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Biomedical subjects

M S Stanton

Publications and source records attributed to M S Stanton.

50 records · Page 3Linked to original sources
PubMed1994

Consistent subcutaneous prepectoral implantation of a new implantable cardioverter defibrillator.

OBJECTIVE: To describe the use of a new implantable cardioverter defibrillator (ICD) that can be placed in the prepectoral region rather than implanted in the abdominal wall. DESIGN: We report the experience of placement of this new ICD in the prepectoral region in 13 patients from Sept. 28, 1993, through Jan. 10, 1994, at the Mayo Clinic. MATERIAL AND METHODS: Thirteen consecutive patients offered this new ICD underwent placement of transvenous defibrillation leads, and the pulse generator was placed in a pocket formed in the subcutaneous, prepectoral space. Testing ensured a defibrillation threshold of 24 J or less. RESULTS: In all 13 patients, the pulse generator could be placed in the subcutaneous, prepectoral space. In all except one patient, acceptable defibrillation thresholds were achieved by using lead systems placed totally transvenously. Only one patient required placement of a subcutaneous patch. All but two patients were dismissed from the hospital within 3 days after the ICD implantation. CONCLUSION: Consistent subcutaneous, prepectoral placement of this new ICD pulse generator is possible. Because the entire procedure can be performed in the pacemaker implantation room, the potential exists for decreasing the duration of the hospitalization and associated costs.

Aged↗
PubMed1994

Torsades de pointes ventricular tachycardia associated with overdose of astemizole.

An overdose of astemizole predisposes the myocardium to ventricular dysrhythmias, including torsades de pointes. Herein we describe a case of astemizole-induced torsades de pointes ventricular tachycardia and also review previous case reports in the literature. All the patients were young, and dysrhythmias developed only in those with corrected QT intervals greater than 500 ms. Although several mechanisms have been postulated, no clear explanation has been provided for why astemizole promotes myocardial dysrhythmias. Treatment of astemizole-induced torsades de pointes includes discontinuing use of astemizole, intravenous administration of magnesium sulfate and isoproterenol, temporary cardiac pacing, and, when necessary, direct current cardioversion. A cardiac cause of syncope or convulsions must not be overlooked, especially in patients taking H1 antagonists because they often have these symptoms before hospitalization or detection of torsades de pointes (or both).

Adult↗
PubMed1994

Pseudo-oversensing of the T wave by an implantable cardioverter defibrillator: a nonclinical problem.

Two patients are described who had pseudo-oversensing of T waves during follow-up testing of the Medtronic PCD. Each patient exhibited appropriate T wave sensing following closely coupled spontaneous QRS complexes to subthreshold stimuli without having T wave sensing following sensed or paced complexes. One patient also revealed T wave sensing following fusion beats. The occurrence of T wave sensing in these unique clinical situations was due to the auto-adjusting sensitivity threshold function used by the PCD. Recognition of this normal sensing function will prevent inappropriate reprogramming of the sensitivity or postpace refractory period, interventions that could potentially lead to ventricular tachyarrhythmia undersensing.

Adult↗
PubMed1993

A population-based estimate of candidacy rates for the implantable cardioverter-defibrillator.

The implantable cardioverter-defibrillator (ICD) increases survival of patients who receive the device. However, candidacy rates have not been calculated for a defined population, and the potential effect of the device on the survival of all patients with heart disease has not been estimated. To make these calculations, medical records were reviewed for 1976 to 1988 in a population demographically similar to the white population of the United States. Definite and possible candidates were identified on the basis of American Heart Association/American College of Cardiology guidelines. Candidacy rates ranged from 3.3/100,000 (counting only definite candidates for the entire period) to 8.7/100,000 (counting definite and possible candidates after 1980). Extrapolated to the 1990 U.S. population, estimates ranged from 8,207 to 21,637 new candidates each year. During an average follow-up of 5 years, half of all deaths among candidates had the potential to be delayed by an ICD. In a similar population that has a death rate from heart disease of approximately 280/100,000, 0.6 to 1.6% of subjects have the potential to have their deaths delayed to some extent by an ICD.

Actuarial Analysis↗
PubMed1993

Five-year follow-up of 589 patients treated with amiodarone.

