Ventricular Stimulation Threshold Research Articles

Стадии артериальной гипертензии и параметры электрокардиостимуляции у пациентов на годовом этапе после имплантации и медикаментозной терапии

Наблюдали 129 пациентов (69 мужчин и 60 женщин) в возрасте (69,5±11,6) лет на годовом этапе поддерживающей медикаментозной терапии после имплантации электрокардиостимуляторов (ЭКС) в режимах DDD/DDDR и VVI/VVIR стимуляции. Пациенты были разделены на 2 группы – II и III стадии артериальной гипертензии (АГ). В раннем послеоперационном, полугодовом и годовом периодах после имплантации, в зависимости от стадии АГ, оценивали такие параметры электрокардиостимуляции: базовую частоту стимуляции, атриовентрикулярную задержку (стимулированную и детектированную), порог стимуляции желудочков, импеданс желудочкового электрода, процент желудочковой стимуляции. Результаты показали отсутствие значимого различия в изменении параметров ЭКС между режимами стимуляции DDD/DDDR и VVI/VVIR у пациентов с имплантированными ЭКС и АГ. Установили, что АГ III стадии требует более высокого порога стимуляции желудочков, импеданса желудочкового электрода, АВ-задержки стимулированного и детектированного комплексов, процента желудочковой стимуляции, чем АГ II стадии на всех этапах наблюдения. Тщательное медикаментозное сопровождение пациентов с АГ и ЭКС с учетом стадии АГ позволяет улучшить параметры ЭКС

Perte de capture par ischémie myocardique : à propos d’un cas

We report the case of a patient with pacemaker who presented chest pain during exercise followed by fainting. He has a history of arterial hypertension and diabetes. The initial examination was normal; the ventricular stimulation threshold was 1.125 volts (V) and cardiac enzymes were normal. Stress test has reproduced chest pain followed by loss of pacemaker capture and asystole. Coronary angiography showed a tight stenosis of the proximal anterior interventricular artery dilated by a drug-eluting stent. The control of stress test was normal. A stent thrombosis eight days later led to an acute coronary syndrome with recurrent syncope due to the loss of ventricular capture. The ventricular pacing threshold was then 2.25V. After revascularization and stabilization of the patient's clinical status, this threshold returned to 1.125V. This clinic case has confirmed that coronary artery disease could increase pacing threshold. It also highlights the usefulness of automatic capture algorithms in coronary patients. The stress test cannot only help to detect coronary artery disease but also allows the optimization of programming the pacemaker.

Single chamber permanent epicardial pacing for children with congenital heart disease after surgical repair

BackgroundTo analyze the 10-year experience of single chamber permanent epicardial pacemaker placement for children with congenital heart diseases (CHD) after surgical repair.MethodsBetween 2002 and 2014, a total of 35 patients with CHD (age: 26.9 ± 23.2 months, weight: 9.7 ± 5.6 kg) received permanent epicardial pacemaker placement following corrective surgery. Echocardiography and programming information of the pacemaker, as well as major adverse cardiac events (MACE) as heart failure or sudden death, were recorded during follow-up (46.8 ± 33.8 months).ResultsAcute ventricular stimulation threshold was 1.34 ± 0.72 V and no significant increase was observed at the last follow-up as 1.37 ± 0.81 V (p = 0.93). Compared with initial pacemaker implantation, the last follow-up didn’t show significant increases in impedance (p = 0.327) or R wave (p = 0.635). Four patients received pacemaker replacement because of battery depletion. 7/35 (20 %) of patients experienced MACE. Although the age and body weight were similar between patients with and without MACE, the patients with MACE were with complex CHD (100 % vs.55.6 %, p = 0.04).ConclusionHigh-degree iatrogenic atrioventricular block was the primary reason for placement of epicardial pacemaker for patients with CHD after surgical repair. Pacemaker placement with the steroid-eluting leads results in acceptable outcomes, however, the pacemaker type should be optimized for the children with complex CHD.

