Ventricular Tachyarrhythmias

Ventricular tachyarrhythmias include a number of different rhythms, which arise in a number of different clinical situations. The ventricular tachyarrhythmias are fast heart rhythms that arise entirely within the lower chambers of the heart (the ventricles). They are faster than 100 beats per minute by definition. Generally, the tachyarrhythmias can be characterized as either monomorphic ventricular tachycardia or polymorphic ventricular tachycardia. Monomorphic ventricular tachycardia would appear on an ECG record with a regular rate and rhythm and fixed shape or morphology of the ECG trace. Each beat of the tachycardia would look the same, hence the designation monomorphic. Polymorphic ventricular tachycardia typically is irregular in rate and rhythm and has varying shapes or morphologies on the ECG. A problem that starts as a monomorphic ventricular tachycardia may deteriorate into polymorphic ventricular tachycardia. The most dangerous rhythm is a form of polymorphic ventricular tachycardia called ventricular fibrillation. The ECG is extremely disorganized and most often leads to death if not corrected very quickly.
Monomorphic Ventricular Tachycardia
Ventricular tachycardia may give rise to symptoms such as palpitations, shortness of breath, or lightheadedness, depending upon the rate of the arrhythmia, its duration, and the underlying heart disease. With faster heart rates and underlying heart disease loss of consciousness (syncope) or sudden death may occur. Episodes lasting only a few beats may produce no or minimal symptoms. Tachycardia rates between 110 and 150 may be tolerated even if sustained for minutes to hours. However, faster rates (>180 beats per minute) may cause drops in arterial pressure and produce syncope. Very fast rates (>220) are imminently dangerous because they rarely terminate spontaneously and invariably cause drops in blood pressure and low cardiac output. Most commonly, sufferers of ventricular tachycardia have underlying cardiac disease. In developed countries, the majority of the patients suffer from coronary artery disease. Although most patients having ventricular tachycardia will have underlying coronary disease or severely depressed heart function some have no demonstrable disease of the heart muscle or coronary arteries.
Medically it is helpful to considered ventricular tachyarrhythmias as either being associated with structural heart disease or not associated with any demonstrable structural problem with the heart.
Structural Heart Disease
VT associated with coronary artery disease is by far the most common form of VT. VT can be associated with acute myocardial infarction or can also appear years after the infarct has healed. In the case of acute myocardial infarction, electrical changes associated with cell starvation and oxygen deprivation or death can result in either ventricular tachycardia or ventricular fibrillation. In the case of VT associated with prior myocardial infarction, scar tissue from the myocardial infarction serves as insulating boundaries that set up anatomic areas where viable tissue can form the reentrant pathway. Reentry within circuits involving or in the vicinity of a healed myocardial infarction arises in response to metabolically-induced changes in impulse conduction or appropriately timed premature beats in otherwise asymptomatic patients. Reentrant VT is typically monomorphic.
VT circuits can also form when patients develop heart disease that results in altered ventricular muscle due scarring, atrophy (wasting away), or hypertrophy (thickening). The likelihood of reentrant arrhythmia is proportional to the degree of myocardial involvement in the underlying disease process, although the correlation is far form perfect.
Right ventricular dysplasia is a rare condition with unclear etiology that produces VT. It is most frequently found in young adult males, but is seen in both sexes and at any age without overt heart disease. With this condition a variable amount of ventricular myocardium is replaced by fatty and fibrous tissue and contractions are abnormal. Symptoms vary from palpitations to syncope. Some individuals who are considered normal on physical examination experience malaise or abrupt extreme weakness. This temporary incapacitation could lead to create major risk for themselves and others. This VT, more common than thought, is emerging as a cause of sudden death in young otherwise healthy adults.
No Structural Heart Disease
Ventricular tachycardia most often occurs in the presence of demonstrable structural heart disease. However, in young patients with ventricular tachycardia it is common no structural heart disease may be found. Two forms of ventricular tachycardia are commonly found and they are right ventricular outflow tract and left posterior septal fascicular ventricular tachycardia. Both of these tachycardia are repetitive monomorphic ventricular tachycardias likely due to an abnormal automatic focus amenable to rf ablation.. These distinctions are based on the location of the abnormal focus causing these tachycardia and the resulting morphology on ECG. These tachycardias are generally well tolerated and the patients complain mainly of episodes of palpitations or fast pulse. These VT's have well defined ECG patterns and are often triggered by exercise or catecholamines. Unlike the VT associated with coronary artery disease, these VT is not associated with an adverse prognosis. This VT seldom degenerates into ventricular fibrillation, and it is often responsive to drug therapy or RF ablation.
Because VT tends to recur and may be fatal, therapy is geared to managing episodes when they occur and if possible, to preventing another episode. RF ablation has been used for repetitive monomorphic VT and offers the only potential cure for VT; it has proven to be effective in many cases. Most types of VT are not readily amenable to ablation, however given the current technology and understanding.
The implantable cardioverter-defibrillator (ICD) has become the treatment of choice for patients with life-threatening VT. The defibrillator is always present and monitors continuously for VT. If an episode of VT commences, the ICD automatically detects and terminates the VT without patient input. Some patients require drug therapy in conjunction with the ICD in order to suppress frequent VT episodes. In general, drug therapy alone is restricted to patients who have well-tolerated arrhythmias or to those whose life expectancy is poor despite aggressive therapy for their arrhythmias.
Polymorphic Ventricular Tachycardia and Ventricular Fibrilation
Ventricular fibrillation results when multiple sites in the ventricles fire impulses very rapidly in an uncoordinated fashion. Although this general scheme appears correct, the exact mechanisms of ventricular fibrillation remain unknown. The ventricles quiver and cease to pump blood effectively, thereby stopping the circulation of blood. Death follows within a few minutes, unless a normal rhythm is restored with emergency treatment. . VF depicts the final common avenue for death in most patients experiencing out of hospital cardiac arrest.
