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A case of ileocecal herniation through the foramen of Winslow is presented. This is an uncommon type of internal hernia and the diagnosis is difficult. From this case, clinical signs, imaging procedures and treatment options are discussed.
This article presents definitions and discusses pathophysiology pertaining to the patent foramen ovale.
This article discusses the ramifications of a hypercoagulable state in patients with a patent foramen ovale.
The platypnea-orthodeoxia syndrome is a rare but important condition caused by a variety of clinical entities. Several mechanisms have been postulated to cause platypnea and orthodeoxia. These mechanisms mainly involve intracardiac shunting, pulmonary vascular shunting, and ventilation-perfusion mismatching. Patent foramen ovale is an important type of intracardiac shunt that can produce platypnea-orthodeoxia in select patients. Concomitant pulmonary hypertension must be ruled out, but symptoms can occur without pulmonary hypertension in cases with altered intrathoracic anatomy and physiology. Diagnosis usually entails transthoracic or trans-esophageal echocardiogram, ideally with postural provocation by the tilt-table test. Treatment with surgical or percutaneous closure may result in symptomatic relief. The decision to intervene is based mainly on the severity of symptoms and potential morbidities associated with the defect.
Migraine headaches have a high prevalence rate in the general population and account for significant morbidity, lost productivity, health care visits, and dollars spent. Increasingly, emerging data show a link between migraine headache, especially migraine headaches with aura, and patent foramen ovale (PFO). Closure of PFO as a cure for migraine headache is a tantalizing idea; this article examines the data supporting that possibility including studies showing improvement in migraine headache after PFO closure and case reports in which migraine headaches worsened after closure of an atrial septal defect.
Patency of the foramen ovale is a risk factor for DCS in SCUBA divers, even if they adhere to the currently accepted and used decompression tables. The primary cause of DCS, however, is the nitrogen bubble, not the PFO. There are a number of techniques any diver can use to minimize the occurrence of nitrogen bubbles after a dive. The authors current practice is to inform civilian sports divers of the increased risk and to advise them to adopt conservative dive profiles. This can be achieved by selecting a more conservative dive computer, performing only dives that do not require obligatory decompression stops, or using oxygen-enriched breathing gas mixtures("nitrox") while still diving on "air profiles" [56].Dive-safety organizations are currently under-taking studies aimed at proposing changes in the decompression algorithms to produce low-bubble dive tables [12]. In the meantime, PFO remains a reason for caution. Whether all divers should be screened for PFOis an ongoing discussion [50] in view of methodologic and practical issues outlined in this article. Any definitive recommendations can be made only after a careful, prospective evaluation of the real relative risk for DCS and long-term cerebral damage.
This article discusses the relationship between patent foramen ovale and stroke, particularly in reference to paradoxical embolism as a cause of cryptogenic stroke.
This article discusses percutaneous patent foramen ovale closure.
This article discusses the role of the pediatric cardiologist in understanding complex patent foramen ovale closure.
OBJECTIVE: We have investigated the localization accuracy of low-resolution electromagnetic tomography (LORETA) for mesial temporal interictal epileptiform discharges (IED) on a statistical basis by using clinical electroencephalographic (EEG) data of simultaneous scalp and intracranial foramen ovale (FO) electrode recordings. METHODS: We retrospectively analyzed the IED of 15 patients who underwent presurgical assessment for intractable temporal lobe epilepsy. All patients have subsequently undergone amygdalohippocampectomy. The scalp signals were averaged time-locked to the peak activity in bilateral 10-contact FO electrode recordings. Source modeling was carried out by using statistical non-parametric mapping (SNPM) of LORETA values and by calculating raw LORETA values of averaged IED. The results were compared to intracranial data obtained from FO electrode recordings. RESULTS: Two thousand six hundred and fifteen discharges could be attributed to 19 different patterns of intracranial mesial temporal IED. SNPM of LORETA revealed confined ipsilateral mesial temporal solutions for 14 (73.7%) and no significant solutions for five (26.3%) of these patterns. Raw LORETA current density distributions of the 19 averaged IED patterns revealed ipsilateral basal to lateral temporal solutions for the 14 IED patterns with a sufficient signal to noise ratio (SNR), but spurious results for those five IED with a low SNR. CONCLUSIONS: SNPM of LORETA but not LORETA analysis of averaged IED patterns accurately localizes the source generators of mesial temporal IEDs. SIGNIFICANCE: SNPM of raw LORETA values might be appropriate for localizing restricted mesial temporal lobe sources.
