Coronary heart disease Flashcards
When does CHD occur?
CHD occurs when the blood flow to the heart muscle is impeded by one of the following:
- atheroma
- thrombosis
- spasm of the coronary arteries
The main clinical manifestations of CHD
Angina and myocardial infarction
Define Angina pectoris
Medical term referring to chest pain caused by reduced blood flow to the heart muscle.
The ischaemia caused by the lack of blood flow and oxygen to the cardiac tissue results in this chest pain or ‘anginal’ pain.
Angina can broadly be divided in to two categories:
- Stable or chronic stable angina, and
- Unstable angina (which comes under the umbrella term ‘Acute Coronary Syndromes’)
Pathophysiology of angina
Angina occurs where there is myocardial ischaemia without any corresponding tissue necrosis.
Myocardial ischaemia occurs when the supply of oxygen to the heart cannot meet the demands of the heart muscle (or myocardium).
Under normal conditions, arterial oxygen saturation and myocardial oxygen demand are relatively constant and myocardial oxygen supply is in balance.
However, myocardial oxygen supply can be reduced if coronary blood flow is reduced, for example when the cross section of a coronary artery or the tone of a coronary artery is reduced. Atherosclerotic plaques can affect both of these.
Narrowed coronary arteries can upset the balance between arterial oxygen saturation and myocardial oxygen demand.
Management of stable angina
Stable angina is a chronic condition which has a lower incidence of acute coronary events, such as heart attack, and mortality. Management is aimed at the following:
The aims of the management of stable angina are to:
Preventing or limiting the symptoms b y reducing the number, severity and severity of the angina attacks.
Reducing the long term morbidity of the condition. This includes reducing the risk of progression of atherosclerosis.
Reducing the risk of mortality. This includes protecting against events such as unstable angina, myocardial infarction, cardiogenic shock and sudden death (NICE CG126).
Management options of stable angina will include:
- Lifestyle advice
- Drug therapy
- Revascularisation procedures
Lifestyle advice
Discussion should be undertaken with the patient regarding their needs in relation to activities, physical activity and exercise, diet and smoking cessation. Discussion should also involve the impact of stress, anxiety and depression which may have an effect on their angina.
Smoking cessation
Smoking still remains one of the most significant causes of preventable disease and early death in the UK. Giving up smoking is therefore one of the most important lifestyle changes a patient can undertake to prevent or limit heart disease and to improve their overall health. Pharmacists have a significant public health role to play in assisting patients to give up smoking.
Both non-pharmacological and pharmacological treatments are available. First-line pharmacological treatment available is nicotine replacement therapy (NRT) of which several formulations exist e.g. transdermal patches, chewing gum, inhalators, lozenges. Choice of treatment will depend on patient preference, previous treatments tried and success rate/s. Other interventions include the use of drugs such as bupropion and varenicline. E-cigarettes are another increasingly popular option to aid smoking cessation although they are not currently classed as licensed medicines.
Drug therapy
The initial drug therapy for the management of stable angina includes offering the patient one or two anti-anginal drugs as needed for regular treatment.
The patient should also be offered drug therapy for secondary prevention of cardiovascular disease.
A short acting nitrate is offered to prevent and treat angina episodes or attacks.
A suggested mnemonic for remembering key factors fundamental to management of angina is the ABCDE approach:
A Aspirin and anti-anginal drugs B Blood pressure lowering therapy C Cholesterol and smoking cessation D Diet and diabetes control E Education and exercise
Anti-anginal drug therapy is aimed at the following:
A reduction of cardiac afterload thereby decreasing oxygen demand on the heart
A reduction of blood pressure and heart rate, thereby decreasing oxygen demand on the heart
Dilation of coronary arteries, reducing preload thereby decreasing oxygen demand on the heart
A reduction in angina pain. [ The pain experienced by the patient increases sympathetic drive leading to an increase in blood pressure and heart rate. This increases the oxygen demand on the heart]
Percutaneous coronary intervention (also known as PCI)
This procedure was formerly known as ‘coronary angiography with stenting’. It involves inserting a catheter via the groin or arm and threading it through the blood vessels and into the coronary artery or arteries which have narrowing. A contrast dye is used to enhance visibility of the arteries and the catheter on the imaging screen which the surgeon then uses as a guide for the procedure. When the catheter tip is in place a balloon tip which is covered with a stent is inflated. This compresses the arterial plaque and expands the stent to widen the artery. Once the stent is in place and the plaque compressed the balloon tip is deflated and withdrawn. The purpose of the procedure is to open up the narrowed artery, restore blood flow and improve symptoms of chest pain and breathlessness.