Medically it is helpful to considered ventricular tachyarrhythmias as either being due to structural heart disease, caused by medicines or no associated with any demonstrable structural problem with the hear of definable cause.
Structural Heart Disease
VF is most commonly associated with structural heart disease. Specifically, coronary artery disease and myocardial infarction or ischemia are the most common underlying heart disease. The next most common group of causative structural heart diseases are the dilated cardiomyopathies. Dilated cardiomyopathy is a condition where the heart is very weakened and enlarged but there is no significant coronary artery disease. Commonly these patients have had exposure to a virus, other infections such as Chagas, or have suffered the consequences of severe congenital heart or acquired valvular problems. Another less common cause of ventricular fibrillation is hypertrophic cardiomyopathy. This disease is when the muscle of the heart thickens significant more than normal without any apparent mechanical reason. This is most likely the cause of the rather well publicized deaths of otherwise very healthy athletes that occurred during exercise.
After resuscitation and hospitalization it is important to identify and correct any reversible arrhythmia prompting factors such as an acute reduction in blood supply to heart muscle (myocardial ischemia), abnormal blood chemistry or drug toxicity. After initial emergency treatment, the cardiac electrophysiologist most likely will perform an EP study to determine the mechanism of the ventricular arrhythmias. An implanted cardioverter-defibrillator (ICD) would be recommended unless there is a strong reason not to implant such a device.
Torsade de pointes is a particular kind of polymorphic VT. It is characterized by onset with an early complex that follows a long pause. Torsades de pointes may be caused as a side effect of certain drugs, including most of the antiarrhythmic drugs. These drugs include commonly prescribed agents such as antiarrhythmias drugs, certain, antibiotics such as erythromycin, psychotropic drugs such as Thorazine, or antihistamines such as Seldane. The combination of Seldane and erythromycin has especially been found undesirable. Episodes of this rhythm are often self-terminating, but can be rapidly fatal if they persist. The treatment is prompt cardioversion if the rhythm is sustained, followed by intravenous magnesium, avoidance of agents that prolong the QT interval, and correction of myocardial ischemia, hypoxia, and electrolyte abnormalities. Torsade de Pointes can occur with or without the presence of structural heart disease.
Long QT Syndrome
Long QT syndrome (LQTS) has created great interest because of its unique and dramatic manifestation. This familial disorder was recognized more than 100 years ago. In 1856 a deaf girl was reported to have collapsed and died while being publicly admonished at school. Previously two of her brothers had died suddenly during under similar stressful situations.
In 1975 A. Jervell and F. Lange-Nielson provided the first complete description of LQTS, a syndrome of deafness and sudden cardiac death and associated with a characteristic ECG abnormality (prolonged Q-T interval). The cardiac arrest in these victims, mostly children and teenagers is due to ventricular tachyarrhythmia. Most episodes of arrhythmias are usually self-terminating, even when they provoke a transient loss of consciousness (syncope). However, when the episodes are prolonged, circulatory failure due to arrhythmia may result in sudden death.
LQTS was previously classified into a non-familial sporadic form and two hereditary types, with deafness (Jervell and Lange-Nielson syndrome, autosomal recessive) and without deafness (Romano Ward syndrome, autosomal dominant). In 1991 M. T. Keating et al. demonstrated linkage between LQTS and chromosome 11. Subsequent genetic studies showed that different LQTS syndromes were due to mutations of different genes (at least 5) localized on chromosomes 3,4,7 & 11. These genes are responsible for the synthesis (encoding) of membrane channel proteins that play a pivotal role in the cellular metabolism and regulation of the electric activity of cardiac cells. LQTSs have thus been recognized as cardiac membrane channel diseases ("channelopathies") that invite syncope and SCD due to ventricular arrhythmias.
The two criteria for diagnosis of LQTS are unexplained transient loss of consciousness and an abnormal ECG. Ventricular arrhythmias and syncope are often provoked by increases in heart rate in response to exercise or emotion. Because such responses involve changes in the autonomic neural (non-voluntary) regulation of the heart, it was believed that LQTS resulted from some imbalance in sympathetic innervation of the heart. However nerve deafness and other possible neural abnormalities associated with LQTSs remain to be elucidated.
The incidence of fully expressed LQTS is probably rare, although variations of the syndrome may remain unrecognized and actually be frequent. Cases have been reported in every continent and in every race. Four factors are associated with an increased risk of SCD: deafness, history of syncope, males before puberty and episodes of sustained females menarche, and sustained (>30sec) and/or very irregular ("polymorphic", torsade de pointes) ventricular tachycardia.
There may be channel gene mutations which by themselves do not seriously affect cardiac cell electric activity, but that may render the heart susceptible to drugs that prolong the QT interval of the ECG. These drugs include commonly prescribed agents such as antiarrhythmic drugs, certain antibiotics (antifungals), psychotropic drugs, or diuretics causing wasting of potassium in the urine.
Ideally, drug treatments should be guided by new genetic and electrophysiologic insights into the different LQTS's. Until recently, anti-adrenergic therapy (beta-blockers) has been the major treatment for LQTS. However based on current information, new targeted treatments may now be considered. The underlying mechanisms of LQT3 are an increase in sodium current, whereas LQT1 and LQT2 arise from deficient potassium currents. These changes in membrane currents can be influenced with specific drugs that selectively block excess sodium currents (sodium channel blockers) or activate potassium currents (potassium channel openers).
In some patients with life-threatening arrhythmias, an implanted cardioverter defibrillator (ICD) may be an appropriate therapy.