Overview: idiopathic ventricular tachycardia (idiopathic ventricular tachycardia, IVT) is Gallavard first reported in 1922. It occurred in patients without structural heart disease based on, the check is a group of no significant abnormal cardiac structure and function of monomorphic ventricular tachycardia.[Cause]
exact cause is unclear, a recent report, believed to be sodium channel gene mutations lead to barriers of the disease. There are reports of 8% to 30% of idiopathic ventricular tachycardia in patients with myocardial biopsy there is focal myocardial lesions, such as subclinical myocarditis, but the extent of the lesion is very small, very light, follow-up is no progress. There are also reports of myocardial biopsy, autopsy heart were normal. Have to prove that even if the patients have mild abnormalities of cardiac function and structure, but also between the two is difficult to ascertain a clear causal relationship. individual patients with sudden death, there are also individual follow-up to become cardiomyopathy. The disease was familial disease may be.
(B) the pathogenesis
1. left bundle branch block in idiopathic ventricular tachycardia must Most originated in the right ventricular outflow tract, a small number originated in the right ventricular inflow tract, apex, right ventricular septal and other parts. It has been proved to be due to triggered activity, and more can be terminated by adenosine. Clinical sensitivity, also known as catecholamines, ventricular tachycardia, adenosine-sensitive ventricular tachycardia, exercise-induced ventricular tachycardia. Electrophysiological characteristics of ventricular process induced by electrical stimulation can be less, only 20% to 30% of patients can be induced, mostly by intravenous infusion of isoproterenol and induced. Program ventricular stimulation induced ventricular tachycardia does not evolve into ventricular fibrillation. Non-sustained ventricular tachycardia electrical stimulation in 15% to 25% of patients can be induced sustained ventricular tachycardia. ventricular late potentials were negative.
2. right bundle branch block in idiopathic ventricular tachycardia was mainly due to its mechanism of micro-reentry excitement caused by the reentrant loop by Purkinje composed of myocardial fibers and local, easily blocked by verapamil. A small number of patients is caused by the delay after depolarization caused by the triggering event, which is characterized by endless attacks, and can be adenosine, β-blockers terminated. Part of the verapamil-sensitive patients may also be terminated by adenosine, suggesting that the Department of cAMP-mediated triggered activity. clinical manifestations of patients with small ventricular contractions or non-sustained ventricular tachycardia. Electrophysiological characteristics of ventricular electrical stimulation of the program about 75% of patients can be induced; program period before the stimulus + induced by isoproterenol infusion rate of 90%. Induced sustained ventricular tachycardia does not evolve into ventricular fibrillation. Exercise can induce sustained ventricular tachycardia, induced rate of 20% to 50%, compared with left bundle branch block idiopathic ventricular tachycardia is less. However, exercise testing is not easy to distinguish two types of idiopathic ventricular tachycardia, could not be sure what kind of research is the mechanism. Intravenous injection of verapamil therapy best, but oral administration of verapamil can not prevent the recurrence of ventricular tachycardia.[Sign]
non-sustained ventricular tachycardia in patients with mostly asymptomatic, short duration of attack, up to 30s. Sometimes attack, palpitations, seizures can be repeated. More common in young or middle-aged, organic heart disease, no clinical basis. Most movement occurs in tension or ventricular tachycardia.
patients with sustained ventricular tachycardia is also more common in young people, mostly aged 20 to 40 years (11 ~ 56 years), mean age of 36.9 years. Duration ranging from an average of 4.1 to 5.5 years. The clinical examination showed no clear basis for structural heart disease. Asymptomatic without attack. When the tachycardia due to longer duration, often heart palpitations, chest tightness, dizziness, nausea, and so on. ventricular rate is too fast or too long duration, there may be syncope or fall in blood pressure. On hemodynamics and cardiac function, are usually mild, but the individual episodes can also occur in patients with hemodynamic disorders. frequency of ventricular tachycardia episodes per year 4 to 48 times. Duration of attack is 0.5 ~ 30h, but there were longer-lasting. Sustained ventricular tachycardia frequency of 115 ~ 250 times / min, left bundle branch block type were more common in women than in men, while the right bundle branch block-type are found in almost all men.
1. there is a history of repeated episodes of tachycardia.
2. clinically asymptomatic, but also palpitations, chest tightness, dizziness, etc., but no syncope.
