Ischaemic Heart Disease

This typically presents as the tight or crushing central chest pain of angina or myocardial infarction. Less commonly, it presents as an arrhythmia or conduction defect, or heart failure.

Myocardial ischaemia is normally caused by atherosclerosis, but cardiac pain is also produced by:

• aortic dissection
  
• paroxysmal tachycardias
  
• severe anaemia, cardiomyopathy, coronary artery embolism and vasculitis – all rare causes.

Coronary Artery Disease

Examination of atherosclerotic plaques indicates an interaction between blood constituents and cellular elements of the arterial wall. Alteration of normal endothelial cell function may allow accumulation of macrophages, which form foam cells and provoke proliferation of smooth-muscle cells and connective tissue. Cholesterol crystals and other lipids accumulate at the base of plaques, which are covered by a fibrous cap. Plaque rupture leads to thrombosis.

Factors associated with coronary artery disease include:

• Sex: it is more common in men than women, particularly before the menopause.
  
• Age: there is a steady increase with age.
  
• Smoking: is a powerful risk factor for coronary heart disease (CHD). Cessation is associated with significant reduction in risk, which decreases by half after 1 year and approaches that of never-smokers after several years.
  
• Hypertension: the risk of coronary heart disease rises progressively with increasing blood pressure. Although most antihypertensive trials have shown a lower than expected reduction in risk, this may reflect the short duration of the trials.
  
• Obesity: central adiposity is a better marker for CHD risk than the overall level of obesity.
  
• Hyperlipidaemia: CHD is associated with raised total cholesterol and high ratio of total cholesterol:high-density lipoprotein (HDL) cholesterol. Hypertriglyceridaemia appears to be associated more with risk of myocardial infarction than coronary atherosclerosis, possibly because it affects coagulation.
  
• Diabetes mellitus: hyperlipidaemia in diabetics is a powerful risk factor. Men with diabetes have 2–3 times and women 4–5 times the background population risk of CHD.
  
• Alcohol: the association between CHD and alcohol is J-shaped – the lowest risk is associated with moderate alcohol intake.

Angina Pectoris

Diagnosis

The diagnosis of angina is clinical, based on the characteristic history:

• site: central chest
  
• character: usually tight, heavy, crushing
  
• radiation: to arms, epigastrium, jaw or back
  
• precipitation: by effort or emotion, particularly after meals or in the cold
  
• relief: within minutes by rest or sublingual or buccal glyceryl trinitrate.

There are no specific physical signs. A non-cardiac cause is favoured by continuation for several days, precipitation by changes in posture or deep breathing, the ability to continue normal activities, and lack of relief by rest. The more common alternatives in the differential diagnosis are oesophageal pain and musculoskeletal pain.

Unstable angina refers to:

• angina of effort of recent onset with no previous history
  
• increased frequency and/or severity of pre-existing angina
  
• angina at rest.

Investigation

Electrocardiogram

The electrocardiogram (ECG) is usually normal between attacks, but may show evidence of old myocardial infarction, T-wave flattening or inversion, bundle branch block or signs of left ventricular hypertrophy. ST segment depression is usually seen during attacks and may be provoked by exercise testing. A negative exercise test, in which there is no chest pain, no ST depression, no arrhythmia and no sustained fall in blood pressure, indicates a good prognosis. Radionuclide studies can be performed if the patient is physically unable to exercise. Images at rest are compared with images obtained after pharmacological stimulation of coronary flow to evaluate the presence of local ischaemia or infarction.

In unstable angina there is ST depression or T-wave change during typical anginal pain but without diagnostic elevation in cardiac enzymes. Nitrates can reverse ST segment elevation.

Coronary arteriography may provide unequivocal evidence of arterial narrowing and define its site to guide revascularisation procedures.

Management of Stable and Unstable Angina

Risk factors should be identified and advice given about stopping smoking, losing weight and taking regular exercise. Treat hypertension and hyperlipidaemia. Anaemia should be investigated and treated.

