Malignant pericardial effusion.

Malignant pericardial effusion is a common and serious manifestation in malignancies. The origins of the malignant process include solid tumors or hematological malignancies, while primary neoplasms of the pericardium are less common. In the oncological patient, pericardial effusion may develop by several different mechanisms, namely by direct or metastatic spread of the primary process or as a complication of antineoplastic therapies. In some cases, pericardial effusion may be the first manifestation of the disease, and that is why malignancy must be excluded in every case of an acute pericardial disease with cardiac tamponade at presentation, rapidly increasing pericardial effusion and an incessant or recurrent course. Thus, the definite differentiation of malignant pericardial effusion and rapid diagnosis are of particular therapeutic and prognostic importance. Management of these patients is multidisciplinary and requires team work, but at present there is a need for further research. An individual treatment plan should be established, taking into account cancer stage, the patient's prognosis, local availability and experience. In emergency cases with cardiac tamponade or significant effusion, initial relief can be obtained with pericardiocentesis. Despite the magnitude of this serious problem, little progress has been made in the treatment of pericardial effusion secondary to malignant disease.

Diagnostic issues in the clinical management of pericarditis.

AIMS: To review the current major diagnostic issues on the diagnosis of acute and recurrent pericarditis. METHODS: To review the current available evidence, we performed a through search of several evidence-based sources of information, including Cochrane Database of Systematic Reviews, Clinical Evidence, Evidence-based guidelines from National Guidelines Clearinghouse and a comprehensive Medline search with the MeSH terms 'pericarditis', 'etiology' and 'diagnosis'. RESULTS: The diagnosis of pericarditis is based on clinical criteria including symptoms, presence of specific physical findings (rubs), electrocardiographical changes and pericardial effusion. Although the aetiology may be varied, most cases are idiopathic or viral, even after an extensive diagnostic evaluation. In such cases, the course is often benign following anti-inflammatory treatment, and management would be not affected by a more precise diagnostic evaluation. A triage of pericarditis can be safely performed on the basis of the clinical and echocardiographical presentation. Specific diagnostic tests are not warranted if no specific aetiologies are suspected on the basis of the epidemiological background, history and presentation. High-risk features associated with specific aetiologies or complications include: fever > 38 degrees C, subacute onset, large pericardial effusion, cardiac tamponade, lack of response to aspirin or a NSAID. CONCLUSIONS: A targeted diagnostic evaluation is warranted in acute and recurrent pericarditis, with a specific aetiological search to rule out tuberculous, purulent or neoplastic pericarditis, as well as pericarditis related to a systemic disease, in selected patients according to the epidemiological background, presentation and clinical suspicion.

Increased insulin resistance and risk of incident cerebrovascular events in patients with pre-existing atherothrombotic disease.

BACKGROUND AND PURPOSE: Diabetes and the metabolic syndrome are known risk factors for ischaemic stroke. Our aim was to examine whether amongst patients with pre-existing atherothrombotic disease, increased insulin resistance is associated with incident cerebrovascular events. METHODS: Patients with stable coronary heart disease included in a secondary prevention trial were followed up for a mean of 6.2 years. Coronary heart disease was documented by a history of myocardial infarction > or =6 months and <5 years before enrollment and/or stable angina pectoris with evidence of ischaemia confirmed by ancillary diagnostic testing. Main exclusion criteria were insulin treated diabetes, hepatic or renal failure, and disabling stroke. Baseline insulin levels were measured in 2938 patients from stored frozen plasma samples and increased insulin resistance assessed using the homeostatic model assessment of insulin resistance (HOMA-IR), categorized into tertiles or quartiles. RESULTS: Crude rates of incident cerebrovascular events rose from 5.0% for HOMA-IR at the bottom tertile to 5.7% at the middle tertile, and 7.0% at the top tertile (P = 0.07). HOMA-IR at the top versus bottom tertile was associated with an unadjusted hazard ratio (HR) of 1.37 (95%CI, 0.94-1.98) and a 1-unit increase in the ln HOMA-IR was associated with a HR of 1.14 (95%CI, 0.97-1.35). In further analyses adjusting for potential confounders, or categorizing baseline HOMA-IR into quartiles, or excluding diabetic patients, we did not identify an increased risk for incident cerebrovascular events conferred by the top category. CONCLUSIONS: Increased insulin resistance did not predict incident cerebrovascular events amongst patients with pre-existing atherothrombotic disease.

