Left anterior fascicular block (LAFB) is presented by irregular contraction of heart muscles, a condition arising as a result of a defect of the anterior half of the bundle of His, a collection of cells which are responsible for electrical transmission from the AV node to the apex of the heart.
People affected by LAFB present with a characteristic scaring along the section of the left ventricle. The major clinical signs which indicate the occurrence of LAFB include:
There is no overall prolonged duration for the ventricular depolarization, and as a consequence a normal duration of less than 0.10 second for the QRS complex can be observed, regardless the location of the fascicular block (in a posterior or anterior position).
The presence of the Q waves in lead I and aVL is explained by the loss of the anterior fascicle. The current, in fact, cannot flow towards these leads and therefore is initially decreased to the left. This in turn brings about the right ventricle depolarization which is duly detected in the electrocardiogram. The depolarization affects the other leads: leads II, III, and aVF produce smaller R waves, and all the limb leads (I, II, and III) produce larger voltages than those normally observed in QRS complexes.
It is possible to observe slight changes in the electrocardiogram also with left posterior fascicular block. In this case, the posterior wall depolarization falls slightly behinds, creating a wave which moves to the right. In the electrocardiogram, left posterior fascicular block is indicated by the following signs:
The criteria to diagnose LAFB on the basis of electrocardiogram can be easily understood by remembering that LAFB occurs when action potentials can no longer be conducted by the anterior fascicle part of the left bundle branch. These criteria are summed up as follows:
To diagnose LAFB quickly, experts suggest to immediately identify the left axis deviation. The deviation is confirmed by the presence of increased QRS complexes in lead I, a decreased QRS complexes in leads II and aVF, and a rS complex in the lead III.
Treatment is largely dependent on the degree of the block and the clinical signs present. In most cases in general, the treatment includes the following clinical protocols:
There is no treatment for bi-fascicular block, which occurs when right bundle branch block and left anterior fascicular block take place at the same time. In particular situations, bi-fascicular block can lead to complete heart block, a condition which requires the implantation of a pacemaker.
LAFB is seen as a benign electrocardiographic finding, even though there is no precise information regarding its consequences in the long run [1]. The block is the result of fibrosis in the conduction system, with a clear association between LAFB and myocardial fibrosis, even if there is complete absence of cardiovascular problems [3] [4]. This is a very useful early sign not only for fibrosis itself, but also for more severe conditions such as atrial fibrillation and congestive heart failure [5] [6].
In the absence of adequate data, the prognostic significance of LAFB is still largely unknown, especially among those who have shown no previous episodes of myocardial infarction and might present with an increased possibilities of coronary artery disease [7] [8]. It is important to notice that no association between LAFB and increased risk of cardiac death has been detected [8]. So far the related data are still limited and largely restricted to a few patients with no long-term clinical follow-up. In those patients for whom LAFB comes as a clinical complication of acute myocardial infarction, this disorder is seen as the consequence of ischemia injury of the anterior fascicle. In this contest, LAFB is also associated with a larger infarct size as well as left anterior descending coronary artery disease, but not with higher mortality rates [9] [10] [11].
All and all, these data seem to indicate that LAFB can be a clinically relevant marker for the propensity of a subject to develop left heart fibrosis, but further studies are needed to find out whether or not LAFB is an important predictor for the coming of other cardiac complications [3] [4].
Many factors have been known as possible causes for the genesis of LAFB. The most common cause is chronic hypertension, followed by aortic stenosis and vascular disorders. Other factors include dilation of aortic root, dilated cardiomyopathy, aging, degenerative fibrotic disease, and even acute myocardial infarction, with around 4% of the cases associated with LAFB.
It is a significant point that isolated episodes of LAFB can also be caused by fibrosis. This means that if fibrosis has occurred LAFB can be associated with an increased possibility of cardiovascular pathological outcomes such as atrial fibrillation or congestive heart failure, even if there are not any clear clinical signs [2]. From this point of view, LAFB can be seen as an early manifestation of diffused cardiac fibrosis which subsequently lead to adverse cardiovascular outcomes [2].
LAFB is more prevalent in men than women, and its frequency tends to increase with ageing. The spontaneous closure of septal defects in ventricles is associated with LAFB, and this might explain the presence of this defect also in young people.
