Maintaining vessel patencyMaintaining vessel patency::

Antiplatelet therapy:Antiplatelet therapy: Oral administration of 75-300 mg aspirin Oral administration of 75-300 mg aspirin daily improves survival (30% reduction in daily improves survival (30% reduction in mortality)mortality)The first tablet (300 mg) should be given The first tablet (300 mg) should be given orally within the first 12 hours and the orally within the first 12 hours and the therapy should be continuedtherapy should be continued indefinitely if indefinitely if there are no unwanted effects. there are no unwanted effects. In combination with aspirin, the early In combination with aspirin, the early (within 12 hours) use of clopidogrel 75 mg (within 12 hours) use of clopidogrel 75 mg daily confers a further 10% reduction in daily confers a further 10% reduction in mortality with no evidence of increased mortality with no evidence of increased adverse bleeding events. adverse bleeding events.

Anticoagulants: Anticoagulants: Subcutaneous heparin (12 500U twice Subcutaneous heparin (12 500U twice

daily), given in addition to oral aspirin, may daily), given in addition to oral aspirin, may prevent reinfarction after successful prevent reinfarction after successful thrombolysis and reduce the risk of thrombolysis and reduce the risk of thromboembolic complications.thromboembolic complications.

Intravenous heparin should be given for 48-Intravenous heparin should be given for 48-72 hours following thrombolysis.72 hours following thrombolysis.

A period of treatment with warfarin should A period of treatment with warfarin should be considered if there is: be considered if there is:

persistent atrial fibrillation persistent atrial fibrillation evidence of extensive anterior infarction, evidence of extensive anterior infarction, if echocardiography shows mobile mural if echocardiography shows mobile mural

thrombus, because these patients are at thrombus, because these patients are at increased risk of systemic increased risk of systemic thromboembolism. thromboembolism.

Adjunctive therapy Adjunctive therapy Beta-blockers: Intravenous β-blockers (e.g. Beta-blockers: Intravenous β-blockers (e.g.

atenolol 5-10 mg or metoprolol 5-15 mg atenolol 5-10 mg or metoprolol 5-15 mg given over 5 minutes) can:given over 5 minutes) can:

relieve pain.relieve pain. reduce arrhythmias and improve short-reduce arrhythmias and improve short-

term mortality in patients who present term mortality in patients who present within 12 hours of the onset of symptoms, within 12 hours of the onset of symptoms, but should be avoided if there is heart but should be avoided if there is heart failure, atrioventricular block or severe failure, atrioventricular block or severe bradycardia. bradycardia.

Chronic oral β-blocker therapy improves Chronic oral β-blocker therapy improves long-term survival and should be given to long-term survival and should be given to all patients who can tolerate it. all patients who can tolerate it.

Nitrates and other agents Nitrates and other agents Sublingual glyceryl trinitrate (300-500 μg) Sublingual glyceryl trinitrate (300-500 μg)

is a valuable first-aid measure in threatened is a valuable first-aid measure in threatened infarction, and intravenous nitrates infarction, and intravenous nitrates (nitroglycerin 0.6-1.2 mg/hour or isosorbide (nitroglycerin 0.6-1.2 mg/hour or isosorbide dinitrate 1-2 mg/hour) are dinitrate 1-2 mg/hour) are useful for the useful for the treatment of left ventricular failure and the treatment of left ventricular failure and the relief of recurrent or persistent ischaemic relief of recurrent or persistent ischaemic pain.pain. Large-scale trials have shown that Large-scale trials have shown that there is there is no evidence of a survival advantage no evidence of a survival advantage from the routine use of oral nitrate therapyfrom the routine use of oral nitrate therapy, , oral calcium antagonists or intravenous oral calcium antagonists or intravenous magnesium in patients with acute MI. magnesium in patients with acute MI.

COMPLICATIONS OF INFARCTIONCOMPLICATIONS OF INFARCTION: : ArrhythmiasArrhythmias::Ventricular fibrillationVentricular fibrillation Ventricular tachycardia Ventricular tachycardia Accelerated idioventricular rhythm Accelerated idioventricular rhythm Ventricular ectopics Ventricular ectopics Atrial fibrillation Atrial fibrillation Atrial tachycardia Atrial tachycardia Sinus bradycardia (particularly after inferior Sinus bradycardia (particularly after inferior

MI) MI) Heart blockHeart block

Pain relief, rest and the correction of hypokalaemia Pain relief, rest and the correction of hypokalaemia can all play a major role in the prevention of can all play a major role in the prevention of

arrhythmias.arrhythmias.

