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Biomedical subjects

J C Luck

Publications and source records attributed to J C Luck.

At least 55 records · Page 3Linked to original sources
PubMed1984

Serial electrophysiologic testing with a permanent pacemaker after acute myocardial infarction.

Electrophysiologic testing in patients after acute myocardial infarction may predict subsequent sudden death. We used a permanent pacemaker for repetitive electrophysiologic testing in a patient after acute infarction. Programmed, twice-threshold ventricular extrastimulation at two weeks after anteroseptal infarction failed to induce ventricular tachycardia. Subsequent programmed extrastimulation induced sustained ventricular tachycardia on four occasions (6, 16, 29 and 65 weeks) after infarction. As yet (20 months), spontaneous ventricular tachycardia has not occurred. Firm conclusions cannot be drawn from a single case. However, our patient developed a stable ventricular tachycardia circuit which was not apparent at two weeks. Thus, a single electrophysiologic study performed acutely after infarction may not accurately describe the potential for ventricular tachycardia or fibrillation. Serial electrophysiologic testing with an implantable externally triggered pacemaker may more accurately describe the potential for sudden death post-infarction in a few high-risk patients. This report shows that induction of ventricular tachycardia after acute infarction may not predict outcome.

Adult↗
PubMed1984

The clinical significance of ventricular arrhythmias after myocardial infarction.

Based on a sound foundation of data in thousands of patients who underwent ambulatory ECG recording after myocardial infarction, it is clear tht ventricular arrhythmias are harbingers of sudden cardiac death. Ambulatory electrocardiography, usually performed for 24 hours, continues to be the standard by which clinicians can identify patients at risk for sudden cardiac death after acute myocardial infarction. Ideally, this test should be performed in the late hospitalization phase of acute myocardial infarction, usually 1 to 2 days prior to discharge from the hospital, and the results made known to the clinician prior to the patient's departure from the hospital. Although performed less frequently, low-level exercise testing prior to discharge from the hospital has been shown in some studies to be of prognostic value in defining a group at high risk for sudden cardiac death. This test offers the additional benefit of allowing the clinician to more knowledgeably prescribe an exercise regimen after hospitalization. The specific role of electrophysiologic testing is presently under clinical investigation. At present, only patients with documented spontaneous sustained ventricular tachycardia or sudden cardiac death after myocardial infarction should be candidates for this study. Although it may be possible in the future that electrophysiologic testing will also be used in patients with high-risk arrhythmia detected on ambulatory electrocardiography, at present this is the subject of clinical investigation in academic medical centers and is not recommended as part of standard therapy.

Ambulatory Care↗
PubMed1984

Investigational antiarrhythmic drugs for the treatment of ventricular rhythm disturbances.

Currently available antiarrhythmic drugs possess very poor therapeutic-to-toxic ratios, and therefore, there is a great deal of interest in the development of new investigational agents to suppress ventricular rhythm disturbances. This article includes most of the investigational ventricular antiarrhythmic drugs in which there has been a great deal of recent active investigation and interest. It stresses the different patient populations that have been tested with each of these antiarrhythmic drugs, pointing out those drugs that have been documented to be effective in nonsustained ventricular tachycardia or sustained ventricular tachycardia and sudden cardiac death.

Amiodarone↗
PubMed1983

Induction of clinical ventricular tachycardia using programmed stimulation: value of third and fourth extrastimuli.

Initiation of ventricular tachycardia (VT) by right ventricular extrastimulation was analyzed in 142 consecutive patients, 53 with electrocardiographically documented episodes of spontaneous VT or ventricular fibrillation (VF) and 68 with no spontaneous VT or VF; 21 patients with a history of sudden death but no documented arrhythmia were excluded from further analysis. All patients received 1 to 4 extrastimuli (S2, S3, S4 and S5) during pacing at fixed cycle lengths of 600 or 500 msec at 1 or 2 right ventricular sites. Clinical VT was reproduced by extrastimulation in 28 of 43 patients (65%) with sustained VT and in 0 of 10 patients with nonsustained VT. Clinical VT was induced by S2 or S3 in 16 patients and by S4 or S5 in 12 patients. Ventricular burst pacing reproduced clinical VT in 3 other patients. Nonclinical VT, which was most often polymorphic and nonsustained, was induced in 24 of 121 patients (20%), in 11 by S2 or S3 and in 13 by S4 or S5. Ventricular burst pacing induced nonclinical VT in 4 other patients. In patients with spontaneous sustained VT, the use of S4 and S5 in the right ventricle increases the yield of inducible clinical VT compared with use of S2 and S3 alone, but at a cost of increased induction of nonclinical VT. Frequent induction of nonclinical VT limits the interpretation of the results of such stimulation in patients without previously documented VT.

