Biomedical subjects
M G Kienzle
Publications and source records attributed to M G Kienzle.
Electrophysiologic evaluation and follow-up characteristics of patients with recurrent unexplained syncope and presyncope.
One hundred nineteen patients with unexplained syncope (82%) or presyncope (18%) underwent complete electrophysiologic study (EPS). Symptoms were recurrent in 72% of the patients. Fifty-two percent of the patients had structural heart disease. Forty-one patients had normal EPS results and 78 had electrophysiologic abnormalities (ventricular tachycardia in 31, induced atrial flutter/fibrillation in 17, vasovagal syncope in 8, hypersensitive carotid sinus syndrome in 7, supraventricular tachycardia in 6, heart block in 5 and sick sinus syndrome in 4). The presence of structural heart disease (p = 0.0033) and previous myocardial infarction (p = 0.05) were the only clinical or electrocardiographic predictors of a positive EPS response. Therapy was guided by EPS and patients were followed for 27 +/- 20 months (mean +/- standard deviation). In the patients with negative EPS results, 76 +/- 11% (mean +/- standard error) were symptom-free at follow-up, compared to 68 +/- 10% in the group with positive EPS responses. No clinical variables helped to predict remission in the absence of therapy. One patient in the negative EPS response group and 2 patients in the EPS positive group died suddenly (cumulative survival 94 +/- 4%). Total cardiovascular mortality was 13% in the positive EPS response group, and 4% in the negative EPS response group. Thus, certain clinical characteristics are helpful in selecting patients for study. Electrophysiologically guided therapy is associated with a recurrence and sudden death rate similar to an untreated control group.(ABSTRACT TRUNCATED AT 250 WORDS)
Use of programmed electrical stimulation to predict sudden death after myocardial infarction.
The use of programmed ventricular stimulation to identify patients at risk for sudden cardiac death following myocardial infarction has not yet been firmly established. The repetitive ventricular response following extrastimuli does not appear to be useful in identifying patients at risk and should not be used to guide antiarrhythmic therapy. Similarly, the response to single and/or double ventricular extrastimuli delivered at twice diastolic threshold from a single right ventricular site during normal sinus rhythm and ventricular pacing also does not appear to be helpful in identifying patients at risk for life-threatening ventricular arrhythmias. A more vigorous stimulation protocol that involves more than one right ventricular site and increased current strength may be necessary to elicit a predictive electrophysiologic response. The need for a more vigorous stimulation is suggested by two preliminary studies. Confirmation of initial reports is necessary. The predictive value of the response to programmed ventricular stimulation must be compared with other noninvasive and invasive measurements of left ventricular dysfunction and the degree of spontaneous ventricular ectopy to determine its superiority or to ascertain multiple variables that can be used together to identify those patients most likely to die suddenly after myocardial infarction. Stimulation protocols used during programmed stimulation must have sufficient sensitivity without sacrificing specificity. A concerted effort using uniform stimulation protocols in large numbers of patients is essential to resolve this important clinical problem.
Discordant results of programmed ventricular stimulation at different right ventricular sites in patients with and without spontaneous sustained ventricular tachycardia: a prospective study of 56 patients.
Programmed ventricular stimulation (PVS) was prospectively performed in 56 consecutive patients from both the right ventricular (RV) apex and the RV outflow tract. Thirty-seven patients had documented clinical sustained ventricular tachycardia (VT) and 19 patients had no sustained spontaneous VT in the absence of antiarrhythmic drugs. The sensitivity of VT induction was 65% from the RV apex, 76% from the RV outflow tract and was 89% with combined stimulation at both RV sites. The specificity from the RV apex, the RV outflow tract and both sites combined was 100%. When sustained VT was induced from both sites (51%), it was usually of the same morphologic characteristics, axis and cycle length. When sustained VT was induced at 1 site and nonsustained VT at the second site, the morphologic characteristics or axis usually differed. Of patients who had VT induced at both RV sites during the baseline study 37% had VT rendered noninducible during treatment with conventional antiarrhythmic agents. No patients whose VT was induced at only 1 RV site responded to conventional drugs. We conclude that programmed ventricular stimulation at a second RV site is frequently helpful in the evaluation of VT. Inducibility at only 1 of 2 RV sites predicts a poor response to conventional antiarrhythmic drugs.
