16-летняя девушка с тахикардией
Модератор: Pyankov Vasily
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Продолжаем следить за регрессом кардиомиопатии у нашей больной. Чувствует она себя хорошо. При осмотре АД 80/55, ЧСС 55 в 1 мин, ритм синусовый, SpO2 99%. КДО ЛЖ уменьшился с 298 мл до 169 мл, масса миокарда — с 247 г до 201 г. ФВ ЛЖ возросла с 37% до 48%. Объем левого предсердия нормализовался (36 мл), митральная недостаточность исчезла. Систолическое ДЛА нормальное (15—20 мм рт. ст.), даже диастолическая функция и та теперь нормальная. Все отменил ей, кроме маленьких доз ингибиторов АПФ. Приедет из своей Молдавии еще через год.
Посмотрите, насколько все стало приличнее выглядеть.
Посмотрите, насколько все стало приличнее выглядеть.
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Спасибо за очень полезную демонстрацию! Наверное, не очень худо было бы проанализиовать, что побудило отказаться от очень удобной версии воспалительной или идиопатической кардиопатии и настаивать на аблации. Может есть какой-нибудь консенсус насчет первоочередного удаления предсердной эктопической или другой тахикардии при признаках дилатационной кардиомиопатии? Насчет тахикардиальной кардиомиопатии известно давно, но случаи такого радикально-успешного решения вопроса довольно редки? Возможно ли было бы в данном случае, медикаментозно урежая ритм, решить проблему?
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У нас как-то и вопроса не было о том, что первично: непароксизмальная (автоматическая) непрерывно рецидивирующая предсердная тахикардия -- самостоятельная болезнь, которая может быть причиной ДКМП. Зачем еще искать причины? Уредить ритм при этой тахикардии очень трудно, в чем мы быстро убедились. Предлагаю прочесть статью из up-to-date по этому поводу.
Incessant atrial tachycardia
Author
Morton F Arnsdorf, MD, MACC Section Editor
Leonard I Ganz, MD Deputy Editor
Gordon M Saperia, MD, FACC
INTRODUCTION — "Incessant" is applied to an atrial tachycardia when it is present for at least 90 percent of the time a patient is monitored. This arrhythmia has been considered as part of primary (including both reentrant and automatic mechanisms), ectopic, or automatic atrial arrhythmias. We are discussing the incessant form separately, since the sustained rapid rate often results in dilatation of the heart and biventricular dysfunction, even in individuals without heart disease. Furthermore, the arrhythmia is resistant to antiarrhythmic therapy.
MECHANISMS — Several mechanisms have been implicated in the genesis of incessant atrial tachycardia including reentry, automaticity, and triggered activity:
• Reentry may involve dual "fast-slow" pathways in the atrioventricular (AV) node (an abnormality which is not strictly an atrial tachycardia), concealed accessory pathways, and occasionally, sinoatrial (SA) nodal and atrial reentry. Macroreentrant, adenosine-resistant circuits have also been described, most of which were in patients with atriotomy scars.
• Automatic atrial tachycardias often originate from the ostia of the pulmonary veins. (See "Focal atrial tachycardia".)
• Atrial tachycardias are common following ablation of atrial fibrillation, and a small portion of these may be incessant.
CLINICAL FEATURES — Incessant atrial tachycardia is often found in otherwise normal young individuals, including children, although it may occur in patients with organic heart disease. The rate tends to be faster during the day than at night, and it may increase with exercise or pregnancy. Heart rate variability, a measure of neural regulation of normal pacemaker tissue, does not seem to differ between ectopic atrial and sinus tachycardias, which suggests that ectopic atrial foci have the same autonomic regulation as normal pacemaker tissue. (See "Heart rate variability: Technical aspects".) A cardiomyopathy has been associated with incessant atrial tachycardia, a result of the chronic, rapid heart rate. (See "Tachycardia-mediated cardiomyopathy".)
One case has been associated with the development of paroxysmal ventricular arrhythmias.
TREATMENT — Pharmacologic therapy is generally ineffective in incessant atrial tachycardia, particularly in children. An occasional success has been reported using beta-blockers in dilated cardiomyopathy, and Class IC antiarrhythmic drugs, such as flecainide, in adults. Lidocaine-sensitive, rate-related, repetitive and nearly incessant atrial tachycardia has been reported, the mechanism of which is poorly understood.
Insertion of a pacemaker is also of little benefit, leading to the presumption that many of these cases are automatic rather than reentrant. Permanent coupled atrial pacing has been used to slow the ventricular rate. DC cardioversion is also ineffective.