3. Following a thorough examination showed no structural heart disease basis.
4. electrocardiogram showed monomorphic ventricular tachycardia LBBB type of qrs waveform was non-sustained ventricular tachycardia, right axis deviation (+90 ° so) individual normal or left side; was sustained LBBB type of idiopathic ventricular tachycardia right axis deviation, the individual left side. RBBB type was sustained idiopathic ventricular tachycardia, left axis deviation, with the right side is rare.
2. comfort with the language of patients, the patients overcome the disease of the determination and confidence.
2. antiarrhythmic drug therapy because of idiopathic ventricular tachycardia and occurrence of different types of mechanisms, the efficacy of antiarrhythmic drugs are also different. Ⅰ C, Ⅱ, Ⅲ, Ⅳ drugs can be selected. Verapamil, propafenone is the type of ventricular tachycardia sensitive drugs. Such as verapamil may be ineffective or insensitive use propafenone, and vice versa. strong efficacy of verapamil, should pay attention to its inhibition of sinus node and atrioventricular node. A small number of patients, especially those associated with hemodynamic disturbance or can not have organic disease other than the need to continue follow-up observer, Ⅲ type of drugs are often recommended. drug therapy and radiofrequency ablation, though not a high success rate, but because of the type of ventricular tachycardia is a relatively benign clinical course, so obvious symptoms or after drug treatment were satisfactory results can continue to use drugs. Some patients after drug treatment, some patients without ventricular tachycardia after drug withdrawal occurs, is unclear.
(1) of the LBBB idiopathic non-sustained ventricular tachycardia treatment: general can be oral verapamil (verapamil) 40 ~ 80mg , 2 to 3 times / d, or propafenone (propafenone) 50 ~ 150mg, 3 times / d. For refractory cases can take amiodarone 100 ~ 200mg, 2 ~ 3 times / d and so on. Also taking β-blockers [such as metoprolol (metoprolol) 12.5 ~ 25mg, 2 ~ 3 times / d].
① Villa Verapamil: the drug of choice. dose of 0.25mg / (kg / time), the total average (18.5 ± 2.8) mg. May also be preferred 5mg, adding 20ml of 5% glucose solution, slow intravenous injection (speed 10min). If invalid, 10min after the additional 5mg, 20mg total no more than is appropriate. Effective rate of 60% to 66.7%.
③ propranolol (Inderal), sotalol: If the treatment does not use this drug. propranolol intravenously 1 ~ 2mg, total <5mg (note can lead to heart failure, hypotension, bradycardia, cardiac arrest). sotalol 0.5 ~ 2mg/kg, slow intravenous injection (side with the former). the efficacy of β blockers in 50%. With β-blockers to prevent ventricular tachycardia recurrence is very poor.
④ amiodarone: the treatment of refractory patients use this drug. dose of 5mg/kg of 5% glucose solution or slow intravenous injection of saline in 20ml. If invalid, 15 ~ 30min after repeated 1 times, but the dose in half. Maintenance dose of 0.5 ~ 0.75mg/min continuous intravenous infusion, the dose appropriate addition and subtraction. This drug can cause bradycardia, conduction block, hypotension, QT interval prolongation with polymorphic ventricular tachycardia.
① verapamil : the drug of choice, dosage as above. Efficiency of 93%. But when the tachycardia lasted longer, there is generated a large number of catecholamines, intravenous verapamil may be invalid. oral verapamil can not prevent tachycardia recurrence.
② propafenone: efficacy similar to verapamil, the dose above. Song with the city reported 10 cases, 9 cases were terminated. Liu Zhiqin other reports (2002), propafenone LBBB-type sensitive type of RBBB ineffective.
③ Procainamide: 87% efficiency, but also report invalid.
(1) Indications: Where the clinical diagnosis of idiopathic ventricular tachycardia, symptoms, repeated seizures, drug seizures and can not effectively prevent significant interference with circulation who are indications.
(2) success criteria: ① ventricular tachycardia soon after the termination of the discharge (<30s); ② can not induce ventricular tachycardia, intravenous infusion of ventricular tachycardia after isoproterenol can not induce: ③ about 1 week after repeated cardiac electrophysiology, ventricular tachycardia is not induced; ④ follow-up without the same type of ventricular tachycardia occurred.