Between 1977 and 1986, 589 patients (age, 57 +/- 13 years; 464 men and 125 women) received amiodarone for ventricular fibrillation (VF; 147 patients), sustained (VT-S; 242 patients) or nonsustained (VT-NS; 80 patients) ventricular tachycardia, or supraventricular tachycardia (SVT; 120 patients). Mean left ventricular ejection fraction was 36 +/- 17%, with 23% in New York Heart Association functional class I, 49% in class II, 25% in class III, and 3% in class IV. Sixty-two percent had ischemic heart disease. Follow-up was 32 +/- 27 months (mean +/- SD). Life table analysis revealed that patients with VF, VT-S, and VT-NS had a cumulative incidence of sudden death of 9% at 1 year, increasing by about 3% per year. By years 2 and 5, the cumulative incidence of sudden death, VF, or VT-S recurrence was 26% and 38% and the percent of patients still taking amiodarone was 54% and 32%. For patients with SVT at years 2 and 5, the cumulative incidence of sudden death was 1% and 3%, and of sudden death or SVT recurrence the cumulative incidence was 20% and 29%. The percent of patients still taking amiodarone was 67% and 43%. Of 14 clinical variables assessed, New York Heart Association functional class was the best predictor of sudden death and arrhythmic failure and no other variable added independent predictive power. Older age and lower left ventricular ejection fraction were independent predictors of drug failure (sudden death or arrhythmic failure or need to discontinue amiodarone because of side effects). We conclude that despite its side effect profile, amiodarone is an effective and reasonably well-tolerated antiarrhythmic drug.

Aged↗
PubMed1993

Prolonged QT syndrome: perioperative management.

Intraoperative cardiac arrhythmias related to prolonged QT syndrome are uncommon. We describe a 26-year-old woman in whom ventricular fibrillation occurred during the final minutes of a partial glossectomy and right supraomohyoid selective neck dissection and discuss the role that this specific operation may have had in the development of the intraoperative event. In addition, we review the perioperative management of patients with prolonged QT syndrome.

Adolescent↗
PubMed1991

Modulation of drug effects by regional sympathetic denervation and supersensitivity.

BACKGROUND: Regional sympathetic denervation, such as that produced by a myocardial infarction, causes electrophysiological heterogeneity in the ventricles. The purpose of this study was to test the hypothesis that such denervation could cause drugs to exert heterogeneous myocardial effects. METHODS AND RESULTS: Sympathetic stimulation increases the amplitude of cesium chloride-induced early afterdepolarizations (EADs). The amplitude of these induced EADs was used to determine whether drug responses were different in innervated versus denervated areas of the heart. A canine model of sympathetic denervation was created at the cardiac apex by either transmural myocardial infarction (n = 19) or phenol application (n = 11). Cesium chloride (84 mg/kg) was infused while monophasic action potential recordings were simultaneously obtained from the base and apex of the left ventricle using an epicardial contact electrode. We found that control (innervated) dogs (n = 17) showed no difference in the EAD amplitude recorded from the apex compared with the base. In dogs with apical sympathetic denervation, the EAD amplitude was greater at the innervated base during ansae subclaviae stimulation than at the denervated apex (25.8 +/- 6.6% at base versus 18.8 +/- 6.7% at apex, p less than 0.001). However, during norepinephrine infusion, the EADs recorded from the denervated apex were greater than those recorded from the innervated base (23.3 +/- 7.6% at apex versus 20.6 +/- 6.0% at base, p less than 0.02) due to denervation supersensitivity. CONCLUSIONS: These data show that regional myocardial denervation creates autonomic and electrophysiological heterogeneity and the substrate for heterogeneous drug actions. This drug-induced electrophysiological heterogeneity may be another mechanism for proarrhythmia.

Action Potentials↗
PubMed1990

Clinical features of amiodarone-induced pulmonary toxicity.

The incidence and clinical predictors of amiodarone pulmonary toxicity were examined in 573 patients treated with amiodarone for recurrent ventricular (456 patients) or supraventricular (117 patients) tachyarrhythmias. Amiodarone pulmonary toxicity was diagnosed in 33 of the 573 patients (5.8%), based on symptoms and new chest radiographic abnormalities (32 of 33 patients) and supported by abnormal pulmonary biopsy (13 of 14 patients), low pulmonary diffusion capacity (DLCO) (nine of 13 patients), and/or abnormal gallium lung scan (11 of 16 patients). Toxicity occurred between 6 days and 60 months of treatment for a cumulative risk of 9.1%, with the highest incidence occurring during the first 12 months (18 of 33 patients). Older patients developed it more frequently (62.7 +/- 1.7 versus 57.4 +/- 0.5 years, p = 0.018), with no cases diagnosed in patients who started therapy at less than 40 years of age. Gender, underlying heart disease, arrhythmia, and pretreatment chest radiographic, spirometric, or lung volume abnormalities did not predict development of amiodarone pulmonary toxicity, whereas pretreatment DLCO was lower in the group developing it (76.0 +/- 5.5% versus 90.4 +/- 1.4%, p = 0.01). There was a higher mean daily amiodarone maintenance dose in the pulmonary toxicity group (517 +/- 25 versus 409 +/- 6 mg, p less than 0.001) but no difference in loading dose. No patient receiving a mean daily maintenance dose less than 305 mg developed pulmonary toxicity. Patients who developed toxicity had higher plasma desethylamiodarone (2.34 +/- 0.18 versus 1.92 +/- 0.04 micrograms/ml, p = 0.009) but not amiodarone concentrations during maintenance therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗
PubMed1989

Regional sympathetic denervation after myocardial infarction in humans detected noninvasively using I-123-metaiodobenzylguanidine.