Adult↗
PubMed1983

Effect of whiskey on atrial vulnerability and "holiday heart".

Vulnerability to atrial fibrillation and flutter was examined in 11 alcohol abusers who did not have cardiomyopathy or manifest heart failure. Atrial extrastimulation was done with rapid pacing (drive cycle length 500 ms) to facilitate induction of atrial vulnerability, seen in four alcohol abusers. The remaining seven were retested 30 minutes after drinking 60 to 120 ml of 86 proof whiskey (ethanol blood levels were 49 to 101 mg/100 ml but pulmonary capillary wedge pressure remained normal in all) and atrial fibrillation or flutter was induced in three of the drinkers. Three nondrinkers, symptomatic with sinus bradycardia but not in heart failure, were found not to be vulnerable to atrial fibrillation or flutter, but flutter was induced in two of the three after drinking whiskey. Whiskey did not alter atrial functional refractory periods (mean +/- standard error of the mean 297 +/- 14 to 290 +/- 12 ms) or widen the dispersion among three disparate right atrial sites (57 +/- 13 to 47 +/- 12 ms). Thus, whiskey enhanced vulnerability to atrial fibrillation and flutter in patients without heart failure or cardiomyopathy, substantiating the "holiday heart" syndrome.

Adult↗
PubMed1983

Analysis of ambulatory electrocardiograms in 15 patients during spontaneous ventricular fibrillation with special reference to preceding arrhythmic events.

Fifteen patients sustained ventricular fibrillation during ambulatory electrocardiographic recording in a period of 3.5 years over which time 16,500 ambulatory electrocardiograms were analyzed (prevalence = 0.09% or 1/1,100). Eight patients died, and seven survived cardiopulmonary resuscitation. Quantitative analysis of hourly ventricular arrhythmias prior to ventricular fibrillation revealed an increased frequency of premature ventricular beats and ventricular tachycardia, especially in the 2 hours immediately before ventricular fibrillation. Ventricular fibrillation was initiated by ventricular tachycardia in all 15 cases. These runs of ventricular tachycardia were characterized by their unusual length (mean = 560 +/- 536 beats) and their rapid rate (241 +/- 45 beats/min). Although an R on T premature ventricular beat initiated ventricular tachycardia and ventricular fibrillation occasionally, the mean prematurity index of the initiating premature ventricular beat was not early (mean = 1.27 +/- 0.28). QT prolongation was present in only 3 of the 15 patients (mean QTc interval = 0.42 +/- 0.06). Left ventricular dysfunction (mean left ventricular ejection fraction = 34.9 +/- 9.9%) and coronary artery disease were nearly always present. The cardiac medications most frequently associated with these patients at the time of ventricular fibrillation were digitalis and quinidine.

Aged↗
PubMed1982

Rapid attenuation of response to nifedipine in primary pulmonary hypertension.

In a 22-year-old woman with primary pulmonary hypertension resistant to all previous attempts to reduce the pulmonary vascular resistance, there was dramatic improvement after the first dose of nifedipine, 20 mg po, which was not sustained with subsequent doses. While there was a persistent reduction in systemic vascular resistance, the initial drug-related reduction in pulmonary vascular resistance was progressively attenuated with the subsequent four doses of nifedipine, 20 mg.

Adult↗
PubMed1980

Modification of ventricular tachycardia by procainamide in patients with coronary artery disease.

Fifteen consecutive patients with coronary artery disease had rapid (158 to 272 beats/min) and sustained ventricular tachycardia induced by the extrastimulus technique, and received procainamide infusion. Before the study, all but one patient had severe symptoms with tachycardia, and six had survived apparent sudden death. Procainamide consistently slowed ventricular tachycardia. However, in traditional doses (1 g infusion, plasma concentration greater than 4 micrograms/ml), it prevented induction of ventricular tachycardia in only 2 of the 15 patients. Induction of ventricular tachycardia was facilitated by procainamide in 10 patients. Larger doses of procainamide (plasma concentration 20.2 micrograms/ml +/- 9.7 [mean +/- standard deviation]) prevented induction of ventricular tachycardia in one of eight patients. Rapid ventricular rates (more than 210 beats/min) that were not slowed (by 50 percent or more) after a 1 g infusion of the drug predicted failure of procainamide to prevent ventricular tachycardia. Therefore, procainamide slowed but did not prevent induced ventricular tachycardia in most of these patients with coronary artery disease at risk of sudden death.

Adult↗
PubMed1979

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↗
PubMed1979

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↗
PubMed1978

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↗
PubMed1976

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↗