mental and physical health conditions. Mental and physical factors related to FTA require further examination, particularly whether pre-enlistment screening or early career intervention could lead to mitigation strategies. Future research should extend this analysis to other services and population subgroups.

Development and Implementation of a Culturally Appropriate Education Program to Increase Cervical Cancer Screening among Maasai Women in Rural Tanzania.

Background: In Tanzania, the incidence of cervical cancer is nearly ten times that found in the US. Tanzanian women of the traditional Maasai tribe are financially and educationally marginalized and face a language barrier that reduces access to health care. While cervical cancer (CACX) screening programs are available locally, in our experience, Maasai women were less likely to use these services compared to local women of other tribal backgrounds. Objectives: A novel patient education program was designed to teach Maasai women about the natural history of cervical cancer and available screening and treatment. The program addressed the importance of preventative health and informed consent. Additionally, we sought to better understand the specific barriers Maasai women face in accessing and utilizing CACX screening services. Methods: The program used simple, scripted language translated into Maa language, the Maasai native language, with accompanying culturally appropriate 3D models. The effectiveness of the program was evaluated through pre and post-intervention surveys administered to Maasai and non-Maasai women as well as local healthcare providers, assessing knowledge of cervical cancer, screening, and treatment. Paired t-test analyses were used to analyze significance. Extensive question and answer sessions followed the education sessions from which additional barriers to screening were identified. Findings: Maasai women had minimal understanding of preventative health services prior to the intervention. While all groups showed an increase in knowledge following the education program, Maasai women demonstrated the greatest statistically significant improvement in knowledge. The proportion of Maasai women in attendance to CACX screening clinics increased by 18% after the intervention. Conclusions: Through a culturally sensitive and accessible patient education program, Maasai women gained knowledge of cervical cancer screening and treatment. This program serves as an adaptable model for other marginalized populations to increase patient understanding and informed consent, and to address issues that pertain to underutilization of health care services.

Treatment of atrioventricular node reentrant tachycardia with encainide: reversal of drug effect with isoproterenol.

To determine the efficacy of encainide in the treatment of atrioventricular (AV) node reentrant tachycardia, Holter electrocardiographic (ECG) monitoring, exercise treadmill testing and programmed electrical stimulation were performed in 16 patients while they were taking no medication and after steady state levels were reached during treatment with encainide (75 to 200 mg/day; mean 117 +/- 47). In addition, to study the possible reversal of drug effects by sympathetic stimulation, AV node conduction and tachycardia induction were reassessed during isoproterenol infusion (1 to 3 micrograms/min), a dose calculated to increase the rest heart rate by 25 +/- 10%. Sustained AV node reentrant tachycardia could be initiated in all 16 patients in the control state, in 2 patients after encainide and in 10 patients during isoproterenol infusion. The shortest mean atrial paced cycle length sustaining 1:1 AV conduction was 358 +/- 57 ms during the control study, which increased to 409 +/- 59 ms with encainide (p less than 0.01 versus control) and decreased to 313 +/- 31 ms during isoproterenol infusion (p less than 0.01 versus control and encainide). The shortest mean ventricular paced cycle length with 1:1 ventriculoatrial conduction was 337 +/- 56 ms in the control study, 551 + 124 ms with encainide infusion (p less than 0.01 versus control) and 354 +/- 72 ms during isoproterenol infusion in the encainide-loaded state (p less than 0.01 versus both control and encainide). During a mean follow-up period of 19 +/- 10 months, significant clinical recurrences occurred in 4 of the 10 patients in whom tachycardia could still be initiated with encainide (with or without isoproterenol).(ABSTRACT TRUNCATED AT 250 WORDS)

Short- and long-term experience with flecainide acetate in the management of refractory life-threatening ventricular arrhythmias.

