Identification of Ventricular Tachycardia Using Intracavitary Ventricular Electrograms: Analysis of Time and Frequency Domain Patterns

Tachycardia detection by implantable antitachycardia devices using rate alone has major limitations. Several alternative methods have been proposed to distinguish ventricular tachycardia or ventricular fibrillation from normal sinus rhythm using intracardiac electrograms. These methods have not been tested, however, for recognition of ventricular tachycardia in patients with abnormal surface QRS conduction during sinus rhythm or with antiarrhythmic drug therapy. In this study, three techniques for the indentification of ventricular tachycardia from intracavitary bipolar ventricular electrograms were examined and compared: correlation waveform analysis, amplitude distribution analysis, and spectral analysis using Fast Fourier transformation. Thirty episodes of induced monomorphic ventricular tachycardia were analyzed and compared sinus rhythm in four groups of patients with: I. Normal surface QRS conduction during sinus rhythm without antiarrhythmic drug therapy (five episodes); II. Intraventricular conduction delay or bundle branch block during sinus rhythm without antiarrhythmic drug therapy (nine episodes); III. Normal surface QRS conduction during sinus rhythm with antiarrhythmic therapy (six episodes); and IV. Intraventricular conduction delay or bundle branch block during sinus rhythm with antiarrhythmic drug therapy (ten episodes). Correlation waveform analysis had 100% sensitivity and specificity in distinguishing ventricular tachycardia from sinus rhythm, even in the presence of an intraventricular conduction delay, bundle branch block, and antiarrhythmic drug therapy. In contrast, amplitude distribution analysis differentiated 15/30 episodes (50.0%) of ventricular tachycardia from sinus rhythm, and a maximum of 18/30 episodes (60.0%) of ventricular tachycardia were identified by specal analysis using Fast Fourier transformation. Correlation waveform analysis appears to be a reliable technique to discriminate ventricular tachycardia from sinus rhythm using intracavitary ventricular electrograms. Its computational demands are modest, making it suitable for consideration in an implantable antitachycardia device.     

Mechanisms of onset of atrial fibrillation: a multicenter,prospective, pacemaker-based study

The aim of this study was to analyze the onset mechanisms of atrial tachyarrhythmias using a dedicated diagnostic system in 83 recipients of DDDR pacemakers implanted for standard clinical indications. The pulse generator was programmed in DDD mode, at 60 beats/min, and the diagnostic instrument was programmed to document atrial tachyarrhythmic episodes at rates >200 beats/min. Onset mechanism was defined as the combination of ambient rhythm and trigger. Various underlying rates and rhythms patterns, including tachycardia, increasing frequency of premature atrial complex (PAC), underlying heart rate increase, restart, and no specific underlying rhythm, and various triggers, including single, multiple, or short runs of PACs, sudden rate decrease, and sudden onset of atrial tachyarrhythmia were included in the combined classification. Atrial tachyarrhythmic episodes were documented on one follow-up interrogation in 48 of the 83 patients. The pacing indications consisted of high degree atrioventricular block in 19 patients, bradycardia-tachycardia syndrome in 22, and isolated sinus node dysfunction in 6 patients. The onset mechanisms of 318 episodes were recorded and analyzed. A variety of triggers were observed in 33 of the 48 patients, and 39 patients had various ambient rhythms. Among 20 documented onset mechanisms, the most common were increasing frequency of PAC + short runs (17%), no specific ambient rhythm + sudden onset (24%), and increasing frequency of PAC + sudden onset (12%). There were wide intra- and interpatient variations in onset mechanisms, suggesting that state-of-the-art pacemakers should represent versatile diagnostic tools and offer flexible pacing methods to refine the management of atrial tachyarrhythmias.     

