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Biomedical subjects

M G Kienzle

Publications and source records attributed to M G Kienzle.

At least 19 recordsLinked to original sources
PubMed1992

Establishment of signal-averaged electrocardiographic criteria with Frank XYZ leads and spectral filter used alone and in combination with ejection fraction to predict inducible ventricular tachycardia in coronary artery disease.

Signal-averaged electrocardiographic criteria are reported for corrected Frank XYZ leads and a spectral filter. The new criteria were used alone and in combination with ejection fraction to predict inducibility of ventricular tachycardia (VT) at electrophysiologic testing. Signal-averaged electrocardiographic criteria were developed in 87 control subjects and validated in 182 patients (aged 63 +/- 10 years) with coronary artery disease and QRS duration less than 118 ms. Patients underwent electrophysiologic testing in which up to 3 extra-stimuli were used during 2 paced drives from 2 right ventricular sites. A positive finding was monomorphic VT lasting 30 seconds or needing intervention. An ejection fraction less than 40% was considered abnormal. Signal-averaged electrocardiographic variables that best characterized control subjects and separated patients with and without inducible VT were filtered QRS duration less than 120 ms, low-amplitude signal duration less than 38 ms and root-mean-square voltage greater than 20 muv. With these criteria, signal-averaged electrocardiographic and ejection fraction sensitivities were 87 and 45%, respectively, and specificities were 65 and 77%, respectively. Combining signal-averaged electrocardiography with ejection fraction improved the predictive accuracy. In conclusion, diagnostic criteria for signal-averaged electrocardiography with use of Frank XYZ leads and a spectral filter produced results similar to those reported for use of bipolar XYZ leads and a Butterworth filter. Signal-averaged electrocardiography was a better predictor of VT than was ejection fraction.

Adult↗
PubMed1992

Effect of direct, reflex and exercise-provoked increases in sympathetic tone on idiopathic ventricular tachycardia.

Exercise treadmill testing and direct enhancement of sympathetic influence with agents such as isoproterenol are often used to reproduce ventricular tachycardia (VT). The cardiac effects of, and arrhythmia responses to, graded exercise, isoproterenol infusion and lower body negative pressure (the latter 2 with and without atrial and ventricular stimulation) were studied in 11 patients with idiopathic VT. During maximal exercise, substantial increases in heart rate and blood pressure occurred, but only 2 of 9 exercised patients had VT (during recovery in both). During programmed stimulation alone, VT was initiated in 6 patients. During maximum levels of lower body negative pressure (-60 cm of water in most), mean systolic blood pressure decreased by 10 mm Hg, heart rate increased by 15 beats/min, and ventricular refractory period decreased by 10 ms. In 4 patients VT occurred spontaneously during lower body negative pressure; in 2, lower body negative pressure was the only intervention producing VT. During isoproterenol infusion VT occurred spontaneously in 2 patients; both had VT initiated during other interventions. Lower body negative pressure and isoproterenol increased VT rate, but did not prolong it. It is concluded that there is significant variability in arrhythmia responses to sympathetic augmentation, suggesting that additional covariables such as parasympathetic input and ventricular volume may also have a role in arrhythmia occurrence.

Adult↗
PubMed1992

Clinical, hemodynamic and sympathetic neural correlates of heart rate variability in congestive heart failure.

Heart rate (HR) variability has long been recognized as a sign of cardiac health. In the presence of heart disease, HR variability decreases, an observation that has been associated with poor prognosis in a number of recent studies. HR variability is particularly altered in congestive heart failure (CHF), a condition associated with a number of typical functional hemodynamic and neurohumoral alterations. The relation of measurements of HR variability to these abnormalities in patients with heart failure has not been carefully examined. Twenty-three patients (19 men, 4 women, mean age 49 years) with New York Heart Association class II to IV CHF were studied prospectively without cardiac medications; radionuclide ventriculography, right-sided heart catheterization, peroneal microneurography, plasma norepinephrine and 24- to 48-hour ambulatory electrocardiography were performed. Average RR interval and its standard deviation, and HR power spectrum (0 to 0.5, 0.05 to 0.15 and 0.2 to 0.5 Hz) were derived from the ambulatory electrocardiographic recordings and compared with left ventricular ejection fraction, thermodilution cardiac output, pulmonary arterial wedge pressure, New York Heart Association class, age, muscle sympathetic nerve activity (peroneal nerve) and norepinephrine level by linear regression. None of the measures of HR variability were significantly related to age, left ventricular ejection fraction, cardiac output or functional classification, whereas the 0.05 to 0.15 and 0.20 to 0.50 Hz components were weakly but significantly related to cardiac output (r = 0.49 and 0.42, p = 0.02 and 0.045, respectively). In contrast, a generally stronger and negative relation was demonstrated between spectral and nonspectral measurements of HR variability, and indicators of sympathoexcitation, muscle sympathetic nerve activity and plasma norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Evaluation of patients with syncope. Separating the 'wheat' from the 'chaff'.

