Avaliação Ecocardiográfica de Pacientes com Forame Oval Patente e Acidente Vascular Cerebral Criptogênico / Echocardiographic Evaluation of Patients with Patent Foramen Ovale and Cryptogenic Stroke

Recentes estudos indicaram que o forame oval patente (FOP) pode ser responsável pelo acidente vascular cerebral criptogênico (AVC) em pacientes jovens que apresentam condições anatômicas favoráveis a essa anomalia e que a oclusão transcateter reduz a incidência do acidente vascular cerebral quando comparada ao tratamento clínico. A injeção de soro agitado durante o estudo ecocardiográfico, associada à manobra de Valsalva, pode evidenciar shunt direita-esquerda com alta sensibilidade (89%) e especificidade (92%) quando se utiliza o ecocardiograma transesofágico. Avaliando as características clínicas de pacientes com acidente vascular cerebral e forame oval patente, o trial Risk of Paradoxical Embolism, conhecido pela sigla RoPE, (Risk of Paradoxical Embolism) estabeleceu um escore de risco para acidente vascular cerebral criptogênico e, por meio de um modelo de regressão multivariada, identificou seis variáveis: idade, presença de isquemia cortical, diabetes, hipertensão, AVC e acidente isquêmico transitório prévio. Os escores mais elevados foram observados em jovens com AVC e sem fatores de risco vascular e os escores mais baixos em idosos com fatores de risco vascular, de modo que o forame oval patente sugere ser acidental. Condições anatômicas do FOP predispõem à embolia sistêmica (separação do FOP > 2 mm; túnel do FOP > 10 mm; ângulo entre a veia cava inferior e o flap do FOP <10°; intensidade do shunt com manobra de Valsalva; presença de aneurisma do septo interatrial e rede de Chiari ou válvula de Eustáquio proeminente). O fechamento do FOP pode prevenir a embolia paradoxal, reduzindo a incidência de acidente vascular cerebral em pacientes considerados com de risco elevado. A relação entre Acidente Vascular Cerebral (AVC) criptogênico e a presença de Forame Oval Patente (FOP) tem despertado particular interesse, baseada em estudos recentes que demonstraram que a oclusão transcateter do FOP reduziu a incidência de AVC criptogênico, quando comparado ao tratamento medicamentoso.1 Trombos atravessando o forame oval podem ser observados em exames ecocardiográficos e em autópsias, confirmando esse mecanismo como responsável pela embolia paradoxal, ou seja, um trombo venoso passando para a circulação arterial por um shunt direita-esquerda. Entretanto, essa visualização ecocardiográfica é rara e existem poucos estudos publicados2,3 (Figura 1). Alguns estudos clínicos demonstram a propensão do FOP ser o responsável pela embolia paradoxal. Pacientes portadores de diabetes, hipertensão arterial sistêmica e doença arterial coronária têm baixa prevalência para o FOP ser o responsável pela embolia paradoxal. Por outro lado, história de trombose venosa profunda, embolia pulmonar, hipertensão pulmonar, viagens prolongadas, manobra de Valsalva precedendo o início de sintomas de AVC, enxaqueca e apneia do sono tem sido descrita como fatores de risco independentes para a associação entre FOP e eventos cerebrovasculares.4 Mesmo sendo pouco frequente a visualização de trombos em forame oval, a observação epidemiológica nos leva a acreditar que o FOP é o responsável por um número considerável de acidentes vasculares cerebrais.5 A prevalência de FOP em um estudo com autópsia em 965 corações normais é de 27%, com similar distribuição entre homens e mulheres. Essa prevalência declina com a idade, sendo de 34% em menores de 30 anos, 25% entre 30 e 80 anos e 20% em maiores de 80 anos.6 Em pacientes com AVC criptogênico, entretanto, a prevalência é particularmente elevada, chegando a 40% em pacientes com idade inferior a 55 anos.7 É importante ressaltar que a presença de FOP em pacientes com AVC criptogênico não é a única etiologia para o embolismo paradoxal. Outros mecanismos podem ser responsáveis, como fibrilação atrial não detectada, tumores cardíacos (mixoma e fibroeslastomas), presença de contraste ecocardiográfico espontâneo em átrio esquerdo, valvopatia mitral reumática, calcificação do anel valvar mitral, próteses cardíacas biológicas e mecânicas, estados de hipercoagulabilidade e ateroma de aorta ascendente.8 O estudo ecocardiográfico é parte da rotina na avaliação do FOP, principalmente o Ecocardiograma Transesofágico (ETE) com utilização de solução salina agitada (macrobolhas). Considera-se um shunt pequeno quando passam de três a dez bolhas, médio de dez a 30 bolhas e grande se mais de 30 bolhas contadas nos primeiros batimentos após a injeção.9 Além da detecção do shunt, o ETE avalia as características anatômicas do FOP, assim como o diagnóstico diferencial com a comunicação interatrial e com o shunt pulmonar.10,11 Trabalhos comparando o ETE utilizando macrobolhas com os achados de autópsia mostram sensibilidade de 89% e especificidade de 92%, sendo que a autópsia é considerada padrão-ouro.12(AU)

