Heiner Langenfeld

The Six-Minute Walk—An Adequate Exercise Test for Pacemaker Patients?

LANGENFELD, H., ET AL.: The Six‐Minute Walk—An Adequate Exercise Test for Pacemaker Patients? In many pacemaker patients bicycle and treadmill ergometry are not practicable. As an alternative, we performed a 6‐minute walk on a 20‐m corridor in 97 pacemaker patients, who were asked to walk as far as possible determining their speed by themselves. Results were compared with those of bicycle ergometry in 42 of these patients and with treadmill exercise of a group of 92 other pacemaker patients. In the 6‐minute walk, performance and maximal heart rate were slightly lower (49 ± 18 W; 96 ± 23 beats/min) than in bicycle (57 ± 16 W; 110 ± 26 beats/min) and treadmill ergometry (50 ± 37 W; 102 ± 35 beats/min). A good correlation was found between walking and bicycling (r = 0.74) and in subgroups of patients with different pacemaker indications. All patients preferred the walk to bicycle ergometry considering it to be more related to daily physical activity. In conclusion, a 6‐minute walk is a simple and physiological exercise test for nearly all pacemaker patients with good correlation to other types of exercise. It seems to be preferable to other tests because of its better acceptance and practicability.

Symptoms, Cardiovascular Risk Profile and Spontaneous ECG in Paced Patients: A Five‐Year Follow‐Up Study

GRIMM, W., ET AL.: Symptoms, Cardiovascular Risk Profile and Spontaneous ECG in Paced Patients: A Five‐Year Follow‐Up Study. Only few data are available about the course of symptoms, cardiac diseases, and spontaneous rhythm in pacemaker patients. Therefore, we followed the course of 308 paced patients (age 72 ± 11 years) with a mean implantation time of 63 ± 45 months. Results: The symptom triad of syncope, dizziness, and dyspnea improved remarkably in 93% of patients. Thirty‐nine percent suffered from coronary heart disease. The risk factors of hypertension (47%), nicotine (37%), and diabetes mellitus (25%) were found significantly more often than in a normal population with the same age and sex profile. In VVI paced patients with sick sinus syndrome (SSS, n = 67) atrial fibrillation (AF) occurred significantly more often (42%) than in patients with AV block (n = 80, 23%, p < 0.05). Only one out of 41 DDD paced patients showed AF at follow‐up. VVI stimulation seems to favor AF due to retrograde conduction in SSS. Only 3% of patients with SSS developed second‐ or third‐degree AV block. Therefore, atrial pacing is preferable in most patients with SSS.

Atrial Fibrillation and Embolic Complications in Paced Patients

Atrial fibrillation (AF) and thromboembolism are discussed to he complications of the WI mode. We reinvestigated the spontaneous ECG and the anamnesis of 246 pacemaker patients with the indications second and third degree atrioventricular block (AV block, n = III), sick sinus syndrome (SSS, n ‐ 101) and other indications (n = 34), all had shown sinus rhythm at implantation. The mean implantation time was 63 ± 45 months (203 VVI and 43 dual chamber pacemkers). The results: (1) Atrial fibrillation was found in 63 patients (26%). Only one of them had a DDD pacemaker inserted, the implantation time of dual chamber devices being shorter, however, (2) The incidence of AF in patients with SSS (37%) was significantly higher (P < 0.01) than in patients with AV block (19%). (3) Three patients suffered from strokes or transitory ischemic attacks in the follow‐up, only one of them had AF at control. Conclusions: Our results confirm that VVI stimulation favors AF long‐term which is most likely due to irritation of the atrial rhythm by retrograde conduction. In our patients the incidence of thromboembolic complications was not higher in the group of patients with AF. However, from this study in surviving patients, we cannot exclude that we Jost some patients due to severe stroke.

Rate Adaptive Pacing—Clinical Experience with Three Different Pacing Systems

Physiological stimulation can be achieved by either bifocal or rate responsive pacing. The latter pacemakers adapt the heart rate to physical activity by biological signals. Out of many possible approaches only three pacemaker systems for rate responsive pacing are available: the QT‐pacemaker (Tx or Quintech), the respiratory biorate pacemaker, and the activity detecting Activitrax. Our own experiences (8 QT, 6 Biorate, 8 Activitrax pacemakers) and a survey of 95 QT‐ and 37 Biorate pacemakers from 11 centers are reported. The Biorate pacemaker functions without any problems; its present disadvantage is limited programmability. With the Tx pacemaker failing, frequency adaptation (26%) was found more often in the early series, mostly due to voltage polarization at the tip of the electrode. The Activitrax pacemaker gives satisfactory frequency adaptation, largely depending on the activity of the muscles of the shoulder and pectoral region.

