Mohd Farid

Mohd Farid
Showing posts with label Atrial Fibrillation. Show all posts
Showing posts with label Atrial Fibrillation. Show all posts

Saturday, March 2, 2019

Certificate No 175 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt-Application In Progress-Memories Never Die

Certificate No 175 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt-Application In Progress-Memories Never Die



EAPCI Webinar On Always Triple Therapy For Afib Patients Undergoing PCI Irrespective Of The Bleeding Risk Status?
European Society Of Cardiology
4 October 2018

Certificate No 162 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt-Application In Progress-Memories Never Die

Certificate No 162 Malaysia Book Of Records "Most Number Of Certificates Received By An Individual" Record Breaking Attempt-Application In Progress-Memories Never Die



EACVI EHRA Webinar On Role Of MMI For Managing Patients With Atrial Fibrillation
European Society Of Cardiology
18 April 2018

Tuesday, February 26, 2019

Sunday, July 30, 2017

Vein Of Marshall And Its Clinical Significant

Vein Of Marshall And Its Clinical Significant




The systemic veins may be arranged into three groups: (1) The veins of the heart. (2) The veins of the upper extremities, head, neck, and thorax, which end in the superior vena cava. (3) The veins of the lower extremities, abdomen, and pelvis, which end in the inferior vena cava.

The Veins of the Heart

Coronary Sinus (sinus coronarius)

Most of the veins of the heart open into the coronary sinus. This is a wide venous channel about 2.25 cm. in length situated in the posterior part of the coronary sulcus, and covered by muscular fibers from the left atrium. It ends in the right atrium between the opening of the inferior vena cava and the atrioventricular aperture, its orifice being guarded by a semilunar valve, the valve of the coronary sinus (valve of Thebesius).

Tributaries.—Its tributaries are the great, small, and middle cardiac veins, the posterior vein of the left ventricle, and the oblique vein of the left atrium, all of which, except the last, are provided with valves at their orifices.
1. The Great Cardiac Vein (v. cordis magna; left coronary vein) begins at the apex of the heart and ascends along the anterior longitudinal sulcus to the base of the ventricles. It then curves to the left in the coronary sulcus, and reaching the back of the heart, opens into the left extremity of the coronary sinus. It receives tributaries from the left atrium and from both ventricles: one, the left marginal vein, is of considerable size, and ascends along the left margin of the heart.
2. The Small Cardiac Vein (v. cordis parva; right coronary vein) runs in the coronary sulcus between the right atrium and ventricle, and opens into the right extremity of the coronary sinus. It receives blood from the back of the right atrium and ventricle; the right marginal vein ascends along the right margin of the heart and joins it in the coronary sulcus, or opens directly into the right atrium.
3. The Middle Cardiac Vein (v. cordis media) commences at the apex of the heart, ascends in the posterior longitudinal sulcus, and ends in the coronary sinus near its right extremity.
4. The Posterior Vein of the Left Ventricle (v. posterior ventriculi sinistri) runs on the diaphragmatic surface of the left ventricle to the coronary sinus, but may end in the great cardiac vein.
5. The Oblique Vein of the Left Atrium (v. obliqua atrii sinistri[Marshalli]; oblique vein of Marshall) is a small vessel which descends obliquely on the back of the left atrium and ends in the coronary sinus near its left extremity; it is continuous above with the ligament of the left vena cava (lig. venæ cavæ sinistræ vestigial fold of Marshall), and the two structures form the remnant of the left Cuvierian duct.

The following cardiac veins do not end in the coronary sinus:

The anterior cardiac veins, comprising three or four small vessels which collect blood from the front of the right ventricle and open into the right atrium; the right marginal vein frequently opens into the right atrium, and is therefore sometimes regarded as belonging to this group;

The smallest cardiac veins (veins of Thebesius), consisting of a number of minute veins which arise in the muscular wall of the heart; the majority open into the atria, but a few end in the ventricles.



Vein Of Interest
The Vein of Marshall, oblique vein of Marshall or the oblique vein of the left atrium is a small vein that descends on and drains the posterior wall of the left atrium. It drains directly into the coronary sinus at the same end as the great cardiac vein, marking the origin of the sinus. It represents the persistent left horn of the sinus venous (left SVC) and is important prenatally, but is of little importance postnatally. 

