Guidelines for the secondary prevention of ischaemic heart ...



Guidelines for the secondary prevention of ischaemic heart disease.

Introduction:

Preventative care in general practice is haphazard. A recent significant event audit in the practice identified less than optimal care of a patient following myocardial infarction. These guidelines have been produced in response to a recommendation of that meeting.

In the six years after myocardial infarction:

• 23% of men and 31% of women suffer a further MI.

• 41% of men and 34% women develop angina.

• About 20% patients are disabled by heart failure.

• 9% of men and 18% women have a stroke.

• 13% of men and 6% women die suddenly.

(Petrie and McMurray, 1998)

There is much strong evidence for the effectiveness of interventions following myocardial infarction:

Aspirin:

(Antiplatelet Trialists’ Collaboration, 1994)

Early administration of aspirin reduces mortality during the acute phase.

Evidence for long term benefit is derived from meta-analysis:

• 12% reduction in all cause mortality

• Reduction in vascular deaths from 9.4 to 8.1%.

• 31% risk reduction in nonfatal reinfarction.

• Risk reduction of 39% in non-fatal stroke.

• Risk reduction of 25% in any serious vascular death.

The higher the absolute risk the greater the gains for giving aspirin, therefore greatest benefits for patients with hypertension, diabetes and aged over 65.

18 patients with a 6% annual risk of coronary heart disease need to be treated for one year with aspirin to prevent one event.

Potential problems:

Aspirin increases the risk of GI bleed 1.5 to 3 fold. Use of 75mg daily in preference to higher doses can reduce the incidence of serious bleeding.

Conclusion:

Unless there are strong contraindications (allergy or GI bleeding) then aspirin should be prescribed to patients with ischaemic heart disease in a dose of 75mg daily.

Remember that patients paying for prescriptions can buy aspirin cheaply. If they are not receiving repeat prescriptions then for audit purposes it is important to record that they are taking the drug.

Beta-blockers:

Taking beta-blockers after myocardial infarction saves lives (reduction in all cause mortality and sudden death by up to 20%) and reduces the likelihood of non-fatal reinfarction. (Yusuf et al, 1988)

Once again, those with highest absolute risk; the elderly, those with left ventricular dysfunction or arrhythmias and diabetic patients benefit most from beta-blockers following myocardial infarction. These patients are often denied these drugs for spurious reasons. (Petrie and McMurray, 1998.)

Potential problems:

Heart failure/left ventricular dysfunction.

Beta-blockers should not be prescribed for patients with acute decompensated heart failure, but those with left ventricular dysfunction should not be denied beta-blockers. If necessary, a small dose of a short acting preparation can be tried initially.

Hypoglycaemia:

Beta-blockers do not increase the incidence of hypoglycaemia in insulin dependant diabetics. The particular benefit to diabetic patients requires that they should be given if at all possible following myocardial infarction.

Intermittent claudication:

Beta-blockers rarely exacerbate intermittent claudication and therefore should be prescribed if at all possible.

15 patients with a 6% annual risk of coronary heart disease need to be treated for one year with a beta-blocker to prevent one event.

The practice uses atenolol as the first choice beta-blocker; there is little evidence on particular dosage or type of drug. To prevent early morning re-infarction and sudden death a longer acting agent seems sensible.

Verapamil may be an alternative to a beta-blocker as routine prophylaxis, its greatest benefit being in patients without heart failure. (Petrie and McMurray, 1998)

Conclusion:

The majority of patients should be prescribed beta-blockers indefinitely following myocardial infarction. Contraindications are asthma and acute decompensated heart failure (until corrected). Consider verapamil if a beta-blocker cannot be prescribed.

ACE inhibitors:

(AIRE, 1993, Ambrosioni et al (SMILE), 1994, ISIS-4, 1995, Swedberg et al (CONSENSUS-II), 1992, GISSI-3, 1994, Pfeffer et al.(SAVE),1992).

ACE inhibitors reduce all cause mortality, the development of heart failure, myocardial re-infarction, sudden cardiac death and revascularisation procedures.

Short and long term trials have shown the largest benefits in patients with large infarcts, left ventricular dysfunction and heart failure.

A considerable proportion of asymptomatic patients with ventricular dysfunction who otherwise might be missed have much to gain from some form of post infarction screening. (The practice has open access to echo-cardiography for assessment of left ventricular function.)

Elderly patients have been shown to have the same relative risk reduction and therefore greater absolute risk reduction and should not be denied therapy.

Patients with a creatinine above 200mmols per litre or patients whose levels rise by 30-50% should not be given ACE inhibitors. Target doses table 1:

|Table 1: target doses of ACE inhibitors in large trials of patients post myocardial infarction. |

|SAVE / captopril |50mg 3 times daily |

|AIRE / ramipril |5mg twice daily |

|GISSI-3 / lisinopril |10mg once daily |

|ISIS-4 / captopril |50mg twice daily |

The practice uses enalapril and lisinopril usually.

Conclusion:

Patients with large infarcts and those with left ventricular dysfunction should be treated with an ACE inhibitor. Consideration should be given to echo-cardiography if it has not been done.