Ventricular fibrillation Ventricular fibrillation This occurs in about 5-10% of patients who This occurs in about 5-10% of patients who

reach hospital, and is thought to be the reach hospital, and is thought to be the major cause of death in those who die major cause of death in those who die before receiving medical attention.before receiving medical attention.

Prompt defibrillation will usually restore Prompt defibrillation will usually restore sinus rhythm. sinus rhythm.

Moreover, Moreover, the prognosis of patients with the prognosis of patients with early ventricular fibrillation (within the first early ventricular fibrillation (within the first 48 hours) who are successfully and 48 hours) who are successfully and promptly resuscitated in this way is promptly resuscitated in this way is identical to the prognosis of patients with identical to the prognosis of patients with acute MI that is not complicated by acute MI that is not complicated by ventricular fibrillation.ventricular fibrillation.

Atrial fibrillation Atrial fibrillation This is common, frequently transient and This is common, frequently transient and

may not require treatment.may not require treatment. However, if the arrhythmia causes a rapid However, if the arrhythmia causes a rapid

ventricular rate with severe hypotension or ventricular rate with severe hypotension or circulatory collapse, circulatory collapse, cardioversioncardioversion by means by means of an immediate synchronised DC shock of an immediate synchronised DC shock should be considered.should be considered.

In other situations, In other situations, digoxin or β-blockers digoxin or β-blockers are usually the treatment of choice.are usually the treatment of choice.

Atrial fibrillation (due to acute atrial Atrial fibrillation (due to acute atrial stretch) is often a feature of impending or stretch) is often a feature of impending or overt left ventricular failure, and therapy overt left ventricular failure, and therapy may be ineffective if heart failure is not may be ineffective if heart failure is not recognised and treated appropriately. recognised and treated appropriately. Anticoagulation may be required if AF Anticoagulation may be required if AF persists. persists.

Sinus bradycardiaSinus bradycardia This does not usually require treatment, This does not usually require treatment,

but if there is hypotension or but if there is hypotension or haemodynamic deterioration, haemodynamic deterioration, atropineatropine (0.6 (0.6 mg i.v.) may be given. mg i.v.) may be given.

Atrioventricular block Atrioventricular block Atrioventricular block Atrioventricular block complicating inferior infarction is usually complicating inferior infarction is usually temporary and often resolves following temporary and often resolves following thrombolytic therapy; it may also respond thrombolytic therapy; it may also respond to to atropine atropine (0.6 mg i.v. repeated as (0.6 mg i.v. repeated as necessary).necessary).

However, if there is clinical deterioration However, if there is clinical deterioration due to second-degree or complete due to second-degree or complete atrioventricular block, a atrioventricular block, a temporary temporary pacemakerpacemaker should be considered. should be considered.

Atrioventricular block complicating anterior Atrioventricular block complicating anterior infarction is more serious because asystole infarction is more serious because asystole may suddenly supervene; a prophylactic may suddenly supervene; a prophylactic temporary pacemaker should be inserted. temporary pacemaker should be inserted.

Ischaemia Ischaemia Post-infarct angina occurs in up to 50% of Post-infarct angina occurs in up to 50% of

patients. Most patients have a residual patients. Most patients have a residual stenosis in the infarct-related vessel stenosis in the infarct-related vessel despite successful thrombolysis, and this despite successful thrombolysis, and this may cause angina if there is still viable may cause angina if there is still viable myocardium downstream; nevertheless, myocardium downstream; nevertheless, there is no evidence that routine there is no evidence that routine angioplasty improves outcome after angioplasty improves outcome after thrombolysis.thrombolysis.

Patients who develop angina at rest or on Patients who develop angina at rest or on minimal exertion following MI should be minimal exertion following MI should be managed in the same way as patients with managed in the same way as patients with unstable angina who are thought to be at unstable angina who are thought to be at high risk. high risk.

Acute circulatory failure Acute circulatory failure Acute circulatory failure usually reflects extensive Acute circulatory failure usually reflects extensive

myocardial damage and indicates myocardial damage and indicates a bad prognosisa bad prognosis. . All the other complications of MI are more likely to All the other complications of MI are more likely to

occur when acute heart failure is present. occur when acute heart failure is present. PericarditisPericarditis: This may occur at any stage of the : This may occur at any stage of the

illness but is particularly common on the illness but is particularly common on the second and second and third days. third days.

