Most likely, there are both patterns present. The endocardium, especially in the papillary muscles, are supplied either through the distal portion of the epicardial coronary arteries or from the left ventricular cavity through luminal channels. In fact arterioluminal channels between the arteriolar arteries and the left ventricular cavity via intertrabecular spaces have been described. Other vessels or channels called sinusoids are thin walled and capillary like, but with lumens of variable size and shape; some of these vessels connect directly to the ventricular chambers and some to venous structures that then empty into the ventricles.
These have been called venoluminal channels. The ostia of these various vessels can be seen on careful inspection of the endocardium of the right and left ventricles, and collectively they are called thebesian veins or, more appropriately, thebesian vessels.
They are more numerous or at least visible in the atria than in the ventricles. Postmortem radiographic and dissection studies have documented subarteriolar collateral connections from about m to over m between the coronary arterial systems. These collateral vessels are most numerous near the apex and through the muscular interventricular septum, but they may also be identified in the interatrial septum, at the crux of the heart, between the sinoatrial nodal artery and other atrial arteries, as well as over the anterior surface of the right ventricle.
In the human with nonobstructed coronary arteries, there are only rarely epicardial collateral vessels. When atherosclerosis results in progressive obstruction to the epicardial coronary arteries, the intramural potential collateral vessels enlarge and become clinically important. There are also extracoronary anastomotic connections between the coronary arteries and the systemic arteries, primarily at the base of the great vessels and around the ostia of the pulmonary veins and vena cavae.
The systemic arteries involved are primarily the pericardial vessels derived from the internal mammary and intercostal arteries, usually at the pericardial reflections. In general, these systemic-to-coronary artery collaterals are clinically unimportant, even in obstructive coronary artery disease.
Another early branch from the right coronary artery is the artery to the superior vena caval orifice that gives rise to the sinoatrial nodal artery Fig. The right coronary artery gives branches superiorly to the right atrial wall and one to three branches inferiorly to the free wall of the right ventricle. At the acute margin of the heart, the acute marginal artery is a large vessel supplying the anterior wall of the right ventricle. The right coronary artery continues inferiorly in the right atrioventricular sulcus, passing under the inferior vena cava at its connection with the right atrium.
The right coronary artery continues posteriorly to the crux of the heart and makes an anterior loop into the posterior atrial septum.
After giving off the AV nodal artery, the right coronary artery turns toward the apex to course in the posterior interventricular sulcus as the posterior descending coronary artery that supplies the posteroinferior surface of the left ventricle, parts of the posterior right ventricle adjacent to the posterior interventricular sulcus and, by small septal perforators, the posterior one-third of the interventricular septum Figs 7 and 9.
In some hearts, the posterior descending coronary artery wraps around the apex and supplies the distal portion of the anterior left ventricular wall. The terminal distribution of the left circumflex and the right coronary arteries posteriorly are reciprocally related, and the blood supply to the posterior wall of the left ventricle depends on whether there is a right dominant or a left dominant circulation.
They lie embedded in epicardial fat and are superficial to the coronary arteries. They receive blood from the myocardial capillaries and carry it back to the right atrium. Most of the venous return to the right atrium is via the coronary sinus Figs 25 and The great cardiac vein accompanies the anterior descending coronary artery in the anterior interventricular sulcus. It drains toward the base of the heart and then follows the left circumflex coronary artery posteriorly in the left atrioventricular sulcus, joining the coronary sinus just beneath the left inferior pulmonary vein.
The great cardiac vein has valves at its connection with the coronary sinus. Throughout its course it receives veins from the anterior muscular interventricular septum, the anterior and lateral walls of the right and left ventricles, and the left atrium.
Coursing on the diaphragmatic surface of the left ventricle, the posterior cardiac vein of the left ventricle accompanies the circumflex coronary artery to connect with the coronary sinus at its distal end. The middle cardiac vein lies in the posterior interventricular sulcus overlying the posterior descending coronary artery; it receives tributaries from the posterior muscular interventricular septum and posterior ventricular walls and empties into the.
