Ventricular Pacing as the Preferable Mode for Long-Term Pacing in Patients with Carotid Sinus Syncope of the Cardioinhibitory Type

This study was designed to determine the efficacy of long-term VVI pacing in patients having the isolated cardioinhibitory type of carotid sinus syncope. The study included 20 patients suffering from repeated syncopal attacks; all were proven by electrophysiological studies to have isolated forms of cardioinhibitory type carotid sinus syncope. Long-term pacing by the VVI mode was carried out in all patients by programming the pacemaker rate well below the patient's sinus rate. The follow-up period after pacemaker implantation, which ranged from 2 to 54 months (average, 20 months), revealed that none of the patients had any recurrence of syncopal attack. Repeated Holter monitoring showed that ten had permanent sinus rhythm without any artificial pacing activity, while in the other ten, pacemaker activity was recorded--predominant in two patients and rare in the other eight. During Holter monitoring, attacks of weakness were reported by four patients; however, they were not related to pacemaker activity. This report indicates the importance of electrophysiological studies in patients suffering from carotid sinus syncope. These studies make possible the diagnosis of the isolated form of cardioinhibitory type syncope for which VVI pacing offers complete relief of symptomatology, thus rendering AV sequential pacing superfluous.     

Intermittent Ventricular Standstill During Chronic Atrial Fibrillation in Patients with Dizziness or Syncope

Thirty-two patients with atrial fibrillation and normal ventricular rates who complained of dizziness or loss of consciousness underwent 24-hour ambulatory electrocardiographic monitoring. A control group of 25 patients in atrial fibrillation but without symptoms of dizziness or loss of consciousness was likewise investigated. All patients remained in atrial fibrillation; periods of ventricular standstill (mean, 2.9; range, 1.8-8.0) were present in 31 symptomatic patients but in only three of the control patients (mean, 1.9 s; range, 1.7-2.4). Twenty-three symptomatic patients with pauses greater than or equal to 2.0 s received a demand pacemaker. Following pacing, nineteen became completely asymptomatic; four patients continued to have dizziness but three of these, who also experienced syncope, no longer did so (mean follow-up, 13 months; range, 6-30). It is suggested that ventricular standstill may commonly occur in patients with controlled atrial fibrillation who complain of dizziness or syncope and that the majority will benefit from permanent cardiac pacing.     

Temperature May Be an Appropriate Sensor for Chronotropically Incompetent Patients with Postural Syncope

Chronotropically incompetent patients benefit most from sensor driven rate response during exercise. Postural syncope may occur despite the chronotropic response because of the failure of currently available sensors to respond physiologically to postural changes. Seven chronotropically incompetent patients with postural syncope who had a dual chamber rate adaptive pacemaker (Circadia^R) that modulates heart rate in response to temperature change were studied with respect to: (1) response to exercise: and (2) head-up tilt (HUT). During exercise, continuous-wave Doppler of aortic velocities and two-dimensional echocardiographic derived measurements of left ventricular systolic function were used to assess cardiac function. Patients exercised longer (by an average of 168 sec) in the DDDF/compared to the DDl mode (P = 0.013). Increase in exercise duration was due mostly to the sensor driven increase during DDDH pacing. During DDDR pacing, heart rate increased from 71 ± 6 to 121 ± 17 ppm compared to 70 ± 1 to 103 ± 21 ppm for the DDl pacing (P = 0.038). Stroke volume as assessed by Doppler derived stroke distance (SD) contributed more significantly to the cardiac output increase during exercise in the DDl mode (SD increased from 13.4 ± 4 to 18 ± 7 cm in DDl compared to 13 ± 4 to 14 ± 2 cm in DDDR mode), although these mechanisms were insufficient to fully compensate for failure of appropriate chronotropic response. In response to the HUT, right ventricular temperature increased from 36.78°C ± 0.29°C to 36.89±± 0.28°C (P = 0.0002), and heart rate increased from 54 ± 3 to 71 ± 8 ppm (P = 0.0003) in the DDDR mode. No significant change in heart rate occurred in the DDl mode in response to the HUT. Strong positive correlation of temperature and heart rate was noted in all patients in response to HUT (P = 0.001, R²= 0.755–0.976). We conclude that temperature sensor responds physiologically to exercise and HUT. Therefore, temperature sensing rate adaptive dual chamber pacing may be appropriate for chronotropically incompetent patients with posture related syncope.     

