Síncope em gestantes - causa arrítimica

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Síncope em gestantes - causa arrítimica

Mensagem  Convidad em Seg Jul 08, 2013 11:27 pm

Arritmias cardíacas em gestantes

Os distúrbios do ritmo cardíaco são observados com frequência durante a gestação, podendo ocorrer tanto em corações normais como em gestantes com cardiopatia prévia, especialmente a insuficiência cardíaca(1).

Significativas mudanças ocorrem na fisiologia materna durante a gestação, como o aumento do débito cardíaco, do volume sanguíneo, da frequência respiratória e do consumo de oxigênio. Além disso, o útero grávido pode causar significativa compressão dos vasos ilíacos e abdominais quando a mãe está em posição supina, resultando em diminuição do débito cardíaco e hipotensão(2,3,4). Associadas a isso, alterações hormonais e influências do sistema nervoso autônomo contribuem para o aumento da incidência de arritmias(5,6). Alterações da velocidade de condução do estímulo pelos átrios e ventrículos e dos períodos refratários teciduais, que sofrem modulações de catecolaminas circulantes, predispõem ao surgimento de arritmias pelo mecanismo de reentrada(7).

Warnes e cols.(Cool advertem que sintomas de uma gestação normal, como fadiga, diminuição da tolerância aos exercícios físicos, pré-síncope e dispnéia podem mascarar doença cardíaca preexistente ou esta pode se manifestar pela primeira vez durante a gestação.

O primeiro e o segundo trimestres são os períodos em que os sintomas tornam-se aparentes, tornando-se mais frequentes entre o segundo e o terceiro, exatamente pela maior intensidade de alterações hemodinâmicas(7).

A terapia com antiarrítmicos durante a gestação é tarefa complexa, porque tanto a arritmia quanto o tratamento podem prejudicar o feto em diferentes escalas(9).

A maioria dos autores concorda que o tratamento medicamentoso seja indicado apenas na dependência de sintomas importantes ou quando do aumento da periodicidade das arritmias, bem como em situações nas quais ocorrem alterações hemodinâmicas com risco para a mãe e para o feto(7,9,10,11).

A conduta não medicamentosa, como observação e repouso, pode ser apropriada em arritmias episódicas e/ou sem repercussão clínica. Manobras vagais como massagem no seio carotídeo, manobra de valsava ou imersão da face em água gelada são bem toleradas e podem constituir uma alternativa segura para esses casos(11,12).

Durante o trabalho de parto, as arritmias cardíacas são extremamente frequentes, tendo sido encontradas em 100% das gestantes normais estudadas por Upsha(13) e em 72,3% das estudadas por Ovando e cols.(14), principalmente no período expulsivo do trabalho de parto, sendo por isso consideradas fisiológicas(13,14,15).

Relação das arritmias com palpitações, tonturas e síncopes

Palpitações, tonturas, pré-síncopes e até mesmo síncopes frequentemente ocorrem durante a gestação(16). A etiologia destes sintomas não está ainda bem elucidada, mas acredita-se que, ao menos em parte, possam se dever aos mecanismos adaptativos inerentes ao período gestacional. Um aumento da incidência das arritmias cardíacas tem sido relatado durante a gestação em pacientes com e sem doença cardíaca identificável(17,18,19,20,21).

Um estudo realizado por Shotan e cols.(22) avaliou a incidência de arritmias na gestação normal e sua relação com palpitações, tonturas, e síncopes. O estudo demonstra alta incidência de arritmias e atividade ectópica ventricular, em mulheres jovens e saudáveis, sendo a palpitação o principal sintoma relatado.

Referência: John Edney dos Santos; Giancarlo Simionatto; Jacy Bruns; Júlio A. Ulhoa Canto; Andrei Lewandowski. Arritmias cardíacas em gestantes.


Ventricular arrhythmias during pregnancy Uptodate.com

Arrhythmias are the most common cardiac complication encountered during pregnancy in women with and without structural heart disease. Arrhythmias may manifest for the first time during pregnancy or pregnancy can trigger exacerbations in women with known preexisting arrhythmias.

The prevalence, clinical presentation and management of ventricular arrhythmias will be reviewed. Cardiac arrest during pregnancy, general management of ventricular arrhythmias and cardiac arrest, electrocardiographic characteristics of ventricular arrhythmias and issues relating to supraventricular arrhythmias during pregnancy are discussed in detail elsewhere.



