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It is said that the coronary artery that gives the posterior descending artery(PDA) determines if the heart is right dominant(most cases) or left dominant. Is there any reason to this? Why PDA?
This is purely an anatomical definition: right dominant is defined as coronary circulation where the PDA (posterior descending artery) is a branch of the RCA (right coronary artery) and left dominant is defined as coronary circulation where the PDA is a branch of the LCX (left circumflex artery). The Wikipedia article on coronary circulation is a reasonable reference for this question.
There's nothing else special about the statement "dominant" and it doesn't have any other importance for cardiac function, except that someone who is left dominant would have more serious issues if there is a blockage in their left main or LCX.
Typical human coronary artery anatomy consists of two ostia off the aorta, right and left. The "left main" branches fairly early on into the LAD (left anterior descending) artery, which follows the septum between left and right ventricles down the anterior side, and the LCX, which follows the 'top' of the left ventricle counter-clockwise (if looking down at the top of heart and rotating the heart so the atria are on top; in an actual human heart the atria actually point towards the midline a bit more than other species). The RCA travels in roughly mirror fashion, following the 'top' of the right ventricle in clockwise fashion. The RCA and LCX nearly meet on the other side of the heart, at the posterior septum.
In a majority of people, the RCA continues and follows the septum down to the apex (kind of like the LAD but on the opposite side). In a non-negligible minority, the supply of the posterior descending artery is either shared by RCA and LCX or is completely supplied by the LCX.
The circulatory system, also called the cardiovascular system or the vascular system, is an organ system that permits blood to circulate and transport nutrients (such as amino acids and electrolytes), oxygen, carbon dioxide, hormones, and blood cells to and from the cells in the body to provide nourishment and help in fighting diseases, stabilize temperature and pH, and maintain homeostasis.
The circulatory system includes the lymphatic system, which circulates lymph.  The passage of lymph takes much longer than that of blood.  Blood is a fluid consisting of plasma, red blood cells, white blood cells, and platelets that is circulated by the heart through the vertebrate vascular system, carrying oxygen and nutrients to and waste materials away from all body tissues. Lymph is essentially recycled excess blood plasma after it has been filtered from the interstitial fluid (between cells) and returned to the lymphatic system. The cardiovascular (from Latin words meaning "heart" and "vessel") system comprises the blood, heart, and blood vessels.  The lymph, lymph nodes, and lymph vessels form the lymphatic system, which returns filtered blood plasma from the interstitial fluid (between cells) as lymph.
The circulatory system of the blood has two components, a systemic circulation and a pulmonary circulation.  While humans and other vertebrates have a closed cardiovascular system (which means that the blood never leaves the network of arteries, veins and capillaries), some invertebrate groups have an open cardiovascular system. The lymphatic system, in contrast, is an open system providing an accessory route for excess interstitial fluid to be returned to the blood.  The more primitive, diploblastic animal phyla lack circulatory systems.
Many diseases affect the circulatory system. This includes cardiovascular disease, affecting the cardiovascular system, and lymphatic disease affecting the lymphatic system. Cardiologists are medical professionals which specialise in the heart, and cardiothoracic surgeons specialise in operating on the heart and its surrounding areas. Vascular surgeons focus on other parts of the circulatory system.
Factors Influencing Coronary Circulation in Human Beings | Biology
The following points highlight the seventeen important factors which influences coronary circulation in human beings. The factors are: 1. Mean Aortic Pressure 2. Cardiac Output 3. Metabolic Factors 4. CO2 and O2 5. Ions 6. Polypeptiedes 7. Adenine Nucleotides 8. Cardiac Sympathetic and Parasympathetic Nerves 9. Heart Rate 10. Hormones 11. Temperature 12. Muscular Exercise and Excitement 13. Anaemia and Few Others.
1. Mean Aortic Pressure:
It is the chief motive force for driving blood into the coronary vessels. Any alteration of aortic pressure will, therefore, because parallel changes in coronary circulation. In a denervated heart-lung preparation of dog, it is observed that a rise of blood pressure from 50 to 130 mm of Hg increases the coronary inflow from 20 to 250 ml per minute.
