Ebook Practical cardiology (2nd edition) Part 2

(BQ) Part 2 book Practical cardiology presentation of content: The revascularisation patient, the patient with palpitations, the patient with dyspnoea, the patient with a murmur, other problems. (BQ) Part 2 book Practical cardiology presentation of content: The revascularisation patient, the patient with palpitations, the patient with dyspnoea, the patient with a murmur, other problems.

C H A P T E R   5

THE REVASCULARISATION

PATIENT

The rather grand term revascularisation refers to the use of coronary angioplasty or surgery to

improve myocardial blood supply

Angioplasty

Balloon dilatation of coronary artery stenoses was first performed in the late 1970s by Andreas Grunzig The technique has undergone many refinements and is now widely used for the treatment of angina not responding to medical treatment Angioplasty has not been shown to improve the prognosis of patients with stable angina Coronary artery bypass grafting (CABG) has similarly not been shown to prolong life for most stable angina patients However, both treat-ments are very successful in relieving the symptoms of angina The COURAGE Trial compared optimal medical treatment of angina with angioplasty but excluded patients with symptoms refractory to medical treatment.1 Not surprisingly, this group of stable mild angina patients had

a similar outcome with angioplasty and medical treatment The trial suggests that compared with optimal medical treatment, angioplasty is a safe and slightly more effective treatment for stable angina Patients can make an informed choice between these two treatments

The majority of patients treated with angioplasty in Australia have acute coronary syndromes and here there is good evidence of prognostic benefit with angioplasty compared with medical treatment In many centres one-, two- and complicated three-vessel disease are managed this way It has been shown to be as effective as coronary surgery for these patients but at the price

of a higher rate of re-intervention This is because the greatest limitation of angioplasty is the rate of restenosis in vessels that have been dilated

Restenosis

Restenosis has been reported in as many as 40% of balloon angioplasties where a coronary stent (p 199) has not been used—plain old balloon angioplasty (POBA) Re-dilatation is usu-ally possible but a similar risk of restenosis occurs after a second dilatation Renarrowing of these vessels is caused by the elastic recoil that occurs over the weeks after dilatation POBA is also associated with a relatively high risk of acute closure of the artery This may result from dissection of the arterial wall during dilatation, leading to thrombus formation or occlusion of the vessel by the dissection flap

Coronary stents

The introduction of coronary stents has revolutionised angioplasty (Fig 5.1) These folded metal structures are crimped onto a balloon catheter They are made from stainless steel or, more recently, cobalt alloys Alloy stents have thinner struts, which make them more flexible and may reduce the rate of restenosis within the stent Dilatation of the balloon expands the stent up against the intima of the artery The stent has enough radial strength to prevent elastic recoil

It will also seal a dissection flap back into place Dissection occurs when damage to the intima separates it from the media This can occur as a result of splitting of the intima following balloon

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The need for urgent coronary artery bypass grafting has fallen from about 5% of cases to much less than 1% In addition, more complicated lesions can be treated safely Sometimes long segments of arteries are stented (video clip 23), although at the cost of a higher risk of restenosis Numerous randomised trials have shown improvement in restenosis rates and in the need for re-intervention when stents are used.2

Angioplasty is increasingly being performed in hospitals without cardiac surgical back-up There remains some controversy about this approach

Bare metal stents

Although stents have eliminated the problem of elastic recoil, restenosis can still occur in up to 30% of patients The mechanism of restenosis within a stent is different from that which occurs after angioplasty It has been shown that stents become lined with new endothelial cells within

has been placed in the circumflex and a long stent is being positioned across the left main and 

into the LAD (arrows). (d) The final result after stenting of the left main and the LAD and balloon 

dilatation through the stent struts into the circumflex. A follow-up angiogram at six months  showed no restenosis and the patient was asymptomatic.

four weeks of being implanted Some of these cells migrate through the struts of the stent from the arterial media For reasons not fully understood, in a proportion of patients they continue

to grow into the lumen of the vessel (neo-intimal proliferation) and gradually cause narrowing that leads to a return of symptoms This is rarely associated with an acute coronary syndrome

or infarct This phenomenon occurs within six months of the stent insertion and it is rare for restenosis to occur after this time Although up to 30% of stents show evidence of restenosis, if patients have routine follow-up angiograms only about 10% develop symptomatic restenosis Certain risk factors for restenosis have been identified (Table 5.1)

Table 5.1 Risk factors for restenosis

1 Diabetes

2 Previous restenosis in that stent

3 A long lesion (and stent) (> 18 mm)

4 A narrow stent (< 3 mm)

5 Dilatation and stenting in a saphenous vein bypass graft

6 A stent not adequately dilated and deployed

Drug-eluting stents

The realisation that restenosis is a neoproliferative process has led to the development of

drug-eluting stents (DESs) These stents are coated with anti-proliferative drugs The drug is held

within a polymer bonded to the metal Drug elution occurs over about four weeks after

implan-tation The two drugs currently available are sirolimus and paclitaxel Sirolimus is used for the

prevention of renal transplant rejection It blocks G1 to S cell cycle progression Paclitaxel is

an anti-proliferative agent that stabilises microtubules and prevents cell division These drugs have almost no systemic absorption when implanted with a stent

The restenosis rate has been reduced dramatically by using these stents Clinical restenosis rates of 2% or 3% are commonly obtained These stents are now implanted in 90% of angio-plasty patients in the United States In Australia the cost of these devices (four to five times that

of a bare metal stent) has kept the implantation rate much lower, but usage varies from state

to state Cardiac surgeons note that the cost of CABG for a patient becomes less than that of angioplasty once more than three or four drug-eluting stents are used

In many hospitals DESs are reserved for patients with a high risk of restenosis They have not been shown to improve mortality compared with bare metal stents

Studies are underway with stents made of materials that are completely absorbed over a period

of months after implantation These include magnesium stents

Indications for angioplasty

Angioplasty is not indicated unless the lesion to be dilated is clearly the cause of the patient’s symptoms, and then usually only if these have not responded to medical treatment If a lesion

is of equivocal significance (< 50% stenosis) or the symptoms are atypical, a sestamibi test or stress echo may be necessary to demonstrate ischaemia in the territory of the suspect vessel.Angioplasty is a very effective treatment for stable angina but has not been proven to improve prognosis when compared with intensive medical treatment It may possibly do so when there

is three-vessel disease suitable for angioplasty or when the patient has a tight lesion in the left anterior descending artery proximal to the first diagonal branch A lesion in this position that threatens a large area of myocardium Successful angioplasty should always be followed by intensive risk factor modification

Treatment of patients with ACS by angioplasty has been shown to improve outcomes, including the risk of death and myocardial infarction (p 157) In busy angioplasty units these patients now provide the majority of the unit’s workload

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Left main stem stenosis is increasingly being managed with angioplasty and stenting There remains some controversy about this approach There is an incidence of sudden death in patients treated in this way This is quite a different outcome from the gradual return of angina that occurs with restenosis in other vessels In experienced centres the outcomes are as good as those for CABG for left main stenosis

The patient who has had bypass surgery and has some patent grafts to the circumflex or LAD is an exception since the vessel is considered ‘protected’ Left main angioplasty is often straightforward for these patients

The technique

The balloon catheter is introduced using a coronary guiding catheter somewhat different from those used for diagnostic angiography (Fig 5.3) Although diagnostic procedures are usually performed with 5 French gauge catheters, angioplasty guiding catheters are often 6 or 7 French They are

designed to provide back-up for the guide wire and balloon catheters—that is, to remain engaged in

the coronary ostium as catheters are passed into the artery A fine guide wire is advanced through the guiding catheter and into the coronary and across the lesion (Fig 5.4) A balloon dilatation catheter

is advanced along this wire until it crosses the lesion The balloon is dilated with contrast solution

to a pressure of up to 18 atmospheres The balloon is kept inflated for about 20 seconds (Fig 5.5)

Since the vessel is completely occluded during the procedure, many patients experience ischaemic chest pain and ST elevation may be visible on the ECG The vessel is injected with contrast and the effectiveness of the dilatation assessed.