Transmural myocardial infarction in dogs produces denervation of sympathetic nerves in viable myocardium apical to the infarct that may be arrhythmogenic. It is unknown whether sympathetic denervation occurs in humans. The purpose of this study was to use iodine-123-metaiodobenzylguanidine (MIBG), a radiolabeled guanethidine analog that is actively taken up by sympathetic nerve terminals, to image noninvasively the cardiac sympathetic nerves in patients with and without ventricular arrhythmias after myocardial infarction. Results showed that 10 of 12 patients with spontaneous ventricular tachyarrhythmias after myocardial infarction exhibited regions of thallium-201 uptake indicating viable perfused myocardium, with no MIBG uptake. Such a finding is consistent with sympathetic denervation. One patient had frequent episodes of nonsustained ventricular tachycardia induced at exercise testing that was eliminated by beta-adrenoceptor blockade. Eleven of the 12 patients had ventricular tachycardia induced at electrophysiologic study and metoprolol never prevented induction. Sympathetic denervation was also detected in two of seven postinfarction patients without ventricular arrhythmias. Normal control subjects had no regions lacking MIBG uptake. This study provides evidence that regional sympathetic denervation occurs in humans after myocardial infarction and can be detected noninvasively by comparing MIBG and thallium-201 images. Although the presence of sympathetic denervation may be related to the onset of spontaneous ventricular tachyarrhythmias in some patients, it does not appear to be related to sustained ventricular tachycardia induced at electrophysiologic study.

3-Iodobenzylguanidine↗
PubMed1989

OPC-88117 suppresses early and delayed afterdepolarizations and arrhythmias induced by cesium, 4-aminopyridine and digitalis in canine Purkinje fibers and in the canine heart in situ.

The effects of OPC-88117, a new investigational antiarrhythmic drug, on early and delayed afterdepolarizations (EAD and DAD, respectively) were assessed in vitro in canine Purkinje fibers and in vivo in the canine right ventricle. OPC-88117 had similar electrophysiologic properties to class I antiarrhythmic agents in that it decreased Vmax. OPC-88117 decreased the amplitude and prolonged the coupling interval of DAD induced by acetylstrophanthidin. Likewise, OPC-88117 suppressed EAD induced in vitro by 4-aminopyridine. In vivo, cesium-induced EAD, ventricular arrhythmia, and atrioventricular block were suppressed by OPC-88117. In summary, OPC-88117 suppressed DAD and EAD in vitro and inhibited EAD and triggered activity in the in situ canine heart.

4-Aminopyridine↗
PubMed1989

Arrhythmogenic effects of antiarrhythmic drugs: a study of 506 patients treated for ventricular tachycardia or fibrillation.

Antiarrhythmic therapy in 506 consecutive patients undergoing 1,268 antiarrhythmic drug trials for ventricular tachycardia or ventricular fibrillation was reviewed for evidence of arrhythmogenic drug effect defined as the occurrence of a new form of ventricular tachyarrhythmia temporally associated with initiation of drug therapy or dosage increase. Arrhythmogenic effects occurred in 6.9% of patients and 3.4% of drug trials. This ranged from a high of 11.8% caused by encainide to none occurring with procainamide, tocainide or beta-adrenergic blocking drugs. The incidence of arrhythmogenesis was significantly greater in patients whose presenting arrhythmia was sustained ventricular tachycardia than it was in those who presented with nonsustained ventricular tachycardia or ventricular fibrillation (p = 0.02). Decreased systolic function measured echocardiographically at the base of the left ventricle was associated with an increased incidence of arrhythmogenic effects (p = 0.006) whereas global left ventricular ejection fraction was not. Age, gender, cardiac diagnosis, location of prior myocardial infarction and New York Heart Association functional class for heart failure were not related to the occurrence of drug-induced arrhythmias. These findings emphasize the need for in-hospital cardiac monitoring during initiation of antiarrhythmic drug therapy for ventricular tachyarrhythmias.

Adolescent↗