[Recurrent acute idiopathic pericarditis: rheumatologic therapy, autoantibodies and long term outcome]. / Pericardite acuta idiopatica recidivante: terapia reumatologica, autoanticorpi e long term outcome.

OBJECTIVE: To evaluate therapy and rheumatologic aspects of recurrent acute idiopathic pericarditis (RAIP). METHODS: We studied 46 patients. We used non-steroidal anti-inflammatory drugs (NSAIDs) at high dosage. We did not start corticosteroid: if already started, we planned a very slow tapering; 37 patients (80.4%) were treated with colchicine. We also assessed the frequency of ANA, anti-SSA and Rheumatoid factor. RESULTS: With our protocol recurrences dropped from 0.46 to 0.03 attacks/patient/month (p<0.00001) within 12 months and remained at the same level (0.024) till the end of the follow-up (mean 8 years). In the 37 patients treated with colchicine recurrences dropped from 0.5 to 0.03 (p<0.0001) within 12 months, and in 9 patients not given colchicine from 0.27 to 0.045 (p<0.005). When colchicine was used the decrease was significantly higher (0.47 vs 0.23) (p<0.001). In 27 (58.7%) patients ANA were positive at a titre >1/80, in 7 (15.2%) >1/160. Rheumatoid factor was positive in 7 (15.2%) and anti-SSA in 4 (8.7%). During the follow-up 4 (8.7%) new diagnosis of Sjogren and 1 (2.2%) of Rheumatoid Arthritis were made. CONCLUSION: NSAIDs at high dosage, slow tapering of corticosteroid and colchicine are very effective in RAIP. The improvement is more dramatic in colchicine treated patients, but also other patients can achieve good control of the disease. The finding of ANA, anti-SSA and the new rheumatological diagnoses support the involvement of autoimmunity.

Therapy for recurrent acute pericarditis: a rheumatological solution?

OBJECTIVE: To assess the efficacy of a multidrug protocol in recurrent acute pericarditis. We tried also to assess the specific role of colchicine. METHODS: We studied 58 patients (34 males) in the largest monocentric observational study. All patients received prolonged courses of non-steroidal anti-inflammatory drugs; generally we do not start a corticosteroid in recurrent acute pericarditis, but if a steroid had already been started, we planned a very slow tapering; if necessary azathioprine, hydroxychloroquine, and other immunosuppressive drugs were used; 44 patients (27 males, 61.4%) were treated also with colchicine and 14 patients (7 males, 50%) were not given this drug. RESULTS: After starting our protocol recurrences dropped from 0.48 to 0.03 attacks/patient/month (p < 0.00001) within 12 months and remained at the same level till the end of the follow-up (mean 8.1 years) in the whole cohort. In the 44 patients treated with colchicine recurrences dropped from 0.54 to 0.03 attacks/patient/month (p < 0.00001) within 12 months, and in 14 patients not given colchicine recurrences decreased from 0.31 to 0.06 attacks/patient/month (p = 0.002). In patients treated with colchicine the decrease was significantly higher (0.51) than in patients not taking this drug (0.25) (p = 0.006). Colchicine was discontinued by 16.3% of patients because of side effects. CONCLUSION: A multidrug protocol including non-steroidal anti-inflammatory drugs at high dosage, slow tapering of corticosteroid, colchicine, reassurance and close clinical monitoring is very effective in recurrent pericarditis; this improvement is more dramatic in colchicine treated patients, but also patients who do not tolerate it can achieve good control of the disease.

The concomitant occurrence of multiple epidermal cysts, osteomas and thyroid gland nodules is not diagnostic for Gardner syndrome in the absence of intestinal polyposis: a clinical and genetic report.

