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PubMed1989

Critical dose of digoxin for treating supraventricular tachycardias after heart surgery.

This study was conducted to ascertain if critical peak body stores of digoxin were needed to protect patients from the debilities that result from supraventricular tachycardias occurring after open heart operations. We gave digoxin peak body stores of 15 micrograms/kg of lean body weight to 100 consecutive patients after open heart operations. If supraventricular tachycardias persisted four hours, we increased peak body stores to 17 or 19 micrograms/kg. The operations included coronary artery bypass grafts, heart valve replacements, and congenital defect correction. After operation, 18 patients had atrial fibrillation or flutter. During supraventricular tachycardias, ventricular rates were 150 beats per minute or slower. In the 100 patients, the median hospital stay after operation was four days. No patient required rehospitalization. The patients who had supraventricular tachycardias stayed in the hospital no longer than the patients who were at all times in regular sinus rhythm. All patients who entered the hospital with regular sinus rhythm went home with regular sinus rhythm. The critical safe peak body stores of digoxin needed to prevent debilities resulting from supraventricular tachycardias after open heart operations were 15 to 19 micrograms/kg of lean body weight.

Aged↗

PubMed1986

A study on entrainment in various forms of tachycardias.

In order to study the entrainment phenomenon in various forms of clinical and experimental tachycardia, overdrive pacing was performed in clinical paroxysmal supraventricular tachycardia (PSVT) of Wolff-Parkinson-White syndrome (6 cases), atrial flutter (AF-6 cases), ventricular tachycardia (VT-2 cases), experimental AF induced by Rosenblueth's method (5 dogs), and in VT induced by aconitine (5 dogs). Progressive fusion was demonstrated in all but aconitine-induced VT. After cessation of pacing, the first tachycardia complex showed no fusion at all, but the timing of the complex varied depending on the recording sites of the electrogram. The tachycardia complex occurred at the pacing rate only when the electrogram was recorded at the upstream of the pacing site along the reentry circuit in PSVT and experimental AF. In clinical VT, the complex appeared progressively later as the pacing rate was increased. In aconitine-induced experimental VT, the complex occurred at its original tachycardia rate originating from the site where aconitine was applied. In reentrant tachycardia, entrainment could be observed even when all three of the diagnostic criteria proposed by Brugada et al. were not fulfilled. The mechanism of tachycardia can be assessed by entrainment, although the proposed criteria should be reevaluated.

Animals↗

PubMed1995

Efficacy of intravenous magnesium sulphate in supraventricular tachyarrhythmias.

This study was conducted to evaluate the clinical efficacy of intravenous (i.v.) magnesium sulphate 2 gm bolus in sustained supraventricular tachycardia (SVT) and atrial flutter-fibrillation with fast ventricular rate of more than 160/min (AF-FVR) and to compare it with i.v. verapamil 5 mg. In this randomised controlled trial, 68 cases of SVT and 86 cases of AF-FVR were studied. Patients with evidence of renal dysfunction and systolic blood pressure less then 90 mm Hg were excluded. Response was considered when the heart rate fell to less than 100/min. In SVT, 33.3% (11 out of 33) responded to magnesium sulphate which was significantly less than verapamil (23 out of 35, 65.7%) p = 0.007. Similarly, in AF-FVR, response was more with verapamil (25 out of 45, 55.6%) than magnesium sulphate (8 out of 41, 19.5%) p < 0.0001. Response to magnesium sulphate was better in patients with IHD. There were no significant side effects, except flushing and sense of warmth with i.v. magnesium sulphate. Serum magnesium rose significantly after i.v. magnesium bolus. Though magnesium sulphate is a weaker antiarrhythmic drug than verapamil, further studies are needed to identify subgroups of supraventricular tachyarrhythmias which would respond to magnesium sulphate.

Adult↗

PubMed1991

Oral propafenone therapy for children with arrhythmias: efficacy and adverse effects in midterm follow-up.

