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Biomedical subjects

J C Luck

Publications and source records attributed to J C Luck.

At least 19 recordsLinked to original sources

Observations on induction and termination of paroxysmal supraventricular tachycardia by external pacing.

Paroxysmal supraventricular tachycardia (PSVT) can be reproducibly induced and terminated by critically timed atrial or ventricular depolarizations. In this study, noninvasive transcutaneous (external) cardiac pacing (NTCP) was compared to endocardial ventricular pacing for the termination and induction of PSVT. In 24 patients, either atrioventricular (AV) nodal reentrant tachycardia or AV reciprocating tachycardia was reproducibly terminated with either critically timed ventricular depolarizations or overdrive ventricular pacing from an endocardial right ventricular site. There were 32 trials of NTCP attempts to interrupt PSVT in the 24 patients. External pacing was successful at terminating PSVT in 23 patients and in 30 of 32 (94%) trials. In 20 patients, there were 26 trials of external pacing attempts to induce PSVT. External pacing initiated PSVT in 21 of 26 trials (81%). The pacing sequences used to induce and terminate PSVT with external pacing were copied from the endocardial sequences. The external pacing threshold averaged 77 +/- 22 mA but the current needed to terminate PSVT was about 1.5 greater than threshold at 117 +/- 27 mA. Serial external pacing studies were performed in seven patients. The thresholds for external pacing were similar from trial to trial as were the mode of termination and induction between the endocardial and external methods. External pacing can terminate most AV reciprocating tachycardias and many AV nodal reentrant tachycardias. It appears promising as a means of inducing PSVT. However, the high stimulation amplitudes needed will prohibit wide acceptance of external pacing for induction and termination of PSVT.

Adult

Acute myocarditis in fulminant systemic sclerosis.

Myositis and myocarditis have been reported in progressive systemic sclerosis, and these patients have had favorable therapeutic responses to intravenous pulse methylprednisolone. Thus far, premortem biopsy documentation of myocarditis and myocardial fibrosis has not been reported in such patients. We report the case of a patient with subacute congestive heart failure six months after she developed Raynaud's phenomenon. Clinical examination was typical of scleroderma but there was no proximal muscle weakness. She had elevated creatine kinase and MB-creatine kinase and laboratory evidence of hypothyroidism. Echocardiogram demonstrated four-chamber dilatation and severe left ventricular dysfunction. Cardiac catheterization revealed normal epicardial coronary arteries and severely decreased cardiac index. A skin biopsy specimen of the forearm was consistent with diffuse systemic sclerosis, and an endomyocardial biopsy specimen demonstrated mild fibrosis and lymphocytic infiltrate. Her heart failure initially improved with digoxin, furosemide, and enalapril. She also received L-thyroxine and intravenous methylprednisolone. The heart failure progressed over the next six weeks and she died. Patients with scleroderma and new-onset heart failure may have acute myocarditis.

Acute Disease

Clarification.

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Cardiac Pacing, Artificial

Clinical applications of external pacing: a renaissance?

It is nearly 40 years since the first reports of noninvasive external pacing for Stokes-Adams syncope. Despite the ease and safety, this method of pacing has yet to flourish despite a recent interest by several authors. At present, external pacing seems best suited for temporary pacing situations that arise as an emergency or for purely prophylactic indications. External pacing is the preferred method of pacing recommended in the advanced cardiac life support guidelines. However, most emergency room and prehospital cardiac arrest trials have not shown any significant benefit from early application of external pacing. The indications have been broadened to include symptomatic bradycardia and termination of some ventricular tachycardias. It may be useful for the termination of AV reciprocating tachycardia and AV nodal reentrant tachycardia. There is a vision that external pacing may be used for serial electrophysiological testing of antiarrhythmic agents. However, there is little data in this regard. More importantly, the external pacing thresholds must be reduced further to allow for sophisticated pacing protocols to be implemented. For practical purposes, external pacing does not capture the atrium. Since the left atrium is easily captured by esophageal pacing, it is likely that noninvasive external pacing will be combined with transesophageal pacing to perform noninvasive electrophysiological testing. The future for external pacing remains in limbo because of the discomfort associated with skeletal muscle contraction. If technical advances can reduce or eliminate this problem, then external pacing may find broader application for bradycardia and tachycardia.

