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Coronary heart disease (CHD) is the manifestation of atherosclerosis in the coronary arteries, so that the oxygen demand of the heart muscle cannot be sufficiently covered by the oxygen supply, because of stenotic coronary vessels. Thus, the myocardium becomes ischemic.
Coronary heart disease has an incidence rate of 0.6 % per year with an increase in the elderly. Men are affected more often than women. Together with its manifestations, it is the leading cause of death in industrialized countries, making up almost 20 % of all deaths.
The international MONICA study (Monitoring of Trends and Determinants of Cardiovascular Diseases) records causes and trends of coronary heart disease.
Causes and risk factors of coronary heart disease
Significant risk factors can be recognized for the occurrence of coronary heart disease. Among the main risk factors, in addition to an increase of LDL cholesterol or a decrease of HDL cholesterol include arterial hypertension, diabetes mellitus, smoking, as well as the family history and male gender.
Other risk factors include an unhealthy, atherosclerosis favoring nutrition, severe obesity and too little physical activity. Metabolic disorders, such as impaired glucose tolerance or lipid metabolism disorder also favor the emergence of coronary heart disease.
In patients who suffer a heart attack at a younger age (< 30 years), other causes may play a role. These include familial lipid metabolism disorders, as well as hypothyroidism, and vasculitis. Coronary anomalies or antiphospholipid syndrome as well as hyperviscosity syndrome should also be excluded. During history taking, possible drug abuse should be inquired about.
We differentiate between asymptomatic and symptomatic coronary heart disease. While the asymptomatic form is a silent ischemia, symptomatic coronary heart disease manifests in different ways. This can range from an unstable angina pectoris to acute coronary syndrome and from ischemic heart muscle damage to cardiac arrhythmia and sudden cardiac death.
If damage to the coronary arteries already exists, for example due to arterial hypertension, endothelium platelets attach themselves to the damaged site. The attract other macrophages among others, with help of mediators. If Macrophages take up LDL cholesterol, they are incorporated as a so-called foam cells into the vessel wall.These remodeling processes, in which fibrotic altered tissue is created, make it impossible to reduce the resulting plaque again. Thus, the calcification process of the coronary vessels has begun. Stenosis of the coronary arteries can lead to an insufficient supply of oxygen to the heart muscle tissue, starting with a narrowing of 50 % on exertion, because the oxygen demand increases by approximately fourfold on exertion.
The so-called coronary reserve, i.e. the difference between the minimum blood flow and the fourfold increased, maximum blood flow during exercise is so severely limited in patients with coronary heart disease, that often not even an increase of blood flow to two times the resting blood flow is possible. The result is ischemic pain.
Symptoms and Clinical Diagnosis
The main symptom of coronary heart disease is angina pectoris, which can be divided into a stable and an unstable form.
The symptoms are often indicated as pain or pressure, which occurs retrosternal. Tightness in the chest is also typical. A radiating pain in the left (or right) arm, reaching up to the lower jaw and neck, is a common symptom.
Stable angina pectorisStable angina can be repeatedly triggered by specific events, such as physical or psychological stress. Heavy food and exposure to the cold contribute to worsening.
Stable angina is responsive to treatment with nitrates within minutes, and is always of the same pain intensity and quality.
Unstable angina pectoris
The unstable angina refers to complaints that persist longer than 20 minutes, are of increasing intensity and occur even at rest. Together with the myocardial infarction, unstable angina pectoris is referred to as an acute coronary syndrome.
Progression and Special Forms
Progressive forms of coronary heart disease
In addition to the typical angina pectoris, with retrosternal discomfort that is triggered by stress and gets better at rest, we have the atypical angina pectoris, which involves only two of the three typical criteria. Angina at rest describes a form, in which the symptoms occur at rest. There is also a nocturnal angina, where complaints manifest only at night.
Special forms of coronary heart diseaseSpecial forms are the so-called variant angina, which is caused by vasospasm occurring at rest. The “walking-through-angina” describes problems that occur at the beginning of an exertion, but improve during the course.
Silent myocardial ischemia can also be a form. Here, the typical symptoms are missing. It occurs frequently in diabetics (due to neuropathy), patients with renal insufficiency, women and elderly patients. The symptoms can be very nonspecific here. Dizziness and nausea as well as shortness of breath and symptoms that radiate into the epigastrium are often at the foreground.
Another special form is the postinfarction angina which may occur within two weeks after a myocardial infarction.
History and laboratory diagnosis of coronary heart disease
For the diagnosis, a history that covers the symptoms and their time of onset, triggering factors and the presence of risk factors has to be explored first. In the physical examination, factors such as hypertension and obesity stand out, but auscultation can also detected an indication of heart disease.
In the laboratory, markers such as CK, CK-MB and troponins indicate myocardial damage, which however is not present in stable angina pectoris. Furthermore, an ECG can be taken at rest, which often remains unchanged, even with severe coronary heart disease. A stress test typically shows a descending or horizontal ST depression of 0.1-0.2 mV.A holter monitor can be useful as well; if for example, the symptoms occur in everyday situations. A transthoracic echocardiography can exclude other causes of angina, such as aortic stenosis, and wall motion abnormalities can give an indication of a myocardial infarction.