Ruptura traumática de músculo papilar da valva tricúspide com forame oval patente adquirido e ruptura atrial direita oculta / Traumatic tricuspid valve papillary muscle case with concomitant acquired patent foramen ovale and covert right atrial rupture

RESUMO O traumatismo cardíaco é comum em acidentes com veículos automotores. Uma mulher com 50 anos de idade foi transportada para nosso hospital após sofrer múltiplos traumatismos em um acidente de automóvel quando dirigia em alta velocidade. Após admissão à unidade de terapia intensiva, uma ultrassonografia cardíaca revelou ruptura traumática de músculo papilar da valva tricúspide e forame oval patente, enquanto se observou, no exame físico, o sinal de Lancisi. Foi realizado tratamento cirúrgico com anuloplastia da valva e fechamento do forame oval patente; durante o ato cirúrgico, diagnosticou-se ruptura oculta do átrio direito.

ABSTRACT Cardiac trauma often occurs in motor vehicle accidents. A 50-year-old female driver was transported to our hospital with multiple trauma after a high-speed car accident. After admission to the intensive care unit, cardiac ultrasound examination revealed traumatic tricuspid valve papillary muscle rupture and patent foramen ovale, while Lancisi's sign was noted on physical examination. Surgical treatment was performed with valve annuloplasty and closure of the patent foramen ovale and a covert right atrial defect that was detected intraoperatively.

Hypercoagulability and Migraine.

BACKGROUND: A growing body of literature suggests that migraineurs, particularly those with aura, have an increased risk for ischemic stroke, but not via enhanced atherosclerosis. The theory that micro-emboli induced ischemia provokes cortical spreading depression (ie, symptomatic aura) in migraineurs but transient ischemic attacks in others highlights a potential role for hypercoagulability as a link between migraine (with aura) and stroke. AIM: Our objective is to summarize the literature evaluating the association of migraine with various acquired or inheritable thrombophilic states, including those related to elevated estrogen levels, endothelial activation and dysfunction, antiphospholipid antibodies (aPL), deficiency of coagulation inhibitors, and presence of certain genetic polymorphisms. FINDINGS: Although definitive studies are lacking, a preponderance of available evidence links migraine, and especially aura, to increased levels of estradiol (eg, oral contraceptive pill [OCP] use, pregnancy), thrombo- and erythrocytosis, von Willebrand factor (vWF) antigen, fibrinogen, tissue plasminogen activator (tPA) antigen, and endothelial microparticles. Studies of a link to migraine are conflicting for aPL, homocysteine, Protein S, and the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism. No association with migraine was found in meta-analyses of Factor V Leiden, and of prothrombin gene mutation. Within a large, young ischemic stroke sample, migraine with aura was associated with a thrombophilic state and with patent foramen ovale (PFO). In the non-stroke population, meta-analyses show an association of PFO and migraine with aura (MA), but two population-based studies do not support the link. RECOMMENDATIONS: For persons with MA and (1) a personal history or family history of thrombosis, or (2) MRI evidence of micro-vascular ischemia or of stroke, an evaluation for hypercoagulability is warranted. In cases of MA alone, consider screening for markers of endothelial activation (eg, vWF, high sensitivity c-reactive protein [hs CRP], and fibrinogen). Rigorous management of other stroke risk factors is paramount, but efficacy of anti-thrombotic agents in the treatment of migraine is unproven. Closure of PFO is not routinely recommended based on negative randomized trials.

Dyspnea following thoracostomy closure after right pneumonectomy: An uncommon echocardiographic diagnosis and therapeutic approach.