Source of Focal AF

In humans, the sinus node is not the only pacemaker. Boineau et al demonstrated widely distributed atrial pacemaker complexes in the human heart. In the isolated, perfused canine right atrium, ectopic pacemaker activity was most often found near the sinus node or the crista terminalis. These pacemakers may exhibit different responses to norepinephrine and acetylcholine. Scherlag et al reported that sympathetic stimulation could also induce left atrial ectopic activity. To study the source of these ectopic activities, we performed a computerized mapping study in the isolated-perfused canine left atrium. Isoproterenol can cause automatic rhythm with this preparation. On the basis of these findings, hypothesized that the Marshall bundle may serve as a source of focal AF in humans.

In the present study, they successfully cannulated the Vein of Marshall and recorded sharp potentials directly from the catheter within the Vein of Marshall. Because the Vein of Marshall is an epicardial structure and the recording site was not close to the pulmonary veins, it is unlikely that these sharp second potentials originated from the extension of the atrial musculature into the pulmonary veins. Rapid activation of the Marshall bundle might serve as a trigger of atrial arrhythmias, including AF. Finally, they were able to use the Vein of Marshall catheter as a guide for radiofrequency ablation. A radiofrequency lesion placed in the posterolateral left atrium between the Marshall bundle insertion and the ostium of the left inferior pulmonary vein resulted in successful treatment of the focal AF. This finding suggests that the trigger of the focal AF episodes resides not within the pulmonary veins, but in the Marshall bundle.
Vein of Marshall And Recurrent AF.

Atrial fibrillation (AF) or flutter can recur after pulmonary vein (PV) antral isolation (PVAI). The Vein of Marshall has been linked to the genesis of AF. The most accepted strategy for catheter ablation of atrial fibrillation (AF) is pulmonary vein (PV) antral isolation (PVAI), since the PVs or neighboring tissues are thought to provide the source of AF-initiating ectopic beats. The vein of Marshall and its associated myocardial fibers and nerves have been implicated in the genesis of AF by multiple mechanisms: as a source of ectopic beats initiating AF,as a connection pathway with neighboring myocardium and left PVs,and as a source of arrhythmogenic autonomic innervation. Given its location on the epicardial surface of the left atrial ridge, it is unclear whether a conventional PVAI reaches the Vein of Marshall sufficiently to ablate it. Therefore, we hypothesized that Vein of Marshall-dependent mechanisms may play a role in AF recurrences after PVAI.
Vein of Marshall as a Mechanism of AF Recurrence

Although a wealth of animal data supports the potential arrhythmogenic role of the Vein of Marshall, its role in human AF has been more elusive. Reports of paroxysmal AF initiating from Vein of Marshall-dependent triggers are abundant in the literature. Based on the potential role of the Vein of Marshall triggering AF; its well-documented sympathetic and parasympathetic innervation that can create a pro-AF physiological state in the atria; and the Vein of Marshall 's fibers connecting to the PVs, which could bypass endocardial ablation lesions and lead to PV reconnections, we had hypothesized that the Vein of Marshall could play a role in PVAI failures. However, aside from atrial ectopic beats and Vein of Marshall tachycardia in a minority of patients, we could not demonstrate AF initiation from Vein of Marshall triggers. This may reflect lack of arrhythmogenicity from the Vein of Marshall, but it also could be due to limitations in the stimulation techniques (isoproterenol, adenosine) used to unmask Vein of Marshall triggers.



Reference

Friday, October 21, 2016

MY RESEARCH PROPOSAL:P WAVE DISPERSION AND ITS ASSOCIATION WITH DIASTOLIC DYSFUNCTION IN ASYMPTOMATIC POPULATION OF THE URBAN AND RURAL MALAYSIA-Introduction Part I


P WAVE DISPERSION AND ITS ASSOCIATION WITH DIASTOLIC DYSFUNCTION IN ASYMPTOMATIC POPULATION OF THE URBAN AND RURAL MALAYSIA






MOHD FARID BIN MOHD TAUFIK






MSc




2016


Chapter One


INTRODUCTION 


1.1         INTRODUCTION


Atrial fibrillation (AF) enforce consequential concern of morbidity and impaired health related to general well-being of individuals, and extremely increases sufferer’s risk of obtaining a cardiovascular event, especially a stroke (apoplexy). Occurrence of atrial fibrillation in Asia and the associated medical care expenses are likely to have been underestimated and are required to improve due to increasing awareness, population ageing and higher prevalence of associated risks and comorbidities [1].