184: A simple method to implant epicardial AICD using two separated coils

Surgical epicardial AICD implantation has been quite abandoned since developpement of endocardial leads and decrease in AICD size. Epicardial patches did not improve since 30 years, are rigid and need to be sewed to the epicard which favors bleeding. In some rare cases, epicardial AICD implantation remains indicated. Therefore we tested a new simple implant technique in 5 patients undergoing open chest surgery trough a median sternotomy. In 3 cases surgery was performed for percutaneous infected lead extraction failure. The two other patients required surgical operation and AICD implant (one for mitral valve regurgitation, one for tricuspid repair). A screw-in bipolar pace/sense lead (St Jude MyodexTM 1084T) was placed on the right ventricular free wall and two defibrillation leads (Medtronic Transvene ® 6937) were respectively sewed on the pulmonary artery trunk and on the diaphragmatic wall of the right ventricle and then connected to an AICD (Biotronik Lumax 540) placed in an abdominal pocket. Best defibrillation configuration (31 J tested) was obtained with a shock delivered between the two coils (AICD passive), from the inferior one to the superior one. There were no major cardiovascular complications. Clinical and telemonitoring follow up (mean 10 months) showed stable ventricular stimulation and detection thresholds as well as lead and coil impedances. No arrhythmias occurred. Epicardial AICD implantation is feasible in a simple way. Long term follow up is needed to confirm post operative results.

An observational study of the effect of coronary artery disease severity on acute pacing threshold and lead impedance in patients with permanent pacemaker

This study investigated the effect of coronary artery disease (CAD) severity, distribution and left ventricular ejection fraction (LVEF) on acute ventricular pacing threshold and lead impedance at the time of pacemaker implantation. One hundred and thirty-two patients who received a ventricular pacemaker or internal cardioverter-defibrilator (ICD) lead in our institution between 2007-2010 were included in this observational study. Patients were divided into ICD and anti-bradycardic pacemaker (PM) groups. Groups were compared for ventricular stimulation threshold, lead impedance and LVEF. Later, groups were sub-grouped according to the severity and distribution of CAD and subgroups were compared in both groups for ventricular stimulation threshold, lead impedance. Quantitative data of groups were compared by means of independent samples t-test. Ventricular pacing thresholds were found significantly higher ICD group compared with PM group (p<0.05). Impedance and LVEF values were significantly lower in ICD group (p<0.05). Impedance and ventricular pacing thresholds were comparable in subgroups of ICD and PM groups. Our study does not confirm any relationship between pacing parameters and severity-distribution of CAD and LVEF. Patients with ventricular ICD lead had higher pacing thresholds but lower pacing impedance values comparing with PM group. This study did not find any significant relationship between pacing parameters at implantation and LVEF, severity and distribution of CAD.

Sudden reversible pacemaker failure in a patient with cardiac sarcoidosis: an unfortunate case of ventricular septal pacing

We report a case of sudden marked deterioration of ventricular stimulation threshold resulting in pacemaker failure 16 months after a ventricular septal lead implantation for atrioventricular block. Echocardiography revealed septal wall thinning at the electrode-tissue interface, which was not detected pre-operatively. Endomyocardial biopsy confirmed cardiac sarcoidosis. The increased threshold was reversible with prednisolone.

Right ventricular stimulation threshold at ICD implant predicts device therapy in primary prevention patients with ischaemic heart disease

