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CAUSES, DIAGNOSIS, AND PREVENTION OF ANGINA PECTORIS
¹Ermatov Farruxjon
²Juraboyev Ozodbek
³Umarov Sherali
Samarkand State Medical University, DKTF, Department of Internal Medicine, Cardiology and
Functional Diagnostics, 2nd year clinical residents
https://doi.org/10.5281/zenodo.14864297
Introduction
: Angina can manifest as a mild, non-distracting pain or can quickly develop
into a strong, intense feeling of pressure in the precordial region. Angina is rarely described by the
patients themselves as "pain". In most cases, patients complain of a feeling of discomfort behind
the sternum, and the localization of these sensations can also vary. The feeling of discomfort can
spread to the left shoulder and extend to the fingertips of the left hand. Pain may occur in the back,
throat, lower jaw and teeth, radiating to the inner surface of the right arm. Sometimes this feeling
of discomfort is localized in the upper abdomen. It is characteristic that with stable angina,
pathological sensations are never localized above the ears and below the navel. Angina pectoris is
a clinical syndrome characterized by discomfort or tightness in the precordial region, which is
caused by transient myocardial ischemia without the development of infarction. In most cases,
angina attacks develop against the background of physical or emotional stress and pass at rest or
after sublingual administration of nitroglycerin. The diagnosis of the disease is established on the
basis of clinical manifestations, ECG changes and various methods of visualization of myocardial
ischemia. Treatment may include antiplatelet drugs, nitrates, beta-blockers, calcium channel
blockers, angiotensin-converting enzyme inhibitors, statins, coronary angioplasty or coronary
artery bypass grafting.
Research methods and materials:
The narrowing of blood vessels in atherosclerosis is
not completely static, the size of the vascular lumen is affected by changes in vascular tone, which
is usually present in all people; It has been found that in most patients, angina attacks occur in the
morning hours, when there is an increase in vascular tone. In addition, endothelial dysfunction
may contribute to changes in arterial tone: for example, in the endothelium affected by
atherosclerosis, a “catecholamine surge” causes more vasoconstriction than vasodilation (the
normal response).
When myocardial ischemia occurs, a decrease in blood pH is observed in the coronary
sinus, the release of potassium ions into the extracellular space, the accumulation of lactate,
changes in the ECG are noted, and a decrease in ventricular contractility (systolic and diastolic) is
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noted. During an attack of angina pectoris, an increase in diastolic pressure in the LV is usually
observed, which is sometimes accompanied by congestion in the lungs and shortness of breath.
The exact mechanism responsible for the feeling of shortness of breath during an angina attack is
unknown, but stimulation of nerve endings by metabolites formed during hypoxia may be
involved.
Results
The frequency of attacks can vary from several attacks per day to prolonged
periods of absence of clinical symptoms lasting weeks, months, or years. The frequency of attacks
can increase (called progressive angina), which leads to myocardial infarction or death.
Conversely, attacks can gradually decrease or disappear, if adequate collateral coronary circulation
develops, a necrotic focus appears at the site of the ischemic area, or heart failure or intermittent
claudication develops, limiting activity.
Nocturnal angina attacks are caused by changes in breathing, heart rate, and blood pressure
that occur during sleep. Nocturnal angina attacks can also be a manifestation of left ventricular
failure, which is equivalent to nocturnal attacks of shortness of breath. In the supine position,
venous return is increased, which leads to myocardial stretching and increased myocardial tension,
which in turn increases myocardial oxygen demand.
Rest angina is angina that occurs spontaneously in the supine position, but not necessarily
at night. It is usually accompanied by a slight increase in heart rate and sometimes a significant
increase in blood pressure, which, accordingly, increases the demand for myocardial oxygen. On
the other hand, an increase in blood pressure and heart rate can provoke the development of an
angina attack, and they can be the result of myocardial ischemia in response to rupture of
atherosclerotic plaque and formation of a thrombus in a coronary artery. If an angina attack lasts
a long time, the imbalance between myocardial oxygen demand and supply increases, which
increases the likelihood of myocardial infarction.If the patient has a normal resting ECG and is
able to exercise, an exercise stress ECG is performed. In men with chest discomfort suggestive of
angina, the sensitivity of the stress ECG is approximately 70% and the specificity is approximately
80% ( 1 ). These values are somewhat lower for women. In addition, women with coronary artery
disease are more likely to have resting ECG changes than men (32% vs. 23%). Despite the high
sensitivity of the exercise stress test, false-negative results are possible in severe forms of coronary
heart disease (main or three-vessel disease). A positive test is the basis for further investigation. In
patients with an atypical clinical presentation, a negative exercise test usually excludes angina and
cardiovascular disease.
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Stress myocardial imaging is performed in conditions where the resting ECG is abnormal,
as false-positive ST-segment elevations are common on the stress ECG. Exercise or
pharmacological therapy (eg, dobutamine and dipyridamole infusions) may be used. Imaging
techniques include stress echocardiography, myocardial perfusion imaging with single-photon
emission CT (SPECT) or PET, and stress MRI. The choice of imaging technique depends on its
availability in the clinic and the experience of the investigators. Imaging techniques allow
assessment of LV contractile function at rest and in response to stress, identification of areas of
ischemia, myocardial infarction, and viable myocardium, and localization and distribution of the
risk zone. Stress echocardiography also allows the diagnosis of mitral regurgitation associated with
ischemic papillary muscle dysfunction.
Conclusion
: Electron beam CT allows us to measure the amount of calcium in
atherosclerotic plaque in the coronary artery. The calcium index is associated with the risk of
developing coronary artery disease. However, because calcium can be detected in the absence of
significant stenosis, this index does not correlate well with the need for PCI or CABG. Based on
these findings, the American Heart Association recommends that CT be performed only in a
limited population of patients and in conjunction with clinical and medical history to assess the
risk of fatal or nonfatal MI ( 4 ). These groups may include asymptomatic patients with an
intermediate 10-year risk estimate for atherosclerotic cardiovascular disease (10–20%) and
symptomatic patients with inconclusive stress test results. The use of electron beam CT is essential
to exclude serious coronary disease in patients presenting to the emergency department with
atypical symptoms, normal troponin levels, and a low probability of hemodynamically significant
coronary artery disease.
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