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group_1_presentation_3_-_atrial_fibrillation [2016/04/01 23:35] dheriaj |
group_1_presentation_3_-_atrial_fibrillation [2018/01/25 15:18] (current) |
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| ''Figure 2: A general outline of the triggers involved in inducing\\ | ''Figure 2: A general outline of the triggers involved in inducing\\ | ||
| - | atrial fibrillation.''</style> | + | atrial fibrillation <sup>[1]</sup>.''</style> |
| - | AF requires a trigger that initiates the arrhythmia, and a substrate that further sustains the arrhythmia and its symptoms [1]. Triggers are extremely diverse and include high blood pressure, abnormal heart structure, infections, diseases that damage the heart, an overactive thyroid, congenital heart diseases, and excessive alcohol [1]. | + | AF requires a trigger that initiates the arrhythmia, and a substrate that further sustains the arrhythmia and its symptoms <sup>[1]</sup>. Triggers are extremely diverse and include high blood pressure, abnormal heart structure, infections, diseases that damage the heart, an overactive thyroid, congenital heart diseases, and excessive alcohol <sup>[1]</sup>. |
| - | Ectopic foci occurring in atrial tissues have also recently been identified as an AF trigger[1]. Once AF occurs, arrhythmias may occur even in the absence of the original trigger [1]. | + | Ectopic foci occurring in atrial tissues have also recently been identified as an AF trigger <sup>[1]</sup>. Once AF occurs, arrhythmias may occur even in the absence of the original trigger <sup>[1]</sup>. |
| - | Some of the substrate that sustains the abnormal heart rhythm include abnormal calcium handling and an altered action potential due to irregular ion currents [1]. | + | Some of the substrate that sustains the abnormal heart rhythm include abnormal calcium handling and an altered action potential due to irregular ion currents <sup>[1]</sup>. |
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| {{:playground:pic_33.jpg?700x400}} | {{:playground:pic_33.jpg?700x400}} | ||
| - | ''Figure 3: An illustration of the improper calcium handling of myocardial cells inflicted with atrial fibrillation. Note that adaptive responses include the upregulation of NCX, a decrease in calcium current, and a decrease in calcium release from the sarcoplasmic reticulum.[1]'' </style> | + | ''Figure 3: An illustration of the improper calcium handling of myocardial cells inflicted with atrial fibrillation. Note that adaptive responses include the upregulation of NCX, a decrease in calcium current, and a decrease in calcium release from the sarcoplasmic reticulum.<sup>[1]</sup>'' </style> |
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| - | As noted as one of the substrates that sustains AF, the mishandling of excessive calcium occurs due to a cascade of abnormal amounts of repetitive atrial excitations [10]. Fundamentally, this mishandling occurs due to ectopic action potentials via afterdepolarizations [10]. | + | As noted as one of the substrates that sustains AF, the mishandling of excessive calcium occurs due to a cascade of abnormal amounts of repetitive atrial excitations <sup>[10]</sup>. Fundamentally, this mishandling occurs due to ectopic action potentials via afterdepolarizations <sup>[10]</sup>. |
| - | As a result of this mishandling of calcium within myocardial cells, the body engages an adaptive response to upregulate NCX channels (Na+-Ca2+ exchanger), decrease the Ca2+ current, and impair the release of Ca2+ from the sarcoplasmic reticulum [10]. As a result of this adaptive response, there is a total decrease in the concentration of Ca2+ within myocardial cells of the atrium, directly resulting in contractile dysfunction due to the reduced activity of myofilament function [10]. | + | As a result of this mishandling of calcium within myocardial cells, the body engages an adaptive response to upregulate NCX channels (Na<sup>+</sup>/Ca<sup>2+</sup> exchanger), decrease the Ca<sup>2+</sup> current, and impair the release of Ca2+ from the sarcoplasmic reticulum <sup>[10]</sup>. As a result of this adaptive response, there is a total decrease in the concentration of Ca<sup>2+</sup> within myocardial cells of the atrium, directly resulting in contractile dysfunction due to the reduced activity of myofilament function <sup>[10]</sup>. |