The patient may recognize that a different pain has The patient may recognize that a different pain has developed even though it is at the same site, and developed even though it is at the same site, and that this pain is positional and tends to be worse or that this pain is positional and tends to be worse or is sometimes only present on inspiration. is sometimes only present on inspiration.

A pericardial rub may be audible.A pericardial rub may be audible. Non-steroidal and steroidal anti-inflammatory drugs Non-steroidal and steroidal anti-inflammatory drugs

should be avoided in the early recovery period as should be avoided in the early recovery period as they may increase the risk of aneurysm formation they may increase the risk of aneurysm formation and myocardial rupture. and myocardial rupture.

Opiate-based analgesia should be used. Opiate-based analgesia should be used.

The post-myocardial infarction syndrome The post-myocardial infarction syndrome (Dressler's (Dressler's syndrome)syndrome)

is characterized by persistent fever, pericarditis and is characterized by persistent fever, pericarditis and pleurisy, and is probably due to autoimmunity. pleurisy, and is probably due to autoimmunity.

The symptoms tend to occur a The symptoms tend to occur a few weeks or even few weeks or even months after the infarctmonths after the infarct and often subside after a and often subside after a few days; prolonged or severe symptoms may few days; prolonged or severe symptoms may require treatment with high-dose aspirin, an NSAID require treatment with high-dose aspirin, an NSAID or even corticosteroids. or even corticosteroids.

Mechanical complicationsMechanical complications Part of the necrotic muscle in a fresh infarct may Part of the necrotic muscle in a fresh infarct may

tear or rupture, with devastating consequences: tear or rupture, with devastating consequences: Papillary muscle damage may cause acute Papillary muscle damage may cause acute

pulmonary oedema and shock due to the sudden pulmonary oedema and shock due to the sudden onset of severe mitral regurgitation, which presents onset of severe mitral regurgitation, which presents with a pansystolic murmur and third heart sound.with a pansystolic murmur and third heart sound.

In the presence of severe valvular In the presence of severe valvular regurgitation, the murmur may be quiet or regurgitation, the murmur may be quiet or absent. The diagnosis can be confirmed by absent. The diagnosis can be confirmed by Doppler echocardiography, and emergency Doppler echocardiography, and emergency mitral valve replacement may be necessary. mitral valve replacement may be necessary.

Rupture of the interventricular septum Rupture of the interventricular septum This usually presents with sudden This usually presents with sudden

haemodynamic deterioration accompanied haemodynamic deterioration accompanied by a new loud pansystolic murmur radiating by a new loud pansystolic murmur radiating to the right sternal border, but may be to the right sternal border, but may be difficult to distinguish from acute mitral difficult to distinguish from acute mitral regurgitation. regurgitation.

However, patients with an acquired However, patients with an acquired ventricular septal defect tend to develop ventricular septal defect tend to develop rightright heart failure rather than pulmonary heart failure rather than pulmonary oedema oedema

Doppler echocardiography and right heart Doppler echocardiography and right heart catheterisation will confirm the diagnosis. catheterisation will confirm the diagnosis. Without prompt surgery, the condition is Without prompt surgery, the condition is usually fatal. usually fatal.

Rupture of the ventricle Rupture of the ventricle may lead to may lead to cardiac tamponade and is usually fatal.cardiac tamponade and is usually fatal.

Embolism: Embolism: Thrombus often forms on the endocardial Thrombus often forms on the endocardial

surface of freshly infarcted myocardium; surface of freshly infarcted myocardium; this may lead this may lead to systemic embolism to systemic embolism and and occasionally causes a stroke or ischaemic occasionally causes a stroke or ischaemic limb. limb.

Venous thrombosis and pulmonary Venous thrombosis and pulmonary embolism embolism may occur but have become less may occur but have become less common with the use of prophylactic common with the use of prophylactic anticoagulants and early mobilisation.anticoagulants and early mobilisation.

Impaired ventricular function: Impaired ventricular function: Acute transmural MI is often followed by Acute transmural MI is often followed by

thinning and stretching of the infarcted thinning and stretching of the infarcted segment (infarct expansion); this leads to segment (infarct expansion); this leads to an increase in wall stress with progressive an increase in wall stress with progressive dilatation and hypertrophy of the remaining dilatation and hypertrophy of the remaining ventricle (ventricular remodelling).ventricle (ventricular remodelling).

