What is Atrial fibrillation ?
Atrial fibrillation (AF) is the most commonly occurring cardiac arrhythmia associated with increased cardiovascular morbidity and mortality. Epidemiological data from the Framingham Heart Study indicate the cumulative incidence of AF over a 22 year follow up was 2.1% in men and 1.7% in women.
The prevalence of AF increases with age, affecting over 1 in 25 persons aged 60 years or older and 1 in 10 persons aged 80 years or older. Even in an ethnic group with a low incidence of coronary artery disease CAD, AF occurs in 1.3% of population with age more than 60 years. Furthermore, recent data suggests that the prevalence of AF is increasing even after adjusting for age and other risk factors.
In conjunction with congestive heart failure CHF, AF has been described as one of the two emerging epidemics of cardiovascular disease due to the aging population. AF is associated with a 3 to 5 fold increase risk of death. In contrast to other risk factors for stroke which decrease with increasing age, risk of AF related stroke remains high at all ages. Although AF is often associated with heart diseases or other risk factors, it can also occur in about 30% of patients without underlying etiological cause.
During AF, the atria activates at more than 350 bpm, resulting in no effective atrial contraction. These chaotic atrial impulses in turn activate the atrio-ventricular AV node at random intervals. As the AV node has a limited capacity in transmitting atrial activations, in most cases the ventricles are beating irregularly at rates between 80-120bpm at rest. Ineffective atrial contraction leads to a reduction in left ventricular LV filling hence decrease stroke volume, a higher left atrial LA pressure and stasis of blood that lead to clot formation.
The ventricles are bystanders during AF. When the ventricular rate VR is inappropriately fast, adequate LV filling does not occur and the depressed stroke volume results in a reduction in forward cardiac output despite the increase in rate. Very often, closely coupled cardiac cycles do not generate a detectable pulse because of small stroke volume and pulse deficit is a feature of AF.
Can We Prevent All Sudden Cardiac Deaths?
In both ischemic and non-ischemic heart disease the severity of LV dysfunction has emerged as the key determinant affecting the decision of which patient should receive an ICD for prophylaxis against a future risk of arrhythmic sudden death. A documented EF of less than 35% in an otherwise suitably treated patient will commonly result in an electrophysiology referral and an ICD implant.
Although such treatment has yielded mortality benefit in the qualifying patient, whether it can significantly impact on overall sudden death in the general population is less clear. A population based study unfortunately showed that only a small proportion of sudden death victims could have benefited from the current primary prevention ICD guidelines.
Of 714 sudden deaths occurring over a two year period, only 121 patients had a previous assessment of LV function and only 36 of these patients (5 % of the total) had an EF of less than 35 %. The concept that only a minority of sudden deaths occurs in patients previously identified as having significant I.V dysfunction has been previously well documented in a number of studies.
So far it remains far less than perfect at predicting at what time and for which patient the unfortunate substrates and triggers cross to result in sudden death. The second corollary is that not all SCDs are from arrhythmias. Clearly, these patients died of AML, which could not be prevented by ICD.
How to Treat Polymorphic Ventricular Tachycardia?
Polymorphic VT arises in different clinical settings. It appears in various genetic syndromes such as the long QT syndrome, the Brugada syndrome, the cahecholaminergic polymorphic VT syndrome, and the short QT syndrome. It can appear in patients with acquired long QT syndromes such as are caused by Class IA and Class III drugs, hypomagnesemia, and hypokalemia.
It also can appear in acute ischemia, so patients with polymorphic VT should be screened for ischemia unless another cause is apparent. The Brugada syndrome also produces episodes of polymorphic VT. It has not been found to reliably respond to anti-arrhythmic drugs, so symptomatic patients and high risk asymptomatic patients are best treated with implantation of an ICD.
What Are The Risk Factors for Atrial Fibrillation
In this modern medical field where you have every solution or treatment for mankind, it is better to learn about the risk factors for Atrial Fibrillation. Generally Atrial fibrillation (AF) is the commonly occurring cardiac arrhythmia associated with increased cardiovascular morbidity and mortality.
The Risk Factors for Atrial Fibrillation is as follows
- Male sex
- Throid dysfunction
- Chronic obstructive lung disease
- Diabetes mellitus
- Cardiovascular diseases
- Valvular heart disease
- Ischaemic heart disease
- Heart failure
- Congenital heart disease
- Wolff-Parkinson-White syndrome
- LV hypertrophy
- Recent cardiac or non-cardiac surgery
Another adverse change is irregularity of the ventricular contraction, and it has been shown that it can further reduce the overall cardiac output compared to a regular rhythm. These ventricular responses are critically dependent on the AV node. For instance, heightened conduction during stress or exercise can worsen the hemodynamic response. On the other hand, appropriate rate control by an AV nodal blocker can ameliorate much of the changes and improve symptomatology. Chronic inappropriately fast VR can lead to impair LV contraction, a condition known as tachycardiomyopathy.
Recent experimental and clinical studies have provided new insights into the mechanisms of AF. The mechanisms of AF are heterogeneous and are likely to differ in different clinical circumstances. However, three basic components are required for the occurrence of AF namely specific trigger, suitable substrate and modifying factors.
Experimental AF could be induced by a single source of very rapid impulses or by available myocardium. If the cycle length of the firing focus is shorter than the refractory period in other parts of atria, rate-dependent functional conduction block occurs and non-uniform excitation will result. This type of AF is actually represented as fibrillatory conduction. One of the important observations from Haissagurere was that a single source of rapid ectopic foci of automatically, mainly originating from the pulmonary veins, can be the trigger for the initiation and maintenance of AF in patients with paroxysmal AF (PAF). Other ectopic foci are in the superior vena cava, coronary sinus, LA posterior wall, vein of Marshall and interatrial septum has also been shown to trigger AF. Furthermore, atrial flutter or any supraventricular tachycardia may also serve to trigger AF.