Myocardial excitability is known (amongst other reasons) to be related to the degree of ischaemia, contractile dysfunction and heart failure. It was hypothesized that the right ventricular (RV) stimulation threshold has prognostic value with respect to the occurrence of ventricular arrhythmias (VAs) and patient survival in recipients of an implantable cardioverter defibrillator (ICD). Ischaemic heart disease patients receiving an ICD at Leiden University Medical Center as primary prevention for sudden cardiac death were included in this study. Right ventricular thresholds were determined at ICD implant. Data were collected on VAs triggering ICD therapy and on all-cause mortality. A total of 689 consecutive patients were included (87% male, age 63 ± 11 years, left ventricular ejection fraction (LVEF) 29 ± 11%) and followed for a median of 28 months. Post-implant RV-threshold was 0.7 ± 0.5 volt (V) at 0.5 ms pulse duration. Best dichotomous separation was reached at a cut-off of 1 V. During follow-up, 167 (24%) patients received appropriate ICD therapy, 88 (13%) had appropriate shocks and 134 (19%) died. Cumulative appropriate shock incidence for patients with RV threshold ≥ 1 V (n = 166) was 16% at 1 year, 24% at 3 years and 34% at 5 years compared with 4, 11 and 17% for patients with an RV-threshold < 1 V (n = 523). Adjusted hazard ratio of RV threshold ≥ 1 V was 2.0 (95% CI: 1.4-2.9) for appropriate therapy, 3.3 (95% CI: 2.0-5.4) for appropriate shocks and 1.6 (95% CI: 1.1-2.5) for mortality. The RV stimulation threshold at ICD implant has a strong independent prognostic value for the occurrence of VAs triggering appropriate ICD therapy, appropriate shocks and mortality.

Seguimiento en fase aguda de catéteres electrodos de estimulación endocavitaria permanente: Comparación de tres modelos

Electrode lead design and materials influence their performance, stability and manipulation characteristics. In our laboratory, we use straight intracardiac, active fixation, steroid eluting leads. These features are shared by three brands of pacemaker distributors. To compare the short term results of three brands of leads used in our laboratory in patients requiring the implant of a pacemaker or cardioverter. One hundred and four patients (mean age 70 years, 59 males) subjected to a pacemaker or cardioverter implant were studied and followed during the first three months post implant. In these patients, 49 Guidant Flextend 4087 or 4088, 27 Saint Jude Tendril 1488T and 10 Medtronic Capsurefix 5076 leads were implanted in the right atrium and 60 Guidant Flextend 4087 or 4088, 29 Saint Jude Tendril 1488T and 19 Medtronic Capsurefix 5076 leads were implanted in the right ventricle. Implant parameters were adequate for all leads. A sub-acute rise in ventricular stimulation threshold was detected in one Flextrend lead. Three atrial leads (two Flextend and one Capsurefix) and one Capsurefix ventricular lead experienced an acute displacement. One patient with a Flextend lead, had a cardiac tamponade caused by an atrial perforation. The three brands of leads tested can be successfully implanted with comparable parameters and without differences in the evolution of patients during the first three months.

Perfil clínico de pacientes chagásicos e não-chagásicos portadores de marca-passo cardíaco artificial

The aim of this study was to compare Chagas and non-Chagas' disease patients using single or dual-chamber pacemaker in relation to the ejection fraction of the left ventricle, the ventricular stimulation threshold and the occurrence of ventricular arrhythmia. From January, 2001 to November, 2002, 45 Chagas' disease patients and 35 non-Chagas' disease patients, all pacemaker users, were evaluated considering clinical history, echocardiographic study, Holter monitoring and analysis of the pacemaker telemetry data. Chagas' disease patients were significantly younger, but both groups were similar when chest X-Ray variables and right ventricular stimulation threshold were analyzed. Chagas' disease patients had a lower left ventricular ejection fraction and more frequent ventricular arrhythmia during Holter monitoring. A positive correlation between the low ejection fraction of the left ventricle and the intensity of ventricular arrhythmia was observed. In conclusion, among pacemaker user patients, Chagas' disease is related to cardiac markers of worse prognosis.

P2-2: Outcomes of six monthly stimulation threshold assessments in patients with pacing systems: A twentieth year follow-up

The purpose of this review was to evaluate the yield of atrial & ventricular stimulation threshold (ST) assessments at each routine six month pacemaker clinic (PC) visit. Since n 1983, and as reported in 1995, six monthly ST have been performed in all 886 actively followed pts: 73.34 ± 0.27 (range 16-102 yrs) with programmable output pacing systems (PS) to establish reduced output levels for safe capture margins while maintaining pulse generator longevity. All records of pts with PS implanted for greater than 24 months were retrospectively reviewed for ST stability.