Detection of Pathological Tachycardia by Analysis of Electrogram Morphology

Pacemaker recognition of pathological tachycardia relies on heart rate analysis. This can lead to misdiagnosis when sinus tachycardia exceeds the preset tachycardia response trigger rate. We have explored a method for automatic tachycardia diagnosis by analysis of bipolar endocardial electrogram morphology. Electrograms were recorded from 11 patients (pts) during sinus rhythm and during a total of 20 abnormal rhythms: retrograde atrial depolarization from ventricular pacing in six patients; atrioventricular reentry tachycardia in five patients with intermittent left bundle branch block in one of those; AV nodal reentry tachycardia in five patients and ventricular tachycardia in three patients. Posture and respiration were varied during all rhythms except ventricular tachycardia. The electrograms were then digitized and converted to a form in which the amplitudes were proportional to the rates of change of the original electrogram (equivalent to a first time derivative); the derived signal was then analyzed by a new gradient pattern detection (GPD) program. Analysis of the processed atrial signals by GPD resulted in automatic recognition of abnormal rhythms from sinus rhythm in all cases except for one patient's retrograde atrial depolarization. At the ventricular level, GPD successfully distinguished all abnormal rhythms from sinus rhythm including recognition of left bundle branch block and varying degrees of preexcitation. Respiratory and postural variation did not affect the recognition process. We conclude that electrogram GPD has successfully and automatically detected a variety of arrhythmias which can be treated by implantable pulse generators and may, therefore, be a useful adjunct to heart rate analysis in future generations of such antitachycardia pacemakers.     

Differentiation Between Monomorphic Ventricular Tachycardia and Sinus Tachycardia Based on the Right Ventricular Evoked Potential

The differentiation between ventricular tachycardia (VT) and smus tachycardia (ST) is problematic in some patients with implantable defibrillators and/ or antitachycardia pacemakers. The Integral of the ventricular endocardial evoked response, or paced depolarization integral (PDI), has been demonstrated to undergo characteristic changes with a variety of stimuli including catecholamines, pacing rate, and exercise. We hypothesized that the PDI recorded from a unipolar transvenous right ventricular endocardial catheter would differentiate VT from ST. The PDI was calculated from a unipolar pacing stimulus, delivered via a cathode in the right ventricular apex, and the reference electrode, a quadripolar catheter positioned in the superior vena cava. PDIs were measured in 22 patients during VT and sinus rhythm. The PDI measured during sinus rhythm was 579 ± 240 μV-sec and the PDI during VT was 894 ± 411 μV-sec (P < 0.001). In a subset of seven patients, PDIs were measured during VT, sinus rhythm, and ST induced by catecholamine infusion or exercise. In this subset, the PDI during sinus rhythm was 645 ± 295 μV-sec, during ST 588 ± 308 μV-sec (9% decrease from sinus, P = 0.05), and during VT 863 ± 342 μV-sec (33.9% increase, P = 0.01). These data indicate that the measurement of the PDI is potentially useful in differentiating VT from ST.     

Paroxysmal Bundle Branch Block of Supraventricular Origin: A Possible Source of Misdiagnosis in Detecting Ventricular Tachycardia Using Time Domain Analyses of Intraventricular Electrograms

Current implantable antitachycardia devices use several methods for differentiating sinus rhythm (SR) from supraventricular tachycardia (SVT) or ventricular tachycardia (VT). These methods include sustained high rate, the rate of onset, changes in cycle length, and sudden onset. Additional methods for detecting VT include techniques based upon ventricular electrogram morphology. The morphological approach is based on the assumption that the direction of cardiac activation, as sensed by a bipolar electrode in the ventricle, is different when the patient is in SR as compared to VT. Whether paroxysmal bundle branch block of supraventricular origin (BBB) can be differentiated from VT has not been determined. In this study, we compared the morphology of the ventricular electrogram during sinus rhythm with a normal QRS (SRNIQRS) or SVT with a normal QRS (SVTNIQRS) with the morphologies of BBB and VT in 30 patients undergoing cardiac electrophysiology studies. Changes in ventricular electrogram morphology were determined using three previously proposed time domain methods for VT detection: Correlation Waveform Analysis (CWA), Area of Difference (AD), and Amplitude Distribution Analysis (ADA). CWA, AD, and ADA distinguished VT from SRNIQRS or SVTNIQRS in 16/17 (94%), 14/17 (82%), and 12/17 (71%) patients, and BBB from SRNIQRS or SVTNIQRS in 15/15 (100%), 13/15 (87%), and 6/15 (40%) patients, respectively. However, the ranges of values during BBB using these methods overlapped with ranges of values during VT in all cases for CWA, AD, and ADA. Hence, BBB may be a source of misdiagnosis in detecting VT when these time domain methods are used for ventricular electrogram analysis.     

