Cardiac drugs used in cross-sectional cardiac imaging: what the radiologist needs to know

Article Outline

• Abstract
• Introduction
• Drugs used primarily in CCT
  • β-blockers
  • Patient selection and preparation
  • Protocols for oral and IV β-blockers
  • Oral β-blockers
  • IV β-blockers
  • Side effects and adverse reactions
  • Esmolol
• Verapamil and diltiazem
• Ivabradine
• Glyceryl trinitrate (GTN)
  • Side effects and adverse reactions
• Drugs used primarily in cardiac stress MRI
  • Adenosine
  • Patient selection and preparation
  • Adenosine infusion protocol
  • Side effects and adverse reactions
• Dobutamine
  • Patient selection and preparation
  • Dobutamine infusion protocol
  • Side effects and adverse reactions
• Dipyridamole
  • Patient selection and preparation
  • Dipyridamole infusion protocol, side effects and adverse reactions
• Atropine
  • Patient selection and preparation
  • Atropine administration protocol
• Conclusion
• References
• Copyright

The demand for cross-sectional imaging of the heart is increasing dramatically and in many centres these imaging techniques are being performed by radiologists. Although radiologists are familiar with the computed tomography (CT) and magnetic resonance imaging (MRI) techniques to generate high-quality images and with using contrast agents, many are less familiar with administering the drugs necessary to perform CT coronary angiography and cardiac MR reliably. The aim of this article is to give an overview of the indications for and the contraindications to administering cardiac drugs in cross-sectional imaging departments. We also outline the complications that may be encountered and provide advice on how to treat these complications when they occur.

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Introduction 

The availability and provision of non-invasive cardiac imaging has expanded considerably in the last decade and a greater number of radiology departments are now providing or looking to establish both cardiac CT (CCT) and cardiac MR (CMR) services. In order to provide the best quality images, cardiac drugs, such as β-blockers, may be needed for CCT and dobutamine or adenosine are required to adequately stress the heart when CMR is used in the assessment of myocardial ischaemia. Radiologists may be reticent about administering cardiac drugs to patients undergoing cardiac imaging and in some centres cardiologists are asked to oversee the administration of cardiac medications. However, with appropriate training, these drugs can be given safely in the majority of patients.

The aim of this review is to demystify the drugs used in cardiac imaging and to provide guidelines to encourage the radiologist to administer these drugs with more confidence. We present a comprehensive guide to the most commonly used cardiac imaging drugs, explain their indications, contraindications, doses and side effects and, where indicated, suggest the appropriate monitoring required when prescribing these drugs. This does not replace the need for cardiological advice, particularly where there is doubt or concern, and a good working relationship with the local cardiologists is important in establishing and running an effective cardiac imaging service. It must also be emphasised that the drugs for these examinations should be administered in a unit with full resuscitation facilities, including oxygen and suction apparatus, and with prompt access to cardiology support.

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Drugs used primarily in CCT 

β-blockers 

β-blockers act on the β-adrenergic receptors, of which there are two main types, β1 and β2. Where possible, agents that are predominantly β1 antagonists are used in cardiac imaging as they are more cardio-selective and have fewer systemic β2 antagonist effects, which can include bronchospasm. β-blockers have a negative inotropic and chronotropic effect and so they reduce myocardial contractility and heart rate respectively. In cardiac radiology, β-blockers are used to slow the heart rate to below 65beats per minute (bpm) for CT coronary angiography. This lower heart rate reduces coronary artery movement artefacts by increasing the length of the diastolic phase and effectively increasing the time that the coronary arteries are motion-free.¹ With higher heart rates, the diastolic phase shortens and the temporal resolution of most current scanners is insufficient to capture the coronary arteries without blurring artefact. With newer CT systems, such as dual-source scanners, the temporal resolution is as low as 83ms and motion-free images may be obtained at higher heart rates.² This is because, with a shorter temporal resolution, the diastolic phase needed to obtain good-quality images of the coronary arteries is shorter and so imaging can be performed with higher heart rates.