In partial clamping of the aorta or in coarctation of the aorta, the central aortic pressure is increased and the coronary flow is also increased. But if this state is kept for some time then the blood flow is not maintained at the same degree.
It has been observed that if the aorta remains in a state of partial occlusion, then the work load of the left heart is increased as the peripheral resistance is increased. This increased work load of the heart ultimately becomes the cause of the congestive heart failure.
2. Cardiac Output:
Obviously, the coronary inflow is directly proportional to the cardiac output.
Increased output raises coronary inflow in two ways:
(a) By raising the aortic pressure, and
(b) By reflex inhi­bition of the vagal vasoconstrictor tone (Anrep).
3. Metabolic Factors:
With the increased metabolism of heart, the O2 requirement is increased and the circulation is greatly increased. There is a causal relationship between the myocardial metabolic activity, oxygen consumption and coronary blood flow. In the normal heart blood oxygen content of coronary sinus is low under a variety of physiological conditions which supports the view of metabolic regulation of coronary blood flow (CBF) by reactive hyperaemia. Adenine nucleotide may be responsible for this reactive hyperaemia.
4. CO2 and O2:
It has been observed by Katz and also by others that if O2 requirement of the heart is increased then the coronary circulation is increased. Furthermore if the O2 supply to the heart muscle is decreased then the coronary flow is increased. But if the O2 is supplied more than it is required, then the coronary circulation is decreased. Similarly, CO2 stimulates the coronary flow. During asphyxia or inhalation of CO2, concentration in the blood is increased coronary flow is also increased at the first stage in order to maintain the total O2 requirement of the cardiac muscle.
It has been observed by Katz that K + in low concentration dilates the coro­nary vessel, whereas K + in higher concentra­tion constricts. Calcium in therapeutic doses increases the flow and O2 consumption of the cardiac muscle.
Bradykinin has been claimed to have vasodilating effect on coronary ves­sels but its normal physiological role is not yet fully known. Angiotensin II is an active octapeptide which causes arteriolar constriction in the skin, kidney, and brain and also in coro­nary vessels.
7. Adenine Nucleotides:
Adenine nucleotides have been known to be potent coronary va­sodilators. ATP and ADP are equally potent vasodilators. AMP is a bit weaker vasodila­tor than those of ATP and ADP. ATP is not permeable to cell membrane, but adenosine can easily pass through the cell membrane.
Berne has described that adenosine, the breakdown product of ATP during hypoxia, perme­ates through the cell membrane to dilate the coronary vessels. Possible metabolic regulation of coronary blood flow by adenosine has been presented schematically by Berne (1963) (Fig. 7.101).
8. Cardiac Sympathetic and Parasympathetic Nerves:
Stimulation of cardiac sympathetic fibres from the stellate ganglion or the ganglion itself produces increased coronary inflow. This is mainly due to the influence of the cardiac sympathetic on coronary blood vessels resulting from the release of norepinephrine which causes vasodilatation of the coronary vessels and increases the coronary inflow.
It has been observed under different experimental conditions that stimulation of sympathetic cardiac nerves causes increase of coronary flow. But the mechanism by which the coronary flow is increased is not yet settled. From the observations of increased flow following intracoronary administration of adrenaline or noradrenaline it is claimed that liberation of noradrenaline from the postganglionic sympathetic nerve ending following stimulation is the probable cause.
Gregg (1963) has described that acute metabolic changes or the cardiac muscle due to increase of cardiac work following sympathetic stimulation is possibly the cause of increased coronary flow. Furthermore, the mediator released at sympathetic postganglionic endings of the cardiac muscle following stimulation increases the O2 consumption and this state causes the cardiac muscle hypoxia, a condition favourable for increasing blood flow through reactive hyperaemia.