Identification of Ventricular Tachycardia Using Intracardiac Electrograms: A Comparison of Unipolar Versus Bipolar Waveform Analysis

Implantable antitachycardia devices suffer a high false-positive rate of delivery of therapy because current detection schemes based upon ventricular rate and rate variations are excessively sensitive at the cost of specificity. Several methods have been proposed for providing complementary information derived from morphologic analysis of intraventricular electrograms in order to increase specificity. The majority of these techniques have utilized bipolar electrogram analysis to detect changes in ventricular activation indicative of ventricular tachycardia. Whether bipolar or unipolar intracardiac electrogram analysis might be preferred for discriminating ventricular tachycardia from sinus rhythm has not been determined. In this study, a previously demonstrated method for identification of ventricular tachycardia using intracardiac electrograms, correlation waveform analysis, was used to analyze both unipolar and bipolar signals during sinus rhythm and ventricular tachycardia recorded during electrophysiology studies of 15 patients with inducible sustained monomorphic ventricular tachycardia. Correlation waveform analysis consistently discriminated between all depolarizations during ventricular tachycardia in 14/15 patients (93%) using either electrogram configuration; 13 of the 14 patients were common to both groups. Of these patients, 8/15 (53%) had greater separation between sinus rhythm and ventricular waveforms with bipolar electrogram analysis while 7/15 (47%) had greater separation with unipolar electrogram analysis. We conclude that morphologic analysis of unipolar and bipolar electrograms may be equally effective in distinguishing ventricular tachycardia from sinus rhythm. For individual patients, either a unipolar or bipolar ventricular configuration may be preferable, and should be chosen on a patient-specific basis during electrophysiology study prior to antitachycardia device implantation.     

The Value of Rate Regularity and Multiplicity Measures to Detect Ventricular Tachycardia in the Presence of Atrial Fibrillation or Flutter

The predominant cause of inappropriate therapy by implantable antitachycardia devices with pacing and nonpacing cardioverter defibrillators, is mistaking a fast ventricular response during atrial fibrillation or flutter with true ventricular tachycardia (VT). The distinction between these arrhythmias is an important consideration in addressing the problem of reducing false-positives in detection mechanisms for implantable devices. Dual chamber analysis that examines atrial and ventricular event ratios has been proposed as a solution to this problem, but would still fail in distinguishing paroxysmal VT requiring treatment from a fast but otherwise benign ventricular response during atrial fibrillation or flutter. In this study, two methods for discriminating these tachyarrhythmias were evaluated. Method 1 examined ventricular rate and rate regularity as a method for VT detection. Method 2 combined rate and regularity as well as an additional multiplicity criterion for recognition of atrial flutter with a fast ventricular response. In 20 patients. Method 1 had 100% sensitivity of VT detection and 80% specificity for detection of atrial fibrillation or flutter. Method 2 had 90% sensitivity and 90% specificity. These results suggest that use of these algorithms in future implantable devices would result in a decrease in false-positive device therapies.     

Significance of Supraventricular Tachyarrhythmias in Patients with Implanted Pacing Cardioverter Defibrillators

Eighty-six patients were treated with an implantable cardioverter defibrillator (ICD) because of sustained ventricalar tachycardia (VT) or ventricular fibrillation (VF). In 27 patients an epicardial system was used, in 59 patients a transvenous system with a subcutaneous patch electrode was implanted. During a mean follow-up time of 17 ± 9 months, inappropriate activations of the ICD due to supraventricular tachycardia were documented by Holter monitoring in 14 patients (16%). In 8 patients paroxysmal atrial fibrillation (AF), in 2 patients chronic AF, in 1 patient atrial flutter, and in 3 patients sinus tachycardia triggered antitachycardia pacing functions (12 patients) or internal defibrillation (2 patients). In 3 patients (5%) VT was induced by inappropriate antitachycardia pacing. In an additional 18 patients (21%) inappropriate activation of antitachycardia functions due to atrial tachyarrhythmias were suspected based on telemetry readouts or the patient's history. Inappropriate activation of ICD therapy triggered by intermittent supraventricular tachyarrhythmias is common. Further improvements of detection algorithms for supraventricular tachycardia are required in future device generations.     

