Disorders of perfusion of the heart muscle are broadly divided according to their severity into:
- Stable angina
- Acute coronary syndrome, which is further subdivided into:
1. Unstable angina
2. Myocardial infarction
Like all body tissues, the heart needs a continuous oxygen-carrying blood supply to function, and for the cells to maintain their metabolism. Cells eventually die without it.
The degree of tolerance to oxygen deficiency varies widely according to the type of tissue. At the extremes of the spectrum lie the nerve cells (neurons) and bone cells (osteocytes).
Neural tissue can’t tolerate oxygen deficiency after 5 minutes, while bone tissue can handle a few hours without irreversible tissue damage. It usually depends on the rate of metabolism of tissues. A factory that produces large amounts of products per hour is more quickly affected by the cessation of its raw materials supplies.
Heart muscle cells are also sensitive to oxygen deficiency, and its effect takes less than 30 minutes to produce an irreversible injury and death to the muscle cells.
How does it happen?
Unstable angina is a supply-demand mismatch of the heart, which means that there are either physiological or pathological conditions that affected the heart, leading to increased oxygen demands. Such conditions range from mild fever to severe valve diseases. This can also be coupled with other health problems that cause the heart muscle’s blood supply to deteriorate. Since oxygen is carried by red blood cells -the better name is red blood corpuscles as they are not “true” cells- through their hemoglobin, which is an oxygen-carrying iron-containing protein. Such conditions include anemia, hypotension, or any other disease affecting breathing or the oxygenation of blood.
Another important mechanism is what is called plaque disruption. When fats are deposited in a gradual manner causing the narrowing of the heart’s blood vessels, they produce stable angina. It increases in severity over a long time and takes years to produce typical symptoms. Such plaques of fat are covered by a layer of the lining of the mentioned blood vessels. In some cases, this cover or “cap” is thin or “unstable” that it becomes liable to rupture, releasing the fatty plaques into the lumen of the blood vessel. This is a catastrophic event because while the cap itself has a smooth surface, it prevents the blood from clotting in the vessel’s wall when released. The cap is ruptured, the smooth surface becomes rough, and clotting occurs, rapidly disrupting the heart’s blood supply. The greatest anticoagulant of the body is the unmatched smoothness of the interior of blood vessels.
An important thing to note here, however, is that muscle cell death does not occur in unstable angina like heart attacks. That’s because the vessel is not completely obstructed but leaves a small portion that allows the cells just to live until it is obliterated.
What does it feel like?
The site and character of pain are very similar to those of stable angina. It is a pressure, fullness, heaviness, or frank pain sensation, felt at the chest either localized to one place or a generalized pressure all over the chest. It can also be felt in the jaw, left arm or shoulder, or the abdomen. It can be associated with:
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- Sweating, but without fever
- Dyspnea (difficulty of breathing)
- Feeling of general weakness
- Vomiting and nausea
- Burning sensation near the stomach
If you are a female, always remember that any of the above symptoms, especially fatigue without pain or chest discomfort, can indicate angina and is enough to warn you to seek medical care.
The main difference between the stable and unstable angina is the duration and severity of the episode. Stable angina tends to be brief and lasts for a few minutes (1-10 minutes), while unstable angina may last for up to 30 minutes. Stable angina recurs in response to physical exertion, while unstable angina can occur at rest. Finally, stable angina has a dramatic reaction to nitroglycerin, while unstable angina is more or less resistant to it. The simple explanation to all these differences is the different mechanisms by which each develops, a narrowed artery by contraction of muscles, or excessive demand can revert by rest or relaxing such muscles. On the other hand, a clogged artery needs more time to remove the blood clot formed and is not related to effort or oxygen demand to be relieved by rest.
Diagnosis
Doctors diagnose angina with the help of several tools. The main challenge here is to differentiate between the several causes of chest pain and differentiate between stable and unstable angina. These tools include:
Medical history: The basis of medicine is medical history. Your doctor will ask you several questions that will help him understand the cause of your discomfort or complaint. Regarding angina, the main questions involve the pattern, site, duration, severity, time of pain, and what alleviates or aggravates it.
Physical examination: A general physical examination is routine, although it doesn’t always show abnormalities. It involves measuring blood pressure and auscultating heart sounds, indicating cardiac abnormalities that either caused or aggravated the condition. Also, signs of heart failure indicate a severe condition that needs more invasive treatment and diagnostic considerations. The doctor may also check your leg edema and auscultate the chest for volume overload evidence, which indicates late-stage heart failure. A physical examination can also be useful in excluding other chest pain causes as muscle pain or problems in the lungs or airways. A reproducible pain usually excludes angina. A general look at the whole body’s blood vessels is also a part of the routine physical examination of patients with cardiac conditions. It includes checking peripheral pulses and carotid auscultation and palpation for signs of occlusion.