. As the ventricle dilates, it becomes less . As the ventricle dilates, it becomes less efficient and heart failure may supervene. efficient and heart failure may supervene. Infarct expansion occurs over a few days Infarct expansion occurs over a few days and weeks but ventricular remodelling may and weeks but ventricular remodelling may take years; heart failure may therefore take years; heart failure may therefore develop many years after acute MI. develop many years after acute MI. ACE ACE inhibitor inhibitor therapy reduces late ventricular therapy reduces late ventricular remodelling and can prevent the onset of remodelling and can prevent the onset of heart failure heart failure

A left ventricular aneurysmA left ventricular aneurysm develops in develops in approximately 10% of patients. Can lead to: approximately 10% of patients. Can lead to:

Heart failure.Heart failure. ventricular arrhythmias.ventricular arrhythmias. mural thrombus.mural thrombus. systemic embolism.systemic embolism. Other clinical features include a Other clinical features include a

paradoxical impulse on the chest wall. paradoxical impulse on the chest wall. persistent ST elevation on the ECG. persistent ST elevation on the ECG. An unusual bulge from the cardiac An unusual bulge from the cardiac

silhouette on the chest X-ray. silhouette on the chest X-ray. Echocardiography is usually diagnostic.Echocardiography is usually diagnostic. Surgical removal of a left ventricular Surgical removal of a left ventricular

aneurysm carries a high morbidity and aneurysm carries a high morbidity and mortality but is sometimes necessary.mortality but is sometimes necessary.

LATE MANAGEMENTLATE MANAGEMENT Patients who have survived an MI are at risk of further Patients who have survived an MI are at risk of further

ischemic events. ischemic events. management should therefore aim to identify those at management should therefore aim to identify those at

high risk and introduce effective secondary high risk and introduce effective secondary prevention . prevention .

Lifestyle modification :Lifestyle modification :Stop smoking Stop smoking Regular exercise Regular exercise Diet (weight control, lipid-lowering) Diet (weight control, lipid-lowering)

Secondary prevention drug therapy :Secondary prevention drug therapy :Antiplatelet therapy (aspirin and/or clopidogrel) Antiplatelet therapy (aspirin and/or clopidogrel) β-blocker β-blocker ACE inhibitor ACE inhibitor Statin Statin Additional therapy for control of diabetes and Additional therapy for control of diabetes and

hypertension hypertension

RehabilitationRehabilitation

If the exercise test is negative and the If the exercise test is negative and the patient has a good effort tolerance, the patient has a good effort tolerance, the outlook is good, with a 1-4% chance of an outlook is good, with a 1-4% chance of an adverse event in the next 12 months. adverse event in the next 12 months.

In contrast, patients with residual In contrast, patients with residual ischaemia in the form of chest pain or ECG ischaemia in the form of chest pain or ECG changes at low exercise levels are at high changes at low exercise levels are at high risk, with a 15-25% chance of suffering a risk, with a 15-25% chance of suffering a further ischaemic event in the next 12 further ischaemic event in the next 12 months. months.

Coronary angiography, with a view to Coronary angiography, with a view to angioplasty or bypass grafting, should angioplasty or bypass grafting, should therefore be considered in any patient with therefore be considered in any patient with spontaneous ischaemia, significant angina spontaneous ischaemia, significant angina on effort, or a strongly positive exercise on effort, or a strongly positive exercise tolerance testtolerance test

ArrhythmiasArrhythmias The presence of ventricular arrhythmias The presence of ventricular arrhythmias

during the convalescent phase of MI may be during the convalescent phase of MI may be a marker of poor ventricular function and a marker of poor ventricular function and may herald sudden death. Although may herald sudden death. Although empirical anti-arrhythmic treatment empirical anti-arrhythmic treatment appears to be of no value and even appears to be of no value and even hazardous, selected patients may benefit hazardous, selected patients may benefit from sophisticated electrophysiological from sophisticated electrophysiological testing and specific anti-arrhythmic therapy testing and specific anti-arrhythmic therapy (including implantable cardiac defibrillators,(including implantable cardiac defibrillators,

Secondary prevention Secondary prevention Smoking: The 5-year mortality of patients who continue to Smoking: The 5-year mortality of patients who continue to

smoke cigarettes is double that of those who quit smoking at smoke cigarettes is double that of those who quit smoking at the time of their infarct. the time of their infarct.