Clinical Performance of a Ventricular Automatic Capture Verification Algorithm

This study was conducted to evaluate the clinical performance of the ventricular automatic capture feature as implemented in the Insignia I Ultra pacemaker system (Guidant) utilizing a variety of ventricular leads. Currently, the optimal programming of the pacemaker output considers both pacemaker efficiency (prolonging battery longevity) and patient safety (adequate safety margin). The ability of a pacemaker to automatically adjust the ventricular output above the pacing threshold while maintaining the appropriate safety margin has been explored since the early 1970s and is only available today in conjunction with a specific low polarization lead system. One hundred and five patients were enrolled from 17 European centers utilizing 31 different types of ventricular leads were followed through their 3-month follow-up visit. There were no restrictions on the type of ventricular leads used. The average mean difference between the commanded autothreshold test (0.652 + 0.335 V) and the manual threshold test (0.651 + 0.335 V) was 0.001 + 0.49 (P < 0.0001). The average mean difference between the ambulatory autothreshold test (0.696 + 0.322 V) and the commanded autothreshold test (0.682 + 0.315 V) was 0.002 + 0.74 (P < 0.0001). Holter recordings confirmed that there were no loss of capture incidences without a backup pulse being delivered. In addition, the mean number of backup pulses delivered in a 24-hour period was less than 0.1% of the total number of paced beats. This study provided that the automatic capture feature while using a variety of leads accurately determines the ventricular stimulation threshold and safely delivers a backup pulse when required.

MRT-Untersuchungen des Hirns bei Patienten mit implantierten Herzschrittmachern. Experimentelle und klinische Untersuchungen an einem 1,5 Tesla-System

In-vitro and In-vivo evaluation of feasibility and safety of MRI of the brain at 1.5 T in patients with implanted pacemakers (PM). 24 PM models and 45 PM electrodes were tested In-vitro with respect to translational forces, heating of PM leads, behaviour of reed switch (activated vs. deactivated) and function at a 1.5 T MRI-system (actively shielded, maximum field gradient: 30 mT/m; rise time: 150 T/m/s). Based on these results, 63 MRI examinations in 45 patients with implanted PM were performed. Prior to MRI the PM were re-programmed in an asynchronous mode. The maximum SAR of MRI-sequences was limited to 1.2 W/kg. Continuous monitoring of ECG and pulse oximetry was performed during MRI. PM inquiry was performed prior to MRI, immediately after MRI and -- to assess long-term damages -- three months after the MRI exams, including determination of stimulation thresholds to assess potential thermal myocardial injuries at the lead tips. Translational forces (F (max) < or = 560 mN) and temperature increase (DeltaT (max) < or = 2.98 degrees C) were in a range which does not represent a safety concern from a biophysical point of view. No changes to the programmed parameters of the PM or damage of PM components were observed neither In-vitro (n = 0/24) nor In-vivo (n = 0/63). Despite the strong magnetic field, the reed switch remained deactivated in 54 % (13/24) of the cases during In-vitro simulated MRI exams of the brain. All patient studies (n = 63/63) could be completed without any complications. Atrial and ventricular stimulation thresholds (expressed as pulse duration at 2-fold rheobase) did not change significantly immediately post-MRI nor in the 3 months follow-up (pre-MRI: 0.17 ms +/- 0.13 ms, post-MRI: 0.18 ms +/- 0.14 ms, 3 months follow-up: 0.17 ms +/- 0.12 ms). MRI of the brain at 1.5 Tesla can be safely performed in carefully selected clinical circumstances when appropriate strategies are used (re-programming the PM to an asynchronous mode, continuous monitoring of ECG and pulse oximetry, limiting the SAR value of the MRI sequences, cardiological stand-by). Based on these studies, implanted PM should not longer be regarded as an absolute contraindication for MRI at 1.5 T.

Left ventricular remodeling during cardiac resynchronization therapy: effect on ventricular dimension and stimulation threshold chronically after biventricular pacing

Left ventricular remodeling during cardiac resynchronization therapy: effect on ventricular dimension and stimulation threshold chronically after biventricular pacing

Long-term follow-up of pacemakers with an Autocapture pacing system.

