Title: Early and Late Outcome of Treated Patients Referred for Syncope to Emergency Department: the EGSYS 2 Follow-Up Study
Topic: Arrhythmias
Date Posted: 2/24/2010
Author(s): Andrea U, Attilio DR, Franco G, et al., on behalf of the Evaluation of Guidelines in Syncope Study 2 (EGSYS 2) Group.
Citation: Eur Heart J 2010;Feb 18:[Epub ahead of print].
Clinical Trial: yes
Study Question: What is the prognosis of patients with syncope?
Methods: This was a multicenter, prospective study of 380 patients (mean age 66 years) with syncope initially evaluated in an emergency department (ED). Therapy was at the discretion of the treating physician. The mean duration of follow-up was 20 months. The 1° endpoint was death from any cause or syncope recurrence.
Results: The most common causes of syncope were neurocardiogenic syncope in 64% of patients, orthostatic hypotension in 17%, cardiac syncope in 15%, and an arrhythmia in 11%. All-cause mortality was 9.2%. The strongest predictors of mortality were structural heart disease or an abnormal electrocardiogram (hazard ratio [HR], 5.6), hypertension (HR, 3.0), and trauma from syncope (HR, 2.24). Mortality in patients with cardiac syncope was significantly higher than in patients with other causes of syncope (37% vs. 7-11%). Syncope recurred in 16% of patients and the recurrence rate was unrelated to the etiology of syncope. The strongest predictors of recurrent syncope were palpitations before syncope (HR, 3.4), male gender (HR, 1.8), and absence of prodrome (HR, 0.4).
Conclusions: The risk of death during follow-up in patients with syncope is related to associated cardiac disease. Syncope recurrence is unrelated to the cause of syncope.
Perspective: A limitation of this study is that left ventricular ejection fraction was not included in the analysis and probably would have been a stronger predictor of mortality than simply the presence of structural heart disease. Fred Morady, M.D., F.A.C.C.
Title: Structural Abnormalities of the Pulmonary Trunk in Tetralogy of Fallot and Potential Clinical Implications: A Morphological Study
Topic: Congenital Heart Disease
Date Posted: 3/1/2010
Author(s): Bйdard E, McCarthy KP, Dimopoulos K, Giannakoulas G, Gatzoulis MA, Ho SY.
Citation: J Am Coll Cardiol 2009;54:1883-1890.
Clinical Trial: No
Study Question: Are intrinsic histological abnormalities present from birth in the pulmonary trunk of patients with tetralogy of Fallot (TOF)?
Methods: A review of 39 formalin-fixed necropsy heart specimens of patients with TOF was performed, and compared with 17 normal control specimens. Histological specimens were studied with light microscopy using standard stains, and findings were graded according to severity.
Results: Of the 39 patients in the TOF group, 11 had undergone palliative surgeries while 10 had undergone complete repair at a median age of 8 years (range 2.5-18 years). Histological changes of grade 2 were common, including medionecrosis in 59%, fibrosis in 36%, cyst-like formation in 56%, and abnormal elastic tissue configuration in 56%. Patients with TOF were found to have higher total histology grading scores (median 6, range 1-9) than controls (median 1, range 1-9). Histological abnormalities were noted in all TOF populations, including infants (median 3.5, range 1-9), patients post-palliative surgery (median score 5, range 2-9), and patients post-complete repair (median score 7.5, range 4-9).
Conclusions: Significant histological abnormalities of the pulmonary trunk in hearts with TOF are present from birth, and are seen in patients prior to and after palliative surgery or complete repair.
Perspective: Previous research has demonstrated histological abnormalities in the aortic root of patients with TOF. This study demonstrates similar abnormalities in the pulmonary tract, and shows them to be present even in fetal life. Although further study will be required to determine the clinical significance of these findings, it is possible that these histological abnormalities might predispose patients to pulmonary regurgitation and/or right ventricular dysfunction. Timothy B. Cotts, M.D., F.A.C.C.