Tachycardias Initiated by Automatic Antitachycardia Pacemakers

Available automatic tachycardia-terminating pacemaker cannot distinguish between physiological and pathological tachycardia and, consequently, electrical stimulation during sinus tachycardia can occur. In order to evaluate whether this might be an arrhythmogenic problem or not the cardiac response in eight patients having paroxysmal supraventricular tachycardia treated with tachycardia-terminating pacemakers was studied during exercise. After tachycardia recognition, the implanted pulse generator automatically emits single or double critically timed premature stimuli for termination of the arrhythmia. Post-implantation examination revealed successful tachycardia termination by the pacemaker at rest, without the addition of any antiarrhythmic drugs, in all eight patients. During exercise tests, the sinus rate in seven patients exceeded the programmed tachycardia trigger rate resulting in triggered pacemaker stimulation. The native supraventricular tachycardia was initialed in four cases. In one of these patients, two short episodes of probable ventricular tachycardia were also recorded. This study demonstrates the clinical value of post-implantation assessments with exercise tests concerning the problem of pacemaker-initiated tachyarrhythmias. Tachycardia-terminating devices can induce tachycardias, and individual precautions must be taken in order to prevent or minimize the risk of pacemaker reversion of sinus rhythm to paroxysmal tachycardia or hazardous arrhythmias.     

Permanent Antitachycardia Pacemaker Therapy for Ventricular Tachycardia

This article describes our experience with an antitachycardia pacemaker alone (N = 3) or in combination with an automatic implontoble cardioverter defibrillator (AICD, N = 8) in the treatment of ventricular tochycardia. EJeven patients (mean ejection fraction 31%, mean oge 67 years) received an antitachycardia pacemaker. Nine had their units programmed for automatic antitachycardia pacing, one unit was programmed to automatic antitachycardia pacing by magnet activation only, and one to tachycardia detection and bradycardia support. Of the nine patients with automatic antitachycardia pacing, seven received appropriate and successful pace termination of spontaneous ventricular tachycardia at up to 120 times per month. Eight of these nine have had AICD implantations as well. There were no operative complications. Over a mean (± SD) follow-up of 12.1 ± 9.3 months (range 3–29 months), there have been two deaths, both due to heart failure. There have been four AICD discharges in three patients. Two units discharged in a clinically appropriate setting. The other two units, both with rate cutoffs <200 beats/min, were inadvertently triggered by the antitachycardia pacemaker and/or the underlying rate. In addition to the careful selection of the defibrillator rate cutoff, adverse device-device interactions were avoided by careful intraoperative lead positioning, and the disabling of bradycardia pacing when not needed or contraindicated. Antitachycardia pacing, with the safety provided by the AICD, is an effective treatment for patients with medically refractory ventricular tachycardia.     

Differentiation of Sinus Tachycardia from Paroxysmal 1:1 Tachycardias Using Single Late Diastolic Atrial Extrastimuli

. Existing antitachycardia devices do not discriminate perfectly between sinus tachycardia and paroxysmal tachycardias with 1:1 atrioventricular relationship (paroxysmal 1:1 tachycardias). The present study tested the hypothesis that the nature of the ventricular response to atrial extrastimulation might distinguish between sinus tachycardia and selected paroxysmal 1:1 tachycardias. In 15 patients, atrial extrastimuli were delivered during sinus tachycardia and in 13 patients during various types of paroxysmal 1:1 tachycardia, and the timing of the next ventricular beat was measured. During sinus tachycardia, in 14 of 15 patients, atrial extrastimuli which were, in turn, early by 80 and 100 ms made the next ventricular beat premature by at least 30 and 50 ms, respectively. In all 13 patients, during paroxysmal 1:1 tachycardia, atrial extrastimuli that were early by 80 and 100 ms failed to make the next ventricular beat premature by more than 10 ms. Single atrial extrastimuli that were premature by less than or equal to 100 ms did not provoke faster tachycardias in any of the patients. In this study, a technique that used single late extrastimuli during tachycardia safely distinguished sinus tachycardia from paroxysmal tachycardias. This technique might be suitable for incorporation into an antitachycardia device. Further investigation of this technique is warranted in a larger number of patients with a wider variety of tachycardias.     