Incidence and Predictors of Syncope in Paced Patients with Sick Sinus Syndrome

In spite of a normal pacemaker/unction, syncope still occurs in some patients with sick sinus syndrome (SSSJ. Causes often remain unknown. To identify predictors and etiologies of this bothersome symptom, we studied 507 patients who received atrial, ventricular, and dual-chamber pacemakers for SSS. During a mean follow-up of 62 ± 38 months, actuarial incidence of syncope was 3% at 1 year, 8% at 5 years, and 13% at 10 years. Causes were vasovagal (18%), orthostatic hypotension (25.5%), rapid atrial tachyarrhythmias (11.5%), ventricular tachycardia (5%), acute myocardial ischemia (2.5%), and pacemaker/lead malfunction (6.5%), In 13 patients (29.5%), syncope remained unexplained. The only preimplant predictor for syncope was syncope as primary indication for pacemaker implant. Electrocardiographic correlation with bradycardia was not a predictor of relief of syncope during the follow-up. In conclusion: (1) syncope in paced patients with SSS has multiple etiologies and may be multifactorial; (2) the only predictor of syncope after pacemaker implant is the occurrence of preimplant syncope as the main indication for pacing; (3) extensive Holier monitoring is not useful to document bradycardic origin of syncope nor to predict its recurrence; (4) SSS probably overlaps with other entities such as autonomic dysfunction, vasovagal syncope, carotid sinus hypersensitivity, and venous pooling, which would provide an explanation for recurrent syncope in patients with normal pacemaker function.     

Neural Monitoring of Vasovagal Syncope

Head-up tilt testing has become a valuable and widely accepted diagnostic tool for evaluation of patients with vasovagal syncope. This test has afforded clinical researchers the opportunity to focus on the hemodynamic, humoral, and neural changes that accompany syncope. We review the animal and clinical studies that provide insight into the possible pathophysiological mechanisms involved in vasovagal syncope. Hemodynamic measurements in patients with vasovagal syncope suggest that a relative decrease in ventricular size and increase in cardiac contractility may be seen in many patients with vasovagal syncope. Patients with vasovagal syncope have also demonstrated numerous "exaggerated" neurohumoral responses to syncope. Differential changes in plasma levels of epinephrine, renin, endothelin, vasopressin, cortisol, prolactin, beta endorphins, and substance P have been reported by some investigators either prior to or during a syncopal episode in patients with vasovagal syncope. The precise pathophysiological significance of these measurements is unknown at the present time. Measurements of autonomic tone may be accomplished indirectly with analysis of heart rate variability or baroreflex slope, or directly by sympathetic neural recordings of the peroneal nerve. We have demonstrated decreased baroreflex slopes in patients with vasovagal syncope. Using microneurography, we and others have demonstrated decreased sympathetic nerve activity occurring 11 ± 3 seconds prior to syncope during bead-up tilt table testing. A variety of other abnormal reflexes, including blunted forearm blood flow responses during exercise, have been demonstrated by others. These observations suggest that pacing instituted after the event may not be as helpful as the use of a hemodynamic sensor that will result in the initiation of pacing prior to sympathetic withdrawal or modify the decrease in sympathetic tone that occurs prior to syncope.     

