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.

I. M. D’IAKONOVA and S. V. SAMOILOVA

References in periodicals archive ?
There is a significant positive correlation between the activities of the endocardial and subendocardial iNOS and eNOS with ventricular contractile performance which suggests a beneficial effect of NO released from the endothelial cells in patients with dilated cardiomyopathy.
Pharmacodynamic parameters such as heart rate, augmentation pressure, augmentation index (Alx), subendocardial viability ratio (SEVR), radial and aortic blood pressure (BP) were recorded before and after the cold pressor test at baseline and at the end of treatment.
There are three cell types identified in the ventricular myocardium: the endocardial, epicardial, and subendocardial M cells (Masonic mid-myocardial Moe cells) [25, 26].
As significant epicardial coronary artery disease was not present in these patients these perfusion defects may result from either significant subendocardial deposition of amyloid protein or possible infiltration of small-calibre coronary vessel walls by amyloid.
ISO administration to rats leads to hypoxia development in the least perfused area of subendocardial layer as result of diastole shortening [7].
Cardiac magnetic resonance imaging (MRI) showed biventricular systolic dysfunction; late gadolinium imaging revealed the presence of left ventricular thrombus and a non-ischaemic subendocardial enhancement with a classical 'zebra sign', compatible with a diagnosis of endomyocardial fibrosis.
Histopathologic lesions included mild diffuse congestion in the pygmy brocket deer's kidneys and extensive subendocardial hemorrhage.
These currents are manifested in the electrocardiogram as a ST segment elevation or depression, as consequence of subepicardial and subendocardial ischemia, respectively (27, 28) In subendocardial ischemia, there is a delay in subendocardial cardiac cells repolarization; in consequence repolarization proceeds as a normal condition, from the epicardium to the endocardium, but is delayed in the ischemic subendocardial area causing a prolonged QT interval and a positive symmetrical, high and pointed T wave (28-32).
These lesions were characterised by the presence of unclotted blood in the abdominal and the thoracic cavity, multifocal hemorrhages in the subcutaneous tissue and the gastrointestinal tract, diffuse pulmonary hemorrhages, subepicardial and subendocardial petechiael hemorrhages and ecchymoses.
An increase in catecholamine level further decreases the subendocardial coronary blood flow.
The most important mechanisms by which hypertension predisposes to sudden cardiac death are: left ventricular hypertrophy, interstitial fibrosis, myocardial or subendocardial scars, silent myocardial ischemia, diastolic dysfunction and high sympathetic nervous activity (1,3-5).