Cholesterol lowering drugs:

(4S, 1994, and Sacks et al (CARE),1996)

The first priority for lipid lowering therapy with a statin is patients who have had a myocardial infarction. Treatment is indicated when the cholesterol level is as low as 4.8 mmol/l (or low density Lipoprotein (LDL) as low as 3.2 mmol/l if measured.)

The second priority for lipid lowering therapy is patients with angina or other clinically overt atherosclerotic disease who have total cholesterol of 5.5 mmol/l or more (or LDL 3.7 mmol/l or more). (Includes peripheral vascular disease or symptomatic carotid disease or patients who have had a bypass graft or angioplasty.) these patients have a risk of major coronary events which averages approximately 3% per year.

Together these two priority groups encompass 4.8% of the population per year.

(Standing Medical Advisory Committee, 1997) – Their advice is summarised as:

1. Consider other methods of reducing the risk of coronary heart before prescribing statins.

2. Prescribe statins to those who have had a heart attack and have total cholesterol of 4.8 mmol/l or more, or have angina and total cholesterol of 5.5 mmol/l or more.

3. Treatment should be started at a low dose and increased as necessary to reduce total cholesterol to 5.0 mmol/l or by 20-25% in those high risk patients (e.g. with a previous MI) who have serum cholesterol below 6.3 mmol/l before starting treatment.

Statins reduce coronary heart disease mortality by 25%. Relative Risk for coronary heart disease mortality = 0.74 (95%CI: 0.66-0.83).

The very long term safety of statins has not been established.

Fibrates reduce coronary heart disease mortality much less: Relative Risk = 0.93 (95%CI: 0.85-1.01) (NHS Centre for Reviews and dissemination, 1998).

13 patients with an annual 6% risk of coronary heart disease would have to be treated with a statin to prevent one event.

Use simvastatin or pravastatin usually.

Blood pressure:

(Sever et al, 1993)

Systematic reviews of RCTs show that for people with high blood pressure, anti-hypertensive medication reduces the risk of all-cause mortality. The British Hypertensive Society advocates aggressive treatment of hypertension in patients with coronary heart disease. Consensus is based on attaining systolic BP below 160 and or diastolic below 90mmHg. Isolated systolic hypertension should definitely be treated.

Lifestyle Advice:

Lifestyle interventions are as important as drug interventions. They may be shown to diminish the need for drug intervention, (particularly lipid lowering).

Smoking:

Evidence for stopping smoking in both primary and secondary prevention is strong, (halving of mortality), Daly, 1983.

Around 2% of patients given nonsmoking advice in a single consultation stop smoking and do not relapse in one year. (Law and Tang, 1995). The use of nicotine gum increases the quit rate to 4% (95%CI 2-6%).

The effect of advice to stop smoking is much greater among those who have had a myocardial infarction with up to 36% stopping, resulting in a 30% reduction in mortality risk. (Burt et al, 1974)

10 patients with a 6% annual risk of coronary heart disease need to receive smoking advice to prevent one event.

Diet:

Dietary advice following MI demonstrates a greater fall in cholesterol than in population based trials, almost certainly due to patient motivation. This fall in blood cholesterol is not mirrored in meta-analysis by a significant coronary heart disease mortality reduction. (NHS Centre for Reviews and dissemination, 1998).

The generally poor performance of some lipid lowering diets may be partly explained by the substitution of complex carbohydrates for total fat, thus reducing both HDL and LDL cholesterol and leaving the LDL/HDL ratio unaffected. (NHS Centre for Reviews and dissemination, 1998).

A) Garlic Oats and Soy protein diets:

Trials severely flawed. No clinical endpoints, NO evidence of decreased CDH risk. (NHS Centre for Reviews and dissemination, 1998).

B) Oily Fish and Mediterranean diet:

1. Oily fish (and Maxepa): Decreased CV morbidity WITHOUT reducing blood Cholesterol Relative Risk = 0.65 (95%CI: 0.5-0.9)

2. Mediterranean diet: No effect on blood cholesterol and again reduced CV morbidity. Relative Risk = 0.25 (95% CI: 0.1-0.8). The most prominent change in the intervention group was an increase in consumption of alpha-linolenic acid from rapeseed margarine as participants found it difficult to consume high intakes of olive oil.

4 patients with 6% annual risk of coronary heart disease need to receive Mediterranean diet to prevent one event. The number needed to treat for oily fish diet is 9.

Weight loss:

Weight loss in obese patients reduces coronary risk both independently and by improving lipid concentrations, blood pressure and glucose tolerance. (Khatzel et al, 1995).

Exercise:

Exercise programmes have reduced death rates following myocardial infarction by 20%, (O’Connor et al, 1989). Many patients with coronary heart disease are afraid of exercise. Advice to promote exercise can improve survival.

Atrial fibrillation:

Non-rheumatic atrial fibrillation is an important risk factor for stroke, increasing the risk factor by five. It is particularly important in the elderly. This risk is largely reversed by anticoagulation, (Atrial Fibrillation Investigators,1994, European Atrial Fibrillation Trial Study Group, 1993). Patients should have atrial fibrillation confirmed by ECG and should be anticoagulated with warfarin aiming for an INR of 2.

