Unexpected ICD pulse generator failure due to electronic circuit damage caused by electrical overstress.

Because it is a lifesaving device, the unexpected failure of an ICD can be catastrophic. We report ICD electronic circuit failure due to electrical overstress damage (EOS) to the high voltage hybird circuit and other electronic components in a series of ICD pulse generator models. Data were obtained from the Multicenter Registry of Pacemaker and ICD Pacemaker and Lead Failures, and from the manufactures' adverse event reports, that were in the FDA's Manufacturer and User Facility Device Experience (MAUDE) database. Of 16 nonbattery Guidant/CPI ICD pulse generator failures reported to the registry, 6 (38%) have been confirmed by the manufacturer to be EOS related, and Guidant/CPI has reported 273 such failures to the FDA as of 12/29/00. The signs of failure included loss of telemetry and inability to deliver therapy, and some patients have experienced serious adverse events. Hybrid circuit damage may have occurred during capacitor charging or reform, and the majority appears to have happened during normal ICD function. While the incidence of this problem is unknown, a management strategy should be adopted that includes routine follow-up every 3 months and device evaluation after a shock or exposure to external defibrillation or electrosurgical devices. This study suggests that additional data are needed to determine the incidence of this problem, and that our present methods for monitoring the performance of ICD's following market release are inadequate.

Feasibility and initial results of an Internet-based pacemaker and ICD pulse generator and lead registry.

The medical community has no independent source of timely information regarding the performance of pacemaker and ICD pulse generators and leads. Accordingly, the authors established an Internet-based registry of pacemaker and ICD pulse generator and lead failures (www.pacerandicregistry.com). During the first year, they found three previously unreported device problems that were promptly communicated to the participants. Of the failures reported, 11% of ICD and 10% of pacemaker pulse generator failures were heralded by signs other than the expected elective replacement indicator (ERI). Average ICD battery longevity was 4.0 +/- 0.7 years, and average dual chamber pacemaker battery longevity was 6.8 +/- 2.6 years. Disrupted insulation accounted for 54% of pacemaker and 29% of ICD lead failures. Compared to pacemaker pulse generator and lead failure, ICD device failures were more likely to cause severe clinical consequences. In conclusion, an Internet-based registry is feasible and capable of providing timely data regarding the signs, causes, and clinical consequences of pacemaker and ICD failures.

Physiotherapists in Balint group training.

BACKGROUND AND PURPOSE: Balint group training (BGT) is a method widely used for enhancing understanding of the relationship and communication between health professionals and their patients. Participants meet in small groups, on a regular basis, with a tutor to discuss their experiences of problem cases. The method was originally developed in the 1950s for enhancing understanding of the doctor-patient relationship. Few studies have focused on BGT and physiotherapists. The aim of the present study was to describe and analyse physiotherapists' experiences of participation in BGT as a means of learning and understanding the physiotherapist-patient relationship. METHOD: Semi-structured, in-depth interviews were conducted with three physiotherapists working in private practice, all participating in BGT. The interviews were transcribed and subjected to a qualitative analysis. RESULTS: The results are presented in a sequential model, featuring eight themes in which the physiotherapists' experiences of the training process are portrayed. CONCLUSIONS: The results suggest that BGT and sharing the experiences of others may be considered a way of enhancing understanding of the patient encounter in clinical practice, possibly to the benefit of physiotherapists and their patients.