GENERAL APPROACH — Women with established arrhythmias or structural heart disease are at highest risk of developing arrhythmias during pregnancy. Due to surgical advances, the number of women of childbearing age with congenital heart disease has increased and this group of women is at particularly high risk for arrhythmias (figure 1). Since arrhythmias are frequently associated with acquired or structural heart disease, any woman who presents with an arrhythmia during pregnancy should undergo clinical evaluation for structural heart disease (including an electrocardiogram and a transthoracic echocardiogram).

In general, the approach to the treatment of arrhythmias in pregnancy is similar to that in the non-pregnant patient. However, due to the theoretical or known adverse effects of antiarrhythmic drugs on the fetus, antiarrhythmic drugs are generally reserved for the treatment of arrhythmias associated with significant symptoms or hemodynamic compromise. Treatment strategies during pregnancy are hampered by the lack of randomized trials in this cohort of women. Choice of therapy, for the most part, is based on limited data from animal studies, case reports, observational studies, and clinical experience.

MECHANISM OF ARRHYTHMOGENESIS IN PREGNANCY — The exact mechanism of increased arrhythmia burden during pregnancy is unclear, but has been attributed to hemodynamic, hormonal, and autonomic changes related to pregnancy.

The hemodynamic changes of pregnancy have been well studied and these changes likely contribute to the development of arrhythmias during pregnancy. Intravascular volume increases, augmenting the preload on the ventricles, and increasing both atrial and ventricular size . Atrial and ventricular myocardial stretch may contribute to arrhythmogenesis due to stretch-activated ion channel activity causing membrane depolarization, shortened refractoriness, slowed conduction and spatial dispersion of refractoriness and conduction. There is also an increase in resting heart rate which has been associated with markers of arrhythmogenesis such as late potentials, premature ventricular contractions, and depressed heart rate variability.

Few studies have been published on the influence of hormonal and autonomic changes on arrhythmogenesis in pregnancy. Although catecholamine levels do not appear to change during pregnancy, there is an increase in adrenergic responsiveness during pregnancy. Estrogen has been shown to increase the number of myocardial alpha-adrenergic receptors. This increased adrenergic activity may contribute to enhanced automaticity and triggered activity.

PALPITATIONS — Palpitations occur frequently during pregnancy and are a common indication for cardiac evaluation during pregnancy. The differential diagnosis of palpitations is extensive and the diagnostic evaluation of pregnant women with palpitations does not differ from nonpregnant women.

One study compared 110 pregnant women with symptoms suggestive of possible arrhythmia (palpitations: 87 percent; dizziness: 13 percent; syncope/presyncope: 6 percent) with 52 pregnant women evaluated for an asymptomatic functional murmur. Prevalence of supraventricular and ventricular ectopic activity on 24-hour Holter ambulatory monitoring was similar in the symptomatic and control groups.

Only 10 percent of symptomatic episodes were accompanied by the presence of an arrhythmia. A sensation of palpitations during pregnancy in the absence of concomitant cardiac arrhythmias may be related to the high output state, including increased heart rate, decreased peripheral resistance, and increased stroke volumes.

VENTRICULAR PREMATURE BEATS — Ventricular premature beats (VPBs) are frequently detected in pregnant women. The prevalence is dependent upon the duration of observation and the clinical presentation.

In the above referenced study of 110 symptomatic and 52 asymptomatic pregnant women, the prevalence of isolated VPBs was similar in symptomatic and asymptomatic women (49 versus 40 percent). However, frequent VPBs (≥50 VPBs per 24 hours) were more common in symptomatic women (22 versus 4 percent). There was a significant reduction in the frequency of combined atrial and ventricular ectopic activity in the 9 women in whom Holter monitoring was repeated postpartum.

Clinical presentation — VPBs produce few or no symptoms in the majority of women, although some women may experience symptoms of palpitations or dizziness.

Management during pregnancy — No therapy is required for VPBs in asymptomatic patients. Pregnant women with symptomatic VPBs should be reassured of the benign nature of VPBs.

Some experts counsel patients with palpitations to discontinue potential precipitant factors such as smoking, coffee intake, alcohol intake, and other stimulants. However the role of caffeine restriction has not been established. Moderate caffeine exposure has not been demonstrated to increase VPBs in patients with or without structural heart disease , and caffeine restriction was not found to improve symptoms or reduce the frequency of VPBs in a small trial .

If ectopic activity continues and is associated with intolerable symptoms, beta blockers can be used. Metoprolol is a preferred beta blocker in pregnant women since atenolol may impair fetal growth. The limited options for treatment of VPBs are discussed further separately.

