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EP-4516240-B1 - ASYMMETRIC SHUNT FOR REDISTRIBUTING ATRIAL BLOOD VOLUME

EP4516240B1EP 4516240 B1EP4516240 B1EP 4516240B1EP-4516240-B1

Inventors

  • EIGLER, NEAL
  • WHITING, JAMES S.
  • NAE, NIR

Dates

Publication Date
20260506
Application Date
20200507

Claims (15)

  1. An asymmetric device (60, 80) for regulating blood volume distribution across a patient's atrial septum, the device (60, 80) comprising: a first expandable end region (61, 81) configured to transition from a contracted delivery state to an expanded deployed state in which the first expandable end region (61, 81) extends into the patient's left atrium and an inlet end (62, 82) of the first expandable end region (61, 81) has a first cross-sectional shape in the expanded deployed state; a second expandable end region (64, 84) configured to transition from a contracted delivery state to an expanded deployed state in which the second expandable end region (64, 84) extends into the patient's right atrium and an outlet end (65, 85) of the second expandable end region (64, 84) has a second cross-sectional shape in the expanded deployed state, the second cross-sectional shape different from the first cross-sectional shape and having a first pair of opposing sides that extend parallel (72, 73, 92, 93) and a second pair of opposing ends that curve (70, 71, 90, 91); and a neck region (63, 83) joining the first expandable end region (61, 81) to the second expandable end region (64, 84), the neck region (63, 83) configured for placement in the patient's atrial septum, wherein one of the first pair of opposing sides (92, 93) that extend parallel of the second cross-sectional shape of the second expandable end region (84) in the expanded deployed state is closest to the first expandable end region (81) in the expanded deployed state, or wherein one of the second pair of opposing ends (70, 71) that curve of the second cross-sectional shape of the second expandable end region (64) in the expanded deployed state is closest to the first expandable end region (61) in the expanded deployed state.
  2. The device (60, 80) of claim 1, wherein the first cross-sectional shape comprises a circle.
  3. The device (60, 80) of claim 2, wherein a distance between the second pair of opposing ends (70, 71) that curve of the second cross-sectional shape of the second expandable end region (64) is larger than or less than a diameter of the circle.
  4. The device (60, 80) of any of the preceding claims, further comprising a central longitudinal axis (69, 89), wherein from a first profile of the device (60, 80) having a first orientation, the central longitudinal axis (69, 89) has a curved shape.
  5. The device (60, 80) of claim 4, wherein from a second profile of the device (60, 80) having a second orientation, the central longitudinal axis (69, 89) is a straight line, and optionally, wherein the second orientation of the second profile is 90 degrees from the first orientation of the first profile when the device (60, 80) is rotated about the central longitudinal axis (69, 89).
  6. The device (60, 80) of any of the preceding claims, wherein the second cross-sectional shape has a cross-sectional area that is less than a cross-sectional area of the first cross-sectional shape, such that blood exits the outlet end (65, 85) at a faster rate than blood entering the inlet end (62, 82), and optionally, wherein the first cross-sectional shape comprises a circle and a distance between the second pair of opposing ends that curve (70, 71, 90, 91) is approximately equal to a diameter of the circle.
  7. The device (60, 80) of any of the preceding claims, wherein the inlet end (62, 82) of the first expandable end region (61, 81) in the expanded deployed state is in a first plane, and the outlet end (65, 85) of the second expandable end region (64, 84) in the expanded deployed state is in a second plane, wherein the first plane intersects the second plane.
  8. The device (60, 80) of claim 7, wherein the first plane intersects the second plane at an angle between 20 and 45 degrees.
  9. The device (60, 80) of any of the preceding claims, wherein the first and second expandable end regions (61, 64, 81, 84) and the neck region (63, 83) are formed by a frame, and wherein the frame is encapsulated with a biocompatible material to form a conduit defining a lumen.
  10. The device (60, 80) of claim 9, wherein the biocompatible material is configured to be resistant to transmural and translational tissue growth.
  11. The device (60, 80) of claim 9 or 10, wherein the conduit has a first end that extends from the neck region (63, 83) a first distance of at least 3 mm into the patient's left atrium and a second end that extends from the neck region (63, 83) a second distance of at least 3 mm into the patient's right atrium, thereby preventing pannus formation from narrowing the lumen of the conduit in the neck region (63, 83).
  12. The device (60, 80) of any of claims 9 to 11, wherein the conduit is configured so that, when implanted, the second end of the conduit extends greater than 5 mm into the right atrium and is located out of a natural circulation flow path of blood entering into the patient's right atrium from an inferior vena cava, thereby reducing a risk of emboli entrained in flow from the inferior vena cava being directed into the second end of the conduit.
  13. The device (60, 80) of any of claims 9 to 12, wherein the lumen has a diameter in the neck region (63, 83) in a range of 5 mm to 6.5 mm.
  14. The device (60, 80) of any of claims 9 to 13, wherein the lumen of the conduit is configured to provide high velocity flow therethrough, and has a length between 10 to 15 mm configured to limit paradoxical emboli passing across the lumen during a transient pressure gradient reversal.
  15. The device (60, 80) of any of claims 9 to 14, wherein the frame comprises a plurality of longitudinal struts interconnected by a plurality of circumferential sinusoidal struts.