Gold standard of diagnostics
The gold standard is the coronary angiography, with access via the femoral artery or the brachial artery or radial artery, to determine the degree of stenosis of the coronary artery. Representations via a multislice spiral CT or dual-source CT or MR angiography are also possible.
To investigate the stress-related ischemia, a stress echocardiography or stress MRI with dobutamine can be performed.
The pathology of coronary heart disease is primarily based on an increased resistance in the coronary arteries. These also include intracoronary additional factors such as cardiac disease or other increased O2 demands during a fever for example, as well as a reduced amount of O2, among other things in lung diseases.
The increased resistance of the coronary vessels can be explained by coronary artery stenosis due to atherosclerosis in 90 % of all cases.These so-called microangiopathies initially only narrow the vessels. But if one of these plaques ruptures, clots that close the vessel completely can form, which in turn leads to a heart attack.
Microangiopathies, where small coronary vessels that are located intramural, are responsible in few cases. Consumption of cocaine for example, can cause coronary spasms, which can lead to angina pectoris, just like coronary anomalies, coronary fistulas or congenital myocardial bridges.
The resistance of the coronary vessel may also be increased in cardiac hypertrophy or hypertension and tachycardia or increased end diastolic valve flow. Thus, these factors may be responsible for angina pectoris as well.
Similar clinical pictures such as coronary heart disease
Since the symptom of coronary artery disease is angina pectoris, the differential diagnosis are numerous. The five most important differential diagnosis to be excluded quickly – as they are immediately life threatening – are acute coronary syndrome, pulmonary embolism, aortic dissection, tension pneumothorax and the spontaneous rupture of the esophagus (Boerhaave’s syndrome).
In general, the differential diagnosis of chest pain can be divided into cardiac and non-cardiac chest pain:
Differential diagnosis of cardiac chest pain in addition to acute coronary syndrome include, for example, hypertensive crisis, valvular heart disease, perimyocarditis or hypertrophic cardiomyopathy, but also Dressler’s syndrome following a myocardial infarction or coronary anomalies.
Non-cardiac causes of chest pain include diseases of the lungs or the pleura, such as pulmonary embolism, and lung carcinoma or pleurisy. An aortic dissection may also be present. Furthermore, there may be diseases of the esophagus or the mediastinum, and diseases of the spine and the ribs or abdominal discomfort.
Therapy can initially be divided into acute therapy and long-term therapy. In acute cases, nitro compounds that are acting as a vasodilator and thus improve the coronary circulation are suitable. They are contraindicated for patients who are taking PDE-5 inhibitors (e.g. sildenafil, Viagra), HOCM, hypotension or present aortic stenosis.
Long-term therapy can be divided into causal and symptomatic therapy. The causal approach is directed towards the main risk factors that support the emergence of coronary heart disease. Lifestyle changes such as weight reduction, smoking cessation, dietary changes to a Mediterranean diet, controlled physical activity and courses on stress management and relaxation are crucial.
This approach aims to control blood pressure and cholesterol, as well as triglyceride levels via a non-drug therapy. Symptomatic treatment on the other hand includes medication and invasive approaches. Drug-based therapy aims to prevent myocardial infarction and reduce mortality. It includes aspirin, beta-blockers, statins, and ACE inhibitors.
Antianginal therapy offers several options: These include beta-blockers to reduce myocardial oxygen demand, nitrates, which hardly find application during long-term treatment, Molsidomine and calcium antagonists, as well as ivabradine and ranolazine.
Revascularization as invasive therapy
Revascularization offers an invasive treatment option. This may on the one hand be achieved by means of PTCA (percutaneous transluminal coronary angioplasty) during which dilation via a balloon catheter, followed by stenting is performed. Impending closures can then be eliminated and the permeability of the vessel can be improved.
A second possibility of revascularization is offered via coronary artery bypass surgery (CABG = coronary artery bypass graft). This can be done via the traditional method with sternotomy access and the use of a heart-lung apparatus. An alternative is the minimally invasive way. The last possibility of therapy that is indicated for coronary heart disease in combination with terminal heart failure is the heart transplant.
Prevention of coronary heart disease includes the elimination of risk factors, especially the main risk factors of cholesterol, arterial hypertension, diabetes mellitus and nicotine abuse. The approaches should initially manifest in the behavior of patients, for example, the diet and sporting behavior. Pharmacological support of these approaches is possible such as statins for the regulation of lipid metabolism.
Popular Exam Questions about Coronary Heart Disease
The answers are below the references.
1. The term coronary heart disease describes…
- …a classic chest pain with radiating pain into the left arm.
- …heart disease of the elderly, in general.
- …the manifestation of atherosclerosis in the coronary arteries.
- …an increased blood flow to the coronary arteries during exercise with resulting chest pain.
- …stable angina pectoris.
2. The gold standard for the diagnosis of coronary heart disease is…
- …the ECG at rest.
- …the stress test.
- …the holter monitor.
- …the cardiac MRI.
- …the cardiac catheterization.
3. Which mechanism is most likely based on the pathophysiology of coronary heart disease?
- Plaque formation with stenosis of the coronary arteries and the risk of rupture
- A limitation of the mechanics of the myocardial tissue
- Terminal heart failure, due to which the coronary arteries are no longer sufficiently supplied with blood.
- Atrial fibrillation with the risk of thrombosis and acute closure of a coronary vessel
- Increased HDL cholesterol levels, which alter the structure of the coronary arteries.