Method for optimizing CRT therapy

Abstract

A method to optimize CRT therapy using ventricular lead motion analysis, either radiographically or with three dimensional electromagnetic mapping, to determine whether focal dyssynchrony is present at baseline, and whether biventricular pacing improves synchronicity and fractional shortening, and if no improvement is evidenced, changing the timing offset, pacing configuration and/or repositioning the ventricular leads to optimize effectiveness of CRT therapy. Various uses of this method include: diagnostic, with temporary leads to determine presence or absence of dyssynchrony and response to pacing; and therapeutic, to guide lead placement and programming during implant of CRT, and to optimize reprogramming of CRT during follow-up.

Description

RELATED APPLICATIONS

This application claims the benefit of U.S. Provisional Patent Application No. 60/998,939 filed on Oct. 15, 2007.

BACKGROUND OF THE INVENTION

1. Field of the Invention

This invention relates to surgery, and more particularly to a method for determining FIG. 22 is a graphic representation of synchronous heart wall movement (FIGS. 7 and 8) and dyssynchronous heart wall movement (FIGS. 9 and 10) showing the correlation with a simultaneous ECG recording (FIG. 4) of plural cardiac cycles by time.The invention provides a method to quantify electromechanical intervals of ventricular systole and diastole to assess dyssynchrony and may also be used to characterize other forms of systolic and diastolic heart failure and may be used as a means to guide therapy.

Our method generally provides a ventricular pacemaker 20 having a left ventricular lead 21, a right ventricular lead 22 and an atrial lead 23; a radiological three dimensional imaging system 24; an image compiling system 25; an analytical processing system 27 and a visual display 26. The left ventricular lead 21 has a lead tip 21a at its terminal end, the right ventricular lead 22 has a lead tip 22a at its terminal end and the atrial lead 23 has a lead tip 23a at its terminal end.

CRT is currently indicated for patients with left ventricular dyssynchrony, an ejection fraction<35%, a prolonged QRS complex 43 having a duration>120 msec and severe heart failure, New York Heart Association (NYHA) classification III or IV, despite maximal medical therapy.

The normal cardiac conduction system is diagramed at FIG. 1. The sinoatrial node 30 (SA node) proximate the right atrium 31 is the pacemaker for heart H. Electrical impulses are generated in and propagate from the SA node 30 to synchronously activate cardiac muscle cells comprising right atrium 31 and left atrium 32. The electrical impulse then propagates downwardly to atrioventricular node 35 (AV node) which is the electrical connection from the right atrium 31 to right ventricle 33 and left ventricle 34.

The AV node 35 distally becomes the HIS bundle 38 which bifurcates into left bundle branch 37 and right bundle branch 36 which conduct the electrical impulse to Purkinje fibers 46 of the right ventricle 33 and the left ventricle 34 so that electrical activation of the right ventricle 33 and left ventricle 34 occurs synchronously resulting in uniform ventricular contraction. (FIGS. 7, 8).

Cardiac muscle cells (not shown) need to be electrically excited to undergo mechanical contraction. During the excitation, known as depolarization, electrical signals are generated that can be recorded with an electrocardiogram (ECG) (not shown). Features of an ECG recording (FIGS. 4, 5) correspond to the origin of the electrical activity. Depolarization in the atria 31, 32 generates a P wave 41. Depolarization in the ventricles 33, 34 generates a wave form known as a QRS complex 43 which consists of a Q-wave 43a, an R-wave 43b and an S-wave 43c. A normal QRS complex 43 has a duration of less than 120 msec. (FIG. 4). A QRS complex 43 having a duration greater than 120 msec (FIG. 5) is abnormal and is one criteria criterion for CRT.

Damage to the conduction tissues below the AV node 35, such as at the level of the bundle branches 36, 37 or lower, can result in dyssynchronous activation of the ventricles 33, 34 which may lead to ventricular dysschrony. Ventricular dysschrony is defined as non-uniform contraction of the ventricles 33, 34 due to delayed activation. (FIGS. 9,10). Damage to the conduction tissues may also cause a prolonged QRS complex 43. Current guidelines use a prolonged QRS complex 43 as a surrogate to identify ventricular dyssynchrony. Unfortunately, a prolonged QRS duration and ventricular dyssynchrony only show a rough correlation to one another.

As shown in FIGS. 2 and 3, the left ventricle 34 starts to contract after an electrical impulse (not shown) propagating down from the left bundle branch excites muscle cells (not shown) of septal wall 39 and lateral wall 40. As the muscle cells contract they become shorter and thicker causing the septal and lateral walls 39 and 40 respectively, to contract inwardly towards each other to pinup blood out of the left ventricle 34 to the body (not shown) through the aorta 48.

As shown in FIG. 6, CRT uses an atrial lead 23 having a lead tip 23a positioned in the right atrium 31, a right ventricular lead 22 having a lead tip 22a positioned on right ventricular apex or septal wall 39 and a left ventricular lead 21 having a lead tip 21a implanted on left ventricular lateral wall 40, left ventricular anterolateral wall (not shown) or left ventricular posterolateral wall (not shown) to provide pacing on both sides of the left ventricle 34 to resynchronize left ventricle 34 activation.