Coronary artery bypass grafting (CABG)
This is a surgical procedure in which a healthy artery is taken from another part of the body, usually chest, leg or arm, and is attached above and below the narrowed part of the diseased coronary artery. One or more grafts may be needed depending on how many diseased arteries there are and the severity. It is a significant procedure lasting several hours and requires the patient to remain in hospital for several days afterwards. patients usually experience significant improvement in their chest pain symptoms and breathlessness however lifestyle improvements should still be the mainstay of recovery and future health.
Acute coronary syndromes - definition and classification
Acute coronary syndromes, also known as ACS, occur when the blood supply to the myocardium suddenly becomes blocked. ACS tend to have a high associated morbidity and mortality. The spectrum of acute coronary syndromes has a common causality, namely, a sudden reduction in blood flow to part of the heart muscle (or myocardium).
ACS is an umbrella term and includes the following:
- Unstable angina
- Non-ST elevation myocardial infarction (known as an NSTEMI)
- ST elevation myocardial infarction (known as a STEMI)
The term ‘ST’ refers to
The term ‘ST’ refers to the ST segment in the section of an ECG trace. It is a key marker in the determination that myocardial ischaemia / infarction has taken place. Click on the link below for an explanation of the ST segment.
Acute Coronary Syndromes - pathophysiology
Myocardial necrosis (cardiac cell death), which occurs during a STEMI or an NSTEMI results in the release of intracellular proteins. For diagnostic purposes the troponins (I and T) are used as a marker of cardiac cell death. In a STEMI a large part of the myocardium is affected possibly involving the full thickness of the ventricular wall. The tissue necrosis is often a result of prolonged myocardial ischaemia. NICE states that nearly half of salvageable myocardium is lost within an hour of occlusion of the coronary artery and two thirds lost within 3 hours.
In an NSTEMI there is often incomplete or temporary occlusion of the coronary blood vessel/s and so the degree of ischaemia and myocardial necrosis may be less. It is usually limited to cardiac tissue surrounding the smaller distal blood vessels.
In unstable angina the coronary obstruction is limited in its extent and time of exposure. This is still enough to cause ischaemia and the symptoms thereof but there is usually no detectable myocardial necrosis present.
Unlike stable angina, the symptoms of unstable angina can come on very suddenly, become more frequent, prolonged and severe, and/or may occur at rest.
Risk factors for ACS include
Non modifiable
- Increasing age
- Male gender
- Family history
- Ethnicity
Modifiable
- Smoking / tobacco use
- Diet
- High cholesterol
- Low daily consumption of fruit and vegetables - Hypertension
- Physical inactivity
- Obesity
- Stress
- Alcohol intake
ACS has a common set of clinical symptoms, not all of which are present in each affected patient. These include:
- Crushing pain which originates at chest, radiates to neck, jaw and/or left arm
- Nausea and vomiting
- Sweating
- Shortness of breath
Management of ACS
Before any diagnosis can be made prompt stabilisation and management of the symptoms are needed.
In nearly 25% of acute myocardial infarction cases death will occur before reaching hospital however this can be preveneteed by rapid access to a defribillator (BMJ, 2015). If medical help does arrive in time, typically the following drugs are used to stabilise the patient:
♥ Morphine or diamorphine intravenously. To treat the pain and also relax the patient.
♥ Anti-emetic e.g. prochlorperazine. To prevent nausea and vomiting which may also be caused by the opioid drug.
♥ Oxygen (only if oxygen saturation levels in the blood are below 94% as per NICE guidance).
♥ Sublingual glyceryl trinitrite (GTN). Used as a vasodilator to decrease heart rate, decrease stress and oxygen demand on the myocardium.
♥ Aspirin 300 mg chewable tablet. Prevents further platelet aggregation and extension of the existing thrombus.
Diagnostics should include:
- Resting 12 lead ECG, a first priority
- Physical examination including pulse, blood pressure and signs of complications e.g. pulmonary oedema.