AF is the most persistent cardiac arrhythmia, and its occurrence in the population is increasing [2]. AF shares many common risk factors with left ventricular diastolic dysfunctio (LVDD), including age [3][4][5], hypertension [3][6][4][7], obesity [8],  and diabetes [9][10]. Patients given the diagnosis of LVDD are more likely to have AF at the time [11]. LVDD has significant pathological effects on atrial structure and atrial function especially LA, many are proarrhythmic that can induce arrhythmias such as AF. Nevertheless, there are so many aspects to be learned about the specific mechanisms through which LVDD induced development of AF [12].

There is growing understanding that congestive heart failure (CHF) caused by a significant LVDD that recognised as diastolic heart failure (HF). Common and causes significant morbidity and mortality is Diastolic HF [5]. Maintainance of sinus rhythm and normal atrial electrical conductions is vital for stability of cardiac output in individual with significant LVDD. Occurrence of AF causing atrial output to decreases. This will results in an increase of LVDD and progression of diastolic HF the patient’s clinical condition deteriorates [6].

There are many noninvasive electrocardiographic parameters have been applied to predict the occurrance of cardiac arrhytmias in individual with LVDD. It has been demonstrates that P wave dispersion as a noninvasive parameter that enables the evaluation of AF risk on the 12 lead surface ECG. This is because of its association to the nonhomogenous and interrupted conduction of sinusal electrical impulses both intra-atrially and inter-atrially [13][14].

LVDD is an important risk factor of AF, because LVDD has fundamental pathological influences on atrial structure and atrial function. Vranka et al. [15] attempted to determine how LVDD increases LAP and LA diameter, both of which influence atrial conduction times measured noninvasively by electrocardiography of P wave.

Researcher will investigate the association between P wave dispersion and the presence of LVDD as detected by Doppler echocardiography, the stage, origin, and other echocardiographic indicators of LVDD that includes LA volume, LA volume index, LA dimension, LA active emptying fraction, LA total emptying fraction and other echocardiography parameters that can represent performance of LA in individual with asymptomatic AF, individual with type 2 diabeties melitus (DM), individual with hypertension and individual that is  asymptomatic healthy individual.

1.2         PROBLEM STATEMENT


P wave dispersion can be used in predicting the risk of AF [13] in LVDD patient. Gunduz et al. [16] in their finding noted that the presence of LVDD is an important factor affecting P wave duration. The goal of the proposed study is to investigate association between LVDD, P wave dispersion and AF. 

P wave measurement by 12 lead ECG have been stated to be applicable tools for assessing the risk of LA enlargement and LVDD [16][17]. Gunduz et al. [16] in their finding noted that prolongation in P wave dispersion is related to LA diameter or to stage of LVDD. Gunduz et al. [16] in their finding also noted as LVDD stage of patient progressed, LA dimensions increased significantly. However, Dilaveris et al. [13] have found that LA diameter is not an important predictor for AF and that P wave duration is unrelated to LA diameter. The purpose of the proposed study is to determine the effect of LVDD on LA diameter and its association with P wave dispersion.

Earlier Tsang et al. [18] have done an early study to examine LVDD and incident AF. They followed 840 elderly men and women, of whom 80 (9.5%) developed atrial fibrillation over a average follow up of 4.1 years. With the use of a derived classification system for LVDD based on transmitral Doppler patterns and LA volume index. They found that more severe LVDD was related with an elevated risk of AF incident. Tsang et al. [18] in their study of 840 elderly men and women also suggest that the strongest predictor of AF was LA volume index.

