Ischaemic Heart Disease and Hypoxia

Question 1

What is ischaemic heart disease (IHD)?

Answer 1

AKA coronary heart disease (CHD) / coronary artery disease (CAD)

Heart problem caused by narrowed heart (coronary) arteries that supply blood to the heart muscle

Mismatch between demand and supply

Most common cause of death in Western cultures

Manifests clinically as myocardial infarction (MI) and ischaemic cardiomyopathy

Sudden death = acute coronary occlusion

Gradual death = progressive weakening of heart pumping process over several years

Question 2

What are the signs and symptoms of IHD?

Answer 2

Angina chest pain
Heart rhythm issues
Nausea, sweating, fatigue, shortness of breath, weakness, dizziness
Reduced exertional capacity 
Leg swelling 
Diaphoresis

Question 3

What are the different characteristics of angina chest pain?

Answer 3

Aching, burning, fullness, heaviness, numbness, pressure, squeezing

Radiation of pain to arms, back, jaw, neck, shoulder

High or low BP

Syncope (fainting)

Question 4

What is IHD often mistaken for and why?

Answer 4

Chest pain may be described by patient in a way that leads to heartburn / indigestion diagnosis

Question 5

What are the characteristics of different heart rhythm problems?

Answer 5

Palpitations (irregular heartbeats or skipped beats)

Heart murmurs

Tachycardia (Acute coronary syndrome
ACS, Acute myocardial infarction AMI)

Atrial fibrillation

Ventricular tachycardia or ventricular fibrillation

S4gallop: A common early finding of diastolic dysfunction

S3gallop: An indication of reduced left ventricular function and a poor prognostic sign

Question 6

IHD is the most common cause of death. Where geographically is IHD death rate high?

Answer 6

East Europe
Middle East
Some of Asia

Question 7

What is a (daily adjusted life year) DALY?

Answer 7

Sum of years a person lost due to death or disability

Question 8

What are some risk factors of IHD?

Answer 8

Non-modifiable (30%):
Age
Sex (male)
Family history of CVD
Ethnicity 
Genetic evidence
Previous history of CVD

Modifiable (70%):
Hypertension
Hyperlipidaemia (/ high cholesterol)
Smoking
Diabetes
High BMI 
Diet 
Exercise 
Stress / Mental ilness
Low socioeconomic state 
Alcohol abuse
Certain medications
Social deprivation

Question 9

Are the modifiable risks/causes of IHD the same around the world?

Answer 9

High income countries = hypertension, cholesterol, tobacco use

Low income countries = poor diet, air pollution, low education

Question 10

What are the 2 causes of IHD?

Answer 10

Myocardial ischaemia occurs when there is an imbalance between the supply of oxygen and the myocardial demand

1. Coronary blood flow to a region may be reduced due to OBSTRUCTION:
Atheroma
Thrombosis
Spasm
Embolus
Coronary ostial stenosis
Coronary arteritis

2. A general decrease of oxygenated blood flow to myocardium:
   Anaemia
   Carboxyhaemoglobulinaemia
   Hypotension causing decreased coronary perfusion pressure

Question 11

What is atherosclerosis and how does it contribute the IHD?

Answer 11

Complex inflammatory process involving accumulation of lipids, macrophages and smooth muscle cells

Plaque formation is initially stable, but becomes unstable over time - leads to thrombus:
Fibrous cap on vulnerable plaque ruptures and pro-thrombotic components are exposed to pro-coagulation factors leading to thrombus formation
[fibrous cap contains macrophages and smooth muscle cells]

Question 12

What are some triggers of atherogenesis?

Answer 12

Endothelial dysfunction
Mechanical sheer stresses (HTN)
Biochemical abnormalities (elevated and modified LDL, DM, elevated plasma homocysteine)
Immunological factors (free radicals from smoking)
Inflammation ( infection such as chlamydia, Helicobacter)
Genetic alteration

Question 13

What is the presentation of IHD depending on the progression of athersclerosis?

Answer 13

Asymptomatic = small, asymptomatic athercosclerotic plaque

Chronic stable angina = stable fixed atherosclerotic plaque (reduced blood flow to heart)

Acute Coronary Syndrome = unstable angina, non ST elevation MI or ST elevation MI

Heart failure

Sudden death

Question 14

What is the role of hypoxia in acute coronary occlusion?

Answer 14

Happens in people with underlying atherosclerotic disease
Local blood clot = thrombus formation

Atherosclerotic plaque breaks through the endothelium –> direct contact with the flowing blood

This can lead to - blood platelets adhering to it, fibrin being deposited, and/or RBCs entrap to form a blood clot

Either or all of these = clot growth until the artery occludes the vessel OR clot breaks away and blocks a more distal artery (coronary embolus)

Question 15

What are collateral blood vessels and what is their role in IHD?