Patient selection and preparation 

The initial assessment of the patient prior to coronary CT includes assessing or palpating the pulse and ensuring the patient has no history of asthma, chronic obstructive pulmonary disease (COPD), severe aortic stenosis or any cardiac rhythm disturbance. The blood pressure should be recorded prior to the administration of β-blockers. Contraindications to β-blockers are listed in Table 1. If β-blockers are given to patients with untreated heart failure, the negative inotropic effect can precipitate pulmonary oedema, so β-blockers should not be administered to patients known to have moderate or severe left ventricular (LV) dysfunction or significant heart failure symptoms without seeking cardiological advice. β-blockers may cause bronchospasm in patients with bronchial hyper-reactivity. Second and third-degree heart block are contraindications to β-blockers and these electrocardiogram (ECG) traces are illustrated in Fig. 1. β-blockers are also contraindicated in patients on verapamil because this drug combination is associated with a risk of asystole or ventricular standstill.

Table 1. β-blockers: contraindications and cautions

Contraindications to β-blockers Hypotension (BP<90/60mmHg) Severe aortic stenosis Asthma, severe chronic obstructive pulmonary disease (COPD) with significant bronchospasm Severe peripheral vascular disease (with claudication) Overt heart failure Sick sinus syndrome Second/third-degree heart block Treatment with verapamil (combination can cause ventricular standstill) Caution to be taken when giving β-blockers Breast feeding and pregnancy First-degree heart block (PR interval >0.2s) Chronic obstructive pulmonary disease (COPD) Severe renal impairment Raynaud’s phenomenon Other rate-slowing agents (e.g., digoxin, diltiazem); use maximum total dose 15mg metoprolol IV and titrate slowly

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• Figure 1 

  (a) First-degree heart block. The PR interval is longer than 0.2s. A QRS complex follows every P wave. (b) Second-degree heart block, Mobitz type 1. There is progressive lengthening of the PR interval until eventually a QRS is dropped. (c) Second-degree heart block, Mobitz type 2. The PR interval is uniform, but the QRS is intermittently dropped. (d) Third-degree heart block. The P waves are completely disassociated from the QRS complexes. All these ECG traces reprinted with permission by Remedica from Arrhythmia (Chapter 8) in E.A. Ashley and J. Niebauer, Editors, Cardiology Explained, © 2004.

Caution should be taken in patients that have COPD, renal impairment, Raynaud’s phenomenon, and first-degree heart block (Table 1). Typically if a patient has first-degree heart block, β-blockers should be given with care as there is a potential risk of the patient developing complete heart block (Fig. 1). Caution should also be taken in patients who are already on heart rate lowering drugs, such as digoxin, calcium channel blockers (e.g. diltiazem) and oral β-blockers as these patients are more susceptible to bradycardia and complete heart block. If patients are on these drugs, intravenous (IV) metoprolol should be given at a slower rate and in lower doses (up to a maximum of 15mg). β-blockers can be given to patients who have a cardiac pacemaker and if the patient’s heart rate slows to the threshold at which the pacemaker is set the patient will become paced. However, it should be noted that the patient with a pacemaker may still become hypotensive and β-blocker administration will reduce the patient’s ability to generate a reflex tachycardia response. It is advisable to seek cardiological advice in patients with pacemakers and, in some situations when the patient is pacemaker-dependent, the threshold may be lowered to produce a bradycardia and hence the required heart rate without the need for β-blockers.

Some of these contraindications are difficult to determine in a cross-sectional imaging department. The likely use of β-blockers in coronary CT needs to be communicated to all referrers, and it is very helpful if the referrer can routinely confirm that there are no known contraindications to β-blockade in each patient.

Protocols for oral and IV β-blockers 

The most commonly used β-blocker in cardiac imaging is metoprolol as it is a cardioselective β1 antagonist which has a rapid onset, can be given either orally or intravenously and has the shortest half-life (T_1/2) of any oral β-blocker (3–4h).³ Other β-blockers are less suitable for use in cardiac CT because of less selective β1 blockade or a longer time to peak absorption for oral preparations.

