Ischemic Cardiac Disease



Ischemic Cardiac Disease





Cardiac MRI for the evaluation of ischemic heart disease has tremendous potential because of its high spatial resolution and image contrast. In considering the different diagnostic strategies that can be used, it is helpful to review the progression of detectable abnormalities in ischemic heart disease, shown in Figure III7-1. The two main diagnostic strategies measure changes in either perfusion or ventricular wall motion under pharmacologic stress compared with rest. Although qualitative perfusion imaging is more sensitive for early ischemic change, it is also less specific than wall motion studies and may be less accurate in patients with global ischemia.

The MR imaging techniques and methods for pharmacologic stress vary considerably across various laboratories. Validation studies of both MR approaches are still being performed, and, in the context of alternative techniques such as stress ECG, SPECT, echocardiography, and PET, the role of MR in the evaluation of patients with ischemic heart disease remains to be defined fully. Some basic principles of stress perfusion and wall motion studies are outlined in this chapter, with the caveat that these methods are continuing to be refined.






FIGURE III7-1. Diagnostic studies for ischemic heart disease.



PHARMACOLOGIC STRESS IN THE MRI SETTING

For the evaluation of ischemic heart disease, all diagnostic techniques are performed with cardiac stress. Stress can be achieved with exercise or with pharmacologic agents. In general, for exercise and sympathomimetic
stress, the goal is to achieve a submaximal target heart rate that depends on age:

Target heart rate = 0.85 × (220 − Age (yrs))

While ergonomic stress is the most physiologic, exercising in the magnet bore is not generally practical. Therefore, cardiac MR studies typically are performed with pharmacologic agents using one of two approaches: (a) dobutamine, a catecholamine that causes increased contractility and oxygen consumption, or (b) either adenosine or dipyridamole, both vasodilators that cause hyperemia. In both cases, changes that are observed are different for regions of myocardium that are supplied by diseased coronary arteries compared with those supplied by normal coronary arteries.

For all stress testing, careful monitoring of patients in the MR setting is vital. A physician experienced in cardiac resuscitation should be present for all examinations. There must be a continuous communication between the subject and operators to ensure prompt attention to symptoms. Monitoring should include frequent blood pressure measurements, continuous pulse oximetry, and continous single-lead ECG tracings for heart rate and rhythm. Although the detection of ST segment changes is problematic in the MR scanner because of the magnetohydrodynamic effect (see Chapter III-1), wall motion abnormalities generally precede ECG changes. With real-time cine MRI early detection of ischemia is possible.


Dobutamine

Dobutamine is a synthetic catecholamine with potent β1-receptor and mild α1– and β2-receptor agonist activity. The effect of dobutamine depends on the dose administered. At low doses (≤ 10 μg/kg body weight/min), dobutamine causes increased contractility. The recovery of wall motion with low-dose dobutamine is one technique for assessing cardiac viability in the setting of resting hypokinesis or akinesis. At high doses of dobutamine, increased heart rate and contractility cause an increase in oxygen consumption. Areas supplied by significantly diseased coronaries develop wall motion abnormalities under these conditions. The stress protocol is based on that used for dobutamine echocardiography (Table III7-1).

Beta-blockers reduce the effects of dobutamine and generally are withheld for 24-48 hours prior to the examination. Similarly, calcium antagonists and nitrates are discontinued for 24 hours prior to the study.

Contraindications for the administration of dobutamine include acute coronary syndrome, severe aortic stenosis, hypertrophic obstructive cardiomyopathy, uncontrolled hypertension, uncontrolled atrial fibrillation, uncontrolled heart failure, and known severe ventricular arrhythmias.