FIGS. 7 and 9 represent a cross-section view of the right ventricle 33 and left ventricle 34 similar to a left anterior oblique (LAO) X-ray view (FIG. 17) and show the relative positions of the right ventricular lead tip 22a and the left ventricular lead tip 21a. Arrows represent direction of ventricular wall movement during synchronous systole/contraction (FIG. 7) and dysschronous dyssynchronous systole/contraction (FIG. 9). Simultaneous electrocardiographic display provides an ability to determine electromechanical measurements of systole and diastole during intrinsic rhythm and in response to pacing.

FIGS. 8 and 10 are graphic representations of the motion of the left ventricular lead tip 21a and the motion of the right ventricular lead tip 22a through plural complete cardiac cycles in the short axis shown in FIGS. 7 and 9. FIGS. 7 and 8 show normal synchronous ventricular contraction and relaxation while FIGS. 9 and 10 show dyssynchronous ventricular contraction and relaxation evidenced by a timing difference of the left ventricular lead tip 21a and right ventricular lead tip 22a at maximum contraction 55 and relaxation 56. As shown, maximal contraction 55 of the left ventricular lead tip 21a occurs at a trough in the graphic representation of the lead tip movement and is 180 degrees out of phase as compared to the maximal contraction 55 of the right ventricular lead tip 22a which occurs at a crest in the graphic representation of the lead tip movement.

FIGS. 11 and 12 are lead tip 21a, 22a motion schematics. Synchronous ventricular contraction (FIG. 11) is evidenced by simultaneous (vertically aligned) right ventricular lead tip 22a and left ventricular lead tip 21a maximal contraction 55. Dyssynchronous ventricular contraction (FIG. 12) is evidenced by a timing delay 50 between maximal contraction 55 of the lead tips 21a, 22a.

The difference in time 50 to between maximal contraction 55 of the right ventricular lead tip 22a and left ventricular lead to 21a is a focal measure of dyssynchrony. FIG. 12 illustrates this measurement at 50. The difference in time 50 from onset of electrical activation (start of the QRS complex 43) to maximal contraction 55 of the right or left ventricular lead (not shown), also provides a measure of electromechanical dyssynchrony. FIG. 22 shows the timing correlation of the electrical activation of the heart H as it relates to the mechanical activation of the heart H. Other electromechanical measures including rate of contraction and/or relaxation and/or duration of contraction and/or relaxation (relative to overall cardiac cycle length) as well as timing of contraction and/or relaxation, may have potential use to guide therapy of systolic or diastolic heart failure.

FIGS. 13 and 14 illustrate quantification of focal contractility by measuring the distance between the right ventricular lead tip 22a and the left ventricular lead tip 21a at time stamped points in a cardiac cycle. Average vertical distance 45 (FIGS. 13, 14) between the lead tips 21a, 22a at the same time stamp is the measure of focal contractility. FIG. 13 shows normal contractility represented by vertically aligned synchronous movement of the left ventricular lead tip 21a and the right ventricular lead tip 22a wherein troughs 52 and representing contraction motion of the left ventricular lead tip 21a are vertically aligned with crests 51 that representing contraction motion of the right ventricular lead tip 22a, and same time stamp relaxations are widely separated 45 vertically while. FIG. 14 shows reduced contractility represented by absence of vertical alignment of the troughs 52 of the left ventricular lead 21a motion with the crests 51 of the right ventricular lead 22a motion and lessened vertical separation 45 between the lead tips 21a, 22a at the same time stamp caused by ventricular dysschrony dyssynchrony 50. Using contractility measures, fractional shortening may also be determined.

Analysis of lead tip 21a, 22a motion in the left ventricular short axis (approximated in the LAO projection) provides data on concentric contraction and radial motion. (FIGS. 7, 9). Left ventricular lead tip 21a and right ventricular lead tip 22a motion in the RAO view provides data to determine longitudinal (Z-axis) motion. Synchronous Z-axis contraction and synchronous Z-axis relaxation of the ventricles 33, 34 is evidenced by parallel lines of motion for the right ventricular lead tip 22a and left ventricular lead tip 21a (FIG. 15) while dyssynchronous Z-axis contraction and dyssynchronous Z-axis relaxation is evidenced by non-parallel lines of motion for the right ventricular lead tip 22a and left ventricular lead tip 21a. (FIG. 16).

With radiologic analysis a cine loop recording (not shown) is made in left anterior oblique (LAO), right anterior oblique (RAO) and anterior posterior (AP) projections (FIG. 17) during plural complete cardiac cycles to document motion of the left ventricular lead tip 21a and the right ventricular lead tip 22a during intrinsic heart rhythm as well as during paced heart rhythm.

The cine loop recording data is exported, preferably in an AVI format, to the image compiling system 25 which is preferably a physics motion analysis program 25 such as Tracker™ software from Open Source Physics, Inc. wherein the X-axis, Y-axis and Z-axis coordinates for the left ventricular lead tip 21a and the right ventricular lead tip 22a are determined for each recorded cine frame and identified by time stamps throughout the plural cardiac cycles. Cine is no less than 15-30 frames per second (fps) to ensure accurate time stamps.

Table 1 sets forth a sample of the data collected by the physics motion analysis program 25 showing left ventricular lead tip 21a positions. For each position the cine frame time is noted as is the X-axis coordinate and the Y-axis coordinate.

