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Biomedical subjects

W A Shapiro

Publications and source records attributed to W A Shapiro.

8 recordsLinked to original sources
PubMed1987

Hemodynamic and electrophysiologic effects of encainide in patients with bundle branch block.

Electrophysiologic studies were performed in 6 consecutive patients with bundle branch block and organic heart disease. All were studied after intravenous (0.9 mg/kg) encainide and 3 of the 6 after 36-72 hours of oral encainide (50 mg every 6 hours). After intravenous encainide, mean H-Q increased from 51 +/- 20 msec to 58 +/- 25 msec (14% p less than or equal to .05). After oral encainide (3 patients) H-Q increased to 90 +/- 39 msec (56% p less than or equal to .05, compared to baseline). Programmed ventricular stimulation was performed in 5. In 1 patient without spontaneous ventricular tachycardia, tachycardia was non-inducible before and after encainide. Of 5 patients with spontaneous arrhythmia, 3 had ventricular tachycardia induced before and after intravenous encainide at mean cycle lengths of 287 +/- 130 msec and 407 +/- 261 msec, (not significant) respectively, while 1 had ventricular tachycardia induced only after encainide. Four patients began chronic treatment with oral encainide (2 patients with inducible rapid ventricular tachycardia after encainide were excluded). All suffered major adverse outcomes. One died suddenly after an electrophysiology study demonstrated inducible ventricular tachycardia, which occurred only after encainide. One experienced new syncope after baseline H-Q increased 75% after encainide. Two patients developed new sustained atrial tachycardias and 1 patient developed persistent ventricular tachycardia on encainide.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1985

Electrophysiologic and anatomic changes in the atrioventricular junction of dogs after direct-current shocks through tissue fixation catheters.

Barb-tipped fixation electrode catheters were inserted under fluoroscopic control in the region of the atrioventricular (AV) node in 6 dogs. A series of direct-current shocks (20 to 240 J) were delivered from the electrode catheter to a back plate. Serial electrophysiologic studies were performed before and 2 to 3 weeks after delivery of the shocks. In general, low-energy shocks--20 to 180 J--resulted in predominant damage to the approaches to the AV node, the AV node and common bundle, whereas larger shocks created diffuse damage involving the His bundle and bundle branches. Despite histologic damage to the AV junction, only minimal changes in AV conduction were observed. Thus, there is a large safety margin for AV conduction.

Animals↗
PubMed1985

Electrophysiologic testing in patients with the long QT syndrome.

Electrophysiologic studies were performed in 15 patients with syncope and/or cardiac arrest who had the long QT syndrome and 11 control subjects who had normal QT intervals. The syndrome was familial in five patients and idiopathic in 10. All patients had a prolonged QT (546 +/- 68 msec, mean +/- SD) and corrected QT (550 +/- 51 msec). Incremental atrial pacing at cycle lengths of 600 to 400 msec resulted in shortening of the QT interval, but there was no significant difference in the magnitude or percent of shortening of the QT interval between patients with the long QT syndrome and control subjects. Intravenous propranolol did not influence the QT interval measured at fixed atrial-paced cycle lengths in patients with either the familial or idiopathic form of the syndrome. Programmed right and left ventricular stimulation with up to three extrastimuli before and during isoproterenol infusion did not induce sustained ventricular tachycardia or ventricular fibrillation in any of the patients. However, rapid polymorphic nonsustained ventricular tachycardia was induced in six of the 15 patients (40%). Neither the inducibility of nonsustained ventricular tachycardia nor the results of electropharmacologic testing with beta-blockers proved to be of any prognostic value during the mean follow-up period of 28 +/- 17 months. Electrophysiologic studies are of limited value in the diagnosis and treatment of patients with the long QT syndrome.

Adolescent↗
PubMed1985

Intraoperative detection of myocardial ischemia in high-risk patients: electrocardiography versus two-dimensional transesophageal echocardiography.

Because acute segmental wall motion abnormalities (SWMAs) of the left ventricle are highly sensitive and specific indicators of myocardial ischemia, this study compared the incidence and significance of ischemia, as detected by two-dimensional transesophageal echocardiography and surface electrocardiography, during anesthesia and surgery in patients at high risk of myocardial ischemia. During surgery, 24 of the 50 patients studied had new SWMAs, whereas only six had ST segment changes. All patients with ST segment changes also had new SWMAs: in three instances, SWMAs occurred before the ST segment change, and in three instances, they occurred simultaneously. All three patients who had intraoperative myocardial infarctions also had persistent intraoperative SWMAs, whereas only one patient had ST segment changes. Ten healthy patients requiring noncardiovascular surgery were monitored similarly; none of these had SWMAs, ST segment changes, or myocardial infarction. This study demonstrates the superiority of two-dimensional transesophageal echocardiography over electrocardiography for the intraoperative detection of myocardial ischemia. Furthermore, when new SWMAs persist to the conclusion of surgery, myocardial infarction is likely to have occurred.