Oral β-blockers 

Two potential protocols for oral metoprolol include: (a) 50–100mg to be taken the evening before and the morning of the scan,⁴ or (b) the patient attends the radiology department an hour before their scan and takes 50–100mg metoprolol orally.⁵, ⁶ Some centres suggest 100mg if the heart rate when the patient attends for the scan is >80bpm and 50mg for heart rates <80bpm.

The first oral protocol relies on the patient receiving the drugs prior to the scan appointment, taking them appropriately and not having any untoward side effects. Additionally, the radiologist is reliant on the referring clinician appropriately assessing the patient’s suitability for β-blockers. The second oral protocol relies on all patients having a normal absorption rate for β-blockers and that the cardiac CT list has the flexibility to allow for the effects on patient flow. An appropriate seating area is required for the patient to wait in until the drugs have taken effect. If β-blockade is inadequate with oral preparations, the patient may require an IV β-blocker. Potentially, with an oral protocol, the radiologist may not need to directly supervise the CT list, given the increasing numbers of nurse practitioners and radiographers with extended roles using patient group directives and departmental protocols.

IV β-blockers 

The IV protocol for metoprolol is commonly 2.5 or 5mg aliquots of metoprolol followed by a saline flush given to the patient while they are on the scanner. Further 2.5–5mg doses are given if no response has occurred after 5min up to a total administered dose of 15mg (although most centres proceed up to a maximum of 30mg) or until the target heart rate has been obtained (Table 2). Blood pressure and continuous ECG monitoring should always be used when giving IV metoprolol.

Table 2. Intravenous metoprolol

IV dose	2.5–5mg aliquots given over 1min at 5min intervals up to a total administered dose of 15mg (although most centres proceed up to a maximum of 30mg)
Patient preparation	Ensure no hypotension or other contraindications (see Table 1)
Side effects	Bradycardia, bronchospasm, heart failure, hypotension
Treating side effects	Bradycardia—atropine or glucagon Bronchospasm—salbutamol

There may be advantages to using the IV method in that it requires less patient co-operation and produces quicker heart rate reduction. However, patient anxiety may increase using an IV drug, which may reduce the drug effect to some degree. The IV protocol will likely prolong the time the patient spends on the scanner and so may reduce the throughput of the department. It is standard practice for a medical practitioner to administer these IV drugs. Patients receiving IV therapy should remain in the department for half an hour after the drug has been administered. It should be noted that the IV preparation is also more expensive, with 5mg metoprolol IV (Betolac) costing 42 pence, while a 100mg tablet (non-proprietary) costs 7 pence.⁷

Side effects and adverse reactions 

At higher doses, there is a potential increased risk of complete heart block, bradycardia and hypotension due to complete blockade of the β-receptors. In some patients where there has been little reduction in heart rate with 15mg of IV metoprolol or who are on long-standing oral β-blockers, increasing the dose further may not yield a significant response. The exact mechanism of this apparent intolerance is not fully understood, but excessive adrenergic stimulation due to anxiety (particularly when administering IV drugs on the scanner) or the presence of β1 receptor polymorphisms are potential reasons.⁸ Patients who are on heart rate lowering drugs should not receive more than 15mg metoprolol IV.

Patients should be warned that they may have symptoms of postural hypotension, which should wear off within a few hours. If a patient develops bronchospasm, oxygen should be given with salbutamol (β2 agonist) either via inhaler or nebuliser (2.5–5mg salbutamol). If a patient’s heart rate becomes excessively low (<40) or the patient is symptomatically bradycardic, IV atropine should be considered at 300–600μg doses up to a maximum dose of 3mg. Patients who have received atropine should be warned that they may experience visual blurring and should not drive for at least 2h. An alternative treatment for severe bradycardia due to β-blocker overdose is glucagon (2–10mg IV). In extreme cases of bradycardia, the patient may require temporary pacing (usually via external pacing) so further assessment by a cardiologist would be required urgently. This emphasises the need for radiologists and radiographers involved in cardiac CT to be trained in immediate life-support (ILS) techniques.

