Ischaemic Heart Disease
Reduced blood supply to heart tissue is the most common cause of death in the world.
Platelet plug formation.
Endothelial cells release prostacyclin and NO (nitric oxide, which also keeps vessel open) which prevents platelets being switched on and becoming adhesive. If you have a tear in the blood vessel wall you get collagen fibres exposed to blood and contents of cells leaking into blood. This gives out a chemical signal to switch on platelets. Local to the break the endothelial cells are damaged so less NO released. Platelets stick together and secrete chemicals which draw in more platelets. This forms a platelet plug which the body uses to prevent blood loss. Atherosclerosis plaques are areas of amaged blood vessels. On these plaques less NO and prostacyclin is released meaning there’s more chance of this occurring.
Prostacyclin is lipid soluble as is NO and so crosses cell membrane and causes the smooth muscle to relax. Switched on platelets produce vasoconstrictive chemicals which cause vasoconstriction, especially as locally the endothelial cells won't produce as much NO or prostacyclin.
Oxygen extraction in the heart is the highest in the body as cardiomyocytes have the highest capillary density. Beta 2 adrenoceptors cause dilation. Coronary arteries also conduct metabolic hyperaemia as some of the metabolic bi products of the heart cause vasodilation. Adenosine is a very important one. Matches blood supply with blood demand. Coronary arteries crushed during systole and fill during diastole. Less flow in cold or when heart is stressed. Note that the layer of muscle closest to the blood in the left ventricle near the apex does the most work so needs most oxygen and is most often ischeamically damaged.
Formation of Atheromatous Plaques
Low density lipoprotein damages endothelial cell and eventually gain access to the sub endothelial space where it gets oxidised. Chemicals are released which attract other things like white blood cells (monocytes) to the plaque. The macrophages which are attracted to the LDL conduct phagocytosis on the LDL. They end up internalising too much and become a foam cell. Primitive plaque formed of foam cells, smooth muscle, lipid and necrotic tissue(due to lack of oxygen). This is a long term process. The endothelial cells become dysfunctional. Contents of plaque eventually leak out and cause a thrombus. When vessels bifurcate the blood flow is turbulent stand this switches off the endothelial cells increasing the chance of aneurysms or clots.
Means chest pain and is a result of temporary denial of oxygen. Stable angina is when you have a plaque which lowers the lumen of the coronary arteries so any time they need to do something which requires the heart to have more blood becomes painful due to the build up of metabolites. Unstable angina is when the plaque ruptures for no apparent reason and causes a thrombus to form. Generally progresses to a myocardial infarction. Note that you can have 70% blockage for flow to be limited and that when oxygen requirement increases problems start. Build up of metabolites causes nerves to fire and give chest pain, myocardium starts to become ischaemic.
The heart can't get oxygen and can't wash away toxic metabolites. ATP production is stopped so muscle is stiffer so cannot contract as well and cannot fill (as this involves stretching) as well. As the metabolites are often ions their build up can cause abnormal firing of a cardiac myocyte (arrhythmia). Stable angina will allow musle to recover from ischaemic.
STEMI is an acute sever episode where you have necrosis, ST elevation myocardial infarction. Stable angina or transient myocardial ischaemia gives you a depression in the ST segment while exercising. Note that the pain often expresses as Levine sign ie bending over and clutching chest. They often also get tachycardia and nausea. Treatment of stable angina is GTN and prevention is GTN, b blockers, ca channel blockers statins. GTN dilates blood vessels (pointless as vessels are maximum dilation) and causes venous dilation lowering the preload and therefore lowering the cardiac workload.
Some muscle dies, some is permanently damaged unlike angina. ST complex is raised due to dying or necrotic tissue acts as a window so you see more parts of the heart. Lower oxygen carrying capacity as the heart is not functioning fully so blood flow to the lungs not entirely optimum therefore oxygen saturation low. Blood pressure can be fine though due to compensatory response.
- Diabetes (+ Diabetic control)
- Oral contraceptive Pill
- Gender (male)
- Family history of IHD (especially age <50 )
Constricting pain & discomfort in the central chest, neck, shoulders, jaw or arms. Not sharp or stabbing. Doesn't change with position or respiration.
- Radiation (favouring left side)
- Down either arm
- Up to jaw
- Down to epigastrium (often confused with indigestion)
- Through to back
- Exacerbating factors
- Exertion (key factor in differentiating stable angina from other forms of chest pain)
- Extremes of weather
- Relieving factors
- GTN spray (within 5 minutes)
The stable pattern of symptoms is due to a narrowed lumen, caused by atherosclerosis, and the atheroma is covered by a fibrous cap. ECG may show ST depression and T wave inversion/flattening but tend to be normal. Look for signs of old infarcts. Consider angiography and PCI (Per Cutaneous Intervention with or without stent insertion).
Management is that of symptoms and risk factors, try to improve quality of life and reduce risk of progression to unstable angina/MI.
The angina pain fits one of the following patterns:
- At rest for > 10 mins
- Severe, new onset
- Change from previous pattern (more severe, longer duration)
The pathophysiology of unstable angina is the reduction of coronary flow, due to
- Transient platelet aggregation on apparently normal endothelium
- Coronary artery spasms
- Or Coronary thrombosis.
In this way, it is the "breaking off" of thrombi, which then settle downstream to induce the unstable pattern of symptoms. This is an Acute Coronary Syndrome, and is likely to lead to MI, so treat in a similar way to Myocardial Infarction.
Blood supply is usually interrupted by occlusion of a coronary artery, following rupture of an atherosclerotic plaque
- Usually more severe pain than angina
- More associated sympathetic symptoms
- Duration > 20 minutes
- Normal relieving factors do not work (GTN/rest)
- Sense of impending doom
- ECG changes-
- ST elevation, new bundle branch block- more likely to represent acute injury
- ST depression, T wave inversion- more likely to be chronic
- Troponin T rise over 12 hours
- Angiography- often performed as a ± Coronary catherisation
- Nitrates (GTN)
- Thrombolysis or
- Primary Percutaneous Coronary Intervention (PCI)
- Cardiac rehabilitation- exercise, driving advice, monitoring for sequelae
Sequelae include heart failure, heart block, atrial fibrillation, ventricular fibrillation, ventricular tachycardia
- Sudden onset of anterior chest pain that is pleuritic (sharp pain when breathing in) and retrosternal
- On examination
- Presence of rub (sounds like sandpaper in chest)
- On ECG
- ST elevation and PR depression
- Pericarditis vs Infarction
- More likely to be sharp and pleuritic
- Increased with coughing, inspiration, swallowing
- Worsened by lying supine, relieved by sitting and leaning forward (easier to breathe)
- Blood splits aortic media with sudden tearing chest pain which can be excruciating
- Often radiates through to the back (imagine where the aorta goes)
- Branches of aorta occlude as dissection unfolds i.e. unequal BP in arms
- If dissection extends proximally MI can occur
- Patient presents in a collapsed state