Lab investigations: Lab investigations offer an excellent “exclusion tool” for unstable angina. The most important of which is cardiac markers. When heart cells die, the various enzymes involved in the mechanism of their contraction “leak” into the bloodstream. Since there is no death or “necrosis” of heart cells in unstable angina, the presence of high levels of such enzymes is strongly suggestive of a heart attack. Other routines -but not insignificant- investigations include:
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- Blood sugar and hemoglobin A1C levels for diabetic patients.
- Lipid profile
- Electrolyte levels, especially potassium and magnesium. A drop in the level of such electrolytes can prove fatal in unstable angina patients, as it can cause arrhythmia.
Electrocardiography: Electrocardiography is the most commonly done investigation for chest complaints, and rightly so. It is easy to do and can exclude many diagnoses, a good portion of which is fatal. In the case of unstable angina, there is no classical finding. However, the ST segment changes -which is when the ventricles restore their electrical polarity and relax- is highly suggestive of a severe episode that needs immediate intervention.
Echocardiography: Both transesophageal and transthoracic echocardiography may be used -although the former is recommended-. Echocardiography can detect abnormalities of the heart’s contraction and sequelae of heart attacks or the presence and assessment of heart failure. It can also exclude other causes of chest pain related to the heart as valvular disorders.
Magnetic resonance imaging: The main advantage of MRI is its high resolution. What can’t be seen by echocardiography can easily be picked by an MRI. It can detect microinfarcts and visualize coronary arteries with great accuracy.
Unstable angina treatment
Treatment of unstable angina focuses on deciding the degree of aggressiveness that the therapy should be according to the condition’s risk. The decision to admit to the ICU is guided by several indications that either point towards or ascertain the presence of myocardial infarction as:
- ECG changes as elevation or depression of ST-segment or evidence of ventricular arrhythmia due to bundle block. All these signs indicate myocardial ischemia that is enough to cause electrical abnormality, which is potentially fatal.
- Any sign of heart failure in development or potentially fatal.
- Elevated cardiac enzymes.
Unlike stable angina, the role of medical therapy in unstable angina is limited to decreasing the number of complications and temporarily controlling the condition’s progression. The invasive interventions remain the definitive therapy for unstable angina.
Medical therapy includes:
- Aspirin: Aspirin remains one of the most important and useful first measures in unstable angina. It prevents further aggregation of platelets, which is the main mechanism by which unstable angina occurs. It also prevents the formation of new clots. With that said, special care should be taken regarding patients who have any bleeding tendencies.
- Other antiplatelet drugs: as Clopidogrel and Ticagrelor may be used instead of aspirin.
- Anticoagulants: A blood clot is formed of platelets and fibrin. Fibrin is formed through a coagulation cascade that starts with the activation of coagulation factors, and while antiplatelets function on platelets alone, anticoagulants act on the coagulation cascade itself. Examples include drugs taken parenterally by injection as heparin and low molecular weight heparin, the latter being the more widely used, and those taken orally as Warfarin. Injectable preparations have a short duration of action, and therefore are used in emergency settings, while oral drugs are primarily used for long-term follow-up therapy.
- Lipid-lowering drugs: Although the main event is the formation of a blood clot, the condition overall is related to atherosclerosis and lipid deposition into the arterial walls. Therefore, the lowering of blood cholesterol levels is paramount in the long-term management of the condition. The most commonly used family of lipid-lowering drugs are called statins, and they act mainly by inhibiting the formation of cholesterol in the body -which is the main source of cholesterol-. In recent studies, it was also proven that they reverse atherosclerosis.
- Beta-blockers: The list of beta-blockers’ uses has expanded recently to include coronary artery diseases from stable angina to myocardial infarction. Doctors widely use such a family because they have multiple effects, most of which are beneficial for cases of supply-demand mismatch in angina. They lower the heart rate and blood pressure and are antiarrhythmics. All the previous effects counteract the sympathetic system overactivity seen in angina or coronary artery disease cases in general, which is one of the leading causes of heart failure in coronary artery diseases. They also lower the demand for oxygen by decreasing the heart’s overall activity, thereby evening the equation of supply and demand. They have relatively few side effects and aren’t contraindicated except in some cases of heart failure.
- Nitrates: Nitrates are a family of drugs whose main action is vasodilation. In angina, they have a dramatic effect on the stable type and can relieve the attack in a matter of minutes. However, they are less effective in unstable angina, but this doesn’t mean that they are useless. They can still increase the caliber of the heart’s blood vessels, improving blood flow to the cardiac muscle to an extent, and lower blood pressure, decreasing the workload on the heart.
Invasive measures
Since the last decade, there has been much debate on the benefit of invasive interventions in the management of unstable angina.
Many doctors still prefer the conventional approach to managing unstable angina by medications since a small number of studies were performed regarding cardiac revascularization, and a few of them came with conclusive results.
However, some of the studies have shown decreased mortality in patients who underwent revascularization by percutaneous intervention as soon as the diagnosis was established. Options include either PCI or coronary artery bypass surgery.