A stent is chosen that is thought to be the correct diameter and length for the artery and the lesion Stents range in size from 2.25 mm diameter to 5.0 mm and in length from 8 mm to

Continues

a

b

Figure 5.5 (a) This 62-year-old man presented to the hospital with chest pain. His initial ECG  showed minor inferior ECG changes. Half an hour later his pain became more intense and his  ECG showed 3 mm of ST elevation in the inferior leads. He was transferred to the catheter  laboratory within 20 minutes of the onset of these ECG changes. The first picture taken showed 

a totally occluded right coronary artery (arrow). (b) The balloon being inflated 

about 38 mm The longer the stent, the more difficult it may be to advance through a tortuous

or calcified artery to the lesion The stent balloon is placed across the lesion and then inflated The nominal size of the stent will be reached when the balloon is inflated to the standard pressure for that balloon This is shown on a chart that comes with the balloon catheter Dilatation to a higher pressure will result in a larger expanded stent diameter If the result looks unsatisfactory, repeat dilatation (post-dilatation) can be performed with a higher pressure (non-compliant balloon)

In some laboratories the lesion and stent expansion are assessed with IVUS (p 137) Further dilatation is performed if the stent struts do not seem adequately opposed to the vessel wall

Closure devices

The femoral artery puncture site can be closed at the end of the procedure using a collagen plug that is inserted into the artery by a sheath or by a stitch also deployed onto the puncture via a sheath This enables the patient to mobilise within an hour or two of the procedure, even when aggressive anticoagulation and anti-platelet treatment have been employed Otherwise, the sheath is withdrawn some hours after the procedure when the ACT has fallen to about

150 seconds Quite prolonged clamping of the site is often required and many patients find this more of an ordeal than the procedure Closure devices are expensive and for that reason are not used for every patient in most hospitals

If the procedure has been performed through the radial artery, the artery is compressed with a velcro strap Stable patients who have had an angioplasty performed via the radial artery may sometimes be discharged on the same day; otherwise they are usually kept overnight

Complications

All the risks associated with coronary angiography apply to the angioplasty procedure Additional possible complications include the following

Dissection of the artery during balloon dilatation

or from the guiding catheter

In most cases stenting will close the dissection flap and lead to a very satisfactory outcome, but a longer stent than would otherwise have been used may be required (Fig 5.2, video clips 20–22)

If dissection has been cause by the guide wire during attempts to cross the lesion, dissection and the creation of a false lumen may make it impossible to wire and stent the true lumen (Fig 5.6) Urgent coronary artery bypass grafting may be needed

Perforation of the artery

This feared complication is most common when attempts are being made to cross a total occlusion with a guide wire Wires designed to cross chronically (more than six months) occluded vessels are very stiff and can perforate the wall of the artery Perforation by a wire may cause only small amounts of bleeding into the pericardium, but if the perforation is not recognised and a balloon is passed over the wire, torrential bleeding into the pericardium may cause cardiac tamponade (p 145) requiring urgent pericardiocentesis The problem may be compounded by the previous administration of IIb/IIIa inhibitors A coronary perforation

or tear may be treated with a covered stent This has a layer of gortex between two layers of metal If this rather bulky stent can be passed across the perforation, it will prevent further bleeding

No reflow

Dilatation of an artery or more often of a degenerated saphenous vein graft can dislodge clot or atheromatous material further down the vessel These fragments can occlude distal arterioles and lead to poor flow into the distal bed and ischaemic symptoms (video clips 24–27) Treatment

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with vasodilators (nitroglycerine, adenosine or verapamil) may eventually restore flow Various devices have been developed to help prevent this problem, especially in vein graft angioplas-ties These include occlusion balloons that can be inflated distal to the lesion After dilatation

of the lesion a suction device is used to remove material before the balloon is deflated Another approach is to use a protection wire These guide wires have a fine mesh basket attached to them This is opened beyond the lesion before dilatation and stenting are performed It is removed after it has been withdrawn into a fine catheter

Side branch occlusion

Some of the most difficult angioplasties involve a lesion close to or involving a large (> 2 mm) side branch Dilatation of the main vessel risks shifting plaque into the branch and compromis-ing it Numerous techniques have been developed to deal with this problem In many cases two guide wires are used so that if dilatation of the main vessel narrows or occludes the origin of the branch a balloon can be passed into the branch (Fig 5.7, video clip 23)

Simultaneous dilatation of two balloons (kissing balloons) may be necessary to keep both

vessels open If, as is usual, the main vessel is stented the side branch needs to be re-wired through the stent struts and dilatation into the side branch performed to open the struts and the proximal part of the branch Other techniques such as stenting the branch first or placing stents into both vessels and dilating them simultaneously can be used Whichever technique is used, there is a higher risk of branch restenosis than for the main vessel The ACT is measured

at the end of the case and additional heparin given if the level is less than about 300 seconds

Figure 5.6 This 40-year-old man presented three days after the onset of ischaemic chest pain.  The ECG showed inferior T wave changes. The right coronary artery was totally occluded and  extensively thrombosed. Attempts to advance the guide wire led to extensive dissection of the  vessel and little blood flow. The wire was in a false lumen.

Stent thrombosis

The thrombotic risk associated with the introduction of foreign material into the coronary artery was at first managed with aggressive anticoagulation with heparin and then with warfarin This led to bleeding complications

Dual anti-platelet therapy

Subacute stent thrombosis is now very uncommon The use of two anti-platelet drugs (aspirin

and clopidogrel) in combination has been very effective in preventing stent thrombosis during the peri-procedural period and afterwards

Aspirin is a cyclo-oxygenase (COX-2) inhibitor and clopidogrel blocks ADP-dependent platelet aggregation Patients having a non-urgent angioplasty should be pre-loaded with both drugs at least 24 hours before the procedure Clopidogrel should be given as a loading dose of 300–600 mg (four to eight tablets) and then 75 mg a day, and the aspirin dose should be up to

300 mg a day

Dual anti-platelet treatment should be continued for at least one month after bare metal stent insertion and single anti-platelet treatment should be continued for ever Patients who receive a DES must continue dual anti-platelet treatment for at least six months, and two years

of treatment is now sometimes recommended This is because re-endothelialisation is delayed

in these stents and thrombosis remains a risk for at least this period

Late stent thrombosis

There are increasing (although rare) reports of late thrombosis in DESs (Fig 5.8) These are ated with a high incidence of myocardial infarction and death They are often reported to have occurred after single anti-platelet treatment has been stopped for some reason Patients given DESs should be warned that they must stop anti-platelet treatment only if absolutely necessary (e.g before surgery involving a high risk of bleeding) and for the shortest possible period.DESs should be avoided for patients likely to need surgery within six months of the procedure and for those who may not be compliant with their treatment

associ-Late stent thrombosis will be an area of intense research over the next few years Since the drug disappears from the stent within a month of implantation, theories as to the cause of late

Figure 5.7 Angioplasty of an LAD/first diagonal bifurcation lesion using two wires

The post-angioplasty visit

This is usually less complicated than the post-surgical visit The patient should be asked how things went Possible problems include a large haematoma over the femoral artery and the recur-rence of chest pain Groin haematomas usually improve spontaneously but can sometimes be spectacular and extend to the knee or even further If there is a lot of discomfort and a pulsatile lump is palpable over the puncture site there is the possibility of a pseudoaneurysm of the artery

An ultrasound examination will confirm or eliminate this possibility This is the only pathology that ultrasonographers can cure as well as diagnose The usual treatment is prolonged (an hour

or more) compression of the artery with a firm blunt object like an ultrasound probe It is also possible to inject a thrombin plug into the aneurysm and close it rather more quickly

Figure 5.8 Thrombosis in a DES placed two years before in the LAD. The lucent area in the  centre of the vessel is due to thrombus (arrow). The patient presented with an acute anterior  infarct. Balloon dilatation in the thrombosed area (in combination with IIb/IIIa platelet inhibition)  led to a return of normal flow.

The recurrence of pain may mean restenosis of the artery but atypical chest pain seems common for a few weeks after angioplasty An ECG should be performed, and if this shows no changes expectant treatment may be all that is needed.

Early complications tend to involve thrombus and are associated with severe symptoms and ECG changes If there is further doubt an exercise test or even repeat angiography is sometimes needed

Restenosis is usually associated with the return of typical exertional angina three to six months after the procedure (Fig 5.9) Although it can begin again quite suddenly, it is rarely associated with infarction or death

Figure 5.9 Severe stenosis inside an LAD stent. The patient had a return of angina but there  was no infarct despite the total occlusion of the artery.