Answer 15

Collateral blood vessels = small capillary-like branches off an artery formed overtime. Collaterals “bypass” the area of narrowing and help to restore blood flow

Dilate within seconds during an acute episode - doubling by the 2nd/3rd day and often reaching normal coronary flow within 1 month

In chronic atherosclerotic patients = slow occlusion = collaterals open at the same time as atherosclerosis begins, and continue to develop as the atherosclerosis gets worse over time

Question 16

Why do you get ACS if collaterals are so effective in helping take over the function?

Answer 16

The collaterals are also blood vessels so they can also get atherosclerosis

OR

The damage becomes so intensive the collaterals cannot cope/keep up

OR

Can cause weakening of the heart = eventually heart failure

Question 17

Why can you restore total heart function after MI?

Answer 17

Collateral formation after acute MI

In about a month - normal coronary flow = normal heart function

Question 18

What are some cardiac muscle stats?

Answer 18

Cardiac muscle require 1.3ml of oxygen per 100g of muscle tissue

8 ml of oxygen per 100 g delivered to normal resting left ventricle each minute so usually muscle do not die

If 15 to 30 percent of blood supply remains, muscle will not die except in the central portion of a large infarct with no collaterals

Question 19

What happens during an MI?

Answer 19

During an acute occlusion = area of muscle has either zero or little flow = cannot sustain cardiac muscle function = infarction

Question 20

What happens soon after infarction? (pathogenesis)

Answer 20

Soon after infarction:

Small amount of collaterals open and blood seeps into the infarcted area

Local blood vessels dilate and area becomes overfilled with stagnant blood

Muscle fibres use all the remaining oxygen, haemoglobin becomes totally deoxygenated giving bluish brown hue & blood vessels appear engorged despite lack of blood flow

Question 21

What happens in the later stages of an MI?

Answer 21

Vessel walls’ permeability increases, fluid leak and local tissue oedematous (excessive accumulation of serous fluid in the intercellular spaces of tissue)

Cardiac muscle cells swell and due to no blood supply, die within few hours

Question 22

What are the 4 different causes of death after an MI?

Answer 22

Decreased cardiac output - due to systolic stretch and cardiac shock = normally heart wall pushes back to exert force during systole, but the weak heart muscle is instead stretched outwards during systole = poor CO that cannot meet body’s needs (cardiogenic shock_

Damming of blood in body’s venous system = poor CO = poor blood flow to kidneys = failure to excrete = increase in blood volume = congestive symptoms = pulmonary oedema

Ventricle fibrillation = can happen during first 10 minutes or after 1 hour or so

Rupture of infarcted area =
Early little danger, but after few days infarcted area begins to degenerate and the heart walls become very thin and stretched. Until it finally ruptures during stretch

Question 23

How does recovery start after an MI?

Answer 23

Tissue is non-functional in the area affected

Small area: little or no death of muscle
Might become non functional temporarily due to lack of nutrients, but recovers

VS

Large area:
Some in the centre die rapidly within 1 to 3 hours due to complete loss of blood supply
Immediately around is non functional area failure of contraction and impulse conduction
But surrounding areas = weak from mild ischaemia, but as collaterals open they go back to functioning
Normal areas of heart gradually hypertrophy to compensate for lost tissue for partial / almost full recovery

Question 24

Does cardiac output stay the same during ischaemia?

Answer 24

Mild = yes, due to cardiac reserve - normal heart can actually pump 300-400% if it wants to; thats how it increases CO during exercise
So problem = when exercising after MI, as reserve is already being use to meet daily needs

Severe = no

Question 25

What is the IHD risk assessment?

Answer 25

All aged 40–74 years, who have not been diagnosed with CVD, diabetes, or CKD = free health check every 5 years

Health check includes CVD risk assessment, alcohol consumption, physical activity, BMI, dementia in 65+, DM, CKD

Person’s 10 year CVD risk assessed using QRISK every 5 years - useful for preventative measures to be put in place for the patient

Question 26

How do you diagnose IHD?

Answer 26

Clinical History:
Symptoms—chest pain type etc, any associated symptoms and signs
Age, sex, Ethnicity, Smoking, Ask about other risk factors, Socioeconomic, family history

Clinical Examination:
Heart auscultation, BP, BMI, GPE

Lab tests:
LDL, HDL, Triglycerides, lipoprotein a, C-reactive proteins etc

Serum markers - esp. in A&E:
Troponins(I or T)
Creatine kinasewith MB isozymes
Lactate dehydrogenase and lactate dehydrogenase isozymes
Serumaspartate aminotransferase

Biomarkers for predicting death e.g. presence of raised:
B-type natriuretic peptide
CRP
Homocysteine
Renin
Urinary albumin-to-creatinine ratio
= more likely of death following MI

Question 27

What are the 3 types of IHD and what are their characteristics?

