Innovations in pacing technology, which include the addition of rate-responsive features to programmable pacemakers, can improve the quality of life of patients suffering from sick sinus syndrome. Among the strategies providing rate-adaptive cardiac pacing, the most attractive is the physiological restoration of closed-loop chronotropic control. This paper describes how autonomic nervous system (ANS) control information is extracted from dynamic measures of myocardial contractile performance obtained from unipolar conductance measurements using the stimulation electrode in the right ventricular cavity. The pacemaker uses the ANS information to modulate pacing rate and restore normal physiological control of heart rate. A new algorithm, regional effective slope quantity (RQ), for isolating the ANS signal was developed. The resulting signal, ventricular inotropic parameter (VIP), is a normalized parameter proportional to the strength of the ANS inotropic signals to the myocardium. The efficacy of the ANS control concept was evaluated in multi-centre studies. Patients with AV block and VIP-controlled pulse generators performed defined exercise protocols. The ANS-controlled pacing rate and the spontaneous sinus rate were closely correlated. Blood pressure and subjective patient reports further indicated that good control of the cardiovascular circulation was achieved.

A multicenter clinical study is presented, which focuses on the reestablishment of closed loop cardiac control in patients with chronotropic insufficiency. Using the information about sympathetic tone contained in the myocardial contractility, it is possible to reconnect the heart rate to the physiological control mechanisms. Intracardiac impedance is measured with the ventricular electrode and the ventricular inotropic parameter (VIP) is derived from that. The VIP serves directly as input to the control of heart rate by the pacemaker. Over 200 patients have received autonomic nervous system (ANS) controlled pacemakers. The patient-pacemaker system was investigated in different ways. This included standard exercise tests, long-term studies of every day activities over 24 hours, psychological, and pharmacological challenges. To prove the validity of the approach we specifically looked at (1) the appropriateness of changes in paced heart rate with sympathetic tone during exercise, (2) the correlation between heart rate and sinus rate, if detectable, and (3) the correlation between the echocardiographically determined preejection period (PEP) and the VIP controlled heart rate.

For studying the hemodynamics of the greater and lesser circulatory system in animals, the impact of general anesthesia upon cardiovascular functions should be as small, as possible. The marked circulation-depressing effect of halothane, which has so far been given preference for experiments on large animals, was confirmed by the present study of the miniature pig. There was a significant decrease in MAP, cardiac index and dp/dtmax/IP, and an increase in PAPp. Useful insights into hemodynamics, derived from experiments modeling the heart, lungs or vascular system cannot be gained for a cardiovascular system, the functions of which are greatly altered by such an anesthesia. As a new form of anesthesia with minimal cardiovascular influence, the ketamine-diazepam N2O combination, which has already been successfully applied in operations on the open human heart, is introduced into experimental surgery.

The potential value of ventricular evoked response (VER) evaluation by implantable pacemakers as clinical marker for disease induced hemodynamic changes in the heart, has so far not been explicitly evaluated. We conducted a study to evaluate the reproducibility of the R spike and T wave measurements (R(VER) and T(VER)) under controlled clinical conditions and examine the correlation between VER parameters and standard echocardiographic measurements in the left ventricle. Additionally, the utility of the VER as a marker for NYHA classification and the presence of cardiomyopathy was investigated. The Physios CTM 01 pacemaker capable of recording authentic VER signal morphology, was used with low polarization fractal coated pacing leads to obtain high-fidelity VER recordings in 26 patients with conventional pacing indications (mean age: 69.1 +/- 11.8 years; 20 men). Three patients suffered from dilative cardiomyopathy (DCM), 14 from hyperthropic nonobstructive cardiomyopathy (HNCM), and nine had no myopathy but suffered from coronary artery disease (CAD). Five patients were in NYHA Class IV, 19 in Class III, and two in Class II. Mean R(VER) and T(VER) amplitudes were calculated from one-minute VER recordings. Standard echocardiography parameters were determined during this recording. Two follow-ups at a mean distance of 11.3 +/- 5.7 month were performed. The reproducibility of R(VER) or T(VER) (correlation factors: 0.992 and 0.981, respectively) was superior to the reproducibility of any echocardiographic parameter (correlation factors 0.404-0.943). There was no strong correlation between VER and any echo parameter. Both R(VER) and T(VER) were significantly reduced in NYHA Class IV patients (P < 0.05), and nearly significantly reduced in DCM versus other patients (P = 0.05-0.09). HNCM made no difference to CAD. The investigation shows that analysis of VER parameters bears a promising potential for dynamic monitoring of diseases affecting the hemodynamics, and of therapeutic effects, by means of regular, nonburdening pacemaker follow-up examinations.

The genesis of arteriosclerosis and, as a consequence, coronary heart disease is put up for discussion. On the basis of morphological considerations, it appears to be absurd to define the cause of arteriosclerosis exclusively on the molecular level. Cholesterol is a functionally important building block in the body. It is regulated by the body. Long-term observations of statin therapy indicate consequential damage, which makes it necessary to rethink this form of therapy. The cause of arteriosclerosis is the result of a chronic ischemic disorder of the arterial vessel wall