Hyperlipidaemia Hyperlipidaemia Lipids should be measured within 24 hours of presentation Lipids should be measured within 24 hours of presentation

because there is often a transient fall in blood cholesterol in because there is often a transient fall in blood cholesterol in the 3 months following infarctionthe 3 months following infarction

Dietary advice should be given but is often ineffective. HMG CoA Dietary advice should be given but is often ineffective. HMG CoA reductase enzyme inhibitors ('statins') can produce marked reductase enzyme inhibitors ('statins') can produce marked reductions in total (and LDL) cholesterol and have been shown reductions in total (and LDL) cholesterol and have been shown to reduce the subsequent risk of death, reinfarction, stroke to reduce the subsequent risk of death, reinfarction, stroke and the need for revascularisation.and the need for revascularisation.

Irrespective of serum cholesterol concentrations, Irrespective of serum cholesterol concentrations, all patients all patients should receive statin therapy after MI. should receive statin therapy after MI. Recent evidence Recent evidence suggests that patients with serum LDL cholesterol suggests that patients with serum LDL cholesterol concentrations greater than 3.2 mmol/l (∼120 mg/dl) benefit concentrations greater than 3.2 mmol/l (∼120 mg/dl) benefit from more intensive lipid-lowering (e.g. atorvastatin 80 mg from more intensive lipid-lowering (e.g. atorvastatin 80 mg daily).daily).

Other risk factorsOther risk factors Maintaining an ideal body weight, Maintaining an ideal body weight, taking regular exercise, taking regular exercise, and achieving good control of hypertension and and achieving good control of hypertension and

diabetes may all improve the long-term outlook.diabetes may all improve the long-term outlook. Mobilisation and rehabilitation.Mobilisation and rehabilitation. There is histological evidence that the necrotic There is histological evidence that the necrotic

muscle of an acute myocardial infarct takes 4-6 muscle of an acute myocardial infarct takes 4-6 weeks to become replaced with fibrous tissue, and it weeks to become replaced with fibrous tissue, and it is conventional to restrict physical activities during is conventional to restrict physical activities during this period. this period.

When there are no complications, the patient can sit When there are no complications, the patient can sit in a chair on the second day,in a chair on the second day,

walk to the toilet on the third day, walk to the toilet on the third day, return home in 5 days return home in 5 days and gradually increase activity with the aim of and gradually increase activity with the aim of

returning to work in 4-6 weeks. returning to work in 4-6 weeks. The majority of patients may resume driving after 4-The majority of patients may resume driving after 4-

6 weeks.6 weeks.

Drug therapy Drug therapy Aspirin and clopidogrel: Low-dose aspirin Aspirin and clopidogrel: Low-dose aspirin

therapy reduces the risk of further therapy reduces the risk of further infarction and other vascular events by infarction and other vascular events by approximately 25% and should be continued approximately 25% and should be continued indefinitely if there are no unwanted effects.indefinitely if there are no unwanted effects.

Clopidogrel should be given in combination Clopidogrel should be given in combination with aspirin for the first 4 weeks. with aspirin for the first 4 weeks.

If patients are intolerant of aspirin, If patients are intolerant of aspirin, clopidogrel is a suitable alternative.clopidogrel is a suitable alternative.

Beta-blockers Beta-blockers Continuous treatment with an oral Continuous treatment with an oral β-β-blocker blocker

has been shown to reduce long-term has been shown to reduce long-term mortality by approximately 25% among the mortality by approximately 25% among the survivors of acute MI. Unfortunately, a survivors of acute MI. Unfortunately, a significant minority of patients do not significant minority of patients do not tolerate β-blockers because of bradycardia, tolerate β-blockers because of bradycardia, atrioventricular block, hypotension or atrioventricular block, hypotension or asthma.asthma.

Patients with heart failure,Patients with heart failure, irreversible chronic obstructive pulmonary irreversible chronic obstructive pulmonary

diseasedisease or peripheral vascular disease derive similar or peripheral vascular disease derive similar

if not greater secondary preventative if not greater secondary preventative benefits from benefits from β-β-blocker therapy if they can blocker therapy if they can tolerate it, and should not be denied this tolerate it, and should not be denied this treatment. treatment.