Coronary artery surgery

Coronary artery bypass grafting may be recommended to patients whose angina cannot be controlled by medical treatment (and who are not suitable for angioplasty)—that is, for symp-toms It is a most effective way of improving these patients and more than 90% will be free of

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angina and off anti-anginal drugs Patients who have severe three-vessel disease and impaired left ventricular function or who have significant left main stenosis (video clip 28) should be offered surgery because it has been shown to improve their life expectancy and risk of infarction—that

is, for prognosis.3 Patients with severe proximal LAD stenosis may also have an improved prognosis following revascularisation In addition, all these patients are usually symptomatic and will have their symptoms relieved

Diabetics with multi-vessel disease have had a better outcome with surgery than with plasty.4 It is possible that the routine use of DESs in diabetics will change this outcome and this

angio-is currently being tested in a multi-centre trial.5

The preoperative assessment

Surgery cannot be performed until a coronary angiogram has demonstrated the coronary anatomy and that the arteries are suitable for grafting In some cases severe disease of the distal vessels may make it impossible for the surgeon to find a suitable area to attach the grafts and surgery is not possible

Other general medical problems may make surgery more difficult, more risky or sible It is not appropriate for patients with a poor life expectancy because of other medical problems to be offered surgery It is important that potential medical problems be identified before surgery

impos-A history should be taken to find out particularly about previous renal disease, malignancy, diabetes or lung disease Patients need to be warned that continued smoking increases consider-ably the postoperative risk of chest infection and, of course, the risk of graft stenosis Some cardiac surgeons will decline to operate on patients who continue to smoke Patients should be asked about the presence of varicose veins or varicose vein surgery Varicose veins cannot be used as bypass grafts and the surgeon needs to be warned that alternative conduits have to be found.The patient needs a physical examination where signs of severe airflow limitation may indicate the need for further respiratory investigations before surgery Varicose veins should

be looked for and their extent noted The presence of carotid bruits is an indication for carotid Doppler studies

Routine investigations should include a blood count to exclude anaemia and serum trolytes, and creatinine to exclude significant renal impairment These problems need to be addressed before surgery if they are uncovered The patient may wish to avoid transfusion with blood from the blood bank Patients can be advised that only a small minority of patients now need perioperative transfusion It is usually preferable for the patient to be discharged from hospital with moderate and usually well-tolerated anaemia (Hb of 80 or 90 g/L) In some cases,

elec-if transfusion seems likely, it is possible for the patient’s blood to be stored by the blood bank

so that it can be used as required during surgery—autologous blood transfusion

In general, patients continue with their usual medications up to the time of surgery The important exception is aspirin, which is often stopped several days before surgery because of the bleeding problems it can cause in the perioperative period Many cardiac surgeons are now prepared to operate on patients who remain on aspirin Patients with moderately severe

or unstable angina may be allowed to continue their aspirin, but dual anti-platelet therapy is usually strongly discouraged by surgeons

Saphenousvein

bypassgraft

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is used to bypass the left anterior descending coronary artery The LIMA is left attached to the left subclavian artery and carefully dissected off the back of the chest wall; the distal end is anastomosed to the LAD beyond the diseased segment Sometimes the LIMA is skipped to the first diagonal branch of the LAD The right internal mammary artery (RIMA) is sometimes used to graft the right coronary artery The radial artery can be used as a free graft One end is attached to the aorta and the other to the distal coronary

Arterial grafts (LIMA, RIMA and probably radial free grafts) have the advantage of a low restenosis rate This is only 5–10% for LIMA grafts, after 10 years Vein grafts have at least a 50% restenosis rate at 10 years Arterial grafts are technically more difficult because the arteries are very sensitive to handling and spasm can occur during or after surgery This can lead to ischaemia or infarction in the immediate postoperative period

Recovery after coronary surgery takes longer than after angioplasty Most patients are in hospital for just under a week and can be back at work after four to eight weeks The mortality for uncomplicated patients is less than 1% but rises considerably if the operation is a second bypass, the patient is diabetic or over 80, or left ventricular function is poor

Management of graft stenosis

Sometimes dilatation and stenting can be performed to re-open narrowed grafts but the nosis rate is high after angioplasty to degenerated vein grafts (Fig 5.11, video clips 29 and 30) The procedure can be technically difficult and the mass of atheromatous material present

reste-in these vessels is such that there is a risk of embolism to the distal vessels and ‘no reflow’ (p 195) Severe graft disease, especially when the LAD graft is affected, is an indication for ‘redo’ coronary surgery This procedure is becoming more common It involves a higher risk than the first operation and there may be technical problems with lack of adequate conduits (no veins left, mammary already used) and with finding suitable ‘target vessels’ for the attachment of the grafts These patients are older and often have diffuse distal disease in their coronary arteries

c

Figure 5.10—conT’d  (c) This patient’s X-ray resembles a metal scrap yard. Sternotomy wires, 

arterial clips and two coronary stents (small arrows) are visible.

Figure 5.11 (a) Severe stenosis (arrow) with little flow in an eight-year saphenous vein graft. 

The patient was a 75-year-old man with recent severe angina. He had been symptom-free after 

his surgery. (b) A guide wire and balloon have been advanced across the lesion. The balloon is  being inflated. (c) There is now normal flow in the graft and on into the native circulation.

b

a

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Minimally invasive coronary artery surgery is now being performed in some units racoscopic equipment is used so that bypass grafting can be performed through a series of small, lateral thoracotomy incisions Most commonly this involves grafting the LIMA to the LAD coronary artery The distal anastomosis can be performed on the beating heart and heart bypass is not required As yet the technique has limited application The operation may take longer than conventional surgery and the disposable equipment is very expensive A series of small lateral thoracotomies may cause more postoperative pain than a median-sternotomy and hospital stay is not dramatically shortened The distal anastomosis is difficult to perform and long-term patency rates are not known

Tho-‘Off-pump’ surgery can be performed on the beating heart This avoids the possible plications of cardiopulmonary bypass (cognitive impairment, ventricular ischaemia) but can be technically difficult Newer techniques involving the use of left and right internal mammary arter-ies grafted off-pump and without the need to clamp the ascending aorta seem very promising

com-Postoperative problems

The risks to the patient in the immediate recovery period include ischaemia or infarction because

of spasm or thrombosis of a graft This may necessitate returning the patient to theatre for regrafting There are occasionally bleeding problems from a graft anastomosis which can also mean re-operation Hypotension or shock can occur because of cardiac ischaemia, hypovolaemia

or pre-existing cardiac failure Inotropic support or even use of the intra-aortic balloon pump (p 281) may be required This device is placed via the femoral artery into the descending aorta and helps support the circulation

Cardiac rhythm disturbances are common following surgery Atrial fibrillation may occur

in up to 30% of patients and for up to a month after the operation In many units digoxin or sotalol (p 228) is given routinely after surgery and for about a month after discharge These drugs are used to prevent rapid ventricular response rates for patients who develop atrial fibril-lation and, in the case of sotalol, to prevent AF Preoperative amiodarone has been shown to reduce the postoperative risk of AF.6

Respiratory complications are also common, especially for patients who have been smokers

Areas of atelectasis occur in most patients and improve gradually over a period of weeks stant physiotherapy and breathing exercises are needed to prevent larger areas of lung collapse This susceptibility is due to the discomfort of deep breathing caused by the chest wound and the fact that the lungs have been deflated during surgery

Con-Wound infection is a relatively uncommon problem It is perhaps more common in the vein

harvesting wounds Small areas of infection may require only the removal of a suture and a course of antibiotics and dressings Larger areas of wound breakdown may mean leaving the wound open and allowing slow healing by secondary intention Sternal wound infections may

be slight and need only dressing and drying out with iodine ointments Severe sternal wound infections, however, can be a disaster since there are foreign bodies (the sternal wires) present Long courses of intravenous antibiotics and eventual removal of the wires may be needed

The postoperative visit

The clinician should express pleasure but not surprise at seeing the patient returned home from

hospital Questions should be asked about the procedure from the patient’s point of view.