Sublingual glyceryl trinitrate remains the mainstay of symptomatic treatment. The major side effect is headache. It should be taken for pain, and prophylactically before known precipitating events. Long-acting nitrates such as isosorbide-5 mononitrate in a 60-mg sustained release formulation given once daily in the morning can give therapeutic plasma nitrate concentrations during the day, and allow a gradual fall during the night to prevent nitrate tolerance without a pre-dose rebound in angina. β-blockers reduce morbidity as well as control symptoms in stable angina. If necessary a dihydropyridine calcium-channel blocker such as amlodipine (not verapamil or diltiazem) can be added. If a β-blocker is contraindicated or not tolerated, diltiazem or verapamil can be used. Nicorandil, a potassium-channel activator, can also be beneficial. ACE inhibitors should be used in patients who also have left ventricular dysfunction or diabetes, unless there are contraindications. Low-dose aspirin (75 mg/day) reduces the risk of acute coronary events and myocardial infarction in patients with stable angina. Clopidogrel, an adenosine diphosphatase (ADP) receptor antagonist, may confer additional benefits but increases the risk of bleeding (see Trials Box 10.1). Diet and statins should be used to reduce LDL cholesterol with a target of < 2.0 mmol/l.

Trials Box 10.1 Anti-platelet and Anti-coagulant Agents in Ischaemic Heart Disease and Myocardial Infarction

The CHARISMA investigators randomly assigned 15,603 patients with either clinically evident cardiovascular disease or multiple risk factors to receive clopidogrel (75 mg/day) plus low-dose aspirin (75–162 mg/day) or placebo plus low-dose aspirin and followed them for a median of 28 months. Overall, clopidogrel plus aspirin was not significantly more effective than aspirin alone in reducing the rate of myocardial infarction, stroke or death from cardiovascular causes. There was a suggestion of benefit with clopidogrel treatment in patients with symptomatic atherothrombosis and a suggestion of harm in patients with multiple risk factors. (New England Journal of Medicine 2006; 354:1706–1717.)

The thrombolysis in myocardial infarction (TIMI) IIB trial randomised 3,910 patients with angina/non-Q-wave myocardial infarction to intravenous unfractionated heparin for ≥ 3 days followed by subcutaneous placebo injections or uninterrupted antithrombin therapy with enoxaparin during both the acute phase and outpatient phase. Enoxaparin was superior to unfractionated heparin for reducing a composite of death and serious cardiac ischaemic events without causing a significant increase in the rate of major haemorrhage. No further relative decrease in events occurred with outpatient enoxaparin treatment, but there was an increase in the rate of major haemorrhage. (Circulation 1999; 100: 1593–1601.)

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Patients with unstable angina (evidence of ongoing myocardial ischaemia without evidence of infarction) should be admitted to hospital and precipitating factors (e.g. anaemia, arrhythmia) identified and treated. Non-ST segment elevation myocardial infarction (NSTEMI) is a closely related condition in which there is sufficient myocardial damage to release a marker of cardiac injury such as troponin or the MB isoenzyme of creatine phosphokinase (creatine phosphokinase has two subunits, which are either B (brain) or M (muscle) types; CK-MB containing B and M subunits is found in cardiac muscle – page 77). Treatment involves bed rest with ECG monitoring whilst pain is ongoing, and escalation of anti-ischaemic therapy. This should include low-dose aspirin, intravenous unfractionated or subcutaneous low-molecular-weight heparin (see Trials Box 10.1) and sublingual nitroglycerin, followed by intravenous nitrates. β-blockade can be added if there is ongoing pain and no contraindication. If β-blockers are contraindicated a non-dihydropyridine calcium antagonist (e.g. verapamil or diltiazem) can be used in the absence of severe left ventricular dysfunction or other contraindications. An ACE inhibitor can be added if hypertension persists despite the above measures. Pain should be controlled with morphine if not relieved, and supplemental oxygen administered if needed to maintain SaO₂ > 90%.

Coronary Angiography and Revascularisation

Indications for coronary angiography differ between units, but angiography with a view to percutaneous coronary intervention or cardiopulmonary bypass surgery should be considered in all patients with evidence of recurrent ischaemia (angina or ST- segment changes at rest or with minimal activity) or a strongly positive stress test despite medical therapy.