Although fairly common, syncope is a frightening symptom that can signal a serious underlying disease. The varying causes present a diagnostic challenge to the examining physician, who needs to assess whether referral for more specialized or invasive study is appropriate. The authors review common cases of syncope and outline a practical approach to rapidly identifying high-risk patients--in other words, to separating the "wheat" from the "chaff."

Heart Diseases↗
PubMed1992

Ventricular tachycardia rate and morphology determine energy and current requirements for transthoracic cardioversion.

BACKGROUND: The electrical current and energy required to terminate ventricular tachyarrhythmias are known to vary by arrhythmia: Ventricular tachycardia (VT) is generally considered to require less energy than ventricular fibrillation (VF). The hypothesis of our study was that current requirements for transthoracic termination of VT are further determined by VT rate and QRS complex morphology. METHODS AND RESULTS: We prospectively studied 203 patients who received a total of 569 shocks for VT or VF by following a current-based protocol. This protocol recommended shocks for VT beginning at 18 A (70 +/- 22 J) and shocks for VF beginning at 25 or 30 A (137 +/- 52 J or 221 +/- 70 J). The ventricular tachyarrhythmias were subclassified as monomorphic VT (MVT): uniform QRS complex morphology on surface electrocardiogram and heart rate greater than 100 beats per minute; polymorphic VT (PVT): nonuniform QRS complex morphology and heart rate less than or equal to 300 beats per minute; or VF: nonuniform QRS complex morphology and heart rate greater than 300 beats per minute. We found that shocks of 18 A and 25 A for terminating MVT had success rates of 69% and 82%, respectively, whereas such low-current shocks were less successful for PVT (33% at 18 A) and for VF (19% at 18 A, 53% at 25 A). High-current shocks of 35 A and 40 A were equally successful for the three ventricular tachyarrhythmias. Subdividing MVT revealed that slower MVT (heart rate less than 200 beats per minute) had a significantly better success rate with low-current shocks of 18 A and 25 A than did faster MVT (greater than 200 beats per minute) (89% versus 72% success, p less than 0.01). Bundle branch block morphology, QRS axis, and duration of ventricular tachyarrhythmia did not alter current requirements. CONCLUSIONS: Heart rate and electrocardiographic degree of organization of ventricular tachycardia are important determinants of transthoracic energy and current requirements for cardioversion and defibrillation. Transthoracic termination of MVT requires relatively low current or energy, but PVT behaves more like VF and requires higher electrical current or energy.

Electric Countershock↗
PubMed1992

Post-mortem observations of a recent radiofrequency catheter ablation site.

The acute and chronic gross and microscopic morphologic changes present in myocardium after radiofrequency catheter ablation have been previously described in animal experiments. Acute changes have also been described in four cadaveric human specimens. We describe post-mortem observations of a recent radiofrequency catheter ablation site in a patient who underwent successful ablation for refractory ventricular tachycardia. Our gross and microscopic observations are similar to those previously described in animal experiments and confirm that the animal experimental results can be extrapolated to human hearts. As the use of radiofrequency becomes more prevalent as an alternative treatment for refractory cardiac tachycardias, pathologists will be called upon to identify post-mortem the lesions described. These lesions can be specifically identified, which can serve as a useful verification for this procedure.

Aged↗
PubMed1991

Pericardial influence on internal defibrillation energy requirements.