The patient should be asked whether there has been any angina and how uncomfortable the chest and leg wound have been The clinician should find out whether there is a productive cough or any sign of wound infection There may have been problems with dyspnoea suggest-ing the possibilities of chest infection, cardiac failure or occasionally pulmonary embolism or pericardial or pleural effusion The clinician should also ask whether the patient’s analgesic regimen has been adequate especially to allow sleep

The list of medications should be studied It is likely to include aspirin, analgesics, any previous

anti-hypertensive drugs, iron supplements and possibly digoxin, sotalol or amiodarone ing on the surgeon’s degree of self-confidence the patient’s previous anti-anginal drugs may or

Depend-The revascularisation patient: points to remember

1  Good  preoperative  assessment  may  prevent  postoperative  complications  or delay in surgery or angioplasty

2  Review of the patient’s medications is appropriate

3 platelet treatment for at least a month (BMS) or at least six months (DES)

4  Long-term low-dose aspirin is also indicated for CABG patients

5  The postoperative visit is an important opportunity to reassess risk factors. All revascularisation patients need appropriate treatment for secondary prevention

may not have been stopped If there has been no chest pain suggestive of angina, anti-anginal drugs should be stopped Anti-arrhythmic drugs and iron supplements are usually continued for about a month Aspirin should be continued indefinitely and the opportunity to talk to the patient about risk factor control should not be lost Reminders about smoking cessation if appropriate and a low-fat diet should be given The serum cholesterol is likely to be lower than usual for the patient during the first couple of months after surgery, but arrangements to check it a few months later should be made All patients will qualify for secondary prevention treatment with a statin

The routine examination should include inspection of the wounds, looking for signs of chest

infection or pleural effusion (bronchial breathing or areas of stony dull percussion note at one

or both lung bases) Examination of the cardiovascular system may reveal atrial fibrillation, high

or low blood pressure, signs of cardiac failure (p 258) or a pericardial rub

An ECG should be performed Widespread T wave changes are common after surgery for up

to a few months The presence of new Q waves suggests a perioperative infarction The patient may be in atrial fibrillation The late development of this, especially in patients not protected

by an anti-arrhythmic drug, can be a cause of dyspnoea and cardiac failure

A chest X-ray is required if there is concern about lung pathology, cardiac failure or a

peri-cardial collection An increase in heart size suggests the need for an echocardiogram to assess left ventricular function and look for a pericardial collection Small pleural and pericardial effusions are common and usually resolve spontaneously, but large ones may need to be drained

Cardiac rehabilitation

This is just as useful for patients recovering from surgery as for those who have suffered an infarct In addition to an exercise program and information about risk factors, advice about management of wound problems and chest physiotherapy can be given

Mrs CS is a 70-year-old with a long history of ischaemic heart disease She had an inferior infarct eight years ago and after investigations was treated medically She has been a type

2 diabetic for six years, treated with oral hypoglycaemic drugs Her HbA1c averages 8 She has a history of hypertension, treated with an ACE inhibitor with only reasonable control (145/80) Her cholesterol when last checked was 8.0 mmol/L; her triglycerides are 3.5 mmol/L Although prescribed a statin she is reluctant to take it because she thinks she saw a report that these drugs cause memory loss She smoked until the time of her infarct She does not take aspirin because she is concerned it might cause gastric ulceration

She has been told she has disease in all three of her coronary arteries and that her heart muscle has been damaged by her previous myocardial infarction Her cardiologist has told her she could have either cardiac surgery or angioplasty and asks her to decide what she wants done

Objectives for the group to understand

The group needs to develop an understanding of the indications for coronary revascularisation and the place of risk factor management for patients undergoing either surgical or interventional revascularisation

Epidemiology and population health

The presenter should ask questions about coronary artery disease epidemiology, including the important risk factors (Ch 1 and 2), disease prevalence and typical age of onset The importance

of combinations of risk factors and of previous ischaemic heart disease as a risk factor should

be identified The influence of diabetes on risk and on future management must be discussed What might have been done to reduce the risk of progression of her coronary disease after her first infarct?

Presenting symptoms and clinical examination

The group should discuss the features of ischaemic chest pain and compare the characteristics

of pain due to myocardial infarction and other ACSs with those of angina Are the symptoms Mrs CS has typical of angina? A differential diagnosis of chest pain should be drawn up by the group (p 176)

Review of pathophysiology

The presenter should ask questions about the difference in pathophysiology of stable angina and the ACSs The group should know how the coronary anatomy (i.e the extent and severity

of coronary disease) correlates with symptoms and prognosis

Evidence-based practice relevant to case

The group should discuss the role and method of risk stratification based on the coronary anatomy and assessment of left ventricular function Which is more important as an indicator

of prognosis?

The presenter should ask for opinions on the role of revascularisation for patients with stable angina Which patients benefit in terms of their prognosis from cardiac surgery and which get only symptom relief (CASS study)? What is the evidence for more aggressive risk factor control for the future (cholesterol, triglycerides, blood pressure, BSLs)?

What is the evidence supporting the use of coronary artery surgery compared with vessel angioplasty (ARTS Trial) with or without DESs, and in diabetics compared with non-diabetics?

multi-What is the place of anti-platelet therapy for patients with stable angina and for patients following cardiac surgery? Which agent should be used (CAPRIE Trial)? When is dual anti-platelet therapy appropriate?

The group should be aware of the major trials of these treatments

Mrs CS’s physical examination

On examination Mrs CS has a BMI of 30 She is not breathless undressing Her blood pressure

is 170/90 mmHg, and her pulse 85 The apex beat is not palpable Her heart sounds are normal Her chest is clear She has a small non-tender bruise over the right femoral artery puncture site There are varicose veins in her left leg and thigh; the right side appears normal

Her ECG shows an old inferior infarct and some anterior T wave flattening

Diagnostic pathology

The presenter should get the group’s opinion about the adequacy of the investigations so far Does this history, ECG and angiogram information provide enough evidence for the recom-mendation of intervention? Is there a place for further tests (e.g sestamibi scanning or calcium scoring)?

Mrs CS’s prognosis

Mrs CS says she would rather not have angioplasty or surgery She would like to know whether there are medical options for her treatment What would the group tell her? What medical treatment might relieve her symptoms? What might improve her prognosis?

Is there evidence to support an attempt to persuade Mrs CS to have surgery or angioplasty? How would the group explain the advantages and disadvantages of each?

What is the relevance of her varicose veins?

Personal and professional development

and medico-legal aspects

The group should discuss the clinician’s place in advising a reluctant patient about drugs or other treatment that may improve prognosis What is the place of the clinician or specialist in explaining the risks associated with procedures and surgical operations? How do the results of trials relate to the treatment of individual patients?

Therapeutics

Mrs CS decides she wants to have a trial of medical treatment even though she has been told surgery would have prognostic benefits for her She is begun on metoprolol 50 mg bd, ceru-vostatin 10 mg daily and aspirin Her diet is reviewed by a dietician and her oral hypoglycaemic medication is increased She promises to test her blood sugars twice a day

After six weeks she has lost 4 kg, her blood sugars average 7 and her blood pressure is 135/85 mmHg Her exercise tolerance has improved slightly She can walk at her own pace on the flat but has to pause and use sublingual nitrates when she walks uphill

What would the group advise? Can Mrs CS expect further improvement if she perseveres?After a family conference Mrs CS decides to have cardiac surgery She spends eight days in hospital She has quadruple bypass—an internal mammary graft to the left anterior descending coronary artery, a saphenous vein graft to the circumflex and first diagonal branch of the LAD, and a radial graft to the right coronary artery There is a small problem with infection in her vein harvesting wound but her stay is otherwise uncomplicated

What should be reviewed at her first outpatient visit?

1 Symptoms—angina, dyspnoea, palpitations

2 Wound problems

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End notes

1 COURAGE Trial investigators Optimal medical therapy with or without PCI for stable coronary

disease New Eng J Med 2007; 356:1503–1516.

2 Serruys P , de Jaegere P , Kiememieij F , et al A comparison of balloon expandable stent tion with balloon angioplasty in patients with coronary artery disease New Eng J Med 1994; 8:489 (Benestent Trial).

high- 3 Medications—usual and anti-arrhythmic

4 Mobility and ability to cope with activities of daily living

5 Involvement in rehabilitation program

What advice should be given about the timing of return to work and sexual activity?Should a patient be encouraged to join a cardiac rehabilitation program? Is there evidence

of such a program’s usefulness (p 176)?

Mrs CS’s long-term management

What would be the group’s approach to the long-term management of Mrs CS with particular reference to her risk factors—her diabetes, weight, cholesterol and hypertension? What is her prognosis and risk of a further ischaemic event with and without aggressive risk factor control?What is the natural history of bypass grafts, and how do vein grafts compare with internal mammary or radial grafts as far as their long-term patency is concerned?