Conversion Rates of Induced Versus Spontaneous Ventricular Tachycardia by a Third Generation Cardioverter Defibrillator

Seventy consecutive patients received the first VENTAK PRx pulse generators (Cardiac Pacemakers, Inc.) implanted in the United States. This multiprogrammable device has therapeutic options that include: (1) antitachycardia pacing; (2) low energy cardioversion; (3) defihrillation shocks; and (4) bradycardia pacing. There were 60 males and 10 females with a mean age of 65.3 ± 9.4 years. The anatomical diagnoses were coronary artery disease in 55 patients, cardiomyopathy in 7 patients, congenital heart disease in 2 patients, and miscellaneous disease in the remaining 6 patients. Thirty-six percent had a history of sudden cardiac death and 90% had documented monomorphic ventricular tachycardia. The mean ejection fraction was 32.7%± 12.2%. Thirty-three (49.3%) had an ejection fraction ≤ 30%. Electrophysiological testing was done preimplant, predischarge, and 1 to 2 months postimplant to define a specific electrical therapy and evaluate the efficacy of the device. Two hundred ninety-three of 367 (80%) episodes of induced ventricular tachycardia were successfully terminated by the VENTAK PRx programmed for antitachycardia pacing. There were 1,794 total therapy episodes for spontaneous ventricular tachycardia; 91% (1,641 episodes) were terminated by antitachycardia pacing and 153 episodes were converted by shocks during a minimal 6-month follow-up per patient. We conclude that documentation of a successful antitachycardia pacing modality in the electrophysiology laboratory predicts conversion of spontaneous episodes of ventricular tachycardia. Furthermore, antitachycardia pacing by the VENTAK PRx can terminate the majority of episodes of ventricular tachycardia.     

A Single Atrial Extrastimulus Can Distinguish Sinus Tachycardia from 1:1 Paroxysmal Tachycardia

We have developed a tachycardia detection scheme for use in an antitachycardia pacemaker in which the use of a properly timed atrial extrastimulus provides a means of discriminating sinus tachycardia from pace-terminable 1:1 tachycardias. An atrial extrastimulus is delivered in late diastole (80 ms premature), and the ventricular response is monitored. In sinus tachycardia, the ventricular response is expected to appear early as well, but in pace-terminable tachycardias, such as AV reentrant and ventricular with VA conduction, the ventricular rhythm will be unperturbed. Testing of the algorithm was performed in 34 patients. In 29 patients, atrial extrastimuli were delivered during sinus tachycardia, and in 22 patients during various types of 1:1 paroxysmal tachycardia. In one patient the procedure was completely automated, i.e., delivery of the atrial extrastimuli and diagnosis were microcomputer controlled. In 28/29 cases, the delivery of an atrial extrastimulus 80 to 120 ms early during sinus tachycardia elicited a ventricular response at least 28 ms early. In 22/22 patients with 1:1 paroxysmal tachycardia, atrial extrastimuli 80 to 120 ms early failed to produce a significant change in ventricular cycle length. This technique appears to be promising for prevention of inadvertent pacing of sinus tachycardia in an antitachycardia pacemaker.     

Pacemaker‐Mediated Tachycardia: Manufacturer Specifics and Spectrum of Cases

Pacemaker‐mediated tachycardia (PMT) is the term used to describe a repetitive sequence of sensed retrograde P waves followed by ventricular pacing at or below the maximum tracking rate. The following events can promote atrioventricular (AV) dissociation, retrograde conduction, and the onset of PMT: ventricular or atrial extrasystole, an excessively long programmed AV delay, external interference or myopotentials sensed by the atrial channel, atrial sensing or pacing failure, the absence of postventricular atrial refractory period extension after removal of a magnet, and VDD pacing at a higher rate than sinus rate. In contemporary devices, each manufacturer has a proprietary algorithm to detect and terminate PMT. Because of the increase in the number and complexity of the pacing algorithms and because of manufacturer‐driven differences, a basic understanding of these new algorithms is important for patient care. We review here the main elements of the physiopathology of this type of tachycardia, describe the specific characteristics of the different manufacturers, and present representative clinical cases.     