Regarding the role of vagus on coronary flow there was conflicting opinion. But recent studies claim that the vagal stimulation, produce vasodilatation of the coronary vessels through liberation of acetylcholine. It is quite unlikely that the vagus will be coronary vasoconstrictor since its chemical mediator acetylcholine is a coronary vasodilator.
9. Heart Rate:
When the heart rate is increased, minute cardiac output, aortic blood pressure may increase but the stroke volume decreases. The phasic coronary inflow and O2 consumption per beat decrease, but minute coronary flow and O2 consumption per minute are increased. With the increase of heart rate, O2 requirement of the heart muscle is increased and is maintained normally through increase of minute flow. It has been observed that with the increase of heart rate the extra-vascular resistance is increased, but the intravascular resistance is actually decreased causing a decrease of resistance, hence increase of minute flow.
In thyrotoxicosis metabolism is increased along with increased coronary inflow and O2 con­sumption per minute. In hypothyroidism the flow is decreased which is possibly related with the al­tered metabolism of the cardiac muscle.
b. Adrenaline and Noradrenaline:
These cause increased coronary inflow along with increased O2 consump­tion per minute. These produce the relaxation of the coronary vessels by acting on the β-receptor of the vessel. Nicotine also increases the coronary flow through the liberation of noradrenaline. Relaxation of coronary blood vessels is prohibited by β-adrenergic blockers.
It causes increased coronary resistance and diminution of coronary inflow. In the open chest or closed chest dog, pitressin causes decrease of coronary flow all throughout the cardiac cycle in the presence of an increased central coronary pressure. This decreased flow is presumably due to direct vasoconstrictor effect on the coronary vascular bed. This vasoconstrictor effect is not due to metabolic effect or due to increase of intracellular and extracellular K + values. It possibly constricts the vessels at arteriolar level.
It increases coronary inflow due to dilatation of the coronary vessels. This increased flow response is completely abolished by atropine. It increases the mean diameter of the coronary vessels.
With the rise of body temperature, the metabolism is increased and for the maintenance of normal O2 need the coronary circulation is increased. But with the fall of body temperature, as in the case of hypothermia, the coronary circulation is greatly decreased along with the decreased metabolic need of the cardiac muscle. The coronary vessels are dilated greatly at that state.
With the increase of body temperature by fever or by external application of heat (hyperthermia), though the heart rate, cardiac output and work of the heart are increased, yet coronary flow possibly remains unchanged. In heart- lung preparation if the myocardial temperature is increased, coronary flow is also increased but if the temperature of blood is increased, then the flow remains unaltered.
12. Muscular Exercise and Excitement:
As mentioned above, coronary inflow is adjusted according to the work done by heart. During heavy exercise the inflow rises about ten times. This is due to the fact that almost all the factors which increase coronary inflow come into action during muscular exercise, viz., O2 lack, CO2 excess, increased H-ion concentration, metabolites, increased temperature, adrenaline secretion, raised blood pressure, etc. During excitement, as the heart rate is increased, the coronary blood flow is also increased greatly, although the diastolic phase is decreased.
In anaemia, the coronary flow is increased sharply in order to maintain the normal O2 need of the cardiac muscle, because the O2 carrying capacity of the blood is decreased under such state. The increase in the coronary flow is related partly to the decreased viscosity of blood and mostly to the active vasodilatation (Reactive hyperaemia) resulting.
(b) Metabolic hypoxia due to compensatory increased heart rate.
14. Intraventricular Pressure:
The increase of intraventricular pressure also alters the coronary flow. The increase of the right ventricular pressure (due to mitral stenosis, emphysema, atelectasis, etc.) affects coronary flow greatly as this pressure is reflected in the coronary venous bed of the right ventricle.
In case of the left ventricle, the coronary flow through this side is initially increased with the rise of intraventricular pressure (due to coarctation of the aorta or increase of peripheral resistance by any means). Under such state the left ventricular work load is increased greatly and ultimately the heart muscle is hypertrophied and coronary flow is gradually decreased. Ultimate fate of the heart is the degeneration of cardiac muscle fibres leading to congestive heart failure.
