Splint assembly for improving cardiac function in hearts, and method for implanting the splint assembly

Abstract

A splint assembly for placement transverse a heart chamber to reduce the heart chamber radius and improve cardiac function has a tension member formed of a braided cable with a covering. A fixed anchor assembly is attached to one end of the tension member and a leader for penetrating a heart wall and guiding the tension member through the heart is attached to the other end. An adjustable anchor assembly can be secured onto the tension member opposite to the side on which the fixed pad assembly is attached. The adjustable anchor assembly can be positioned along the tension member so as to adjust the length of the tension member extending between the fixed and adjustable anchor assemblies. The pad assemblies engage with the outside of the heart wall to hold the tension member in place transverse the heart chamber. A probe and marker delivery device is used to identify locations on the heart wall to place the splint assembly such that it will not interfere with internal heart structures. The device delivers a marker to these locations on the heart wall for both visual and tactile identification during implantation of the splint assembly in the heart.

Description

FIELD OF THE INVENTION [0001] The present invention pertains to a device, and a method for placing the device, for treating a failing heart. In particular, the device and its related method of the present invention are directed toward reducing the wall stress in a failing heart. The device reduces the radius of curvature and / or alters the geometry or shape of the heart to thereby reduce wall stress in the heart and improve the heart's pumping performance. BACKGROUND OF THE INVENTION [0002] Heart failure is a common course for the progression of many forms of heart disease. Heart failure may be considered as the condition in which an abnormality of cardiac function is responsible for the inability of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues, or can do so only at an abnormally elevated filling pressure. There are many specific disease processes that can lead to heart failure. Typically these processes result in dilatation of the ...

AI Technical Summary

Benefits of technology

[0014] One aspect of the present invention pertains to a non-pharmacological, passive apparatus and method for the treatment of a failing heart due to dilatation. The device is configured to reduce the tension in the heart wall, and thereby reverse, stop or slow the disease process of a failing heart as it reduces the energy consumption of the failing heart, decreases isovolumetric contraction, increases isotonic contraction (sarcomere shortening), which in turn increases stroke volume.

[0018] According to yet another aspect of the present invention an apparatus for improving cardiac function includes an elongate member attached to a leader member at one end thereof and being configured to extend transverse a heart chamber, a first heart-engaging assembly attached to the other end of the elongate member and configured to engage a first exterior location of a heart wall, and a second heart-engaging assembly configured to slidably receive the leader member and the elongate member and to thereby be secured to the elongate member and to engage a second exterior location of the heart wall. The second heart-engaging assembly is configured to be secured to the elongate member such that a length of the elongate member between the first and second heart-engaging assemblies can be adjusted during placement of the elongate member transverse the heart chamber.

Problems solved by technology

Typically these processes result in dilatation of the left ventricular chamber.

With damage to the myocardium or chronic volume overload, however, there are increased requirements put on the contracting myocardium to such a level that this compensated state is never achieved and the heart continues to dilate.

The basic problem with a large dilated left ventricle is that there is a significant increase in wall tension and / or stress both during diastolic filling and during systolic contraction.

However, in a failing heart, the ongoing dilatation is greater than the hypertrophy and the result is a rising wall tension requirement for systolic contraction.

This is felt to be an ongoing insult to the muscle myocyte resulting in further muscle damage.

Additionally, because of the lack of cardiac output, a rise in ventricular filling pressure generally results from several physiologic mechanisms.

These drug therapies offer some beneficial effects but do not stop the progression of the disease.

Heart transplantation has serious limitations including restricted availability of organs and adverse effects of immunosuppressive therapies required following heart transplantation.

However, this extremely invasive procedure reduces muscle mass of the heart.

Finally, mitral regurgitation is a condition whereby blood leaks through the mitral valve due to an improper positioning of the valve structures that causes it not to close entirely.

If the infarcted or aneurysmal region is located in the vicinity of the mitral valve, geometric abnormalities may cause the mitral valve to alter its normal position and dimension, and may lead to annular dilatation and the development of mitral regurgitation.

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