Research

Are there any aspects of the patient’s management that lack an appropriate evidence base? If

so, how can these deficiencies in knowledge be addressed by research? What research is being conducted comparing angioplasty with surgery for patients with three-vessel disease? n

C H A P T E R   6 THE PATIENT WITH

PALPITATIONS

The history

Palpitations are perhaps best defined as an inappropriate awareness of the heart’s beating It is

not really a medical term but patients often feel that use of the word to describe their symptoms should be enough to give the clinician the diagnosis Taking the history from patients who complain of palpitations may therefore be difficult, as patients may resent having to describe their symptoms in more detail

The first questions should be directed at finding out what the patient actually means and whether there is really an awareness of the heart beating or some quite different symptom Ask the patient to describe what happens and assess whether the abnormality is noticed only if the patient takes his or her own pulse (gratuitously) or takes the blood pressure with an electronic device that beeps in time with the heart beat

Then ask about the speed and regularity or irregularity of the perceived heart beat The heart beat may be fast or slow, regular or irregular, or some combination of these

Next ask about the onset and offset of the abnormality The instantaneous onset of a very rapid

and regular heart beat is typical of supraventricular tachycardia (SVT) (Fig 6.1) or less often of ventricular tachycardia (VT) (Fig 6.2) The offset may also be instantaneous, but sometimes the anxiety associated with the attack will cause a sinus tachycardia (ST) (Fig 6.3), which subsides

more gradually The gradual onset and offset of a more moderate tachycardia is more suggestive

of the awareness of sinus rhythm, which may be a symptom of anxiety or occasionally due to

an abnormality like thyrotoxicosis

The frequency of attacks is important as an indication of their effect on the patient’s life and

also because very frequent attacks are easier to record on an ECG and diagnose Very infrequent attacks may require no treatment, particularly if the patient’s description is suggestive of SVT This condition may begin causing symptoms at any age but often does so in the late teens There may be a history of episodes of sudden onset of tachycardia for many years Some patients’ attacks may occur less than once a year

The duration of the attacks is not especially helpful as far as the diagnosis goes, but very

long attacks may give the patient time to have an ECG recorded during the episode Prolonged attacks are clearly more disturbing than brief ones

There may be associated symptoms during the episodes Very rapid heart rates of any aetiology

are likely to cause some dizziness and dyspnoea Marked dizziness or syncope is suggestive of, but not specific for, ventricular tachycardia Chest pain may occur and is sometimes due to myo­cardial ischaemia brought on by the increased oxygen demands of the rapidly beating heart

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The patient may have noticed precipitating or relieving factors SVT and VT are usually of

spontaneous onset, sinus tachycardia may be precipitated by anxiety or the consumption of caffeine, and occasionally symptoms are predictably associated with exercise Some patients may have learnt or been taught to terminate attacks by deep breathing, the Valsalva man­ oeuvre or carotid sinus massage Immediate and reliable response to one of these suggests that the problem is SVT

A history of recent or even remote ischaemic heart disease increases the possibility of VT

as the cause of the symptoms

Occasionally patients have an incessant moderate tachycardia This seems to be a normal variant The patient is rarely aware of the heart rate and it tends to come to medical attention because of a routine examination or ECG Certain underlying conditions (anaemia, heart fail­ure, thyrotoxicosis, use of bronchodilators and beta­blocker withdrawal) need to be excluded before this diagnosis is made

to AF is not fast (Fig 6.5)

AF is a very common rhythm disturbance It becomes more common with age but can occur

at any age In the Framingham study the incidence of paroxysmal or chronic AF was 2% for people over the age of 22; while the prevalence of persistent or chronic AF was 0.5% for people aged 50–59, increasing to 8.8% for people aged 80–89

Ask about precipitating or aetiological factors (Table 6.1) These include recent heavy alcohol intake (usually a drinking binge 12–18 hours beforehand in a young man), thyrotoxicosis (there may be symptoms of this but thyroid function tests are necessary to make the diagnosis) and mitral valve disease Recent surgery is also a common cause, especially thoracic surgery, and AF can complicate myocardial infarction Sometimes it can be part of sick sinus syndrome These patients have periods of palpitations due to AF and periods of bradycardia or heart block which can cause dizziness or syncope

When patients with AF ask ‘Why me?’ Remember: ‘AF happens’

Patients vary greatly in the way they tolerate AF, especially when it is paroxysmal Some people are quite unaware of the heart rhythm and it is picked up incidentally, while others find epi­sodes intolerably distressing The symptomatic response is only partly explained by the variation

Figure 6.3 thyroidism. The RAA is common in thyrotoxicosis. Note that the PR and ST segments are part of a   single arc: the apparent ST segment depression is partly due to atrial repolarisation (PT or TA wave).

Figure 6.5 AF with a slow ventricular response (38/minute) in a hypertensive 55-year-old man  with angina pectoris on metoprolol. It is difficult to ascribe the ST/T changes to LVH alone.  Metoprolol is probably responsible for some of the AV block in this patient.

Slower irregular rhythm

The awareness of intermittent irregularities of the heart beat or pulse that are not associated with tachycardia is very common Patients may describe a hollow feeling in the chest followed by a thump or sometimes the need to cough (they may present to a chest physician) The episode lasts only a few seconds but may be repeated every few beats or less frequently There is often the sensation of a missed beat If the patient is taking the pulse it may be felt to miss Many people describe a ratio of normal to missed beats When every third beat is ectopic the rhythm is called trigeminy; when every second beat is ectopic the rhythm is called bigeminy Two ectopic beats in a row are called a couplet

This symptom is very suggestive of the awareness of ectopic beats that may be supraven­tricular (Fig 6.6) or ventricular (Fig 6.7) in origin Some people find these very distressing but others are entirely unaware of them, and they are an incidental finding Prolonged recording of ECGs of people who appear to be normal (usually medical students) reveals that ectopic beats are very common indeed

Table 6.1 Conditions associated with AF

Hypertension

Ischaemic heart disease (including

myocardial infarction)

Valvular heart disease (especially mitral)

Cardiomyopathies and myocarditis

Conduction system disease

Thoracic or cardiothoracic surgery

Congenital heart disease

Atrial masses

Pericarditis (rarely on its own)

Familial

Thyrotoxicosis Lung disease (e.g COPD, pulmonary embolism, fibrosing alveolitis) Neurological diseases

Idiopathic 2 (‘lone fibrillation’)

Figure 6.6 Sinus rhythm and sinus arrhythmia with four atrial premature (ectopic) beats 

(arrows). All the QRSs have the same LBBB morphology. The patient, an 80-year-old man with  urinary retention, was unaware of his irregular heart beat.

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Ask when the episodes are worst The usual pattern is for the palpitations to occur at rest and disappear on exertion This is because an increase in the sinus rate suppresses the ectopic focus and also because exercise is a distraction Consumption of large amounts of caffeine (a cup of coffee contains 150 mg of caffeine and a cup of tea about half that amount) may make the ectopic beats more frequent

It is not uncommon for people to go through periods of weeks or months when ectopic beats are frequent and then have them settle down, only to return years later Therefore, there may be a history of previous episodes Ask whether the attacks are bad enough to prevent sleep since this is one of the few indications for attempting treatment

Ventricular ectopic beats seem to be benign, except for those that occur in the weeks or months after a myocardial infarction (p 168) In these patients they indicate a somewhat increased risk of sudden death In some population­based studies, however, they may be a marker of increased risk of cardiovascular events generally.3 Frequent atrial ectopic beats may sometimes be a precursor of AF

Bradycardia

Occasionally patients may be aware of a slow pulse rate These are usually people who regularly count their pulse for sporting or introspective reasons A regular resting bradycardia (Fig 6.8) may be a normal variant, a sign of physical training (due to increased vagal tone), caused by beta­blockers or some calcium channel antagonists, or due to hypothyroidism In such cases the rhythm is sinus bradycardia

Patients with more severe bradycardia due to heart block are more likely to present with dizziness

or syncope than palpitations, but Möbitz type I (Fig 6.9) or even type II heart block is an occasional incidental finding in athletes or people on beta­blockers However, it is more often a sign of signifi­cant conduction system disease It can be a complication of myocardial infarction (p 168)

The examination

If the patient reveals that the usual palpitations are present at the time of the consultation, the opportunity must be seized to take the pulse at once (and if possible perform a 12­lead ECG) Certain arrhythmias may be diagnosed (fairly) confidently when the radial pulse is assessed

Figure 6.7 The same patient as in  Figure 6.2 : the frequent VEBs (ventricular ectopic beats)   (in bigeminy and trigeminy) (arrows) have the same morphology and axis as the VT in  Figure 6.2   The sinus rhythm is conducted with LBBB.

1 Premature ectopic beats (extra-systoles) After a number of normal pulses there is a miss fol­

lowed by a more forceful impulse (the next sinus beat, which is more forceful because there has been a longer diastolic filling period) Sometimes the extra­systole itself is palpable as a weak impulse detected earlier than expected The pauses may occur unpredictably or in a fixed ratio to sinus beats Occasionally second degree heart block (as in Fig 6.9) can cause

Figure 6.8 Sinus bradycardia (43/minute) with LAA in a 79-year-old woman on atenolol for  angina. The interpolated VEB (arrow) has no visible effect on the subsequent PR interval because 

of bradycardia. Note the evidence of old anterior and lateral infarctions with RAD and small  frontal plane voltage.