Surgery — Surgery with excision, exclusion, and cryoablation has been used with some success to treat incessant atrial tachycardia. In one case, we found that the excised focus demonstrated triggerable automatic activity that could be initiated and terminated by extrastimuli. It is not known if this observation is more generally applicable.
Ablation — Ablative techniques have been used to interrupt the bundle of His, thereby slowing the ventricular response, to eliminate an ectopic atrial focus, or to interrupt a reentrant pathway. A nonfluoroscopic catheter-based electroanatomic mapping system, CARTO, has a magnetic field emitter and sensor and can create a replica of the anatomy of the cardiac chamber in which the tachycardia focus, in either the right or left atria, is located, permitting more precise localization of the arrhythmia focus (figure 2 and figure 3). Electroanatomic mapping images also allow identification of areas of interest around an arrhythmia focus.
One study used radiofrequency ablation in 15 patients (11 adults, 4 children). The site of origin of the tachycardia was in the right atrium in 14 and the left atrium in 1; 11 patients had an ectopic atrial tachycardia, while 4 had a reentrant SA nodal tachycardia. Ablation was successful in all cases; the arrhythmia recurred in 3 (2 ectopic, 1 SA reentrant), with a second successful ablation in one. The electrophysiologic map of the right atrium and the site of the ectopic tachycardia can also be identified (figure 4).
Ablation was also highly successful in a second study of 23 patients without structural heart disease who had 27 right atrial tachycardias. Radiofrequency ablation was effective in 96 percent of cases. In addition, utilizing intracardiac echocardiography during electrophysiologic mapping, 67 percent of the tachycardias were found to originate on the crista terminalis.
RECOMMENDATIONS — Primary therapy of incessant atrial tachycardia should be either surgical or ablative, procedures which should be performed at an experienced center. Flecainide can be tried in individuals without apparent heart disease; its proarrhythmic properties make it contraindicated in patients with heart disease, except for the treatment of potentially life-threatening ventricular arrhythmias.
Incessant atrial tachycardia
Author
Morton F Arnsdorf, MD, MACC Section Editor
Leonard I Ganz, MD Deputy Editor
Gordon M Saperia, MD, FACC
INTRODUCTION — "Incessant" is applied to an atrial tachycardia when it is present for at least 90 percent of the time a patient is monitored. This arrhythmia has been considered as part of primary (including both reentrant and automatic mechanisms), ectopic, or automatic atrial arrhythmias. We are discussing the incessant form separately, since the sustained rapid rate often results in dilatation of the heart and biventricular dysfunction, even in individuals without heart disease. Furthermore, the arrhythmia is resistant to antiarrhythmic therapy.
MECHANISMS — Several mechanisms have been implicated in the genesis of incessant atrial tachycardia including reentry, automaticity, and triggered activity:
• Reentry may involve dual "fast-slow" pathways in the atrioventricular (AV) node (an abnormality which is not strictly an atrial tachycardia), concealed accessory pathways, and occasionally, sinoatrial (SA) nodal and atrial reentry. Macroreentrant, adenosine-resistant circuits have also been described, most of which were in patients with atriotomy scars.
• Automatic atrial tachycardias often originate from the ostia of the pulmonary veins. (See "Focal atrial tachycardia".)
• Atrial tachycardias are common following ablation of atrial fibrillation, and a small portion of these may be incessant.
CLINICAL FEATURES — Incessant atrial tachycardia is often found in otherwise normal young individuals, including children, although it may occur in patients with organic heart disease. The rate tends to be faster during the day than at night, and it may increase with exercise or pregnancy. Heart rate variability, a measure of neural regulation of normal pacemaker tissue, does not seem to differ between ectopic atrial and sinus tachycardias, which suggests that ectopic atrial foci have the same autonomic regulation as normal pacemaker tissue. (See "Heart rate variability: Technical aspects".) A cardiomyopathy has been associated with incessant atrial tachycardia, a result of the chronic, rapid heart rate. (See "Tachycardia-mediated cardiomyopathy".)
One case has been associated with the development of paroxysmal ventricular arrhythmias.
TREATMENT — Pharmacologic therapy is generally ineffective in incessant atrial tachycardia, particularly in children. An occasional success has been reported using beta-blockers in dilated cardiomyopathy, and Class IC antiarrhythmic drugs, such as flecainide, in adults. Lidocaine-sensitive, rate-related, repetitive and nearly incessant atrial tachycardia has been reported, the mechanism of which is poorly understood.