(b) the prognosis
as idiopathic ventricular tachycardia without a clear heart, tachycardia tolerance strong, long-term clinical follow-up showed arrhythmic deaths (sudden death) has reported very little, so the prognosis is good. Brugada 54 cases of idiopathic ventricular tachycardia were followed up for 7 years, 50% of patients despite repeated episodes of ventricular tachycardia, but no case of sudden death. In contrast, 35 patients with acute myocardial infarction in patients with ventricular tachycardia after an average follow-up period of 20 months, 11% of patients sudden death. Ohe report four cases of idiopathic left ventricular tachycardia in patients with oral verapamil follow-up 2.8 years, 1 case of ventricular tachycardia remission, 3 patients become non-sustained ventricular tachycardia, no significant improvement in clinical symptoms. Some patients with idiopathic ventricular tachycardia, ventricular tachycardia episodes has a natural tendency to ease and disappear, so patients with no obvious symptoms, seizures not frequent, long-term use of antiarrhythmic drugs is not necessary, but should be followed up regularly.
is no relevant information reported.
mainly based on ECG.
A. repeated short episodes of array of monomorphic ventricular tachycardia: three consecutive lines of each episode or three or more ventricular contraction. Mostly in the 30s and continued to self-termination. Generally 3 to 20 consecutive ventricular contractions, so non-sustained ventricular tachycardia (Figure 1).
B. ventricular tachycardia was LBBB-type qrs wave shape: the first ventricular tachycardia one after the qrs QRS graphics with the same graphics. qrs wave duration> 0.12s, but widened to a lesser extent. To 0.13 ~ 0.14s up to see more in the 0.16s or less.
D. Most episodes of ventricular rate in patients with 110 to 160 beats / min, often without temperature wake phenomenon. Most of ventricular rate and uniform rules together, and a few may be irregular, sometimes before the termination of ventricular tachycardia has gradually reduced its perimeter first.
E. seizures and heart rate related: When sinus rhythm is easy to attack fast, exercise can induce. Low period before the stimulation procedure, intravenous infusion of isoproterenol may induce or facilitate the application period before stimulation.
F. largely determine the right ventricle of origin: Ⅱ, Ⅲ, aVF ecg R wave as the main person, originated in the right ventricular outflow tract or free wall, Ⅱ, Ⅲ, aVF lead to S-wave were mainly originated in the right ventricular inflow tract or apex.
G. intermittent episodes of normal sinus rhythm: also often single or in pairs ventricular contraction associated with. ventricular contractions and ventricular tachycardia qrs wave forms exactly the same.
H. Signal average ecg is normal.
E. period before the stimulus program may be terminated for some patients with persistent or induced LBBB-type idiopathic ventricular tachycardia. Sometimes still need to under isoproterenol infusion, easier to succeed.
F. largely determine the right ventricle of origin: with non-persistent characteristics.
H. Signal average ecg is normal.
LBBB idiopathic ventricular tachycardia between the two types: the majority of the performance of only one type. A small number of patients may be non-persistent repeated attacks, and then evolved into persistent: the first performance of some patients with sustained ventricular tachycardia, and then naturally stop the attack, but also between the two attacks were not sustained, then After a longer length of time ranging from ventricular tachycardia, sinus rhythm changes.
(2) RBBB type of persistent idiopathic ventricular tachycardia: This type accounts for idiopathic ventricular tachycardia of 30%, compared with the occurrence of LBBB-type much lower rates. Most were sustained, the individual was non-persistent. The ecg features are as follows:
② spontaneous or induced atrial and ventricular programmed stimulation in RBBB idiopathic ventricular tachycardia is sustained monomorphic ventricular tachycardia. qrs complex showed RBBB (Figure 3), QRS> 0.12s.
⑤ qrs wave of the amount of surface ecg showed left axis deviation 85%: 15% were highly skewed to the right. Point of origin, mostly in the left posterior branch of the left ventricle at intervals, a few in the left branch office. Another originated in the left ventricular free wall, may be associated with right axis deviation, is less common. Some originated in the left ventricular outflow tract and so on.
⑥ aVL leads showing R or RS graphics.
(1) branch of the ventricular heart too speed: more common in young people, the general examination showed no structural heart disease based on repeated episodes of ventricular tachycardia, but the onset of the hemodynamic effects of small, does not deteriorate into ventricular fibrillation, severe symptoms can be no special, not only the usual misdiagnosed as supraventricular tachycardia. As the effect of verapamil treatment significantly, so that its mechanism mostly triggered activity, and the after-depolarization. In recent years, electrophysiological studies support the reentry mechanism. ecg Features:
② qrs wave of mostly right bundle branch block with left anterior branch block or left posterior branch graph: the point of origin were located in the left ventricle in the lower part of the interval. A few patients showed a qrs complex with left bundle branch block left axis deviation or right side graphics, point of origin were located in the right ventricular outflow tract or right bundle branch high (Figure 5).