Coronary revascularisation can be achieved by coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI) using catheter-borne devices (usually a balloon or laser) to open stenotic areas within coronary arteries (see Trials Box 10.2). CABG tends to be recommended in patients with three vessel disease, significant left main coronary artery disease or two vessel disease with significant proximal left anterior descending coronary artery disease and abnormal left ventricular function. PCI was initially only used for more proximal one vessel disease. Improved techniques, the advent of drug eluting stents and improved pharmacological therapies following PCI have reduced the risk of restenosis or occlusion, and PCI is now used in more complex situations. Patients should receive dual antiplatelet treatment with aspirin and clopidogrel following PCI with stent placement. The recommended duration of clopidogrel therapy depends on the type of stent.

Trials Box 10.2 Revascularisation for Coronary Artery Disease

The Bypass Angioplasty Revascularisation Investigation (BARI) investigators compared angioplasty with coronary artery bypass surgery as initial treatment in 1,829 patients with multivessel disease. Initial treatment by angioplasty did not compromise 5-year survival, although subsequent revascularisation was required more often than in patients treated by surgery in the first instance. In those with diabetes 5-year survival was better in patients treated initially by surgery. (New England Journal of Medicine 1996; 335: 217–225.) In an analysis of 10-year clinical outcomes there was no significant long-term disadvantage regarding mortality or myocardial infarction associated with an initial strategy of PTCA compared with CABG. Among patients with treated diabetes, CABG conferred long-term survival benefit, whereas the two initial strategies were equivalent regarding survival for patients without diabetes. (Journal of the American College of Cardiology 2007;49(15):1600–1606.)

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Myocardial Infarction

The size and location of the infarct depend on which artery is involved (Fig. 10.1) and the presence of any collateral supply. Occlusion of:

• left anterior descending affects the anterior wall of the left ventricle, and sometimes the septum
  
• right coronary artery involves the inferior part of the left ventricle, as well as part of the septum and right ventricle
  
• left circumflex involves the lateral or posterior walls of the left ventricle.

The infarct may extend from endocardium to epicardium (transmural) or involve only the subendocardial region.

Figure 10.1 Anatomy of the coronary arteries. Note that the right coronary artery supplies both the SA and AV nodes.

There may be a

• past history of hypertension, stroke, intermittent claudication, diabetes mellitus, hyperlipidaemia, smoking
  
• family history of cardiovascular disease, hyperlipidaemia.

Symptoms

• Pain: onset, duration (usually over 20 min), character (often tight or compressing), site and radiation (usually chest going to arms or neck). Associated sweating, breathlessness, nausea and vomiting are common. There may be a previous history of angina or myocardial infarction.

NB: Intensity is no guide to the extent of the infarct, especially in the elderly and in diabetics where pain may be absent. If there is interscapular pain associated with a ‘myocardial infarction’ syndrome, consider dissection of the thoracic aorta.

Examination

Once any distress has been alleviated by pain control there may be no signs. Examine:

• for associated diseases:

xanthelasmata and xanthomata of hyperlipidaemia

evidence of diabetes, thyroid disease, diabetes mellitus, gout, cigarette smoking (smell and finger staining)

• pulse for small volume (low cardiac output), arrhythmia
  
• blood pressure (hypotension usually indicates low cardiac output; hypertension may not be long-standing)
  
• jugular venous pressure (JVP) is usually normal – elevation suggests heart failure
  
• listen to heart for:

fourth heart sound (common); third heart sound if there is heart failure

pericardial friction rub

mitral regurgitation (papillary muscle dysfunction or ventricular dilatation)

ventricular septal defect (VSD) caused by a ruptured septum (rare)

• listen to lungs for basal crackles of heart failure.

Investigations

ECG (see p. 78 and Box 10.1)

Serial ECGs typically show ST segment elevation and T-wave inversion, with the development of Q waves indicating full-thickness myocardial necrosis. Changes occur in the anterior chest (V) leads in anterior myocardial infarction (Fig. 10.2) and in leads II, III and augmented voltage foot (AVF) in inferior myocardial infarction (Fig. 10.3).

Figure 10.2 Anterior myocardial infarction.

Figure 10.3 Inferior myocardial infarction.

Box 10.1 ECG Patterns in Common Clinical Conditions

Myocardial infarction

A characteristic pattern of ECG changes typically evolves:

• First few minutes – peaked T waves.
  
• First few hours – ST segment elevation, inversion of T waves, development of Q waves.
  
• After a few days the ST segment returns to normal (persistent elevation raises the possibility of left ventricular aneurysm).
  