Echocardiography↗
PubMed1984

Bupivacaine-induced cardiac arrhythmias in sheep.

Controversy persists about the cardiac toxicity of bupivacaine if accidentally administered intravenously during regional anesthesia. Using awake, unanesthetized sheep, we evaluated the cardiac effects of low and high equivalent doses of lidocaine and bupivacaine given intravenously over 10 s. All animals convulsed within 30 s of injections. Although both drugs significantly increased heart rate and systemic and pulmonary arterial blood pressure for up to 10 min, cardiac output was affected variably. The magnitude of hemodynamic changes that each drug produced did not differ significantly from each other at either dose level. However, of the sheep receiving intravenous lidocaine, none developed arrhythmias other than mild sinus tachycardia and minimal ST-T wave changes (which occurred in 25% of the animals). After intravenous bupivacaine injection, all sheep had transient changes on the EKG and/or arrhythmias (e.g., supraventricular tachycardia; atrioventricular condition blocks; ventricular tachycardia; multiform premature ventricular contractions; wide QRS complexes; ST-T wave changes; and in one animal, fatal ventricular fibrillation). Normal sinus rhythm usually returned within 8-10 min. Arterial blood gas and acid-base values stayed within the normal range during the studies, and serum potassium did not change significantly from control. In conclusion, in conscious adult sheep, equivalent doses of lidocaine or bupivacaine produced similar central nervous system (CNS) toxicity when rapidly injected intravenously. In the absence of marked hypoxia, respiratory or metabolic acidosis, hyperkalemia, or hypotension, serious cardiac arrhythmias occurred after bupivacaine but not lidocaine.

Animals↗
PubMed1983

Extent of atrial participation in atrioventricular-reciprocating tachycardia.

Twenty-one patients with atrioventricular (AV) bypass tracts underwent electrophysiologic studies. The bypass tract was left-sided in 15 patients, septal in five and right-sided in one patient. Orthodromic AV-reciprocating tachycardia was induced in all 21 patients, with a mean tachycardia cycle length of 342 +/- 59 msec. The introduction of single stimuli in the high right atrium during tachycardia resulted in simultaneous dissociation of the high right atrial and low septal atrial electrograms in nine patients. In six patients, high right atrial overdrive pacing during tachycardia resulted in simultaneous dissociation of the high right atrial and low septal atrial electrograms for two to five consecutive beats. All patients in whom the low septal atrial electrogram was dissociated from the tachycardia had a left-sided bypass tract. In no patient was the coronary sinus atrial electrogram dissociated from the tachycardia by high right atrial pacing. Dissociation of the low septal atrial electrogram (as recorded in the His bundle electrogram) from AV-reciprocating tachycardia suggests that the portion of the right atrium adjacent to the AV node may not be a necessary link in the tachycardia circuit. This observation suggests that the site of entry of left-sided impulses into the AV node may be different from that of right-sided impulses.

Cardiac Pacing, Artificial↗
PubMed1983

Effects of verapamil on ventricular tachycardias possibly caused by reentry, automaticity, and triggered activity.

To define the role of verapamil in the treatment of ventricular tachycardia (VT), we studied 21 patients with chronic recurrent VT. Electrophysiologic studies were performed before and during intravenous infusion of verapamil (0.15 mg/kg followed by 0.005 mg/kg per min). On the basis of the mode of VT initiation and termination, we identified three groups of patients: (a) 11 patients had VT suggestive of reentry, as VT could be initiated with ventricular extrastimulation and terminated with overdrive ventricular pacing. Verapamil did not affect the inducibility and cycle length of VT. (b) 7 patients had VT suggestive of catecholamine-sensitive automaticity as VT could not be initiated with programmed electrical stimulation but could be provoked by isoproterenol infusion. Moreover, the VT could not be converted to a sustained sinus rhythm with overdrive ventricular pacing and it resolved only with discontinuing isoproterenol infusion. Verapamil exerted no effects on VT. (c) 3 patients had VT with electrophysiologic characteristics suggestive of triggered activity related to delayed afterdepolarizations. Characteristically, after attaining a range of cycle lengths, the sinus, atrial or ventricular paced rhythm could initiate VT without ventricular extrastimulation. The first beat of VT invariably occurred late in the cardiac cycle with a premature coupling interval 0-80 ms shorter than the preceding QRS cycle length; the premature coupling interval gradually decreased as the sinus, atrial or ventricular paced cycle length progressively shortened. Of note, verapamil completely suppressed VT inducibility in these three patients. These observations lead us to suggest that verapamil does not affect VT caused by reentry and catecholamine-sensitive automaticity but is effective in suppressing VT caused by triggered activity related to delayed afterdepolarizations in humans.

Adolescent↗