The aim of this study was to evaluate the safety and performance of the Autocapture pacing system during a 5-year follow-up period. The study was conducted retrospectively between May 1996 and May 2001. Sixty consecutive patients who had undergone VVI pacemaker implantation using an Autocapture program with leads 1402T (n: 31) and 1452T (n: 29) were included in the study. Intraoperative measurements including a ventricular stimulation threshold test, sensing of intrinsic R wave (mV), and lead impedance (W) were done by a standard pacing system analyzer. Evoked responses (ER, mV) and polarization signals (PS, mV) were measured after the pocket was closed. Pacing thresholds by Autocapture (AC thrd, V) and Vario (Vario thrd, V), battery current (mA), and battery impedance (kW) were also repeated during predischarge and 1, 6, 12, 18, 24, 30, 40, 50, and 60 months after discharge. According to the ER and PS values an Autocapture algorithm could be activated in 49 patients (88%). The Autocapture algorithm remained active during the follow-up in all of these patients. In patients with inappropriate ER and PS values (11 patients, 12%), pacemakers were programmed to a VVIR pacing mode and Autocapture algorithm was inactivated. ER and PS values did not reach appropriate values to activate the Autocapture algorithm in any of these patients in consecutive follow-ups. Twenty-four-hour Holter monitoring could be conducted in 32 patients (53%). In all recordings, when the loss of capture occurred, it was confirmed that back-up pacing continued. When the first measurements recorded during implantation were compared to approximately the 5th year measurements; ER (9.2 mV vs 9.6 mV), PS signal (1.13 +/- 0.30 mV vs 1.15 +/- 0.72 mV), AC thrd (0.4 V vs 1.2 V), Vario thrd (0.7 V vs 1.3 V), and lead impedance (502 ohm vs 620 ohm) were not changed significantly. Battery impedance increased 1 kOhm between 30-40 months of the implantation. Seven deaths occurred during follow-up. Three patients had fatal myocardial infarction, one died due to a non-cardiac event, and the remaining three died due to progressive heart failure. ER, R wave amplitude, and PS, which are the main parameters for the continuation of Autocapture function, did not change significantly during long-term follow-up. High output back up pacing provided additional safety for sudden rises in threshold. The Autocapture pacing algorithm was found to be effective and reliable during long-term follow-up.

Influence of Acute Exposure to High Altitude and Hypoxemia on Ventricular Stimulation Thresholds in Pacemaker Patients

Cardiac stimulation threshold of implanted pacemakers may be influenced by a variety of endogenous and exogenous factors. High altitude provokes hypoxemia, which may change stimulation thresholds, besides causing other important physiological changes. The aim of our study was to investigate the influence of high altitude on ventricular stimulation thresholds in pacemaker patients. Thirteen patients (10 men; aged 65.5 +/- 4.8 years) with implanted single chamber pacemakers (nine with Pacesetter Regency SR+ with the Autocapture feature) were exposed to an altitude of 4,000 m above sea level, as simulated in a hypobaric chamber. Stepwise ascension was performed with a speed of 5 m/s starting at 450 m above sea level. A 5-minute rest was performed every 500 m to measure stimulation threshold at each step. After a stay of 30 minutes at 4,000 m stimulation threshold was measured, followed by a stepwise descent. Pacemaker interrogation and arterial blood gas analysis were performed at 450 and at 4,000 m, and a strength-duration curve was determined. Blood pressure, heart rate, and oxygen saturation were monitored continuously during the study. Ascent to 4,000 m above sea level induced a significant decrease in arterial pO2 (10.7 +/- 1.1 vs 5.5 +/- 0.3 kPa), pCO2 (5.3 +/- 0.3 vs 4.7 +/- 0.4 kPa), oxygen saturation measured by arterial blood gas analysis (95.5% +/- 1.2% vs 79.1% +/- 2.5%), and increase in pH (7.39 +/- 0.02 vs 7.45 +/- 0.04) (P < 0.0001). Stimulation thresholds and the strength-duration curve remained unchanged in all patients throughout the study. In conclusion, exposure to an altitude of 4,000 m above sea level with resultant hypobaric hypoxemia has no impact on ventricular stimulation thresholds. Therefore, in regard to the safety of pacing, pacemaker patients can safely be exposed to this altitude.