OBJECTIVE: We introduce a monopole model to examine the sources of ictal and interictal activity in mesial temporal lobe epilepsy (MTLE) recorded using foramen ovale electrodes (FOE). METHODS: Classical electrostatic theory was applied to derive mathematical expressions. Interictal and ictal activity was acquired using FOE and scalp video-electroencephalography (v-EEG) during awake and sleep states. A total of 2057 interictal spikes and 712 ictal spikes were analyzed. Thirty-five seizures from several consecutive episodes were examined. MRI and clinical data were correlated with voltage source localization. RESULTS: Patients (20) were grouped according to the spatial distribution of voltage sources of interictal activity. Voltage sources were located over 3.4 and 21.6mm in the anterior-to-posterior axis of mesiotemporal structures and separated no more than 7 mm from this axis. In most patients (16), sources were restricted to 11.1+/-1.5mm, whereas other patients (4) exhibited a wider distribution (29.6-43.5mm). Sources of ictal and interictal activity partially overlapped, with ictal sources exhibiting a posterior localization at 20-40 mm. Both interictal and ictal sources were anterior to MRI atrophy. No difference between awake and sleep states were found, neither correlation between source scattering and history of epilepsy. CONCLUSIONS: Voltage source analysis applied to FOE suggests that, in most MTLE patients, interictal activity emerges from very restricted areas. Some patients, however, exhibited sources which are distributed all along the mesiotemporal structures. Our data suggest an anterior-to-posterior alignment of the irritative, ictal and atrophic zones. SIGNIFICANCE: The voltage source model applied to FOE can help to map the extension of the irritative and ictal areas in mesiotemporal structures.
OBJECTIVE: We have investigated intracerebral propagation of interictal epileptiform discharges (IED) in patients with mesial temporal lobe epilepsy (MTLE) by using spatiotemporal source maps based on statistical nonparametric mapping (SNPM) of low resolution electromagnetic tomography (LORETA) values. METHODS: We analyzed 30 patterns of IED recorded simultaneously with scalp and intracranial foramen ovale (FO) electrodes in 15 consecutive patients with intractable MTLE. The scalp EEG signals were averaged time-locked to the peak activity in bilateral 10-contact FO electrode recordings. SNPM was applied to LORETA values and spatiotemporal source maps were created by allocating the t-values over time to their corresponding Brodmann areas. Propagation was defined as secondary statistically significant involvement of distinct cortical areas separated by >15 ms. The results were correlated with intracranial data obtained from FO electrode recordings and with scalp EEG recordings. All patients underwent subsequent amygdalo-hippocampectomy and outcome was assessed one year after surgery. RESULTS: We found mesial to lateral propagation in 6/30 IED patterns (20%, four patients), lateral to mesial propagation in 4/30 IED patterns (13.3%, four patients) and simultaneous (within 15 ms) activation of mesial and lateral temporal areas in 6/30 IED patterns (20%, five patients). Propagation generally occurred within 30 ms and was always limited to ipsilateral cortical regions. Nine/30 IED patterns (30%) showed restricted activation of mesial temporal structures and no significant solutions were found in 5/30 IED patterns (16.7%). There was no clear association between the number or characteristics of IED patterns and the postsurgical outcome. CONCLUSIONS: Spatiotemporal mapping of SNPM LORETA accurately describes mesial to lateral temporal propagation of IED, and vice versa, which commonly occur in patients with MTLE. SIGNIFICANCE: Intracerebral propagation must be considered when using non-invasive source algorithms in patients with MTLE. Spatiotemporal mapping might be useful for visualizing this propagation.
