QRS dispersion an electrocardiographic index of systolic left by nikeborome


									QRS dispersion: an electrocardiographic index of systolic left
 ventricular dysfunction in patients with left bundle branch

 Protocol of a thesis submitted in partial fulfillment of the degree of
                         master of cardiology

              Ehab Ahmed Mohamed Ahmed Beshry
              Minstery of health and population hospitals

        Professor Doctor. Wagdy Abd-Elhamid Galal
                Professor of Cardiology and Angiology
              Faculty of medicine - Ain-Shams University

                  Doctor. Rania Samir Ahmed
                Lecturer of Cardiology and Angiology
              Faculty of medicine - Ain-Shams University

             Doctor. Mohamed Amin Abd-Elhamid
                Lecturer of Cardiology and Angiology
              Faculty of medicine - Ain-Shams University
        A widely known definition of heart failure is "a pathophysiological state in which
an abnormality of cardiac function is responsible for the failure of the heart to pump
blood at a rate commensurate with the requirements of the metabolizing tissues."[1] This
definition places the emphasis on the physiology of the circulation. More recent
definitions have taken a clinically useful approach. One American definition is "Heart
failure is a complex clinical syndrome that can result from any structural or functional
cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. The
cardinal manifestations of heart failure are dyspnea and fatigue, which may limit exercise
tolerance, and fluid retention, which may lead to pulmonary congestion and peripheral
edema."[2] A recent European definition is similar: "Heart failure is a complex syndrome
that can result from any structural or functional cardiac disorder that impairs the ability of
the heart to function as a pump to support a physiological circulation. The syndrome of
heart failure is characterized by symptoms such as breathlessness and fatigue, and signs
such as fluid retention."[3]

        Although the mortality rate from heart disease is declining as a consequence of
improved treatment and primary prevention in industrialized countries [4] the number of
patients affected by congestive heart failure is still increasing. This is a consequence of
increased longevity and of the age-associated increase in the prevalence of heart diseases
in general, and of congestive heart failure in particular. [5]

        Among the many clinical and pathophysiologic factors that have been proposed as
prognostic indicators in congestive heart failure, reduced left ventricular ejection
fraction,[6,7] neurohormonal activation,[6] and reduced exercise tolerance expressed as
peak oxygen consumption,[6,8,9] or performance in the 6-minute walk test,[10] have been
identified as independent predictors of mortality rate. In patients with congestive heart
failure due to ventricular systolic dysfunction, intraventricular conduction delays are
frequently observed, in such patients, QRS duration of ≥ 120 ms is prevalent in 25-50%,
and left bundle branch block is found in 15-27%. [11] Despite this, data concerning the
prognostic significance of intraventricular conduction defects and, in particular, of
complete left bundle branch block in congestive heart failure are more conflicting.

       Atrioventricular and intraventricular conduction delays both further aggravate left
ventricular dysfunction in patients with underlying heart failure. Notably, left bundle
branch block alters the sequence of left ventricular contraction, causing wall segments to
contract early or late, with redistribution of myocardial blood flow, non-uniform regional
myocardial metabolism, and changes in regional molecular processes, such as calcium
handling and stress kinase proteins.[12-16] Intraventricular dyssynchrony partly favors
mitral valve incompetence and shortening of left ventricular filling. In addition to
intraventricular conduction, delays in atrioventricular timing also influence the
mechanical function of the four cardiac chambers, in which optimal timing of the atrial
systole is linked to an increase in cardiac output and the duration of diastolic filling and a
decrease of pre-systolic mitral regurgitation. Thus dyssynchrony seems to represent a
pathophysiological process that directly depresses ventricular function, causes left
ventricular remodeling and congestive heart failure, and as a consequence causes a higher
risk of morbidity and mortality.

        Even though left bundle branch block morphology with QRS duration > 120
milliseconds is included in the current recommendations for biventricular pacing in
congestive heart failure patients, several studies have shown that the mechanical
improvement after electrical resynchronization does not closely relate to QRS
duration.[17,18] Therefore several investigators claim that surface electrocardiogram is not
sensitive enough to detect electromechanical delay that leads to ventricular
dysynchronization.[19-20] QRS dispersion, measured as the difference between maximal
and minimal QRS duration on the 12-lead surface electrocardiogram, has been recently
proposed to be associated with increased mortality in congestive heart failure patients.[21]
The impact of this electrocardiographic index on systolic performance of the heart needs
to be studied.
                             AIM OF THE WORK
        The aim of this prospective study is to investigate whether QRS dispersion is
related to left ventricular systolic dysfunction, in patients with complete left bundle
branch block.

       The study will be conducted on 40 consecutive patients with complete left bundle
branch block presenting to the cardiology department of Ain-Shams University hospital.

Inclusion criteria:
1. Gender; males and females.
2. Age; more than 18 years old.
3. Electrocardiogram findings; complete left bundle branch block diagnosed according
   to standard definitions:[22] QRS-duration greater than or equal to 0.12 seconds,
   predominantly upright QRS complexes with slurred R waves in leads I, V5, and V6,
   and QS or rS pattern in V1.

Exclusion criteria:
1. Patients with acute myocardial infarctions/acute coronary syndromes.
2. Patients with atrial fibrillation.
3. Patients with decompensated heart failure.
       Each of the selected patients will be subjected to the following:

•   Complete history taking.
•   Complete clinical examination.
        o General examination
        o Local examination
•   Standard 12-lead electrocardiogram performed before the study, with simultaneous
    recording of the 12-leads at a velocity of 50 millimeters/second, the QRS duration
    will be measured manually from the beginning of the first appearing Q or R wave to
    the end of the last appearing R, S, or R’ wave [23] and QRS dispersion will be
    estimated as the difference between maximal and minimal QRS intervals in
•   Transthoracic echocardiography to estimate global left ventricular systolic function
    by left ventricular ejection fraction. The ejection fraction will be calculated from two
    dimensional echocardiography images used for measuring left ventricular volume.
    The volume of the left ventricular is calculated from the dimension and area obtained
    from two orthogonal apical views (four-chamber and two-chamber views). The left
    ventricular volume then is calculated electronically with the modified Simpson
    method or disk summation method where the left ventricular endocardial border is
    traced from the two orthogonal apical views to create multiple (usually 20) cylinders
    whose volume is summated to provide left ventricular volume.
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