Gardner syndrome, a phenotypic variant of familial adenomatous polyposis, is characterized by the classical clinical triad of skin and soft tissue tumours, osteomas and intestinal polyposis, but disease patterns with pairs of these findings have also been reported. Different mutations in the adenomatous polyposis coli (APC) gene have been shown to be associated with Gardner syndrome disease phenotypes. A 36-year-old patient presented with multiple epidermal cysts on the face, left ear lobe and neck, and the possible diagnosis of Gardner syndrome was based on the additional findings of two classical osteomas in the left radius and ulna and a cold non-malignant nodule of the thyroid gland. Intestinal polyposis was lacking at the time of examination. Major deletions but not microdeletions were excluded by a cytogenetic analysis with 650 chromosomal bands per haploid set. Systematic sequencing of the entire coding region of the APC gene (> 8500 bp) of the patient and five healthy controls was also performed. As a results, new APC gene polymorphisms were identified in exons 13 [A545A (A/G)] and 15 [G1678G (A/G), S1756S (G/T), P1960P (A/G)]. We also detected D1822V (A/T) which has recently been reported to be potentially related to colorectal carcinoma, and genotyped 194 randomly chosen healthy individuals from the Glasgow area for this as well as for the above variants in exons 13 and 15. Interestingly, of the 194 controls, 112 carried the DD (57.7%), 71 the DV (36.6%), and the remaining 11 (5.7%), including our patient, the VV genotype. It is therefore unlikely that APC D1822V serves as an important marker for colorectal carcinoma. In conclusion, we failed to identify obvious germline candidate mutations in > 8500 bp of the coding region of the APC gene in a patient with multiple epidermal cysts, osteomas and a thyroid gland nodule; major chromosomal deletions were excluded. Therefore, we assume that only the presence of intestinal polyposis is a marker for Gardner syndrome.

Adamantiades-Behçet's disease with inner ear involvement.

Adamantiades-Behçet's disease is a chronic recurrent inflammatory disorder involving the small and large vessels. Typical loci of manifestations are the mucous membranes, skin and eyes, as well as the joints and central nervous system. Other organs are not commonly involved. We present two patients, one with ocular and the other with mucocutaneous manifestation of Adamantiades-Behçet's disease. In addition, the first patient reported three episodes of sudden hearing loss while under immunosuppressive therapy for his eye involvement. The second, therapy-naive patient complained of tinnitus in his left ear. Careful examination revealed vestibular involvement in the first patient and retrocochlear involvement in the second. Inner ear involvement is an uncommon manifestation of Adamantiades-Behçet's disease. In case of relevant signs or history, such as hearing disturbance, tinnitus and/or vertigo, patients should be examined for inner ear involvement.

Evidence for fractal correlation properties in variations of peripheral arterial tone during REM sleep.

Previous studies utilizing detrended fluctuation analysis (DFA) of heart rate variability during sleep revealed a higher fractal exponent during rapid eye movement (REM) sleep than non-REM sleep. The aim of this study was to determine whether the same difference exists in the variations of peripheral arterial tone (PAT). Finger pulse wave measured by a novel plethysmographic technique was monitored during sleep in 12 chronic heart failure patients, 8 heavy snorers, and 12 healthy volunteers. For each subject, at least two 15-min time series were constructed from the interpulse intervals and from pulse wave amplitudes during REM and non-REM sleep. Fractal scaling exponents of both types of time series were significantly higher for REM than non-REM sleep in all groups. In each of the groups and in both sleep stages, the fractal scaling exponents based on pulse wave amplitude were significantly higher than those based on pulse rate variability. A repeat of the analysis for short-, intermediate-, and long-term intervals revealed that the fractal-like exponents were evident only in the short- and intermediate-term intervals. Because PAT is a surrogate of sympathetic activation, our results indicate that variations in sympathetic activation during REM sleep have a fractal-like behavior.

Mycophenolate mofetil is ineffective in the treatment of mucocutaneous Adamantiades-Behçet's disease.

BACKGROUND: Cyclosporine A and azathioprine are effective on mucocutaneous lesions in Adamantiades-Behçet's disease. Mycophenolate mofetil (MMF) is a drug resembling their activity but with comparably negligible adverse reactions. OBJECTIVE: A prospective clinical proof-of-principle study was conducted to investigate the effectiveness and toxicity of MMF in mucocutaneous Adamantiades-Behçet's disease. METHODS: Thirty patients were to be treated with MMF 2 g/day p.o. for 6 months, in combination with prednisolone 30 mg/day p.o. during the first month of treatment. Inefficacy was followed by an increase in MMF dose to 3 g/day. The primary efficacy variable was the decrease in the disease activity index (DAI) according to a modified variant of the Iran Behçet's Disease Dynamic Activity Measure system. RESULTS: The study was interrupted due to inefficacy of the compound after the intermediate evaluation of the first 6 patients (aged 37.0 +/- 7.7 years with disease duration of 10.0 +/- 8.9 years) as required by the ethical committee. Although an improvement of the DAI from 5.2 +/- 3.5 to 1.3 +/- 0.5 was found after the first month of combination treatment, withdrawal of prednisolone led to quick relapses with a new index increase (3.0 +/- 3.5). The treatment was discontinued in 3 patients after 3 months, in 2 patients after 4 months and in another one after 5 months due to deterioration of the disease. Introduction of interferon alpha(2a) (3 x 9 million IU 3x/week s.c.) in 3 patients decreased the activity index from 4.0 +/- 1.0 to 0.0 +/- 0.0. No adverse effects were detected under MMF treatment. CONCLUSION: MMF (2-3 g/day) is unable to control the signs of mucocutaneous Adamantiades-Behçet's disease.