ACE inhibitors:ACE inhibitors: Several clinical trials have shown that long-Several clinical trials have shown that long-

term treatment with an ACE inhibitor (e.g. term treatment with an ACE inhibitor (e.g. enalapril 10 mg 12-hourly or ramipril 2.5-5 enalapril 10 mg 12-hourly or ramipril 2.5-5 mg 12-hourly mg 12-hourly

can counteract ventricular remodelling, can counteract ventricular remodelling, prevent the onset of heart failure, prevent the onset of heart failure, improve survival and reduce hospitalisation. improve survival and reduce hospitalisation. The benefit of treatment is greatest in The benefit of treatment is greatest in

those with overt heart failure (clinical or those with overt heart failure (clinical or radiological)radiological)

but extends to patients with asymptomatic but extends to patients with asymptomatic LV dysfunction and those with preserved LV LV dysfunction and those with preserved LV function. function.

In patients intolerant of ACE inhibitor In patients intolerant of ACE inhibitor therapy, angiotensin receptor blockers (e.g. therapy, angiotensin receptor blockers (e.g. valsartan 40-160 mg daily or candesartan 4-valsartan 40-160 mg daily or candesartan 4-16 mg daily) are suitable alternatives and 16 mg daily) are suitable alternatives and are better tolerated. Patients with acute MI are better tolerated. Patients with acute MI complicated by heart failure and LV complicated by heart failure and LV dysfunction appear to benefit from dysfunction appear to benefit from additional aldosterone receptor antagonism additional aldosterone receptor antagonism (e.g. eplerenone 25-50 mg daily).(e.g. eplerenone 25-50 mg daily).

Device therapy : Implantable cardiac Device therapy : Implantable cardiac defibrillators are of benefit in preventing defibrillators are of benefit in preventing sudden cardiac death in patients who have sudden cardiac death in patients who have severe left ventricular impairment (ejection severe left ventricular impairment (ejection fraction ≤ 30%) after MI. fraction ≤ 30%) after MI.

PROGNOSIS: In almost one-quarter of all PROGNOSIS: In almost one-quarter of all cases of MI, death occurs within a few cases of MI, death occurs within a few minutes without medical care. minutes without medical care.

Half the deaths from MI occur within 24 Half the deaths from MI occur within 24 hours of the onset of symptomshours of the onset of symptoms

and about 40% of all affected patients die and about 40% of all affected patients die within the first month. within the first month.

The prognosis of those who survive to reach The prognosis of those who survive to reach hospital is much better, with a 28-day hospital is much better, with a 28-day survival of more than 80%.survival of more than 80%.

Early death is usually due to an arrhythmia Early death is usually due to an arrhythmia but later on the outcome is determined by but later on the outcome is determined by the extent of myocardial damage.the extent of myocardial damage.

Unfavourable features includeUnfavourable features include poor left ventricular function, poor left ventricular function, atrioventricular block atrioventricular block and persistent ventricular arrhythmias. and persistent ventricular arrhythmias. The prognosis is worse for anterior than for The prognosis is worse for anterior than for

inferior infarcts. Bundle branch block and inferior infarcts. Bundle branch block and high enzyme levels both indicate extensive high enzyme levels both indicate extensive myocardial damage. Old age, depression myocardial damage. Old age, depression and social isolation are also associated with and social isolation are also associated with a higher mortality. Of those who survive an a higher mortality. Of those who survive an acute attack, more than 80% live for a acute attack, more than 80% live for a further year, about 75% for 5 years, 50% for further year, about 75% for 5 years, 50% for 10 years and 25% for 20 years. 10 years and 25% for 20 years.

MYOCARDIAL INFARCTION IN OLD AGE:MYOCARDIAL INFARCTION IN OLD AGE:

Atypical presentation: often with anorexia, Atypical presentation: often with anorexia, fatigue or weakness rather than chest pain. fatigue or weakness rather than chest pain.

Case fatality: rises steeply. Hospital mortality Case fatality: rises steeply. Hospital mortality exceeds 25% in those over 75 years old, exceeds 25% in those over 75 years old, which is five times greater than that seen in which is five times greater than that seen in those aged less than 55 years. those aged less than 55 years.

Survival benefit of treatments: not influenced Survival benefit of treatments: not influenced by age. The absolute benefit of evidence-by age. The absolute benefit of evidence-based treatments may therefore be based treatments may therefore be greatest in older people. greatest in older people.

Hazards of treatments: rise with age (e.g. Hazards of treatments: rise with age (e.g. increased risk of intracerebral bleeding increased risk of intracerebral bleeding after thrombolysis) and is due partly to after thrombolysis) and is due partly to increased comorbidity. increased comorbidity.

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