Esmolol 

For cardiac imaging, an alternative IV agent to metoprolol is the ultra-short acting β1-selective β-blocker esmolol.⁵, ⁹ Esmolol is quick acting with an extremely short half-life of 9min. It is expensive compared with metoprolol and rather cumbersome to administer as it is usually given as an infusion.

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Verapamil and diltiazem 

Diltiazem and verapamil are calcium channel blockers that are available both in oral and IV preparations. These can be used to slow the heart rate in cardiac imaging, particularly in patients in whom β-blockers are contraindicated.⁶ Unfortunately, in practice, the efficiency of rate reduction in this setting has been disappointing.⁴ These drugs are contraindicated where there is a history of heart failure or significantly impaired LV function because they can reduce myocardial contractility.

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Ivabradine 

Ivabradine (Procorolan©) is a novel anti-anginal agent that is a pure negative chronotrope. It reduces the heart’s natural pacemaker activity by inhibiting the I_f (funny) ion channels, which are abundantly expressed on the sinoatrial node. Therefore, it is useful in patients in sinus rhythm, but not in other rhythms such as atrial fibrillation. Although not routinely used at present, ivabradine may yet play an important role in cardiac CT. It is generally well tolerated, but patients may complain of some visual disturbance such as enhanced brightness. Ivabradine has a relatively short half-life of around 2h and is currently only available as an oral preparation. The usual starting dose for patients with ischaemic heart disease is 5mgbd. Significant bradycardia occurs in only 2% of patients taking 7.5mg.¹⁰ The oral dose usually does not give a sufficiently rapid onset of bradycardia to be of use acutely and it has yet to be reliably demonstrated as of practical value in clinical CT practice but an IV preparation may overcome this. Ivabradine is contraindicated in sick sinus syndrome and should not be used in patients who are already taking CYP 3A4 inhibitors such as ketoconazole, macrolides (such as erythromycin), and nefazadone [used in the treatment of human immunodeficiency virus (HIV)].

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Glyceryl trinitrate (GTN) 

GTN causes smooth muscle relaxation of vessel walls resulting in vasodilatation. In CT coronary angiography it is used to improve image quality by increasing the luminal diameter of the coronary arteries.¹¹ This is important in patients who have small calibre vessels, particularly females. There is evidence that GTN particularly improves visualisation of the right coronary artery and septal branches,¹² but there are no published data that it definitely increases diagnostic yield. Although there has been some debate about GTN causing reflex tachycardia, evidence suggests that in practice this does not occur.¹² A recent survey in the United States found that 84% of centres routinely use GTN.¹³ GTN is a fast acting nitrate and is quickly metabolised by the body. It is typically given as two sprays of 0.4mg sublingual GTN just before the scan is performed, ideally with the patient on the scanner table. No monitoring is required for sublingual GTN administration.

Side effects and adverse reactions 

It is advisable to warn the patient that they may experience a headache but this usually resolves quickly. Uncommonly, GTN may precipitate vasovagal symptoms that usually require simple supportive measures, such as elevating the patient’s legs. Patients that have taken a phosphodiesterase type 5 inhibitor, e.g., sildenafil, vardenafil, or tadalafil within the preceding 24–48h should not be given GTN.¹⁴ Both of these drug types work on different parts of the nitric oxide cyclic GMP pathway and hence amplify the effects of blood pressure reduction,¹⁴ potentially inducing a hypotensive crisis. If the blood pressure becomes very low, this may precipitate a stroke or a myocardial infarction.

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Drugs used primarily in cardiac stress MRI 

Adenosine 

Adenosine is commonly used as a stress agent in cardiac MRI and nuclear cardiology studies. At high doses, adenosine causes a transient blockade of the atrioventricular (AV) node and many clinicians have experience of using IV adenosine to treat supraventricular tachycardia in the acute or emergency setting. At the lower doses used in diagnostic imaging, adenosine principally acts by stimulating the A2 receptors in the heart, causing smooth muscle relaxation and significant vasodilatation. Normal coronary arteries dilate in response to adenosine and consequently there is increased coronary blood flow.¹⁵ In areas of stenotic coronary artery disease, the vessel has much less ability to dilate and there is reduced coronary flow reserve. Therefore, adenosine induces a heterogeneous coronary blood supply in patients with coronary artery disease and this can be used to demonstrate regions of reduced coronary artery flow reserve as inducible perfusion defects. The blood supply to areas supplied by a stenotic coronary artery is not usually reduced by adenosine.¹⁶ However, in the presence of a severe stenosis, the myocardium in this territory may become ischaemic, possibly due to a steal phenomenon of blood towards regions of myocardium with a better blood supply.¹⁷