Arrhythmogenesis in experimental models of heart failure: the role of increased load.

To assess the effects of cardiac failure due to doxorubicin cardiotoxicity or chronic myocardial infarction on arrhythmia induction, ventricular repolarization and refractoriness in isolated perfused rabbit hearts under different loading conditions. Cardiac failure was induced by doxorubicin injection (1-1.25 mg.kg-1 twice weekly for 8 weeks, n = 16) or coronary ligation (n = 12), with 12 controls. Cardiac failure was defined by an echocardiographic ejection fraction < or = 0.40. Arrhythmia susceptibility was assessed by programmed ventricular stimulation and fibrillation threshold measurement during Langendorff and during working heart perfusion under baseline conditions and at maximum tolerated preload and afterload. Monophasic action potential duration, dispersion of refractoriness, conduction time and effective refractory period were measured at each level of load. During unloaded (Langendorff) perfusion, there was a low incidence of arrhythmia induction in all hearts. Increasing load did not alter arrhythmogenesis significantly in normal hearts, but led to increases in arrhythmia inducibility and falls in fibrillation threshold which were significantly greater in failing than in non-failing hearts. Monophasic action potential duration was significantly (P < 0.05) shorter in failing than in non-failing hearts in the doxorubicin-treated [mean (s.e.m.) 140(2) vs. 147(2) ms] and post-infarction groups [146(2) vs. 154 (3) ms] during working heart perfusion. The shortening in action potential duration and effective refractory period during increased preload tended to be greater in failing than in non-failing hearts. There were no changes in conduction times in response to changes in loading. The inducibility of ventricular arrhythmias is greater in failing than in non-failing hearts and is further enhanced by increases in preload. Shortening of repolarization and refractoriness due to increased preload may contribute to the increased risk of ventricular tachyarrhythmias and sudden death in cardiac failure.

Transthoracic DC Shock May Represent a Serious Hazard in Pacemaker Dependent Patients

External defibrillation is widely used for the termination of various atrial and ventricular tachyarrhythmias, including pacemaker patients. Our study was intended to evaluate the effects of DC shocks in 36 patients with unipolar pacemakers implanted in the right pectoral region (25 DDD, 10 VVI, 3 AAI). The shocks were delivered with paddles on the anterior surface of the thorax, as far as possible away from the pacemaker. The pacing output was programmed at 0.5 msec and 5 V (25 patients), 4 V (1 patient), and 2.5 V (10 patients). Transient loss of capture occurred in 18 patients (50%). These patients, compared with those without capture failure, received higher peak and cumulative shock energies, respectively, 216 +/- 99 versus 123 +/- 50 joules (P < 0.002) and 352 +/- 62 versus 147 +/- 98 joules (P < 0.004) and had a lower pacemaker pulse amplitude (4.0 +/- 1.2 vs 4.6 +/- 1.0 V, P = 0.11). Failure to capture lasted from 5 seconds to 30 minutes (mean 157 sec). In 15 patients the ventricular stimulation threshold was measured before and serially after cardioversion. A six-fold threshold increase was observed 3 minutes after the shock (P < 0.004) with gradual recovery to nearly baseline values at 24 hours. Transient sensing failure occurred in 7 of the 17 patients in whom it could be evaluated (41%). Furthermore, three cases of shock induced pacemaker malfunctions were observed requiring replacement of the stimulator in two patients. In conclusion, the incidence of loss of capture in pacemaker patients subjected to electrical cardioversion/defibrillation is high.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute and long-term ventricular stimulation thresholds with a new, iridium oxide-coated electrode.

