الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Heart failure can be defined as a complex clinical syndrome coming from both functional and structural disability of blood ejection or ventricular filling. Although that clinical syndrome of heart failure could arise as a result of disorders or abnormalities of all element of function and structure of the heart, most heart failure patients have impairment of myocardial performance, with wide range of findings from normal ventricular size and function to noticeable ventricular dilatation and decreased function.
Adverse ventricular remodeling is considered as the explanation element in the deterioration of cardiac function, contributing to the downward progression toward heart failure. The increased stress on the myocardial wall during the diastolic phase is the cause of the develop, and consequently the progression of that adverse cardiac remodeling.
The electrical activation of the heart is a coordinated rapid process, in which electrical signals travel via the His-Purkinje system and activate the two ventricles in approximately 50 to 80 milliseconds. The excitation advances from the endocardium to the epicardium also from the apex to the base, leading to a coordinated efficient contraction where all walls contribute to generate pressure. It ensures an appropriate activation of papillary muscles, optimizing the mitral valve’s function as well as preventing regurgitation. An abnormal His- Purkinje activation could impair the spreading of the electrical impulse diffusely, slow the intramyocardial conduction and subsequently cause a heart failure. More noticeable regional delays, like those resulting from a conduction block, lead to a regional delay in contraction, consequently, cause ventricular dyssynchrony.
LV dyssynchrony commonly is a consequence of altered activation the lateral left ventricular free wall and manifests often, though not always, by left branch bundle block on the electrocardiogram. Early systolic contraction of the anterior left ventricle and septum causes the lateral wall, which is still passive, to prestretch, which delays the rise in intracavitreal pressure and closure of the mitral valve. The left ventricular lateral free wall’s delayed systolic activation causes the anteroseptal area to stretch in response, which competes with aortic ejection and reduces the net cardiac output. This leads to mechanical inefficiency, where the ventricular blood pool is transmitted between two intracavitary sinks (the anteroseptal region in the late systole and the stretched lateral wall in the early systole). Functional mitral regurgitation, which is caused by the delayed increase of left ventricular intracavitary pressure and the absence of coordinated papillary muscle contraction, may exacerbate that inefficiency.
CRT is considered as non-pharmacological option for HF patients left in NYHA functional classification II, III, and IV in defiance of optimum medical therapy, LVEF < 35%,also manifest ventricular desynchrony appeared as a wider QRS >150 ms on ECG. CRT is responsible for improvement in morbidity and mortality in cases with severely reduced LV function through synchronized biventricular pacing and consequently reverse remodeling.
Despite biventricular pacing, Just two thirds of patients who have CRT implants respond; the