BACKGROUND: The eustachian valve (EV) (valvula venae cavae inferioris) is a remnant of the embryonic right valve of the sinus venosus. Embryologically, the EV directs oxygenated blood from the inferior vena cava across the patent foramen ovale (PFO) into the systemic circulation. Transthoracic echocardiography shows the EV in the majority of newborns, but the prevalence of EV in adults studied with transesophageal echocardiography is unknown. We studied whether the presence of an EV is associated with PFO or with cryptogenic stroke. METHODS: The frequency and size of the EV was studied in 211 consecutive patients undergoing transesophageal echocardiography after a cryptogenic stroke and in 95 consecutive patients without cerebrovascular events. In all 306 patients, the presence of a PFO was studied with 2-dimensional transesophageal echocardiographic, color Doppler, and contrast echocardiographic studies. RESULTS: An EV was seen in 174 of 306 patients overall (57%). The mean size was 1.0 +/- 0.4 cm (range: 0.5-2.0); 70% of patients with an EV had a PFO (Cohen's kappa = 0.75; P <.001). This relationship was not significantly influenced by a cryptogenic stroke. The prevalence of PFO was 30% in the control group and 61% for those with presumed paradoxical embolism (P <.001). Thus, an EV was more common for patients with presumed paradoxical embolism than in control patients (143 of 211 68% vs 31 of 95 33%, respectively, P <.001). There was no significant difference in the size of the EV between the 2 groups (1.1 vs 1.0 cm; P =.24). CONCLUSION: A persisting EV is a frequent finding in patients with a PFO. By directing the blood from the inferior cava to the interatrial septum, a persisting EV may prevent spontaneous closure of PFO after birth and may, therefore, indirectly predispose to paradoxical embolism.
BACKGROUND: The choice of the optimal echo contrast agent could be of relevance for the detection of a patent foramen ovale (PFO). This study compares agitated saline solution and oxypolygelatine (OXY) with respect to their ability to detect a PFO. METHODS: A total of 34 patients (13 women, age 45 +/- 16 years) underwent both transthoracic and transesophageal echocardiography. The appearance of contrast and the presence of a PFO was assessed visually and by acoustic densitometry for both agents. RESULTS: The sensitivity of the detection of a PFO (22 patent, 65%) was 71% with saline versus 84.6% for OXY. Maximum, mean acoustic densitometry grayscale intensity values and the duration of opacification was significantly higher for OXY versus saline for all chambers. CONCLUSIONS: OXY has superior echo properties that translate into a higher sensitivity for the detection of a PFO. The choice of the optimal agent must be considered for clinical routine and research studies.
BACKGROUND: Recent studies have suggested that a higher mobility of the fossa ovalis membrane (FOM) may be associated with an increased risk for stroke in patients with patent foramen ovale (PFO). The current study analyzed whether Doppler tissue echocardiography is useful for quantitation of FOM motion velocities. METHODS: FOM dynamics were prospectively studied in 107 consecutive patients (average age 50.7 +/- 15.3 years, 48 men) with in sinus rhythm who underwent transesophageal echocardiography for various indications. With pulsed wave Doppler tissue echocardiography interrogation, a characteristic quadrophasic signal was recorded in all patients, consisting of a positive wave toward the left atrium (A-wave) at late diastole, followed by a negative wave (B-wave) toward the right atrium, a pronounced, again positive wave during midsystole (C-wave), and a final negative wave (D-wave). RESULTS: Peak velocities of A-wave, B-wave, C-wave, and D-wave were 0.08 +/- 0.02 m/s, 0.11 +/- 0.05 m/s, 0.17 +/- 0.07 m/s, and 0.14 +/- 0.06 m/s, respectively. In 21 of 107 (19.6%) patients, PFO was detected. Patients with PFO had significantly higher C-wave and D-wave peak velocities compared with the 86 patients without PFO (0.23 +/- 0.10 m/s vs 0.15 +/- 0.05 m/s, P < .001 and 0.16 +/- 0.07 m/s vs 0.12 +/- 0.06 m/s, P = .04, respectively). CONCLUSIONS: Assessment of FOM dynamics using Doppler tissue echocardiography is feasible. It allows definition of a characteristic quadrophasic FOM motion pattern, thereby providing new insights into the physiology of FOM mobility. Patients with PFO were found to have increased FOM mobility compared with patients without PFO.