EPIDEMIOLOGY OF VT AND VF — Ventricular tachyarrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF]) are rare during pregnancy. VT has been reported in pregnant women without apparent structural heart disease, but is usually associated with structural heart disease. The risk of recurrent VT during pregnancy is particularly high (27 percent) in women with structural heart disease and a history of VT. Types of structural heart disease associated with VT in pregnancy include hypertrophic cardiomyopathy, peripartum cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, congenital heart disease , and valvular heart disease. Myocardial infarction with or without coronary artery disease has been observed during pregnancy and may be complicated by VT or VF. Women with primary electrical diseases such as long QT syndrome (LQTS) and Brugada syndrome are also at risk of VT.

Other medical conditions associated with ventricular tachycardia (VT) during pregnancy are hypomagnesemia, hypertensive crises, and thyrotoxicosis.

The management of ventricular arrhythmias needs to be tailored to the individual. The following are among the clinical factors that should be considered:

Presence and severity of underlying heart disease
Ventricular function
Etiology of the VT (catecholamine sensitive versus noncatecholamine sensitive)
Frequency and duration of VT (nonsustained versus sustained)
Severity of associated symptoms
The following section will review issues regarding VT during pregnancy in women with and without structural heart disease.

IDIOPATHIC VT — Monomorphic VT without apparent structural heart disease is considered idiopathic. The most common type of idiopathic VT is repetitive monomorphic VT which usually originates from the right ventricular outflow tract (ECG "signature": left bundle branch block and inferior axis) or, less often, from the left ventricular outflow tract (ECG pattern: right bundle branch block and inferior axis or left bundle and inferior axis but earlier precordial transition than for right ventricular outflow tract tachycardia). Another type is idiopathic left ventricular tachycardia which originates from the inferior aspect of the midseptum and has the morphologic pattern of right bundle branch block with left axis deviation (QRS axis around -60°).
A study of seven women presenting with new-onset idiopathic VT during pregnancy found that the VT was often catecholamine sensitive and that the VT was often suppressed in women who received beta blockers. There were no maternal or fetal complications in this series. There is one case report of sudden death in a woman with idiopathic VT who died in the third trimester, three weeks after initiation of procainamide therapy.

Management during pregnancy — Idiopathic VT rarely degenerates into an unstable rhythm and usually has a benign prognosis.

Treatment of repetitive monomorphic VT with cardioselective beta blockers may be effective in pregnant women with idiopathic VT even in the absence of a clear relationship to adrenergic tone. Sotalol can be used as an alternative.
The less common idiopathic left ventricular tachycardia appears to respond well to verapamil, both for the termination of acute episodes and the prevention of recurrences.

LONG QT SYNDROME — Although VT during pregnancy has been reported in women with long QT syndrome (LQTS), the increase in heart rate seen during pregnancy may serve to shorten the QT interval and therefore may be partially protective.
In women with LQTS, the risk of VT is especially high in the postpartum period. Increased risk of VT during the postpartum period may be related to a decrease in the heart rate and an associated increase in the QT interval. The physiologic stress and altered sleep patterns associated with caring for a newborn infant may also contribute to an increase in adrenergically mediated cardiac events.

The effect of pregnancy was evaluated in a retrospective analysis of 422 women (111 probands and 311 first-degree relatives) entered into the International LQTS registry [56]. Most of the probands had a personal history of syncope or aborted cardiac arrest. The following findings were noted:

Probands were significantly more likely to have cardiac events (syncope, aborted cardiac arrest, or SCD) in the 40-week postpartum interval than during the prepregnancy period of 40 weeks (23.4 versus 3.8 percent). The increase in risk was distributed throughout the postpartum period. The incidence of first cardiac events during pregnancy was slightly but not significantly increased compared to the prepregnancy period (9.0 versus 3.8 percent)
The postpartum increase in risk also applied to first cardiac events (9.0 versus 1.8 and 0 percent during and before pregnancy).
Treatment with beta blockers was independently associated with a decrease in risk for cardiac events in probands during all three intervals (odds ratio 0.023).
The average probability of having a cardiac event during the postpartum period in probands was 2 percent (one in 50 pregnancies). Treatment with a beta blocker lowered the risk to one in 2500 pregnancies.
The risks associated with pregnancy may be different among various LQTS genotypes. The influence of genotype is illustrated by the following observations:

In a series of 388 LQTS patients referred for genetic testing, postpartum cardiac events were more commonly reported in patients with LQT2 mutation (13 of 80, 16 percent) than in patients with LQT1 (1 of 103, <1 percent).
In a series limited to women with a single LQT1 mutation, cardiac event rates associated with pregnancy were low (2.6 percent). These events occurred only in women with a prior history of symptoms who were not taking beta blockers.

