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Prevention of cardiovascular disease

Prevention of Cardiovascular Disease
See separate articlesand The revised Joint British Societies' (JBS 3) guidelines on prevention of cardiovascular disease (CVD) in clinicalpractice recommend that CVD prevention should focus equally on the following three groups of patients who areat high risk of CVD: [1] Apparently healthy individuals with 20% or greater risk over 10 years of developing symptomaticatherosclerotic disease.
People with diabetes mellitus (type 1 or 2).
People with established atherosclerotic CVD.
Cardiovascular risk calculation
Whenever risk factors are identified they should not be considered in isolation, but the 10-year CVD risk should
be calculated and used as the basis for recommendations to reduce the risk.
Risk assessment should include ethnicity, smoking habit history, family history of CVD and measurements ofweight, waist circumference, blood pressure, lipids (total cholesterol and high-density lipoprotein (HDL)cholesterol) and glucose. The American Heart Association (AHA) guidelines also recommend recording the pulserate and rhythm to screen for atrial fibrillation. [2] More recently the European Society of Cardiology (ESC) recommends a total CVD risk assessment using the
SCORE (= Systemic Coronary Risk Evaluation) project approach. [3] This consists of charts which provide a risk
assessment over a patient's lifetime, with different charts for high- and low-risk countries. This replaces the
notion of primary and secondary CVD prevention. For example, patients with CKD and no other cardiac risk
factors should be treated as very high-risk.
For further details see separate article.
The healthy individual[3]
The European Health Charter in 2007 made a public health announcement describing the healthy to have the
following characteristics:
No use of tobacco.
Physical activity - at least 30 minutes, five times a week.
Healthy eating.
Not overweight.
BP <140/90 mm Hg.
Total cholesterol <5 mmol/L.
Normal glucose metabolism.
Avoidance of stress.
Reduction of risk of developing CVD involves lifestyle modifications, drug treatment and effective management ofany overt underlying medical condition - eg, diabetes, hypertension, hyperlipidaemia. [2] [3] [4] Lifestyle modifications [3]
All patients with CVD can benefit from programmes to encourage behavioural change. [5] [3] However, greater
access for patients could be achieved through the automatic referral of all eligible patients to cardiac
rehabilitation; [6] hospital-based programmes are effective, and evidence suggests that patients who choose not
to access them can also benefit from home-based or community-based schemes. [7]
Consider setting up a disease register and systematic recall with a nurse-led secondary preventionclinic. Evidence supports their efficacy in the short term, but is lacking over a 10-year follow-up. [8] all patients should be actively discouraged from smoking - repeated briefsupportive advice, combined with nicotine replacement therapy when needed. [9] Passive smokingmay also increase risk but this remains contentious. [3] Keep total dietary intake of fat to a maximum of 30% of total energy intake, with intake of saturated fats10% or less of total fat intake and the intake of dietary cholesterol to less than 300 mg/day. Saturatedfats should be replaced with an increased intake of monounsaturated fats.
Consumption of fresh fruit and vegetables should be increased to at least five portions per day. AMediterranean diet has been shown to reduce mortality. Regular intake of fish (twice a week) and atleast one of those to be oily fish. [3]Limit the intake of salt to less than 100 mmol/L per day (less than 5 g of salt per day). [3] [10] Alcohol consumption should be limited to three units per day (21 units per week) for men and two unitsper day (14 units per week) for women.
Patients should be encouraged to exercise regularly: Exercise training has been shown to slow the progression or partially reverse the severity ofcoronary atherosclerosis.
Aerobic exercise can modify all the components of the metabolic syndrome with adecrease in blood pressure and triglycerides, increase in HDL, and an improvement ofinsulin sensitivity.
Overweight patients should be encouraged to lose weight through a combination of diet andexercise.
Maintain an ideal body weight for adults (body mass index 20-25 kg/m2) and avoid centralobesity (waist circumference in white Caucasians less than 102 cm (40 inches) in men andless than 88 cm (circa 34½ inches) in women); in Asians, the recommended targets areless than 90 cm (35 inches) in men and less than 80 cm (circa 31½ inches) in women.
