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This paper reports on frequency tunable MEMS magnetoelectric (ME) sensors. Different designs are studied in respect to ME voltage coefficient and frequency tunability. Compared to state-of-the-art ME sensors, the presented ME resonators display a highly reversible and linear frequency tuning, enabled by applying a DC voltage to piezoelectric actuators. A frequency shift of up to 0.2 Hz V-1 is demonstrated for a sensor with a limit of detection of 128 pT/Hz0.5 at resonance frequency of 13 kHz. This sensor type is of particular interest for vector field sensors and sensor arrays in bio-magnetic applications, where sensors with either identical resonance frequencies or precisely defined frequency spacing are required.

MEMS sensors based on magnetoelectric composites have attracted great interest due to their capability to detect weak magnetic fields, showing high potential in applications like biomagnetic field detection and magnetic particle imaging. This paper reports on a scandium aluminum nitride thin film-based MEMS magnetoelectric sensor. The sensor consists of a polycrystalline silicon cantilever with a size of 1000 mm × 200 mm covered by a piezoelectric Al0.73Sc0.27N and a magnetostrictive (Fe90Co10)78Si12B10 thin film. The performance of the presented sensor is investigated based on the magnetoelectric (ME) voltage coefficient, voltage noise density, and limit of detection and compared to the characteristics of the aluminum nitride thin film-based ME sensor with the same layout and fabrication technology. By using an Al0.73Sc0.27N thin film with a higher piezoelectric activity instead of AlN in MEMS ME sensors, the ME voltage coefficient of (1334 ± 84) V/cm Oe in resonance is almost double, thereby lowering the requirements for the electronic system. The limit of detection of (60 ± 2) pT/Hz0.5 remains unchanged due to the dominant thermomechanical noise in resonance.

Background: The prevalence of heart failure (HF) is gaining epidemic proportions. Recent data stress the importance of multidisciplinary strategies for the management of HF patients, but the practical consequences of such programmes remain unclear. Objective: To describe our experience with a dedicated heart failure programme involving two HF nurses and a cardiologist. Method: All patients admitted to the cardiology department with NYHA class III-IV heart failure were included. After admission, patients received optimal medical therapy according to current guidelines, and extensive instructions from a dedicated HF nurse. On discharge they were given comprehensive lists of medications and symptoms, and a weighing list. They were advised to call a nurse in case of questions or problems. Results: 861 patients were included: 63% >75 years, 47% with LVEF >45%. From 2000 onwards, the number of patients admitted once a year increased but seemed to level off in 2004. Most phone calls involved weight changes as well as general physical complaints. In 1266 (46%) of calls, the medication change was a consequence of a problem raised by the patient. The nurse received and answered almost all phone calls. Conclusion: The patient group will grow substantially during the first years of the programme, but the number of patients seen in the outpatient clinic appears to stabilise after five years. Many issues regarding the care of these patients can be handled by the HF nurse

Background Antiarrhythmic therapy of ventricular tachycardia is associated with decreased efficacy and increased proarrhythmia in patients with congestive heart failure, but the explanation for these observations is not known. This study examined the interaction of ventricular dilatation and d-sotalol in a model of reentry ventricular tachycardia. Methods and Results Thin epicardial layers of anisotropic myocardium were created in Langendorff-perfused rabbit left ventricles by a cryoprocedure. A fluid-filled, latex balloon was secured within the left ventricle to change ventricular volume. Sustained reentrant ventricular tachycardia, around a central cryolesion, was induced by rapid pacing in ah preparations (n=7). Epicardial mapping was performed through 248 electrodes. Single premature beats introduced within the reentry circuit were used to define the excitable gap. Dilatation did not influence ventricular tachycardia cycle length or conduction velocity. A 1.25-mL increase in left ventricular volume widened the excitable gap by 12% (range, 5% to 29%) (P