Insertion of a pacemaker is also of little benefit, leading to the presumption that many of these cases are automatic rather than reentrant. Permanent coupled atrial pacing has been used to slow the ventricular rate. DC cardioversion is also ineffective.
Surgery — Surgery with excision, exclusion, and cryoablation has been used with some success to treat incessant atrial tachycardia. In one case, we found that the excised focus demonstrated triggerable automatic activity that could be initiated and terminated by extrastimuli. It is not known if this observation is more generally applicable.
Ablation — Ablative techniques have been used to interrupt the bundle of His, thereby slowing the ventricular response, to eliminate an ectopic atrial focus, or to interrupt a reentrant pathway. A nonfluoroscopic catheter-based electroanatomic mapping system, CARTO, has a magnetic field emitter and sensor and can create a replica of the anatomy of the cardiac chamber in which the tachycardia focus, in either the right or left atria, is located, permitting more precise localization of the arrhythmia focus (figure 2 and figure 3). Electroanatomic mapping images also allow identification of areas of interest around an arrhythmia focus.
One study used radiofrequency ablation in 15 patients (11 adults, 4 children). The site of origin of the tachycardia was in the right atrium in 14 and the left atrium in 1; 11 patients had an ectopic atrial tachycardia, while 4 had a reentrant SA nodal tachycardia. Ablation was successful in all cases; the arrhythmia recurred in 3 (2 ectopic, 1 SA reentrant), with a second successful ablation in one. The electrophysiologic map of the right atrium and the site of the ectopic tachycardia can also be identified (figure 4).
Ablation was also highly successful in a second study of 23 patients without structural heart disease who had 27 right atrial tachycardias. Radiofrequency ablation was effective in 96 percent of cases. In addition, utilizing intracardiac echocardiography during electrophysiologic mapping, 67 percent of the tachycardias were found to originate on the crista terminalis.
RECOMMENDATIONS — Primary therapy of incessant atrial tachycardia should be either surgical or ablative, procedures which should be performed at an experienced center. Flecainide can be tried in individuals without apparent heart disease; its proarrhythmic properties make it contraindicated in patients with heart disease, except for the treatment of potentially life-threatening ventricular arrhythmias.
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Версия удобная лишь с точки зрения оправдания ничегонеделания. Побудил здравый смысл: лечить надо устранимые факторы (тахикардия), а не неустранимые (миокардит). Медикаментозное лечение не давало никакого значимого эффекта, как и должно быть при предсердных тахикардиях. Подобные случаи описаны в литературе, можно поискать в пабмеде, на них и ориентировались (помимо здравого смысла).Sergey Chevychelov писал(а):Спасибо за очень полезную демонстрацию! Наверное, не очень худо было бы проанализиовать, что побудило отказаться от очень удобной версии воспалительной или идиопатической кардиопатии и настаивать на аблации. Может есть какой-нибудь консенсус насчет первоочередного удаления предсердной эктопической или другой тахикардии при признаках дилатационной кардиомиопатии? Насчет тахикардиальной кардиомиопатии известно давно, но случаи такого радикально-успешного решения вопроса довольно редки? Возможно ли было бы в данном случае, медикаментозно урежая ритм, решить проблему?
update: пока я отвечал, Максим Александрович меня опередил исчерпывающей цитатой.
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Спасибо за ответ и за информацию. Эта часть ответа весьма логична и ожидаема. Но, пациентка случайно (?) попала в хорошие руки. До этого она прошла через один как минимум (?) институт Кардиологии. Более того ей отказывали в аблации уже с Вашей подачи и отказывала совсем не периферийная катлаборатория. Дело не в морали (хотя это тоже важно), в Молдавии не читают пубмед и не знакомы с аптудатой (как и в головных педиатрических учреждениях РФ)? Или есть стандарты МЗ и СР РФ, ну для Молдавии сойдет и 2003 ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias, придерживаясь которых, можно избавить наших пациентов от поисков хороших рук? Впрочем, извините,вероятно, резонерство мой конек.
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Девушка продолжает чувствовать себя хорошо и уже ничего не принимает, вот ее картинки в августе 2011 г. Митральной недостаточности нет, дефект после транссептального доступа не обрнаружен.
Рад сообщить, что этот замечательный случай удостоился устного доклада на Европейском кардиологическом конгрессе в Париже.
Рад сообщить, что этот замечательный случай удостоился устного доклада на Европейском кардиологическом конгрессе в Париже.