The use of oral propafenone was assessed in 57 children. Mean age was 4.8 +/- 5.2 years (range 1 day to 17 years). Twenty-three patients were less than 1 year of age (40%) and 10 were less than 1 month of age (18%). Arrhythmias included supraventricular tachycardia in 32 patients (57%), atrial flutter in six (10%), and ventricular tachycardia in 19 (33%). Cardiac diagnoses included: an otherwise normal heart in 30 (53%); unoperated congenital heart defect in 11 (19%); cardiomyopathy in nine (16%); and an operated congenital heart defect in seven (12%). Mean dose of propafenone was 13.1 mg/kg/day (range 8 to 15). Success (assessed by relief of symptoms and serial 24-hour ECGs) was achieved in 16 of 32 patients with supraventricular tachycardia (50%), three of six with atrial flutter (50%), and 8 of 19 with ventricular tachycardia (42%). Drug efficacy in patients with and without organic heart disease was 30% (8 of 27) and 63% (19 of 30), respectively (p less than 0.05). Mean duration of therapy in patients in whom the drug was effective was 22.9 +/- 13.2 months (range 6 to 60). Growth was unimpaired in all patients. A neonate with nonsustained monomorphic ventricular tachycardia had sustained ventricular tachycardia during the second day of propafenone therapy at a dose of 13 mg/kg/day. Sustained ventricular tachycardia disappeared when the drug was discontinued. Another patient had an asymptomatic and transient increase in the glutamic pyruvic transaminase level. No adverse hemodynamic effects were observed. In conclusion, propafenone is an effective antiarrhythmic drug in children with normal hearts; it is less effective in patients with heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1979

Acebutolol in supraventricular arrhythmias.

The effect of intravenous acebutolol on supraventricular arrhythmias was evaluated in 20 patients, 5 with chronic obstructive pulmonary disease. A rapid ventricular rate in atrial fibrillation was slowed greater than 15% in all of 10 patients by acebutolol and in none of 5 patients by saline. A rapid ventricular rate in atrial flutter was slowed greater than 15% in all of 6 patients by acebutolol and in none of 3 patients by saline. Frequent premature atrial beats were abolished or reduced by greater than 75% in each of 2 patients by acebutolol and not in a patient by saline. Acebutolol converted multifocal atrial tachycardia to sinus rhythm in a patient. Digitalis-induced nonparoxysmal atrioventricular junctional tachycardia was not affected by saline but was abolished by acebutolol in a patient. Acebutolol was well tolerated in each of 5 patients with chronic obstructive pulmonary disease. Acebutolol is useful in the treatment of supraventricular arrhythmias.

Acebutolol↗

PubMed1978

Echocardiographic features in a case of intrapericardial teratoma.

An infant presented with symptoms of congestive heart failure. Ultrasound examination revealed a dense layer of echoes at the root of the aorta, a large anterior pericardial effusion, and coarse fluttering of the right ventricular wall. The clinical diagnosis of intrapericardial teratoma was confirmed by cineangiography and surgical resection. The pathological examination was consistent with benign teratoma. A postoperative ultrasound examination revealed absence of pericardial effusion and tumor echoes. This appears to be the first echocardiographic report of a pericardial tumor in an infant.

Angiography↗

PubMed1992

Spinal fusion in Duchenne muscular dystrophy: a multidisciplinary approach.

We studied 27 Duchenne muscular dystrophy patients having spinal fusion for scoliosis. One patient died intraoperatively of cardiac arrest; all others have done well with no instances of malignant hyperthermia, postoperative ventilatory system dependence, pneumothorax, persisting infection, neurologic damage, nonunion, or pain. The anesthetic management included primarily intravenous general anesthetics with minimal myocardial depressant effects, avoiding succinylcholine and inhalation agents. Preoperative cardiac studies aided anesthetic management intra-operatively. There was an almost universal sinus tachycardia. Holter monitoring defined 4 of 16 with ventricular premature beats, 4 of 16 with atrial premature beats, and no ventricular tachycardia or atrial flutter or fibrillation. Echocardiogram demonstrated mitral prolapse in 2 of 22, frequent abnormal systolic performance with abnormal shortening fraction less than 28% in 7 of 16, and reduced rate-corrected velocity of fiber shortening in 9 of 15. Afterload was elevated in 7 of 15. The mean forced vital capacity (FVC) preoperatively was 45.3 +/- 15.9% with continuing diminution to 28.7 +/- 14.9% at 3.3 +/- 2.2 years after surgery. The main benefit of surgical stabilization is the relative ease and comfort of wheelchair seating compared with those nonoperated patients who develop progressive deformity. We have not seen lasting improvement or stabilization in FVC following surgery as decreasing function is related primarily to muscle weakness.

Adolescent↗

PubMed2005

First report of supraventricular tachycardia after intravenous pulse methylprednisolone therapy, with a brief review of the literature.