Dual Chamber Pacing Aborts Vasovagal Syncope Induced by Head-Up 60° Tilt

To determine if pacing might prevent syncope in cardioinhibitory 'Malignant Vasovagal Syndrome' (also known as 'Neurally-Mediated Bradycardia/Hypotension'), a study of dual chamber pacing during head-up 60 degrees tilt was undertaken. Paired invasive tilts were performed in 10 patients who had a history of recurrent syncope, normal routine investigations including electrophysiological study and prior tilt-induced vasovagal syncope. Vasovagal reactions of identical severity were produced by prolonged 60 degrees head-up tilt on consecutive days in seven out of 10 patients. On day 2, without pacing, seven patients had tilt-induced vasovagal reactions and six became syncopal during the reaction. On day 3, with temporary DVI pacing with rate hysteresis, seven patients had tilt-induced vasovagal reactions and 1 patient was syncopal. Syncope was aborted in the other five patients. DVI pacing significantly improved cardiac index (CI) (one +/- 0.2 to 1.6 +/- 0.3 L/min/m2, P less than 0.01) and mean arterial blood pressure (MABP) (30 +/- 11 to 48 +/- 12 mmHg, P less than 0.01) during vasovagal reactions on day 3 compared with day 2. The mean period of time that patients could tolerate in the tilted position after the onset of the tilt-induced vasovagal reaction was significantly prolonged by pacing from 0.9 +/- 1.2 to 3.2 +/- 1.6 min (P less than 0.01). Dual chamber pacing may abort syncope in 85% of patients with cardioinhibitory malignant vasovagal syndrome. Pacing may prolong consciousness sufficiently during a vasovagal reaction to allow injury to be avoided.     

Recognizing Cardiac Syncope in Patients Presenting to the Emergency Department with Trauma

Background

Cardiac syncope is associated with poor outcomes and may result in traumatic injuries. In patients presenting to the emergency department (ED) with trauma, recognizing the cause of syncope is particularly challenging. Also, clinical markers to identify cardiac syncope are not well established.

Study Objectives

We sought to evaluate clinical markers that could identify cardiac syncope in patients with traumatic falls derived from a large urban trauma database.

Methods

All patients presenting to the ED during a 10-year study period with a traumatic fall were identified retrospectively. The subset of patients with syncope was ascertained by chart review and defined as cardiac syncope (e.g., presence of dysrhythmia, valvular abnormality), non-cardiac syncope (e.g., vasovagal, neurological), or syncope of unknown cause.

Results

Of the 5420 patients with traumatic falls, 180 (3.3%) patients with syncope were identified. Among the 180 patients with syncope, the cause was identified as cardiac in 24 (13%), noncardiac in 58 (32%), and unknown in 98 (54%). Three independent predictors (i.e., risk factors) of cardiac syncope were identified: age >65 years, presence of coronary artery disease, and pathological Q waves. Presence of at least one risk factor accurately predicted cardiac syncope in this population, with a sensitivity of 100%, a specificity of 43%, and a negative predictive value of 100% (area under the receiver operating characteristic curve: 0.80 ± 0.04).

Conclusion

In patients with traumatic falls and syncope, simple clinical and electrocardiographical variables may identify patients with cardiac causes of syncope. Proper identification of cardiac syncope in this population can potentially prevent recurrence of life-threatening traumatic injury.     

The Role of Electrophysiologic Studies in the Management of Patients with Unexplained Syncope

We evaluated the frequency and type of electrophysiologic abnormalities in an unselected population of consecutive patients with unexplained syncope. Fifty patients were entered in the study; all had 24-hour dynamic electrocardiographs (Holter) recordings and underwent complete electrophysiological studies. An abnormal electrophysiologic study was found in 74% of the patients. Sinus node abnormality was observed in 30%, abnormal AV node function in 14%, long HV in 10%, block distal to H during rapid atrial pacing in 6%, paroxysmal supraventricular tachycardia in 12%, ventricular tachycardialfibrillation in 8%, and hypersensitive carotid sinus syndrome in 24%. There was no correlation between Holter and electrophysiologic study findings except for the presence of paroxysmal sustained supraventricular tachycardia. Based on clinical, Holter monitoring, and electrophysiologic findings, 38% were treated by antiarrhythmic drugs, 40% received permanent pacemakers, and. 22% were not treated at all. During follow-up (23 ± 13 months), 9 patients (18%) experienced recurrent syncope or death.     

Cardiac Syncope: A Case Exhibiting Dichotomy Between Clinical Impression and Electrophysiologic Evaluation

This case report illustrates the value of electrophysiologic study in patients presenting with graphically unmonitored syncope and/or sudden cardiac death, and who have clinical markers of both bradycardia and ventricular tachycardia. In our patient, a wide QRS on the electrocardiogram and Holter monitor documented high grade ventricular ectopic activity. In this case, had therapy been solely guided by the clinical impression that the patient had ventricular tachycardia, the treatment would have resulted in increasing the risk of recurrence of syncope and/or sudden cardiac death.     

