Ventricular arrhythmias are a broad category of conditions that include premature ventricular contractions (PVCs), ventricular tachycardia, accelerated idioventricular rhythm, torsades de pointes, ventricular flutter and
fibrillation.
Premature Ventricular Contractions. Prudent medical practice dictates that therapy for PVCs be based on "the company they keep". They are common in the general population, and if no heart disease is present, they are generally benign. Accompanying conditions that increase catecholamine levels, as well as hypoxia, electrolyte abnormalities, and drug toxicity, should be treated.
If, however, the PVCs occur with acute ischemic heart disease or any other organic heart disease, they may be of greater signifi-cance. PVCs themselves are not a cause of mortality, unless they lead to sustained VT or VF. Clinically, one should look first for disorders associated with increased catecholamine levels, hypoxia, electrolyte abnormalities, drug toxicity, HF, and ischemia. These conditions should be corrected if they exist. If PVCs persist, Holter monitoring could be considered in an attempt to determine if more malignant forms are present. In the absence of underlying heart disease, PVCs, even if frequent, are generally benign and need not be treated. If the patient is symptomatic from such PVCs, a beta-blocker is the antiarrhythmic agent of choice.
In contrast, if PVCs occur in a patient who does not have underlying heart disease, cardiovascular risk is increased. The problem is that with rare exceptions, antiarrhythmic therapy has not been shown to increase survival in such patients. If treatment is deemed necessary, a beta-blocker is again the agent of choice. It should be kept in mind that antiarrhythmic drugs are not benign and, in 5 to 10 percent of cases, may be associated with a proarrhythmic effect, in which they paradoxically exacerbate the arrhythmia. This is a major reason for the reluctance to treat PVCs in recent years.
Ventricular tachycardia. When short episodes of VT occur in a normal heart, they are usually benign. However, once VT is found, intensive cardiac evaluation is usually indicated to assess the patient for underlying heart disease. If heart disease is not present, no therapy may be needed.
On the other hand, when VT occurs with organic heart disease, the risk of VF is higher and, therefore, the risk of sudden cardiac death increases. Full evaluation with echocardiography, cardiac catheterization, and/or electrophysiologic studies should be strongly considered. Treatment options include amiodarone or other antiarrhythmic therapy or an implantable defibrillator, depending upon the LVEF and how inducible the VT is with electrophysiologic studies. For example, VT is much more likely to be inducible in a patient with ischemic cardiomyopathy compared to one with a nonischemic cardiomyopathy. In appropriately selected patients, use of an implantable cardioverterdefibrillator (ICD) may result in a greater than 90-percent survival rate at five years in those patients who otherwise would be at very high risk for sudden cardiac death.
Recently, the Multicenter Automatic Defibrillator Implantation Trial (MADIT) was completed, in which prophylactic implantation of an ICD appeared to benefit a select group of patients with nonsustained VT and impaired left ventricular function following myocardial infarction. Although additional data are needed to confirm these results, it would seem that patients with sustained VT and underlying heart disease should be referred for extensive cardiac evaluation including electrophysiologic study. Management decisions are less clear at this time for patients with asymptomatic episodes of nonsustained ventricular tachycardia (NSVT) who have underlying heart disease. At the least, control of potentially exacerbating causes of ventricular arrhythmias (whenever possible) is essential in such patients, including correction of electrolyte abnormalities and treatment of ischemia, heart failure and/or hypoxia. Preference should be given to use of ACE inhibitors and beta-blockers when appropriate for treatment of these underlying conditions. Whether or not patients with asymptomatic NSVT and underlying heart disease hould be routinely referred for electrophysiologic study remains controversial at this time, and is a decision that should be individualized for each patient depending on specific circumstances of the particular case at hand.
Finally, for patients who develop either cardiac arrest from ventricular fibrillation and/or sustained ventricular tachycardia associated with hemodynamic compromise that is not the result of acute myocardial infarction, recent data suggest the superiority of treatment with an ICD over treatment with antiarrhythmic drugs. Patients with these presentations should be referred for electrophysiologic evaluation unless extenuating circumstances exist.
fibrillation.