Comparative analysis of the association of HLA-B*51 suballeles with Behçet's disease in patients of German and Turkish origin.

The distribution of the different HLA-B*51 suballeles among patients with Behçet's disease (BD) of German (n=33) and Turkish (n=92) origin in comparison to their presence in the respective ethnically matched healthy control groups (German: n=325, Turkish: n=93) was studied. HLA-B*51x was significantly increased in both patient groups in comparison to the controls (Germans: 58% vs. 12%, OR 9.76, P<0.001; Turkish: 75% vs. 25%, OR 9.13, P<0.001). Molecular subtyping of B*51x revealed HLA-B*51011 and B*5108 as the predominant suballeles in both patient groups and controls although with a slightly increased frequency of HLA-B*5108 in the diseased individuals. HLA-B*5105 was the only further HLA-B*51x subtype detected in one Turkish patient heterozygous also for HLA-B*5101. HLA-B*5107 although present in a Turkish as well as German control was absent in the patient groups. There was also a tendency towards a higher degree of homozygosity for HLA-B*51x in both patient groups versus the matched controls (Germans: 10% in patients vs. 2,5% in controls; Turkish: 27% in patients vs. 13% in controls). Our study further supports previous hypothesis of an association of BD with B51 suballeles which share amino-acid residues at positions 63 and 67 as well as at positions 77-83 for specific peptide binding and natural killer (NK)-cell interactions. This applies to HLA-B*5101 and B*5108, but not to HLA-B*5107 different at position 67, which could be negatively associated with BD.

[Association between mitral annulus calcification and atherosclerosis].

Mitral annulus calcification (MAC) is best diagnosed by transthoracic echocardiography. MAC is associated with known atherosclerotic risk factors such as diabetes mellitus, hypertension and hypercholesterolemia. It is also known from the literature that patients with MAC have higher prevalence of left atrial and left ventricular enlargement, hypertrophic cardiomyopathy, atrial fibrillation, aortic valve calcification and stenosis, various cardiac conduction defects, bacterial endocarditis, cardiovascular events and stroke, though the etiological basis is unknown. Pathological studies from the 80's present a theory that MAC is a form of atherosclerosis. During the past few years we conducted a few clinical studies in order to test this theory and to examine the association between MAC and known atherosclerotic phenomena. We found higher prevalence of aortic atheroma in patients with MAC, especially complex atheroma, and we also found a continuous correlation between the MAC and atheroma thickness. We also noted that MAC patients have a higher prevalence of carotid artery stenosis, coronary artery stenosis, peripheral artery stenosis and higher levels of anti beta 2-Glycoprotein I antibodies in patients with MAC thickness equal or greater than 5 mm. These studies support the theory that MAC is a form of atherosclerosis and define a group of patients with higher prevalence of atherosclerotic disease in multiple blood vessels.

The effects of streptokinase and hydroxyethyl starch on in vitro clot disruption by ultrasound.

BACKGROUND: In vitro studies showed that low-frequency ultrasound (US) causes blood clot dissolution. This effect is augmented with thrombolytics, microbubbles and microparticles. However, in animal models of transcutaneous delivery, US alone is not effective, probably due to attenuation of US energy by overlying skin. When combined with thrombolytics or microbubbles, transcutaneous US is highly effective. PURPOSE: To assess the synergistic effect of low-intensity low-frequency US and saline, hydroxyethyl starch (HAES) (a non-gas filled microparticle containing solution), streptokinase (STK), and their combination on blood clot disruption. METHODS: Human blood clots from 4 healthy donors, 2-4 hours old, were immersed for 0, 15, or 30 min in 37 degrees C in 10 ml of the above-mentioned solutions, and then were randomized to 10 sec of 20 kHz US or no US. The % difference in weight was calculated. RESULTS: Immersion for 30 min without US resulted in 13.8 +/- 1.2% clot lysis in saline, and 22.0 +/- 1.3%, 21.7 +/- 2.1%, and 23.2 +/- 1.9% in STK, HAES, and STK + HAES, respectively (p = 0.002). US augmented clot lysis in all groups and at all time points. With low-intensity US, HAES was not better than saline. However, the combination of HAES + STK with US resulted in larger clot disruption at 15 sec incubation time (46.7 +/- 3.2%) than with saline (29.6 +/- 2.1%), HAES (29.6 +/- 2.5%), and STK (32.8 +/- 3.6%) (p < 0.001). CONCLUSION: low-frequency, low-intensity US combined with HAES and STK resulted in greater clot disruption at short incubation times. This combination may assist in achieving faster reperfusion in in vivo models.