- Detailed clinical history including cardiovascular history and previous treatments
- Pain characteristics and onset
- Determination of cardiovascular risk factors
What does NICE recommend for ACS
NICE recommends the use of high sensitivity (hs) troponin testing for patients presenting with suspected ACS. The first blood sample is taken on initial assessment in the hospital’s emergency department. A second blood sample is taken 3 hours later. Determination of a positive sample ( a result which is above the lower limit of detection of troponin) can support a diagnosis of ACS (NSTEMI or STEMI).
Clinical assessment should also be used to confirm the diagnosis since troponin levels can be raised in other conditions, for example, in pulmonary embolism.
Continued monitoring is required such as BP, pulse, ECG monitoring, oxygen saturation using pulse oximetry and checking that pain relief is effective.
Assessment and treatment algorithm: ACS
Diagnosis of the presenting ACS must initially be made and the appropriate treatment strategy applied as indicated below.
Risk tools such as the TIMI risk score tool are used to estimate mortality risk for patients with ischaemic pain and suspected unstable angina or NSTEMI. The tool stratifies patients according to a scoring system with higher scores indicating a higher risk patient who may require more aggressive medical or procedural interventional.
[Newer chest pain risk scores such as the Heart Score have shown better ability to stratify patients according to severity or mortality risk]
Management of a STEMI (ST elevation myocardial infarction)
The aim of treatment in the case of a STEMI is to reperfuse the occluded blood vessels/ supplying the myocardium as soon as possible. This can be done either by thrombolysis or physical intervention.
The most effective way to reperfuse the heart is through primary angioplasty. This involves inserting a fine wire into the coronary artery which positions a catheter with a balloon tip at the site of the occlusion. The balloon is then inflated to 10-20 times atmospheric pressure which forces the atheroma back into the blood vessel wall and opens the lumen. The balloon is surrounded by a wire meshwork known as a stent which when inflated prevents collapse of the vessel wall.
The process of angioplasty and stent insertion is known as ‘percutaneous coronary intervention’ or PCI (see previous note on PCI).
Thrombolytic (fibrinolytic) agents
There are several thrombolytic agents available for the treatment of STEMI. These include streptokinase and the tissue plasminogen activators (tPAs) such as alteplase, reteplase and tenecteplase. Choice of thrombolytic may vary depending on local policy however tPAs are generally preferred to streptokinase. This is due to streptokinase’s lack of fibrin specificity (see link to the pharmacology above) and its antigenicity. Patients can produce antibodies to streptokinase after first administration thereby reducing the drug’s potency if it should ever be administered for the second time to the same patient.
NSTEMI (Non-ST elevation myocardial infarction) and unstable angina - management
The initial stabilisation therapy for patients presenting with NSTEMI and unstable angina is the same as for STEMI.
Patients who are considered to have a high mortality risk should be considered for PCI, but thrombolysis is never indicated for NSTEMI or unstable angina.
Unfractionated heparin or low molecular weight heparin along with antiplatelet therapy is indicated instead.
As an example of antiplatelet therapy, aspirin and clopidogrel and aspirin both at 75 mg daily, are given for 12 months only. Typically, a loading dose of 300 mg of each drug is given on presentation.
Further management of ACS
Once an episode of ACS has been treated, the risk of a second episode should be carried out before risk management strategies, interventional treatments and rehabilitation starts.
Assessing risk is known formally as risk stratification. There are several scoring systems available however NICE CG94 recommends the use of an established risk scoring system such as the Global Registry of Acute Cardiac Events (GRACE) tool which predicts 6-month mortality. The GRACE tool predicts the 6 month mortaility risk for the patient following their myocardial infarction.
The risk score obtained from GRACE ACS risk and mortality indicator tool is based upon the following:
Age Heart rate Systolic blood pressure Serum creatinine (renal function) The presence of congestive heart failure ST segment deviation on the ECG Cardiac arrest at admission Abnormal cardiac enzymes (e.g. elevated troponins)
The GRACE risk stratification tool
The risk is calculated as a predicted 6-month mortality score as shown below.
Predicted 6-month mortality
Risk of future adverse CV events
< 1.5%
Lowest
> 1.5 – 3.0%
Low
> 3.0 – 6.0%
Intermediate
> 6.0 – 9.0%
High
> 9.0%
Very high
ECG findings Unstable angina (UA)
May be normal or may show ST depression or T wave inversion.