The occurrence of supraventricular tachycardia after high-dose intravenous methylprednisolone pulse therapy (HIVMPT) in a patient with active rheumatoid arthritis is described for the first time. This case report further expands the range of arrhythmias that can occur with HIVMPT. Other arrhythmias previously reported to occur after HIVMPT include atrial fibrillation, atrial flutter, junctional rhythm, and ventricular tachycardia. To the best of our knowledge, supraventricular tachycardia has not been reported previously, although severe bradycardia, hypotension, asystole, cardiovascular collapse, and sudden death have been documented. A review of the literature indicates that these case reports not withstanding, HIVMPT is generally safe, and cardiovascular toxicity is rare. However, close supervision with repeated measurements of blood pressure, electrocardiogram, and blood electrolytes is mandatory during and immediately after HIVMPT, especially for patients with pre-existing cardiovascular disease, and the lowest effective dose of methylprednisolone should be infused at a slow rate.

Arthritis, Rheumatoid↗

PubMed1984

Antegrade conduction and AV node function in patients with unidirectional retrograde accessory pathways.

In 26 patients with unidirectional retrograde accessory pathways (URAP), antegrade conduction properties were evaluated. During electrophysiologic study the interval from the low septal right atrial potential to the His bundle potential (LSRA-H) in sinus rhythm (SR) was found to be less than 60 msec in 7 out of the 18 patients with left-sided URAP and in one out of two patients with septal URAP. Each of the six patients with right-sided URAP had an LSRA-H equal to or greater than 70 msec. During atrial extrastimulus testing, LSRA-H failed to prolong more than 100 msec (LSRA-H increment equal to or less than 100 msec) in four of six patients with left-sided URAP and LSRA-H of less than 60 msec in SR as well as in the one of two patients with septal URAP in whom the LSRA-H in SR was less than 60 msec. During rapid atrial pacing, we found 1:1 AV node conduction at a pacing rate of more than 200 bpm in the one patient with septal URAP and in 7 out of 14 patients with left-sided URAP who could be assessed. Three of these patients had progression from 1:1 AV conduction to 2:1 AV block without intervening Wenckebach. In conclusion, accelerated AV node conduction in SR and reduced AV node function during rapid atrial pacing or extrastimulus testing was found in 44% of our patients with left-sided or septal URAP. Since these patients are at higher risk for faster ventricular response to atrial flutter and fibrillation and for high frequency during supraventricular tachycardia, these findings were of clinical relevance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1984

Torsade de pointes due to quinidine: observations in 31 patients.

We performed a mail solicitation and obtained the records of 31 patients with documented torsade de pointes (TDP) due to quinidine. All 31 patients had heart disease: ischemic = 11 patients (36%), rheumatic = five patients (16%), hypertensive = four patients (13%), cardiomyopathic = four patients (13%), other = seven patients (22%). Quinidine was administered to these patients for the following reasons: atrial fibrillation or flutter = 22 patients (71%), ventricular premature beats = six patients (19%), ventricular or supraventricular tachycardia = three patients (10%). The 31 patients were receiving quinidine, 650 to 2400 (mean 1097) mg/day, and 14 patients had serum quinidine levels of 1.4 to 10.6 (mean 3.7) micrograms/ml. TDP occurred within 1 week of initiation of quinidine therapy in 23 (74%) of the patients. Twenty-eight (90%) of the 31 patients were receiving digoxin, and 5 (24%) of 21 patients had hypokalemia at the time of TDP. Off of quinidine therapy, corrected QT (QTc) intervals in 24 patients ranged from 390 to 580 (mean 470) msec and were prolonged in 17 patients (71%). On quinidine therapy, QTc intervals in 23 patients ranged from 390 to 630 (mean 510) msec and were prolonged in 21 patients (91%). In summary, patients with TDP due to quinidine usually had heart disease complicated by atrial fibrillation, were receiving digoxin, and were receiving moderate dosages of quinidine for less than 1 week prior to TDP. Approximately two thirds of patients with TDP due to quinidine had long QT intervals while off of quinidine.

Adolescent↗

PubMed1987

Amiodarone efficacy in a young population: relationship to serum amiodarone and desethylamiodarone levels.

Serum amiodarone and desethylamiodarone levels were measured in children and young adults receiving chronic amiodarone therapy. The study population consisted of 34 children and young adults with ventricular tachycardia (36%), atrial flutter (36%), and recurrent supraventricular tachycardia (27%). The mean age was 12.9 +/- 8.6 years (range 4 months to 23 years) and the mean daily dose of amiodarone was 6.6 +/- 3.7 mg/kg/day (range 2.5 to 25 mg). Serum amiodarone and desethylamiodarone levels after 10.1 months (range 1 to 40 months) were 0.85 +/- 0.63 microgram/ml and 0.67 +/- 0.42 microgram/ml, respectively. In three patients for whom amiodarone therapy was unsuccessful, serum amiodarone levels were 0.27, 0.85, and 1.18 micrograms/ml. There was no significant correlation between serum amiodarone or desethylamiodarone levels and dosage of amiodarone. Four patients, all 13 years or older, developed toxicity (skin rash [one patient], keratopathy [two patients], and hyperthyroidism [one patient]). There was no correlation between serum amiodarone and desethylamiodarone levels and toxicity; although there was a trend toward elevated reverse serum triiodothyronine levels in patients who developed toxicity, the values fell within the range of those patients without toxic side effects. Serum amiodarone levels do not appear to be of great value in predicting efficacy and toxicity of amiodarone in children and young adults receiving chronic drug therapy.