Later Tsang et al. [19] have done follow-up study that examined only patients with impaired relaxation based on transmitral peak E/A (0.75) and deceleration time (240ms) and found an increased risk of the combined outcome of AF and HF with impaired relaxation, although this effect was not significant in the absence of an increased LA volume index (27 mL/m2). This finding again suggesting that it was LA size, rather than any particular diastolic parameter, that increases risk of AF. In addition, normal LA volume in a patient with advanced LVDD is most unusual unless the LV filling pressure increase abruptly because of the sudden onset of a structural abnormality, such as severe mitral regurgitation or aortic regurgitation due to sudden valvular disruption or valvular abnormalities. LA volume is a good predictor of the development of AF and long term outcome in various cardiac disorder [19]. The purpose of the proposed research is to determine the effect of LVDD on LA volume and LA volume index and its association with P wave dispersion.

Faggiano et al. [20] in their study show the relationship between LAP or pulmonary capillary wedge pressure (PCWP) obtain by right sided heart catheterization and obtain by echocardiography to signal averaged P wave duration in patients with CHF. The author believes that in patients with chronic HF, P wave duration in signal average ECG seems to depend more on the level of LAP compare to LA dimension. Vranka et al. [15] supports Faggiano et al. [20] with their result that high left atrial pressure expressed by increased E/E’ ratio, may be play an important role in prolonging P wave duration, as was shown by Doppler parameters. The author suggest that prolonged atrial conduction was not associated with LA enlargement. The goal of the proposed study is to examine association between LVDF and its effect on P wave dispersion and LA.

Morris et al [21] mentions that individuals with HF with normal LVEF had more impaired LA systolic function compared to asymptomatic population. The author states that noninvasive LV filling pressure were modestly related with LA systolic function. The goal of the proposed study is to investigate association between LVDD and its effect on P wave dispersion and LA systolic function.
In essential hypertension in adult individuals, a significant relationship has been showed between changes in LV geometry and P wave dispersion.  P wave dispersion is the difference between maximum and minimum P wave duration measured on 12 lead ECG [13]. Hypertension is one of the causes of AF. LVDD in a hypertrophic LV results in an increase in LV end diastolic pressure and in LA dimension [22]. De Marchi et al. [23] showed an important association between the extent of hypertrophy and LVDD. The target of the proposed study is to examine the relationship between LVDD, LV hypertrophy, P wave dispersion and its effect on LA dimension, LA volume and LA volume index in hypertensive population.

Patil and colleagues [10] in their finding stated that preclinical LVDD is common in patient with DM. Soldatos et al. [24] in their case control study of individuals with Type 2 DM found that LVDD, present in a significant proportion with Type 2 DM. Boyer et al. [25] stated that the prevalence of LVDD in asymptomatic, normotensive patients with Type 2 DM disease is high. Yazici et al. [26] also manage to show that prolongation of P wave dispersion can be seen in Type 2 DM cases without hypertension and ischemic heart disease. They found that slightly prolong P wave dispersion in the Type 2 DM group compare to the control group but diastolic relaxation parameters, such as early diastolic rapid filling and isovolumic relaxation time (IVRT) were within normal value and mean LA diameter were similar in both groups. Depends on these findings, P wave dispersion is not affected by these diastolic parameters. The aim of the proposed study is to examine the relationship between LVDD, LV hypertrophy, P wave dispersion and its effect on LA dimension, LA volume and LA volume index in diabetic population.


1.3         OBJECTIVES


1.3.1        Main Objective


To investigate association between Left Ventricular Diastolic Dysfunction (LVDD), P wave dispersion and AF.


1.3.2        Objectives


1.      To investigate association between LVDD and its effect on P wave dispersion, LA dimension, LA volume and LA volume index.

2.      To investigate association between LVDD and its effect on P wave dispersion, LA systolic function and LAP.

3.      To examine the effect of LVDD on LA dimension, LA volume, LA volume index, LA systolic function and LAP with presence of increased P wave dispersion compared to healthy controls.

4.      To examine the effect of LVDD on LA dimension, LA volume, LA volume index, LA systolic function and LAP with presence of increased P wave dispersion compared to hypertensive population.

5.      To examine the effect of LVDD on LA dimension, LA volume, LA volume index, LA systolic function and LAP with presence of increased P wave dispersion compared to diabetic population.