Background Double-wave reentry (DWR) can be a mechanism for acceleration of ventricular tachycardia (VT) with a large excitable gap (EG). The purpose of this study was to determine the effects of heptanol, class Ic, and class III drugs on the inducibility of DWR. Methods and Results In 11 Langendorff-perfused rabbit hearts, a thin ring of anisotropic left ventricular epicardium was created by a cryoprocedure. VT with a revolution time of 180+/-26 milliseconds and an EG of 106+/-8 milliseconds was induced by incremental pacing. During control, entrainment with 10 stimuli at a 99+/-15-millisecond interval terminated VT in seven hearts. In four hearts VT was accelerated from 205+/-24 to 115+/-14 milliseconds by introduction of a second circulating wave in the ring. In the seven VTs that could not be accelerated, 0.5 mu mol/L Org7797 (class Ic) and 1.0 mmol/L heptanol (uncoupling agent) prolonged the cycle length of VT by 32% and 37%, respectively. Because the refractory period (RP) only increased by 11%, the EG prolonged by 71% and the ratio between EG and RP was increased from 0.66 to 1.00. Under these conditions, DWR could be induced in all seven hearts. In the four VTs that could be accelerated during control, administration of the class III drug D-sotalol (35 mu mol/L) only slightly slowed VT by 6%. Because the RP was prolonged by 15%, the ratio between the EG and the RP decreased from 0.76 to 0.63. Entrainment now failed to accelerate VT in two of four hearts, whereas in the two other hearts, double-wave reentry self-terminated within eight cycles. Conclusions Drugs that increase the ratio of EG and RP enhance the susceptibility to acceleration of VT, whereas drugs that decrease this ratio prevent induction of sustained double-wave reentry

Background. Entrainment of ventricular tachycardia can either terminate or change the rate and/or morphology of ventricular tachycardia. The purpose of this study was to elucidate the underlying mechanisms by mapping of entrainment of ventricular tachycardia. Methods and Results. In 10 Langendorff-perfused rings of anisotropic rabbit left ventricular epicardium created by a cryoprocedure, ventricular tachycardia with a cycle length of 167+/-17 milliseconds was induced by incremental pacing. During transient entrainment (10 stimuli), the circulating wave was extinguished by collision with the paced antidromic wave, whereas ventricular tachycardia was reset by the paced orthodromic wave. At shorter pacing intervals, the site of collision shifted deeper into the circuit. Entrainment at high rates (104+/-11 milliseconds) resulted in either termination (n=54), a change in morphology (n=8), or acceleration (n=6) of ventricular tachycardia. Termination of ventricular tachycardia was due to complete (84%) or partial (16%) block of the paced orthodromic wave. Partial block induced microreentry within the circuit, resulting in a reflected echo wave that terminated ventricular tachycardia. A change in morphology of ventricular tachycardia was due to reversion of the direction of propagation of the circulating wave around the obstacle. Acceleration of ventricular tachycardia was caused by double-wave reentry induced by block of the paced antidromic wave. In 28 cases, the sequence of activation during entrainment was not stable but changed from beat to beat due to varying arcs of conduction block. Block occurred predominantly (86%) during slow transverse propagation. Before termination, local oscillations in interval occurred, resulting in a shortening of the last local interval at the site of block by 10+/-6 milliseconds. Conclusions. Termination of ventricular tachycardia by entrainment was due either to complete orthodromic block or to a reflected echo wave. A change in morphology occurred when the direction of the circulating wave reversed. Acceleration of ventricular tachycardia was due to initiation of double-wave reentry. All changes were preceded by conduction block during one or more stimuli at one or multiple sites in the circuit. Block occurred predominantly during slow transverse propagation and was preceded by local oscillations in interval at the site of block