There is no consensus regarding optimal positioning of patch leads for implantation of automatic implantable cardioverter defibrillators. We compared the energy (in joules) required for 50% and 80% successful termination of ventricular fibrillation with titanium-mesh patch leads outside intact normal pericardium and directly on the epicardium in 13 open-chest dogs. Talc was then instilled into the pericardial space to stimulate adhesion formation and pericardial thickening. After 3 weeks of recovery, thoracotomy and defibrillation testing were repeated in nine dogs with the patch leads outside the thickened, adherent pericardium. There were no significant differences in defibrillation energy requirements between locations (p greater than 0.10). In addition, a comparison of electrical impedance measurements at 10 joules showed no significant differences (p greater than 0.30). In this animal model, defibrillation energy requirements were not altered by positioning the patch leads outside normal intact pericardium rather than placing them directly on the epicardium. Furthermore, thickened, adherent pericardium interposed between the patch leads and the heart does not increase defibrillation energy requirements. These data suggest that placement of automatic implantable cardioverter defibrillator patch leads outside the pericardium in patients (including those with pericardial adhesions from previous cardiac operations) will not adversely affect defibrillation efficacy and thus can simplify the implantation procedure.

Animals↗
PubMed1990

Syncope: mechanisms and manifestations.

Patients who have had syncopal episodes--even one episode--should be carefully evaluated. Of special concern is identifying those with a cardiovascular cause of syncope, in whom the one-year mortality is high and death is frequently sudden. An understanding of syncope's various potential mechanisms provides the key to the diagnosis.

Cardiovascular Diseases↗
PubMed1990

Polymorphous ventricular tachycardia: a side effect of intracoronary papaverine.

Polymorphous ventricular tachycardia occurred in 1.3% of patients (5 of 391) who received intracoronary papaverine over a 47 month period. The arrhythmia lasted less than 1 min in all five patients, converting spontaneously in four and requiring electrical cardioversion in one. Ventricular tachycardia occurred in 4.4% of women (4 of 90) and 0.3% of men (1 of 301) (p less than 0.0025). Only one of the patients with ventricular tachycardia had coronary artery disease. To determine whether other clinical or procedural factors predispose patients to this side effect of papaverine, these 5 patients were compared with 25 control patients who were matched for gender and extent of coronary artery disease. The following variables were analyzed: age, baseline serum potassium and calcium levels, left ventricular ejection fraction, baseline heart rate, mean arterial pressure, corrected QT interval, the change in corrected QT interval produced by papaverine and the maximal dose of the drug per kilogram of body weight. Of these variables, only baseline heart rate differed significantly in the two groups of patients. Thus, polymorphous ventricular tachycardia is an infrequent, but important, side effect of papaverine that is usually self-limited. Women with a relatively slow heart rate appear to be predisposed to this side effect.

Coronary Vessels↗
PubMed1989

Induced sustained ventricular tachycardia in nonischemic dilated cardiomyopathy: dependence on clinical presentation and response to antiarrhythmic agents.

Thirty-one patients with nonischemic dilated cardiomyopathy either idiopathic or due to regurgitant valvular disease were studied in the cardiac electrophysiology lab. The indications for study were sustained ventricular tachycardia (VT) in 16, ventricular fibrillation (VF) in 11, and syncope of unknown etiology in 4. Sustained VT was reproducibly induced in 17 patients, including 12 with a history of sustained VT, 2 with VF and 3 with syncope. Of 15 patients undergoing serial antiarrhythmic drug studies, sustained VT was rendered noninducible or nonsustained in 13. Three had recurrent arrhythmic events while on therapy predicted to be effective. One of 2 patients discharged on a regimen predicted to be ineffective had a recurrence of sustained VT that resulted in cardiac arrest. Of 14 patients in whom sustained VT could not be reproducibly induced, 2 subsequently had spontaneous occurrences of sustained VT, and 2 experienced aborted sudden death. These results suggest the following: (1) the induction of sustained VT in the setting of nonischemic dilated cardiomyopathy is dependent on the clinical presentation; (2) antiarrhythmic drugs frequently render sustained VT noninducible or nonsustained; (3) antiarrhythmic drug suppression of inducible sustained VT predicts long-term prevention of spontaneous recurrences; and (4) noninducibility of sustained VT in the baseline state does not predict freedom from subsequent episodes of VT or sudden death.

Adult↗
PubMed1989

Sympathoinhibitory responses to digitalis glycosides in heart failure patients. Direct evidence from sympathetic neural recordings.