Management during pregnancy — We agree with the 2006 American College of Cardiology/American Heart Association/European Society of Cardiology (ACC/AHA/ESC) guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death and the 2011 European Society of Cardiology guidelines on the management of cardiovascular diseases during pregnancy. The guidelines recommended that pregnant women with LQTS who have had symptoms benefit from continued beta-blocker therapy throughout pregnancy and postpartum, unless there are definite contraindications.

VT IN WOMEN WITH STRUCTURAL HEART DISEASE

Hypertrophic cardiomyopathy — In general, women with hypertrophic cardiomyopathy (HCM) tolerate pregnancy well, although several case reports have described cardiac complications and sudden death during pregnancy.

The largest study investigating mortality and morbidity in pregnant women with HCM included 100 women who had a total of 199 live births. Two sudden cardiac deaths occurred during pregnancy in women with high risk features. One of the women had severe left ventricular hypertrophy (30 mm maximal wall thickness) and a resting outflow gradient of 115 mmHg. She died suddenly four days after delivery after complaining of palpitations. The other woman had a family history of eight deaths in young relatives, five of which were sudden. This patient developed recurrent episodes of sustained VT during labor.

Management of pregnancy and delivery in women with HCM is discussed separately.

Congenital heart disease — The prevalence of sustained VT during pregnancy in women with CHD has been reported to range from 4.5 to 15.9 per 1,000 pregnancies. Prevalence rates are strongly influenced by the types of cardiac lesions in the study population.

In a large prospective multicenter study in women with CHD, two cases of sustained VT occurred in 445 pregnancies. One woman had an unrepaired intracardiac shunt and the other had repaired congenital aortic stenosis.
A multicenter study from Japan reported two cases of sustained VT during 126 pregnancies. Both cases of VT occurred in women with repaired tetralogy of Fallot and both were successfully treated with intravenous lidocaine. Seven pregnancies were complicated by nonsustained VT, none of which were treated.
Peripartum cardiomyopathy — Peripartum cardiomyopathy is a rare and sometimes life-threatening condition defined as development of systolic heart failure in the last month of pregnancy or within five months of delivery. The incidence varies widely among various populations. The clinical presentation includes symptoms of new-onset heart failure such as dyspnea, cough, orthopnea, and hemoptysis. The prevalence of sustained VT in patients with peripartum cardiomyopathy is unknown; few cases have been reported in the literature [43,44,81]. These ventricular arrhythmias can be refractory to pharmacologic treatment (eg, lidocaine, metoprolol, amiodarone) and DC cardioversion

MANAGEMENT OF VT DURING PREGNANCY IN WOMEN WITH STRUCTURAL HEART DISEASE

Management of acute episodes — Acute treatment of sustained ventricular arrhythmias in pregnant women is similar to that in nonpregnant women. Ventricular arrhythmias in the presence of structural heart disease are potentially life-threatening and require immediate evaluation for hemodynamic instability to determine whether electrical cardioversion or defibrillation is indicated.

In hemodynamically well tolerated VT, pharmacological cardioversion may be acceptable. Pharmacological options include intravenous procainamide, amiodarone, or lidocaine; the choice of pharmacological agents should be tailored to the individual case. For women at risk for VT during labor and delivery, it is important to ensure that appropriate cardiac medications and external defibrillators are available in the delivery suites.

Electrical cardioversion — Emergent or elective electrical cardioversion can be performed at all stages of pregnancy. Electrical cardioversion is indicated for any sustained VT with hemodynamic compromise and can be considered for drug-refractory VT. Electrical cardioversion does not result in compromise of blood flow to the fetus  While there is a theoretical risk of inducing an arrhythmia in the fetus, this risk is very small due to the high fibrillation threshold and small amount of energy reaching the fetus. Nonetheless, fetal rhythm monitoring is recommended, because of rare reported cases of cardioversion precipitating fetal distress requiring emergency cesarean delivery. In the third trimester, some physicians prefer to perform electrical cardioversion under general anesthesia and intubation considering the more difficult airway and increased risk of gastric aspiration during pregnancy.

Prophylactic pharmacologic therapy during pregnancy — The risk of recurrent VT and sudden death in women with structural heart disease can be substantial and the benefits of prophylactic drug therapy may outweigh the potential fetal adverse effects of these drugs. The risk of sudden death is further increased when concomitant left ventricular dysfunction is present.

