Systems for heart treatment

Abstract

Described are devices and methods for treating degenerative, congestive heart disease and related valvular dysfunction. Percutaneous and minimally invasive surgical tensioning structures offer devices that mitigate changes in the ventricular structure (i.e., remodeling) and deterioration of global left ventricular performance related to tissue damage precipitating from ischemia, acute myocardial infarction (AMI) or other abnormalities. These tensioning structures can be implanted within various major coronary blood-carrying conduit structures (arteries, veins and branching vessels), into or through myocardium, or into engagement with other anatomic structures that impact cardiac output to provide tensile support to the heart muscle wall which resists diastolic filling pressure while simultaneously providing a compressive force to the muscle wall to limit, compensate or provide therapeutic treatment for congestive heart failure and / or to reverse the remodeling that produces an enlarged heart.

Description

CROSS-REFERENCE TO RELATED APPLICATIONS [0001] This application claims the benefit of Provisional Application Ser. No. 60 / 329,694 entitled “Percutaneous Cardiac Support Structures and Deployment Means” filed Oct. 16, 2001 and Provisional Application Ser. No. 60 / 368,918 entitled “Percutaneous Vascular Tensioning Devices and Methods” filed Mar. 29, 2002, each of which is incorporated herein by reference.FIELD OF THE INVENTION [0002] The present invention relates generally to minimally invasive medical devices for treating or preventing congestive heart failure and related or concomitant valvular dysfunction. More specifically, the invention relates to tensioning structures and related deployment devices to mitigate changes in the ventricular structure and geometry and deterioration of global left and right ventricular performance related to tissue damage from myocardial ischemia, acute myocardial infarction (AMI), valve related disease or dysfunction, or other instigators of deteriora...

AI Technical Summary

Benefits of technology

[0022] The present invention meets these needs with tensioning structures that can be utilized locally (e.g., left ventricular anterior wall only versus about the entire heart) to reduce wall stresses, reinforce the walls, and reduce / limit volume of the heart muscle as required using percutaneous, minimally invasive surgical (MIS), and open surgical means or a combination thereof. Devices according to the present invention may be used to facilitate operator controlled “tailoring” of localized treatment using various embodiments of the invention at various chosen target zones (i.e., left ventricle, mitral valve annulus, or sub-valvular apparati). Custom tailoring of each tensioning structure enables application of compression against specific regions of tissue in one, two or three dimensions relative to the heart's surface and patient specific adjustability of the amount of compression applied to the tissue to optimize the heart's overall hemodynamic performance.

[0023] Tensioning structures according to the invention can be individually placed within or about the heart (intravascularly or extravascularly) working in concert to provide reinforcement against myocardial stretch (or infarct expansion) and additionally to facilitate contraction of tissue previously subject to such myocardial degeneration. In doing so, the contractile and expansion energies of the heart can be transferred to and across the weakened sections of the heart from the more viable sections of the heart muscle. Such devices provide localized dynamic support or reinforcement and are active throughout the cardiac cycle unlike previous device approaches that generally only reduce the stress in the heart wall during diastole. Diastolic compliance can also be regulated or controlled with structures according to the invention. Also, the tensioning structures facilitate and maintain a more efficient and perhaps optimal wall motion through the cardiac cycle thereby aiding in diastolic filling and systolic contraction at the tissue area that has been compromised by ischemia, infarct or other abnormalities. The tensioning structures are implanted in target heart regions using standard cardiovascular, interventional techniques using guiding catheters and introducing sheaths or less invasive surgical techniques involving port access or small incisions into the thoracic cavity to eliminate the need for more radical surgery (e.g., median sternotomy) to provide a potential, palliative or therapeutic response to the disease.

Problems solved by technology

While the exact etiology of the syndrome that causes heart failure is not fully understood, the primary cause of CHF is left ventricular dysfunction (i.e., the inability of the heart to properly and adequately fill or empty blood from the left ventricle with adequate efficiency to meet the metabolic needs of the body).

These include neuro-hormonal stimulation, endothelial dysfunction, vasoconstriction, and renal sodium retention-all of which can cause dyspnea, fatigue and edema rendering patients unable to perform the simplest everyday tasks.

With existing pharmacological, surgical and device-based therapies symptoms can be alleviated, but the quality of a patient's life remains significantly impaired.

Further morbidity and mortality associated with the disease is exceptionally high.

Decreases in systolic contraction can lead to cardiomyopathy, which further exacerbates the localized, ischemia damaged tissue or AMI insult into a global impairment, thereby leading to episodes of arrhythmia, progressive pump failure and death.

Ischemia-damaged and / or infarct damaged heart muscle tissue results in progressive softening or degeneration of cardiac tissue.

These ischemic and infarcted zones of the heart muscle wall have limited, if not complete loss of tissue contractile functionality and overall physical integrity and present an analogous situation to those presented by vascular aneurysms.

With this enlargement, the heart's burden is increased to pump more blood with each pump cycle.

With this bulging, the heart's natural contraction mechanism is dissipated and attenuated, resulting in a marked and progressing decrease in cardiac output.

Any damage or impairment in function of any of these key components can render the valve structure incompetent.

Impairment of valve function, due to independent factors (i.e., a concomitant valve pathology) or dependent factors (i.e., valve dilation related to dilated cardiomyopathy), can result in valvular insufficiency further exacerbating the degenerative CHF cycle.

However, there still remains no definitive cure for CHF.

These kinds of vasodilators relax both arterial and venous smooth muscle, thereby reducing the resistance to left ventricular ejection.

The procedure is known to provide some symptomatic improvement, but is controversial with regard to its ability to enable active improvement of cardiac performance.

In spite of the positive outcome on relieving some of the symptoms, the procedure is highly invasive, requiring access to the heart via a sternotomy, expensive, complex and of unknown durability (due to the muscle wrap blood flow requirements and fibrosis issues).

While innovative, the procedure is highly invasive, traumatic and costly.

Further, the actual volume reduction results in a reduction in valve competence and elicits the associated regurgitation.

While being generally successful and routine in surgical practice today, these procedures are also costly, highly invasive and are still have significant associated morbidity and mortality.

Still, the use of such devices is limited by high costs and a lack of substantial, clinical evidence warranting their use.

As a result, these types of approaches require unnecessary positioning of the devices over healthy (non local, undamaged) areas or zones of the heart affecting the entire organ when the primary treatment is usually focused is on the left ventricle or the mitral valve annulus.

Such non-localized treatment can elicit iatrogenic conditions such as undesired valvular dysfunction and / or constrictive physiology due to over restriction of the heart by such restraints.

While appealing, the clinical efficacy of this approach is unknown at this time.

Transplants represent a massive challenge with donor hearts generally in short supply and with the transplant surgery itself presenting a high risk, traumatic and costly procedure.

In spite of this, transplants present a valuable, albeit limited, upside, increasing life expectancy of end stage congestive heart failure patient from less than one year up to a potential five years.

In view of the above, it should be evident that there is currently no ideal treatment among the various surgical, pharmacological, and device-based approaches to treat the multiple cardiac and non-cardiac factors implicated with the syndrome of CHF.

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