Dyspnea and hypoxemia are common postoperative problems after pneumonectomy. One of the rarer causes of respiratory distress after right pneumonectomy is the development of a significant right-to-left shunt across a patent foramen ovale (PFO), which can evolve at a variable interval of time after the operation. We report here our experience with a patient who underwent right pneumonectomy, followed by several complications, and who presented severe dyspnea 7 months later, after the closure of a right thoracostomy. This report outlines the management of this challenging clinical condition; transesophageal echocardiography (TOE) provided a clear diagnosis and guided an effective percutaneous treatment.

Decompression illness with hypovolemic shock and neurological failure symptoms after two risky dives: a case report.

Hypovolemia is known to be a predisposing factor of decompression illness (DCI) while diving. The typical clinically impressive neurological symptoms of DCI may distract from other symptoms such as an incipient hypovolemic shock. We report the case of a 61-year-old male Caucasian, who presented with an increasing central and peripheral neural failure syndrome and massive hypovolemia after two risky dives. Computed tomography (CT) scans of the chest and Magnetic resonance imaging scans of the head revealed multiple cerebral and pulmonary thromboembolisms. Transesophageal echocardiography showed a patent foramen ovale (PFO). Furthermore, the patient displayed hypotension as well as prerenal acute kidney injury with elevated levels of creatinine and reduced renal clearance, indicating a hypovolemic shock. Early hyperbaric oxygen (HBO) therapy reduced the neurological deficits. After volume expansion of 11 liters of electrolyte solution (1000 mL/h) the cardiopulmonary and renal function normalized. Hypovolemia increases the risk of DCI during diving and that of hypovolemic shock. Early HBO therapy and fluid replacement is crucial for a favorable outcome.

[Hypoxemia 4 month after right-sided pneumonectomy]. / Hypoxämie 4 Monate nach rechtsseitiger Pneumektomie.

A 64-year-old male reported worsening dyspnea four months after right-sided pneumonectomy, due to lung cancer. Platypneu-or-thodeoxie syndrome was suspected due to a decrease in oxygen-saturation while the patient was in upright position. The shift of the right hemidiaphragm and liver caused compression of the right atrium and a shunt over a persistent foramen ovale. The right-to-left shunt was proven during right heart catheter. Interventional closure of the shunt resulted in immediate improvement of arterial oxygenation and a decrease in dyspnea.

Forame oval permeável e sua relação com acidente vascular cerebral isquêmico (AVC) e enxaqueca / Permeable foramen ovale and its relation to ischemic stroke (stroke)and migraine

O forame oval permite, durante o período fetal, a passagem de sangue oxigenado oriundo da placenta para o átrio direito, possibilitando oxigenação adequada do cérebro e do coração. Após o nascimento, com o início da respiração e com a desconexão da placenta, há um aumento da pressão do lado esquerdo e uma diminuição do lado direito do coração, empurrando a lâmina do forame oval para a direita, o que ocasiona o seu fechamento funcional. Entretanto, em aproximadamente 25% da população ele pode permanecer patente. Sua relação com o acidente vascular isquêmico e com enxaqueca com aura tem sido sugerida em várias publicações. Na presença de acidente vascular isquêmico idiopático, tem sido sugerido por vários autores o fechamento percutâneo do forame oval patente (FOP), quando comprovada a existência de shunt da direita para a esquerda, espontaneamente ou com manobra de Valsalva. Contudo, hã necessidade de maior tempo de observação para avaliar a sua superioridade em relação ao tratamento clínico.

Foramen ovale allows the passage, during the fetal period, of oxygenated blood coming from the placenta to the right atrium, supplying adequate oxygenation for brain and heart. After birth, with onset of breathing and disconnection of the placenta, there are an increased pressure on the left side ofthe heart and a decreasing in its right side pushing the blade of the foramen ovale to the right, causing its functional closure. However, the patent foramen ovale (PFO) occurs in approximately 25% of the population. The relationship between cryptogenic stroke, migraine with aura and PFO has been suggestedin several publications. In the presence of cryptogenic stroke, percutaneous closure of PFO, when shown the existente of a shunt from right to left spontaneously or with the Valsalva maneuver, has been suggested by several authors. However, there is need of more observation time to assess its superiority over medica1 treatment.

Platypnea-orthodeoxia, an uncommon presentation of patent foramen ovale.

The platypnea-orthodeoxia syndrome is a rare clinical presentation. The differential diagnosis is short and includes cardiac, hepatic, and pulmonary causes, with right-to-left intracardiac shunt being the most common. A secondary process is usually present in conjunction with an intracardiac shunt in order for platypnea and orthodeoxia to develop. We present a 63-year-old man in whom the platypnea-orthodeoxia syndrome was associated with a patent foramen ovale and symptoms were manifested by the subacute development of pulmonary arterial hypertension mediated by pulmonary tumor emboli. On postmortem examination, the patient had an underlying poorly differentiated lung adenocarcinoma. This case provides a concise review of the platypnea-orthodeoxia syndrome and pulmonary tumor emboli and stresses the importance of looking for a secondary process in conjunction with an intracardiac shunt in establishing the underlying diagnosis.