Cardiac Pacing, Artificial

Description of the strength-interval relation with external noninvasive pacing.

The strength-interval relationship obtained by external pacing (EXP) was compared to curves obtained by endocardial pacing from a right ventricular site. There were 17 patients, age 45 +/- 17 years. Effective and functional ventricular refractory periods (ERP, FRP) were determined during a ventricular drive train of 8 stimuli at a cycle length 500 msec. Endocardial pacing threshold current averaged 0.5 +/- 0.3 mA (range 0.2-1.0 mA) and EXP threshold current averaged 64 +/- 14 mA (range 40-80 mA). At twice threshold, endocardial ventricular ERP was 235 +/- 32 msec and FRP was 262 +/- 29 msec. At 10 mA above threshold, EXP ventricular ERP was 276 +/- 29 msec and was significantly longer than endocardial ERP at twice threshold (P less than 0.001). EXP ventricular FRP shortened to 237 +/- 39 msec at twice threshold and was similar to endocardial ERP (P = 0.55). EXP ventricular FRP was significantly longer than endocardial ERP (280 +/- 29 vs 262 +/- 29 msec, P less than 0.001) at twice threshold. EXP strength-interval curves were similar to endocardial curves in 14 of 17 (82%) patients. We conclude, that at twice threshold, similar coupling intervals can be obtained with both endocardial and EXP. Therefore, EXP can provide critically coupled extrastimuli for programmed ventricular stimulation.

Adolescent

Amiodarone: a postmarketing evaluation of monitoring for drug-induced toxicity.

Amiodarone, an antiarrhythmic drug with predominantly class III effects, has demonstrated serious adverse drug reactions and interactions. The Departments of Pharmacy and Cardiology retrospectively evaluated the monitoring parameters at this institution. Criteria based on current literature were developed. Twenty-six patients were administered amiodarone, qualifying for entry into the audit. Of these patients, seven were excluded because their medical records were unavailable or incomplete. The 19 eligible patients were hospitalized during initiation of therapy and followed in the Outpatient Cardiology Clinic. The collected data extracted from the medical charts were compared with the following elements of the criteria selected: baseline evaluation prior to the start of therapy; monitoring for signs of pulmonary, hepatic, thyroid, cardiac, ophthalmologic, neurologic, and dermatologic toxicity; and evaluation of potential drug interactions with digoxin and warfarin-type anticoagulants. The percentage of criteria elements appropriately monitored on each patient ranged from 82 to 100 percent, with an average of 91 percent. The most frequently overlooked parameters were warning the patient of a possible photosensitivity reaction, decreasing the digoxin dose if the patient was concurrently taking amiodarone, and performing a slit-lamp examination every six months. Frequent examination of the patient's total organ system and laboratory tests, in addition to patient education, are essential to safe monitoring of amiodarone therapy.

Amiodarone

Termination of sustained ventricular tachycardia by external noninvasive pacing.

Cardiac pacing has proven useful in the termination of sustained ventricular tachycardia (VT). In this study, the effectiveness of external noninvasive temporary pacing was compared with traditional endocardial burst ventricular pacing for the termination of sustained and hemodynamically stable VT. In 14 patients, 16 VT morphologies induced by programmed right ventricular extrastimulation were reproducibly terminated by endocardial burst pacing (3 to 9 complexes). VT cycle lengths averaged 392 +/- 97 ms (standard deviation) and ranged from 300 to 690 ms. The endocardial burst pacing cycle length used to terminate VT averaged 298 +/- 93 ms (range 220 to 600 ms). External burst pacing terminated 14 of 16 VT morphologies (88%). The pacing cycle length used to terminate these 14 VTs averaged 282 +/- 44 ms. The number of ventricular captures ranged from 5 to 20 beats. Failure to terminate 2 VT morphologies probably represented a failure of the device to capture the ventricle. Acceleration of VT occurred in 1 patient with burst external noninvasive pacing. These observations suggest that external burst pacing may be an effective means of terminating sustained VT in some patients.