Efforts have been made to design electrodes that significantly reduce not only the acute and chronic stimulation thresholds, but also attenuate the early peaking phenomenon and polarization. At two voltage levels (2.7 V and 5.4 V, respectively), we evaluated the right ventricular stimulation thresholds obtained with a new, iridium oxide-coated electrode in ten patients who received a VVI pacemaker. Measurements were made at implant and at multiple intervals for 1 year. Pulse width stimulation thresholds at implant were as follow: 0.04 +/- 0.008 msec at 2.7 V, 0.03 +/- 0.004 msec at 5.4 V; values at 2 weeks were 0.14 +/- 0.06 msec at 2.7 V, 0.07 +/- 0.025 msec at 5.4 V; values at 3 months were 0.09 +/- 0.03 msec at 2.7 V, 0.05 +/- 0.01 msec at 5.4 V; values at 1 year were 0.08 +/- 0.02 msec at 2.7 V, 0.04 +/- 0.01 msec at 5.4 V. The maximal increase of 0.11 +/- 0.05 msec occurred at 2.7 V, 2 weeks after implant. Our results indicate that this new electrode provides low acute and long-term stimulation thresholds, as well as an attenuated early peaking phenomenon, being able to stimulate safely at 2.7 V even early after implant.

Effects of oral propafenone therapy on chronic myocardial pacing threshold.

The effects of oral propafenone therapy on pacing threshold were studied in 36 patients chronically paced for sick sinus syndrome or AV block. The pacemakers, all unipolar models and with noninvasive threshold measurement facilities, were: 9 VVI, 15 AAI, and 12 DDD. Each patient received an initial propafenone dose of 450 mg/day, that in 18 cases was increased to 900 mg/day. Threshold was tested at baseline and at each dosage after 7 days of therapy. With the lower propafenone dosage the threshold, measured at 2.5 V, rose from 0.14 +/- 0.10 to 0.21 +/- 0.16 msec (+55%) in the atrium (P less than 0.0001) and from 0.10 +/- 0.08 to 0.15 +/- 0.09 msec (+63%) in the ventricle (P less than 0.0001). In the 18 patients who received both dosages, the mean atrial and ventricular threshold increased from 0.12 +/- 0.10 to 0.17 +/- 0.14 msec with the lower dose and to 0.27 +/- 0.22 msec (+125%) with the higher dose (P less than 0.0001 for both increments). With the 900 mg/day dose, a threshold increment greater than or equal to 300% was observed in 15% of the stimulated chambers. A good linear correlation (r = 0.76) was found between the ventricular threshold increment and the drug induced QRS widening. In conclusion, treatment with oral propafenone increases atrial and ventricular stimulation threshold in pacemaker patients. Threshold increment is dose dependent and proportional to the drug induced QRS widening. In the majority of the cases the threshold increment is not clinically significant, but caution must be used in prescribing high doses of the drug to patients with high baseline threshold.

Atrial and Ventricular Stimulation Threshold Development: A Comparative Study in Patients with a DDD Pacemaker and Two Identical Carbon‐Tip Leads

The atrial and ventricular pacing threshold development during the first postoperative year was studied in a group of patients receiving DDD pacemakers. Identical carbon-tip endocardial leads were implanted in atrium and ventricle. Atrial and ventricular voltage stimulation thresholds were measured at implantation, and noninvasively at 1 and 12 months thereafter. The atrial amplifier sensitivity required for adequate P wave sensing during follow-up was also determined. The possible influence of a number of factors upon atrial and ventricular threshold evolution was statistically assessed. The threshold data were complete in 57 patients (mean age +/- SD, 65.2 +/- 12.4 years). Thirteen patients had a diagnosis of sinus node disease, whereas 44 had not. Patient age and diagnosis did not significantly influence atrial or ventricular stimulation threshold development. Atrial sensing thresholds were not related to atrial stimulation thresholds during follow-up. Atrial pacing thresholds were higher than ventricular thresholds at pacemaker implantation (P less than 0.00005), but the postoperative threshold rise and thresholds at 1 and 12 months postoperatively did not differ significantly between the atrium and ventricle. The ratio of chronic to acute stimulation thresholds was higher on the ventricular than on the atrial level (0.001 greater than P greater than 0.0005). The chronic atrial threshold showed a logarithmic relation to the threshold at implantation (P = 0.0006); postoperative threshold rise was not a significant determinant of the chronic atrial threshold (P = NS). On the ventricular level, the reverse was seen: The chronic threshold was related to the postoperative threshold rise (P = 0.0015, logarithmic relation), but not to the implantation threshold (P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)