TABLE 1
t	x	y
0	116.426	22.788
0.066	115.926	17.283
0.132	112.422	20.285

The X axis coordinate data, the Y axis coordinate data and the time data for each lead tip 21a, 22a, 23a in each view is then exported to analytical processing system 27 having a computer operating system, such as Origin™ software manufactured by Origin Lab Corp. of Northhampton, Mass., USA. Paired analyses comparing the intrinsic heart rhythm data and the paced heart rhythm data, is performed for each radiographic view. (LAO, RAO and AP). The motion of the left ventricular lead tip 21a and the motion of the right ventricular lead tip 22a motion is then visually presented, such as by graphing, showing the time difference 50 to maximum contraction 55 between the right ventricular lead tip 22a and left ventricular lead tip 21a which provides a focal measure of dysschrony dyssynchrony (FIGS. 11, 12) and the percentage of shortening from maximum diastole to maximal systole between the left ventricular lead tip 21a and the right ventricular lead tip 22a providing a measure of contractility and shortening fraction. These measures can also be correlated with simultaneous electrocardiographic (ECG) recording to provide electromechanical intervals of ventricular systole and diastole to assess dyssynchrony and may also be used to consider other forms of systolic and diastolic heart failure and may be used as a means to guide therapy. Baseline dysschrony dyssynchrony, baseline contractility and, baseline shortening fraction and ventricular heart wall motion in systole and diastole are then compared with paced dysschrony dyssynchrony, paced ventricular heart wall motion, paced contractility and, paced shortening fraction and ventricular heart wall motion in systole and diastole at the current lead 21, 22 positions to determine the effectiveness of CRT. (FIGS. 18-20 22). Using the measures it is possible to assess whether there is focal improvement in dysschrony dyssynchrony, contractility and, shortening fraction and ventricular heart wall motion in systole and diastole with pacing at the current lead locations and pacing configuration. Other pacing configurations such as isolated right ventricular or left ventricular pacing, or pacing with RV-LV offset could also be similarly assessed.

This method is also applicable using a three dimensional mapping system such as St Jude Medical NAVX to document lead tip motion without x-ray use. In such an application, the 3D mapping patches are placed system is set up for standard use and the left and right ventricular leads 21, 22 are connected to the NAVX monitor monitoring system allowing 3-Dimensional recording of the motion of the monitored lead tips 21a, 22a during multiple cardiac cycles during intrinsic and paced rhythm. This technique allows correlation with ECG and allows measurement of electromechanical intervals (time from onset of QRS complex to peak contraction, through plural complete cardiac cycles) of either lead 21, 22 and limits respiratory interference. (FIG. 22).

FIG. 18 shows dysschronous lead tip 21a, 22a movement during intrinsic heart rhythm at a plurality of time stamps. FIG. 19 shows motion of the lead tips 21a, 22a during paced rhythm at a plurality of time stamps showing improvement and more synchronous ventricular contraction 55.

In the absence of an ECG recording, systole is defined as earliest maximal contraction 55 of either ventricular lead tip 21a, 22a or in the case of severe akinesis, by the maximal two dimensional shortening between the two ventricular lead tips 21a, 22a. Similarly, diastole is defined as earliest maximal relaxation 56 of either ventricular lead tip 21a, 22a or in the case of severe akinesis, by the maximal two dimensional lengthening between the ventricular lead tips 21a, 22a. When ECG recording is available, electromechanical intervals can be determined such as the onset of QRS to peak contraction or relaxation, duration of contraction and relaxation intervals of the left or the right ventricular lead tips 21a, 22a respectively during intrinsic and paced rhythms.

Left ventricle lead tip 21a motion and right ventricle lead tip 22a motion are assessed in the LAO view during intrinsic heart rhythm. The position of both lead tips 21a, 22a is identified at each time stamped cine frame using the image compiling system 25. The lead tip 21a, 22a positions are documented at time intervals in two-dimensions (the X-axis correlates roughly with the short axis of the left ventricle 34 in the LAO view; the Y-axis, although also in the short axis of the left ventricle 34, correlates more directly with respiratory cardiac motion). The lead tip 21a, 22a motion data is then transferred to the analytical processing system 27.

In the X-axis, the motion of the left ventricular lead tip 21a and motion of the right ventricular lead tip 22a is plotted showing systole and diastole, lead excursion and the relation of right ventricle 33 to left ventricle 34 upon contraction 55. The time differential 50 from maximal right ventricle 33 contraction 55 to maximal left ventricle 34 contraction 55 is used to quantify local dyssynchrony 50. (FIG. 11, 12). A zero timing difference (FIG. 11) is consistent with synchronous ventricular contraction 55. A positive timing difference indicates right ventricle 33 maximal contraction 55 precedes left ventricle 34 maximal contraction 55 while a negative timing difference indicates left ventricle 34 maximal contraction 55 precedes right ventricle 33 maximal contraction 55. (FIG. 12). Multiple measurements are taken and averaged for consistency.

In two-dimensional analysis (FIGS. 13, 14 and 20) fractional shortening is determined for each contractile cycle. Fractional shortening is a measure of heart contractility and is measured using two-dimensional LAO view data to calculate the maximal distances between the lead tips 21a, 22a at the start and end of each cardiac cycle using the following formula: Shortening Fraction (%)=(maximal distance from right ventricle lead tip 22a to left ventricle lead tip 21a−minimal distance from right ventricle lead tip 22a to left ventricle lead tip 21a)×100/(maximal distance from right ventricle lead tip 22a to left ventricle lead tip 21a).