Adolescent↗

PubMed1994

Physiologic role of atrio-Hisian and nodo-Hisian bypass tracts in supraventricular tachycardia.

Atrio-Hisian bypass tracts are considered to be rare electrophysiologic curiosities. The prevalence and functional significance of these tracts are unknown. We examined the incidence of atrio-Hisian and nodo-Hisian bypass tracts, their electrophysiologic manifestations, and their physiologic role in supraventricular tachycardia in 200 consecutive patients referred for evaluation of supraventricular tachycardia. In one patient it was demonstrated for the first time that a concealed (retrograde only) nodo-Hisian bypass tract functioned as the retrograde limb of orthodromic reciprocating tachycardia. The VA interval was negative during tachycardia, similar to that sometimes observed in atrioventricular nodal reentry. In a second patient an anterograde and retrograde conducting pathway resulted in a pseudo Wolff-Parkinson-White electrocardiographic pattern and served as an "innocent bystander," permitting a rapid ventricular response during atrial flutter. In conclusion, although atrio-Hisian and nodo-Hisian bypass tracts are rare, they are sufficiently prevalent to make them observable in a larger referral series. Most importantly, they may participate as bystanders during supraventricular tachycardia or as either the anterograde or retrograde limbs of reciprocating tachycardia. They may possess features that mimic Wolff-Parkinson-White syndrome and/or AV nodal reentry.

Adult↗

PubMed1981

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of Wolff-Parkinson-White Syndrome.

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-"distal" His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the "proximal" His bundle was stimulated. In these two patients, having as "common denominators" short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possible due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the "slow" nodal pathway.

Adolescent↗

PubMed1985

Site of conduction delay and electrophysiologic significance of first-degree atrioventricular block in children with heart disease.

Associated electrophysiologic abnormalities and site of delay were studied in 20 patients, aged 1.5 to 16.5 years, with congenital heart disease and first-degree atrioventricular (AV) block (PR interval above the 98th percentile for age and heart rate). Eight of the 20 patients with first-degree AV block were studied after 1 or more cardiovascular operations. Refractory periods of the atrium, AV node, His-Purkinje system and ventricle were determined. As a further test for AV nodal integrity, rapid atrial pacing was performed and the cycle at which Wenckebach periodicity occurred was noted. Four groups were identified. Group I included 4 patients (20%) with intraatrial conduction delay (long PA interval). Three patients had depressed sinus nodal function and 1 had depressed AV nodal function. Group II included 7 patients (35%) with AV nodal delay (long AH interval). One patient had sinus nodal depression and 2 had AV nodal depression (prolonged AV nodal refractory period or Wenckebach at a long paced cycle length). Group III included 3 patients (15%) with His-Purkinje delay (long HV interval). Measured functions were normal in all patients. Group IV included 6 patients (30%) with normal or high normal intracardiac intervals with long PR. One patient had sinus nodal dysfunction, 2 patients had long atrial refractory periods, 1 had AV nodal depression; 2 had long refractory period of the His-Purkinje system, and 1 had long ventricular refractory period. Atrial flutter was induced in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1979

Right-sided infective endocarditis: an echocardiographic study.

Echocardiographic observations are described in 10 patients with right-sided bacterial endocarditis. Six of the nine patients with tricuspid regurgitation had shaggy echoes on the tricuspid valve, which were confirmed to be vegetations on autopsy in two patients. In six patients, right ventricular dilatation was present, and paradoxic septal motion was seen in four. In one of the patients with pulmonic valve endocarditis, the pulmonic valve and right ventricular outflow tract revealed the shaggy echoes in diastole, along with systolic fluttering of the pulmonic valve, right ventricular dilatation and paradoxic septal motion. When the findings are supplemented to the clinical picture, echocardiography is found to be a useful noninvasive adjunct in the diagnosis of acute vegetative bacterial endocarditis involving the right side of the heart, especially if other clinical features, e.g., fever, leukocytosis and positive blood cultures are absent.

Adult↗

PubMed1990

Clinical experience with a new catheter for His bundle ablation.

