Previous research has shown that the risk of sudden death due to cardiac arrhythmias can be predicted by observing the shape of recorded endocardial electrograms in response to pacing, and in particularly detecting certain small deflections in the recorded electrogram following early stimulation of the heart. A long standing problem has been the reliable detection of these small individual potentials because of the presence of noise in the recorded electrical signals created by other electrical equipment within a typical catheter laboratory. The solution described involves deriving a model of noise from a first portion of the electrogram in which a physiological signal is presumed to be absent, and transforming a second portion of the electrogram, presumed to contain a physiological signal, into the model of noise. The physiological signal can then be identified by identifying portions of signal within the second portion of the electrogram that do not conform to the model of noise.

Methods and/or devices may be configured to monitor ventricular activation times and modify an atrioventricular delay (AV delay) based on the monitored ventricular activation times. Further, the methods and/or devices may determine whether the AV delay should be modified based on the measured activation times before modifying the AV delay.

According to some embodiments, a device operates by comparative morphological analysis of depolarization signals collected in spontaneous rhythm on separate respective channels, with two temporal components combined into a single 2D parametric VGM vectogram characteristic. Similarity quantification methods evaluate a variation over time of a descriptor parameter of a current VGM compared to a stored previous reference VGM. This variation is compared with predetermined thresholds to diagnose an occurrence of remodeling or reverse remodeling in a patient, and/or to detect a lead failure or an occurrence of ischemia. The descriptor parameter is a function of a velocity vector of the VGM, a comparison relating to a correlation coefficient between respective magnitudes of a current VGM velocity vector and of a reference VGM velocity vector, and an average angle between these respective velocity vectors.

Embodiments of device for monitoring pressure in the left atrium are provided. The device is delivered to the left atrium via the coronary sinus. A first portion of the device is deployed in the left atrium, the first portion of the device comprising a pressure sensor. A second portion of the device is deployed in the coronary sinus. Monitoring left atrial pressure via coronary sinus access can provide a safer, less invasive way to monitor a patient for heart failure.

A method for determining the degree of parallel activation of a heart undergoing pacing includes calculating vectorcardiogram (VCG), or electrocardiogram (ECG), or electrogram (EGM) waveforms from right ventricular pacing (RVp) and left ventricular pacing (LVp). A synthetic biventricular pacing (BIVP) waveform is generated by summing the VCG of the RVp and LVp, or by summing the ECG of the RVp and the LVp, or by summing the EGM of the RVp and the LVp. A corresponding EGM or ECG or VCG waveform from real BIVP is calculated. The method includes comparing the synthetic BIVP waveform and the real BIVP waveform and calculating time to fusion by determining the point in time in which the activation from RVp and LVp meets and the synthetic and the real BIVP curves start to deviate. A delay in time to fusion indicates a higher degree of parallel activation.

Brugada syndrome and related forms of ion channelopathies, including ventricular asynchrony of contraction, originate in the region near the His bundle or para-Hisian regions of the heart. Manifestations of Brugada syndrome can be corrected by delivering endocardial electrical stimulation coincident to the activation wave front propagated from the atrioventricular (AV) node early enough to compensate for the conduction problems that start in those region. The stimulation can include waveforms of the same or different polarity delivered to a site within the region near the His bundle or para-Hisian regions of the heart associated with a low cardiac electrical asynchrony level or can include at least two single-phased superimposed waveforms of opposite polarity delivered through a pair of pacing electrodes relative to a reference electrode, which can be delivered to any site within the region near the His bundle or para-Hisian regions of the heart.

Methods, apparatus, and systems are provided to control contraction of the heart. At least one sensing element receives signals indicating electrical activity of sinus rhythm of the heart. Based on the received signals, the progress of contraction of the heart is determined. Based on the progress of contraction, the chamber of the heart may then be stimulated at a plurality of locations. In another embodiment, a plurality of electrodes are implanted in the left ventricle to stimulate at multiple locations in the left ventricle for the purpose of improving hemodynamic performance and increasing cardiac output in a patient who is suffering from congestive heart failure.

The present disclosure relates generally to pacing of cardiac tissue, and more particularly to adjusting delivery of His bundle or bundle branch pacing in a cardiac pacing system to achieve synchronized ventricular activation. Bundle pacing may be delivered in response to determining whether the QRS parameter or activation interval is greater than a threshold. A set of AV delays may be generated, and an optimal AV delay may be selected from the stored set of AV delays. His-bundle or bundle-branch pacing may be selectively delivered based on RV or LV activation time. Pacing may also be adjusted based on dyssynchrony detected or the type of bundle branch block pattern detected.

Methods and devices are provided for, under control of one or more processors within an implantable medical device (IMD), delivering cardiac resynchronization therapy (CRT) at one or more pacing sites. The processors obtain cardiac signals, associated with a candidate beat, from multi-site left ventricular (MSLV) electrodes distributed along a left ventricle and analyze the cardiac signals to collect at least one of a MSLV conduction pattern or a MSLV morphology. The processors compare at least one of the MSLV conduction pattern or MSLV morphology to one or more associated templates. The processors then label the candidate beat as a pseudo-fusion beat based on the comparing and adjust the CRT based on the labeling.

Systems and methods for ambulatory detection of medical events such as cardiac arrhythmia are described herein. An embodiment of an arrhythmia detection system may include a detection criterion circuit that determines a patient-specific detection criterion using a baseline cardiac characteristic when the patient is free of cardiac arrhythmias. The detection criterion circuit generates a patient-specific threshold of a signal metric by adjusting a population-based threshold of the signal metric, where the manner and the amount of adjustment is based on information about patient baseline cardiac characteristic. The arrhythmia detection system detects an arrhythmia episode using a physiologic signal sensed from the patient and the patient-specific arrhythmia detection threshold.