Answer 27

Stable angina = angina symptoms during moderate physical activity

Unstable angina / NSTEMI = angina symptoms while doing very little / at rest

Acute MI / STEMI = angina symptoms while
at rest

Question 28

How does the ECG change is the 3 types of IHD:

Stable angina
Unstable angina / NSTEMI
Acute MI / STEMI

Answer 28

Stable Angina =
Pretty much normal ECG if you want to see the changes do an exercise stress test
During stress test might see ST depressions indicating IHD

Unstable Angina/ NSTEMI =
ST depressions and T wave inversion, non-Q-wave MI
[NSTEMI = positive cardiac markers, unstable = negative cardiac markers]

Acute MI/ STEMI =
ST segment elevation with T wave inversion, and Q-wave MI
[positive cardiac markers]

Question 29

What are some types of echocardiography, what can they detect and what can they diagnose?

Answer 29

Transthoracic echo = helps to assess:
Left ventricular function
Wall-motion abnormalities in the setting of ACS
Mechanical complications of ACS

Transoesophageal echo = most often used for assessing possible aortic dissection in the setting of ACS.

Stress echo = used to evaluate haemodynamically significant stenoses in stable patients who are thought to have CAD

Question 30

What is coronary angiography and why is it used?

Answer 30

In vivo assessment of coronary arteries

Iodinated contrast agent injected through catheter placed at the ostium of the coronaries - contrast agent is visualized through radiographic fluoroscopic examination of the heart

Used to detecting stenoses that may be revascularized through percutaneous or surgical intervention

Coronary CT angiography = used to detect presence and extent of CAD, and independent predictors of significant coronary stenosis and other cardiovascular events

Question 31

What is ultrasonography and why might it be used?

Answer 31

Ultrasonography (AKA Doppler US) of the common and internal carotid arteries = non-invasive measure of arterial wall anatomy

Can be performed repeatedly and reliably in asymptomatic individuals

Combined thickness of intima and media of the carotid artery = associated with prevalence of CVD and risk factors, and increased risk of MI and stroke

Question 32

What are doppler velocity probes and why might they be used?

Answer 32

Doppler Velocity probes = measures coronary flow

Doppler guidewire measures phasic flow velocity patterns and tracks flow rates in small, straight coronary arteries

Doppler velocity probe = used to determine the severity of intermediate stenosis (40-60%)

Helps evaluate whether normal blood flow has been restored after percutaneous transluminal coronary angioplasty (PTCA)

Question 33

What is the pharmacological treatment in stable or some unstable anginas?

Answer 33

HMG-CoA reductase inhibitors =
Lower LDL-C and triglyceride levels, and raise serum HDL levels
e.g. Atorvastatin (Lipitor)

Bile Acid Sequestrants =
Block enterohepatic circulation of bile acids and increase the fecal loss of cholesterol
e.g. Cholestyramine (Questran, LoCholest, Prevalite)

Calcium channel blockers =
Relaxes coronary smooth muscle and produces coronary vasodilation = improved myocardial oxygen delivery
e.g. Amlodipine (Norvasc)

ACE Inhibitors =
Helps hypertension = reduces vascular endothelial dysfunction
e.g. Captopril (Capoten), enalapril (Vasotec), and lisinopril (Zestril)

Beta-blockers =
Inhibit sympathetic stimulation of heart = reduced HR and contractility; decreased myocardial oxygen demand

Antianginal Agents =
Inhibition of late sodium current of cardiac action potential = reduced myocardial cellular sodium and calcium overload

Platelet aggregate inhibitors = 
Inhibition of platelet function = protection against atherosclerosis 
e.g. Clopidogrel, Aspirin 

Nitrates =
Decrease myocardial oxygen demand by producing systemic vasodilation

Question 34

Which of these is useful in treating acute angina pain?

Answer 34

Nitrates = very helpful for acute angina pain

Question 35

What are some revascularisation therapies?

Answer 35

Percutaneous coronary Intervention
(PCI) - given to all patients with stable CAD who have areas that can be revascularised - use angiography to place stent, which compresses plaque and improves blood flow

Coronary Artery Bypass Graft (CABG) - graft from vessel from vein in leg = placed on heart to bypass narrowed artery
Recommended to those with several narrowed coronary arteries

Question 36

What are some recommendations to help prevent CAD and IHD?

Answer 36

Moderate physical activity for a total of 30 minutes on most days of the week

Avoid tobacco use and exposure to environmental smoke; make plans to quit if you already smoke

Choose a diet rich in fruits, vegetables and potassium, and avoid saturated fats and calorie-dense meals

Maintain a normal body weight; if you are overweight, lose weight by increasing physical activity and reducing calorie intake

Reduce stress at home and at work