Figure 6.9 A 67-year-old man with 4:3 Wenckebach AV block, admitted for insertion of a  permanent pacemaker. The average rate here is 65/minute but was documented at 40/minute  during 2:1 block. Note the LAA (left atrial abnormality), commonly associated with both  

SA (sino-atrial) and AV (atrioventricular) nodal disease.

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a similar pattern, but here there are no palpable or audible extra­systoles If there is any doubt, listening to the heart will confirm the presence of heart sounds and thus a contrac­tion during the pause in the pulse, and exclude heart block as the cause (Fig 6.10)

2 Atrial fibrillation This common chronic or paroxysmal arrhythmia is characterised by a pulse

that is irregular in timing and amplitude The pulse may be fast, especially if the rhythm

is of recent onset and uncontrolled There is often a pulse deficit; that is, the heart rate as counted at the wrist is lower than that counted by listening to the heart sounds at the apex This is because some of the cardiac contractions occur after such a short diastolic filling period that the volume of blood ejected is insufficient to produce an impulse at the wrist

It may sometimes be difficult to distinguish AF from frequent ectopic beats

3 Supraventricular tachycardia and ventricular tachycardia These arrhythmias both cause a

rapid (often very rapid) pulse rate which may be difficult to count In most cases of VT there

is atrioventricular dissociation That is, the atria and ventricles contract independently This means that some ventricular contractions will occur at the same time as the atria contract This results in intermittent right atrial contraction against a closed tricuspid valve, and

therefore in intermittent cannon a waves These may be visible in the neck when the JVP is

assessed (p 257) It is said that in many cases of VT the heart sounds are of varying intensity because of changes in the relative timing of atrial contraction However, it is usually very difficult to distinguish VT and SVT clinically

4 Heart block and profound sinus bradycardia There may be obvious slowing of the pulse

permanently or intermittently in patients with dizziness or syncope The clinician who is fortunate enough to be present when a patient has a syncopal attack must feel the pulse at once The disappearance of the pulse during syncope followed by the return of consciousness and the pulse is characteristic of Stokes–Adams attacks These are syncopal episodes caused

by intermittent complete heart block or ventricular standstill—complete heart block with

no ventricular escape rhythm (Fig 6.11)

As a matter of routine, a cardiovascular and general examination (p 293) must be under­taken for patients with palpitations even if no symptoms are present There may be a rhythm disturbance even though no symptoms are present Otherwise an underlying cardiac abnormality (e.g mitral valve disease or AF) may suggest a cause for the palpitations (Table 6.2)

The above signs are not mutually exclusive

Figure 6.11 Ventricular standstill in an 80-year-old woman with aortic stenosis and episodes of  syncope previously ascribed to the valve disease. The asystole is associated with transient slowing 

of the sinus rate, suggesting a reflex mechanism.

presence of an intra­nodal accessory pathway This is called Lown–Ganong–Levine syndrome.4

Fibres close to, or within, the atrioventricular node bypass the normal slow conduction between the atria and ventricles and allow impulses to overtake the normal conduction The atrial impulse reaches the ventricles early and the PR interval is short During an episode of SVT one pathway conducts impulses anterogradely—that is, from the atria to the ventricles—and the other conducts impulses retrogradely This enables a circuit of electrical activity to cause atrial and then ventricular contraction independently of the sinus node and very fast (Fig 6.13).Sometimes the accessory pathway lies away from the AV node The ECG in these patients

shows a pattern called pre-excitation (Fig 6.14 and p 65) The abnormal electrical connection allows the impulse from the atrium to reach the ventricles early Because the fibre deposits the impulse in the ventricle away from the fibres of the His­Purkinje system, its passage through the ventricles is slower than the rival (normal) impulse spreading slowly through the AV node The normal impulse reaches the His­Purkinje fibres and then spreads rapidly within the ventricles The ECG reflects this The beginning of the QRS complexes is close to the P wave

Table 6.2 The examination of the patient with palpitations

1 Signs of thyrotoxicosis or lung disease (AF or sinus tachycardia can complicate these conditions)

2 Signs of cardiac failure (p 258) (VT and AF can complicate failure)

3 Signs of valvular heart disease (p 297) (AF can complicate mitral valve disease or

hypertrophic cardiomyopathy, and heart block and syncope can occur with severe aortic stenosis)

Figure 6.12 Sinus rhythm with a PR interval of 0.11 seconds in a 57-year-old woman with  recurrent SVT

Ion channelopathies

There are increasingly recognised inherited abnormalities of the cardiac ion channels that are associated with sudden death from ventricular arrhythmias These abnormalities mostly affect repolarisation About 5% of people resuscitated from VF or VT have a structurally normal heart and many have one of these conditions

SN

Atria

AVN Anterograde

Free wall pathway

Figure 6.14 The SVT circuit in WPW tachycardia

Long QT syndrome

The most common of the ion channelopathies is long QT syndrome A number of different mutations that affect the sub­units of sodium or potassium transport can be responsible These abnormalities lead to a prolongation of the recovery phase of the ECG (repolarisation) This creates a dispersion of electrical activity and the opportunity for re­entrant circuits to occur within the ventricle The typical rhythm disturbance that results is polymorphic VT

or torsade de pointes The three most frequent mutations—long QT 1, long QT 2 and long

QT 3—account for 90% of cases They are inherited in an autosomal dominant pattern The presentation of each type is different Patients with long QT 1 often have episodes of syncope

or documented VT during exercise (especially swimming) or when angry or emotional, whereas those with long QT 3 are more often affected during rest or sleep There is often a family history of sudden death

The rhythm may be difficult to confirm, even during an attack of tachycardia, but broad complex tachycardias should usually be considered due to VT (Fig 3.45 and p 76) unless there is good reason to suspect otherwise Some supraventricular tachycardias may be conducted with a bundle branch block pattern and appear wide, and since this is a much nicer diagnosis than VT

it is tempting to call these tachycardias SVT with aberrant conduction This temptation should

be resisted, particularly if the patient has any reason to be at risk of VT (a history of ischaemic heart disease or infarction, a history of cardiac failure or surgery for congenital heart disease)

Brugada syndrome

This condition results from a mutation that affects sodium channel function It is also of autoso­mal dominant inheritance Repolarisation is shortened in the epicardial layers of the heart This leads to a persistent ST elevation pattern in the right precordial leads (Fig 3.111 on p 110) Again, re­entrant circuits can occur between areas at different stages of repolarisation and lead to VT or

VF The risk of sudden death is high in some subgroups (e.g those with episodes of syncope)

Acquired long QT syndrome

Certain electrolyte disturbances, bradycardia, the use of anti­arrhythmic drugs or some combi­nation of these factors can prolong the QT interval These patients are at risk of sudden death

or syncope from polymorphic VT The mechanism seems to be related to inhibition of potas­sium channels Important anti­arrhythmic drugs with this risk include quinidine, flecainide and sotalol The risk is between 0.5% and about 5% It is higher during the first few weeks of treat­ment but can occur even after years of uneventful treatment Other drugs with QT prolongation effects include cisapride, some of the tricyclic antidepressants, non­sedating antihistamines and the phenothiazines It should be routine to repeat the ECG and remeasure the QT interval in patients who have begun treatment with these drugs

Ectopic beats

The presence of VEBs or AEBs (atrial ectopic beats) on the ECG is very common in asymp­tomatic patients but their association with the patient’s usual symptoms is most helpful in confirming the diagnosis

Atrial fibrillation

Recording AF on the ECG when a patient has symptoms is also most helpful The ventricular response rate must be noted since this may determine the need for drug treatment to slow it down If the ventricular response rate is already slow a more complicated problem such as sick sinus syndrome may be present

Heart block

First degree heart block (a prolonged PR interval) (Fig 3.9 on p 56) is not a cause of symptoms

It is often a harmless normal variant but can be a sign of intermittent higher degrees of heart block or be due to anti­arrhythmic drugs

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Second degree heart block—Möbitz type I (Fig 6.9) or Möbitz type II (Fig 6.15 and

p 56)—may cause the awareness of missed beats or be associated with dizziness or syncope It

is usually abnormal and can complicate inferior wall myocardial infarction It is sometimes a normal variant in athletes with high vagal tone

Third degree heart block (Figs 6.9 and 6.16) is usually associated with dizziness or syncope but if the ventricular escape rate is not very slow it may cause no symptoms Some patients complain more of tiredness or dyspnoea than dizziness Children with congenital complete heart block may be asymptomatic and require no treatment

Other investigations

Ambulatory (Holter) monitoring

The resting ECG is often frustratingly normal between episodes of palpitations If symptoms occur on most days and the diagnosis is not very obvious from the patient’s description (e.g occasional extra­systoles), a 24­hour Holter monitor should be arranged This small device

Figure 6.15 3:2 Möbitz type II AV block in an 85-year-old man with pre-syncope and a history of  remote myocardial infarction. All the PR intervals are the same. Note the associated RBBB and LAHB.

