Chest Pain / Angina Pectoris
In 1772 doctor William Heberden first described angina pectoris, he wrote: “They who are afflicted with it are seized, while they are walking (more especially if it be up hill), with a painful and most disagreeable sensation in the breast, which seems as if it would extinguish life if it were to increase or to continue, but the moment the patient stands still all this uneasiness vanishes”.
Three major coronary arteries provide the heart with oxygenated blood, the right coronary artery (RCA), the left coronary artery (LCA) and the circumflex artery (Cx). When the coronary arteries are affected by atherosclerosis and the lumen of the coronary arteries narrows, the heart receives less oxygenated blood and becomes hypoxic, which results in angina pectoris.
Complete history and physical examination are essential to determine angina pectoris as diagnosis and to exclude other causes of chest pain, such as aorta dissection, arrhythmias, pulmonary embolism, pneumonia, heartburn, hyperventilation or musculoskeletal problems.
Patients often experience angina pectoris as if a elephant stands on their chest. Because the heart itself has very few nerves the pain can be sensible elsewhere in the upper body, mainly arms, jaw and/or back. Some patients only complain about stomach ache so the presentation can be very a specific.
Angina pectoris however has some characteristics that can help to differentiate between other causes of (chest) pain. Angina pectoris is gradual in onset and offset, with the intensity increasing and decreasing over several minutes. The pain is constant and does not change with respiration or position. If patients had angina pectoris before they will recognize the pain immediately.
Angina pectoris usually occurs during exercise when the demand for oxygenated blood increases. Coronary arteries with a narrowed lumen can not meet the demand of oxygenated blood during exercise. As soon as the exercise is aborted angina pectoris decreases. This is called stable angina pectoris. Unstable angina pectoris means angina pectoris at rest which consists less than two months. Over time the angina pectoris develops to more often, severe and prolonged, so that symptoms are to occur at less and less effort than before. Stable angina pectoris responds to nitro-glycerine spray, unstable angina pectoris does not. Nitro-glycerine spray is a venodilator which reduces venous return to the heart and therefore decreases the workload and therefore oxygen demand. It also vasodilates the coronary arteries and increases coronary blood flow.
Nitro-glycerine is however not specific for angina pectoris, a similar response may be seen with oesophageal spasm or other gastrointestinal problems because nitro-glycerine also relaxes smooth muscle.
During angina pectoris so called vegetative symptoms can occur, this includes sweating, nausea, paleface, anxiety and agitation. The idea is that the vegetative nerve system is more active in a reaction to stress.
Oxygen deficiency of the heart leads to ischemia, ischemia and the discomfort the patient experiences lead to sympathetic activation of the nervous system. This is detectable during physical examination by an increase in heart rate and elevation in blood pressure. Ischemia can also cause a temporarily impairment in myocardial function, on auscultation you could hear a paradoxically split second heart sound, a third or fourth heart sound and a mitral regurgitation murmur. All these findings however disappear with resolution of the ischemia
The electrocardiogram (ECG) is an easy and important tool to differentiate between myocardial ischemia and infarction. Patients with unstable angina pectoris will show abnormalities on the ECG at rest, in particular ST depression. Patients with stable angina pectoris are likely to have a completely normal ECG at rest, exercise ECG testing will be necessary to show any abnormalities. During exercise ECG testing an ECG is made during cycling on a home trainer or walking on a treadmill. While exercising the oxygen demand of the heart increases, if the narrowed coronary arteries are unable to supply enough oxygenated blood, the patient develops pain on the chest and the ECG will show abnormalities.
If the ECG made during exercise testing does not show any abnormalities angina pectoris becomes very unlikely. If the ECG does show abnormalities during exercise testing additional research needs to be done. Depending on the hospital one of the below standing research will be done.
- Exercise echocardiography means that an echocardiography is made directly after exercise. The poorly perfused parts of the heart will show less activity.
- Myocardium Perfusion Scintigraphy (MPS) is able to show the perfusion of the heart during exercise and at rest.
- MRI can be done with vasodilatory dobutamine or stimulating adenosine to assess how the heart behaves during exercise.
If abnormalities are found a coronary angiography (CAG) will be necessary.
In addition to an ECG it is common to take blood samples and run the blood for elevated cardiac markers. Elevated CK MB and Troponin I indicate ischemia. It can however take 4-8 hours, after the symptoms started, before CK MB is elevated. The same applies to Troponin I, the advise is to repeat the measurements after 4-6 hours. A pitfall concerning elevated Troponin I can be patients with renal failure or pulmonary embolism. Positive cardiac markers indicate non ST elevation MI (NSTEMI), negative cardiac markers indicate unstable angina pectoris.
In patients with stable angina pectoris with little or no symptoms and no abnormalities found during additional research, treatment focuses on preventing angina pectoris and reducing the risk of a heart attack to a minimum. Therefore medication, all aimed to keep the workload of the heart as low as possible, will be necessary. β blockers lower heart rate and blood pressure, this decreases the oxygen demand of the heart. Nitrates dilatate the coronary arteries so the heart receives more oxygenated blood. Anticoagulants reduce the risk of development of a thrombus in the coronary arteries. Statins to lower cholesterol levels.
Apart from starting medication the patient needs to minimize any present risk factors like smoking, overweight and drinking alcohol. See chronic coronary diseases.
Coronary angiography (CAG) is an X ray examination of the coronary arteries, a catheter is inserted into the femoral artery or into the radial artery. The tip of the catheter is positioned at the beginning of the coronary arteries and contrast fluid is injected. Contrast is visible by X ray and the images that are obtained are called angiograms. On an angiogram stenoses will be visible, if the stenosis is significant coronary intervention will take place. Ideally this happens immediately following the CAG but not all hospitals that are entitled to carry out CAG are qualified to perform percutaneous coronary intervention (PCI).
Percutaneous Coronary Intervention
The procedure of PCI is similar to a CAG, except this time a catheter with an inflatable balloon will be brought at the site of the stenosis. Inflation of the balloon within the coronary artery will crush the atherosclerosis and eliminate the stenosis. To prevent that the effect of the balloon is only temporarily a stent is often positioned at the site of the stenosis.
Coronary Artery Bypass Graft
When the coronary arteries contain too many or too severe stenoses for PCI a coronary artery bypass graft (CABG) is indicated. Especially when the stenoses are located proximally of the three major coronary arteries, causing occlusion of many ramifications and high risk of severe myocardial damage.
CABG does not eliminate the stenosis like PCI does. Using the internal thoracic arteries or the saphenous veins from the legs a bypass is made around the stenosis. The bypass originates from the aorta and terminates directly after the stenosis. Thereby restoring the blood supply to the ramifications.
A bypass can be single or multiple, multiple meaning that there are several coronary arteries bypassed using the same bypass.