Method and apparatus to improve myocardial infarction...

Surgery – Diagnostic testing – Detecting nuclear – electromagnetic – or ultrasonic radiation

Reexamination Certificate

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C600S420000

Reexamination Certificate

active

06526307

ABSTRACT:

BACKGROUND OF INVENTION
The present invention relates generally magnetic resonance imaging (MRI), and more particularly, to a method and apparatus, including a new pulse sequence, to achieve greater sensitivity in detecting infarcted myocardial tissue.
MRI utilizes radio frequency pulses and magnetic field gradients applied to a subject in a strong magnetic field to produce viewable images. When a substance containing nuclei with net nuclear magnetic moment, such as the protons in human tissue, is subjected to a uniform magnetic field (polarizing field B
0
), the individual magnetic moments of the spins in the tissue attempt to align with this polarizing field (assumed to be in the z-direction), but precess about the direction of this magnetic field at a characteristic frequency known as the Larmor frequency. If the substance, or tissue, is subjected to a time-varying magnetic field (excitation field B
1
) applied at a frequency equal to the Larmor frequency, the net aligned moment, or “longitudinal magnetization”, M
Z
, may be nutated, or “tipped”, into the x-y plane to produce a net transverse magnetic moment M
t
. A signal is emitted by the excited spins after the excitation signal B
1
is terminated (as the excited spins decays to the ground state) and this signal may be received and processed to form an image.
When utilizing these signals to produce images, magnetic field gradients (G
x
G
y
and G
z
) are employed. Typically, the region to be imaged is scanned by a sequence of measurement cycles in which these gradients vary according to the particular localization method being used. The resulting MR signals are digitized and processed to reconstruct the image using one of many well-known reconstruction techniques.
Myocardial infarction is a type of cardiac syndrome in which oxygen is deprived from a portion of the heart. The size of the myocardial infarct has been demonstrated to have a strong correlation with patient outcome/recovery. Myocardial perfusion imaging is a technique in which regions of abnormal or impaired blood flow to the heart are detected by tracking the passage of a tracer or contrast agent through myocardial tissue. Regions of impaired blood flow or poor perfusion would not exhibit the presence of the contrast material or tracer whereas in tissues with normal perfusion, the presence of the contrast material or tracer would be indicated.
The imaging of tissue (blood) perfusion is closely related to the imaging of blood flow in vascular structures, such as in MR angiography (MRA). As with MRA, MR perfusion imaging is performed by injecting a volume a contrast agent, such as gadolinium chelate, into the blood stream, conventionally via an intravenous injection. The volume or mass of contrast agent administered is typically referred to as a bolus as it is delivered in a tight volume at a relatively high volume delivery rate (usually 1-5 ml/sec). Differing agents can either decrease the T
1
of blood to enhance the detected MR signal, or decrease the T
2
of blood to attenuate the detected MR signal. As the bolus passes through the body, the enhanced or attenuated signal increases or decreases the signal intensity observed in perfused tissue, but not in the non-perfused tissue. The degree of signal change in the observed tissue as compared with baseline images acquired prior to the arrival of the contrast material can be used to determine the degree of tissue perfusion. Since perfusion measurements are based on the change in tissue signal intensity between the baseline and during the first pass passage of the contrast material, it is important that the MR signal strength be made insensitive to variations from other factors unrelated to the primary mechanism for signal intensity changes due to perfusion. One such variable is the magnitude of the longitudinal magnetization M
z
, which is tipped into the transverse plane by the RF excitation pulse in the MR pulse sequence. After each excitation, the longitudinal magnetization is reduced and recovers magnitude at a rate determined by the T
1
constant of the particular spins being imaged. If another pulse sequence is played out before the longitudinal magnetization has fully recovered, the magnitude of the acquired MR signal will be less than the signal produced by a pulse sequence which is delayed long enough to allow full recovery of the longitudinal magnetization. Moreover, if the delay time varies as a result of variations in the patient's cardiac heart rate, the amount of longitudinal magnetization available will vary between heartbeat to beat heartbeat. This will cause fluctuations or variations in the signal intensity in the myocardial tissue independent of perfusion. It is known that the use of a saturation rf pulse with a flip angle of 90° will set the longitudinal magnetization to zero. Thus by waiting a pre-determined and fixed time after the saturation rf pulse before imaging, the re-growth the longitudinal magnetization is dependent on the tissue spin-lattice relaxation time, T
1
. Since the contrast agent effects T
1
, the use of a saturation rf pulse will yield a signal intensity that is dependent on the concentration of the contrast material present in a region of myocardial tissue and not variations in the patient's heart rate. The same technique is also applicable to T
2
or T
2
* shortening agents.
Typically, perfusion imaging is a technique used to rapidly acquire images during the first pass of the contrast agent/bolus through the blood stream by using carefully optimized pulse sequence parameters. The goal of myocardial perfusion imaging is to detect and characterize any abnormal distribution of myocardial blood flow. Perfusion deficits are indicative of areas of compromised blood flow. These perfusion deficits may be transient, whereby the region of myocardial tissue is still viable and continues to receive some supply of blood, or acute where the blood flow to that region has been compromised sufficiently to render cellular damage to the myocardial tissue (i.e., myocardial infarction). Non-viable infarcted tissue undergoes cellular changes that damage the ability of the myocardial tissue or muscle to contract. Hence, regions of myocardial infarction are often characterized by having abnormal cardiac wall motion at rest. Under certain conditions where the tissue is still viable, with increased blood flow to that region, the myocardial tissue begins normal contractile motion. This type of characteristic is attributed to stunned or hibernating myocardium where the tissue is still viable but severely under perfused.
The area of cellular damage or myocardial infarction is often assessed to better determine the course of patient management. In some cases, in the periphery of the infarcted tissue, some recovery of function may be possible. However, in regions where the damage leads to micro-vascular obstruction, no recovery is possible. The use of imaging of myocardial infarcted regions allows the assessment of the extent of the cardiac injury and permits the monitoring of the patient's response to a specific treatment regimen.
In order to assess for the presence of myocardial infarction, an inversion recovery pulse sequence is routinely employed to suppress normal myocardial tissue subsequent to the administration of the contrast bolus, which is typically between 0.1 and 0.2 mmol/kg of gadolinium contrast material. In this application, the bolus has the effect of shortening the T
1
time of the blood.
During the first pass of the contrast material, under resting conditions, the infarcted region may be identified by regions of abnormal perfusion. That is to say, the infarcted zones, having very low blood perfusion would be hypo-intense relative to normal, healthy myocardium. With recirculation of the contrast material, transport of the contrast material to the site of the myocardial infarct is by the limited blood flow to the affected region or by diffusion into the extra-cellular space. Consequently, the uptake of contrast material by infarcted tissue occurs at a much slower ra

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