Figure 6.16 A lead 2 strip of a 71-year-old woman with complete AV block. The junctional  escape rhythm persists unchanged through sinus bradycardia with atrial ectopic beats, AF and  flutter. Pacemaker rhythm with 1:1 capture ends the strip. Note the short QT interval: this  patient, with sick sinus syndrome, was digoxin-toxic.

is able to record 24 hours of ECG The patient is given a diary to record the times of any symp­toms The tape can be used to print out a real­time (Fig 6.17(a)) or compressed version of the events (Fig 6.17(b)), or it can be scanned automatically to pick up abnormalities like pauses

or periods of bradycardia or tachycardia If an abnormality is found, it is important to ask the patient if typical symptoms occurred at that time If the recording shows normal sinus rhythm during a typical episode this is most reassuring Many palpitations are due to nothing more than the awareness of forceful normal beats

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It is more difficult to investigate patients whose symptoms are very infrequent If episodes are prolonged when they occur, arranging for an ECG recording during an attack is probably the best approach It may be useful to give the patient a letter directed to the accident and emergency department of the closest hospital, asking that an ECG be performed without too much delay if the patient presents with palpitations

If the symptoms suggest a potentially life­threatening arrhythmia, such as syncope preceded

by rapid palpitations in a patient with known ischaemic heart disease, further and more urgent investigations may be required It is probably appropriate to monitor such patients in a coro­nary care unit until the problem is resolved If episodes cannot be recorded or if self­limiting

or sustained VT is recorded, electrophysiological (EP) studies may be needed.

EP studies

This investigation involves the use of pacemaker­type cardiac catheters that are inserted into the heart through the femoral vein to reach the right atrium and ventricle, and sometimes through the femoral artery to reach the left ventricle These catheters can be used to measure intra­cardiac electrograms The conduction times of the various parts of the cardiac conduction system can be measured Slowing of conduction or recovery times after the conduction of impulses may suggest that conduction system disease is responsible for intermittent heart block and syncope.The catheters can also be used to stimulate the ventricle with trains of impulses These will induce VT in patients susceptible to this rhythm, and inability to induce VT with vari­ous established protocols of extra stimuli is reassuring Patients with inducible VT may then

be retested after treatment to ablate the focus of the arrhythmia (if there is one) Suppression

of the VT suggests a good prognosis Many ventricular arrhythmias are due to diffuse disease and are unsuitable for ablation treatment These patients may be candidates for an implanted cardioverter defibrillator (p 246)

EP studies are also used for patients with WPW who have symptoms, or for those who have had WPW found on a routine ECG and have a dangerous occupation Patients with WPW have an increased risk of developing AF Some of those who develop AF are at risk of sudden death because their accessory pathway is able to conduct impulses at a very rapid rate If AF develops, the refractory period of the accessory pathway may be short enough for extremely rapid ventricular rates to occur, and these can lead to the development of ventricular fibrilla­tion During EPS both the inducibility of AF and the refractory period of the accessory pathway can be measured It is also possible in many cases to ablate the pathway during the same study using radiofrequency energy

Treatment

Ectopic beats (PVCs and PACs)

Reassurance should be the mainstay of treatment for these annoying symptoms An explanation

to the patient of what is going on and reassurance about the symptoms’ benign and often self­limiting nature is often enough treatment Temporary or permanent reduction in caffeine intake may help, and the occasional patient may feel better after a course of magnesium supplements.Patients who are kept awake at night may be given a trial of treatment with beta­blockers if there are no contraindications to their use Other anti­arrhythmic agents such as class I drugs (e.g quinidine, flecainide) (Table 6.3) should be avoided if possible These drugs can have serious pro­arrhythmic effects and the patient has a small risk of developing new ventricular arrhythmias or even of sudden death because of treatment for a benign condition

The occurrence of frequent VEBs after an infarct is a more difficult problem These patients are at a small but increased risk of developing serious ventricular arrhythmias No particu­lar treatment has been shown specifically to reduce this risk but the use of beta­blockers in

post­infarct patients may help and should be routine Trials with drugs such as amiodarone have not been shown to confer definite benefit, but trials with class I drugs such as flecainide have shown an increased risk of sudden death for treated patients.5

SVT

If a patient presents with an episode of SVT, reversion should be attempted first using the Valsalva manoeuvre and then, as long as there are no carotid bruits, firm carotid sinus massage Press first on one side and then on the other The carotid artery is compressed with the thumb

or fore­ and middle fingers by pushing it back against the cervical spine Compression should

be at the point just below the angle of the jaw (Fig 6.18)

Less practical in adults but often useful for small children is stimulation of the diving reflex

by plunging the patient’s forehead into very cold water Testicular traction is equally effective but has failed to gain popularity as a treatment for SVT Eyeball pressure, even if tolerated, risks detaching the retina All these manoeuvres cause a temporary increase in vagal tone which may alter the refractory period of one of the pathways enough to terminate the rhythm

Failure of these methods means drug treatment is required Intravenous adenosine is the treatment of choice because of its very short half­life and absence of negative inotropic effects Adenosine attaches to receptors in the sinus and atrioventricular nodes where it causes interrup­tion or profound slowing of conduction This transient AV block will almost always interrupt the re­entrant circuit The drug is safe to use if there is some doubt about the diagnosis It will not harm patients who are really in AF, atrial flutter or VT Adenosine is given as a rapid bolus starting with 6 mg and increasing to 12 mg if reversion does not occur More than 90% of SVT cases will be reverted rapidly in this way The drug often causes a brief flush and feeling of severe malaise, and some patients are reluctant to use the drug a second time

The more traditional treatment for an episode is IV verapamil This drug has negative inotropic effects and can be dangerous if given for AF or for VT misdiagnosed as SVT.6 It should be given slowly (1 mg/minute) and the blood pressure checked after every 5 mg or so Pre­treatment with IV calcium may prevent hypotension.7 It may be worth repeating carotid sinus massage after every 5 mg Most SVT cases will revert with IV verapamil

The confirmed diagnosis of intermittent SVT is an indication for prophylactic treatment only if episodes are frequent enough to warrant daily drug treatment This choice should be the patient’s It should be explained to the patient that attacks of SVT, although very unpleasant, are

Table 6.3 The Vaughan Williams classification of anti-arrhythmic drugs

Class I

IA: quinidine, procainamide, disopyramide These drugs prolong the action potential by an

effect on the sodium channel.

IB: lignocaine, mexiletine These drugs predominately affect Purkinje fibre and ventricular

muscle action potential duration and the effective refractory period by sodium channel blockade.

IC: flecainide Flecainide prolongs conduction in all cardiac fibres again by sodium channel

Amiodarone, bretylium and sotalol (also has class II activity) These drugs prolong the

action potential and refractory period of cardiac fibres.

Class IV

Calcium channel antagonists These drugs all block the slow calcium channel.