Digitalis glycosides exert both excitatory and inhibitory autonomic actions in animals and produce vasoconstriction in normal humans but produce vasodilation in heart failure patients. To determine whether or not these contrasting vascular responses are due to differing autonomic actions of the drug, we compared the responses to intravenous administration of Cedilanid-D (0.02 mg/kg) in eight normal subjects (mean age, 23 +/- 1 years) and eight patients with moderate-to-severe heart failure (mean age, 52 +/- 5 years, NYHA Class III-IV). Hemodynamics and efferent sympathetic nerve activity to muscle (MSNA) were measured during 5-minute periods before (control) and 20 minutes after drug administration. In the heart failure patients, Cedilanid-D significantly increased systolic and pulse pressures, whereas mean arterial pressure was unchanged. There was a decrease in right atrial pressure and a tendency for a decrease in pulmonary artery diastolic pressure with a slowing of heart rate. Cardiac index increased by 24 +/- 7%. Short-term administration of digitalis in these heart failure patients produced a fall in forearm vascular resistance (from 37.6 +/- 8.2 to 31.8 +/- 8.1 units, p less than 0.05) and an early, profound, and sustained decrease in MSNA (from 831.0 +/- 118.4 to 474.4 +/- 103.6 units/100 heart beats, p less than 0.01). Digitalis glycosides produced different vascular and MSNA responses in the normal subjects. In the normal volunteers, the drug significantly increased systolic, mean, and pulse pressures and decreased central venous pressure and heart rate. Despite the significant increase in arterial pressure, there was no change in forearm vascular resistance (from 11.7 +/- 1.0 to 12.7 +/- 1.0 units, p = NS) or MSNA (from 494.8 +/- 88.5 to 369.1 +/- 60.5 units/100 heart beats, p = NS), suggesting a sympathoexcitatory response in normal subjects. To determine whether or not the digitalis-induced sympathoinhibition in the heart failure patients was simply due to an inotropic effect (stimulation of inhibitory cardiac mechanoreceptors), we studied the responses of seven additional patients with heart failure before and during administration of dobutamine (3.4 +/- 0.4 micrograms/kg/min). Dobutamine produced a 34 +/- 3% increase in cardiac index, no significant change in systemic arterial pressures, a decrease in pulmonary artery diastolic and right atrial pressures, and no change in heart rate or forearm vascular resistance (from 30.2 +/- 4.3 to 26.5 +/- 4.7 units, p = NS).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1988

Enhanced efficacy of oral sotalol for sustained ventricular tachycardia refractory to type I antiarrhythmic drugs.

Sotalol is a nonselective beta-adrenergic blocking agent with Vaughn-Williams class III activity. Its efficacy was tested in 9 patients with sustained ventricular tachycardia (VT) that had previously remained inducible during electrophysiologic testing of type I drugs (procainamide or quinidine). Eight patients had coronary artery disease with remote myocardial infarction and 1 had cardiomyopathy (ejection fraction 0.34 +/- 0.08, mean +/- standard deviation). Type I drugs prolonged the effective refractory period of the right ventricle 12 +/- 14% and prolonged the VT cycle length 41 +/- 24%. In contrast, despite an equivalent effect on the effective refractory period, a sustained VT could no longer be initiated in any of the 8 patients ultimately tested while taking oral sotalol. Daily doses averaged 600 +/- 103 mg and blood levels associated with VT suppression in electrophysiologic studies were generally greater than 3,000 ng/ml. In addition, sotalol was moderately effective at reducing ventricular ectopic activity measured by ambulatory electrocardiography. Over a mean follow-up of 23 months (range 1 to 37), mild heart failure (3 patients), symptomatic brady-cardia requiring pacemaker (1) and drug-related polymorphous VT (1) have occurred. Sudden death occurred in 1 patient and nonfatal VT recurrence was noted in 2. Five of 8 chronically treated patients currently are successfully treated with minimal side effects. Sotalol appears to be a promising antiarrhythmic drug in the treatment of serious ventricular arrhythmias, even in patients refractory to type I antiarrhythmic agents.

Administration, Oral↗
PubMed1988

Usefulness of isoproterenol in facilitating atrioventricular nodal reentry tachycardia during electrophysiologic testing.