BACKGROUND: Patent foramen ovale (PFO) is commonly demonstrated by transesophageal echocardiography (TEE) in patients with a recent transient ischemic attack or stroke. Our purpose was to determine how the TEE visualization of a PFO alters anticoagulation therapy. METHODS: We retrospectively identified 100 patients with transient ischemic attack or stroke referred for TEE; 50 had a PFO and 50 did not (control patients). RESULTS: Both groups were similar in regard to age, sex, the occurrence of transient ischemic attack versus stroke, and history of stroke. The PFO group had a higher incidence of a mobile interatrial septum, interatrial septal aneurysm, or both ( P < .001 by Fisher exact test). Both groups had similar pre-TEE aspirin, other antiplatelet, and warfarin use. After TEE, warfarin was instituted in 8 of 50 patients with PFO versus 2 of 50 in the control group ( P = .05) and aspirin use was discontinued in 9 of 50 patients with PFO versus 3 of 50 in the control group ( P = .12). CONCLUSION: The main effect of demonstrating a PFO by TEE after an ischemic cerebral event was the institution of warfarin; there was a trend toward discontinuing aspirin.
BACKGROUND: Surgical closure of patent foramen ovale (PFO) has been considered definitive and the gold standard for preventing recurrent paradoxical embolism. However, in contrast to transcatheter PFO closure, patients undergoing operation have not systematically been re-evaluated for residual shunting. This study aimed to assess the efficacy of surgical PFO closure during follow-up by transesophageal echocardiography (TEE). METHODS: Eleven adult patients with diagnosis of a PFO by contrast and/or color Doppler TEE underwent PFO closure by thoracotomy and direct suturing because of paradoxical embolism (n = 4), because of impending paradoxical embolism (n = 1), or during valve operation (n = 6). RESULTS: TEE performed 5 days to 7 months after PFO closure revealed residual shunting in 8 of 11 patients (73%). The shunt size was unchanged in two patients. According to the color Doppler jet width across the atrial septum, the postoperative PFO diameter was smaller in 5 of the remaining 6 patients. Right-to-left shunting by contrast TEE, however, had newly developed (n = 1) or increased (n = 2) for patients with concomitant valve operation. Despite therapeutic anticoagulation a cerebrovascular event occurred in one patient 4 weeks after attempted PFO closure. The mechanism for persistent shunting was incomplete sealing of septum primum and septum secundum by the suture line (n = 6) or a new iatrogenic defect of the fossa ovalis caused by surgical manipulation (n = 2). In two patients a second TEE after 12 and 41 months revealed enlargement of the PFO diameter. CONCLUSIONS: Surgical PFO closure can not be regarded as the gold standard for definitive treatment of interatrial shunts. Residual shunting present in a high proportion of patients may partly explain the recurrence of embolic events.
Saline and indocyanine green dye were the first agents noted to produce a contrast effect when injected peripherally during M-mode echocardiographic imaging, although it was subsequently found that almost any type of injected solution would have this effect. These first-generation contrast agents were limited to opacification of right heart structures, and they prompted subsequent development of agents that traverse pulmonary circulation. Although opacification limited to right heart structures is considered a limitation of these first-generation agents, this is an advantage when attempting to identify the presence of right-to-left shunt. First-generation air contrast is considered the gold standard for identification of patent foramen ovale (PFO). However, PFO investigators have used varying criteria to define abnormal contrast studies. There are also multiple mechanisms by which saline contrast studies may produce both false-positive and false-negative results for presence of PFO. There is mounting experimental evidence that PFO is associated with cerebral ischemia and migraine headache, with a resulting evolution of devices for percutaneous closure of these shunts. Echocardiographic physicians must be aware of potential pitfalls of the air contrast technique to avoid exposing patients to unnecessary risk of closure devices, and missing the potential benefit of shunt closure in appropriately selected patients.