Efficacy of implantable cardioverter-defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy is a genetic disease associated with a risk of ventricular tachyarrhythmias and sudden death, especially in young patients. METHODS: We conducted a retrospective multicenter study of the efficacy of implantable cardioverter-defibrillators in preventing sudden death in 128 patients with hypertrophic cardiomyopathy who were judged to be at high risk for sudden death. RESULTS: At the time of the implantation of the defibrillator, the patients were 8 to 82 years old (mean [+/-SD], 40+/-16), and 69 patients (54 percent) were less than 41 years old. The average follow-up period was 3.1 years. Defibrillators were activated appropriately in 29 patients (23 percent), by providing defibrillation shocks or antitachycardia pacing, with the restoration of sinus rhythm; the average age at the time of the intervention was 41 years. The rate of appropriate defibrillator discharge was 7 percent per year. A total of 32 patients (25 percent) had episodes of inappropriate discharges. In the group of 43 patients who received defibrillators for secondary prevention (after cardiac arrest or sustained ventricular tachycardia), the devices were activated appropriately in 19 patients (11 percent per year). Of 85 patients who had prophylactic implants because of risk factors (i.e., for primary prevention), 10 had appropriate interventions (5 percent per year). The interval between implantation and the first appropriate discharge was highly variable but was substantially prolonged (four to nine years) in six patients. In all 21 patients with stored electrographic data and appropriate interventions, the interventions were triggered by ventricular tachycardia or fibrillation. CONCLUSIONS: Ventricular tachycardia or fibrillation appears to be the principal mechanism of sudden death in patients with hypertrophic cardiomyopathy. In high-risk patients with hypertrophic cardiomyopathy, implantable defibrillators are highly effective in terminating such arrhythmias, indicating that these devices have a role in the primary and secondary prevention of sudden death.

Clinical course of hypertrophic cardiomyopathy in a regional United States cohort.

CONTEXT: Hypertrophic cardiomyopathy (HCM) has been regarded as a disease that causes substantial disability, with annual mortality rates of up to 6%, based largely on reports from tertiary referral centers. OBJECTIVE: To assess the clinical course of HCM in a patient cohort more closely resembling the true disease state. DESIGN: Retrospective cohort study. SETTING: A regional cohort from Minnesota and adjoining regions, free of referral center bias, studied at Minneapolis Heart Institute. PATIENTS: Two hundred seventy-seven consecutively studied HCM patients, none referred for specialized HCM care, managed clinically in a standard fashion. MAIN OUTCOME MEASURES: Mortality and clinical course of HCM. RESULTS: During a mean (SD) follow-up of 8.1 (6.6) years, 45 patients died and 29 of these deaths were directly related to HCM; however, 8 of the 29 HCM deaths were not premature (occurring >75 years of age). Annual HCM mortality rate was 1.3% (0.7% for sudden cardiac death). Patients identified in adulthood (n = 234) showed no statistically significant difference in mortality when compared with expected mortality, as calculated for the general US or Minnesota populations (P=.17). Patients identified as children (n=43) showed decreased survival compared with the general population (P<.001). At most recent clinical evaluation, 192 patients (69%) had no or mild symptoms and 69 (25%) experienced incapacitating symptoms or HCM-related death; 53 (19%) of the patients had achieved estimated life expectancy of 75 years or older. More advanced symptoms at diagnosis-occurrence of atrial fibrillation (often associated with stroke), the presence of basal outflow obstruction of at least 30 mm Hg, and marked left ventricular wall thickness of more than 25 mm-were clinically important independent predictors of HCM mortality. CONCLUSIONS: In a regionally selected patient population most closely resembling the true disease state, HCM did not significantly increase the risk of premature death or adversely affect overall life expectancy. Prevailing misconceptions of HCM as a generally unfavorable condition may largely be related to the skewed patient referral patterns characteristic of tertiary care centers. Hypertrophic cardiomyopathy is nevertheless a highly complex disease capable of serious clinical consequences and premature death in some patients.

Implantation of the implantable cardioverter defibrillator in the heart transplant candidate.

Because the major cause of death in patients awaiting heart transplantation results from out-of-hospital sudden cardiac arrest, the use of the implantable cardioverter defibrillator has been proposed as a bridge to transplantation. To provide a safe and simple implantation procedure that also easily allows access to cardiopulmonary bypass at the time of transplantation, a modified subxiphoid approach is reported.