• The T waves may eventually become upright, but in full thickness untreated myocardial infarction Q waves persist indefinitely.
  
• Rhythm abnormalities are common.
  
• Left bundle branch block (Fig. 10.8, p. 79) may occur at any stage, making further interpretation of the site, timing or extent of an infarct impossible.

Pulmonary embolism (Fig. 10.4)

Figure 10.4 Acute pulmonary embolism with S1, Q3, T3 pattern, a mean frontal QRS axis towards the right (+90°) and right ventricular (RV) strain pattern in leads V1–3.

• Tachycardia and transient arrhythmias (particularly AF).
  
• Right axis deviation.
  
• Right ventricular strain pattern – dominant R wave and inverted T waves in V1–4.
  
• RBBB.
  
• Occasionally S1, Q3, T3 pattern (S wave in lead I, Q and inverted T in III).

Ventricular hypertrophy

Large R waves occur over the appropriate ventricle in the chest leads (V1–2 for right ventricular hypertrophy and V5–6 for left ventricular hypertrophy). There tend to be large negative S waves in reciprocal leads (e.g. large S in V1 in left ventricular hypertrophy). A number of voltage criteria for left ventricular hypertrophy have been identified; for example, with normal QRS complexes if the sum of the S in V1 plus the R in V5 is greater than 35 mm, left ventricular hypertrophy is present on voltage criteria.

Digoxin

Sagging (reverse tick) ST segments, T-wave inversion.

Metabolic abnormalities

Hyperkalaemia (Fig. 10.5). Flattened P wave, broad QRS complex, peaked T wave.

Figure 10.5 Hyperkalaemia.

Hypokalaemia (Fig. 10.6). Prolonged PR, depressed ST, flattened T wave and prominent U wave.

Figure 10.6 Hypokalaemia.

Hypocalcaemia (Fig. 10.7). Prolonged QT interval.

Figure 10.7 Hypocalcaemia. Normal complexes apart from a prolonged QT_c (QT interval corrected for heart rate). Rate 95/min, QT 0.4, QT_c 0.5.

Bundle branch block

• The QRS complex is greater than 0.12 s.
  
• In left bundle branch block (LBBB) the complex is negative (V- or W-shaped) in V1 (Fig. 10.8). Causes include ischaemic heart disease, myocardial infarction, cardiomyopathy, hypertension and aortic stenosis.
  
• In right bundle branch block (RBBB) the complex is positive (M-shaped) in V1 (Fig. 10.9). In addition to occurring in conditions associated with LBBB, RBBB occurs in conditions that put a strain on the right ventricle (e.g. COPD, pulmonary embolism). RBBB can occur in an otherwise normal heart.

Figure 10.8 Left bundle branch block. RSR (M-shaped QRS complex) is visible in some of the left ventricular leads, I, AVL and V4–6, and notched QS complexes in the right ventricular leads, V1–2.

Figure 10.9 Right bundle branch block. RSR in the right ventricular leads V1–2 and slurred S waves in the left ventricular leads I, AVL and V4–6.

Fascicular block

There are three fascicles to the bundle of His: right, left anterior and left posterior. Block of one of the left bundles (unifascicular block) produces the following patterns with QRS complexes of normal width:

• In left anterior hemiblock there is left axis deviation.
  
• In left posterior hemiblock there is right axis deviation.

Sinoatrial disease (sick sinus syndrome)

This is a chronic disorder often associated with ischaemic heart disease in which sinus bradycardia and/or episodic sinus arrest can alternate with episodes of rapid supraventricular arrhythmia. Symptoms include dizziness, syncope, palpitations and dyspnoea. Permanent pacing may be necessary. Diagnosis is most easily made using 24-h ambulatory ECG monitoring.

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Sub-endocardial myocardial infarction leads to ST segment and T-wave changes, but not Q waves. A normal ECG does not exclude myocardial infarction. Posterior infarction is rare and does not produce Q waves, but gives a tall R wave in V1.

Right ventricular infarction is usually associated with inferior infarction, and produces ST elevation which can be detected if right ventricular leads (V3R and V4R) are recorded by placing chest electrodes on the right side of the chest in positions equivalent to V3 and V4.