In the subendocardial connective tissue of all four cardiac chambers there is a plexus of valved lymphatic vessels. These channels drain through a web of anastomosing lymphatic vessels that envelop the myocardial fibers. The lymphatics. The preganglionic neurons of the sympathetic chain are located in the upper five or six thoracic levels of the spinal cord and synapse with second-order neurons in the cervical sympathetic ganglia.
The postganglionic sympathetic axons terminate in the heart and on the adventitia of the great vessels. The parasympathetic preganglionic neurons are located in the dorsal efferent nucleus of the medulla; these axons project as branches of the vagus nerve to the heart and great vessels where they synapse with second-order neurons in epicardial ganglia and adventitia of the great vessels Fig. Both sympathetic and parasympathetic fibers enter the heart for the most part by common autonomic nerve trunks from the mediastinum by way of the dorsal mesocardia.
The autonomic nerves are interdigitated within two neuroplexuses, divided for convenience into a superficial cardiac plexus on the anterior. In: Anson BJ Ed.
Lehrbuch der Systematischen Anatomie. Berlin: Springer-Verlag; These vessels join on the epicardium to form several large lymphatic vessels that follow the course of the epicardial coronary arteries and veins. The major lymphatic trunks drain into the atrioventricular sulcus and form a single large trunk that passes over the top of the left main coronary artery and under the arch of the main pulmonary artery. This trunk courses to the left of the aortic root where it exits the pericardial sac to join the left mediastinal lymphatic plexus, draining into the mediastinal lymph nodes and finally into the thoracic duct.
The small cardiac vein on the surface of the right ventricle accompanies the acute marginal artery and drains the anterolateral wall of the right ventricle. It follows the course of the right coronary artery in the right atrioventricular sulcus, receives tributaries from the right atrium and empties into the coronary sinus near its ostium at the right atrium. On the anterior aspect of the right ventricle there are anterior cardiac veins that empty through the ventricular wall in the conal region, into the small cardiac vein, or directly into the right atrium through separate orifices.
The coronary sinus is the continuation of the great cardiac vein; it is 35 mm in diameter and 25 cm in length. It courses in the left atrioventricular sulcus inferiorly, receiving veins from the left atrial and ventricular walls. A small vein draining from the roof of the posterior left atrium between the left and right pulmonary veins, called the oblique vein of the left atrium or vein of Marshall, is the remnant of the embryologic left common cardinal vein.
When this cardinal vein remains patent, it is called a persistent left superior vena cava and connects the left innominate vein with the coronary sinus. This is clinically important in that catheters passed through the left median basilic vein enter the right atrium through the coronary sinus and are difficult to maneuver into the right ventricle and out the pulmonary artery.
Since the left fourth and sixth embryonic aortic arches develop into the left aortic arch and the ductus arteriosus, cardiac branches of the left vagus nerve and left-sided sympathetic nerves distribute primarily to the aortic arch and pulmonary trunk, forming the arterial and conotruncal plexi.
Embryologically the venous side favors the right-sided structures, since the right superior vena cava is retained, and the sinus venosus shifts to the right from midline and is incorporated into the right atrium.
Therefore, the venous part of the heart is associated with cardiac nerves from the right cardiac sinoatrial plexus. The sympathetic nerves arise from the superior and middle cervical ganglia, giving off the superior and middle cardiac nerves respectively.
The inferior cardiac nerve originates from the fusion of the inferior cervical ganglion and the first thoracic ganglion, called the stellate ganglion. Each vagus nerve contributes to the cardiac plexuses by way of the superior and inferior cervical nerves, as well as a thoracic cardiac branch arising from the recurrent laryngeal nerve. The superficial cardiac plexus receives its contributions from the inferior cervical cardiac branch of the left vagus and the left superior cardiac nerves of the sympathetic nervous system.
The ganglion of Wrisberg is associated with this plexus and lies between the aortic arch and the pulmonary trunk to the right of the ligamentum arteriosum. The deep cervical plexus receives contributions from three right-sided sympathetic cardiac nerves, three cardiac branches of the right vagus nerve, three superior cervical and thoracic cardiac branches of the left vagus nerve, the middle and upper cardiac nerves from the sympathetic trunk, and direct branches from the five or six thoracic sympathetic ganglia.