Percutaneous transluminal coronary angioplasty in the setting of large intracoronary thrombi.

A cohort of 112 consecutive patients with angiographically defined intracoronary thrombi was treated with percutaneous transluminal coronary angioplasty and followed prospectively to determine early and late outcomes. Coronary angioplasty using a treatment modality of intravenous and intracoronary heparin, antiplatelet agents and prolonged inflations with oversized balloons (balloon:vessel ratio, 1.2:1) resulted in clinical success in 103 patients (92%) at hospital discharge. No periprocedural thrombolytic therapy was used and prolonged pretreatment with heparin was not routinely used. Four patients (3.5%) required elective coronary bypass surgery, and 4 patients (3.5%) required emergency coronary artery bypass grafting because of abrupt closure. Late clinical follow-up (mean 7 months) was available in 99 of the 103 successfully treated patients (96%). Seventy-three percent of patients were asymptomatic at follow-up, and 27% had class I or II angina. No patients had a late myocardial infarction. Elective coronary artery bypass surgery was required in 3 patients (3%) and repeat coronary angioplasty in 17 patients (17%). There were 2 late cardiac deaths at 7 months. Ninety-four patients (95%) had an event free follow-up defined as absence of coronary artery bypass surgery, myocardial infarction or death. In conclusion, coronary angioplasty alone, using intracoronary heparin and prolonged balloon inflations with relatively oversized balloons may be helpful to achieve a high initial success rate, low incidence of in-hospital complications and excellent long-term results in patients with intracoronary thrombus.

Cardiovascular complications of thrombolytic therapy in patients with a mistaken diagnosis of acute myocardial infarction.

Thrombolytic drugs given to patients with a mistaken diagnosis of acute myocardial infarction could produce adverse effects, although no such cases have been reported. Two patients treated with intravenous streptokinase for presumed but nonexistent acute myocardial infarction are described. Pericardial tamponade developed in both patients, in one after aortic dissection and in the other after pericarditis. Both required surgery; one died. Symptoms and electrocardiographic abnormalities mimicking acute myocardial infarction may be caused by non-coronary syndromes. In such cases, treatment with thrombolytic agents may exacerbate the underlying disease process and produce cardiovascular complications.

Cardiac electrophysiologic effects of orally administered DPI 201-106 in conscious canines: effects of pharmacologic autonomic blockade or cardiac transplantation.

This study assessed the cardiac electrophysiologic effects of DPI 201-106 (DPI), a novel orally absorbable positive inotropic agent, the administration of which has been associated with electrocardiographic (ECG) QT and T-wave changes. In the intact conscious dog, oral administration of both 8 and 16 mg/kg DPI produced marked sinus cycle length prolongation (8 mg/kg, + 11%; 16 mg/kg, + 9%) within 60 min of DPI administration (p less than 0.05 vs. baseline). DPI also tended to prolong right atrial refractory periods, and increase sinus node recovery time. In addition, DPI exhibited a negative dromotropic effect on the atrioventricular (AV) node, prolonging both AV node effective and functional refractory periods and tending to increase the minimum atrial paced cycle length at which AV conduction of 1:1 was maintained. DPI also significantly increased right ventricular effective refractory period (ERP) at both doses studied and increased ventricular functional refractory period (FRP) at the 16-mg/kg dose. Finally, although DPI administration was associated with QT interval prolongation, this effect was slight when corrected for sinus cycle length (SCL) (QTc, +3%). When administered concomitantly with propranolol and atropine or after surgical cardiac denervation, DPI-induced electrophysiologic changes were largely attenuated or abolished. Thus, findings in this study indicate that the apparent cardiac electrophysiologic effects of DPI are predominantly of neurally mediated origin in this animal model.

Intravenous amiodarone for the rapid treatment of life-threatening ventricular arrhythmias in critically ill patients with coronary artery disease.

