Typical signs of angina pectoris
The first signs of angina pectoris usually become apparent during physical exertion or psychological stress. In such situations, the oxygen demand of the body increases. As a result, the heart has to perform increased pumping work, which in turn requires a better blood supply to the heart.
However, the increased blood supply to the heart muscles is not possible due to coronary artery disease, which causes a lack of oxygen to the heart. This causes sudden stabbing or dull pain in the chest area. Typically, a strong feeling of tightness in the chest occurs at the same time, which causes additional breathing difficulties.
If coronary heart disease worsens, angina pectoris attacks occur at lower levels of stress. In particularly severe stages, symptoms may also occur at rest. An increase in pain and tightness with each attack also indicates that the disease is progressing. If the symptoms do not change over time, this is more likely to indicate stable angina pectoris, in which the disease does not progress.
Causes of angina pectoris
Angina pectoris (chest pain) is the leading symptom of coronary heart disease (CHD), a disease in which the coronary arteries become increasingly clogged and thus narrow due to arteriosclerosis (calcification of the arteries). These narrowings limit the blood flow to the heart and are called coronary stenoses. Due to the poorer blood flow, there is a mismatch between the oxygen demand of the heart and the supply of oxygen, this fact is called coronary insufficiency.
In the following, you will find an overview of the main factors of angina pectoris, which will then be discussed in more detail. – Arteriosclerosis and elevated blood lipid levels
- High blood pressure
- Psychosomatic causes
- Cold as a risk factor
- Other possible causes
The cause of angina pectoris is therefore arteriosclerosis. In the case of arteriosclerosis, the risk factors mentioned below lead to damage to the endothelium, which is the innermost layer lining the arterial wall.
The endothelial damage alters the properties of the arterial wall: blood components can now adhere more easily to the vessel wall. In addition, messenger substances are released which mediate inflammation and tissue growth. This leads to an inflammatory process and tissue growth in the arterial wall.
In addition, different cell types and fats are deposited in the affected vessel wall. The deposition is called “fatty streak” and does not yet lead to a significant vasoconstriction. Over the years, the deposits become larger and larger and are incorporated into the vessel wall under a cell cap.
The diameter of the artery is now significantly smaller, and the affected vessel cannot expand if necessary. If there is an increased oxygen demand, as is the case during physical exertion, the heart receives too little oxygen due to the poor blood circulation, which manifests itself as angina pectoris. The risk factors for arteriosclerosis thus largely correspond to the risks for angina pectoris.
The main causes of arteriosclerosis are elevated blood lipid levels, arterial hypertension, diabetes mellitus, smoking and an age above 45 years for men and 55 years for women. Other risk factors for calcification of the arteries are lack of exercise, overweight and metabolic disorders of fat and sugar regulation. This topic might also be of interest to you: AtheromatoseStress is a very high risk factor for all kinds of heart disease.
Whether the stress has physical or psychological causes, it has an equally negative effect on the cardiovascular system. The hormone cortisol, which is secreted more frequently under stress, leads to an increased production of vascular-damaging molecules. Cortisol thus leads to increased fat deposition on the vessel walls.
Over time, the deposits develop into plaques and calcifications that constrict the vessels. If such a deposition takes place in the coronary arteries, it can quickly lead to an undersupply of the heart muscles behind them, causing angina pectoris symptoms. An elevated blood pressure is responsible for the development of cardiovascular diseases in many patients.
It will cause a faster blood flow in the vessels, whereby greater forces act on the vessel walls, which promotes the development of arteriosclerotic plaques. In addition, the increased blood pressure causes many small turbulences in the blood flow, which in turn means that greater forces act on the vessel walls. On the other hand, these turbulences can cause cells from the blood to settle on the plaques.
This makes the constricting calcifications on the vessel walls larger. The more plaques there are in the coronary arteries, the worse the blood circulation is, which can lead to angina pectoris. Psychosomatic causes are psychological factors that have an influence on the development of physical (=somatic) diseases.
Psychological stress plays a major role in angina pectoris. It leads to the release of the stress hormone cortisol, which accelerates the production of vascular-damaging substances. These harmful substances lead to the increased formation of plaques in the coronary vessels, which promotes the development of angina pectoris.