Effectiveness of Noninvasive Programmed Stimulation for Initiating Ventricular Tachyarrhythmias in Patients with Third-Generation Implantable Cardioverter Definrillators

Previous generations of implantable cardioverter defibrillators (ICDs) required invasive electrophysiological testing to assess defibrillator function. Newer third-generation ICDs include the capability for performing noninvasive programmed stimulation (NIPS) and may reduce the need for invasive studies to assess tachycardia recognition and antitachycardia therapy algorithms. The effectiveness of ICD-based NIPS for the induction of ventricular arrhythmias has not, however, been formally assessed. Third-generation ICDs were implanted in 79 patients, who underwent a total of 166 postoperative defibrillator tests. NIPS with rapid ventricular pacing was performed in all patients in an attempt to induce ventricular fibrillation. In patients with prior sustained uniform ventricular tachycardia, programmed stimulation with up to three extrastimuli was performed in order to attempt to initiate the clinical ventricular tachcardia. Ventricular fibrillation was induced with NIPS in 146 of 166 studies (88%). Ventricular tachycardia was initiated with NIPS in 104 of 123 studies (85%). The type of defibrillator and the use of endocardial or epicardial rate sensing/ pacing leads did not influence the efficacy of NIPS. NIPS with third-generation ICDs is generally effective at inducing ventricular fibrillation and clinically relevant ventricular tachycardias, and reduces the need to perform invasive electrophysiological testing following device implantation. In a minority of patients temporary transvenous pacing catheters must still be used to facilitate arrhythmia induction.     

Automatic Recognition of Ventricular Arrhythmias Using Temporal Electrogram Analysis

Future antitachycardia devices must be able to deliver a variety of therapies according to the requirements of the underlying arrhythmia. To ensure that appropriate treatment is prescribed the device must use a detection algorithm that is able to discriminate between multiple arrhythmias. Current criteria such as rate, change of rate, duration at high rate, and high rate stability are inadequate for this purpose. Many algorithms that evaluate the morphology of the endocardial electrogram are of too great a complexity to be incorporated in implantable devices that require real-time analysis without undue power consumption. In this study the sensitivity of a simple morphological technique (temporal electrogram analysis) is examined. The method sets threshold 'rails' above and below the isoelectric line and classifies ECG complexes according to the sequence and duration of rail excursions. A total of 27 ventricular tachyarrhythmias were induced in 25 patients (17 with a history of recurrent arrhythmias and eight undergoing risk stratification postmyocardial infarction). Temporal electrogram analysis (TEA), initially detected the onset of the ventricular arrhythmia in all patients whose surface ECG showed polymorphic or right bundle branch block pattern tachycardia, in 5/8 of cases with left bundle branch block pattern and in 4/5 of patients with concordant complexes across the precordial leads. After minor modifications the overall sensitivity of the method was improved to 95% (26/27 arrhythmias detected). TEA is a technique of low computational demands, which in this study, reliably discriminated between resting sinus rhythm and ventricular arrhythmias.     

A Hierarchical Approach to the Treatment of Ventricular Tachycardias

Electrical management of ventricular tachycardias with an implanted device is greatly complicated by reduced hemodynamic tolerance to the tachycardia with increasing rate, and by the risk of accelerating the tachycardia into fibrillation. Pacing (extrastimuli, bursts), low-energy cardioversion, and high-energy defibrillation therapies are all useful in safely treating a ventricular tachycardia. A implantable device is described which allows the classification of up to four different arrhythmias each having their own detection criteria (including high rate, sudden onset, rate stability and sustained high rate). For each classified arrhythmia, up to four, therapies may be programmed to be sequentially delivered. This scheme allows for increasing on the aggressiveness of the therapy based on elapsed time, increased rate, or both; and provides a large amount of flexibility for tailoring the desired therapies to individual patients.     