Aged

Clinical suppression of refractory ventricular tachycardia with oral bretylium not predicted by electrophysiologic drug testing.

We report the findings in a patient in whom intravenous bretylium was the only effective agent to suppress refractory ventricular tachycardia and ventricular fibrillation. After attempts to switch the patient to amiodarone and bethanidine (an oral analogue of bretylium) caused proarrhythmic effects, he was successfully converted to oral therapy with bretylium. Electrophysiologic testing was not predictive of the clinical response from oral bretylium. To our knowledge, this is the first report of a proarrhythmic effect from bethanadine and it suggests a divergence in the actions of various class 3 antiarrhythmic agents.

Administration, Oral

Two different patterns of entrainment of ventricular tachycardia.

In a patient with two morphologic forms of ventricular tachycardia, rapid pacing from different ventricular sites produced two distinctively different patterns of entrainment. Pacing from sites contralateral to the site of emergence of ventricular tachycardia caused progressive fusion. Following pacing, the interval (return interval) between the first tachycardia beat (return beat) and the preceding beat was equal to the pacing cycle length. Near the site of emergence, the local electrogram of the return beat was morphologically identical to that of the preceding paced beats. In contrast, pacing from sites ipsilateral to the site of emergence did not cause fusion. The return intervals increased with decreasing pacing cycle lengths. The local electrogram of the return beat was morphologically different from that of the preceding paced beats. Using a model of ventricular reentrance, both patterns of responses can be explained. Pacing impulses arising from sites contralateral to the site of emergence activate the latter orthodromically. Fusion occurs between the emerging tachycardia wavefront and the next pacing wavefront. In contrast, pacing impulses arising from sites ipsilateral to the site of emergence activate the latter antidromically. Fusion is not observed because collision within the area of slow conduction prevents the emergence of the tachycardia during pacing.

Adult

Termination of sustained tachycardia by external noninvasive pacing.

Invasive cardiac pacing has proved useful in the induction and termination of reentrant sustained tachycardias. In one of our two cases, programmed ventricular extra-stimulation was used to induce sustained ventricular tachycardia from the endocardial surface of the right ventricle. Induced ventricular tachycardia was terminated by burst ventricular pacing with an external cardiac pacemaker. In our second patient, external pacing was effective at inducing and terminating sustained supraventricular tachycardia. These patients illustrate that the principles of terminating sustained reentrant tachycardia with invasive pacing may also apply to noninvasive external pacing. The usefulness of this approach in treating reentrant tachycardias needs further evaluation.

Adult

Emergency defibrillation using a temporary pacing electrode catheter.

Direct application of electrical current to the heart utilizing special equipment such as implantable defibrillators or specially designed catheters has been useful in patients with recurrent ventricular tachyarrhythmias. We describe a patient who developed intractable ventricular fibrillation (VF) during the course of electrophysiologic testing. VF continued for 50 minutes, during which time multiple transthoracic shocks of 360 joules failed to convert the arrhythmia. Intracardiac shocks were then delivered via a transvenous 6 French standard quadripolar pacing catheter positioned in the right ventricular apex by direct application of the defibrillator paddle to the catheter, with the patient lying on the posterior paddle. Energy of up to 300 joules failed to defibrillate the patient, but use of 360 joules delivered in this fashion defibrillated the patient twice. Despite the protracted time of cardiac arrest, the patient recovered without sequelae. We report this case to demonstrate that VF refractory to transthoracic defibrillation may be converted by intracardiac shocks using a temporary pacing catheter without special equipment.

Cardiac Catheterization

Diagnostic implications of atrial vulnerability.