Conversely, heart disease (somatic=physical disease) can also have an influence on the psyche. Thus, angina pectoris attacks often trigger fear and panic in those affected. This fear also falls under the term psychosomatics, as the psyche and body interact with each other.
Cold is a major risk factor for the occurrence of angina pectoris attacks, especially in winter. Due to the low temperatures, the blood vessels on the skin surface contract. This mechanism is designed to bring as little heat as possible to the surface.
However, the contraction of the blood vessels results in increased resistance in these vessels. The heart has to pump against this resistance and therefore increases blood pressure. In order to maintain the higher blood pressure, the heart has to work harder, which in turn requires an improved blood supply to the heart muscles.
Due to the narrowing of the coronary arteries, however, increased blood flow is not possible, which results in a reduced supply of blood to the heart tissue. This causes angina pectoris symptoms. Angina pectoris is divided into the following forms: There are also different degrees of severity (CCS classification CanadianCardiovascularsociety):
- Stable angina pectoris
- Unstable angina pectoris
- Prinzmetal angina
- Angina decubitus
- Other forms such as stress angina or pre-infarct angina
- 0: silent angina pectoris, rather than incidental
- 1: AP symptoms only occur during the most severe physical exertion (shovelling snow, heavy gardening)
- 2: AP symptoms occur easily during normal to heavy physical exertion (e.g.
rapid climbing of stairs)
- 3: AP symptoms are more pronounced during normal physical activity
- 4: AP symptoms even at the slightest physical exertion (e.g. severe pain even while dressing) or at physical rest
In stable angina pectoris, 90% of all cases are caused by a narrowing of at least one of the coronary arteries. It is characterised by the fact that the symptoms always occur at the same strain and always subside with the same countermeasures. The countermeasures include physical rest and the taking of medication.
Unstable angina pectoris is first of all any newly occurring angina pectoris or any change in symptoms of stable angina pectoris. If the seizures occur, for example, even at low levels of exertion or at rest, or if the seizures occur more frequently, or if the pain persists despite taking medication, this is called unstable angina pectoris. This is usually caused by a narrowing of several coronary vessels or a narrowing of a larger coronary vessel (often a so-called left-sided main stem stenosis).
Unstable angina pectoris carries a very high risk of heart attack. Patients with unstable angina pectoris must therefore receive medical treatment immediately. Prinzmetal’s angina (angina pectoris) got its name from its first describer Myron Prinzmetal (1908 – 1987).
He described the disease for the first time in 1959 as a special form of angina pectoris. In this case, the heart is not less supplied with oxygen due to a narrowing, but due to a so-called vasospasm. This is a spasm of one or more coronary vessels, which leads to a narrowing of the vessels.
The cause of the cramps is still unclear. A connection with the parasympathetic nervous system is suspected. This is a part of the vegetative (involuntary) nervous system, which is responsible for all things like digestion (parasympathetic nervous system) or escape reflexes (sympathetic nervous system).
Prinzmetal angina occurs completely independently of stress. However, it is more likely to occur in the early hours of the morning, as the parasympathetic nervous system is most active at this time. It is typical for Prinzmetal angina to occur as early as the 3rd to 4th decade of life.
Like the other forms of angina pectoris, it can trigger a heart attack. This form of angina pectoris occurs mainly at night or after lying down for a long time. It is a form of unstable angina pectoris.
When lying down, there is an increased backflow of venous blood into the heart. If the heart muscle cells have been previously damaged, this is the trigger for the angina decubitus/nocturna. Occasionally one hears or reads other names for angina pectoris.
However, these names are only synonyms or other terms for the forms of angina pectoris described above. For example, stress angina is only a description of the fact that angina pectoris only occurs under stress. (i.e. at least a degree of severity 1) Pre-infarction angina is also more frequently referred to. This describes an angina pectoris that occurred before a heart attack and is therefore likely to have caused it. Therapy-resistant angina pectoris describes a severe form of unstable angina pectoris that is difficult or impossible to treat.