Comparative analysis of the action of class I antiarrhythmic drugs (lidocaine, quinidine, and prajmaline) in rabbit atrial and ventricular myocardium

Effects of three class I antiarrhythmic drugs (quinidine, lidocaine, and prajmaline) on transmembrane resting (RMP) and action potentials (AP) of isolated rabbit atrial and ventricular myocardium were studied at different stimulation rates. The frequency-dependent depression of the maximal upstroke velocity (Vmax) of the AP (sodium channel block) was analyzed according to the “guarded receptor” hypothesis. The resting block (Vmax depression after a resting period) induced by prajmaline (10−6 M), quinidine (2.2 × 10−5 M), and lidocaine (4.3 × 10−5 M) was more expressed in the atrium (44, 28, and 19%, respectively) than in the ventricle (32, 9, and 0%, respectively). There were also significant (p < 0.05) atrioventricular differences in the frequency-dependent extra block (Vmax reduction on stimulation at 3.3 Hz) for quinidine (39 vs. 26%) and lidocaine (4 vs. 25%). From the analysis, according to the guarded receptor hypothesis, it follows that the three compounds bind preferentially to inactivated sodium channels with about the same affinity to the atrium and ventricle, except for quinidine which shows a significantly smaller dissociation constant in the atrium (5 × 10−6 M vs. 2.7 × 10−5 M; p < 0.001). We conclude that the atrioventricular differences in the resting block are mainly due to atrioventricular differences in the RMP, whereas the differences in the frequency-dependent extra block are based on the shorter atrial AP duration (lidocaine) or are due to higher affinity to atrial sodium channels (quinidine).

Course of Symptoms and Spontaneous ECG in Pacemaker Patients: A 5-Year Follow-up Study

We investigated the course of symptoms and the spontaneous ECG retrospectively in 308 patients who had received a pacemaker because of atrioventricular (AV) block fn = 115), sick sinus syndrome (SSS, n = 107), bradyarrhythmic atriai jibriJiation (bradyarrhythmia, n = 51). carotid sinus syndrome (CSS, n = 16), complete bifascicular block associated with 1st degree AV block (n = 13) and with other indications fn = 6). The mean implantation time was 63 months. The clinical state of 93% of all patients improved after pacemaker implantation; their symptoms decreased markedly. Persisting syncopy in some patients with SSS, however, supports a restricted implantation policy. We rarely saw improved AV conduction in patients with AV block fn%). Furthermore, in patients with SSS, atrial fibrillation occured significantly more often (35%) than in those with AV block (17 %; P < 0.01). Only 3% of patients with SSS developed 2nd and 3rd degree AV block within the observation period. In all patients with Initial bifascicular block and additional 1st degree AV block, pacing prevented further syncopal attacks; four of them showed 3rd degree AV block at control, indicating that pacemaker implantation is mandatory in symptomatic patients with bifascicular disease and 1st degree AV block.

New Concept in Activity-Controlled Pacemakers: Clinical Results With an Accelerometer-Based Rate Adaptive Pacing System

An accelerometer‐based rate adaptive generator (EXCEL(tm) VR) has been introduced. A preclinical group of 22 subjects with strap‐on devices was observed and reported. A clinical protocol including observation of rate adaptive response to typical daily activities and incremental exercise on a treadmill was administered in seven implanted patients. Indications for implantation in these patients was either second‐ or third‐degree atrioventricular block (five patients, VVIR pacing mode) and sick sinus syndrome (two patients, AAIR pacing mode). Mean pacing rates were 50 ppm (supine), 56 ppm (standing), 77 ppm (descending the stairs), 81 ppm (slow walk), 83 ppm (slow stair climb), 91 ppm (fast walk), and 92 ppm (fast stair climb). When the arm proximal to the pulse generator was exercised, the rate rose to 92 ppm. When the distal arm was strained, the rate was 63 ppm. During treadmill testing, rates between 82 ppm (2 km/hour) and 104 ppm (5 km/hour) were observed. This accelerometer‐based rate adaptive pulse generator provided a proportional response to graded activities of treadmill exercise and daily living in these groups of preclinical and clinical subjects.

Reverse Use Dependence of Antiarrhythmic Class la, Ib, and Ic: Effects of Drugs on the Action Potential Duration?