Long-Term Performance of Epimyocardial Pacing Leads in Adults: Comparison with Endocardial Leads

The long-term performance of epimyocardiaJ pacing leads in children is well established, but few studies have analyzed the performance in adults. This issue has clinical relevance in view of the increased use of epimyocardial leads with implantable cardioverter defibrillator and antitachycardia pacing systems. We analyzed 93 epimyocardial pacing "systems" (121 leads: 65 unipolar, 28 bipolar) in adult patients (age 57 ± 16 years), implanted since January 1980. Two different models were studied: Medtronic 4951 "Stab–on" (n = 35) and Medtronic 6917/6917A "Screw-in" (n = 58). A control group was created by randomly matching each epimyocardial system with two endocardial leads, according to age and year of implant. Epimyocardial and endocardial leads were followed-up for 44 ± 35 and 43 ± 35 months, respectively (P = NS). Freedom from failure for epimyocardial leads was 0.91 (95% Confidence Interval [95% CI] = 0.82 to 0.96) at 5 years, and 0.91 f95% CI = 0.69 to 0.98) at 10 years. No difference was found between the two analyzed models. Freedom from failure for endocardial leads was 0.97 (95% CI = 0.93 to 0.99) and 0.90 (95% CI = 0.61 to 0.97) at 5 and 10 years, respectively. Epimyocardial Jeads had a significantly poorer short-term survival than endocardiaJ leads, secondarily to earlier "technique related" failures (P = 0.03; relative riskc 3.0; Wilcoxon test). However, overall long-term performance was similar to endocardial leads. Epimyocardial pacing leads, meticulously implanted and tested, have a long-term performance similar to endocardial pacing leads.     

A New Pacemaker for Monitoring Asystole and Prevention of Adams-Stokes Syndrome and Sudden Cardiac Death

Patients with suspected Adams-Stokes syndrome are examined by Holter monitoring. During the monitoring, there is the danger of syncopes occurring and there are even reports of sudden cardiac death. We therefore developed a pacemaker for cardiac arrest monitoring and the prevention of Adams-Stokes syndrome and sudden cardiac death, which has the following functions: (1) the longest escape interval of the pacemaker not exceeding the value at which syncope is induced is determined by the decline of the mean heart rate including the asystole to a certain threshold rate; (2) once the pacemaker escapes from the interval it continues pacing for a while at a physiological rate to allow recover from ischemias in organs or tissues; and (3) to prevent overdrive suppression to the heart, the pacing rate gradually declines and stops pacing until the next asystole. This pacemaker is useful not only in the diagnosis of Adams-Stokes syndrome but also in pharmacological and pathophysiological studies and in determining when pacing should cease.     

Electrocardiographic Recognition of Variant Angina During Permanent Pacing

We present a patient with a permanent venlricular pacemaker who was investigated for episodes of chest pain associated with syncope. Ambulatory electrocardiographic monitoring showed essentially paced rhythm. ST segment elevation of the paced beats was observed during spontaneous chest pain, but the significance of this finding was initially unclear in the context of the abnormal repolarization associated intrinsically with paced rhythm. At angiography, coronary spasm was demonstrated after ergonovine, and this was associated with ST segment elevation during paced rhythm and with chest pain. We conclude that ST segment elevation may indicate myocardial ischemia even when observed in the face of abnormal repolarization associated with paced rhythm.     

Electrocardiographic patterns during: pacing the great cardiac and middle cardiac veins

BACKGROUND: The electrocardiogram (ECG) patterns during pacing from the great cardiac vein (GCV) and the middle cardiac vein (MCV) are not well known. METHODS: We recorded 12-lead ECGs during GCV and MCV pacing in 26 patients undergoing implantation of a cardiac resynchronization device. The left ventricular (LV) lead was passed down the GCV (n = 19) or MCV (n = 7) prior to moving it to a lateral or posterolateral vein for permanent implantation. RESULTS AND CONCLUSIONS: Pacing within the GCV resulted in a left bundle branch block (LBBB) morphology with no or minimal R-wave in V(1) in 14 patients and a right bundle branch block (RBBB) pattern (R > S in lead V(1)) in four patients. In one patient, lead V1 during GCV pacing was isoelectric (R = S). A more distal pacing site in the GCV yielded a LBBB pattern in all the patients. All leads placed in the MCV resulted in a LBBB configuration. An ECG pattern with a RBBB pattern was invariably recorded during LV pacing in 125 consecutive outpatients with biventricular pacemakers and LV leads in the posterolatral and lateral coronary veins. Knowledge of the ECG patterns from various pacing sites in the coronary venous system may be helpful for troubleshooting all types of pacing systems, especially those where the coronary venous pacing site is unintentional.     