The distance measurements are repeated and assessed during biventricular pacing, during right ventricular pacing and during left ventricular pacing, as well as with left ventricular/right ventricular pacing offsets and differing left ventricular pacing configurations. The pacing measurements are then compared with the distance measurements taken during intrinsic heart rhythm.

If there is no significant improvement in dyssynchrony or significant improvement in shortening fraction, consideration is given to altering the pacing offset, changing the pacing configuration, or changing left or right ventricular lead tip 21a, 22a position.

Three-dimensional lead tip 21a, 22a motion analysis may be performed by using simultaneous bi-plane imaging in left anterior oblique (LAO) and right anterior oblique (RAO) views. In the three-dimensional application of the method, the LAO view is adjusted to represent the true short axis of the left ventricle 34 and represents radial shortening. (FIG. 7). The RAO view is obtained at a 90° angle. With simultaneous cine in these two views, the left ventricular lead tip 21a motion data is plotted to determine short axis movement (X and Y axis) and right ventricular lead tip 22a motion data is plotted to obtain longitudinal motion (Z axis). (FIGS. 15, 16). Using X, Y and Z axis coordinates, three-dimensional left ventricular lead tip 21a motion and three dimensional right ventricular lead tip 22a motion is determined. Using the three-dimensional technique and analysis thereof, individual lead tip 21a, 22a motion, dysschrony dyssynchrony and fractional shortening can also be determined and graphed.

Three-dimensional lead tip 21a, 22a, motion analysis may be obtained using a series of topical patches (not shown) applied to the patient's chest (not shown) using a global three dimensional positioning approach to document the ventricular lead tip 21a, 22a positions by time. Commercially available motion analysis systems three dimensional imaging systems, such as a NAVX system, by St. Jude Medical Inc. may be used to perform the three dimensional lead tip motion analysis and avoid X-ray exposure. The data is collected using the right ventricular lead tip 22a as a reference and the left ventricular lead tip 21a as input during intrinsic ventricular rhythm and paced ventricular rhythm. Lead tip 21a, 22a motion is documented throughout the cardiac cycle including systole and diastole during intrinsic heart rhythm and during the paced biventricular rhythm, paced right ventricular rhythm and paced left ventricular rhythm. Other left ventricular pacing configurations and left ventricular/right ventricular pacing offsets may also be documented and assessed. Simultaneous ECG input allows electromechanical measurements of timing from QRS onset to peak mechanical contraction 55 of left or right ventricles 34, 33 respectively during intrinsic and paced rhythms throughout plural complete cardiac cycles.

Having described our method for optimizing CRT, its operation may be understood.

FIG. 22 is a compilation of FIGS. 4, 8, 10, 11 and 12 showing an ECG recording of three successive cardiac cycles showing the P-wave 41, the QRS complex 43 and the T-wave 42 by time. Left ventricular heart wall movement is graphically shown by left ventricular lead 21a movement, and right ventricular heart wall movement is graphically shown by right ventricular lead 22a movement. Maximal ventricular heart wall contraction is shown at 55 (which also marks the beginning of mechanical relaxation) and maximal ventricular heart wall relaxation is shown at 56 (which also marks the beginning of mechanical contraction). 60 is a measure of electromechanical delay between onset of the QRS complex 43 (beginning of electrical depolarization of the heart H) to the beginning of mechanical contraction 56. 61 is a measure of electromechanical delay between onset of the QRS complex 43 (beginning of electrical depolarization of the heart H) to the beginning of mechanical contraction when there is a timing abnormality leading to dyssynchrony which is shown by dashed line 21b having a maximal delayed contraction at 55b and maximal delayed relaxation at 56b. 62 is a measure of the electromechanical delay between end of the QRS complex 43 (beginning of electrical repolarization of the heart H) to the beginning of mechanical relaxation 55. 63 is a measure of the electromechanical delay between end of the QRS complex 43 (beginning of electrical re-polarization of the heart H), to the beginning of mechanical relaxation 55b when there is a timing abnormality as illustrated by dashed line 21b.

The electromechanical delays 60, 61, 62 and 63 shown in FIG. 22 are only two examples of timing delays that may be identified and examined using our described and claimed method. Other timing delays and periods such as, but not limited to, rate and duration of contraction and/or relaxation and the corresponding phase relationships are likewise contemplated herein and may also be used for therapy, treatment and management of timing disorders of the heart H.

A patient is identified as having perceived ventricular systolic dyschrony dyssynchrony. The patient may be identified by diagnostic use of our method using temporary pacing catheters in the right ventricle 33 and coronary sinus (for left ventricular pacing) similar to a diagnostic electrophysiologic study to assess for baseline dyssynchrony and to predict potential response to CRT.

Alternatively, in a patient identified as a candidate for CRT under the current guidelines, our method may be used to optimize lead tip 21a, 22a, 23a positions and improve CRT response during follow-up.

The first step of the method is the implantation of the leads 21, 22, 23 into the patient's heart H. Initially, the lead tip 21a, 22a, 23a implantation positions are determined empirically using prior studies that have identified the locations typically generating the greatest physiologic benefit from pacing.