Cardiac Biomarkers

Troponin T, from cardiac muscle breakdown, is cardiac specific and the marker of choice.

Creatine kinase (CK) is formed by dimerisation of two polypeptide chains, B and M, giving rise to three different isoenzymes. The predominant isoenzyme in skeletal muscle is MM, whereas in brain it is BB. Cardiac muscle contains both MM and MB, and the MB isoenzyme is used in diagnosis of myocardial infarction, although it is also elevated in skeletal muscle disease and by muscle trauma.

Management

Early mortality (within 4 weeks) is chiefly within the first 2 h and usually from ventricular fibrillation. Any patient suspected of having a myocardial infarction requires:

• pain relief – usually in the form of opiates plus antiemetics
  
• oxygen
  
• aspirin 300 mg to chew immediately
  
• nitrates should be administered for relief of ongoing ischaemic pain and can be used to control blood pressure and treat heart failure
  
• transfer to specialist facilities for reperfusion therapy.

Reperfusion Therapies

Shortening the time between recognition of symptoms and seeking medical help, and initiation of reperfusion treatment with thrombolysis or primary percutaneous coronary intervention is a key element of management (see Trials Box 10.3).

Trials Box 10.3 Myocardial Infarction

In the Comparison of Angioplasty and Prehospital Thrombolysis in Acute Myocardial Infarction study, 840 patients who presented within 6 h of acute myocardial infarction with ST-segment elevation were assigned to prehospital fibrinolysis (n = 419) with alteplase or primary angioplasty (n = 421) and all were transferred to a centre with access to emergency angioplasty. The median delay between onset of symptoms and treatment was 130 min in the prehospital-fibrinolysis group and 190 min (time to first balloon inflation) in the primary-angioplasty group. There was no difference in primary endpoint, which was a composite of death, non-fatal reinfarction and non-fatal disabling stroke at 30 days between the two groups. (Lancet 2002; 360(9336): 825–829.) Further analysis of the data indicated that prehospital thrombolysis may be preferable to primary PCI for patients treated within the first 2 h after symptom onset. (Circulation 2003; 108(23): 2851–2856.)

The PRAGUE-2 study randomised 850 patients with acute ST elevation myocardial infarction presenting within < 12 h to the nearest community hospital without a catheter laboratory to either thrombolysis in that hospital (TL group, n = 421) or immediate transport for primary percutaneous coronary intervention (PCI group, n = 429). The study showed that long-distance transport from a community hospital to a tertiary PCI centre in the acute phase of myocardial infarction was safe. The strategy markedly decreased mortality in patients presenting > 3 h after symptom onset. For patients presenting within < 3 h of symptoms, thrombolysis results were similar to those subjected to long-distance transport for PCI. (European Heart Journal 2003; 24(1): 94–104.) The early benefit from the PCI strategy over thrombolysis was sustained during 5 years’ follow-up. (European Heart Journal 2007; 28(6): 679–684.)

Immediate angioplasty was compared with standard therapy with rescue angioplasty after thrombolysis in the Combined Abciximab REteplase Stent Study in Acute Myocardial Infarction (CARESS-in-AMI). Immediate transfer for PCI improved outcome in high-risk patients with ST elevation myocardial infarction treated at a non-interventional centre with half-dose reteplase and abciximab. (Lancet 2008; 16(371): 559–568.)

Keeley et al. performed a meta-analysis of 23 trials, which together randomly assigned 7,739 thrombolytic-eligible patients with ST-segment elevation AMI to primary PTCA (n = 3,872) or thrombolytic therapy (n = 3,867). Primary PTCA was better than thrombolytic therapy at reducing overall short-term death, non-fatal reinfarction, stroke and the combined endpoint of death, non-fatal reinfarction and stroke. The results seen with primary PTCA remained better than those seen with thrombolytic therapy during long-term follow-up, and were independent of both the type of thrombolytic agent used and whether or not the patient was transferred for primary PTCA. (Lancet 2003;361(9351): 13–20.)

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Several studies in the late 1980s showed that intravenous streptokinase reduced mortality in patients reaching hospital with myocardial infarction from just over 10% to around 8%. ISIS-2 (Second International Study of Infarct Survival) showed that aspirin gives additional benefit, and subsequent trials showed that alteplase had similar effects.