Patient selection and preparation 

Adenosine is contraindicated in patients with severe asthma because of the risk of inducing bronchospasm. Sick sinus syndrome and symptomatic bradycardia, heart block and a history of myocardial infarction within the preceding 72h are also contraindications to the use of adenosine (Table 3). A relative contraindication is in patients with mild asthma and COPD. Most centres will cautiously administer adenosine to patients with mild, stable asthma but not to severe asthmatics. Some centres use a titrating regimen if there is doubt over the severity of reactive airways disease, starting off at a low dose and gradually building up to full dose over 6min.

Table 3. Adenosine

Dose	140μg/kg/min (160 or 210μg/kg/min in some centres)
Contraindications	Severe asthma, sick sinus syndrome, heart block, myocardial infarction within previous 3 days
Relative contraindications	Mild asthma or chronic obstructive pulmonary disease (COPD) on regular bronchodilators
Patient preparation	Stop nitrates, caffeine and dipyridamole for 24h. Theophyllin drugs should be stopped for 48h
Side effects	Flushing sensation, shortness of breath, chest pain, headache. Rarely bronchospasm, complete heart block
Treating side effects	Stopping infusion usually results in resolution of side effects as half-life is very short (around 10s)

Caffeine contains a purine structure that is pharmacologically similar to adenosine and can reduce its effects by a process of competitive antagonism. Patients are, therefore, required to abstain from caffeine for 24h prior to imaging. This includes tea, coffee, cola and fizzy drinks and chocolate. Most labelled decaffeinated drinks contain a low level of caffeine. Theophyllin drugs (e.g., aminophyllin) used in the treatment of airways diseases are also similar to caffeine and these must also be stopped for 48h prior to imaging. Long-acting nitrates (such as isosorbide mononitrate) and dipyridamole (which can increase endogenous adenosine levels) should also be stopped for 24h prior to the investigation. If patients are unable or forget to follow this preparation, an alternative stress agent such as dobutamine could be considered, although there is some evidence that higher doses of adenosine (up to 210μg/kg/min) can be used to produce an adequate response in patients that have had coffee shortly before the scan.¹⁸

Adenosine infusion protocol 

For CMR, separate IV lines are used for gadolinium and adenosine infusions and patients have ECG and blood pressure (BP) monitoring. BP monitoring is useful to assess for a small drop in BP that is often seen during adenosine infusion due to vasodilatation. In some centres, BP monitoring is omitted as it is felt that an increase in heart rate is sufficient to assess for an adequate response. However, it is useful in case there is a more significant episode of hypotension during stress. Adenosine is typically administered via a continuous pump injection for ≥3min at a dose of 140μg/kg/min. Some centres routinely use slightly higher doses of 160μg/kg/min to ensure adequate stress.

Side effects and adverse reactions 

Patients should be warned prior to scanning that they will feel unwell while the adenosine is being infused. Patients often become flushed, breathless and have chest pain. This chest pain is often different from the patient’s normal chest pain and may be due to adenosine A1 receptor effects. Some patients get a sensation of “impending doom,” whereas others complain of lower limb numbness. All these sensations resolve within a few seconds after the infusion has been stopped as adenosine is metabolised very quickly (half-life 10s). More serious side effects are uncommon (less than 0.1% of patients¹⁹) and include bronchospasm, bradycardia or heart block and very rarely pulmonary oedema and myocardial infarction.

If bradycardia or bronchospasm does occur, stopping the adenosine infusion usually results in resolution. If bronchospasm persists, inhaled salbutamol and an aminophyllin infusion can be considered.

