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3. 4. 5. 6. 7. 33 beta subunit) to create the IKs ion channel, which is responsible for the delayed potassium rectifier current of the cardiac action potential [84]. Homozygous mutations in KVLQT1 leads to severe prolongation of the QT interval (due to near-complete loss of the IKs ion channel), and is associated with increased risk of ventricular arrhythmias and congenital [87, 84]. LQT2: It is the second most common gene location that is affected in long QT syndrome, making up about 35 to 45 percent of all cases.

18 . 8) 2 Theoretically, Lead III as well as the augmented unipolar limb leads do not need to be recorded, but instead they can be computed from Lead I and Lead II. aV F = φLL − 16 3. 15. The generation of the ECG signal in the Einthoven limb leads. 17(a). 17(b). The Unipolar Precordial Leads are called also Wilson Unipolar Chest Leads. V6 . They yield a positive deflection when facing positive charges and negative when facing negative charges according to what Wilson called the the solid-angle concept [41].

They are located in the sinoatrial node, SA or sinus node, in the right atrium at the superior vena cave. These cells are also called pacemaker cells in the way they are able to generate an action potential without any influence from other cells and in the way their discharge determines the rate of the heart. Their self-extracting action is actually controlled by sympathetic and parasympathetic autonomic nervous systems. The sympathetic system dominates a high heart rate during activity, exercise and stress, whereas the parasympathetic system maintains much lower heart rate during relaxation.

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