Depending on the underlying cardiac condition, beta-1 selective beta-blockers alone, amiodarone alone, or both in combination can be effective in preventing VT during pregnancy as noted in the 2006 ACC/AHA/ESC ventricular arrhythmia guidelines. Gestational exposure to amiodarone is associated with neonatal hypothyroidism and hyperthyroidism. Small-for-gestational-age infants are reported with gestational exposure to the combination of amiodarone and beta blockers. In some cases, sotalol can be considered if beta-blocker therapy is ineffective. Because of potential side effects, all women should be counseled about the potential risks and benefits of drug therapy.

Although some have used class IA (eg, quinidine, procainamide) or IC (eg, flecainide) drugs as prophylactic treatment for VT during pregnancy, these drugs are not generally recommended since they have not improved survival in the nonpregnant population with structural heart disease, presumably because of proarrhythmic effects.

Implantable cardioverter-defibrillator — Women with an implantable cardioverter-defibrillator (ICD) can have a successful pregnancy with good fetal outcome [96,97]. Indications for ICD placement are discussed separately.

In a retrospective multicenter study of pregnancy outcomes in women with ICDs (n = 44), 25 percent (11 of 44) of the pregnancies were complicated by at least one shock. All ICDs were implanted for secondary prevention and the underlying cardiac diseases were primary electrical diseases (ie, LQTS, idiopathic ventricular fibrillation) or structural heart diseases (ie, cardiomyopathy, congenital heart disease, arrhythmogenic right ventricular dysplasia). Pregnancy was not associated with an increase in ICD-related complications or an increase in the number of shocks (0.07 versus 0.06 shocks per month) compared to the preconception period.

The experience with ICD implantation during pregnancy is limited [98], however, pacemaker implantation during pregnancy can be accomplished and total radiation dose can be reduced by using echocardiographic guidance.

If a pregnant patient is determined to be at high risk of sudden death, placement of an implantable defibrillator is generally deferred until after delivery of the baby. In this setting, an external wearable automatic defibrillator (LifeVest) is often prescribed for the duration of the pregnancy.

Radiofrequency catheter ablation — The success rate of radiofrequency catheter ablation of monomorphic VT is between 80 to 100 percent  and may be considered in women who are using antiarrhythmic therapy and are contemplating pregnancy.

Experience with radiofrequency catheter ablation during pregnancy has been limited to cases of SVT. These procedures are generally not performed during pregnancy, mainly due to concerns of ionizing radiation exposure to the fetus. However, in rare cases, women with severe and drug-resistant VT during pregnancy may be considered for an ablation procedure. The risk of radiation exposure for the fetus during a typical ablation is small (<1 mGy at all periods of gestation), and is mainly attributable to scatter from the thorax of the mother.

ISSUES REGARDING ANTIARRHYTHMIC DRUG TREATMENT — Use of antiarrhythmic drugs in pregnancy requires attention to potential alterations in pharmacokinetics as well as fetal risk. For most antiarrhythmic drugs, adequate and well-controlled studies in pregnant women are lacking and most drugs are categorized as class C drugs by the US Food and Drug Administration [115,116] (table 1 and table 2). Another consideration is potential adverse effects in the infant during breast feeding (table 2). Antiarrhythmic drug safety during pregnancy, teratogenic risk, pharmacokinetic changes and breast feeding are discussed further separately.

SUMMARY AND RECOMMENDATIONS

Ventricular tachyarrhythmias are frequently associated with acquired or structural heart disease and therefore any woman who presents with a ventricular arrhythmia during pregnancy should undergo clinical evaluation for structural heart disease (including an electrocardiogram and a transthoracic echocardiogram).
Monomorphic ventricular tachycardia without apparent structural heart disease is considered idiopathic. The most common type originates from the right ventricular outflow tract, and this form of ventricular tachycardia can often be successfully treated with beta blockers or verapamil.
Women with the long QT syndrome are at risk for ventricular tachycardia, especially in the postpartum period. Pregnant women with long QT syndrome should be treated with beta-blocker therapy throughout pregnancy and postpartum.
Acute treatment of sustained ventricular arrhythmias in pregnant women is similar to that in nonpregnant women. Ventricular arrhythmias in the presence of structural heart disease are potentially life-threatening and require immediate evaluation for hemodynamic instability to determine whether electrical cardioversion or defibrillation is indicated.
In women with structural heart disease and a history of ventricular tachycardia, the benefits of prophylactic drug therapy may outweigh the potential fetal adverse effects of these drugs.
Women with an implantable cardioverter-defibrillator can have a successful pregnancy with good fetal outcome.

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