During transfusion, ventricular load is increased due to rapid venous return and the systolic and diastolic heart size, ventricular stroke volume and work and also arterial blood pressure are all increased. Under such state the heart rate decreased causing greater increase of stroke volume, diastolic pause and thus the coronary flow per beat and per minute is increased.
16. Extravascular Pressure:
This is an important determinant of the coronary flow as the coronary vascular resistance is increased due to rhythmical compression of the myocardial vessels during contraction.
17. Viscerocardiac Reflex:
The coronary flow is markedly altered during visceral distention and it is often encountered in a patient with ischaemic heart disease. Anginal pain, following a meal in such cardiac patient, is the consequence of decreased coronary flow. The reflex pathways for the manifestation of this pain following visceral distention are possibly lying in the vagi and the sympathetic. Thorough works in this line are required.
The heart receives its own supply of blood from the coronary arteries. Two major coronary arteries branch off from the aorta near the point where the aorta and the left ventricle meet. These arteries and their branches supply all parts of the heart muscle with blood.
Left Main Coronary Artery (also called the left main trunk)
The left main coronary artery branches into:
The left coronary arteries supply:
- Circumflex artery - supplies blood to the left atrium, side and back of the left ventricle
- Left Anterior Descending artery (LAD) - supplies the front and bottom of the left ventricle and the front of the septum
Right Coronary Artery (RCA)
The right coronary artery branches into:
The right coronary artery supplies:
- Right atrium
- Right ventricle
- Bottom portion of both ventricles and back of the septum
The main portion of the right coronary artery provides blood to the right side of the heart, which pumps blood to the lungs. The rest of the right coronary artery and its main branch, the posterior descending artery, together with the branches of the circumflex artery, run across the surface of the heart's underside, supplying the bottom portion of the left ventricle and back of the septum.
What is collateral circulation?
Collateral circulation is a network of tiny blood vessels, and, under normal conditions, not open. When the coronary arteries narrow to the point that blood flow to the heart muscle is limited (coronary artery disease), collateral vessels may enlarge and become active. This allows blood to flow around the blocked artery to another artery nearby or to the same artery past the blockage, protecting the heart tissue from injury.
Electronic supplementary material is available online at https://dx.doi.org/10.6084/m9.figshare.c.4161107.
Published by the Royal Society. All rights reserved.
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Coronary artery disease is the leading global cause of mortality. Long recognized to be heritable, recent advances have started to unravel the genetic architecture of the disease. Common variant association studies have linked approximately 60 genetic loci to coronary risk. Large-scale gene sequencing efforts and functional studies have facilitated a better understanding of causal risk factors, elucidated underlying biology and informed the development of new therapeutics. Moving forwards, genetic testing could enable precision medicine approaches by identifying subgroups of patients at increased risk of coronary artery disease or those with a specific driving pathophysiology in whom a therapeutic or preventive approach would be most useful.
Angina, or chest pain and discomfort, is the most common symptom of CAD. Angina can happen when too much plaque builds up inside arteries, causing them to narrow. Narrowed arteries can cause chest pain because they can block blood flow to your heart muscle and the rest of your body.
For many people, the first clue that they have CAD is a heart attack. Symptoms of heart attack include
- Chest pain or discomfort (angina)
- Weakness, light-headedness, nausea (feeling sick to your stomach), or a cold sweat
- Pain or discomfort in the arms or shoulder
- Shortness of breath
Over time, CAD can weaken the heart muscle. This may lead to heart failure, a serious condition where the heart can&rsquot pump blood the way it should.
Learn the facts about heart disease, including coronary artery disease, the most common type of heart disease.
What Is the Function of the Coronary Circulation?
Coronary circulation refers to the circulation of blood in blood vessels of the human heart. It is an essential process that delivers oxygen-rich blood to the coronary arteries. In addition to supplying the heart with blood, coronary circulation provides drainage systems to remove deoxygenated blood.