Background. The goal of this study was to investigate the nature and electrophysiological mechanisms of the proarrhythmic effects of flecainide in Langendorff-perfused rabbit hearts. Methods and Results. A thin layer of epicardium was obtained by an endocardial cryotechnique in 10 Langendorff-perfused rabbit hearts. Six other hearts were kept intact. Programmed electrical stimulation using up to three closely coupled premature stimuli and burst pacing was used to test the inducibility of arrhythmias both during control and administration of 1-mu-g/ml flecainide. During control, in the thin layer of epicardium, application of one to three premature stimuli induced nonsustained ventricular tachycardia in one out of 10 hearts, and burst pacing induced nonsustained ventricular tachycardia in four hearts and sustained ventricular tachycardia in two hearts. During administration of 1-mu-g/ml flecainide, application of one to three premature stimuli induced sustained ventricular tachycardia in five hearts, and burst pacing induced sustained ventricular tachycardia in nine hearts. All tachycardias were based on circus movement of the impulse around arcs of functional block. During administration of flecainide, different locations of the arc of block could be found in the same heart, leading to different reentrant circuits with different cycle lengths. In the control group of six intact hearts, application of up to three closely coupled premature stimuli in all cases induced ventricular fibrillation both during control and administration of flecainide. Conclusions. Flecainide alters propagation of the impulse in thin surviving layers of myocardium in a manner that facilitates the induction of functionally determined reentry

Background. The aim of this study was to test the hypothesis that electrical uncoupling and depression of the fast sodium channels have differential effects on propagation of the electrical impulse relative to the fiber orientation. Methods and Results. In a model of reentrant ventricular tachycardia (VT) (mean cycle length, 144 +/- 13 msec) around a ring of anisotropic myocardium in 10 Langendorff-perfused rabbit hearts, the effects of extracellular K+ concentration ([K+]o) and hepatanol were studied. [K+]o and heptanol each had a dose-dependent effect on VT cycle length. However, high [K+]o slowed the VT mainly by depressing longitudinal conduction, whereas heptanol preferentially depressed transverse conduction. The ratio between longitudinal and transverse conduction velocities progressively decreased with high [K+]o and progressively increased with heptanol. Heptanol terminated VT at a mean concentration of 3.5 +/- 0.5 mM. The cycle length before termination was 446 +/- 120 msec (p

Background. The pathophysiological mechanisms leading to acceleration of ventricular tachycardia (VT) are still unclear. Methods and Results. High-resolution epicardial mapping was used to study the mechanisms of VT acceleration by programmed electrical stimulation (PES) in a model of sustained reentrant VT in Langendorff-perfused rabbit hearts (n = 40). Three different mechanisms responsible for acceleration of VT were identified: 1) induction of double-wave reentry (n = 6), defined as the occurrence of two successive activation waves circulating in the same direction in the same circuit; 2) change to a functionally determined circuit (n = 4), defined as reentry of the impulse around a functional line of block without involvement of a fixed obstacle; and 3) change of the reentrant circuit to reentry within a different, faster anatomic pathway (n = 3). Analysis of 81 episodes of sustained monomorphic VT induced by PES in 74 patients with clinically documented sustained VT in the setting of chronic coronary artery disease showed that in 22 episodes VT was suddenly accelerated by PES (mean cycle length, from 345 +/- 73 to 277 +/- 71 msec, p

The purpose of this study was to study the role of anisotropic distribution of conduction velocity in the initiation and perpetuation of ventricular tachycardia in an experimental model of sustained reentrant ventricular tachycardia in the Langendorff perfused rabbit heart. The hearts of 30 rabbits were used in the study. The right ventricle, the interventricular septum and the endocardial and intramural layers of the left ventricle were destroyed by freezing. In the surviving epicardial layer an obstacle was created using a cryoprobe. Thus, the final preparation consisted of a perfused ring of epicardium in the left ventricle. In 27 of 30 experiments programmed electrical stimulation induced sustained reentrant excitation around the obstacle. The cycle length of the tachycardia ranged from 128 to 197 ms in different experiments (mean 162 +/- 17 ms). During tachycardia in some segments of the ring the impulse propagated parallel to fiber orientation at a mean conduction velocity of 61 +/- 7 cm/s whereas in other segments of the ring the impulse propagated perpendicular to fiber orientation at a mean conduction velocity of 22 +/- 4 cm/s. An excitable gap was present during all episodes of tachycardia. In conclusion, conduction velocity during reentrant tachycardia depends on the relation between direction of propagation and fiber orientation. This anisotropic distribution of conduction velocity can play an important role in the initiation and perpetuation of ventricular tachycardia