Blood pressure management
See also separate article:
The optimal blood pressure target is less than 140 mm Hg systolic and less than 85 mm Hgdiastolic. [3] In selected higher-risk people (eg, established atherosclerotic disease, diabetes, and chronic kidneydisease) a lower blood pressure target of less than 130 mm Hg and less than 80 mm Hg may be moreappropriate. [11] Beta-blockers: Recommended for all people following myocardial infarction unless there are contra-indications.
Angiotensin-converting enzyme (ACE) inhibitors: Recommended for people with symptoms or signs of heart failure at the time of myocardialinfarction, or for those with persistent left ventricular systolic dysfunction (ejection fractionless than 40%) following infarction.
Should be considered for others with coronary artery disease, especially if the bloodpressure is not below the target of less than 130 mm Hg systolic and less than 80 mm Hgdiastolic.
An angiotensin-II receptor antagonist is an alternative to an ACE inhibitor if an ACE inhibitoris associated with side-effects.
An ACE inhibitor should be considered in combination with a thiazide diuretic in all peoplewith an established stroke, especially if the blood pressure is not below the target of lessthan 130 mm Hg systolic and less than 80 mm Hg diastolic.
Calcium-channel blockers (CCBs) and diuretics: These should be considered in all high-risk people if the blood pressure is not below thetarget (although purely as secondary prevention agents, CCBs are ineffective).
Lipid management
See also separate article
The optimal total cholesterol target is less than 4.0 mmol/L and low-density lipoprotein (LDL)cholesterol less than 2.0 mmol/L, or a 25% reduction in total cholesterol and a 30% reduction in LDLcholesterol, whichever gets the person to the lowest absolute value. [3] [4] Fasting lipids should be estimated at least eight weeks after an acute cardiovascular event and, ifnecessary, the dose of statin up-titrated to achieve the total and LDL cholesterol targets. HDLcholesterol and fasting triglycerides should be measured and considered at the same time.
Statins are recommended for: All high-risk people with established atherosclerotic disease.
In the following people with diabetes: All those who are aged 40 years or more with either type 1 or type 2 diabetes.
People aged 18-39 years with either type 1 or type 2 diabetes and who have atleast one of the following: Retinopathy (preproliferative, proliferative, maculopathy).
Nephropathy, including persistent microalbuminuria.
Poor glycaemic control (HbA1c greater than 9%).
Elevated blood pressure requiring antihypertensive therapy.
Raised total blood cholesterol (greater than 6.0 mmol/L).
Features of metabolic syndrome (central obesity and fastingtriglyceride greater than 1.7 mmol/L (non-fasting >2.0 mmol/L) and/orHDL cholesterol less than 1.0 mmol/L in men or less than 1.2 mmol/Lin women).
Family history of premature CVD in a first-degree relative.
Primary prevention for those who are at >10% risk of developing CVD. [4] There is a greater risk of developing muscle problems when the patient is also taking amlodipine ordiltiazem. [12] The dose of statin may need adjusting.
Other classes of lipid-lowering drugs (particularly fibrates, bile acid sequestrants, cholesterolabsorption inhibitors, nicotinic acid, omega-3 (n-3) fatty acids) should be considered in addition to astatin if the total and LDL cholesterol targets have not been achieved, or if there are other lipidabnormalities - eg, HDL cholesterol or triglycerides.
Blood glucose and diabetes
In all high-risk people the optimal fasting glucose is less than 6.0 mmol/L. [3]For people with impaired fasting glycaemia or impaired glucose tolerance: review annually to reassessglucose regulation and all other cardiovascular risk factors.
People with types 1 and 2 diabetes mellitus: rigorous control of glycaemia. The optimal target forglycaemic control in diabetes is a fasting or preprandial glucose value of 4.0-6.0 mmol/L and an HbA1cless than 6.5%.
Coronary or peripheral atherosclerosis: Aspirin 75 mg daily is recommended for life for all people with coronary or peripheralatherosclerotic disease. If aspirin is contra-indicated, or there are side-effects, thenclopidogrel is appropriate.