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not life­threatening, and that an otherwise normal heart will tolerate many hours of tachycardia without harm Some patients with frequent attacks are able to terminate them rapidly with the Valsalva manoeuvre and are happy with this approach

If drug treatment is necessary, this is usually applied empirically It may be useful to begin with verapamil (160–240 mg/day) This is well tolerated The main side effect tends to be consti­pation Digoxin (125–250 μg/day) is also well tolerated and moderately successful in preventing attacks Beta­blockers (e.g atenolol 50 mg/day) can be used in those without contraindications Class IC drugs like flecainide (100–150 mg bd) are effective but considered second­line choices because of their pro­arrhythmic potential They are usually safe for patients without ischaemic heart disease or impaired left ventricular function

The availability and success of catheter ablation techniques for SVT have meant that the majority of patients with more than occasional attacks now have this curative treatment Most patients can be cured of their SVT with a single treatment requiring only a day in hospital Radiofrequency energy is used to make a tiny burn (1 mm in diameter) in the area of the acces­sory pathway The procedure still takes a number of hours but experience with the technique is leading to constant refinements and increases in success rates and speed

Problems with catheter ablation are uncommon but include damage to the AV node and the induction of heart block that needs permanent pacemaker insertion Very rarely, the cardiac wall may be perforated and cause cardiac tamponade

Ablation treatment is now a routinely accepted treatment for SVT Patients with WPW­type SVT who are symptomatic may be at risk of atrial fibrillation and sudden death and should

be encouraged to have ablation treatment The surface ECG returns to normal (delta wave disappears) in these patients after successful treatment

Prevention of VT is perhaps more difficult Evidence concerning the pro­arrhythmic effects

of anti­arrhythmic drugs has led to pessimism about their use In any event, except for patients with other severe medical problems or extreme old age, an attempt should be made to find the cause of the VT This means assessment of left ventricular function (usually by echocardiography) and investigations for ischaemic heart disease (exercise testing or coronary angiography) The presence of very poor LV function not only suggests a reason for the VT but also limits other treatment, such as the use of anti­arrhythmic drugs that reduce left ventricular contractility (which is most of them)

Patients found to have severe ischaemic heart disease and VT may benefit from revascularisa­tion, although there is no guarantee this will prevent attacks If there is a ventricular aneurysm and EP studies have shown this to be the source of the ventricular arrhythmias, resection of this and coronary artery surgery may be useful Occasionally patients with an infarct but no aneurysm can be shown to have VT originating from a small area around this scar and will benefit from catheter ablation of the focus

One approach to drug treatment is to use EPS­guided therapy The ability of a drug to pre­vent the induction of previously inducible VT suggests an improved prognosis with that drug The class I drugs (e.g flecainide, quinidine, disopyramide and procainamide) (Table 6.3) have

a high potential for pro­arrhythmia and should probably not be used without EPS guidance for VT In general, EPS­guided drug treatment has been used less frequently since cardioverter defibrillators became available

Sotalol, a class III drug with beta­blocker activity, has a somewhat lower pro­arrhythmic potential and may sometimes be used empirically Its use is often limited by its negative inotropic activity It cannot be used for patients with a poor left ventricular ejection fraction (a common problem for these patients)

Amiodarone, a class III drug with some beta­blocker activity, has a low but not zero potential for pro­arrhythmia It has very little negative inotropic effect and can be used empirically for patients considered too unwell for invasive investigations Some studies have suggested a slight improvement in prognosis (i.e reduced risk of death) for patients treated with amiodarone in this way The drug has many exotic and difficult side effects Its half­life is very long and when

it is used orally a loading dose (e.g 200 mg three times a day) must be given for several days before it becomes effective After that, the lowest possible dose should be used to reduce the risk of side effects (Table 6.4)

Drug treatment of ventricular arrhythmias has been very disappointing, even when guided by EPS,8 and is mostly used now as a back­up to an implanted cardioverter defibrillator (ICD)—that

is, to guide treatment to reduce the frequency of episodes that need to be treated by the device.Patients who have been resuscitated from VF clearly need aggressive treatment to prevent recurrence Their prognosis is relatively poor with drug treatment and they are now usually candidates for an ICD (p 246) Young patients with recurrent malignant arrhythmias and poor left ventricular function on the basis of either ischaemic heart disease or dilated cardiomyopathy may be candidates for a heart transplant as a solution to both problems

Patients with documented VF or hypotensive VT have an improved prognosis with an ICD, but it is not indicated for syncope of uncertain cause, for those with incessant VT or for those with a very limited life expectancy for other reasons

Patients with long QT or Brugada who are thought to be at high risk are candidates for an ICD

Outflow tract VT

There is another group of patients with a benign form of recurrent ventricular tachycardia The majority of these tachycardias have a left bundle branch block morphology (Fig 6.19) and arise from a small area in the right ventricular outflow tract (RVOT VT) A few have a right bundle branch block appearance and arise from within the left ventricle These arrhythmias appear very alarming and typically the patient has very frequent or incessant episodes Patients are usually only moderately symptomatic The VT often responds to treatment with verapamil and is also readily cured by catheter ablation

Acute AF: recent onset (< 48 hours)

Some patients may require no treatment An episode of AF in a young adult, especially if there has been a possible precipitating event such as a drinking binge, will usually be self­limiting Treatment during the attack need only be symptomatic Digoxin is probably the safest drug

Figure 6.19 Runs of RVOT tachycardia

Table 6.4 Important side effects of amiodarone

1 Skin sensitivity to sunlight This occurs in all patients and advice needs to be

given about skin protection to prevent sunburn.

2 Corneal deposits These also occur in all patients They are often

visible only to the ophthalmologist and do not usually interfere with vision They gradually disappear when the drug is withdrawn.

3 Amiodarone hepatitis This is uncommon but means regular checking

of liver function tests may be sensible The effect is usually reversible The risk seems dose-related.

4 Interference with thyroid function This is relatively common This is thought to

occur because the drug contains iodine Patients may become hypo- or hyperthyroid Sometimes,

if continued use of the drug seems essential,

it may be continued and the thyroid problem treated separately.

5 Pulmonary fibrosis This is the most feared complication of

amiodarone since it may be progressive, even when the drug is stopped It is very uncommon and said to be very rare at doses of 300 mg/day

or less.

6 Peripheral neuropathy This is also unusual at low doses.

to use for these patients It can be given orally in a loading dose of 500 μg followed by 250 μg six­hourly for two or three more doses Most patients will revert over 48 hours whether treated

or not, but digoxin helps to slow the ventricular response rate and makes the patient more comfortable Beta­blockers or non­dihydropyridine calcium antagonists (e.g verapamil) are

a reasonable alternative if not contraindicated Some authorities prefer anti­adrenergic drugs, since new­onset AF, like exercise­induced tachycardia in AF, may be associated with high adrenergic tone.9 In coronary care units, IV amiodarone is most commonly used for immedi­ate rate control

Chemical and electrical cardioversion

When spontaneous reversion is common, the effectiveness of drug treatment can be difficult

to judge The current ESC guidelines recommend flecainide (class I) or amiodarone (class IIa) Flecainide can be given as a single 300 mg oral dose; amiodarone needs to be given intravenously unless delayed cardioversion is acceptable Flecainide should not be used if there is a history of ischaemic heart disease or cardiac failure

Sotalol is commonly used for these patients but is not recommended Its intravenous use is particularly associated with the risk of precipitating acute heart failure

As a routine, an echocardiogram to exclude mitral valve disease or a cardiomyopathy is probably indicated on a non­urgent basis If spontaneous reversion occurs, it only remains for the clinician to warn against possible AF precipitants For most patients the risk of long­term medication may be greater than that of recurrent AF.10 There is probably, however,

an increased incidence of AF in the future for these patients, and drugs that help maintain sinus rhythm such as amiodarone should be considered for patients whose tolerance of AF

is poor

If reversion has not occurred within 48 hours a decision should be made about an attempt

at direct current (DC) cardioversion Under a very brief general anaesthetic or heavy sedation a shock synchronised to the R wave of the ECG and starting at about 150 joules is given Modern defibrillators administer biphasic shocks These are more effective than monophasic shocks The chances of success depend on the aetiology of the AF and its chronicity AF of very recent onset in patients with a structurally normal heart has a very high success rate However, the presence of a large left atrium (especially if larger than 50 mm) is associated with low initial and sustained success

This treatment is very safe and the only important precaution is to ensure the patient is not hypokalaemic Hypokalaemia, especially when the patient is on digoxin, is associated with a risk of induction of ventricular arrhythmias during cardioversion

If cardioversion is performed within about two days of the onset of AF, the risk of embolus from the left atrium or atrial appendage is minimal After about three days this risk begins to increase (up to 7% and usually within the first week after cardioversion) so that it is not safe

to perform cardioversion (electrical or chemical) until the patient has been anticoagulated with warfarin for four weeks This then needs to be continued for at least another four weeks afterwards

If more urgent cardioversion is desirable, a transoesophageal echocardiogram (TOE) can

be performed The patient should be begun on heparin and warfarin If no atrial or left atrial appendage thrombus is seen, cardioversion appears to be safe.11 The patient is then routinely anticoagulated for four or five weeks afterwards

Paroxysmal AF

For patients with confirmed paroxysmal AF, these episodes are often associated with intoler­able symptoms This may be the time to prevent disillusionment and explain to the patient that complete prevention of episodes of AF may be very difficult with drug treatment or may require the use of drugs with unacceptable side effects The patient can be reassured, however, that the heart rate can usually be controlled during episodes and that this will considerably reduce their unpleasantness