Platypnea-orthodeoxia syndrome: a rare complication after right pneumonectomy.

Platypnea is characterized by breathlessness in the upright position. Orthodeoxia is defined by arterial desaturation on standing. Herein we describe a case of platypnea-orthodeoxia syndrome in a patient who underwent a right pneumonectomy for adenocarcinoma of the lung. Closure of a patent foramen ovale, causing a right-to-left shunt, with an Amplatzer device, produced immediate symptomatic relief.

Endomyocardial fibrosis mimicking Ebstein's anomaly: a diagnostic challenge.

Endomyocardial fibrosis is a rare disease that is seen most commonly in tropical countries. It usually presents with characteristics of right-heart failure. Herein, we report the case of a 14-year-old adolescent boy who experienced endomyocardial fibrosis. Upon transthoracic echocardiography, the condition was mistakenly diagnosed as Ebstein's anomaly of the tricuspid valve. Sixteen months after undergoing tricuspid annuloplasty and receiving a bidirectional Glenn shunt, the patient showed no echocardiographic evidence of valvular regurgitation. We discuss imaging and surgical techniques that enable the diagnosis and treatment of endomyocardial fibrosis.

Development of severe and persistent hypoxemia seven months after orthotopic heart transplantation.

We report the case of a 57-year-old man who underwent orthotopic heart transplantation because of prior myocardial infarction and cardiogenic shock. The patient developed refractory hypoxemia 7 months after transplantation, secondary to a right to left shunt across a patent foramen ovale related to severe tricuspid regurgitation resulting from repeated control biopsies. Percutaneous closure of the foramen ovale was performed.

Haemodynamic complications after pneumonectomy: atrial inflow obstruction and reopening of the foramen ovale.

BACKGROUND: Haemodynamic impairments after pneumonectomy are rare complications and present in different forms. Due to a low awareness of these potential complications their diagnosis is difficult and often established late. The most important forms are: firstly reopening of a previously closed foramen ovale (PFO) caused by a combination of changed anatomic position of the left atrium and elevated pulmonary artery pressure leading to a significant right-left shunt; secondly diaphragmatic relaxation can lead to a dislocation of the liver into the right hemithorax, compressing the right atrium with subsequent inflow obstruction. METHODS: We retrospectively analysed our patient cohort from 1997 to 2006 for occurrence of haemodynamic complications requiring surgical intervention after pneumonectomy. RESULTS: Five hundred and forty-six pneumonectomies were performed in our centre during the observation period. Five patients (1 female, 4 male, age 59+/-9 years) with haemodynamic complications were identified. Two of those patients were referred with haemodynamic complications after pneumonectomy was performed in a peripheral centre. All patients had undergone right pneumonectomy for NSCLC (n=4) or atypical carcinoid (n=1). Two patients were readmitted 3 months and 2 years postoperatively due to increasing platypnoea and orthodeoxia. After closure of the reopened foramen ovale, which was found as the underlying pathological mechanism, respiratory symptoms were resolved. One patient required reintubation 2h postoperatively; after surgical closure of a PFO the respiratory situation significantly improved. One patient was readmitted due to right atrial inflow obstruction 17 months after right pneumonectomy. Underlying cause was a severe diaphragmatic relaxation with compression of the atrium by the liver. After diaphragmatic plication all symptoms resolved. However 1 year thereafter reoperation for recurrence of diaphragmatic elevation was required. One patient was readmitted 3 months after pneumonectomy and partial atrial resection for cyanosis and dyspnoea. Diagnostics revealed a PFO and a massive raise of the right diaphragm with compression of the right atrium. After surgical correction of the contorted foramen ovale and diaphragmatic plication, symptoms vanished. CONCLUSION: Haemodynamic alterations due to a reopened foramen ovale or right atrial inflow obstruction are rare, however they are severe complications after pneumonectomy. They occur at variable points in time after pneumonectomy. Diagnostic efforts are often made at a late stage due to a low awareness of the problem. Closure of the PFO either surgical or interventional and/or plication of the elevated diaphragm are mandatory. In our experience these complications occur only after right pneumonectomy.