Coronary Circulation

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Coronary Circulation


the blood supply to the cardiac muscle, carried by the intercommunicating arteries and veins that run throughout the myocardium.

In man, arterial blood is supplied mainly by the right and left coronary arteries, which begin at the base of the aorta. There are three types of blood supply—right coronary, left coronary, and general—which in some measure determine the nature of the pathology of the coronary circulation in the event of disease of the heart vessels. The coronary veins are both larger and greater in number than the arteries. The veins empty into the right atrium. The principal arterial and venous trunks are connected by a well-developed network of anastomoses, which facilitates collateral (shunt) circulation in cases of impairment of blood supply to the heart.

The great intensity of the blood supply to the myocardium is provided by a dense network of capillaries (approximately twice the number per unit volume than in the skeletal muscles). The level of the coronary circulation in a healthy body corresponds exactly to the force and frequency of the heartbeat. It is regulated both by physical factors (for example, blood pressure in the aorta) and by neural and humoral mechanisms. Coronary circulation is influenced by physical and mental condition and by the degree and character of stress or load. It is sharply impaired by nicotine and certain factors that lead to atherosclerosis, hyper-tension, and cardiac ischemia, such as overstrain of the nervous system, negative emotions, improper nutrition, and the absence of constant physical excercise. Coronary insufficiency and disturbances of coronary circulation are among the most frequent causes of death in economically developed countries, and there-fore their prevention and treatment (mainly of infarction) are the most pressing problems of modern medicine.


References in periodicals archive ?
It is important to note that the distribution of these changes varied in the studied groups in subendocardial, intramuscular, and subepicardial layers of the myocardium (Figure 3).
[94] ADMA and subendocardial viability ratio 201 No association between Dimitroulas et al.
Although the reasons for the absence of abnormal Q waves are not fully understood, they are associated with subendocardial rather than transmural infarction, inferior rather than anterior infarcts, and smaller rather than larger infarcts in adults.[10],[11]
Myocytolysis or myofibrillar degeneration denotes acute myocardial stress and is characterized by foci of subendocardial hemorrhage surrounding epicardiac nerves [33].
Cardiac MRI is helpful in diagnosing subendocardial perfusion defects, assessing the size as well as localization of noncompaction [20].
Left ventricular EF is commonly preserved in the early stages of the disease process as it is primary calculated from the contraction of the heart along its short axis, while the subendocardial myocytes that are prone to damage are longitudinally oriented and therefore the longitudinal contraction will be impaired [31].
Such abnormalities in troponin concentration may occur in the absence of ischemic heart disease; indeed multiple mechanisms besides coronary artery disease have been invoked for release of troponin in patients with HF, including subendocardial stress, myocyte degeneration, and toxic effects of non-CV disorders such as renal failure.
The latter were placed in all 17 AHA segments in the left ventricle and varied in size to include subendocardial and transmural scenarios [31].
A gadolinium-enhanced cardiac MRI revealed circumferential subendocardial edema from the mid cavity to apex, most prominently in the lateral wall (Figure 1).
Previous studies indicated that myxoma cells arise from remnants of subendocardial vasoformative reserve cells or multipotential primitive mesenchymal cells in the fossa ovalis and surrounding endocardium, which can differentiate into a variety of cell lineages including endothelial, fibroblastic, hematopoietic, glandular, neurogenic, and smooth muscle cells [1-3].
Previously, in nondiabetic animal models, it was shown that the subendocardial area was more vulnerable than the interstitial area to cardiac dysfunction, due to differences in blood flow between the two areas [9-11].
The experienced pathologist evaluated endocardium (thickness, subendocardial fat, fibrosis, and inflammation); myocardium (muscle fiber number, size, and damage); interstitium (fibrosis, fat, edema, and inflammation); and intramural vessels (size, signs ofinflammation, damage, and luminal stenosis).