Thirty-eight patients with organic heart disease and history of sudden cardiac arrest or recurrent sustained ventricular tachycardia were treated with flecainide. Coronary artery disease was present in 33 patients. Previous antiarrhythmic therapy consisted of two to eight drugs (mean four). Fourteen patients were resuscitated from sudden cardiac death and 24 patients had chronic recurrent sustained ventricular tachycardia. Twenty-eight patients had electrophysiologic testing before and during flecainide treatment. Sustained ventricular tachycardia became noninducible in 5 patients, nonsustained in 5 patients and slowed in 13 patients (cycle length increased from 278 +/- 64 to 395 +/- 91 ms; p = 0.002). Three of the 14 patients with sudden cardiac death and 15 of the 24 patients with recurrent sustained ventricular tachycardia remained on long-term flecainide treatment. The mean left ventricular ejection fraction in 16 of these 18 patients was 37%. Nonlimiting side effects occurred in seven patients (18%). Proarrhythmic effects were seen in four patients (10%). At a mean follow-up time of 11 +/- 3 months, 15 patients (39%) had had no recurrence, including 5 who had inducible sustained ventricular tachycardia and 5 who did not on retesting during treatment. In the 18 patients who received long-term therapy, 3 late deaths occurred, 1 of which was of arrhythmic origin. These data suggest that flecainide is effective in about 40% of patients with severe refractory ventricular arrhythmias. Its value as a single drug in the treatment of sudden cardiac death remains to be defined.

Efficacy and safety of class IC antiarrhythmic agents for the treatment of coexisting supraventricular and ventricular tachycardia.

Thirty-three patients with concurrent supraventricular (SVT) and ventricular tachycardia (VT) were treated with class IC antiarrhythmic agents. Twenty-two patients had atrial fibrillation (17 with paroxysmal and 5 with chronic fibrillation), 1 patient had ectopic atrial tachycardia and 11 patients had reentrant paroxysmal SVT (8 with atrioventricular node reentrant tachycardia, 3 with atrioventricular reentrant tachycardia). Of 5 patients with Wolff-Parkinson-White syndrome, 2 had only atrial fibrillation. Six patients had sustained VT and 27 had nonsustained VT. Twenty-nine patients had organic heart disease (16 with coronary artery disease, 8 with cardiomyopathy and 5 with valvular heart disease) and 4 had primary electrical disease. The mean ejection fraction was 40 +/- 14% (range 15 to 66%). The study population's arrhythmias were not controlled despite having received 2 to 5 (mean 3.1) previous drug trials. Eighteen patients were referred for treatment of SVT and 15 were referred for treatment of VT (mean symptom duration 107 months). Efficacy was determined in 13 of 33 patients with sustained SVT or VT by programmed electrical stimulation and in 20 of 33 by telemetry and 24-hour Holter response. Twenty-two flecainide and 15 encainide trials were conducted in the 33 patients. Four patients underwent trials with both drugs. Of 33 patients with coexisting SVT and VT, 15 (45%) were controlled with an IC agent alone and 3 continued therapy with an IC agent plus additional therapy (2 drugs, 1 antitachycardia pacing). During the follow-up period (mean 10.4 months), flecainide produced a complete response in 9 patients and encainide in 9 patients. SVT was not controlled in 7 patients and VT was not controlled in 7 patients. One patient had neither arrhythmia controlled. Atrial or ventricular proarrhythmia was seen in 9 of 33 patients (27%) (5 with ventricular and 4 with atrial arrhythmia). Noncardiac side effects were uncommon. Oral class IC agents may be effective therapy for some patients with coexisting VT and SVT of different mechanisms. Patients with such complex arrhythmias should be evaluated carefully because there is a potential for both atrial and ventricular proarrhythmia.

Assessment of antiarrhythmic drug efficacy in the treatment of supraventricular arrhythmias.

Few guidelines exist for judging the efficacy of antiarrhythmic drugs in patients with supraventricular arrhythmias. Useful definitions concerning the frequency and duration of supraventricular arrhythmias are offered, and complete and partial efficacy criteria are outlined for noninvasive electrocardiographic and invasive electrophysiologic techniques. Several open label, double-blind, parallel and crossover study designs are suggested for efficacy studies concerning the termination and prevention of supraventricular tachycardia. These recommendations are useful for designing new drug trials needed to evaluate properly the efficacy of antiarrhythmic agents in the treatment of various supraventricular arrhythmias.

Effect of pharmacologic autonomic blockade on ventriculoatrial conduction.

