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Biomedical subjects

M G Kienzle

Publications and source records attributed to M G Kienzle.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1988

Energy, current, and success in defibrillation and cardioversion: clinical studies using an automated impedance-based method of energy adjustment.

The purposes of this study were two. First, we wanted to evaluate in patients a technique for automated adjustment of selected energy for defibrillation or cardioversion based on transthoracic impedance. Second, we wanted to define the relationship of peak current and shock success in various arrhythmias. Applying a previously validated method of predicting transthoracic impedance in advance of any shock, we modified defibrillators to automatically double the operator-selected energy if the predicted impedance exceeded 70 omega. Success rates of shocks given for ventricular and atrial arrhythmias from these modified energy-adjusting defibrillators were compared with success rates for shocks given from standard defibrillators. We prospectively collected data on 347 patients who received a total of 1009 shocks. Low-energy (100 J) shocks given to high-impedance (greater than or equal to 70 omega) patients had a poor success rate; in such high-impedance patients significant improvement in shock success rate was achieved by the energy-adjusting defibrillators. For example, when 100 J shocks were selected for high-impedance patients in ventricular fibrillation the energy-adjusting defibrillators achieved a shock success rate of 75%, whereas standard defibrillators achieved a shock success rate of only 36% (p less than .01). Similar improvements were seen for ventricular tachycardia and atrial fibrillation. Thus, automated energy adjustment based on transthoracic impedance is a beneficial approach to defibrillation and cardioversion. For ventricular fibrillation, atrial fibrillation, and atrial flutter there was a clear relationship between peak current and shock success.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1988

Predictors of failure after endocardial resection for sustained ventricular tachycardia.

This study was designed to identify characteristics that might be predictors of failure of surgical treatment alone (endocardial resection) for sustained ventricular tachycardia. Thirty-three consecutive patients with sustained ventricular tachycardia were studied by standard techniques preoperatively, intraoperatively, and 7 to 36 days postoperatively. Standard endocardial resection was guided by intraoperative mapping in all patients. Adjuvant cryoablation was used in areas that were not accessible to excision. Patients were divided into two groups on the basis of the results of the postoperative electrophysiologic study. Group I (14) were patients who still had ventricular tachycardia (failure) and Group II (19) were those who did not have ventricular tachycardia (success). On the basis of the postoperative electrophysiologic testing, the time from myocardial infarction to surgical treatment (less than 3 months) was a powerful predictor of failure of operation alone to prevent ventricular tachycardia (p less than 0.01). This may indicate a different mechanism of ventricular tachycardia in this group of patients. Another possible predictor of surgical failure was three-vessel disease. The site of origin of ventricular tachycardia, the use of cryoablation, the number of morphologies, and the amount of tissue resected were not significant predictors of success or failure. The result of the postoperative electrophysiologic study was also a strong prognostic predictor of subsequent arrhythmias.

Aged↗
PubMed1987

Alterations in endocardial activation of the canine papillary muscle early and late after myocardial infarction.

Permanent coronary occlusion produces time-dependent changes in surviving subendocardial cellular properties. We compared the functional alterations in Purkinje (P) and ventricular muscle (VM) activation early (24 hr) and late (4 weeks or greater) after permanent coronary occlusion in an in vitro preparation of canine papillary muscle. High-density extracellular (1 to 2 mm resolution) and selected intracellular recordings were made in five animals early and seven animals late during stimulation of a free-running P strand. Activation patterns of P and VM layers from ischemic and unaffected papillary muscles were compared in the same animal. Average P layer conduction velocity was determined in normal and ischemic regions with the use of a linear array of recording and stimulating electrodes. Purkinje activation was altered little in the early phase of infarction, while healing was associated with a generalized 25% reduction in P layer conduction velocity and localized block and fragmentation of P waveforms. Intracellular recordings at sites of nonsynchronous P activation revealed electrotonic interaction between cell groups. At 24 hr, small groups of VM were present but with abnormal activation patterns in regions of necrosis with fragmented and delayed extracellular waveforms produced by partially uncoupled groups of cells. Local delay and block could be modulated by rate and site of stimulation. After healing, VM activation abruptly stopped at the visual infarct border, marked by a characteristic "end potential." These studies demonstrate important differences in the functional attributes of the P and VM layers studied early and late after coronary occlusion. Alterations in cell-to-cell relationships are likely very important in determining abnormalities of activation in both settings.

Animals↗
PubMed1986

Electrophysiologic sequelae of chronic myocardial infarction: local refractoriness and electrographic characteristics of the left ventricle.

Ventricular tachycardia (VT) has been shown to arise from ischemically damaged left ventricular myocardium, which possesses heterogeneity of refractoriness and activation. Catheter techniques were used to study left ventricular refractoriness using the strength-interval relation and activation by local electrographic characteristics in 8 patients with and 6 patients without previous myocardial infarction (MI). Noninfarcted myocardium in patients with and without previous MI was similar overall with respect to refractoriness and excitability, whereas local electrographic duration in MI patients was longer (66 +/- 2 vs 52 +/- 3 ms, p less than 0.005) and amplitude lower (3.9 +/- 2.1 vs 6.1 +/- 2.0 mV, p less than 0.05). Comparisons of infarcted and noninfarcted regions in MI patients revealed an increased threshold of excitability at infarct sites (e.g., 1.9 +/- 1.0 vs 0.7 +/- 0.4 mA, p less than 0.05) and prolongation of refractory periods (375 +/- 118 vs 275 +/- 13 ms, p less than 0.05) at the lowest level of stimulating current. Shortening of refractory period as a result of change in pacing cycle length was not affected by infarction. The local electrographic duration (95 +/- 17 ms) was significantly longer in infarcted regions than at noninfarcted sites (p less than 0.005), but the electrographic amplitude (3.4 +/- 3.0 mV) differed significantly only in noninfarct patients. It is concluded that considerable electrophysiologic disparity exists between infarcted and noninfarcted myocardium. Whether or not arrhythmogenic tissue possesses unique alterations in electrophysiologic characteristics remains to be established.

Adult↗