Streptokinase 1,500,000 units is given by intravenous infusion over 1 h. It is cheaper than alternatives but can cause allergic reactions. Its potential for repeated use is limited by antibody formation. Alteplase (recombinant tissue plasminogen activator, rtPA) is not antigenic but is expensive. It is critically important to start thrombolysis within 12 h of myocardial infarction; additional benefit is obtained if started within 6 h.

Contraindications to thrombolysis are recent bleeding, severe hypertension (blood pressure > 200/120 mmHg), active peptic ulceration, recent stroke (within the last 2 months), proliferative diabetic retinopathy, severe liver or renal disease, pregnancy/lactation, bacterial endocarditis and acute pancreatitis.

Primary percutaneous coronary intervention (PCI) is the preferred treatment if it is rapidly available (Box 10.3). The European Society of Cardiology and the American College of Cardiology/American Heart Association Task Forces all recommend a target for the time from arrival in the emergency department to angioplasty (door-to-balloon time) of 90 min.

β-Blockade

ISIS-1 (First International Study of Infarct Survival) showed that intravenous β-blockade in the early stages of myocardial infarction may confer benefit, but is contraindicated if there is bradycardia, hypotension, heart failure, asthma, sick-sinus syndrome or heart block (second- or third-degree or bifascicular). Long-term β-blockade post-infarction is routine in the absence of contraindications.

Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE) inhibitors are beneficial, particularly in patients with anterior myocardial infarction, but their use may be limited by hypotension.

Anticoagulant and Antiplatelet Therapy

NICE Technology Appraisal 230 recommends the thrombin inhibitor bivalirudin in combination with aspirin and clopidogrel for the treatment of adults with ST-segment-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI).

Complications

• Heart failure (p. 88).
  
• Shock: the patient is hypotensive, pale, cold, sweaty and cyanosed. Arrhythmias are common. Treatment is with:

oxygen

diuretics if pulmonary oedema

vasodilators – ACE inhibitors (arterial and venous) or nitrates (venous) if blood pressure allows

inotropes – dopamine and dobutamine increase cardiac contractility by stimulating β₁-receptors in cardiac muscle. Low doses of dopamine (< 5 mcg/kg/min) induce vasodilatation and increase renal perfusion, whereas higher doses cause vasoconstriction and may exacerbate heart failure.

• Arrhythmias (see p. 84 and Table 10.1).
  
• Sinus tachycardia: usually requires no treatment.
  
• Supraventricular extrasystoles: common, but rarely requires treatment.
  
• Supraventricular tachycardia: arise from the atria or atrioventricular junction. Management depends on the nature of the tachycardia.
  
• Sinus or nodal bradycardia: may be caused by sedation, particularly with opiates. If the rate is < 50 beats/min and the patient is hypotensive, give atropine 0.6 mg intravenously and repeat twice if necessary. If unsuccessful, consider cardiac pacing.
  
• Heart block: all degrees of heart block are more serious if they complicate anterior rather than inferior infarcts.

first-degree: requires no therapy

second-degree: monitor and consider atropine. Many physicians would consider cardiac pacing for Mobitz type II with anterior infarcts (p. 88)

third-degree (complete heart block): atropine and isoprenaline may be helpful while awaiting cardiac pacing.

Table 10.1 Cardiac arrhythmias

NB: Complete heart block is more common in inferior myocardial infarctions because the atrioventricular nodal artery is a branch of the right coronary artery; complete heart block complicating anterior infarction is ominous because it implies a large muscle infarction.

• Ventricular tachycardia: this can respond to intravenous amiodarone, but proceed to direct current (DC) cardioversion without delay if no success or there is haemodynamic collapse.
  
• Ventricular fibrillation: this is frequently within 6 h of myocardial infarction (see Cardiorespiratory arrest, p. 88).
  
• Electromechanical dissociation (complexes on ECG with no pulse – see Cardiorespiratory arrest, p. 88).

Late Complications

Ventricular aneurysm can cause heart failure, angina, arrhythmias and emboli from thrombi within the aneurysm. There may be cardiac enlargement and abnormal cardiac pulsation (e.g. an impulse at the left sternal border). Its presence is suggested by ST-segment elevation persisting in convalescence. The aneurysm may be demonstrated by echocardiography, radionuclide studies or left ventriculography. Surgical removal is indicated for heart failure or arrhythmias. Anticoagulants reduce the risk of emboli.