Premature Ventricular Contractions. Prudent medical practice dictates that therapy for PVCs be based on "the company they keep". They are common in the general population, and if no heart disease is present, they are generally benign. Accompanying conditions that increase catecholamine levels, as well as hypoxia, electrolyte abnormalities, and drug toxicity, should be treated.
If, however, the PVCs occur with acute ischemic heart disease or any other organic heart disease, they may be of greater signifi-cance. PVCs themselves are not a cause of mortality, unless they lead to sustained VT or VF. Clinically, one should look first for disorders associated with increased catecholamine levels, hypoxia, electrolyte abnormalities, drug toxicity, HF, and ischemia. These conditions should be corrected if they exist. If PVCs persist, Holter monitoring could be considered in an attempt to determine if more malignant forms are present. In the absence of underlying heart disease, PVCs, even if frequent, are generally benign and need not be treated. If the patient is symptomatic from such PVCs, a beta-blocker is the antiarrhythmic agent of choice.
In contrast, if PVCs occur in a patient who does not have underlying heart disease, cardiovascular risk is increased. The problem is that with rare exceptions, antiarrhythmic therapy has not been shown to increase survival in such patients. If treatment is deemed necessary, a beta-blocker is again the agent of choice. It should be kept in mind that antiarrhythmic drugs are not benign and, in 5 to 10 percent of cases, may be associated with a proarrhythmic effect, in which they paradoxically exacerbate the arrhythmia. This is a major reason for the reluctance to treat PVCs in recent years.
Ventricular tachycardia. When short episodes of VT occur in a normal heart, they are usually benign. However, once VT is found, intensive cardiac evaluation is usually indicated to assess the patient for underlying heart disease. If heart disease is not present, no therapy may be needed.
On the other hand, when VT occurs with organic heart disease, the risk of VF is higher and, therefore, the risk of sudden cardiac death increases. Full evaluation with echocardiography, cardiac catheterization, and/or electrophysiologic studies should be strongly considered. Treatment options include amiodarone or other antiarrhythmic therapy or an implantable defibrillator, depending upon the LVEF and how inducible the VT is with electrophysiologic studies. For example, VT is much more likely to be inducible in a patient with ischemic cardiomyopathy compared to one with a nonischemic cardiomyopathy. In appropriately selected patients, use of an implantable cardioverterdefibrillator (ICD) may result in a greater than 90-percent survival rate at five years in those patients who otherwise would be at very high risk for sudden cardiac death.
Recently, the Multicenter Automatic Defibrillator Implantation Trial (MADIT) was completed, in which prophylactic implantation of an ICD appeared to benefit a select group of patients with nonsustained VT and impaired left ventricular function following myocardial infarction. Although additional data are needed to confirm these results, it would seem that patients with sustained VT and underlying heart disease should be referred for extensive cardiac evaluation including electrophysiologic study. Management decisions are less clear at this time for patients with asymptomatic episodes of nonsustained ventricular tachycardia (NSVT) who have underlying heart disease. At the least, control of potentially exacerbating causes of ventricular arrhythmias (whenever possible) is essential in such patients, including correction of electrolyte abnormalities and treatment of ischemia, heart failure and/or hypoxia. Preference should be given to use of ACE inhibitors and beta-blockers when appropriate for treatment of these underlying conditions. Whether or not patients with asymptomatic NSVT and underlying heart disease hould be routinely referred for electrophysiologic study remains controversial at this time, and is a decision that should be individualized for each patient depending on specific circumstances of the particular case at hand.
Finally, for patients who develop either cardiac arrest from ventricular fibrillation and/or sustained ventricular tachycardia associated with hemodynamic compromise that is not the result of acute myocardial infarction, recent data suggest the superiority of treatment with an ICD over treatment with antiarrhythmic drugs. Patients with these presentations should be referred for electrophysiologic evaluation unless extenuating circumstances exist.
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