Methods and devices for reducing ventricle filling volume are disclosed. In some embodiments, an electrical stimulator may be used to stimulate a patient's heart to reduce ventricle filling volume or even blood pressure. When the heart is stimulated in a consistent way to reduce blood pressure, the cardiovascular system may over time adapt to the stimulation and revert back to the higher blood pressure. In some embodiments, the stimulation pattern may be configured to be inconsistent such that the adaptation response of the heart is reduced or even prevented. In some embodiments, an electrical stimulator may be used to stimulate a patient's heart to cause at least a portion of an atrial contraction to occur while the atrioventricular valve is closed. Such an atrial contraction may deposit less blood into the corresponding ventricle than when the atrioventricular valve is opened throughout an atrial contraction.

Systems, apparatus, methods and computer-readable storage media that facilitate monitoring the integrity of telemetry connectivity between an implantable device and an external device are provided. In one embodiment, an implantable device includes a monitoring component that monitors advertisement signal information identifying an amount of advertisement signals transmitted to the external device within a defined time period, and telemetry session information identifying an amount of the telemetry sessions that are established between the external device and the implantable device within the defined time period. A connectivity assessment component of the implantable device further determines whether a telemetry connectivity problem exists between the external device and the implantable device based on a degree of miscorrelation between the advertisement signal information and the telemetry session information.

In one example, this disclosure is directed to a kit for intravascular implantation of an implantable medical device within a patient, the kit comprising an elongated outer sheath forming an inner lumen with a distal opening, the outer sheath sized to traverse a vasculature of the patient, and an elongated inner sheath with an enlarged distal portion, wherein the enlarged distal portion is configured to substantially fill the inner lumen and close-off the distal opening of the outer sheath. The enlarged distal portion is slidable relative to the outer sheath. The inner sheath further includes a tether with a helical element that is remotely controllable from a proximal end of the inner sheath to release the implantable medical device from a distal portion of the outer sheath.

One embodiment provides a system for determination and utilization of cardiac electrical asynchrony data. The system includes an analysis circuitry including a processor and a memory, the analysis circuitry configured to: obtain a plurality of sets of cardiac signals collected in at least two locations of a heart of a patient, the signals comprising at least one of surface electrocardiography signals and pseudo-surface ECG signals; detect one or more QRS complexes for each of the sets based on the cardiac signals for that set; obtain one or more cross-correlation signals, each of the cross-correlation signals being between at least two of the signal sets and being obtained using the detected QRS complexes from the signal sets; and calculate one or more asynchrony indices using one or more of the cross-correlation signals, each of the asynchrony indices being indicative of a level of asynchrony between the at least two locations.

Pacing parameters may be adjusted to increase the cardiac output of a patient's heart while a patient is awake and/or active and the demand placed on the heart may be greatest, and to decrease or hemodynamic efficiency while a patient is at rest so that the heart itself has time to rest before the next period of higher demand for efficiency begins. This may aid in lessening the strain placed on the heart by making the heart work hard when needed such as when the patient is active, and by permitting the heart to “rest” when the patient is relatively inactive.

A method for identifying reversible cardiac dyssynchrony (RCD) of a patient and treating the RCD measures an event relating to a rapid increase in the rate of pressure increase within the left ventricle. The method calculates a first time delay between the event and a first reference time. If the first time delay is longer than a set fraction of electrical activation of the heart, then the presence of cardiac dyssynchrony in the patient is identified. Pacing is applied to the heart, and a second time delay between the event following pacing and a second reference time following pacing is calculated. If the second time delay is shorter than the first time delay, the method identifies a shortening of a delay to onset of myocardial synergy, OoS, thereby identifying the presence of RCD in the patient. Treatment of the RCD is performed.

In some examples, an electromechanical disassociation state (EMD) of a heart of a patient can be treated by delivering electrical stimulation to a tissue site to at least one of modulate afferent nerve activity or inhibit efferent nerve activity upon determining that the heart is in an electromechanical dissociation state, where the tissue site comprises at least one of a nonmyocardial tissue site or a nonvascular cardiac tissue site. The delivery of electrical stimulation may effectively treat the EMD state of the heart, e.g., by enabling effective mechanical contraction of the heart. In another example, an electromechanical disassociation state of a heart of a patient can be treated by determining autonomic nervous system activity associated with a detected EMD state of the heart of a patient, and delivering electrical stimulation therapy to the patient based on the determined autonomic nervous system activity of the patient associated with the EMD state.

There is provided a method for controlling a flow of fluid and/or other bodily matter in a lumen formed by a tissue wall of a patient's organ. The method comprises gently constricting (i.e., without substantially hampering the blood circulation in the tissue wall) at least one portion of the tissue wall to influence the flow in the lumen, and stimulating the constricted wall portion to cause contraction of the wall portion to further influence the flow in the lumen. The method can be used for restricting or stopping the flow in the lumen, or for actively moving the fluid in the lumen, with a low risk of injuring the organ. Such an organ may be the esophagus, stomach, intestines, urine bladder, urethra, ureter, renal pelvis, aorta, corpus cavernosum, exit veins of erectile tissue, uterine tube, vas deferens or bile duct, or a blood vessel.

Guidewires and methods for transmitting electrical stimuli to a heart and for guiding and supporting the delivery of elongate treatment devices within the heart are disclosed. A guidewire can comprise an elongate body, including first and second elongate conductors, and at least first and second electrodes. A distal end portion of the elongate body can include a preformed bias shape, such as a pigtail-shaped region, on which the first and second electrodes can be located. The preformed bias shape can optionally be non-coplanar relative to an intermediate portion of the elongate body. The first and second elongate conductors can be formed of a single structure or two or more electrically connected structures. The conductors can extend from proximal end portions to distal end portions that electrically connect to the first and second electrodes. A corewire can extend the length of the elongate body, can at least partially form the first conductor, and can be at least partially surrounded by the second conductor.

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.