[right half black circle] TABLE III7-1




















Dobutamine Dose


Duration Until Target Heart Rate Is Reached (or Other Criteria, Table III7-2)


10 μg/min/kg body weight


3 min


20 μg/min/kg body weight


3 min


30 μg/min/kg body weight


3 min


40 μg/min/kg body weight


3 min


Optional atropine 0.25 mg × 4 (1-2 mg total)









[right half black circle] TABLE III7-2

















Criteria for Stopping Dobutamine Infusion


Target heart rate achieved


Systolic blood pressure decrease more than 40 mm Hg


Blood pressure increase greater than 240/120 mm Hg


Intractable symptoms


New or worsening wall motion abnormalities in at least two adjacent left ventricular segments


Complex cardiac arrhythmias


As shown in Table III7-1, the conventional protocol involves incremental increases in dobutamine doses in steps of 10 μg/min/kg body weight, up to a maximum dose of 40 (or even 50) μg/min/kg. If target heart rate is not reached, additional atropine can be administered at doses of 0.25 mg, up to 1-2 mg total, during the ongoing infusion of dobutamine. Criteria for termination of the study are shown in Table III7-2 and include the development of signs and symptoms of ischemia—including wall motion abnormalities in at least two adjacent ventricular segments or anginal symptoms.

Side effects of the dobutamine can be reversed with a β-blocker such as intravenous esmolol or metoprolol if signs and symptoms do not resolve after infusion is stopped. The half-life of dobutamine is short—approximately 2 min. In patients who develop angina, sublingual nitroglycerin can also be used.


Dipyridamole and Adenosine

Dipyridamole (Persantine) and adenosine have almost identical vasodilatory effects. Adenosine is a naturally occuring vasodilator. Dipyridamole blocks the cellular uptake and metabolism of adenosine and consequently also causes vasodilation. With both agents, a four- to five-fold hyperemia is seen in normal myocardial territories but not in regions subtended by stenotic coronary arteries. With significant coronary artery disease, dipyridamole
and adenosine cause a steal phenomenon, and the differential perfusion changes with vasodilation are used to diagnose ischemic heart disease.








[right half black circle] TABLE III7-3 Doses of Adenosine and Dipyridamole















Pharmacologic Agent


Dose


Duration


Adenosine


140 μg/kg body weight/min


6 min (start imaging after 3 min)


Dipyridamole


0.56 mg/kg body weight total


4 min (start imaging after 2 min)


Contraindications include asthma, high-grade atrioventricular block, sinus arrhythmia, aortic or mitral valvular stenosis, and carotid artery stenosis. Medications that contain aminophylline, theophylline, and other xanthines (such as caffeinated products) are withheld for 12-24 hours before the study.

Assessment of perfusion is performed using first-pass gadolinium-enhanced perfusion. The standard dosing regimens for the two vasodilatory agents are shown in Table III7-3.

Reasons for stopping the infusion of these agents include bronchospasm, ventricular arrhythmias, and the onset of second- or third-degree atrioventricular block and bradycardia. Low-workload exercise (such as handgripping exercises) have been shown to reduce the side effects associated with the vasodilators. Intravenous aminophylline is an antidote to both adenosine and dipyridamole and should be available for immediate administration. The plasma half-life of adenosine is less than 10 sec. For intravenous dipyridamole, it is 5 min.


Pharmacologic Stress in the Diagnosis of Ischemic Heart Disease

Both categories of pharmacologic agents—sympathomimetics such as dobutamine or vasodilators such as adenosine or dipyridamole—improve the diagnosis of ischemic heart disease by accentuating differences between territories supplied by normal coronary arteries and those that receive inadequate blood supply. In the clinical setting, the most common imaging strategies for detecting these differences are stress radionuclide perfusion examination and stress echocardiography. The MR tools recapitulate these approaches. MRI can be used either to measure perfusion, typically with first-pass gadolinium-enhanced Tl-weighted imaging, or to detect changes in wall motion with fast cine gradient echo imaging. Each class of stressor agent can be used with either MRI approach. However, most commonly, perfusion imaging is performed with vasodilators and contractility studies are performed with dobutamine. Whether to use perfusion or contractility methods remains the subject of active research. Some considerations include the extent of coronary disease, tradeoffs between sensitivity and specificity, tolerance by patients, cost, and ease of administration.