Morphologically distinct sustained ventricular tachycardias in coronary artery disease: significance and surgical results.
One hundred patients with drug-refractory recurrent sustained ventricular tachycardia associated with coronary artery disease who underwent mapping-directed subendocardial resection for ventricular tachycardia were retrospectively evaluated with respect to a number of morphologically distinct tachycardias on a 12 lead electrocardiogram. Of 91 operative survivors, 18 patients had only one configuration of tachycardia, whereas 73 (81%) had multiple distinct tachycardia configurations; 36 had multiple configurations clinically. Patients with multiple clinical configurations had a longer mean HV interval (65 +/- 11 versus 53 +/- 10 ms, p less than 0.005) and a higher failure rate of surgery alone (47 versus 25% for single clinical tachycardia, p less than 0.05). The 13 patients whose multiple clinical tachycardias originated in disparate sites in the heart (greater than 5 cm between sites of origin) were less often cured by surgery alone than were those whose multiple tachycardias originated in the same or adjacent sites (83 versus 38% failure rate of surgery alone, p less than 0.05). On the basis of mapping data, multiple configurations of ventricular tachycardia appear to originate in the same or adjacent sites in the majority of patients, although in 16% of patients with multiple tachycardias, the tachycardias originate at widely separated sites.
Limited role of intravenous propafenone hydrochloride in the treatment of sustained ventricular tachycardia: electrophysiologic effects and results of programmed ventricular stimulation.
The electrophysiologic effects and response to programmed ventricular stimulation of intravenous propafenone, an experimental antiarrhythmic agent, were studied in a group of 14 patients with both clinical and induced sustained ventricular tachycardia. Twelve of the 14 patients had not responded to conventional antiarrhythmic drug therapy. Propafenone had no significant effect on sinus cycle length (836 +/- 170 ms before and 750 +/- 124 ms after propafenone), P wave duration (108 +/- 24 ms before and 106 +/- 23 ms after propafenone) or PR interval (181 +/- 45 ms before and 194 +/- 53 ms after propafenone). QRS duration and ventricular effective refractory periods increased significantly (109 +/- 20 to 130 +/- 21 ms and 235 +/- 24 to 256 +/- 19 ms, respectively). Ventricular tachycardia remained inducible or occurred spontaneously in 13 of 14 patients after propafenone administration. Neither mode of initiation nor mode of termination of ventricular tachycardia was predictably altered. Additional forms of ventricular tachycardia were seen in six patients. Cycle length of ventricular tachycardia was 303 +/- 73 ms before and 346 +/- 143 ms after propafenone (p = NS). In conclusion, intravenous propafenone does not significantly affect sinus rate, intraatrial conduction or atrioventricular conduction. Ventricular refractoriness and intraventricular conduction are prolonged. The mode of initiation, mode of termination and ventricular tachycardia cycle length are not predictably altered, but ventricular tachycardia occasionally occurs spontaneously after propafenone. Intravenous propafenone rarely prevents induction of ventricular tachycardia in patients with sustained ventricular tachycardia refractory to conventional antiarrhythmic agents.
Subendocardial resection for ventricular tachycardia: predictors of surgical success.