Management of acute ischaemic stroke in the elderly: tolerability of thrombolytics.

Stroke and its consequences are of global concern. Although stroke can affect individuals of any age, it primarily affects the elderly. It is among the leading causes of severe disability and mortality. In recent years, acute stroke has become a medical emergency requiring urgent evaluation and treatment. Effective management of patients with acute stroke starts with organisation of the entire stroke care chain, from the community and prehospital scene, through the emergency department, to a dedicated stroke unit and then to comprehensive rehabilitation. Intravenous thrombolysis with alteplase (recombinant tissue plasminogen activator; rt-PA) 0.9 mg/kg (maximum dose 90 mg) was shown to significantly improve outcome of acute ischaemic stroke, despite an increased rate of symptomatic intracerebral haemorrhage, if treatment is initiated within 3 hours after the onset of symptoms to patients who meet strict eligibility criteria. Post-marketing studies have demonstrated that intravenous alteplase can be administered appropriately in a wide variety of hospital settings. However, strict adherence to the published protocol is mandatory, as failure to comply may be associated with an increased risk of symptomatic intracerebral haemorrhage. Intra-arterial revascularisation may provide more complete restitution of flow than intravenous thrombolytic therapy and improve the clinical outcome if it can be undertaken in patients with occlusion of the middle cerebral artery, and possibly the basilar artery, within the first hours from stroke onset. However, further data are needed. Although intravenous alteplase is recommended for any age beyond 18 years, elderly patients, in particular patients aged > or = 80 years, were often excluded or under-represented in randomised clinical trials of thrombolysis, so that available data on risk/benefit ratio for the very elderly are limited. Small post-marketing series suggest that despite elderly patients over 80 years having greater pre-stroke disability, the use of intravenous alteplase in this patient group does not significantly differ in effectiveness and complications compared with the same treatment in patients aged under age 80 years. Further studies are necessary and elderly patients with acute stroke should be included in future trials of the merits of thrombolytic therapy.

Long-term diuretic therapy in patients with coronary disease: increased colon cancer-related mortality over a 5-year follow-up.

OBJECTIVES: Recent studies have suggested that long-term diuretic therapy may be associated with increased risk of renal cell carcinoma. This carcinoma is not a common malignancy, but it shares risk factors with the considerably more widespread colon cancer (CC). However, there are no data whether or not a relationship between long-term diuretic therapy and CC mortality exists. In this study we tested the hypothesis that long-term diuretic therapy may be associated with increased CC mortality over a 5.6-year follow-up period. SUBJECTS AND METHODS: The study sample comprised 14 166 patients aged 45 to 74 years with a previous myocardial infarction and/or stable anginal syndrome, screened for participation in the bezafibrate infarction prevention (BIP) study. There were 2153 patients receiving diuretics and 12 013 patients receiving no diuretics. RESULTS: During the follow-up 139 (6.5%) new cases of cancer were diagnosed in the diuretic-treated group compared with 622 (5.2%) in the group receiving no diuretics (P = 0.02). Colon cancer mortality was significantly higher in the diuretic-treated patients (0.1 vs 0.5%, P = 0.001), whereas mortality differences for other cancer types were not documented. Multivariate analysis identified diuretics as an independent predictor of increased colon cancer incidence and colon cancer mortality with a hazard ratio (HR) of 2.0 (95% CI 1.2-3.2) for colon cancer incidence and 3.7 (95% CI 1.7-8.3) for mortality. However, the association between diuretic therapy and higher incidence of colon cancer was observed only among non-users of aspirin. A relatively lower colon cancer incidence was observed in the furosemide subgroup, and higher in the small combined amiloride/hydrochlorthiazide subgroup (HR 3.15, 95% CI 1.15-8.65). CONCLUSION: Long-term exposure to diuretic therapy may be associated with an increased colon cancer-related mortality.

Mitral annulus calcification with a mobile component as a possible source of embolism.