Papillary muscle dysfunction or rupture may cause heart failure. There is a pansystolic or late sysytolic mitral regurgitant murmur. Echocardiography confirms the diagnosis. Surgery may be indicated.

Ruptured ventricular septum is rare. Urgent surgical repair may be required for severe heart failure.

Myocardial rupture leads to death from tamponade (unless immediate surgery is available). Dressler (post-myocardial infarction) syndrome occurs weeks or months after myocardial infarction or cardiac surgery. It is characterised by fever, pleurisy and pericarditis, and the presence of antibodies to heart muscle.

Invasive and Non-Invasive Assessment Post Myocardial Infarction

Patients with ongoing angina (or other evidence of ischaemia) at rest or on minimal exertion or left ventricular dysfunction should undergo coronary angiography to evaluate the need for coronary revascularisation. Patients in whom angiography is not planned should undergo exercise testing towards the end of the hospital admission or early after discharge to assess functional capacity and look for evidence of inducible ischaemia. Echocardiography should be performed to assess left ventricular function. Dipyridamole or adenosine stress myocardial perfusion imaging can be used in patients unable to exercise or if baseline abnormalities compromise ECG interpretation during exercise testing.

Rehabilitation

Cardiac rehabilitation programmes reinforce the importance of secondary prevention and promote adoption of a healthy lifestyle. Dietary education is given to achieve normal BMI and reduce dietary cholesterol and saturated fat. Active involvement in self-rehabilitation should be encouraged. The importance of stopping smoking must be stressed and strategies to help smokers used.

Patients should be encouraged to increase activity gradually over 1–2 months, when return to work can be considered. Patients should be advised about driving restrictions (p. 88).

Long-Term Pharmacological Treatments

Unless contraindicated, aspirin, β-blockade, angiotensin blockade and statins (Trials Box 10.4) should be started in all patients and continued indefinitely. Target LDL cholesterol should be less than 2.0 mmol/l.

Trials Box 10.4 Statins

The Incremental Decrease in Endpoints through Aggressive Lipid lowering (IDEAL) study enrolled 8,888 patients aged 80 years or younger with a history of acute MI: 4,439 patients were randomly assigned to receive a high dose of atorvastatin (80 mg/day) and 4,449 patients were randomised to usual-dose simvastatin (20 mg/day). During treatment, mean LDL cholesterol levels were 104 mg/dl in the simvastatin group and 81 mg/dl in the atorvastatin group. More intensive lowering of LDL cholesterol did not result in a significant reduction in the primary outcome of major coronary events, but did reduce the risk of other composite secondary endpoints and non-fatal acute MI. There were no differences in cardiovascular or all-cause mortality. (JAMA 2005; 294(19): 2437–2445.)

In the Treating to New Targets (TNT) study, 10,001 patients with coronary heart disease and LDL cholesterol levels of less than 3.4 mmol/l were randomly assigned to receive either 10 mg or 80 mg of atorvastatin per day. The mean LDL cholesterol levels were 2.0 mmol/l during treatment with 80 mg of atorvastatin, and 2.6 mmol/l during treatment with 10 mg of atorvastatin. There was an absolute reduction in the rate of major cardiovascular events of 2.2% and a 22% relative reduction in risk in patients receiving more intensive lipid-lowering therapy. This occurred with a greater incidence of elevated aminotransferase levels. (New England Journal of Medicine 2005; 352: 1425–1435.)

The Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction-22 (PROVE IT TIMI-22) study enrolled 4,162 patients who had been hospitalised for an acute coronary syndrome within the preceding 10 days and compared 40 mg of pravastatin daily (standard therapy) with 80 mg of atorvastatin daily (intensive therapy). The intensive lipid-lowering statin regimen provided greater protection against death or major cardiovascular events than the standard regimen. (New England Journal of Medicine 2004; 350: 1495–1504.)