The leads 21, 22, 23 are positioned using known catheters and known procedures. As shown in FIG. 1, the atrial lead 23 is positioned in the right atrium with the atrial lead tip 23a affixed to the right atrium 31. The right ventricular lead 22 is positioned in the right ventricle with the right ventricular lead tip 22a attached to the right ventricular apex or septum 47. The left ventricular lead 21 is generally placed in a lateral wall 40 position of the left ventricle 34 via the coronary sinus (allowing for anatomic constraints) or epicardially on the left ventricular epicardium. The pacemaker or defibrillator 20 is connected to the leads 21, 22, 23 opposite the lead tips 21a, 22a, 23a.

A radiographic imaging system 24 is used to make cine loop image recordings (not shown) of the heart H in the LAO, RAO and AP views (FIG. 17) through at least three complete cardiac cycles during intrinsic heart rhythm. The cine is at a minimum of 15-30 frames per second and time stamps are recorded on each cine frame. The positions of the left ventricular lead tip 21a and the right ventricular lead tip 22a are tracked throughout the cardiac cycles.

The intrinsic rhythm cine loop recordings are converted into an AVI format and transferred to the image compiling system 25, such as a Tracker™ system from Open Sources Physics, Inc. The X-axis, Y-axis and Z-axis coordinates for the left ventricular lead tip 21a and the right ventricular lead tip 22a are determined by the image compiling system 25 and the appropriate time stamps are accorded to each set of coordinates. The compiled data of intrinsic heart rhythm is transferred to the analytical software program 27 to provide a baseline measure of dysschrony and contractility.

The pacemaker 20 is activated and electrical pacing impulses generated within the pacemaker 20 are sent through the leads 21, 22, 23 to the lead tips 21a, 22a, and 23a for paced activation of the heart H. Biventricular pacing, right ventricular pacing and left ventricular pacing may be performed and various left ventricular pacing configurations or left ventricular/right ventricular timing offsets may also be assessed and utilized.

The radiographic imaging system 24 is again used to make cine loop image recordings (not shown) of the heart H in the LAO, RAO and AP views through at least three complete cardiac cycles during the paced heart rhythm configurations. The cine is at a minimum of 15-30 frames per second (fps) and time stamps are recorded on each cine frame. The position of the left ventricular lead tip 21a and the right ventricular lead tip 22a are tracked throughout the cardiac cycles.

The paced rhythm cine loop recordings are converted into an AVI format and transferred to the image compiling system 25. The X-axis, Y-axis and Z-axis coordinates for the left ventricular lead tip 21a and the right ventricular lead tip 22a are determined by the image compiling system 25 and the appropriate time stamps are accorded to each set of coordinates. The compiled results of paced heart rhythm are transferred to the analytical software program 27 to provide a measure of paced dysschrony dyssynchrony and contractility and ventricular heart wall motion throughout systole and diastole.

The analytical software program 27 plots the data from the intrinsic heart rhythm and plots the data from the paced heart rhythm on graphs and generates a visual display 26 showing the motion of the lead tips 21a, 22a by time. The visual display 26 may be printed or electronically displayed graphs and will show the measures of dysschrony and dyssynchrony, contractility and ventricular heart wall motion throughout systole and diastole for both intrinsic heart rhythm and the paced heart rhythm.

The visual display is interpreted by the physician performing the procedure to determine if there has been improvement in dysschrony dyssynchrony and an improvement in contractility or ventricular heart wall motion as a result of the pacing.

If assessment of the results shows no significant improvement in contractility, or significant improvement in dysschrony dyssynchrony or ventricular heart wall motion, the physician may re-assess pacing with an alternative left ventricular pacing configuration, such as using left ventricular/right ventricular pacing offsets, or move the left ventricular lead tip 21a to another position on the heart H such as to a more atypical position on the lateral wall 40, and/or the physician may change the position of the right ventricular lead tip 22a. The physician may also change offset of the pacemaker 20 to change the timing of the electrical impulses directed to the ventricular lead tips 21a, 22a.

The procedure for making a cine loop recording of the paced heart rhythm is repeated for the new lead tip 21a, 22a positions in the LAO, RAO and AP views and the data is exported for compiling, analysis and comparison against the intrinsic heart rhythm data. If no significant improvement is shown as a result of the new lead tip 21a, 22a position, the procedure may be repeated until improvement is achieved or patient condition requires the procedure be discontinued.

If assessment of the results shows only minimal improvement in contractility or minimal improvement in dysschrony, the physician will record the positions of the lead tips 21a, 22a in the heart H and then may change the positions of the lead tips 21a, 22a to improve the effects of pacing. The procedure for making a cine loop recording of the paced heart rhythm is repeated for the new lead tip 21a, 22a positions in the LAO, RAO and AP views and the data is exported for compiling, analysis and comparison against the intrinsic heart rhythm data. If no significant improvement is shown as a result of the new placement, the procedure may be repeated again or the lead tips 21a, 22a may be repositioned to the earlier position that showed some improvement with pacing.

If assessment of the results shows significant improvement in contractility and significant improvement in dysschrony dyssynchrony and ventricular heart wall motion, the physician will end the procedure.

Use of our method with a three dimensional mapping system such as NAVX (St Jude Medical Inc) allows three dimensional lead tip motion assessment in similar fashion without the detrimental effects of X-ray exposure and also provides ECG correlation as previously described.