Conclusions:

Virtually all patients in general practice with coronary heart disease have at least one aspect of medical management which would benefit from change and at least half have two, Campbell et al, 1998.

References:

Ambrosioni E. Borghi C. Magnani B (1994). Survival of myocardial infarction long term evaluation (SMILE) study; rationale, design, organisation and outcome definitions. Controlled Clinical Trials; 15: 201-10

Antiplatelet Trialists’ Collaboration, (1994) Collaborative overview of randomised trials of antiplatelet therapy. 1. Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ; 308: 81-106

Atrial Fibrillation Investigators (1994) Risk factors for stroke and efficacy of antithrombotic therapy in atrial fibrillation. Analysis of pooled data from five randomised controlled trials. Arch Intern Med; 154: 1449-57

Burt A. Thornley P. Illingworth D. White P. Shaw TR. Turner R (1974) Stopping smoking after myocardial infarction. Lancet; 1(7852):304-6, Feb 23.  

Campbell N, Thain J, Deans H, Ritchie L, and Rawles J. (1998) Secondary prevention in coronary heart disease: baseline survey of provision in general practice. BMJ; 316: 1430-4

European Atrial Fibrillation Trial Study Group, (1993) Secondary prevention in non-rheumatic atrial fibrillation after transient ischaemic attack or minor stroke. Lancet; 342:1255-62

NHS Centre for Reviews and Dissemination, University of York. (1998) Cholesterol and Coronary heart disease: screening and treatment. Effective Health care; 4(1): 1-15

Daly L, (1983) Long term effect on mortality of stopping smoking after unstable angina and myocardial infarction. BMJ; 287: 324-6

ISIS-4 Collaborative Group,(1995) A randomised factorial trial assessing early captopril, oral mononitrate, and intravenous magnesium sulphate in 58050 patients with suspected acute myocardial infarction. Lancet; 345: 990-5

Khatzel L, Bleecker E, Colman E, Rogus E, Sorkin J, Goldberg A, (1995) Effects of weight loss vs aerobic exercise training on risk factors for coronary disease in healthy obese, middle aged and older men. A randomized controlled trial. JAMA; 274: 1915-21

Law M, Tang J, (1995) An analysis of the effectiveness of interventions intended to kelp people stop smoking. Arch Int Med; 155:1933-41.

O’Connor G, Buring J, Yusuf S, Godhaber S, Olmstead E, (1989) An overview of randomised controlled trials of rehabilitation with exercise after myocardial infarction. Circulation; 80: 234-44

Petrie M, McMurray J, (1998) Secondary prevention of myocardial infarction. Prescriber; Vol 9, issue 9:75-88

Pfeffer MA. Braunwald E. Moye LA. Basta L. Brown EJ Jr. Cuddy TE. Davis BR. Geltman EM. Goldman S. Flaker GC. et al.(1992). Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Trial. NEJM; 327(10):669-77, Sep 3.

Sacks FM. Pfeffer MA. Moye LA. Rouleau JL. Rutherford JD. Cole TG. Brown L. Warnica JW. Arnold JM. Wun CC. Davis BR. Braunwald E. (1996) The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators (CARE). NEJM; 335(14):1001-9, Oct 3.  

Swedberg K, Held P, Kjekshus J, Rasmussen K, Ryden L and Wedel H, (1992) Effects of the early administration of enalapril on mortality in patients with acute myocardial infarction. Results of the Cooperative New Scadinavian Enalapril Survival Study II (CONSENSUS II). NEJM; 327(10): 678-84 Sep 3.

Scandinavian Simvastatin Study Group (1994) Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet; 344: 1383-89

Sever P, Beevers G, Bulpitt C, Lever A, Ramsay L, Reid J, (1993) Management guidelines in essential hypertension: report of the second working party of the British Hypertension Society. BMJ; 306: 983-7

Standing Medical Advisory Committee, (1997) The use of Statins. London: Department of Health, (11061 HCD Aug97(04))

The Acute Infarction Ramipril Efficacy (AIRE) Investigators (1993). Effects of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. Lancet; 342:821-8

Third Gruppo Italiano per lo Studio della Sopravvienza nell’infarcto Myocardio, (1994). GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singularly and together on six week mortality and ventricular function after acute myocardial infarction. Lancet; 343: 1115-22

Yusuf S, Wittes J, Friedman L, (1988) Overview of randomised clinical trials in heart disease. 1. Treatments following myocardial infarction. JAMA; 260: 2088-93

Guidelines produced by:

John Potter

Steve Holmes

Adrian Dunbar

Sheena McMain

Shirley Brierley

Simon Towers

Alison Evans

Consultation with:

Keith Collett, General Practitioner

Julien Clark, General Practitioner

Barry Clarson, General Practitioner

Tony Salisbury, General Practitioner

Rob Bain, Cardiologist

Sian Burton, Dietician

Sheila Popplewell, Health Visitor

Sharman Burchell, Practice Nurse

Barbara Rafiuddin, Practice Nurse

To be reviewed after one year or before if new scientific evidence or professional consensus.

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