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Dobutamine 

Dobutamine is a synthetic catecholamine that causes positive inotropic and chronotropic effects and hence increases myocardial contractility and heart rate. This results in an increased myocardial oxygen demand and simulates the effects of exercise reasonably well. Clinically a rise in blood pressure is also often seen. Dobutamine mainly works as a β1 agonist but it also has some β2 agonist activity, which causes coronary artery vasodilatation. At higher doses, there is some α-blocking activity that can result in a fall in blood pressure.

Dobutamine can be used at lower doses to determine the presence of myocardial viability by looking for contractile reserve in segments of myocardium that have impaired function at rest.²⁰ It can also be used to identify inducible ischaemia by looking for inducible wall motion abnormalities at higher doses.²¹

Patient selection and preparation 

Dobutamine can be used as a stress agent where there is a contraindication to adenosine. It is also likely to be more accurate than adenosine perfusion when there is known or suspected triple vessel disease because a visual assessment of perfusion in balanced global ischaemia may be interpreted as normal. Dobutamine allows for a graded step-wise assessment that can identify ischaemic territories in turn. It should not be used in patients with severe hypertension (systolic BP >220mmHg and diastolic BP >120mmHg) or in hypertrophic cardiomyopathy (Table 4). It is also contraindicated in those patients with aortic stenosis (AS) with a peak gradient of over 50mmHg, but as some patients with AS have impaired LV function and hence a reduced ability to generate a peak aortic valve gradient of this magnitude, dobutamine should not be administered to a patient with moderate or severe AS. In addition, dobutamine should not be used following a recent myocardial infarction, in patients with unstable angina or in those patients with a history of ventricular arrhythmia.

Table 4. Dobutamine

Dose	10μg/kg/min increasing by 10μg/kg/min to a maximum of 40μg/kg/min
Contraindications	Severe hypertension (>220/120mmHg), moderate to severe aortic stenosis, severe hypertrophic cardiomyopathy, recent myocardial infarction, complex dysrhythmia, unstable angina, active endo/myo/pericarditis
Patient preparation	Stop β-blockers for 48h
Side effects	Anxiety, chest pain, nausea, ventricular ectopics, atrial fibrillation. Myocardial infarction and ventricular dysrhythmias are rare
Treating side effects	Stopping infusion usually results in resolution of side effects (half-life is 120s). Consider sublingual glyceryl trinitrate or IV metoprolol if needed

Patients undergoing a dobutamine stress study should stop their β-blockers for 48h prior to the investigation, as these drugs will counteract the effects of dobutamine. The referring clinician should be made aware that β-blockers are routinely stopped for a dobutamine stress scan as, for example, some patients with heart failure that are prescribed β-blockers for prognostic purposes may become rapidly symptomatic if these are withdrawn suddenly.

Dobutamine infusion protocol 

In the assessment of inducible ischaemia, dobutamine is typically infused at 10μg/kg/min for 3min and the dose is increased by 10μg/kg/min every 3min up to a maximum of 40μg/kg/min. The dobutamine infusion may be stopped before this maximal level if the target heart rate has been reached [(220–age)×0.85] or for other reasons as shown in Table 5. If the target heart rate is not reached at a maximal level of dobutamine, boluses of IV atropine (0.3mg up to a total of 1.5mg) can be given. The dose of dobutamine may be started at 5μg/kg/min with initial 5μg/kg/min incremental increases in patients with impaired LV function at rest to assess myocardial contractile reserve and viability. Where only information on viability is required, the dose of dobutamine is increased up to a maximum of 10–15μg/kg/min. Blood pressure and ECG monitoring are recommended throughout the study.