In some patients with documented atrioventricular (AV) nodal supraventricular tachycardia (SVT), the arrhythmia is not inducible during a standard stimulation protocol. In these patients the level of sympathetic activity may be an important factor. This study evaluates the influence of isoproterenol on anterograde and retrograde pathway properties in patients with AV nodal SVT and the mechanism by which this SVT is facilitated. Group 1 consisted of 8 consecutive patients, ages 23 to 85 years (mean +/- standard error, 57 +/- 8) who had no inducible AV nodal SVT during electrophysiologic testing until isoproterenol (0.5 to 3.0 micrograms/min) was infused. These patients were compared with 6 patients in the same age range (45 to 78 years, mean +/- standard error, 64 +/- 5) who had inducible AV nodal SVT without isoproterenol and who comprised group 2. In comparing group 1 (before isoproterenol) with group 2, there was no significant difference in the refractory periods of the anterograde slow and fast pathways, although the anterograde block cycle length was longer in group 1 patients (421 +/- 18 vs 362 +/- 14 ms, p less than 0.05). The retrograde block cycle length was also longer in 7 of the 8 group 1 (before isoproterenol) patients in whom it could be measured versus those in group 2 (411 +/- 14 vs 318 +/- 27 ms, p less than 0.05). During isoproterenol, the anterograde and retrograde block cycle lengths in group 1 were not different from group 2. Therefore, AV nodal SVT may not be inducible in some patients during routine electrophysiologic testing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1988

Alterations in the initial portion of the signal-averaged QRS complex in acute myocardial infarction with ventricular tachycardia.

This study was designed to examine 2 hypotheses: that acute myocardial infarction (AMI) alters early cardiac activation measured by signal-averaging; and that the magnitude of abnormality of early activation may be greater in patients with post-AMI ventricular tachycardia (VT). We examined the root-mean square voltage amplitude in 10-ms intervals over the first 80-ms of the signal-averaged QRS complex. Data from 42 healthy volunteers were compared with those from 52 patients with previous AMI (24 anterior) but no VT and 46 post-AMI patients (33 anterior AMI) with recurrent sustained VT. Patients with VT differed from other post-AMI patients because of lower left ventricular ejection fraction, more frequent aneurysm formation and higher levels of ventricular ectopic activity. A significant decrease in initial voltage amplitude occurred at 30 to 40 ms after the beginning of the QRS in both anterior and inferior AMI patients compared with the normal group. A further significant decrease in initial amplitude occurred in VT patients both after anterior and inferior AMI. These differences persisted for the remainder of the 80-ms interval. These changes were weakly related to QRS duration (r = 0.45), ejection fraction (r = 0.50) and poorly correlated with the presence of Q waves on 12-lead electrocardiogram (r = 0.21). Direct endocardial catheter recordings performed in VT patients confirmed abnormalities of local septal activation after anterior and inferior AMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Propranolol blocks ventricular refractory period changes with orthostatic stress in humans.

The purpose of this study was to test the hypothesis that orthostatic stress shortens the right ventricular effective refractory period by reflex activation of beta-adrenergic receptors. Twelve patients undergoing electrophysiologic testing for standard clinical indications were studied. After a full electrophysiologic study, patients underwent graded lower body negative pressure before and after administration of either propranolol (0.2 mg/kg intravenously) in Group I or atropine (0.035 mg/kg intravenously) in Group II. Before the addition of drugs, lower body negative pressure produced decreases in systolic blood pressure and significant increases in sinus rate. The effective refractory period shortened from 214 +/- 8 (mean +/- SEM) to 206 +/- 7 ms at -40 cm H2O and to 197 +/- 4 ms at -60 cm H2O lower body negative pressure. After propranolol, Group I patients had no change in right ventricular effective refractory period despite similar changes in sinus rate and systolic blood pressure. In group II patients, atropine did not alter effective refractory period responses to lower body negative pressure. Thus, reflex adjustments to orthostatic stress result in shortening of right ventricular effective refractory period mediated by way of beta-adrenergic mechanisms. These findings constitute the first evidence that sympathetic influences mobilized by the body can directly modulate ventricular electrophysiologic changes.

Adult↗
PubMed1988

Possible proarrhythmic effects of tocainide in dilated cardiomyopathy.

A patient with a dilated cardiomyopathy experienced a cardiac arrest when taking tocainide for asymptomatic nonsustained ventricular tachycardia. After successful resuscitation from ventricular fibrillation and exclusion of a myocardial infarction, an electrophysiological evaluation was performed. Drug-free study #1 revealed no induction of ventricular tachycardia. A tocainide study revealed induction of sustained monomorphic ventricular tachycardia. Drug-free study #2 revealed induction of nonsustained ventricular tachycardia. This report illustrates a possible proarrhythmic effect of tocainide.

Cardiomyopathy, Dilated↗