| - | This can be quantitatively seen in a group showing the relationship between pressure and time of the atrial contraction; compared to normal sinus rhythms, atrial myocardial cells demonstrate a significant depression of the action potential plateau[10]. Potential effects stemming from AF include stasis of the atria, leading to thromboemboli, and further downstream a cardiac infarction (also known as a heart attack) [10]. | + | This can be quantitatively seen in a group showing the relationship between pressure and time of the atrial contraction; compared to normal sinus rhythms, atrial myocardial cells demonstrate a significant depression of the action potential plateau<sup>[10]</sup>. Potential effects stemming from AF include stasis of the atria, leading to thromboemboli, and further downstream a cardiac infarction (also known as a heart attack) <sup>[10]</sup>. |
| <style float-left> | <style float-left> | ||
| - | {{:playground:pic_2.jpg?400x390}} | + | {{:playground:pic_2.jpg?410x390}} |
| - | ''Figure 4: The relationship between pressure and time of the atrial \\ contraction, comparing the normal sinus rhythm (left) with the sinus \\ rhythm suffering from atrial fibrillation (right). [10]'' </style> | + | ''Figure 4: The relationship between pressure and time of the atrial \\ contraction, comparing the normal sinus rhythm (left) with the sinus \\ rhythm suffering from atrial fibrillation (right) <sup>[10]</sup>.'' </style> |
| === Normal Sinus Rhythm === | === Normal Sinus Rhythm === | ||
| - | The sinoatrial (SA) node, located in the right atrium is known as the pacemaker of the heart and is responsible for initiating action potentials via spontaneous firing. The pathway of the action potential is as follows: the action potential begins in the atria, then travels to the AV node, and finally to the ventricles. Together, this triggers coordinated contraction of the heart, and pushes blood out of the heart and into systemic circulation [1]. | + | The sinoatrial (SA) node, located in the right atrium is known as the pacemaker of the heart and is responsible for initiating action potentials via spontaneous firing. The pathway of the action potential is as follows: the action potential begins in the atria, then travels to the AV node, and finally to the ventricles. Together, this triggers coordinated contraction of the heart, and pushes blood out of the heart and into systemic circulation <sup>[1]</sup>. |
| === Normal Excitation Coupling === | === Normal Excitation Coupling === | ||
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| **Cardiac excitation** - contraction coupling is the manner in which electrical excitation generates contraction of the heart. | **Cardiac excitation** - contraction coupling is the manner in which electrical excitation generates contraction of the heart. | ||
| - | Calcium plays a key role in the regulation of cardiac contractility, and is the activator of myofilaments; the key structures responsible for contraction. During the onset of an action potential within cardiomyocytes, intracellular calcium enters through depolarized activated calcium channels contributing to the characteristic cardiac action potential plateau. Subsequently, calcium entry prompts calcium release from the sarcoplasmic reticulum via the ryanodine receptors [1]. Thus, the intracellular concentration of calcium rises and calcium then binds to the myofilament protein troponin C. | + | Calcium plays a key role in the regulation of cardiac contractility, and is the activator of myofilaments; the key structures responsible for contraction. During the onset of an action potential within cardiomyocytes, intracellular calcium enters through depolarized activated calcium channels contributing to the characteristic cardiac action potential plateau. Subsequently, calcium entry prompts calcium release from the sarcoplasmic reticulum via the ryanodine receptors <sup>[1]</sup>. Thus, the intracellular concentration of calcium rises and calcium then binds to the myofilament protein troponin C. |