1.4         RESEARCH QUESTION


Does prolonged P wave dispersion cause AF?What is the relationship between P wave dispersion and LVDF?

3.      What is the association between LVDD and its effect on P wave dispersion, LA dimension, LA volume and LA volume index?

4.      What is the association between LVDD and its effect on P wave dispersion, LA systolic function and LAP?

      What is the effect of LVDD on LA dimension, LA volume, LA volume index, LA systolic function and LAP with presence of increased P wave dispersion compared to healthy controls?

What is the the effect of LVDD on LA dimension, LA volume, LA volume index, LA systolic function and LAP with presence of increased P wave dispersion compared to hypertensive population?

What is the the effect of LVDD on LA dimension, LA volume, LA volume index, LA systolic function and LAP with presence of increased P wave dispersion compared to diabetic population?

1.5         RESEARCH HYPOTHESIS



1.      Normal P wave duration, LVDD, LA dimensions, LA area, LA volume, LA volume index, LA active emptying fraction and LA total emptying fraction in control group.

2.      Prolong P wave duration and dispersion in study group with hypertension.

3.      Prolong P wave duration and dispersion study group with type 2 diabetes mellitus.

4.      Prolong P wave duration and dispersion with evidence of LV hypertrophy in study group with hypertension and diabetes mellitus.

5.      The LVDD worsens in study group with hypertension.

6.      The LVDD worsens in study group with type 2 diabetes mellitus.

7.      LA dimensions, LA area, LA volume, LA volume index and LAP were significantly increased in study group with hypertension.

8.      LA dimensions, LA area, LA volume, LA volume index and LAP were significantly increased in study group with type 2 diabetes mellitus.

9.      LA active emptying fraction and LA total emptying fraction were significantly reduced in study group with hypertension.

10.  LA active emptying fraction and LA total emptying fraction were significantly reduced in study group with type 2 diabetes mellitus.

1.6         SIGNIFICANCE OF THE STUDY


AF is the most common persistent cardiac arrhythmia, and increasing in prevalence. AF occurs in 0.3% to 0.4% of the adult group [9]. The impact of AF on morbidity and mortality is high. It will give socioeconomic burdened to the society. AF is most commonly seen in patients with underlying structural heart disease, including hypertensive population, cardiomyopathy, ischemic heart disease, valvular heart abnormalities and HF [27].

Early identification of patients at risk of AF may help to reduce potential health risks, costs and other related complications. P wave dispersion analysis has been shown to classified between individuals at risk of AF and those without risk of AF. P wave prolongation on may be associated with left ventricular diastolic dysfunction and following an increase of LAP, LA enlargement and reduced LA systolic function; therefore, P wave  prolongation should be assessed in individuals at risk of AF. Combining P wave duration with other predictors of AF may improve the diagnostic value of P wave dispersion analysis [15].

In condition of ncreased in LV end diastolic pressure with LVDD, the maintainance of normal sinus rhythm and atrial contractions is essential for the maintainance of cardiac output. If AF occurs, the loss of efficient atrial contraction, which accounts for 40% of atrial output during diastolic phase. This will results in worsening of LVDD and in progression of diastolic HF [6].

Identifying association of P wave dispersion with early echocardiographic changes especially on LVDF assessment allow physicians to intervene and manage underlying illnesses more aggressively to reduce risk of development of AF. Potential health risk such as hypertension and Type 2 DM nowadays have increasing in Malaysia population has been proved to be risks factors of LVDD and P wave dispersion. Early treatment of this potential risk can also reduced risk of developing AF.

1.7         DELIMITATIONS OF THE STUDY


The study will be limited to an investigation of respective knowledge specifically on non invasive LVDD evaluation by 2D echocardiography and Doppler echocardiography modalities analysis. The study also will be limited to an investigation of respective knowledge on non invasive 12 lead surface ECG analysis specifically on P wave characterictic. Invasive LVDD and intra cardiac electrophysiology study evaluation will not be obtain and tested.

1.8         LIMITATIONS OF THE STUDY


The LA function will only focusing on systolic function. Left atrial diastolic function evaluation has to be done by strain imaging. Strain imaging did not included in raw database to be obtain, test and evaluate.