Heart Rate Monitoring in Implanted Pacemakers

Increasing pacemaker memory allows integration of heart rate monitoring into the pacemaker. Two main methods can be distinguished. 1. Heart rate monitoring in histograms. 2. Heart rate monitoring in the time domain (heart rate holter). Method 1 is useful in antitachycardia and diagnostic pacemakers when short specific events must be detected (tachycadia, bradycardia). For the analysis of a rate adaptive pacemaker this method is less appropriate as it does not give any information about the dynamics of rate changes or its time relations. For this purpose Method 2 will give more information about the functioning of the pacemaker as it does not only store the heart rate but also the timing of the heart rate so that changes in heart rate can be correlated to the activity of the patient. An algorithm was developed to store the average heart rate over 7.8 minute periods in a pacemaker. On interrogation of the pacemaker the information will always reveal the heart rate over the 24 hours prior to interrogation. This monitor can also be temporarily programmed to store the average heart rate in 20 second intervals to monitor the response to an exercise test for a period of 1 hour. The time needed for a standand follow-up procedure of a rate adaptive pacemaker can be dramatically reduced to a value close to the follow-up time of a standard WI pacemaker.     

Radioisotopic Pacemaker: Long-Term Clinical Results

In order to prolong the service life of the generator, the isotopic pacemakers, powered by Pu²³⁸, have been developed and implanted since 1970. We report the follow-up of 325 patients (mean age 39 ± 18 years) implanted with an isotopic pulse generator (Medtronic 9000/9090) between April 1970 and July 1982. The mean follow-up was 12 years (range 6 days to 18.5 years). The generator was highly reliable; the mean value of pacing rate between implantation and last follow-up decreased significantly but no more than 1 beat/min (72.7 vs 71.8 beats/ min; P < 0.001) and the pulse width did not change significantly. The actuarial survival of the device was 97% at 18.5 years. During the follow-up period, 122 reoperations were performed in 85 patients: 88 explanations of the entire pacing system and 34 modifications of the lead system. Lead dysfunction accounted for 68% of the 122 reoperations, generator failure for 6%, and miscellaneous reasons for 26%. However, 72% of patients remain free of intervention during the follow-up period and 61 patients (20%) died during this period. Most deaths (52%) were of nonsudden cardiovascular origin, 17% were related to cancer, and 13% to sudden death. After 5, 10, and 18.5 years, 94%, 89%, and 73% of the patients were alive, respectively. No side effect could be attributed to the radioisotope. We conclude that this isotopic pacemaker demonstrated its reliability for long-term cardiac pacing.     

Recurrent Symptoms after Ventricular Pacing in Unexplained Syncope

We report clinical and hemodynamic data in two cases of recurrent syncope. Both patients received permanent demand ventricular pacing (VVI) for unexplained syncope. Both patients experienced recurrent syncope after pacemaker implantation. They later underwent 60 degrees head-up tilt testing, initially noninvasively and then with hemodynamic profile. A vasovagal response to tilt occurred with bradycardia and was complicated by the onset of ventricular pacing and retrograde atrioventricular conduction (RAVC) with hemodynamic deterioration and rapid reproduction of syncope. Limited intracardiac electrophysiological study (EPS) excluded atrioventricular (AV) conduction disease, sinus node disease, and carotid sinus syndrome, and confirmed RAVC. Both patients were upgraded to dual chamber pacing, DDI mode, with 50/80 rate hysteresis. One patient was asymptomatic at repeat tilt testing; the other experienced continued symptoms due to the vasodepressor component of vasovagal syncope. Cardiac pacing alone is ineffective treatment for this phenomenon, and no proven therapy is presently available. Ventricular pacing applied to patients with unexplained syncope may lead to an increase in or continuation of symptoms rather than an amelioration. There is a need for full investigation of such patients, which must include tilt testing, to allow for the most accurate diagnosis possible and guide the most appropriate therapy.     