ECG findings - NSTEMI
ST depression or deep T wave inversion
ECG findings - STEMI
ST segment elevation
Raised Troponin levels? Unstable angina (UA)
No
Raised Troponin levels? - NSTEMI
+
Raised Troponin levels? - STEMI
++
Occlusion of a coronary artery Unstable angina (UA)
No
Occlusion of a coronary artery - NSTEMI
Likely partial
Occlusion of a coronary artery -STEMI
Full occlusion
Myocardial necrosis (myocyte cell death) - Unstable angina (UA)
No
Myocardial necrosis (myocyte cell death) -NSTEMI
Yes
Myocardial necrosis (myocyte cell death) -STEMI
Yes
Mortality risk -Unstable angina (UA)
Low compared with NSTEMI & STEMI
Mortality risk -NSTEMI
Potentially High
Requires risk stratification.
Mortality risk - STEMI
High
Secondary prevention of myocardial infarction
- Physical activity
- Diet
- Safe alcohol limits
- Smoking cessation
- Weight management
- Drug treatment for secondary prevention
All patients who have had an acute myocardial infarction should be offered the following combination of drugs:
- ACE inhibitors (or ARB if intolerant of ACE inhibitors)
- Dual antiplatelet therapy consisting of aspirin and a second antiplatelet drug
- Beta blocker
- Statin
ACE inhibitors and beta blockers should be titrated carefully to their target doses with close monitoring. Refer to the BNF for further information.
Determine whether the chest pain may be cardiac and therefore whether this guideline is relevant, by considering
the history of the chest pain
the presence of cardiovascular risk factors
history of ischaemic heart disease and any previous treatment
previous investigations for chest pain
Initially assess people for any of the following symptoms, which may indicate an ACS
pain in the chest and/or other areas (for example, the arms, back or jaw) lasting longer than 15 minutes
chest pain associated with nausea and vomiting, marked sweating, breathlessness, or particularly a combination of these
chest pain associated with haemodynamic instability
new onset chest pain, or abrupt deterioration in previously stable angina, with recurrent chest pain occurring frequently and with little or no exertion, and with episodes often lasting longer than 15 minutes
Immediate management of a suspected acute coronary syndrome
GTN
300mg aspirin
Preventing and treating episodes of angina
Offer a short-acting nitrate for preventing and treating episodes of angina
When a short-acting nitrate is being used to treat episodes of angina, advise people:
- to repeat the dose after 5 minutes if the pain has not gone
- to call an emergency ambulance if the pain has not gone 5 minutes after taking a second dose.
Drugs for secondary prevention of cardiovascular disease
Consider aspirin 75 mg daily for people with stable angina, taking into account the risk of bleeding and comorbidities.
Consider angiotensin-converting enzyme (ACE) inhibitors for people with stable angina and diabetes. Offer or continue ACE inhibitors for other conditions
Offer statin treatment in line with Lipid modification
Offer treatment for high blood pressure in line with Hypertension
Drugs for treating stable angina
Offer either a beta blocker or a calcium channel blocker as first-line treatment for stable angina. Decide which drug to use based on comorbidities, contraindications and the person’s preference.
If the person cannot tolerate beta blockers and calcium channel blockers or both are contraindicated, consider monotherapy with one of the following drugs:
- a long-acting nitrate or
- ivabradine or
- nicorandil or
- ranolazine.
as part of the early management for patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission
Consider intravenous eptifibatide or tirofiban (Glycoprotein IIb/IIIa inhibitors)
Antithrombin therapy for NSTEMI and unstable angina
- Offer fondaparinux to patients who do not have a high bleeding risk, unless coronary angiography is planned within 24 hours of admission.
- Offer unfractionated heparin as an alternative to fondaparinux to patients who are likely to undergo coronary angiography within 24 hours of admission.
- Consider unfractionated heparin, with dose adjustment guided by monitoring of clotting function, as an alternative to fondaparinux for patients with significant renal impairment
Consider bivalirudin for patients who:
- are at intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3%), and
- are not already receiving a GPI or fondaparinux, and
- are scheduled to undergo angiography (with follow-on PCI if indicated) within 24 hours of admission.