To determine the influence of autonomic tone on retrograde ventriculoatrial (VA) conduction, incremental atrial and ventricular pacing was performed before and after pharmacologic autonomic blockade in 28 patients. VA conduction during ventricular pacing was demonstrated, with highest frequency in patients capable of 1:1 atrioventricular (AV) conduction at atrial paced cycle lengths of 300 ms or less (7 of 7, 100%). In subjects with 1:1 AV conduction at minimum cycle lengths of 300 to 500 ms, 14 of 21 (67%) demonstrated VA conduction in the control state; however, only 12 of 21 (57%) did so after autonomic blockade. The lowest frequency was observed in those capable of 1:1 AV conduction at minimum cycle lengths of 505 ms or more before and after autonomic blockade (2 of 7, [29%], p less than or equal to 0.02 compared with values in the first group). No change in the mean minimum ventricular paced cycle length at which 1:1 VA conduction could be maintained was demonstrated after autonomic blockade. In individual subjects, incremental change in this cycle length after autonomic blockade correlated positively with the corresponding change in minimum atrial cycle length at which 1:1 AV conduction could be maintained (r = 0.62, p less than 0.005), and was concordant in direction in 18 of 21. In conclusion, the sympathetic and parasympathetic modulation of VA conduction is balanced and concordant in direction to the effect on AV nodal conduction.

Congestive heart failure with normal systolic function.

Although there have been isolated reports of congestive heart failure (CHF) with normal systolic function, the prevalence and characteristics of this condition have not previously been described. Accordingly, 188 patients with CHF undergoing radionuclide ventriculography were prospectively evaluated. Sixty-seven (36%) had a normal ejection fraction (EF) of 0.45 or greater, and 121, an abnormal EF of less than 0.45. Of these, 72 (55 with an abnormal EF [group I] and 17 with a normal EF [group II]) were also reviewed for clinical characteristics. There was no demographic difference between groups, except that systemic hypertension appeared to be a contributing factor in 65% of the patients in group II, compared with 23% of the patients in group I (p less than 0.002). Echocardiographic left atrial emptying index, reflecting left ventricular compliance, was determined in 72 patients and 14 normal subjects. Left atrial emptying index in normal control subjects was 0.93 +/- 0.11 (+/- standard deviation), compared with 0.41 +/- 0.18 in group I and 0.44 +/- 0.19 in group II patients (p less than 0.001 vs control in both groups). Thus, normal systolic function is common among patients with CHF. Diastolic dysfunction, consistent with a noncompliant left ventricle, was found in both CHF groups.

Amrinone: acute electrophysiologic and hemodynamic effects in patients with congestive heart failure.

Amrinone is an effective inotropic agent, but its electrophysiologic effects in humans have not been previously determined. Fifteen patients with congestive heart failure (CHF) New York Heart Association functional class II to IV, underwent an electrophysiologic study after withdrawal of all other cardioactive drugs before and after 10 to 20 micrograms/kg/min of intravenous amrinone (doses that increased cardiac index and decreased pulmonary capillary wedge pressure and systemic vascular resistance, p less than 0.002). Amrinone caused no change in PR, QRS, QTc, AH or HV intervals or maximal corrected sinus node recovery time and had no significant effect on the ventricular effective refractory periods. Amrinone decreased the atrial effective refractory period from 256 +/- 40 to 240 +/- 38 ms (p = 0.015), and the atrioventricular (AV) nodal functional refractory period from 374 +/- 65 to 356 +/- 64 ms (p less than 0.05), and enhanced maximal 1:1 AV nodal conduction from 371 +/- 46 to 334 +/- 47 ms (p = 0.006). Nine patients had baseline HV prolongation; this was not affected by amrinone. The frequency of inducible ventricular tachycardia was not significantly affected by amrinone. Holter recordings (24 to 48 hours) were obtained from 10 patients before and after acute oral amrinone dosing (75 to 150 mg every 8 hours). There was no change in the number of ventricular premature contractions per 24 hours (2,197 +/- 3,305 vs 2,616 +/- 2,436) or number of runs of ventricular tachycardia per 24 hours (10 +/- 12 vs 12 +/- 13); however, the number of ventricular couplets per 24 hours increased from 22 +/- 34 to 52 +/- 55 (p = 0.054).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of adrenergic stimulation by isoproterenol in reversal of effects of encainide in supraventricular tachycardia.