Bradycardia and Syncope in Children Not Controlled by Pacing: Beta-Adrenergic Hypersensitivity

Cardiac pacing is frequently employed in the therapy of children with syncope and documented bradycardia. This report describes two children, ages 7 and 9 years, who underwent placement of demand ventricular pacing systems for documented bradycardia and syncope. Cardiac catheterization and intracardiac electrophysiological studies failed to show evidence of structural abnormalities, sinus node or conduction system disease, inducible arrhythmias, or VA conduction in each patient. Both patients had persistent symptoms after pacemaker implantation. Autonomic function testing with continuous heart rate and blood pressure monitoring revealed exaggerated beta-adrenergic responses to simple standing and small doses of isoproterenol. Symptoms were completely eliminated with atenolol. In these two children, cardiac pacing alone was not adequate for relief of symptoms. Autonomic mechanisms of bradycardia and hypotension should be considered prior to implantation of permanent pacing systems in children.     

Long-Term Performance of Endocardial Pacing Leads

To assess the performance of endocardial pacemaker leads and to identify factors associated with structural lead failure, medical records of 2,611 endocardial pacing leads (in 1, 5W patients) implanted between 1980 and 1991, having at least 1 month of follow-up, were reviewed. Leads without structural failure had normal function at the last follow-up date, or were discontinued for reasons other than structural failure (patient death, infection, dislodgment, lead-pacemaker incompatibility, operative complication, or abandonment by telemetry not related to failure). Leads with suspected structural failures were invasively or noninvasively disconnected because of clinical malfunction (loss of capture or sensing, oversensing, elevated thresholds, or skeletal muscular stimulation). Leads with verified structural failures met the criteria for suspected lead failure and also had a visible defect seen in the operating room or on chest roentgenograms, a change in the impedance interpreted by the physician as lead disruption, or a manufacturer's return product report that confirmed structural failure. Variables analyzed included patients’ age and gender, paced chamber, venous access, insulation materials, fixation mechanism, coaxial design, polarity, and different lead models. The cumulative lead survival at 5 and 10 years were 97.4% and 92.9%, respectively, for suspected failures; and 98.7% and 97.3%, respectively, for verified failures. Leads in older patients (≥ 65 years old), and leads in atrial position had fewer verified failures (P = 0.014 and P = 0.007, respectively). Unipolar leads also tended to perform better according to the verified definition (P = 0.07). The lead Medtronic 4012 had more suspected (P < 0.05) and more verified failures (P < 0.01), the lead CPI 4010 had more verified failures (P < 0.05) than the entire group of ventricular leads. Conclusions: Endocardial pacing leads implanted in atrial position, and implanted in older patients (> 65 years old) seems to have better long-term survival. Some lead models (Medtronic 4012 and CPI 4010) had poor survival rates, that could not be explained by the analyzed variables. The expected performance of endocardial pacing leads varies according to how failure is defined.     

Clinical Evaluation of Automatic Tachycardia Diagnosis by an Implanted Device

Reliable discrimination between sinus tachycardia (ST) and pathologic tachycardia has been a major problem for automatic implantable antitachycardia devices. In patients whose sinus response to activity is as rapid or faster than their pathologic tachycardia (rate crossover), these unsophisticated devices deliver the programmed tachycardia response to either the pathologic or sinus tachycardia. Over a one-year period, 50 Intermedics Intertach Model 262–12 antitachycardia pulse generators were implanted to evaluate the specificity of a new group of tachycardia recognition algorithms. Patients were subjected to exercise testing and noninvasive programmed stimulation to demonstrate the efficacy of this new approach. The five recognition algorithms tested were various combinations of the following criteria: high rate HR), sudden onset (SO), rate stability (RS), and sustained high rate (SHR). False positive rates (tachycardia response inappropriately triggered by ST) were as follows: HR (93%); HR + SO (3%); HR + RS (63%); HR + (RS or SHR) (87%); HR + HS + SO (8%). Pair-wise significance testing between HR only and HR + SO (p < 0.001), HR + RS (p = 0.01) and HR + SO + RS (p < 0.001), demonstrated a significant reduction in the rate of false positives through the use of the sudden onset and rate stability criteria in concert with the standard high rate criterion.