From these autonomic nervous system plexi, the sympathetic and vagal nerves distribute to the walls of the great vessels, including the SA and AV nodes and the bundle of His.
Sympathetic nerves and some parasympathetic nerves accompany the coronary arteries and innervate the ventricles. In the same nerves and through the same pathways, both afferent sympathetic and parasympathetic fibers pass back to the central nervous system.
The field has evolved over centuries, and information continues to accrue, stimulated in large part by clinical advances. This chapter provides an overview of cardiac anatomy that is relevant to.
This anatomical information forms the basis for an understanding of not only radiographic studies but also cardiac pathophysiology and the approach to therapeutic interventions. For various subspecialty works, more detailed information is available in the published literature.
Molecular pathway for the localized formation of the sinoatrial node. Circ Res. Sinus node revisited in the era of electroanatomical mapping and catheter ablation.
Atrial structure and fibres: morphologic bases of atrial conduction. Cardiovasc Res. Kent AFS. Observations on the auriculoventricular junction of the mammalian heart. Q J Exp Physiol. Mahaim I. Paris: Masson; James TN. The connecting pathways between the sinus node and AV node and between the right and left atrium in the human heart. Am Heart J. The nature of the vascular communications between the coronary arteries and the chambers of the heart.
Barry A, Patten BM. The structure of the adult heart. In: Goul SE Ed. Pathology of the Heart, 3rd edition. Springfield, lL: Charles C Thomas; Licata RH.
Anatomy of the heart. In: Liusada AA Ed. Development and Structure of the Cardiovascular System. New York: McGrawHili; McAlpine WA. Berlin: Springer; Netter FH. Summit, NJ: Ciba; Patten BM. The heart. Philadelphia: Blakiston; Examination of the heart.
Hum Pathol. The receptor then can recycle to the cell surface. These uncoupling proteins also target receptors to clathrincoated pits resulting in receptor downregulation and eventual proteolysis. It has recently been shown that GRKs by themselves can activate parallel signaling pathways such as stretchassociated angiotensin-II activation. This hypothesis led to the idea that blocking -adrenoceptors might be a useful strategy in heart failure. Although it took many years to prove this hypothesis, -blocker therapy is now routine in heart failure patients.
Along the way, much was learned about receptors. There are two principal types of -receptors: 1 and 2. Early studies by Bristow and his colleagues in tissue obtained from advanced heart failure patients revealed that 1 receptor density was reduced, while 2 receptor density actually increased and switched its coupling to a guanine nucleotide inhibitory protein Gi. What adverse mechanisms are mediated by -receptors in heart failure? Polymorphisms in the 1- and 2C-adrenergic receptors may play a role in some patients.
In heart failure, where 1 signaling induces cell remodeling and programmed cell death, this spatial restriction is lost, such that 1 and 2 signaling resemble each other. Synchronous cardiac contraction and relaxation require the coordination of numerous complex systems both within and without the cardiac myocyte.
The human heart has evolved to integrate these pathways to provide efficient energy production and utilization in order to maintain blood supply to other vital organs as well as to the heart itself. Disruption of these pathways can be both cause and effect of cardiac injury and failure. Among the two most prominent pathways that require moment to moment coordination and integration are the betaadrenergic signaling pathway and calcium handling. Both are central to cardiac contraction and relaxation, are abnormal in pathophysiologic states, and are targets for therapeutic intervention.
Located on the cell surface, -adrenoceptors are prototypical G-protein coupled receptors. They are liganded by the naturally occurring catecholamines, norepinephrine and epinephrine. Norepinephrine is released from synaptic vesicles of sympathetic nerves that innervate the heart and is principally responsible for cardiac chronotropy and contractility. Signaling results from the downstream activation of cyclic adenosine monophosphate cAMP , initiated by liganding of the receptor by the catecholamine.
Through a series of complex interactions, cAMP activates the contractile apparatus and also influences the conductance of ion channels that govern heart rate. Numerous studies have established that the -adrenergic receptor is highly regulated.