This study examined the effectiveness of intravenous amiodarone for rapid control and prevention of recurrent life-threatening ventricular tachyarrhythmias associated with cardiovascular collapse. In 22 critically ill patients with coronary artery disease (mean ejection fraction 27 +/- 13%), recurrent ventricular tachyarrhythmias proved refractory to 3.7 +/- 1.1 (mean +/- standard deviation) conventional antiarrhythmic drugs. In the 24-hour period before intravenous amiodarone treatment, patients experienced 2.4 +/- 2.3 (range 1 to 9) episodes of life-threatening ventricular tachycardia, ventricular fibrillation or both, requiring 4.0 +/- 3.9 direct current cardioversions. Within the 24 hours after initiation of intravenous amiodarone therapy (900 to 1,600 mg/day), 20 of 22 patients remained alive and had 1.1 +/- 1.6 episodes of life-threatening ventricular arrhythmias, requiring 1.9 +/- 3.1 direct current cardioversions. In the second 24-hour period, there were 19 survivors and life-threatening arrhythmias were reduced to 0.4 +/- 0.7 episode/patient requiring 0.4 +/- 0.9 direct current cardioversion. Overall, arrhythmias were controlled in 11 of 22 (50%) patients within the first 24 hours, and in 14 of 22 (64%) in the second 24 hours. Intravenous amiodarone therapy was well tolerated. Twelve patients were discharged from the hospital and 8 remained alive at a mean follow-up of 22 +/- 14 months. Thus, in critically ill patients, intravenous amiodarone may be useful for rapid control of spontaneous, refractory, life-threatening ventricular tachyarrhythmias.

Provocation of bradycardia and hypotension by isoproterenol and upright posture in patients with unexplained syncope.

Neurally mediated hypotension and bradycardia are believed to be common causes of syncope. We used the "upright-tilt test" (duration, less than or equal to 10 minutes) with or without an infusion of exogenous catecholamine (isoproterenol [1 to 5 micrograms per minute], given intravenously) to elicit bradycardia, hypotension, or both in 24 patients with recurrent syncope and in 18 control subjects. A conventional electrophysiologic test performed before the tilt test was positive in 9 of the 24 patients, revealing arrhythmias that may have caused recurrent syncope, but was negative and thus nondiagnostic in 15 patients. The tilt test alone (i.e., without isoproterenol) induced symptomatic bradycardia or hypotension in 1 of the 9 patients with positive electrophysiologic tests (11 percent), 4 of the 15 patients with negative electrophysiologic tests (27 percent), and none of the controls. When the isoproterenol infusion was administered during the tilt test, 9 of the 11 patients with negative electrophysiologic and tilt tests had syncope, marked slowing of the heart rate, and hypotension. In contrast, isoproterenol was associated with tachycardia and only a slight decline in arterial pressure in the 8 remaining patients with positive electrophysiologic tests and the 18 control subjects, and syncope developed in only 1 of the 8 patients with positive electrophysiologic tests and negative tilt tests (13 percent) and 2 of the 18 control subjects (11 percent). We conclude that an isoproterenol infusion administered in conjunction with the upright-tilt test may be useful for identifying susceptibility to neurally mediated recurrent syncope.

Cardiac electrophysiologic and hemodynamic correlates of neurally mediated syncope.