This method may also be utilized during routine follow-up of patients with CRT, utilizing external patches and CRT analysis to provide lead tip motion analysis during office reprogramming to maximize CRT therapy. This method, by either X-Ray or three dimensional mapping system, may be utilized diagnostically or therapeutically to define electromechanical measures of contraction and ventricular heart wall motion, including responses to pacing, to uniquely assess systolic and diastolic heart failure and guide medical and CRT therapy.

The foregoing description of our invention is necessarily of a detailed nature so that a specific embodiment of its best mode may be set forth as is require, but it is to be understood that various modifications of details, and rearrangement, substitution and multiplication of steps and apparatus may be resorted to without departing from its spirit, essence or scope.

Having thusly described our invention, what we desire to protect by Letters Patent, and

Claims

1. A method for determining and optimizing left ventricular synchrony during cardiac resynchronization therapy comprising in combination:

identifying a patient as having perceived ventricular systolic dyssynchrony who may benefit from cardiac resynchronization therapy;

implanting left ventricular and right ventricular leads in the patient's heart, each lead having a lead tip at a first end portion;

positioning each lead tip initially at a location prior published studies have shown generate the greatest physiologic benefit from pacing;

connecting a pacemaker to the plural leads opposite the lead tips;

using a radiographic imaging system to make cine loop image recordings of the patient's heart in left anterior oblique, right anterior oblique and anterior-posterior views through at least three complete cardiac cycles during intrinsic heart rhythm and assigning time stamps to each cine frame to ascertain the position of each lead tip throughout the intrinsic cardiac cycles;

transferring the intrinsic rhythm cine loop image recordings to an image compiling system for compiling into intrinsic heart rhythm data and for determining an X-axis, a Y-axis and a Z-axis coordinate for each lead tip for each time stamped cine frame;

transferring the X-axis, the Y-axis and the Z-axis coordinate for each lead tip for each intrinsic rhythm time stamped cine frame to an analytical software program to determine a baseline measure of dyssynchrony and contractility at the current lead tip locations in the patient's heart;

activating the pacemaker to send electrical pacing impulses through the ventricular leads to the lead tips for paced activation of the patient's heart;

using the radiographic imaging system to make cine loop image recordings of the heart in left anterior oblique, right anterior oblique and anterior-posterior views through at least three complete cardiac cycles during the paced heart rhythm and assigning time stamps to each cine frame to ascertain the position of each lead tip throughout the paced cardiac cycles;

transferring the paced rhythm cine loop image recordings to the image compiling system for compiling into paced heart rhythm data and for determining the X-axis, Y-axis and Z-axis coordinate for each lead tip for each paced time stamped cine frame;

transferring the X-axis, the Y-axis and the Z-axis coordinate for each lead tip for each paced rhythm time stamped cine frame to the analytical software program to determine a measure of paced ventricular dyssynchrony and paced ventricular contractility at the current lead tip locations in the patient's heart;

plotting the intrinsic heart rhythm coordinate data and plotting the paced heart rhythm coordinate data and generating a visual display showing the motion of the lead tips by time so that the intrinsic heart rhythm coordinate data may be compared against the paced heart rhythm coordinate data;

interpreting the intrinsic heart rhythm coordinate data and the paced heart rhythm coordinate data to determine if the paced activation of the patient's heart decreases the ventricular dyssynchrony relative to the intrinsic ventricular dyssynchrony and increases ventricular contractility relative to the intrinsic contractility; and

ending the cardiac resynchronization therapy if the interpretation of the paced heart rhythm data compared against the intrinsic heart rhythm data shows increased contractility and increased synchrony with paced activation of the patient's heart at the current lead tip locations.

2. The method for determining and optimizing left ventricular synchrony of claim 1 wherein a right ventricular lead tip is located on the patient's heart's right ventricular septum.

3. The method for determining and optimizing left ventricular synchrony of claim 1 wherein a right ventricular lead tip is located on the patient's heart's right ventricular apex.

4. The method for determining and optimizing left ventricular synchrony of claim 1 wherein: a left ventricular lead tip is located on a left ventricular lateral wall.

5. The method for determining and optimizing left ventricular synchrony of claim 1 wherein: a left ventricular lead tip is located on a left ventricular anterolateral wall.

6. The method for determining and optimizing left ventricular synchrony of claim 1 wherein: a left ventricular lead tip is located on a left ventricular posterolateral branch of the coronary sinus.

7. The method for determining and optimizing left ventricular synchrony of claim 1 further comprising:

if interpretation of the results shows no improvement in contractility and no improvement in synchrony, documenting the position of the lead tips in the heart;

changing the position of at least one lead tip; and

repeating the steps of claim 1 for activating the pacemaker, imaging, compiling, identifying coordinate positions and comparing the paced heart rhythm data against the intrinsic heart rhythm data.

8. The method for determining and optimizing left ventricular synchrony of claim 1 further comprising:

if interpretation of the results shows minimal improvement in contractility and minimal improvement in synchrony, documenting the position of the lead tips in the heart;

changing the position of at least one lead tip; and

repeating the steps of claim 1 for activating the pacemaker, imaging, compiling, identifying coordinate positions and comparing the paced heart rhythm data against the intrinsic heart rhythm data.

9. The method for determining and optimizing left ventricular synchrony of claim 1 further comprising:

if interpretation of the results shows minimal improvement in contractility and minimal improvement in synchrony, documenting the position of the lead tips in the heart;

changing the pacing configuration; and

repeating the steps of claim 1 for activating the pacemaker, imaging, compiling, identifying coordinate positions and comparing the paced heart rhythm data against the intrinsic heart rhythm data.