LACK OF PRESYNAPTIC EFFECTS OF KETANSERIN ON CARDIAC NORADRENERGIC NERVE TERMINALS IN THE SHR

The potential cardiac presynaptic effects of ketanserin (K) (0.01-3.00 mg/kg IV) were investigated in pithed SHR in 4 experimental conditions: (a) basal heart rate (HR); (b) HR increased by selective cardiac sympathetic stimulation (SS); (c) HR increased by aminophylline infusion; and (d) HR increased by SS and brought back to basal value by clonidine. Control groups were treated with saline. In the 4 types of experiments, K, starting from 0.3 mg/kg, induced almost identical and dose-dependent decreases in HR (maximal reduction: 45 beats/(min at 3 mg/kg). Thus we conclude: (1) that K is devoid of any presynaptic facilitatory effect on norepinephrine release since it was unable to raise HR in experiment D; (2) that K is devoid of any presynaptic inhibitory effect on norepinephrine release since it lowered HR to the same extent in both experiments B (noradrenergic tachycardia) and (non-noradrenergic tachycardia); and C (3) that the bradycardia which was induced by high doses of K (much above those required to block 5-HT2 and alpha 1-adrenergic receptors) and which was of similar magnitude in the 4 experimental conditions is probably due to a direct, nonspecific depressant effect of K on the sinus node.     

RESTRAINING EFFECTS OF LOSARTAN ON BLOOD PRESSURE AND HEART RATE VARIABILITY INDUCED BY STRESS

Summary— The effects of chronic treatment with losartan on blood pressure (BP) and heart rate (HR) variability responses during air-jet stress were studied in WKY and SHR. In untreated animals, air-jet stress induced an increase in systolic BP (SBP) (9 ± 2 mmHg for WKY and 8 ± 2 mmHg for SHR) and HR (56 ± 19 bpm for WKY and 76 ± 8 bpm for SHR). These changes were accompanied by an increase of the mid frequency (0.2–0.6 Hz, MF) component of HR in WKY (183%) and by an increase of the MF component of SBP in SHR (65%). Chronic suppression of the renin-angiotensin system (RAS) by losartan reduced resting BP only in SHR (-20 mmHg for SBP) without affecting HR and did not modify the resting MF components of BP and HR. This pretreatment did not alter the BP response in WKY to stress but impaired it in SHR. In both strains, treatment with losartan abolished all BP and HR variability changes, whereas the tachycardia response was unaltered. Losartan caused inhibition of BP and HR variability changes in response to stress in WKY and SHR. We provided evidence for the importance of the angiotensin II-sympathetic interaction in the BP and HR variability responses to a stressful environment.     

Efficacy of Pacemaker Tachycardia Termination Algorithms: Is Electrophysiological Testing Alone Adequate?

Selection of an optimal pacemaker tachycardia reversion algorithm is generally performed utilizing programmed electrical stimulation (PES). Multiple tachycardias are induced and various tachycardia termination protocols are tested for reversion success. However, PES may induce nonclinical tachycardia and result in an inaccurate assessment of subsequent reversion effectiveness for spontaneous tachycardia. To investigate this question, we compared tachycardia reversion protocol success for PES-induced tachycardia versus spontaneously occurring tachycardia in 16 patients with atrially placed Intermedics 262–12 antitachycardia pacemakers. The pacemaker has tachycardia response counters, and the reversion success was calculated from these counters. This was performed by comparing the percent of time 1° versus 2° modality use occurred; crossover to the 2° modality implied failure of the 1° modality to convert the tachycardia. PES was used to induce multiple episodes of tachycardia and spontaneous episodes of tachycardia were recorded over time by pacemaker counters. The pacemaker 1° modality success was then compared for spontaneous and induced arrhythmias. Results: A total of 53 discrete data comparisons of PES versus spontaneous tachycardia counters were performed in the 16 patients. PES reversion success occurred 85%± 22% of the time versus a spontaneous reversion success of 88%± 22%. However, the Spearman rank correlation coefficient test demonstrated nonsignificant overall correlation (P < 0.1), and Pearson correlation on an individual patient basis varied widely (r value from < 0.1 to 1.0). Conclusions: When utilizing the same termination algorithm, the percentage conversion of tachycardias occurring spontaneously and induced by PES is similar but does not correlate well overall. This suggests that PES may not be a good linear predictor of the long-term success of antitachycardia pacing algorithms.