The prolongation of the action potential duration (APD) induced by sotalol has been shown to be diminished with increasing heart rate. This phenomenon is called “reverse use dependence.” We examined the la, Ib, and Ic effects of different Class I drugs on the APD under normal and fast stimulation rates (1.0 and 2.5 Hz) in isolated rabbit atria) and ventricular muscles by means of intracelular microelectrodes. Results (n = 98): With 1.0 Hz lidocaine fib, 4.3 ? 10−5 M) shortened the APD at 90% repolarization (APD90) in the atrium by 9% and in the ventricle lay 8% (NS), whereas quinidine (la, 2.2 ? 10 −5 M) and prajmaline (la, 10 −6 M) prolonged the APD90 in the atrium (quinidine +45%; prajmaline +10%, P < 0.001) and in the ventricle (+ 42%, P < 0.001; +17%, P < 0.05J. Propafenone (Ic, 2.6 ? 10 −6 M) showed this effect only in the atrium (APD90 + 33%; P < 0.01). With the faster stimulation rate of 2.5 Hz we could not find a significant influence of any drug on the APD90 in the ventricle and only quinidine prolonged the APD90 in the atrium by 16% (P < 0.05). Conclusions: The subclassification of Class I antiarrhythmic drugs that is based on APD modifying influences is only valid under normal heart rates (1.0 Hz). During tachycardia these actions are absent and the phenomenon of “reverse use dependence” is found in Class I drugs. Therefore, an additional antiarrhythmic effect due to APD modification by the examined drugs should not be expected at rapid heart rates.

Dissimilar Action of Two Cyclic Adenosine- Monophosphate Analogues on the Sodium Current in Intact Rat Papillary Muscle

In intact papillary muscles from rat we have found with the loose‐patch‐clamp technique an increase of the fast cardiac sodium current (INa+) by isoproterenol (ISO). In this study we have tested two membrane permeable analogues of the intracellular second messenger cyclic adenosine‐monophosphate (cAMP) to investigate the intracellular pathway: 8‐Br‐cAMP (50 μM) and the newer developed Sp5,6‐Dichloro‐1‐β‐D‐ribofuranosylbenzimidazole‐3′, 5′‐cyclic‐monophosphor‐othioate (5,6‐DCl‐cBiMPS, 20 μM). The availability of INa+ was determined with test pulses to ± 0 mV every 3.5 seconds after 2.5‐second conditioning between ‐130 mV and‐50 mV and a holding potential at the resting potential of the cell under examination, and after wash‐in of either compound. The peak currents were fit to a Boltzmann equation, and expressed by the maximal attainable current INa+Na,max the mid‐point potential V½, and a steepness parameter a. Values are given by mean ± SEM. 8‐Br‐cAMP showed a significant shift of the availability curve in the hyperpolarized direction (V½= ‐82 ± 2 mV vs ‐ 66 ± 2 mV, n = 5, P < 0.05) with only minor changes of I+No,max and a. In contrast, 5,6‐DCI‐cBiMPS had no significant effect on V½ but increased I+Na,max by 8%± 2% versus control (n = 5. P < 0.05). In an intact muscle preparation we have found that 5,6‐DCI‐cBiMPS has a similar effect as that observed with the β‐adrenergic agonist ISO (100 nM), whereas 8‐Br‐cAMP exhibited a dissimilar action. This indicates, that ihe effects of ISO are transmitted by the cAMP system. On the other hand, 8‐Br‐cAMP, which is not as permeable and specific an activator of the cAMP dependent proteinkinase, may have other effects on the sodium channel, perhaps mediated through purinergic receptors.

Influence of Cardiac Dysfunction on Fast Sodium Current Regulation by Forskolin

There are several reports of an altered β‐adrenergic pathway in heart failure. Since the fast cardiac sodium current (INA+) is also subject to β‐receptor dependent regulation, we investigated its regulation in a model of cardiac dysfunction. Adenylyl cyclase was stimulated directly with forskolin as one step in the β‐adrenergic pathway. Twelve‐week‐old Wistar rats were infarcted by ligation of the left anterior descending coronary artery. Eight weeks later, the induced hemodynamic changes were evaluated. The left ventricular end‐diastolic pressure (LVEDP) was used as a measure of the hemodynamic effects of the myocardial infarction. With the loose patch clamp technique, INa+ was measured in intact papillary muscles at an external sodium concentration of 150 mmol/L. Potential dependent availability was tested with pulses to 0 mV from various conditioning potentials. In animals with minor infarction (n = 7, LVEDP = 7.7 ± 0.9 mmRgj, forskolin (3 mmol/L) increased the maximal available INa+ to 109%± 13% of baseline values. This increase was nearly the same in the group with significant infarctions (n = 7, LVEDP = 15.7 ± 1.6 mmHg) to 113%± 6%. Thus, although we previously observed a reduction of the isoproterenol induced increase of INA + in rats with significant myocardial infarctions, this increase remalns the same when adenylyl cyclase is stimulated directly. This is consistent with a direct β‐receptor down‐regulation or desensitization.