Reversal of the electrophysiologic effects of oral encainide with isoproterenol was evaluated in 16 patients with atrioventricular (AV) nodal reentry (group A) and in another 16 patients with Wolff-Parkinson-White syndrome (group B). Sustained AV nodal reentry was induced in all group A cases before administration of encainide, in 2 cases after oral encainide, and in 12 patients during infusion of isoproterenol. Among group B cases, 14 of 16 had sustained AV reentry during control, 6 of 16 after receiving encainide, and 8 of 16 with addition of isoproterenol. During a mean follow-up of 19 +/- 10 months in group A and 17 +/- 9 months in group B, clinical tachycardia recurred in 8 patients (4 from each group). These 8 patients were among the 20 patients who demonstrated (1) isoproterenol-induced reversibility of encainide-suppressed tachycardia, or (2) acceleration of tachycardia rate slowed by encainide. No recurrences were seen among any of the 12 cases in which isoproterenol failed to reverse the encainide-induced tachycardia suppression. Patients with clinical recurrences were controlled with a variety of means, which included beta blockers in 3 and nonpharmacologic methods in the remaining 5. In patients with AV junctional tachycardia treated with oral encainide, our findings suggest that lack of tachycardia inducibility with isoproterenol predicts freedom from clinical recurrences. Furthermore, addition of a beta blocker to oral encainide may prevent clinical recurrence in some who demonstrate adrenergic reversal of encainide effect.

Efficacy and safety of flecainide acetate for atrial tachycardia or fibrillation.

Thirty-nine patients with symptomatic ectopic atrial tachycardia (9 paroxysmal, of which 5 were incessant) and atrial fibrillation (AF) (25 paroxysmal, 5 chronic) were treated with oral flecainide acetate (100 to 400 mg/day). Thirty-two patients had organic heart disease (16 coronary artery disease, 6 valvular, 10 cardiomyopathy, 7 primary electrical abnormality). Previous antiarrhythmic trials consisted of 0 to 5 drugs (mean 2.2). Of 39 patients with atrial tachycardia or AF, a complete response (no recurrent symptomatic atrial arrhythmia) was achieved in 22 (56%), a partial response (more than 95% reduction in arrhythmia occurrence) in 3 (8%) and no response in 14 (36%). Left atrial size, ejection fraction, underlying heart disease, duration of symptoms before treatment and drug levels were not useful for predicting clinical response. Therefore, during the follow-up period of 5.4 +/- 6.7 months (range 4 weeks to 2.5 years), flecainide had a complete or partial effect in 25 patients (64%). Complete or partial responses were noted in 8 of 9 patients (90%) with ectopic atrial tachycardia and 17 of 30 (57%) with AF. In 14 patients with concurrent ventricular arrhythmias, a significant reduction in episodes of nonsustained ventricular tachycardia was also achieved. Treatment was discontinued in 8 patients (20%) because of cardiac adverse reactions, including pulmonary edema and ventricular or atrial proarrhythmic response. Thus, oral flecainide acetate is effective therapy for some patients with ectopic atrial tachycardia or AF.

Electrophysiologic effects of amrinone.

Patients with congestive heart failure (CHF) have a high prevalence of complex ventricular arrhythmias. Accordingly, the electrophysiologic effects of new drugs for the treatment of CHF should be studied to determine whether they are safe in this population of patients. Fifteen patients with New York Heart Association functional classes II to IV CHF underwent hemodynamic and electrophysiologic testing during control conditions, and after 10 to 20 micrograms/kg/min of intravenous amrinone (dosages that increased cardiac output and decreased left ventricular filling pressures). All cardioactive drugs were stopped for at least 5 half-lives before entry into the study. Amrinone decreased the atrial effective refractory period from 256 to 240 ms (p = 0.015) and the AV nodal functional refractory period from 374 to 356 ms (p less than 0.05), and enhanced maximal 1:1 AV nodal conduction from 371 to 334 ms (p = 0.006). Prolonged HV intervals were present in 9 of 15 patients and were not affected by amrinone. Holter monitoring was performed in 10 patients during acute oral administration of amrinone. There were no significant changes in the frequency of ventricular extrasystoles or ventricular tachycardia, although the frequency of ventricular couples tended to increase slightly. Amrinone therefore enhances AV conduction and does not appear to have significant arrhythmogenic potential during acute administration.

Acute conversion of paroxysmal supraventricular tachycardia with intravenous diltiazem. IV Diltiazem Study Group.