10. The method for determining and optimizing left ventricular synchrony of claim 1 further comprising:

if interpretation of the results shows minimal improvement in contractility and minimal improvement in synchrony, documenting the position of the lead tips in the heart;

changing the ventricular pacing offsets; and

repeating the steps of claim 1 for activating the pacemaker, imaging, compiling, identifying coordinate positions and comparing the paced heart rhythm data against the intrinsic heart rhythm data.

11. The method for determining and optimizing left ventricular synchrony of claim 1 further comprising:

if interpretation of the results shows minimal improvement in contractility and minimal improvement in synchrony, documenting the position of the lead tips in the heart;

changing the timing of the electrical impulses; and

repeating the steps of claim 1 for imaging, compiling, identifying coordinate positions and comparing the paced heart rhythm data against the intrinsic heart rhythm data.

12. The method for determining and optimizing left ventricular synchrony of claim 1 further comprising wherein:

using a three dimensional mapping system is used to generate a three dimensional lead tip motion assessment without instead of X-ray to avoid the detrimental effects of X-ray exposure to provide ability to determine electromechanical measurements related to dyssynchrony.

13. The method for determining and optimizing left ventricular synchrony of claim 1 wherein 12 further comprising:

the method is utilized during routine follow-up care of patients having previously undergone cardiac resynchronization therapy; using plural topical heart monitor patches to provide three dimensional analysis and the present method to provide lead tip motion analysis during office reprogramming of the pacemaker to maximize long term benefits of cardiac resynchronization therapy.

14. The method for determining and optimizing left ventricular synchrony of claim 1 12 wherein:

three-dimensional lead tip motion analysis is performed using simultaneous bi-plane imaging in left anterior oblique and right anterior oblique imaging views;

the left anterior oblique view is adjusted to represent short axis of the left ventricle to show radial shortening;

the right anterior oblique view is obtained at a 90° angle;

simultaneous cine is performed in the two views;

the left ventricular lead tip motion data is plotted to determine short axis movement (X and Y axis) and right ventricular lead tip motion data is plotted to obtain longitudinal motion (Z axis);

using the X, Y and Z axis coordinates, three-dimensional left ventricular lead tip motion and three dimensional right ventricular lead tip motion is determined without the detrimental effects of x-ray to determine left ventricular lead tip motion and right ventricular lead tip motion to graph and analyze dyssynchrony and, fractional shortening, and heart wall movement.

15. The method for determining and optimizing left ventricular synchrony of claim 1 12 wherein:

three-dimensional lead tip motion analysis is obtained using plural topical patches applied to the patient's chest using a global positioning approach to document the ventricular lead tip positions by time;

data is collected using the right ventricular one lead tip as a reference and the left ventricular a second lead tip as input during intrinsic ventricular rhythm and various configurations of paced ventricular rhythm;

lead tip motion is documented during intrinsic heart rhythm and during the paced biventricular rhythm including assessing right and left ventricular pacing offsets, paced right ventricular rhythm and paced left ventricular rhythm, at differing right and left ventricular lead locations and differing pacing configurations; and

simultaneous ECG input provides electromechanical measurements of timing from QRS onset to peak mechanical contraction of left and right ventricles during intrinsic and paced rhythms.

16. The method for determining and optimizing left ventricular synchrony of claim 1 wherein:

the patient is identified as a candidate for cardiac resynchronization therapy by diagnostic use of the method using temporary pacing catheters in the right ventricle and coronary sinus to assess for baseline dyssynchrony and to predict potential response to cardiac resynchronization therapy.

17. The method for determining and optimizing left ventricular synchrony of claim 1 wherein:

the cine is not less than 15 frames per second and time stamps are recorded on each cine frame.

18. A method for determining and optimizing ventricular heart wall motion in a patient having ventricular heart wall movement dysfunction comprising in combination:

identifying a patient as having perceived ventricular heart wall movement dysfunction who may benefit from therapy;

placing pacing leads having electrodes at a lead tip end portion in the patient's heart;

positioning each lead initially at a location published studies have shown to generate physiologic benefit from pacing;

using radiographic imaging to make recordings of the heart in multiple views through plural complete cardiac cycles including systole and diastole during intrinsic heart rhythm and assigning a time stamp to ascertain the position of a lead throughout the cardiac cycles including systole and diastole;

determining an X-axis, a Y-axis, and a Z-axis coordinate for the lead position for the time stamp;

compiling the intrinsic heart rhythm data;

analyzing the compiled intrinsic heart rhythm data to determine a baseline measure of dyssynchrony contractility and/or ventricular heart wall motion through the plural complete cardiac cycles including systole and diastole;

applying an electrical signal to the leads to pace the heart;

using radiographic imaging to make recordings of the heart in multiple views through plural complete cardiac cycles including systole and diastole during paced heart rhythm and assigning a time stamp to ascertain the position of each lead throughout the plural complete cardiac cycles including systole and diastole;

determining an X-axis, a Y-axis, and a Z-axis coordinate for each lead position for each time stamp;

compiling the paced heart rhythm data;

analyzing the compiled paced heart rhythm data to determine a measure of dyssynchrony and contractility through plural complete cardiac cycles including systole and diastole;