The ventricular conduction system is made of three major divisions or fascicles, which include: the right bundle branch and the two left divisions, the anterior and the posterior one. Since the left anterior division is frequently smaller than the posterior one, it is usually more often affected by fascicular blocks. The anterior divisions leads electrical signals to the upper parts of the ventricle, the anterior part and the lateral walls, while the posterior division mainly leads electrical signals to the lower part towards the posterior wall. When a left anterior fascicular block occurs, the initial septal activation and the activation of the inferior and apical areas are oriented anteriorly and inferiorly, with the first one to the right and the second one to the left. Then follows the activation of the anterolateral and posterobasal areas of the left ventricular wall, which is oriented superiorly and posteriorly to the left.
The trifascicular form of the intraventricular conduction system and the associated concept of triventricular block were first observed back in 1968, and since then the pathological, electrophysiological, and clinical aspects of this disorder have constantly been confirmed by the subsequent studies conducted on this subject. However, it should be noted that LAFB might simulate or even mask the electrocardiographic signs of myocardial infarction and myocardial ischemia, as well as mask or simulate those of ventricular hypertrophy. Therefore, electrocardiogram findings must be interpreted carefully. In this regard, it is very helpful to remember that LAFB is often associated with anteroseptal myocardial infarction, arterial hypertension, and other heart diseases.
As previously stated, LAFB develops when an interruption of the electrical activity in the left bundle anterior fascicle occurs, which subsequently causes a delay in the related depolarization for the left ventricle upper part. This condition is classically revealed by a left axis deviation in the electrocardiogram, which usually is less than -60°, together with smaller Q waves in leads I and aVL, R waves in leads II, III, and aVF, and a shorter QRS that usually becomes less than 0.12 second for all leads.
LAFB tends to become more frequent with the advancement of age, even though it might follow the spontaneous closure of ventricular septal defects. Isolated case of left posterior fascicular block, instead, is very rare, with a prognostic significance that still remains largely unknown and is usually associated with right bundle-branch block. In this case, prognosis might be very serious and frequently result in complete atrioventricular block and Adams-Stoke seizures.
It is important to note that left anterior fascicular block can also provoke the block of more than one fascicle, in the contest of a bifascicular or trifascicular block.
People having the presence of LAFB but apparently having no signs of known cardiovascular disease are faced with a greater risk to sufferer from it. In order to reduce the risk of developing such pathological cardiovascular conditions, the following drugs can be prescribed:
While planning a regime to reduce the risk of developing cardiovascular diseases, the following factors should be taken into consideration:
The left bundle splits into two branches called left anterior fascicle and left posterior fascicle, which spread in the left ventricle to conduct electrical signals. If this cardiac region is damaged, electrical conduction is slowed down and results in a delay in the heart pumping activity. This condition is called fascicular block, or specifically left anterior fascicular block (LAFB) or left posterior fascicular block (LPFB), according to the bundle branch concerned. It is also referred to as left anterior hemiblock. LAFB is considered a benign electrocardiographic finding, even though its clinical consequences in a long run have not been completely understood yet [1].
It is well known that fascicular block does not prolong ventricular depolarization, and depolarization of the rest of the ventricle continues as it would in normal clinical conditions. This is a significant aspect to remember, as it determines the electrocardiographic appearance usually observed in fascicular blocks. LAFB is frequently associated with other cardiac pathologies such as valvular disorder, hypertension, cardio-myopathies, and degenerative fibrotic disease, and can be easily diagnosed by using ECG.
Left anterior fascicular block (LAFB) is defined as a cardiovascular disease in which electrical impulses are slowed down in their movement around the cardiac muscles, in a condition which results in a delay of the heart pumping activity. This pathology is the consequence of a defect on the anterior half of the bundle of His, a special group of cell specialized in transmitting electrical impulses from the AV node to the apex of the heart, which determines the appearance of an irregular heart contraction. Although patients affected by LAFB are frequently asymptomatic, those who do report clinical signs often show the following symptoms:
In the worse cases the pathology leads to the development of myocardial infarction episodes. Treatment largely depends on the severity and degree of the blockage, even though the most frequently protocols include the following procedures: