Background Long-term risk factor control after myocardial infarction (MI) is currently inadequate and there is an unmet need for effective secondary prevention programmes. Design and methods It was the aim of the study to compare a 12-month intensive prevention programme (IPP), coordinated by prevention assistants and including education sessions, telephone visits and telemetric risk factor control, with usual care after MI. Three hundred and ten patients were randomized to IPP vs. usual care one month after hospital discharge for MI in two German heart centres. Primary study endpoint was the IPP Prevention Score (0-15 points) quantifying global risk factor control. Results Global risk factor control was strongly improved directly after MI before the beginning of the randomized study (30% increase IPP Prevention Score). During the 12-month course of the randomized trial the IPP Prevention Score was improved by a further 14.3% in the IPP group ( p < 0.001), while it decreased by 11.8% in the usual care group ( p < 0.001). IPP significantly reduced smoking, low-density lipoprotein cholesterol, systolic blood pressure and physical inactivity compared with usual care ( p < 0.05). Step counters with online documentation were used by the majority of patients (80%). Quality of life was significantly improved by IPP ( p < 0.05). The composite endpoint of adverse clinical events was slightly lower in the IPP group during 12 months (13.8% vs. 18.9%, p = 0.25). Conclusions A novel intensive prevention programme after MI, coordinated by prevention assistants and using personal teachings and telemetric strategies for 12 months, was significantly superior to usual care in providing sustainable risk factor control and better quality of life.

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Objective-To investigate the incidence of sinus node disease after pacemaker implantation for exclusive atrioventricular (AV) block. Design-441 patients were followed after VDD (n = 219) or DDD pacemaker (n = 222) implantation for AV block over a mean period of 37 months. Sinus node disease and atrial arrhythmias had been excluded by Holter monitoring and treadmill exercise preoperatively in 286 patients (group A). In 155 patients with complete AV block, a sinus rate above 70 beats/min was required for inclusion in the study (group B). Holter monitoring and treadmill exercise were performed two weeks, three months, and every six months after implantation. Sinus bradycardia below 40 beats/min, sinoatrial block, sinus arrest, or subnormal increase of heart rate during treadmill exercise were defined as sinus node dysfunction. Results-Cumulative incidence of sinus node disease was 0.65% per year without diVerences between groups. Clinical indicators of sinus node dysfunction were sinus bradycardia below 40 beats/min in six patients (1.4%), intermittent sinoatrial block in two (0.5%), and chronotropic incompetence in five patients (1.1%). Only one of these patients (0.2%) was symptomatic. Cumulative incidence of atrial fibrillation was 2.0% per year, independent of the method used for the assessment of sinus node function and of the implanted device. Conclusions-In patients undergoing pacemaker implantation for isolated AV block, sinus node syndrome rarely occurs during follow up. Thus single lead VDD pacing can safely be performed in these patients. (Heart 1999;81:580-585)

In dual chamber pacemakers, atrial sensing performance is decisive for maintenance of AV synchrony. Particularly, the efficacy of mode switching algorithms during intermittent atrial tachyarrhythmias depends on the sensitive detection of low potential amplitudes. Therefore, a high atrial sensitivity of 0.18 mV, commonly used in single lead VDD pacemakers, was investigated for its efficacy and safety in DDD pacing. Thirty patients received dual chamber pacemakers and bipolar atrial screw-in leads for sinus node syndrome or AV block; 15 patients suffered from intermittent atrial fibrillation. Pace makers were programmed to an atrial sensitivity of 0.18 mV. Two weeks, 3, 9, and 15 months after implantation, P wave sensing threshold and T wave oversensing thresholds for the native and paced T wave were determined. The myopotential oversensing thresholds were evaluated by isometric contraction of the pectoral muscles. Automatic mode switch to DDIR pacing was activated when the mean atrial rate exceeded 180 beats/min. The patients were followed by 24-hour Holter monitoring. Two weeks after implantation, mean atrial sensing threshold was 1.81 +/- 0.85 mV (range 0.25-2.8 mV) without significant differences during further follow-up. Native T wave sensing threshold was < 0.18 mV in all patients. In 13% of patients, paced T waves were perceived in the atrial channel at the highest sensitivity. This T wave sensing could easily be avoided by programming a postventricular atrial refractory period exceeding 300 ms. Myopotential oversensing could not be provoked and Holter records showed no signs of sensing dysfunction. During a 15-month follow-up, 1,191 mode switch events were counted by autodiagnostic pacemaker function. Forty-two of these events occurred during Holter monitoring. Unjustified mode switch was not observed. In DDD pacemakers, bipolar atrial sensing with a very high sensitivity is efficient and safe. Using these sensitivity settings, activation of the mode switch algorithm almost completely avoids fast transmission of atrial rate to the ventricle during atrial fibrillation.

Atrial undersensing occurs in a considerable number of patients, both with single lead VDD pacemakers and with DDD devices. The aim of this study was to investigate the diagnostic efficacy of electrocardiographic methods and autodiagnostic pacemaker features to detect atrial sensing dysfunction. Two hundred and thirty-one patients with AV block received single lead VDD pacemakers or DDD devices. Atrial sensitivity was programmed to 0.1 or 0.18 in VDD devices and to 0.5 mV in DDD devices; the rate limits were set to 40 and 160 beats/min. Twelve-lead ECG recording for 1 minute during deep respiration and change of body position, 24-hour Holter ECG recording, and treadmill exercise were performed 2 weeks and 15 months after pacemaker implantation. AV synchrony and, if available, P wave amplitude histogram were sampled by autodiagnostic pacemaker features and compared to electrocardiographic findings. Atrial undersensing was assumed, if AV synchrony was below 100% or if minimal P wave amplitude (PWA) was equal to the programmed atrial sensitivity. Intermittent atrial undersensing occurred in 20.7% of patients. The diagnostic sensitivities of the various methods used to detect atrial sensing failures were: 24-hour Holter monitoring 97.5%, P wave amplitude histogram 90.0%, stored AV synchrony 68.0% without significant difference between the various devices, treadmill exercise testing 58.8%, and 12-lead ECG recording 21.3%. In one patient, atrial undersensing was exclusively detected by exercise testing. In conclusion, autodiagnostic pacemaker features facilitate the evaluation of atrial sensing performance. However, to exclude intermittent atrial malesensing, routine Holter monitoring and treadmill exercise are still needed.