Table 5. Reasons for terminating dobutamine infusion

Target heart rate reached [(220–age)×0.85] Blood pressure increase to >240/120mmHg Fall in blood pressure by 40mmHg from previous systolic level or to 20mmHg below baseline systolic level Patient request such as chest pain or intractable symptoms Ventricular arrhythmia Evidence of ischaemia (new wall-motion abnormality)

Side effects and adverse reactions 

Most patients develop mild symptoms, such as anxiety, nausea, flushing and breathlessness. Atrial arrhythmias, such as atrial fibrillation (AF), and ventricular ectopics can occur and the patient’s typical chest pain can be induced. More severe complications such as ventricular dysrhythmia (ventricular tachycardia and ventricular fibrillation) and myocardial infarction are very uncommon.²², ²³ Dobutamine has a short half-life of 120s so if a complication occurs, stopping the infusion usually results in gradual resolution of the side effects. The clinical effects can take about 10min to resolve completely. If side effects persist or the patient develops anginal symptoms, GTN can be administered sublingually or a β-blocker may be given, such as 2.5–5mg metoprolol IV slowly.

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Dipyridamole 

Dipyridamole is a thromboxane synthase inhibitor that is commonly used in patients with ischaemic heart disease who are unable to take aspirin. It is also used with aspirin for secondary prevention in stroke patients. When administered intravenously for stress imaging, it causes vasodilatation by inhibition of cellular uptake of adenosine and inhibition of adenosine breakdown. This results in an increase in local adenosine concentration and it thus causes indirect vasodilatation. Adenosine is now the more widely used agent in stress MR because there tend to be more significant adverse effects with dipyridamole.

Patient selection and preparation 

Patient preparation, contraindications and side effects are the same as for adenosine. Dipyridamole should not be given to patients with myasthenia gravis, as it may precipitate a myasthenic crisis due to its anti-cholinesterase activity, and it should not be used when the systolic blood pressure is less than 90mmHg.

Dipyridamole infusion protocol, side effects and adverse reactions 

Dipyridamole is given as a continuous infusion at a dose of 0.57mg/kg over 4min,²⁴ which is increased to 0.84mg/kg over 6min in some centres.²⁵

ST segment depression on the ECG can occur, although this may not be identified on the ECG trace used for triggering the MR scan. Dipyridamole has a longer half-life than adenosine (10h) so aminophyllin is more likely to be required to counteract side effects than for adenosine stress tests.

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Atropine 

Atropine is an anticholinergic drug. It blocks the activity of the vagus nerve causing a rise in heart rate due to increased conduction through the sinoatrial (SA) node.

Patient selection and preparation 

It is used routinely in dobutamine stress tests if the target heart rate has not been achieved at the peak dose of dobutamine. It may also be required in cardiac CT if β-blocker administration results in excessive bradycardia. The main contraindication to atropine is narrow angle glaucoma and it can cause urinary retention in patients with prostatic hypertrophy. It should not be given to patients with myasthenia gravis.

Atropine administration protocol 

When atropine is used in dobutamine stress imaging, the dose is 0.3mg slow IV boluses up to a maximum of 1.5mg. The dose is administered incrementally until target heart rate is achieved. Patients should be warned that they may notice dryness of the mouth and blurred vision.

When given for symptomatic bradycardia in patients receiving β-blockers in CT, the maximum dose is higher with 300–600μg aliquots given up to a maximum dose of 3mg.²⁶ This dose completely blocks the vagus nerve. IV boluses are given every few minutes to maintain an adequate heart rate. If atropine has little or no effect on the heart rate and the patient remains symptomatically bradycardic, cardiological advice should be sought urgently.

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Conclusion 

Cardiac imaging is one of the most rapidly expanding areas of modern cross-sectional imaging practice and it is likely that the demand for these techniques will increase dramatically over the next decade. As a result, more radiologists are starting local programmes and, therefore, administering the drugs required to obtain robust diagnostic images. While for some this is a daunting prospect, the guidance in this article should enable radiologists to use these drugs with more confidence. The nature of the drugs to be given should be discussed with local cardiologists prior to starting a cardiac imaging programme and it is useful for these cases to be performed during a regular session initially so that the cardiologists can provide support as required. Although in the majority of patients these drugs can be given quite safely, it is clearly preferable for the radiologist to gain experience from visiting regional teaching centres or attending formal courses prior to embarking on their own programmes. Even when suitably trained and with significant experience, there will be cases where there is doubt over the safety of administering these drugs, highlighted as areas of caution in this article. Where there is doubt, the case should be discussed with a cardiologist and their presence in the scanning suite for these cases can provide further reassurance.

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