Results in primary prevention are inconclusive. [13] Recent studies have found that aspirindoubles the risk of gastrointestinal bleeding and current opinion is that this outweighs anybenefits which might be conferred in reducing the onset of CVD. [14]Anticoagulation should be considered for selected people at risk of systemic embolisationfrom large myocardial infarctions, heart failure, left ventricular aneurysm, or paroxysmaltachyarrhythmias.
Cerebral atherosclerotic disease (non-haemorrhagic): All people with a history of cerebral infarction, or transient ischaemic attack, and who are insinus rhythm, should take low-dose aspirin plus modified-release (MR) dipyridamole for twoyears following the initial event to prevent stroke recurrence as well as other vascularevents.
For those who have a further ischaemic cerebrovascular event while taking aspirin and MRdipyridamole, then changing aspirin for clopidogrel should be considered.
Anticoagulation with warfarin should be considered for all people with atrial fibrillation whoare at moderate (aged 60-75 years without additional risk factors) to high risk (over 75years, or over 60 years with other risk factors such as hypertension, diabetes, or leftventricular dysfunction) to reduce the risk of a further stroke.
If oral anticoagulation is contra-indicated, or cannot be tolerated, antiplatelet therapy shouldbe considered instead.
There is no evidence of benefit for anticoagulation in people with ischaemic stroke who arein sinus rhythm.
Amiodarone significantly reduces the risk of cardiac mortality after myocardial infarction in those withhigh risk of arrhythmic death. [15]Beta-blockers (see above) have a favourable interaction with amiodarone, with additional reduction inmortality (however, sotalol increases mortality after myocardial infarction in those with left ventriculardysfunction).
Surgery
After assessment with an exercise tolerance test, echocardiography, angiography, and scanning, the following
may be beneficial where appropriate:
Coronary artery bypass grafting: reduces mortality compared with medical treatment alone,particularly in those with poor left ventricular function.
Percutaneous transluminal coronary angioplasty (PTCA).
Intracoronary stent: particularly useful for restenosis after PTCA.
Atherectomy by various methods, and transmyocardial laser revascularisation are less commonprocedures used.
Psychosocial risk factors [3]
Increased CVD death and disability have been associated with:
Low socio-economic statusSocial isolationWork-related stressDepressionPanic attacks Some of these risk factors can be difficult to control for and require intervention at a government level.
Future aspects of CVD prevention [3]
Effective CVD prevention depends in part on accurate determination of risk. Risk determination is more difficult in
those who are asymptomatic. Newer aspects of risk determination include:
Biomarkers of CVD - eg, high-sensitivity C-reactive protein and homocysteine.
Imaging for atherosclerotic disease - this includes looking for plaques (eg, CT scan of the coronaryarteries looking at calcium levels and/or imaging the carotid artery intima-media thickness).
Further reading & references NICEPublic Health Guideline (June 2010) ; NICE CKS, December 2007 (UK access only) 1. ; JBS3, 20142. ; American Heart Association, 20093. ; European Society of Cardiology (2012)4. 5. Effect of tailored practice and patient care plans on secondary prevention of BMJ.
2009 Oct 29;339:b4220. doi: 10.1136/bmj.b4220.
6. British Heart Foundation7. ; Effectiveness of secondary prevention programmes in CHD. Lancet. 2009 May 16;373(9676):1671; author reply 1671.
8. Secondary prevention clinics for coronary heart disease: a 10-year follow-up of a Heart. 2008 Nov;94(11):1419-23. Epub 2008 Jan 15.
9. NICE CKS, December 2008 (UK access only) 10. ; Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials. BMJ. 2013 Apr 3;346:f1325. doi: 10.1136/bmj.f1325.
11. ; ESH/ESC Clinical Practice Guidelines, European Society of Cardiology (2013) 12. Medicines and Healthcare products Regulatory Agency (MHRA), October 201213. Aspirin in the primary and secondary prevention of vascular disease: Lancet. 2009 14. Don't use aspirin for primary prevention of cardiovascular disease. BMJ. 2010 Apr 21;340:c1805. doi: 10.1136/bmj.c1805.
15. ; Randomised trial of effect of amiodarone on mortality in patients with Lancet. 1997 Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical
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