Eleven patients aged 33-66 years were referred for treatment of refractory supraventricular arrhythmias. Each patient had failed to respond to medical treatment. One patient had a paroxysmal atrial flutter with a rapid ventricular response. Six patients had a chronic atrial fibrillation. Two others had a supraventricular tachycardia due to reentry in the atrioventricular (AV) node, and two patients suffered from circus movement tachycardia using a concealed left free wall accessory pathway. A specially built United States Catheter and Instruments (USCI) women Dacron polyurethane electrode catheter (bipolar 8F with an internal lumen, 90 A, 5,000 V, 5.5 omega) was positioned in the His bundle area to record unipolar large atrial and His signals. When the maximal ratio low right atrium/His spike was recorded, the pole was connected to the output of a standard defibrillator. A shock of 200-250 J was delivered through this pole. Ten patients developed complete AV block (CAVB) immediately. After 72 hours, these patients were implanted with a rate-responsive pacemaker. The procedure was without side effects. Nine patients remain in CAVB after 3-17 months; in one case AV conduction resumed but the patient is free of arrhythmia. Another patient needed a second catheter ablation after 1 month.

Adult↗

PubMed2004

Calcium chloride before i.v. diltiazem in the management of atrial fibrillation.

Diltiazem is commonly used to treat atrial fibrillation or flutter (AFF) with rapid ventricular response (RVR). Although it is very effective for rate control, up to an 18% prevalence of reported diltiazem-induced hypotension [defined by systolic blood pressure (SBP) < 90 mm Hg], and a mean of 9.7% hypotension have been reported from several studies totaling over 450 patients. This hypotension may complicate therapy. Our objective was to determine if calcium chloride (CaCl(2)) pre-treatment would blunt a SBP drop after i.v. diltiazem, while allowing diltiazem to maintain its efficacy. A prospective, randomized, double-blind, placebo-controlled study was conducted. Seventy-eight patients with AFF and a ventricular rate of >/= 120 beats per minute were enrolled. Half received i.v. CaCl(2) pre-treatment; the other half received placebo. All patients then received i.v. diltiazem in a standard, weight-based dose. A second dose of CaCl(2) pre-treatment or placebo and diltiazem was given if clinically indicated for additional rate control. Both CaCl(2) and placebo pre-treatment groups had equal lowering of heart rate (p < 0.001). There were no adverse events in the calcium pre-treatment study arm. One patient in the placebo group became paradoxically more tachycardic and apneic after the diltiazem infusion. Although i.v. CaCl(2) seems to be equally safe compared to placebo as a pre-treatment in the management of AFF with RVR, we were unable to find a statistically significant blunting of SBP drop with CaCl(2) i.v. pre-treatment. Until further research determines a benefit exists, we cannot recommend i.v. CaCl(2) pre-treatment before diltiazem in the treatment of AFF with RVR.

Adult↗

PubMed2004

Late pacemaker requirement after pediatric orthotopic heart transplantation may predict the presence of transplant coronary artery disease.

BACKGROUND: Few data are available regarding pacemaker implantation after pediatric orthotopic heart transplantation. The purpose of this study was to assess the incidence, indications and associations with regard to pacemaker placement in children who have undergone orthotopic heart transplantation. METHODS: We performed a retrospective study of all patients undergoing orthotopic heart transplantation at our institution from October 1984 to March 2001. Data obtained included demographics, indications for pacemaker, presence of transplant coronary artery disease and long-term follow-up. Patients were divided into: Group 1, patients requiring a pacemaker within 3 months of transplantation; and Group 2, patients requiring a pacemaker beyond 3 months. RESULTS: Pacemakers were required in 7 of 106 (6.6%) transplant recipients. Pacing indications for patients in Group 1 (n = 2) were persistent bradycardia with pause-related ventricular arrhythmia and atrial flutter with resultant sinus pauses of up to 4 seconds. In Group 2 patients (n = 5), indications for pacing were high-grade atrioventricular (AV) block in 1 patient and episodic sinus pauses up to 3.3 seconds associated with syncope/dizziness in the remaining 4 patients. All patients in Group 2 had transplant coronary disease diagnosed within 1 year of pacemaker implantation. All had resolution of symptoms and no complications after implantation. CONCLUSIONS: Pacemakers are infrequently required after cardiac transplantation in children. Despite not meeting classic symptomatic sinus bradycardia criteria, pacemaker placement should be considered post-transplantation in patients with episodic sinus pauses and dizziness or syncope. Patients who present with the aforementioned symptoms or high-grade AV block should be evaluated closely for the presence or development of transplant coronary artery disease, as it may be their first symptom.

Bradycardia↗