Coronary circulation is achieved through the heart’s blood vessels. These vessels are paramount to provide the myocardium with the blood, oxygen and nutrients required to pump blood throughout the human body.
Coronary circulation occurs in the coronary arteries, which extend from the aorta to carry blood to the heart muscle. The human heart consists of two coronary arteries that arise from the aorta. During the coronary circulation process, blood is transferred into the coronary arteries and then returned through the coronary veins to the chambers of the heart.
The pulmonary and systemic loops are the primary coronary circulation systems in the cardiovascular system. Pulmonary circulation transports the deoxygenated blood from the heart to the lungs, where the blood absorbs oxygen and dumps it off to the left side of the heart. The right ventricle and right atrium are the pumping chambers that support pulmonary coronary circulation.
Systemic circulation transfers oxygenated blood from the left side of the heart to the body’s tissue systems. This form of coronary circulation is essential for eliminating waste from the body’s tissues and returning deoxygenated blood to the right side of the heart muscle. The left ventricle and left atrium are essential for carrying out systemic circulation.
Coronary circulation - Biology
Evolution of Lungs in Fishes
Conventional wisdom has held that lungs in fishes are an adaptation that allowed them to live in oxygen-poor, freshwater habitats. However, consideration of the evolutionary history of the respiratory system of the protovertebrate and early vertebrates, the fossil record of bony fishes, and the anatomy and physiology of extant lung breathing fishes may indicate that lungs are an adaptation for supplying the heart with oxygen (Farmer 1997, 1998, 1999). Thus lungs may have allowed early fishes to become large and active animals in a marine environment.
Schematic of circulatory system of larval lamprey and hagfish, a model of the protovertebrate
Oxygen-rich blood from cutaneous respiration mixes with the oxygen-poor blood returning to the heart from the muscle and other organs, before the admixture enters the heart. Thus the heart, which lacks a coronary circulation and relies entirely on the oxygen in luminal blood is downstream (efferent) from the gas exchange organ.
Schematic of the circulatory system of a gill-breathing fish
As fishes became larger the skin was no longer adequate as the sole gas exchanger. When gills became the site of gas exchange, replacing the skin, the heart was left upstream (efferent) the gas-exchanger. Thus, oxygen-poor blood returning to the heart from the muscle and other organs is not enriched. These fish may be limited in their aerobic performance a potential selective pressure for the evolution of a coronary circulation.
Schematic of the circulatory system of Amia calva, a basal air breathing fish.
Oxygen-rich blood from the lung mixes with the oxygen-poor blood returning to the heart from the muscle and other organs, before the admixture enters the heart. Thus the heart, which lacks a coronary circulation and relies entirely on the oxygen in luminal blood is downstream (efferent) from the gas exchange organ. Lung breathing fishes with this type of circulatory arrangement (e.g., the Australian lungfish, Neoceratodus forsteri, the gar, Lepisosteus, and tarpon, Megalops) are very active fish and airbreath while active independent of the tension of oxygen in the water.
Schematic of circulatory system in the South American lungfish, Lepidosiren paradoxa
These fish are obligate airbreathers. Imagine fish that drown when held underwater! They live at times in oxygen-poor water and their gills have degenerated, especially the filaments of the 3rd and 4th gill arches, which prevents oxygen-rich blood that has passed through the lung and flows through these gill arches from losing oxygen to the water. The 5th and 6th gill arches receive oxygen-poor, carbon dioxide-rich blood. The streams of blood are kept separate by septation of the atrium into a right and left side, by a partial septum in the cardiac ventricle, and by a spiral valve in the conus arteriosus. The gill filiments of the 5th and 6th arches are used to remove carbon dioxide from the blood. One half of the heart lacks enrichment of luminal blood with oxygen, and these fishes are not highly active.
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Farmer, C. 1997. Did lungs and the intracardiac shunt evolve to oxygenate the heart in vertebrates? Paleobiology 23(3):358-72 PDF