After the receptor binds to a stimulatory guanine nucleotide regulatory protein Gs , adenylyl cyclase is activated to hydrolyze ATP and produce cAMP. The G-protein-receptor complex can be uncoupled from its downstream signaling effectors by a molecule called G-protein.
Calcium was first found to exert an influence on the heart in the second decade of the 20th century. Subsequently it has become clear that calcium is a universal second messenger and in the heart exerts effects on contractility, mitochondrial function, transcriptional regulation and action potential generation.
Calcium control is tightly linked to adrenoceptor signaling via intracellular mechanisms that take up and release ionic calcium. The sarcoplasmic reticulum SR , equivalent to the endoplasmic reticulum in other cells, lies just beneath the sarcolemma, which consists of the cell surface and invaginated T tubules.
Each junction between the sarcolemma and the SR, where L-type calcium channels and ryanodine receptors are clustered, constitutes a local calcium signaling complex or couplon. When calcium enters the cell via sarcolemmal L-type calcium channels, adjacent ryanodine receptors are activated. This leads to SR calcium release and a marked increase in intracellular calcium concentration. This process has been termed calcium-induced calcium release and results in enhanced cardiac muscle contraction.
This inhibition decreases the rate of muscle relaxation and contractility. Most of the remaining cytoplasmic calcium is removed via the sodium-potassium exchanger. Inhibition of this exchanger resulting in increased cytosolic calcium is the basis of the action of digitalis glycosides, which for almost two centuries was the only effective heart failure treatment available.
In addition, since SERCA is more active, the next action potential will cause increased calcium release, resulting in augmented contraction. It has been found that SERCA protein and activity are diminished in heart failure, and replenishing this protein using gene therapy is a current therapeutic goal.
Animal experiments have been successful, and a human clinical trial is under way. As noted above, -adrenergic blockade has emerged as successful conventional therapy for heart failure.
Why this should be so has elicited considerable interest. In a canine model of myocardial infarction, upregulation of previously downregulated -receptors in response to -blockade has been reported. This involves the consequences of altered ryanodine receptor function and SR calcium loss. Studies have described increased ryanodine receptor open probability in isolated preparations and increased calcium loss from SR vesicles isolated from failing hearts. These findings point to a possible common mechanism underlying alterations of systolic and diastolic function seen in heart failure.
Calcium channel hyperphosphorylation can also result in increased calcium current that predisposes to arrhythmias. Excess phosphorylation in the SR complex can result in depletion of SR calcium stores, causing impaired cytosolic calcium transients resulting in systolic and diastolic dysfunction. Thus, inhibition of excess -adrenergic drive would be expected to reduce these responses and improve cardiac function, which indeed appears to be the case as documented by randomized, controlled clinical trials.
As CamKII is upregulated both in hypertrophy and in heart failure, small molecule inhibitors of CamKII are being developed but to date remain at the preclinical stage. Calcium is also involved in myofilament function via a calcium-dependent ATPase.
Thus, augmented or reduced mitochondrial generation of ATP under normal and pathological circumstances is dependent on calcium availability, and the relation between calcium flux and ATP generation is critical for fundamental processes such as contraction, relaxation and electrical activity. The localization of mitochondria near calcium release sites on the SR places these organelles in position to accumulate calcium, thereby regulating the level of calcium in the cytosol.
Conversely, mitochondria can prevent SR calcium depletion by recycling this ion to the SR. The role of calcium in oxidative phosphorylation and the production of ATP in the mitochondria are exquisitely balanced with the energy required for myocyte crossbridge cycling that is fueled by the hydrolysis of MgATP and regulated by calcium.
Mitochondria have two membranes: an outer membrane permeable to molecules of 10 kilodaltons or less and an inner membrane permeable only to oxygen, carbon dioxide and water. The inner membrane, which is layered and invaginated, forms cristae, thereby markedly increases its surface area. The space between the two membranes intermembrane space has an important role in the mitochondrions. From succinate, there is a similar pathway, but protons are not translocated at complex II. What is the purpose of this complicated schema?
