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.

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 (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.

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.

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.

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.

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.

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.

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

Stay updated, free articles. Join our Telegram channel

Join