Extrastimulation in the atrial vulnerable zone may result in atrial fibrillation or flutter (AFF), especially with stimulation of multiple atrial sites. However, the clinical relevance of such vulnerability to AFF is unknown. Therefore, single twice-threshold extrastimuli were applied at three disparate right atrial sites in 45 consecutive unmedicated patients without overt heart failure. Group I consisted of 12 patients with documented spontaneous paroxysms of AFF. AFF was duplicated in 9 to 12 patients using extrastimulation in the vulnerable zone (5 in sinus rhythm, 4 requiring atrial pacing at 120 beats/min). Group II consisted of 33 patients without documented AFF dispite monitoring. Vulnerability to AFF was found in 12 of 33 patients (4 in sinus rhythm, 8 requiring atrial pacing). The duration of induced AFF did not discriminate between the two groups. Among the 12 Group II patients vulnerable to AFF, 3 had rapid palpitations, 2 had undiagnosed rapid tachycardias, 1 had atrial tachycardias and 1 junctional tachycardias. In vulnerable patients, the pause after AFF correlated with the pause after atrial pacing, but only 1 of 11 Group II patients with sick sinus syndrome was vulnerable. Thus, paroxysmal AFF may be duplicated with the extrastimulus technique if sufficient arial sites are stimulated, providing a model for evaluation of these arrhythmias. But atrial vulnerability, even to extrastimulation at normal heart rates, may be seen in patients suspected of atrial tachyarrhythmia in the absence of documented AFF, and does not contribute to the diagnosis of sinoatrial dysfunction.

Atrial Fibrillation

Dispersion of atrial refractoriness in patients with sinus node dysfunction.

Abnormal atrial refractoriness was examined as a cause of atrial fibrillation/flutter (AFF) in patients with bradycardia. Refractory periods at three disparate right atrial sites were compared in 17 patients with sinus node dysfunction (SND) and 16 controls. Atrial pacing shortened refractory periods, but failed to decrease dispersion of refractoriness significantly. During sinus rhythm, duration and dispersion of refractoriness were greater in SND patients than in controls. These differences persisted with atrial pacing. For example, at the paced rate, dispersion of effective refractory periods in SND patients was greater than in controls (62.9 +/- 34 vs 36.6 +/- 21 msec, p less than 0.01). Six SND patients had AFF, but they did not have greater dispersion than other SND patients, or unusually short or long refractory periods. Thus, prolonged and nonuniform refractoriness were features of SND. Abnormal refractoriness in SND reflected atrial disease and persisted with pacing. These abnormalities were not unique to patients with AFF.

Adult

Arrhythmias from fiberoptic bronchoscopy.

The electrocardiogram was monitored in 51 patients during fiberoptic bronchoscopic procedures and was compared to recordings made before premedication. Sixteen of the patients had heart disease. During the bronchoscopic procedure, the heart rate increased by 154 "/- 5 percent (+/- SE). The frequency of atrial ectopic beats was minimally increased, by an average 0.15 +/- 0.12 beats per minute (not significant). Ventricular ectopic beats became less frequent during the bronchoscopic procedure (-0.17 +/- 0.41 beats per minute; not significant), and there was no ventricular tachycardia. Frequent ventricular ectopic beats were seen mainly during bronchoscopic procedures in patients with coronary heart disease, but even in this group, ventricular ectopic beats became less frequent than at rest (-1.13 +/- 1.46 beats per minute; not significant). The nearly uniform sinus tachycardia that was observed was well tolerated but could predispose coronary patients to ischemia; however, the fiberoptic bronchoscopic procedure per se does not enhance prior ectopy.

Adult

The effect of emboli upon intrapulmonary receptors in the cat.

The effect of successive injections (on the activity from pulmonary stretch, irritant and type J receptors) of 0.1 g aliquots of either potato starch or plastic sheres was examined in artificially ventilated, anaesthetized, open chested cats. The discharge from nineteen pulmonary stretch receptors was altered after embolisation and mean maximum changes of 10% were observed in peak frequency and spike count per respiratory cycle. The activity from twelve of fourteen irritant receptors was changed after embolisation, mainly in the form of an increase of an existing, respiratory modulated discharge. O f ten type J receptors examined, six were stimulated after embolisation to produce an erratic pattern of discharge. The response of the three groups of receptors appeared to be independent of the size of the emboli. Histological examination showed scattered emboli in capillaries and columns in arterioles, according to particle size. It is likely that all three receptor types are involved in the reflex tachypnoea induced by pulmonary embolisation, since the changes in afferent vagal discharge occurred at or before the onset of the reflex respiratory events.

Animals