We retrospectively evaluated the first 100 patients who underwent mapping-guided subendocardial resection (SER) at our hospital for drug-refractory sustained ventricular tachycardia caused by coronary artery disease. There were 91 survivors of surgery with 200 morphologically distinct types of ventricular tachycardia. Eighty-three patients (91%) were cured of ventricular tachycardia by SER alone (60 patients or 66%) or by SER in combination with antiarrhythmic drug therapy (23 patients or 25%) (mean follow-up, 28 +/- 19 months). There were four late sudden deaths and four patients continued to have rare episodes of spontaneous ventricular tachycardia after surgery despite receiving antiarrhythmic drugs. Factors associated with failure of SER alone to cure ventricular tachycardia were presence of disparate sites of ventricular tachycardia origin (greater than 5 cm between mapped sites of origin; 64% vs 30% failure rate) and presence of multiple morphologically distinct spontaneous tachycardias (47% vs 25% failure rate). A log-linear model of multivariate analysis identified disparate sites of origin of ventricular tachycardia and the absence of a discrete left ventricular aneurysm as the only independent variables associated with failure of surgery alone. Inferior wall site of origin (41% vs 12% failure) and right bundle branch block morphology of ventricular tachycardia (20% vs 7% failure) were also significantly associated with failure of surgery to cure ventricular tachycardia. Mapping-guided SER is a highly effective mode of treatment for drug-refractory ventricular tachycardia, despite the existence of subgroups of patients with higher-than-average surgical failure rates.
Intraoperative endocardial mapping during sinus rhythm: relationship to site of origin of ventricular tachycardia.
Mapping-guided endocardial resection has proved to be an effective therapy for recurrent sustained ventricular tachycardia. However, some patients cannot be mapped during ventricular tachycardia, so that guidance from findings during normal sinus rhythm would be highly desirable. We examined the frequency, timing, and duration of several abnormal types of electrograms recorded endocardially during sinus rhythm and related these findings to activation mapping during sustained ventricular tachycardia. Thirteen patients with extensive myocardial infarction complicated by recurrent sustained ventricular tachycardia were studied intraoperatively during sinus rhythm and induced ventricular tachycardia with a standardized mapping scheme involving the entire endocardial surface. Fractionated electrograms (multicomponent with amplitude less than 1 mV and duration greater than 50 msec) were recorded in all patients. This type of electrogram could be recorded at up to 36% of mapped sites. Split electrograms (two components separated by isoelectric period) were also frequently seen but involved only a mean of 5.8% of mapped sites. Late electrograms (inscribed entirely after the QRS complex) were only recorded in four of 13 patients at a mean of 5% of mapped sites. The location of these electrograms was related to an arbitrary 8 cm2 zone around the earliest site of endocardial activation recorded during ventricular tachycardia. The longest fractionated electrogram was closely related to nine of 22 morphologies of induced ventricular tachycardia, split electrograms were related to seven of 16 morphologies, and late electrograms to two of four morphologies. We have concluded that extremely abnormal electrograms recorded endocardially during sinus rhythm are widespread in patients with extensive myocardial infarction complicated by ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)
Antiarrhythmic drug therapy for sustained ventricular tachycardia.
VT may be observed to accompany a wide variety of heart diseases and occasionally no heart disease at all. The efficacy of drug therapy is dependent on antiarrhythmic effects and the mechanism underlying the patient's VT. Conventional antiarrhythmic agents appear to be effective in no more than one third of patients, but a substantial number of other potentially useful antiarrhythmic agents exist. Unfortunately, their effectiveness in treating sustained VT for the most part must still be proved. Other agents such as amiodarone appear effective, but ways to predict which patients will benefit remain unknown. Invasive and noninvasive techniques exist for assessing therapeutic efficacy, but determination of which is more appropriate awaits a wider experience and more direct comparison.
Programmed ventricular stimulation at a second right ventricular site: an analysis of 100 patients, with special reference to sensitivity, specificity and characteristics of patients with induced ventricular tachycardia.