comparing the intrinsic heart rhythm data and the paced heart rhythm data and generating a visual display showing the motion of the leads throughout the plural complete cardiac cycles by time;

interpreting the intrinsic heart rhythm data and the paced heart rhythm data to determine if there is an improvement in dyssynchrony, contractility or ventricular heart wall movement throughout the plural complete cardiac cycles resulting from pacing;

if interpretation of the paced heart rhythm data shows no improvement or minimal improvement in synchrony, contractility, or or ventricular heart wall movement, documenting the position of the lead tips in the heart;

changing the pacing configurations, and/or changing a lead tip position and repeating the imaging, compiling, identifying coordinate positions, and comparing the paced heart rhythm data and intrinsic heart rhythm data; and

ending the procedure if assessment of the paced heart rhythm data shows improvement in synchrony, contractility, or ventricular heart wall movement.

19. The method for determining and optimizing ventricular heart wall motion of claim 18 further comprising:

simultaneous electrocardiographic (ECG) monitoring to determine electromechanical and mechanical measurements of ventricular heart wall movement, electrical depolarization and re-polarization throughout the plural complete cardiac cycles, rates of systolic and diastolic ventricular wall motion, duration of systole and diastole, during intrinsic and paced rhythm, for diagnostic assessment of systolic and diastolic heart failure, and to guide therapy.

20. A method for determining and optimizing ventricular heart wall motion in a patient having ventricular heart wall movement dysfunction comprising in combination:

identifying a patient as having perceived ventricular heart wall movement dysfunction who may benefit from therapy;

placing pacing leads having electrodes at a lead tip end portion in the patient's heart;

positioning each lead initially at a location published studies have shown to generate physiologic benefit from pacing;

using three dimensional imaging to make recordings of the lead electrodes movement through plural complete cardiac cycles including systole and diastole during intrinsic heart rhythm and assigning a time stamp to ascertain the position of each electrode throughout the cardiac cycles;

determining an X-axis, a Y-axis, and a Z-axis coordinate for each electrode position for the time stamps;

compiling the intrinsic heart rhythm data;

analyzing the compiled intrinsic heart rhythm data to determine a baseline measure of dyssynchrony, contractility and ventricular heart wall motion throughout the plural complete cardiac cycles including systole and diastole;

applying an electrical stimulus to the leads to pace the heart;

using three dimensional imaging to make recordings of the lead electrodes movement through plural complete cardiac cycles including systole and diastole during paced heart rhythm and assigning a time stamp to ascertain the position of each electrode position throughout the plural complete cardiac cycles;

determining an X-axis, a Y-axis, and a Z-axis coordinate for each electrode position for the time stamps;

compiling the paced heart rhythm data;

analyzing the compiled paced heart rhythm data to determine a measure of dyssynchrony, contractility and ventricular heart wall motion throughout the plural complete cardiac cycles including systole and diastole;

comparing the intrinsic heart rhythm data and the paced heart rhythm data and generating a visual display showing the motion of the lead throughout the plural complete cardiac cycles by time;

interpreting the intrinsic heart rhythm data and the paced heart rhythm data to determine if there is improvement in dyssynchrony, contractility and ventricular heart wall motion throughout the plural complete cardiac resulting from the pacing; and

if interpretation of the intrinsic heart rhythm data and the paced heart rhythm data shows no/minimal improvement in synchrony, contractility, or ventricular heart wall movement, documenting the position of the leads in the heart;

changing the lead position and/or changing a pacing configuration and/or changing ventricular pacing offsets; and

repeating the steps of claim 20 for imaging, compiling, identifying coordinate positions, and comparing the intrinsic heart rhythm data and the paced heart rhythm data; and

ending the procedure if assessment of the results shows improvement in synchrony, contractility, or ventricular heart wall movement.

21. The method for determining and optimizing ventricular heart wall motion of claim 20 wherein: one lead is positioned in the patient's right ventricle to optimize ventricular synchrony, ventricular contractility, and/or ventricular heart wall motion.

22. The method for determining and optimizing ventricular heart wall motion of claim 20 wherein: one lead is positioned in the patient's coronary venous system to optimize ventricular synchrony, ventricular contractility, and/or ventricular heart wall motion.

23. The method for determining and optimizing ventricular heart wall motion of claim 20 wherein: one lead is positioned on the patient's left ventricular epicardium to optimize ventricular synchrony, ventricular contractility, and/or ventricular heart wall motion.

24. The method for determining and optimizing ventricular heart wall motion of claim 20 further comprising:

simultaneous ECG to determine electromechanical and mechanical measurements of ventricular heart wall movement related to dyssynchrony, contractility, and electrical depolarization and repolarization ventricular heart wall motion throughout the plural complete cardiac cycles, as a diagnostic tool during lead implant and during cardiac resynchronization therapy follow up.

25. The method for determining and optimizing ventricular heart wall motion of claim 20 further comprising:

simultaneous electrocardiographic (ECG) monitoring to determine electromechanical and mechanical measurements of contraction and ventricular heart wall motion including electrical depolarization and re-polarization throughout the plural complete cardiac cycles, rates of systolic and diastolic ventricular heart wall motion and relative duration of systole and diastole during intrinsic and paced rhythm for diagnostic assessment of systolic and diastolic heart failure to guide therapy.