It is to drive the activity of ATP synthase complex V which is dependent on the proton chemiosmotic gradient created by the ETC between the matrix and the intermembrane space. ATP forms spontaneously in the presence of ATP synthase, but the chemiosmotic gradient is necessary to cause the release of bound ATP, so that the cycle can continue and ATP can be continuously generated. When there is a threat that the gradient will be dissipated by the need for more ATP, electron transport is increased so that the gradient is maintained.
As oxygen is the ultimate electron acceptor, the process of ATP generation is termed oxidative phosphorylation. All of the above reactions are summarized schematically in Figure 1. Much of mitochondrial pathophysiology revolves around the inability to maintain the chemiosmotic gradient and the consequences of this failure.
For mitochondria to maintain this proton-mediated pH gradient and the resulting membrane potential m necessary to drive oxidative phosphorylation, the inner mitochondrial membrane must remain impermeable to all, but a few ions and metabolites for which specific transport mechanisms have evolved. It has been hypothesized that water and restricted metabolites can pass through the inner membrane via a pore, also called the permeability transition pore.
The physical characterization of this permeability barrier remains controversial. Nevertheless, persistent opening of this barrier under oxidative stress causes collapse of the proton gradient and m across the inner mitochondrial membrane, resulting in uncoupling of oxidative phosphorylation and initiation of a series of biochemical changes which lead to cell death.
As a normal byproduct of the electron transfer activity described above, mitochondria generate reactive oxygen species ROS. The primary sources are complexes I and III. The inner membrane surrounds another compartment called the matrix which contains the enzymes responsible for citric acid Krebs cycle reactions. The folded cristae provide both a large surface area and intimate contact with the matrix, so that matrix components can rapidly diffuse to inner membrane complexes.
It should be noted that the only Krebs cycle reaction that occurs in the inner membrane itself is the oxidation of succinate to fumarate catalyzed by succinate dehydrogenase. This succinate dehydrogenase complex, which is composed of the enzyme, succinate and the energy carrier flavin adenine dinucleotide FAD , is also called complex II of the ETC.
This system accepts energy from carriers in the matrix and stores it in a form that can be used to phosphorylate ADP. Two carriers donate free energy to the ETC. FMN receives the resulting hydrogen from NADH and two electrons; it also garners a proton from the matrix and passes the electrons to iron-sulfur clusters that are part of the complex and forces two protons into the intermembrane space.
Electrons pass to a carrier located in the membrane Coenzyme Q and are passed to complex III, which is associated with a further hydrogen translocation event. The next step in the pathway is cytochrome C and then further on to complex IV cytochrome oxidase , where more protons are translocated. It is at this site that oxygen binds along with protons.
Using the remaining pair of electrons and free energy, oxygen is reduced to water. This last step is diatomic, requiring two electron pairs and two cytochorme oxidase complexes. Thus, oxygen serves as an electron acceptor so that electron. We do not store files not owned by us, or without the permission of the owner. We also do not have links that lead to sites DMCA copyright infringement. If You feel that this book is belong to you and you want to unpublish it, Please Contact us. Cardiology: An Illustrated Textbook 2nd Edition.
Rashid, M. Ross Fuente: Angelfire. Know the symptoms. Here ends our selection of free Cardiology books in PDF format. We hope you liked it and already have your next book! Medical books in PDF. Do you want to read about another topic? Art and Photography. Alternative Therapy. Business and Investment. Food and drinks. Mystery and Thriller. Molecular imaging and three-dimensional echocardiography and intravascular ultrasound imaging have been introduced.
Advances have occurred in nuclear, cardiovascular computerized tomographic and magnetic resonance imaging. In the textbook, the advances in these diagnostic techniques and their clinical applications in the practice of cardiology have been extensively discussed. The role of rest and stress and electrocardiography and echocardiography has been emphasized.
During last two decades, we have witnessed enormous advances in the understanding of the genesis of atrial and ventricular arrhythmias, in the techniques of electrophysiologic and the pharmacologic and nonpharmacologic treatment of arrhythmias.
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