| - | In order for relaxation to occur, the intracellular concentration of calcium must decrease, which allows for calcium to dissociate from troponin. Calcium is then transported out of the cytosol by four pathways++| utilizing the sarcoplasmic reticulum ATPase, sarcolemma Na+/Ca2+ exchange, sarcolemma Ca2+ transport ATPase or mitochondrial CA2+ uniport [1]. ++ | + | In order for relaxation to occur, the intracellular concentration of calcium must decrease, which allows for calcium to dissociate from troponin. Calcium is then transported out of the cytosol by four pathways++| utilizing the sarcoplasmic reticulum ATPase, sarcolemma Na<sup>+</sup>/Ca<sup>2+</sup> exchange, sarcolemma Ca<sup>2+</sup> transport ATPase or mitochondrial CA<sup>2+</sup> uniport <sup>[1]</sup>. ++ |
| <style float-right> | <style float-right> | ||
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| {{:playground:pic_44.jpg?400x400}} | {{:playground:pic_44.jpg?400x400}} | ||
| - | http://users.atw.hu/blp6/BLP6/HTML/common/M9780323045827-013-f003.jpg </style> | + | Figure 5: The role of calcium in normal excitation coupling |
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| === Normal Excitation Coupling === | === Normal Excitation Coupling === | ||
| - | Excitation within the heart is characterized by two phases; systole and diastole. During systole, calcium is released inside the sarcomere leading to an increase of intracellular calcium. Calcium then binds to [[wp>troponin]] initiating contraction of the heart, and blood from the heart is pumped throughout the body. Subsequently, during diastole there is an uptake of calcium into the sarcoplasmic reticulum via the Ca2+ ATPase. This then results in relaxation of the heart [1]. | + | Excitation within the heart is characterized by two phases; systole and diastole. During systole, calcium is released inside the sarcomere leading to an increase of intracellular calcium. Calcium then binds to [[wp>troponin]] initiating contraction of the heart, and blood from the heart is pumped throughout the body. Subsequently, during diastole there is an uptake of calcium into the sarcoplasmic reticulum via the Ca<sup>2+</sup> ATPase. This then results in relaxation of the heart <sup>[1]</sup>. |
| === Sinus Rhythm in Atrial Fibrillation === | === Sinus Rhythm in Atrial Fibrillation === | ||
| - | Atrial fibrillation is characterized by an irregular heart rhythm that begins in the atria. Contrary to normal sinus rhythm where the SA node is responsible for initiating [[wp>action potentials]], in atrial fibrillation there are many different impulses that all rapidly fire at once leading to a very rapid rhythm in the atria. The consequence of this rapid rhythm is that the atria cannot contract or squeeze blood into the ventricle. Thus, in affected patients there is a large number of impulses that get into the ventricle leading to irregular contraction and subsequently an irregular and rapid heartbeat [2]. | + | Atrial fibrillation is characterized by an irregular heart rhythm that begins in the atria. Contrary to normal sinus rhythm where the SA node is responsible for initiating [[wp>action potentials]], in atrial fibrillation there are many different impulses that all rapidly fire at once leading to a very rapid rhythm in the atria. The consequence of this rapid rhythm is that the atria cannot contract or squeeze blood into the ventricle. Thus, in affected patients there is a large number of impulses that get into the ventricle leading to irregular contraction and subsequently an irregular and rapid heartbeat <sup>[2]</sup>. |
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| ==== Concluding Remarks ==== | ==== Concluding Remarks ==== | ||
| - | Continued research in determining the relative roles of ectopic activity, single-circuit reentry and multiple-circuit reentry in maintaining clinical AFib is important to better understand the mechanisms underlying AFib. Answering these questions will lead to new and improved possibilities in prevention and therapy. | + | There are many questions that need to be answered in order to better understand the mechanisms underlying AFib, such as the genes responsible for familial Afib and how they lead to arrhythmia. Continued research in determining the relative roles of ectopic activity, single-circuit reentry and multiple-circuit reentry in maintaining clinical AFib is important to better understand the mechanisms underlying AFib. Answering these questions will lead to new and improved possibilities in prevention and therapy. |
| ====== References ====== | ====== References ====== | ||