Diltiazem has electrophysiologic effects similar to those of verapamil. Its efficacy and safety in 4 doses for treatment of induced supraventricular tachycardia (SVT) were examined and compared with those of placebo in 87 patients (25 with atrioventricular [AV] nodal reentry tachycardia, 60 with AV reentry associated with an accessory AV connection, and 2 with atrial tachycardia). Conversion to sinus rhythm occurred in 4 of 14 patients (29%) with 0.05 mg/kg of diltiazem, 16 of 19 (84%) with 0.15 mg/kg, 13 of 13 (100%) with 0.25 mg/kg, and 14 of 17 (82%) with 0.45 mg/kg compared with 6 of 24 (25%) treated with placebo. Conversion rates in groups receiving doses of 0.15 to 0.45 mg/kg of diltiazem were superior to that in the placebo group (p less than 0.001). Time to conversion was 3.0 +/- 2.6 minutes in responding diltiazem patients compared with 5.9 +/- 6.1 minutes in responding control patients. Diltiazem administration resulted in significant lengthening of SVT cycle length, AH interval, and AV nodal effective refractory period and block cycle length. The most frequent adverse response to diltiazem was hypotension (7 of 63 patients); however, only 4 patients had symptoms related to hypotension. Thus, intravenous diltiazem in doses of 0.15, 0.25 and 0.45 mg/kg is an effective and safe treatment for the acute management of SVT.

Encainide for atrial fibrillation associated with Wolff-Parkinson-White syndrome.

Thirty-six patients with a history of atrial fibrillation and Wolff-Parkinson-White syndrome were treated with oral encainide, 175 +/- 44 mg/day, after undergoing baseline drug-free electrophysiologic studies. The mean age was 38 +/- 15 years, with structural heart disease present in only 3 patients. Nine patients had only paroxysmal atrial fibrillation and 27 patients had both atrial fibrillation and atrioventricular reciprocating tachycardia (AVRT). Symptoms were present for a mean of 195 +/- 168 months and were treated with an average of 2.7 +/- 1.6 drugs before encainide. Anterograde block in the accessory pathway occurred in 12 of 30 patients (40%) and retrograde block accessory pathway occurred in 10 of 24 patients in whom comparison could be made. AVRT was initiated in 29 of 36 patients during the control study and could be initiated in 19 of 29 patients while receiving encainide. Drug efficacy was determined by the clinical response judged completely effective, partially effective or ineffective. During a mean follow-up of 30.1 +/- 25 months, 24 patients (67%) continued to take encainide. Encainide was completely effective in 14 of 24 patients and partially effective in another 7 patients. Noncardiac side effects were mild and generally resolved, and required discontinuance in only 1 patient. More frequent AVRT occurred in 2 patients, but was managed with dose reduction and the addition of a beta blocker. Three patients had ventricular tachycardia requiring discontinuance; however 2 of 3 patients had a history of ventricular tachycardia before receiving encainide. Encainide is an effective and safe agent for treating atrial fibrillation in patients with Wolff-Parkinson-White syndrome.

Encainide for treatment of atrioventricular reciprocating tachycardia in the Wolff-Parkinson-White syndrome.

Oral encainide, varying from 75 to 300 mg/day (mean 174 mg/day), was administered to 52 patients with drug-resistant atrioventricular reciprocating tachycardia (AVRT) associated with the Wolff-Parkinson-White syndrome. Electrophysiologic studies were performed before and during drug treatment. Encainide resulted in anterograde accessory pathway block in 15 of 37 (41%) and retrograde accessory pathway block in 11 of 46 (24%) patients. In patients with residual accessory pathway conduction, encainide significantly prolonged the shortest pacing cycle length maintaining anterograde (261 +/- 26 to 404 +/- 85 ms) and retrograde (279 +/- 46 to 436 +/- 87 ms) accessory pathway conduction, as well as the anterograde accessory pathway effective refractory period (271 +/- 32 to 329 +/- 73 ms). AVRT could not be induced during encainide therapy in 20 of 49 patients (41%). In the remaining patients, AVRT cycle length increased (319 +/- 44 to 426 +/- 90 ms, p less than 0.001) due to prolongation of HV and ventriculoatrial intervals. During follow-up (mean 38.5 months), 30 patients continued to take the drug and 7 patients with favorable drug response subsequently elected to undergo surgical accessory pathway ablation (71% overall favorable response). Encainide was ineffective in 11 patients, was discontinued because of drug intolerance in 2 patients and exacerbated ventricular tachycardia in 2 patients. Lack of AVRT inducibility at encainide electrophysiologic study did not always predict recurrence-free follow-up. Encainide is an effective and well-tolerated drug to prevent recurrence of AVRT in patients with Wolff-Parkinson-White syndrome.

Efficacy and electrophysiologic effects of encainide for atrioventricular nodal reentrant tachycardia.