The prospective studies collaboration performed a meta-analysis of 61 prospective observational studies consisting of almost 900,000 adults without previous disease and with baseline measurements of total cholesterol and blood pressure. During nearly 12 million person years at risk between the ages of 40 and 89 years, there were more than 55,000 vascular deaths (34,000 ischaemic heart disease, 12,000 stroke, 10,000 other); 1 mmol/l lower total cholesterol was associated with about a half, a third and a sixth lower ischaemic heart disease mortality in both sexes at ages 40–49, 50–69 and 70–89 years, respectively, with no apparent threshold. (Lancet 2007; 370: 1829–1839.)

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Arrhythmias

(See Table 10.1.)

Supraventricular Tachycardias

Supraventricular tachycardias arise from the atria or atrioventricular junction. QRS complex is normal unless there is also bundle branch block.

Sinus Tachycardia

In sinus tachycardia the rate is >100 beats/min. An underlying cause (anxiety, exercise, fever, anaemia, heart failure, thyrotoxicosis) can usually be identified.

Atrial Fibrillation

Atrial fibrillation (AF) is predominantly a disease of the elderly, occurring in 0.2% of men aged 47–56 and 3% of those aged 77–86 (Framingham study, 1949). Rheumatic AF occurs in association with rheumatic valve disease, whereas in non-rheumatic AF there is an underlying metabolic disorder or other form of cardiac disease. Lone AF occurs in the absence of valvular, myocardial or other identifiable disease. The common causes are:

• ischaemic heart disease
  
• thyrotoxicosis
  
• mitral valve disease
  
• cardiomyopathy.

Management

Check serum potassium, echocardiogram and thyroid function. The aims are to restore sinus rhythm or control the ventricular rate and minimise the risk of embolisation.

Direct current (DC) cardioversion can establish sinus rhythm in 90% of patients, but relapse is common. Long-term amiodarone reduces the frequency of relapse, although side effects can limit its use. Anticoagulant treatment is recommended for 3 weeks before and at least 4 weeks after successful cardioversion (see Box 10.2).

Box 10.2 Anti-thrombotic Therapy in Patients with Atrial Fibrillation, Including Paroxysmal Atrial Fibrillation, and Atrial Flutter

The American College of Chest Physicians Evidence-Based Clinical Practice Guidelines on antithrombotic therapy in atrial fibrillation (CHEST 2008; 133 (Suppl 6): 546S–592S) recommend long-term anticoagulation with warfarin (or other vitamin K antagonist) with an INR target of 2.5 (range 2.0–3.0) in patients with AF, including those with paroxysmal AF, who have had a prior ischaemic stroke, transient ischaemic attack (TIA) or systemic embolism, and in patients who have two or more of the following risk factors: age > 75 years, history of hypertension, diabetes mellitus, moderately or severely impaired left ventricular systolic function and/or heart failure. In patients with only one of these risk factors long-term antithrombotic therapy with either warfarin or aspirin at a dose of 75–325 mg/day is recommended, and in patients with none of these risk factors long-term aspirin therapy at a dose of 75–325 mg/day is recommended. Recommendations for patients with atrial flutter are similar, although the evidence base is less strong. Long-term anticoagulation with warfarin is also recommended for patients with AF and mitral stenosis, and with AF and prosthetic heart valves.

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NB Side effects of amiodarone are reversible corneal microdeposits, photosensitivity, skin discolouration, hypothyroidism, hyperthyroidism, diffuse pulmonary alveolitis and fibrosis, peripheral neuropathy and myopathy.

Medical Therapy

Quinine, flecainide and amiodarone have all been used to restore and maintain sinus rhythm. Digoxin does not restore sinus rhythm, but is effective in controlling the ventricular rate, either alone or in combination with β-blockers.

The incidence of ischaemic stroke (embolic or thrombotic) is increased in patients with AF, and anti-thrombotic treatment is recommended (Box 10.2 and Table 10.2).

Table 10.2 Summary of recommendations for antithrombotic therapy in atrial fibrillation

Atrial Flutter

The atria discharge at around 300/min, giving the characteristic ‘saw-tooth’ baseline on ECG (see Fig. 10.10). There is usually atrioventricular block, leading to a ventricular rate of 150/min (2 : 1) or 100/min (3 : 1). The rate is basically regular but is affected by 2 : 1, 3 : 1 and variable block. The causes are similar to AF, although atrial flutter is less common.

Figure 10.10 Atrial flutter with ‘saw-tooth’ atrial waves (arrows) and 4 : 1 block.

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