Description

FIELD OF THE INVENTION This application generally relates to percutaneously placed asymmetric implants and methods for redistributing blood from one cardiac chamber to another to address pathologies such as heart failure ("HF"), myocardial infarction ("MI") and pulmonary arterial hypertension ("PAH"). BACKGROUND OF THE INVENTION Heart failure is the physiological state in which cardiac output is insufficient to meet the needs of the body or to do so only at a higher filing pressure. There are many underlying causes of HF, including myocardial infarction, coronary artery disease, valvular disease, hypertension, and myocarditis. Chronic heart failure is associated with neurohormonal activation and alterations in autonomic control. Although these compensatory neurohormonal mechanisms provide valuable support for the heart under normal physiological circumstances, they also play a fundamental role in the development and subsequent progression of HF. For example, one of the body's main compensatory mechanisms for reduced blood flow in HF is to increase the amount of salt and water retained by the kidneys. Retaining salt and water, instead of excreting it via urine, increases the volume of blood in the bloodstream and helps to maintain blood pressure. However, the larger volumes of blood also cause the heart muscle, particularly the ventricles, to become enlarged. As the heart chambers become enlarged, the wall thickness decreases and the heart's contractions weaken, causing a downward spiral in cardiac function. Another compensatory mechanism is vasoconstriction of the arterial system, which raises the blood pressure to help maintain adequate perfusion, thus increasing the load that the heart must pump against. In low ejection fraction ("EF") heart failure, high pressures in the heart result from the body's attempt to maintain the high pressures needed for adequate peripheral perfusion. However, as the heart weakens as a result of such high pressures, the disorder becomes exacerbated. Pressure in the left atrium may exceed 25 mmHg, at which stage, fluids from the blood flowing through the pulmonary circulatory system transudate or flow out of the pulmonary capillaries into the pulmonary interstitial spaces and into the alveoli, causing lung congestion and if untreated the syndrome of acute pulmonary edema and death. Table 1 lists typical ranges of right atrial pressure ("RAP"), right ventricular pressure ("RVP"), left atrial pressure ("LAP"), left ventricular pressure ("LVP"), cardiac output ("CO"), and stroke volume ("SV") for a normal heart and for a heart suffering from HF. In a normal heart beating at around 70 beats/minute, the stroke volume needed to maintain normal cardiac output is about 60 to 100 milliliters. When the preload, after-load, and contractility of the heart are normal, the pressures required to achieve normal cardiac output are listed in Table 1. In a heart suffering from HF, the hemodynamic parameters change (as shown in Table 1) to maintain peripheral perfusion. Table 1ParameterNormal RangeHF RangeRAP (mmHg)2-66-20RVSP (mmHg)15-2520-80LAP (mmHg)6-1215-50LVEDP (mmHg)6-1215-50CO (liters/minute)4-82-6SV (milliliters/beat)60-10030-80 HF is generally classified as either systolic heart failure ("SHF") or diastolic heart failure ("DHF"). In SHF, the pumping action of the heart is reduced or weakened. A common clinical measurement is the ejection fraction, which is a function of the blood ejected out of the left ventricle (stroke volume) divided by the maximum volume in the left ventricle at the end of diastole or relaxation phase. A normal ejection fraction is greater than 50%. Systolic heart failure generally causes a decreased ejection fraction of less than 40%. Such patients have heart failure with reduced ejection fraction ("HFrEF"). A patient with HFrEF may usually have a larger left ventricle because of a phenomenon called "cardiac remodeling" that occurs secondarily to the higher ventricular pressures. In DHF, the heart generally contracts normally, with a normal ejection fraction, but is stiffer, or less compliant, than a healthy heart would be when relaxing and filling with blood. Such patients are said to have heart failure with preserved ejection fraction ("HFpEF"). This stiffness may impede blood from filling the heart and produce backup into the lungs, which may result in pulmonary venous hypertension and lung edema. HFpEF is more common in patients older than 75 years, especially in women with high blood pressure. Both variants of HF have been treated using pharmacological approaches, which typically involve the use of vasodilators for reducing the workload of the heart by reducing systemic vascular resistance, as well as diuretics, which inhibit fluid accumulation and edema formation, and reduce cardiac filling pressure. No pharmacological therapies have been shown to improve morbidity or mortality in HFpEF whereas several classes of drugs have made an important impact on the mana