One hundred patients without ventricular tachycardia (VT) initiated from the right ventricular (RV) apex were subjected to stimulation at the RV outflow tract. Sixty-two patients had no clinical arrhythmias, and 38 had sustained VT, ventricular fibrillation (VF) or cardiac arrest. Of the 38 patients with clinical arrhythmias, 22 (58%) had VT or VF induced from the RV outflow tract. Among the 62 patients without arrhythmias, 5 (13%) had polymorphic nonsustained VT or VF induced, which occurred with triple extrastimuli in all 5 patients. The 22 patients with VT initiated at the RV outflow tract were a heterogeneous group; 10 (45%) patients had cardiac diagnoses other than coronary artery disease (CAD). In contrast were patients whose VT was initiated at the RV apex (n = 84); in this group, 20 patients (22%) had diagnoses other than CAD (p less than 0.05). These 22 patients also were younger (mean age 46 years) than patients whose VT was initiated at the RV apex (mean age 58; p less than 0.01). Of the 16 patients with clinical VT and no induced arrhythmia from either RV site, 7 had CAD (4 with cardiac arrest), 5 had the long QT syndrome, 3 had dilated cardiomyopathy and 1 had valvular heart disease. In conclusion, stimulation at a second RV site increases the sensitivity of RV stimulation in patients with known VT and seldom initiates VT in patients without clinical VT.
Clinical characteristics and long-term follow-up in 119 survivors of cardiac arrest: relation to inducibility at electrophysiologic testing.
Electrophysiologic studies were performed in 119 survivors of cardiac arrest. Sustained ventricular arrhythmias were initiated by programmed ventricular stimulation in 72 patients (61%). Coronary artery disease patients with induced sustained ventricular arrhythmias had a higher incidence of prior myocardial infarction (95 versus 72%) and ventricular aneurysm (59 versus 28%) and a lower ejection fraction (37 versus 50%) than those with no inducible sustained ventricular arrhythmias. Of the 72 patients with inducible ventricular arrhythmias, 11 (15%) died suddenly during a mean follow-up of 18 months (range 15 days to 58 months). In this group, 6 of 41 patients (15%) discharged on a successful antiarrhythmic regimen and 5 of 27 patients (19%) discharged on an unsuccessful regimen or without a predischarge study have died suddenly. Of these 27 patients, 1 of 12 patients treated with amiodarone and 4 of 15 (27%) with conventional antiarrhythmic therapy died suddenly. The remaining 4 patients died of nonarrhythmic causes in the postoperative period. Of 47 patients without inducible sustained ventricular arrhythmias, 15 (32%) died suddenly at a mean follow-up of 20 months, 10 (34%) with and 15 (28%) without empiric therapy. It is concluded that sustained ventricular arrhythmias can be initiated in most patients resuscitated from cardiac arrest. Patients with inducible arrhythmias have greater left ventricular dysfunction than those without inducible arrhythmias. Medical or surgical therapy that prevented the induction of sustained ventricular arrhythmias was predictive of a successful outcome in 85% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Relation of mode of induction and cycle length of ventricular tachycardia: analysis of 104 patients.
One hundred four consecutive patients with ventricular tachycardia (VT) were examined to correlate the cycle length with the mode of initiation of VT (single, double, and triple extrastimuli and rapid pacing). Tachycardias induced with a single extrastimulus were slower (342 +/- 72 ms, mean cycle length) than those induced with double (295 +/- 60 ms) or triple (282 +/- 56 ms) extrastimuli or rapid pacing (293 +/- 40 ms). There were no differences among the last 3 groups. In 38 patients who had endocardial catheter mapping to determine the site of origin of VT, distance from stimulation site to the site of origin was estimated and correlated with mode of initiation. There was no difference in mode of initiation when the stimulation site was close (less than 3 cm), intermediate (3 to 5 cm), or distant (greater than 8 cm) from the site of origin. To address the issue of distance from stimulation site to the site of origin somewhat differently, mode of initiation was correlated with site of previous myocardial infarction in 69 patients with VT initiated from the right ventricular apex. Again, mode of initiation did not differ among patients with septal, inferior, lateral, or multiple myocardial infarctions. Thus, cycle length of VT initiated with a single extrastimulus was slower than that initiated with double or triple extrastimuli or rapid pacing and the mode of initiation of VT was unrelated to site of myocardial infarction or distance between stimulation site and site of origin of VT.
Subendocardial resection for refractory ventricular tachycardia: effects on ambulatory electrocardiogram, programmed stimulation and ejection fraction, and relation to outcome.
