8.2 Myocardial supply and demand

8.2.1 Supply

In the normal heart, several factors contribute to myocardial oxygen supply and demand.
Coronary blood flow is the primary means by which the myocardial tissue meets its metabolic needs. It stands to reason, then, that anything that impedes blood flow from the coronary vessels will cause a reduction in the supply of oxygen. Although an atherosclerotic plaque is the most likely cause, recall that coronary arteries are compressed during systole, and the majority of coronary blood flow occurs during diastole. Therefore, any condition that affects diastole also affects coronary blood flow (e.g. aortic regurgitation). Additionally, within the blood itself, any condition affecting the oxygen-carrying capacity of the blood, such as anaemia, will also result in a reduction of oxygen supply and cause ischaemia.

8.2.2 Demand

On the other hand, oxygen and nutrients are required to adequately meet myocardial demand. Factors that contribute to or increase demand include thickness of the ventricular wall (increasing the energy demands of cardiac myocytes) and an increased heart rate or blood pressure. These factors force the heart to pump harder and, as such, myocardial demand for oxygen and ATP goes up.

The interplay between supply and demand can be thought of as a dynamic process, and an imbalance in the scale will result in some of the symptoms seen in the section below and the chapter ahead.

8.3 Angina pectoris

8.3.1 What is angina?

Angina refers to the squeezing, vice-like gripping sensation associated with cardiac chest pain. It is often described as a ‘crushing sensation’ or ‘pressure’ retrosternally – “It’s like there’s someone sitting on my chest, doctor!”.

Many conditions exhibit angina as a presenting symptom, but coronary artery disease is the most common causative pathophysiological process. Angina, particularly when there is an underlying ischaemic cause, is rarely positional or sharp, and chest pain of that nature should prompt the clinician to reconsider the diagnosis.

Ischaemic heart disease may manifest in several conditions, some of which are discussed in this chapter, and others in the chapters ahead:

• Stable angina
  
• Unstable angina (refer to Chapter 9)
  
• Myocardial infarction (refer to Chapter 9)
  
• Heart failure (refer to Chapter 10)

• Arrhythmia (refer to Chapter 11)

8.4 Stable angina

8.4.1 Definition

• Stable angina results from a fixed narrowing of the coronary arteries normally resulting in a fixed threshold for symptoms, which are typically associated with one or more of: exertion, emotion, eating, cold weather, and occasionally recumbency (angina decubitus).

8.4.2 Epidemiology

• Prevalence: 38 per 100 000 in men and 21 per 100 000 in women
  
• Male predominance; men are affected almost twice as much as women
  
• Risk factors include diabetes mellitus, hypertension, hyperlipidaemia, smoking and South Asian ethnicity
  
• Lower socioeconomic status is also a risk factor.

8.4.3 Aetiology

• Primarily related to atherosclerosis.

8.4.4 Pathophysiology

• The pathophysiological basis of stable angina is twofold in nature:
  
  
  
  • fixed vessel narrowing by an atherosclerotic plaque, reducing blood flow
    
  • endothelial dysfunction caused by the atheroma, reducing release of the vasodilators nitric oxide (NO) and prostacyclin, decreasing antithrombotic properties of the endothelium.

8.4.5 Clinical features

• Consider history and risk factors to elicit the diagnosis

GUIDELINES: Chest pain of recent onset: assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin (NICE, 2010)

Key features

• Central chest pain (in actuality, stable angina is rarely described as frank ‘pain’; rather, the nature of the discomfort may be heaviness, pressure, squeezing, smothering, or choking)

• Precipitated by exertion (or other exacerbating factors, as listed above)

• Relieved by rest or nitrates (including GTN) within 5 minutes

• NICE considers a patient with all of the above factors to have typical angina, a patient with two to have atypical angina, and a patient with one or none of the factors to have non-anginal pain.

Examination findings:

• Features on examination are relatively non-specific
  
• Findings should be tailored to assessing risk factors e.g. xanthelasma in hyperlipidaemia.

8.4.6 Investigations

First-line:

• Electrocardiogram (ECG)
  
• Blood tests: FBCs, LFTs (for baseline LFT before any introduction of statin therapy), U&Es, glucose, cholesterol and triglycerides (TGs)
  
• While the ESC guidelines still recommend stress tests in their algorithm, NICE does not recommend the use of stress testing in the evaluation of a patient with stable angina.

GUIDELINES: Chest pain of recent onset: assessment and diagnosis of recent onset chest pain or discomfort of suspected cardiac origin (NICE, 2010; CG95)

NICE recommends stratifying patients with clinical assessment, ECG and typicality of angina to estimate the likelihood of coronary artery disease.

• Estimated likelihood of coronary disease less than 10% – consider alternative causes of chest pain other than coronary artery disease (e.g. hypertrophic cardiomyopathy) before considering an alternative diagnosis.

• Estimated likelihood of coronary disease 10–29% – offer CT calcium scoring. If the calcium score is 0, consider an alternative diagnosis. For a calcium score from 1–400, offer CT coronary angiography. If the calcium score is >400, invasive angiography should be considered.

• Estimated likelihood of coronary disease 30–60% – offer non-invasive functional testing, e.g. myocardial perfusion scan, stress echocardiography.

• Estimated likelihood of coronary disease 61–90% – coronary angiography if revascularisation is considered and functional testing if revascularisation is not deemed appropriate.

• Estimated likelihood of coronary disease >90% – proceed straight to management for patients in this group. Typical angina also falls within this group. Further diagnostic testing is unnecessary.

Second-line

• ESC guidelines still recommend stress testing (refer to Chapter 3)
  
• Additionally, offer invasive coronary angiography as a second-line investigation when the results of non-invasive functional imaging are inconclusive.

8.4.7 Management

GUIDELINES: The management of stable angina (NICE, 2011; CG126)

1. Explanation and lifestyle

• It is important to ensure that the patient understands the condition and the factors that may provoke it (including emotional stress and eating heavy meals)

• Optimise lifestyle factors e.g. physical exercise, diet and smoking

• Do not offer acupuncture in the treatment of stable angina

2. Pharmacological therapy

• Glyceryl trinitrate (GTN) spray should be used as and when necessary. Repeat in 5 minutes if the pain persists. Call for an ambulance if the pain continues 5 minutes after a second dose.

• Use a beta-blocker or calcium channel blocker (CCB) first line (consider patient’s comorbidities – use a rate-limiting CCB such as verapamil if used as monotherapy).

• If symptoms are still not controlled, switch the initial drug or use both in combination. If a CCB is used in combination with a beta-blocker, use a slow long-acting dihydropyridine e.g. nifedipine.

• If a patient is on a beta-blocker or CCB and is unable to tolerate either as the second therapy, offer either a long-acting nitrate, ivabradine, nicorandil or ranolazine (refer to Chapter 5).

• Only consider a third drug if a patient is considered for PCI or CABG. It is important to acknowledge that the evidence for third and fourth anti-anginals is poor.

• The patient should also be given aspirin and a statin.

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