③ ventricular rate less than 180 times / min: after the termination of ventricular tachycardia, ecg returned to normal . Part of the ecg ST-segment depression may occur and t wave inversion, that is due to electrical tension adjustment mechanism.
(2) catecholamine-sensitive ventricular tachycardia (catecholamine sensitive VT): The onset of ventricular tachycardia and sympathetic nerve activity, increased secretion of adrenaline on , exercise and stress can trigger episodes of ventricular tachycardia. 50% to 70% of patients by exercise test-induced ventricular tachycardia. intravenous infusion of isoproterenol-induced ventricular tachycardia is the most reliable diagnostic method. Period before the stimulus program generally does not induce or terminate the attack.
(3) idiopathic ventricular tachycardia with electrical tension modulation of t wave changes: ecg characteristics: When idiopathic ventricular tachycardia, ventricular branch tachycardia after restoration of sinus rhythm, the electrocardiogram before the onset of tachycardia compared with the same lead to inverted t wave (ie, t wave in Ⅱ, Ⅲ, avF, V3 ~ V6 leads inversion, the amplitude can be deep up to 0.1 ~ 1.0mV), known as the electrical modulation of T-wave changes (ST segment depression can be associated) (Figure 6). A transient change in this system, more than a few days or ten days to restore. The mechanism is unclear. Some people think that ventricular tachycardia in myocardial involvement, myocardial fiber stretch, even to stop ventricular tachycardia, cardiac repolarization is not normal, can lead to t wave changes.
(4) idiopathic ventricular tachycardia with exit block: In a few cases, ventricular tachycardia, ventricular ectopic pacemaker exit block around the place, mostly for the second time, was 2:1,3:2 exit block, resulting in RR interval range (Figure 7).
1. idiopathic ventricular tachycardia and paroxysmal ventricular tachycardia pathological identification of the ECG, although both belong to the same monomorphic ventricular tachycardia, the ecg characteristics were similar, but the etiology and clinical significance is decidedly different, not difficult to identify the two. arrhythmia in the clinical differential diagnosis must be combined with a comprehensive analysis. pathological paroxysmal supraventricular tachycardia is characterized by: ① 90% of patients with structural heart disease, 70% to 80% occur in patients with coronary heart disease; ② often ischemic ecg ST-segment depression, t wave abnormalities or myocardial infarction graphics; ③ program period before stimulation can induce sustained ventricular tachycardia was induced by the sudden death rate; ④ serious prognosis. And idiopathic ventricular tachycardia occurred in normal subjects, the vast majority of patients with good prognosis.
2.LBBB idiopathic ventricular tachycardia after myocardial infarction in patients with paroxysmal supraventricular tachycardia and rational arrhythmogenic right ventricular dysplasia ventricular tachycardia on the ecg identification
(1) LBBB idiopathic ventricular tachycardia ecg qrs frontal plane axis of most of the right side, a small number of normal or left side; and myocardial infarction pathological paroxysmal supraventricular tachycardia ecg mostly left axis deviation: arrhythmogenic right ventricular dysplasia ventricular tachycardia mostly left side, a small number of normal.
(2) LBBB idiopathic ventricular tachycardia was QS-type lead aVL, and myocardial infarction pathological paroxysmal supraventricular tachycardia lead aVL United were R-type; right ventricular dysplasia lead aVL was R or S-type.
(3) LBBB idiopathic ventricular tachycardia limb lead R wave amplitude sum ≥ 40mV accounted for 70.9%, does not appear QR-type (but sometimes exceptions), and pathological paroxysmal supraventricular tachycardia limb lead R wave amplitude ≥ 40mV were only 5% and 75% of patients QR graphics. right ventricular dysplasia ≥ 40mV and only 20%.
3. with paroxysmal supraventricular tachycardia with room to identify differences in conduction as idiopathic sustained ventricular tachycardia episodes were paroxysmal, long duration, so in young patients is often misdiagnosed as paroxysmal supraventricular tachycardia. At this point the main basis for identifying whether the atrioventricular separation, such as with the tips of idiopathic ventricular tachycardia. Do esophageal ECG, in order to fully display atrioventricular separation.[Disease]
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