Cardiac electromechanics

Details Cardiac electromechanics Cardiac electromechanics

1998-07-07

2001-09-04

Dvorak, Linda C. M. (Department: 3739)

Surgery

Diagnostic testing

Structure of body-contacting electrode or electrode inserted...

C600S407000, C600S424000, C600S508000, C128S899000, C128S922000

Reexamination Certificate

active

06285898

ABSTRACT:

FIELD OF THE INVENTION
The present invention relates to the field of cardiac medicine and more particularly to diagnosing and treating diseased hearts based on the interaction between cardiac electro-physiological and cardiac bio-mechanical activity.
BACKGROUND OF THE INVENTION
Cardiovascular diseases accounted for approximately 43 percent of the mortality in the United States of America in 1991 (923,000 persons). However, many of these deaths are not directly caused by an acute myocardial infraction (AMI). Rather, many patients suffer a general decline in their cardiac output known as heart failure. Once the overt signs of heart failure appear, half the patients die within five years. It is estimated that between two and three million Americans suffer from heart failure and an estimated 200,000 new cases appear every year. In many cases heart failure is caused by damage accumulated in the patient's heart, such as damage caused by disease, chronic and acute ischemia and especially (~75%) as a result of hypertension.
A short discussion of the operation of a healthy heart is useful in order to appreciate the complexity of the functioning of the heart and the multitude of pathologies which can cause heart failure.
FIG. 1A
is a schematic drawing of a cross-section of a healthy heart
20
. In general heart
20
comprises two independent pumps. One pump comprises a right atrium
22
and a right ventricle
24
which pump venous blood from an inferior and a superior vena cava to a pair of lungs (not shown) to be oxygenated. Another pump comprises a left atrium
26
and a left ventricle
28
, which pump blood from pulmonary veins (not shown) to a plurality of body systems, including heart
20
itself. The two ventricles are separated by a ventricular septum
30
and the two atria are separated by an atrial septum
32
.
Heart
20
has a four phase operational cycle in which the two pumps are activated synchronously.
FIG. 1B
shows a first phase, called systole. During this phase, right ventricle
24
contracts and ejects blood through a pulmonic valve
34
to the lungs. At the same time, left ventricle
28
contracts and ejects blood through an aortic valve
36
and into an aorta
38
. Right atrium
22
and left atrium
26
are relaxed at this point and they begin filling with blood, however, this preliminary filling is limited by distortion of the atria which is caused by the contraction of the ventricles.
FIG. 1C
shows a second phase, called rapid filling phase and indicates the start of a diastole. During this phase, right ventricle
24
relaxes and fills with blood flowing from right atrium
22
through a tricuspid valve
40
, which is open during this phase. Pulmonic valve
34
is closed, so that no blood leaves right ventricle
24
during this phase. Left ventricle
28
also relaxes and is filled with blood flowing from left atrium
26
through a mitral valve
42
, which is open. Aortic valve
36
is also closed to prevent blood from leaving left ventricle
26
during this phase. The filling of the two ventricles during this phase is affected by an existing venous pressure. Right atrium
22
and left atrium
26
also begin filling during this phase. However, due to relaxation of the ventricles, their pressure is lower than the pressure in the atria, so tricuspid valve
40
and mitral valve
42
stay open and blood flows from the atria into the ventricles.
FIG. 1D
shows a third phase called diastatis, which indicates the middle of the diastole. During this phase, the ventricles fill very slowly. The slowdown in filling rate is due to the equalization of pressure between the venous pressure and the intra-cardiac pressure. In addition, the pressure gradient between the atria and the ventricles is also reduced.
FIG. 1E
shows a fourth phase called atrial systole which indicates the end of the diastole and the start of the systole of the atria. During this phase, the atria contract and inject blood into the ventricles. Although there are no valves guarding the veins entering the atria, there are some mechanisms to prevent backflow during atrial systole. In left atrium
26
, sleeves of atrial muscle extend for one or two centimeters along the pulmonary veins and tend to exert a sphincter-like effect on the veins. In right atrium
22
, a crescentic valve forms a rudimentary valve called the eustachian valve which covers the inferior vena cave In addition, there may be muscular bands which surround the vena cava veins at their entrance to right atria
22
.
FIG. 1F
is a graph showing the volume of left ventricle
24
as a function of the cardiac cycle.
FIG. 1F
clearly shows the additional volume of blood injected into the ventricles by the atria during atrial systole as well as the variance of the heart volume during a normal cardiac cycle.
FIG. 1G
is a graph which shows the time derivative of
FIG. 1F
, i.e., the left ventricle fill rate as a function of cardiac cycle. In
FIG. 1G
two peak fill rates are shown, one in the beginning of diastole and the other during atrial systole.
An important timing consideration in the cardiac cycle is that the atrial systole must complete before the ventricular systole begins. If there is an overlap between the atrial and ventricular systoles, the atria will have to force blood into the ventricle against a raising pressure, which reduces the volume of injected blood. In some pathological and induced cases, described below, the atrial systole is not synchronized to the ventricular systole, with the effect of a lower than optimal cardiac output.
It should be noted that even though the left and the right sides of heart
20
operate in synchronization with each other, their phases do not exactly overlap. In general, right atrial systole starts slightly before left atrial systole and left ventricular systole starts slightly before right ventricular systole. Moreover, the injection of blood from left ventricle
26
into aorta
38
usually begins slightly after the start of injection of blood from right ventricle
24
towards the lungs and ends slightly before end of injection of blood from right ventricle
24
. This is caused by pressures differences between the pulmonary and body circulatory systems.
When heart
20
contracts (during systole), the ventricle does not contract in a linear fashion, such as shortening of one dimension or in a radial fashion. Rather, the change in the shape of the ventricle is progressive along its length and involves a twisting effect which tends to squeeze out more blood.
FIG. 2
shows an arrangement of a plurality of muscle fibers
44
around left ventricle
28
which enables this type of contraction. When muscle fibers
44
are arranged in a spiral manner as shown in FIG.
2
and the activation of muscle fibers
44
is started from an apex
46
of left ventricle
28
, left ventricle
28
is progressively reduced in volume from the bottom up. The spiral arrangement of muscle fibers
44
is important because muscle fibers typically contract no more than 50% in length. A spiral arrangement results in a greater change of left ventricular volume than is possible with, for example, a flat arrangement in which the fibers are arranged in bands around the heart. An additional benefit of the spiral arrangement is a leverage effect. In a flat arrangement, a contraction of 10% of a muscle fiber translates into a reduction of 10% of the ventricular radius. In a spiral arrangement with, for example, a spiral angle
48
of 45°, a 10% contraction translates into a 7.07% contraction in ventricular radius and a 7.07% reduction in ventricular length. Since the ventricular radius is typically smaller than the ventricular length the net result is that, depending on spiral angle
48
, a tradeoff is effected between a given amount of contraction and the amount of force exerted by that contraction.
Spiral angle
48
is not constant, rather, spiral angle
48
changes with the distance of a muscle fiber from the outer wall of the ventricle. The amount of force produced by a muscle fiber is a function of its contraction, thus, each la

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