Mitral annulus calcification has been associated with embolic events, but the precise pathophysiology has not been elucidated. The authors describe four patients who experienced embolic events whose transesophageal echocardiograms showed a mitral annulus calcification, with a mobile component that exhibited the same echogenicity as the calcification. Three patients had no other conditions known to be associated with embolism. On follow-up transesophageal echocardiography, the mobile component of the mitral annulus calcification had disappeared in three patients. These findings support the hypothesis that mitral annulus calcification not only is associated with but also is possibly a direct cause of embolic events in some patients.

Oral antidiabetic treatment in patients with coronary disease: time-related increased mortality on combined glyburide/metformin therapy over a 7.7-year follow-up.

BACKGROUND: A sulfonylurea--usually glyburide--plus metformin constitute the most widely used oral antihyperglycemic combination in clinical practice. Both medications present undesirable cardiovascular effects. The issue whether the adverse effects of each of these pharmacologic agents may be additive and detrimental to the prognosis for coronary patients has not yet been specifically addressed. HYPOTHESIS: This study was designed to examine the survival in type 2 diabetics with proven coronary artery disease (CAD) receiving a combined glyburide/metformin antihyperglycemic treatment over a long-term follow-up period. METHODS: The study sample comprised 2,275 diabetic patients, aged 45-74 years, with proven CAD, who were screened but not included in the bezafibrate infarction prevention study. In addition, 9,047 nondiabetic patients with CAD represented a reference group. Diabetics were divided into four groups on the basis of their therapeutic regimen: diet alone (n = 990), glyburide (n = 953), metformin (n = 79), and a combination of the latter two (n = 253). RESULTS: The diabetic groups presented similar clinical characteristics upon recruitment. Crude mortality rate after a 7.7-year follow-up was lower in nondiabetics (14 vs. 31.6%, p<0.001). Among diabetics, 720 patients died: 260 on diet (mortality 26.3%), 324 on glyburide (34%), 25 on metformin alone (31.6%), and 111 patients (43.9%) on combined treatment (p<0.000001). Time-related mortality was almost equal for patients on metformin and on combined therapy over an intermediate follow-up period of 4 years (survival rates 0.80 and 0.79, respectively). The group on combined treatment presented the worst prognosis over the long-term follow-up, with a time-related survival rate of 0.59 after 7 years, versus 0.68 and 0.70 for glyburide and metformin, respectively. After adjustment to variables for prognosis, the use of the combined treatment was associated with an increased hazard ratio (HR) for all-cause mortality of 1.53 (95% confidence interval [CI] 1.20-1.96), whereas glyburide and metformin alone yielded HR 1.22 (95% CI 1.02-1.45) and HR 1.26 (95% CI 0.81-1.96), respectively. CONCLUSIONS: We conclude that after a 7.7-year follow-up, monotherapy with either glyburide or metformin in diabetic patients with CAD yielded a similar outcome and was associated with a modest increase in mortality. However, time-related mortality was markedly increased when a combined glyburide/metformin treatment was used.

Role of transesophageal echocardiography in the evaluation of patients with retinal artery occlusion.

OBJECTIVE: To evaluate the role of transesophageal echocardiography (TEE) in detecting cardiac and thoracic aortic sources of retinal emboli. DESIGN: Retrospective observational case series. PARTICIPANTS: The study population consisted of 18 patients who were initially seen with retinal artery occlusion (7 central, 11 branch) and underwent TEE as part of the systemic evaluation. INTERVENTION: All patients underwent TEE, consisting of complete two-dimensional and Doppler color flow examinations. TEE was done immediately after transthoracic echo (TTE) examination. The medical records were reviewed. MAIN OUTCOME MEASURE: Detection of a possible cardiac or thoracic aortic source of retinal embolus. RESULTS: Cardiac or thoracic aortic pathologic conditions, which were a possible source of the retinal emboli, were detected by TEE in 13 of the 18 patients (72%). They included aortic arch atheroma (n = 7), mitral annulus calcification (n = 4), left atrial appendage thrombus (n = 2), valvular abnormalities (n = 5), left atrial smoke (n = 3), and patent foramen ovale (n = 3). In 11 patients (61%), at least one cardiac or aortic source of emboli detected by TEE was missed by TTE. Significant carotid artery disease (>or=40% stenosis) was present in 3 of 16 patients (17%). CONCLUSIONS: TEE is a potentially useful modality for detecting possible sources of retinal artery emboli and may be considered as an adjunct to the routine evaluation of affected patients.