This study assessed the temporal relation of RR interval, AH interval and systemic blood pressure changes during induced symptomatic bradycardia-hypotension episodes in 14 patients with recurrent syncope suspected of being neurally mediated. Upright tilt with isoproterenol reproduced symptoms in 9 of 14 patients (positive response) and was negative in 5 of 14 (negative response). Isoproterenol alone shortened supine RR intervals in all patients. With tilt, however, isoproterenol prolonged RR intervals in those with positive results (supine 519 +/- 124 ms vs tilt 845 +/- 212 ms, p less than 0.005) while further shortening RR intervals among negative responders (supine 436 +/- 90 ms vs tilt 377 +/- 82 ms, p less than 0.05). Similarly, tilt with isoproterenol prolonged AH intervals in patients with positive responses despite RR prolongation, while shortening AH in negative responders. Additionally, with combined tilt and isoproterenol, systemic arterial pressure decreased significantly in patients with positive responses (systolic 99 +/- 13 vs 57 +/- 13 mm Hg, p less than 0.001, diastolic 62 +/- 17 vs 28 +/- 9 mm Hg, p less than 0.001) but not in patients with negative responses. Further, onset of hypotension (42 +/- 14 seconds after tilt) preceded onset of RR interval prolongation (52 +/- 23 seconds after tilt). Syncope (142 +/- 72 seconds after tilt) coincided closely with nadir of systemic pressure (136 +/- 74 seconds) and both tended to precede maximum RR prolongation (152 +/- 87 seconds). Thus, the bradycardia and hypotension associated with neurally mediated syncope exhibit characteristic but distinctly different time courses, with arterial pressure changes developing earlier and coinciding more closely with symptom development.

Plasminogen activator inhibitor 1 (PAI) is bound to vitronectin in plasma.

Functionally active plasminogen activator inhibitor 1 (PAI) is bound to a discrete binding protein in plasma [(1988) Thromb. Haemost. 59, 392-395]. The binding protein has now been partially purified using conventional chromatographic techniques. After addition of active PAI its complex with the binding protein was purified by chromatography on insolubilized monoclonal antibodies towards PAI. Dodecylsulphate (polyacrylamide gel electrophoresis revealed two main compounds with molecular masses of 50 and 75 kDa respectively. NH2-terminal amino acid sequence analysis and immunoblotting analysis suggested that the two compounds were PAI (50 kDa) and vitronectin (75 kDa). We conclude that the PAI-binding protein is identical to vitronectin.

Pharmacy newsletters--the journalistic approach.

Pharmacy newsletters are an important communication tool for the majority of pharmacy operations across the country. They are used by pharmacists for basically two purposes: 1) to disseminate information to physicians, nurses and other hospital staff; and 2) for public relations. An enormous amount of time is spent by pharmacists in preparing newsletters but their effectiveness with respect to the above two purposes may vary from hospital to hospital. It is believed that a journalistic approach to the creation and publication of pharmacy newsletters can increase their effectiveness and acceptance by the hospital staff.

Role of extrastimulus site and tachycardia cycle length in inducibility of atrial preexcitation by premature ventricular stimulation during reciprocating tachycardia.

Preexcitation of the atria during reciprocating tachycardia (RT) by a premature ventricular complex occurring when the His bundle is refractory provides direct evidence of the presence of accessory atrioventricular (AV) connection. The impact of ventricular stimulation site and RT cycle length on inducibility of atrial preexcitation was assessed in 38 patients with RT utilizing a single accessory AV connection (right free wall in 5 patients, left free wall in 21 and posterior septal/paraseptal in 12). Extrastimuli were inserted at right ventricular (RV) apical, left ventricular (LV) septal and LV free wall sites. Inducibility of and magnitude of atrial preexcitation increased as stimulation site approached accessory AV connection site. Thus, for RV free wall connections, RV extrastimuli preexcited the atria in 5 of 5 patients, LV septal in 1 of 5 and LV free wall in 0 of 4. For LV free wall accessory connections, RV extrastimuli preexcited the atria in only 3 of 21 patients, compared with 12 of 17 with LV septal and 20 of 21 with LV free wall stimulation. Additionally, the magnitude of atrial preexcitation achieved was related to RT cycle length, diminishing as cycle length shortened. Finally, in a few instances both RV apical and LV free wall extrastimuli failed to elicit preexcitation in patients with a posterior septal connection. Thus, ventricular pacing site and RT cycle length contribute importantly to induction of atrial preexcitation by ventricular extrastimulation technique and should be considered during evaluation of patients with RT in whom accessory AV connections may be present.