PERFUSION IMAGING

The controversies in cardiac perfusion imaging span virtually the entire range of protocol options: from the imaging sequence to the rate and amount of contrast injection to the post-processing analysis of the images. This section begins with a brief discussion of the desired features of perfusion imaging sequences. Characteristics of different commonly used imaging methods are described in the remainder of this section.


Desired Features of MR Perfusion Imaging

The underlying principle of first-pass myocardial perfusion MR imaging is that differences in blood flow to the myocardium can be tracked by the direct visualization of enhancement with gadolinium contrast agents. The diagnosis of myocardial ischemia or infarction is based on its lower blood flow, recognized by slower rates of both uptake and washout of contrast material during the first pass through the myocardial circulation (Figure III7-2). To maximize detection of ischemia, particularly subendocardial ischemia, several features of the imaging technique are necessary (Table III7-4).

Most cardiac perfusion sequences are T1-weighted fast gradient echo sequences or echo planar sequences performed with magnetization preparation to improve image contrast. Considerations in optimizing MR perfusion sequences include the design of the magnetization preparation prepulse (Chapter I-9), selection of a fast gradient echo readout, gadolinium contrast material injection protocol, and image analysis, each of which is discussed next.


Magnetization Preparation Prepulses

The goal is to differentiate areas of normal perfusion and hypoperfusion during first-pass contrast-enhanced MR imaging using gadolinium contrast agents. Magnetization preparation prepulses are used to accentuate T1 differences. Typically either a 90° saturation prepulse, referred to as saturation recovery, or a 180° inversion recovery prepulse is used (Figure III7-3). The prepulse is nonsliceselective to minimize in-flow effects and is typically applied at a fixed time after the R wave. After a selected inversion time, data acquisition is performed with either a gradient echo or an echo planar readout.

The higher the flip angle of the prepulse, the greater the T1 contrast. However, high flip angles require a longer time for recovery between the prepulse and data acquisition,
called the inversion time. Ideally, the inversion time is selected so that the unenhanced myocardium is relatively low in signal, or nearly nulled, compared to the enhancing myocardium. The time required for recovery of longitudinal magnetization restricts the number of slices that can be imaged. Additionally, because this sequence is an ECG-gated sequence, recovery of longitudinal magnetization depends on the heart rate, and therefore arrhythmias are detrimental to good image contrast.






FIGURE III7-2. Schematic of first-pass tracer kinetics in coronary artery disease. Ischemic myocardium demonstrates a lower rate of enhancement and a lower peak compared with nonischemic myocardium. Enhancement of infarcted myocardium is significantly slower than that of ischemic tissue.








[right half black circle] TABLE III7-4 Desired Features of First-Pass MR Perfusion



























Features


Desired Attributes


Spatial coverage


Entire left ventricular myocardium


Temporal resolution


High resolution to detect differences during first-pass (<1-2 sec)


Spatial resolution


High resolution to detect subendocardial ischemia (<2 mm)


Signal-to-noise ratios


High SNR to differentiate normal and ischemic myocardium


Image contrast


High contrast to differentiate normal and ischemic myocardium


Motion artifact


Minimum


Gadolinium contrast concentration vs. SI


A known and quantifiable relationship between gadolinium contrast concentration and signal intensity


An interleaved notched saturation perfusion method builds in a longer inversion time between the prepulse and the readout without lengthening the acquisition time. The magnetization prepulse is designed to have a notched slice profile so that all but a central notch is saturated (Figure III7-4). As shown in Figure III7-4, rather than performing the readout shortly after the saturation pulse, the readout is delayed until the subsequent slice, which allows for a longer inversion time and consequently better image contrast.


Readout Sequences

Following the prepulse, data are acquired. For sufficient spatial coverage and temporal resolution, three slices are acquired per heartbeat, or 6-7 slices every two heartbeats. The readout for each image is therefore constrained to less than 200 msec

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Jun 7, 2016 | Posted by in VASCULAR SURGERY | Comments Off on Ischemic Cardiac Disease
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