The inducibility of ventricular tachycardia by programmed stimulation was correlated with ventricular ectopic activity on ambulatory electrocardiogram, ejection fraction and clinical outcome in 36 patients after endocardial resection for medically refractory ventricular tachycardia. Ventricular tachycardia was noninducible postoperatively in 25 patients and was inducible in 11. After administration of antiarrhythmic drugs, ventricular tachycardia could no longer be induced in four patients and remained inducible in the other seven patients. All 36 patients had postoperative and 20 had preoperative ambulatory electrocardiograms obtained while they were not receiving drug therapy. Pre- and postoperative ambulatory electrocardiograms did not differ in mean hourly ventricular premature depolarization frequency, Lown arrhythmia grade or change in grade (pre- vs. postoperative). The majority of postoperative patients had repetitive forms of ventricular arrhythmia postoperatively and there was no difference between patients with inducible and noninducible ventricular tachycardia in regard to Holter monitoring characteristics. There was no significant difference in postoperative ejection fraction between patients with inducible and noninducible ventricular tachycardia postoperatively. Ventricular tachycardia has recurred in 2 of 29 patients who had no inducible tachycardia at the time of hospital discharge and were followed up for a mean of 1 year; it has recurred in one of seven patients in whom it was still inducible at the time of hospital discharge and who were followed up for a mean of 7 months.(ABSTRACT TRUNCATED AT 250 WORDS)
Electrocardiographic changes following endocardial resection for ventricular tachycardia.
The ECG changes resulting from endocardial resection, with or without aneurysmectomy and coronary artery bypass grafting (CABG), are reported in 82 patients. Angiographic and surgical features and peak creatine kinase (CK) levels are correlated with ECG findings. Twenty-three of 82 patients (28%) had the following ECG changes postoperatively: decreased ST segment elevation = 3 (4%), loss of R wave amplitude = 4 (5%), increased R wave amplitude = 5 (6%), new Q wave = 4 (4%), axis shift greater than or equal to 45 degrees = 6 (7%), and new bundle branch block = 6 (7%). Five of six new cases of bundle branch block were left bundle type and resulted from resection of the inferoposterobasal and contiguous septal endocardium. ECG anterior infarction, anterior aneurysm, and anteroseptal endocardial resection were associated with a significantly lower incidence of postoperative ECG changes. Aneurysmectomy and the performance of CABG were not significantly associated with postoperative ECG changes, but more bypass grafts per patient grafted appeared in the group with postoperative ECG changes, suggesting that coronary artery disease may be more severe in that group. Peak CK did not correlate with postoperative ECG findings. We conclude that ECG changes occur infrequently after endocardial resection and that the factors responsible are not clear, although severity of coronary artery disease may be contributory. Left bundle branch block is a significant complication of inferoposterobasal resection, but complete heart block appears not to be. The diagnosis of myocardial necrosis is difficult in these patients.
Effect of an ulcer on the gastric mucosal barrier in dogs.
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Studies of anti-inflammatory drugs and aliphatic alcohols on antral mucosa.
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Circadian control of heart rate in young insulin-dependent diabetes mellitus patients.
Our objective was to determine whether young insulin-dependent diabetes mellitus (IDDM) patients without complications have abnormal circadian patterns of sympathetic or parasympathetic control of heart rate. Twenty-four-hour electrocardiographic recordings in 26 IDDM patients without complications and 27 control subjects were obtained. Patients were in good health and participated in their usual daily activities. Power spectral analysis was performed to determine the amount of heart rate variability due to all (0.01-1.0 Hz), low (0.04-0.15 Hz), and high (0.15-0.40 Hz) frequency input signals hourly and throughout the entire 24-h period. Overall 24-h heart rate power did not differ between control and IDDM subjects. In IDDM subjects high-frequency power decreased with increasing diabetes duration (r = -0.49, p = 0.013). A significant difference in circadian variation of heart rate power was only found for low frequency power (p = 0.014). These results demonstrate that young IDDM subjects without diabetic complications have normal or near normal parasympathetic and sympathetic circadian patterns of heart rate control.
Syncope: pursuing the common and prognostically important causes.
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