To prospectively determine the clinical efficacy and electrophysiologic effects of encainide in atrioventricular nodal reentrant tachycardia (AVNRT), 49 patients refractory to 2.7 +/- 1.5 previous antiarrhythmic drug trials underwent electrophysiologic study before and 47 did so after administration of oral encainide (75 to 240 mg/day). Encainide prolonged the minimum atrial pacing cycle length maintaining 1:1 atrioventricular (AV) nodal conduction from 334 +/- 55 to 391 +/- 55 ms (p = 0.0001). Encainide induced ventriculoatrial (VA) block in 12 patients (25%) and slowed the minimum ventricular pacing cycle length maintaining 1:1 VA conduction from 315 +/- 46 to 485 +/- 89 ms (p = 0.0001) in the remaining 35 patients. After encainide, AVNRT was not inducible in 32 of 47 patients (68%) primarily because of the effects on retrograde AV nodal conduction. In the remaining 15 (32%) patients, AVNRT remained inducible; however, the tachycardia cycle length slowed from 397 +/- 86 to 492 +/- 90 ms (p = 0.0001). There was no significant difference in the baseline minimum ventricular pacing cycle length maintaining 1:1 VA conduction in patients whose inducible tachycardia was or was not suppressed. Forty-seven patients were treated for 18.9 +/- 12.9 months (range 1 to 50) with oral encainide. Encainide was completely effective in eliminating recurrences of supraventricular tachycardia in 26 of 47 patients (55%) and partially effective in an additional 42%. Recurrences of arrhythmia occurred in 15 of 32 patients (47%) whose inducible tachycardia was suppressed by encainide and 7 of 15 patients (47%) whose inducible tachycardia was not suppressed by encainide (p = not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic effects of milrinone in patients with congestive heart failure.

The electrophysiologic effects of milrinone, a new inotropic agent, have not been characterized in humans. Accordingly, 10 patients with class III or IV congestive heart failure underwent hemodynamic and electrophysiologic testing before and during an infusion of milrinone (0.5 micrograms/kg/min). Cardiac index increased from a mean of 1.65 +/- 0.51 to 2.19 +/- 0.68 liters/min/m2 (p less than 0.03) and pulmonary artery capillary pressure decreased from 30 +/- 9 to 22 +/- 9 mm Hg (p less than 0.01), without a significant change in systemic arterial pressure. Holter monitoring was performed for 48 hours at baseline and during infusion of milrinone. Frequency of ventricular premature complexes and ventricular couplets did not change significantly. Frequency of ventricular tachycardia (VT) increased significantly, although no patients would be classified as having a proarrhythmic effect based on a clinical model. PR, QRS, QTc, heart rate, AH, HV, atrial, atrioventricular and ventricular effective and functional refractory periods were not affected. Milrinone decreased 1:1 atrioventricular maximal conduction from 399 +/- 133 to 374 +/- 111 ms (p less than 0.01); ventriculoatrial conduction was not significantly affected. During programmed right ventricular stimulation, 5 patients had inducible VT at baseline (3 sustained, 2 non-sustained), whereas after drug administration, none had it (p less than 0.05). Thus, intravenous milrinone is an effective inotropic drug that also enhances atrioventricular conduction and may decrease the incidence of inducible VT in patients with congestive heart failure.

Amiodarone: pharmacology and antiarrhythmic and adverse effects.

Amiodarone is a benzofuran derivative that has been effective for the treatment of both supraventricular and ventricular tachyarrhythmias. It has a large volume of distribution, moderate bioavailability and a long half-life. Its pharmacokinetics are not well understood and its tissue distribution is not typical of a 2-compartment model. Due to ocular, dermatologic, gastrointestinal, neurologic, cardiovascular, thyroid and pulmonary toxicity, amiodarone should be reserved for use in patients with refractory and/or life-threatening arrhythmias.

Stochastic aspects of one-dimensional discrete dynamical systems: Benford's law.

Benford's law owes its discovery to the "Grubby Pages Hypothesis," a 19th century observation made by Simon Newcomb that the beginning pages of logarithm books were grubbier than the last few pages, implying that scientists referenced the values toward the front of the books more frequently. If a data set satisfies Benford's law, then it's significant digits will have a logarithmic distribution, which favors smaller significant digits. In this article we demonstrate two ways of creating discrete one-dimensional dynamical systems that satisfy Benford's law. We also develop a numerical simulation methodology that we use to study dynamical systems when analytical results are not readily available.