Cardiovascular Imaging in Stress Cardiomyopathy (Takotsubo Syndrome).

Stress cardiomyopathy (Takotsubo syndrome) is a reversible syndrome stemming from myocardial injury leading to systolic dysfunction and is usually noted in the setting of a stressful event, be it an emotional or physical trigger. While the exact pathophysiology behind stress cardiomyopathy is yet unknown, there is ample evidence suggesting that neurocardiogenic mechanisms may play an important role. Although historically stress cardiomyopathy was generally thought to be a relatively benign condition, there is growing recognition of the cardiovascular complications associated with it despite its reversibility. Our review aims to shed light onto key cardiovascular imaging modalities used to diagnose stress cardiomyopathy while highlighting the role that imaging plays in assessing disease severity, identifying complications, dictating treatment approaches, and in short-term and long-term prognosis.

Relation of the Mitral Annular Plane Systolic Excursion to Risk for Intervention in Initially Asymptomatic Patients With Aortic Stenosis and Preserved Systolic Function.

Aortic valve intervention (AVI) in patients with a severe aortic stenosis (AS) and a preserved left ventricular ejection fraction (LVEF) is controversial. Mitral annular plane systolic excursion (MAPSE) is an easily acquired metric of left ventricular longitudinal shortening. We sought to investigate if an asymptomatic decrease in MAPSE preceded the need for AVI in asymptomatic patients with AS and a preserved LVEF. In this retrospective cohort study, we identified 205 consecutive patients (56% male, 73 ± 11 years) with at least a moderate AS and a normal LVEF who underwent a serial outpatient transthoracic echocardiography (TTE) from 2006 to 2013. Apical TTE images were reviewed and (the average of septal, lateral, anterior, and inferior) MAPSE was measured. We examined the association of change in MAPSE with aortic valve area and LVEF over time and used time-varying Cox models to examine the risk of AVI. MAPSE correlated with aortic valve area (Spearman r = 0.18, p = 0.02) and decreased with subsequent TTE, whereas LVEF was "maintained." For each 1-mm reduction in MAPSE, the age- and gender-adjusted hazard ratio (HR) for AVI was 1.15 (95% confidence interval [CI] 1.01 to 1.31, p = 0.04). A MAPSE decrease of >2 mm/TTE was significantly associated with an increased risk of AVI, with an adjusted HR of 1.95 (95% CI 1.04 to 3.66, p = 0.04), whereas a MAPSE decrease of >1.5 mm/year trended toward an association with an increased risk of AVI (HR 1.61, 95% CI 0.95 to 2.74, p = 0.08). In conclusion, in asymptomatic patients with at least a moderate AS and a preserved LVEF, an asymptomatic decrease in MAPSE was associated with the clinical need for AVI despite ongoing preservation of LVEF.

Interaction of hookworm 14-3-3 with the forkhead transcription factor DAF-16 requires intact Akt phosphorylation sites.

BACKGROUND: Third-stage infective larvae (L3) of hookworms are in an obligatory state of developmental arrest that ends upon entering the definitive host, where they receive a signal that re-activates development. Recovery from the developmentally arrested dauer stage of Caenorhabditis elegans is analogous to the resumption of development during hookworm infection. Insulin-like signaling (ILS) mediates recovery from arrest in C. elegans and activation of hookworm dauer L3. In C. elegans, phosphorylation of the forkhead transcription factor DAF-16 in response to ILS creates binding cites for the 14-3-3 protein Ce-FTT-2, which translocates DAF-16 out of the nucleus, resulting in resumption of reproductive development. RESULTS: To determine if hookworm 14-3-3 proteins play a similar role in L3 activation, hookworm FTT-2 was identified and tested for its ability to interact with A. caninum DAF-16 in vitro. The Ac-FTT-2 amino acid sequence was 91% identical to the Ce-FTT-2, and was most closely related to FTT-2 from other nematodes. Ac-FTT-2 was expressed in HEK 293T cells, and was recognized by an antibody against human 14-3-3beta isoform. Reciprocal co-immunoprecipitations using anti-epitope tag antibodies indicated that Ac-FTT-2 interacts with Ac-DAF-16 when co-expressed in serum-stimulated HEK 293T cells. This interaction requires intact Akt consensus phosphorylation sites at serine107 and threonine312, but not serine381. Ac-FTT-2 was undetectable by Western blot in excretory/secretory products from serum-stimulated (activated) L3 or adult A. caninum. CONCLUSION: The results indicate that Ac-FTT-2 interacts with DAF-16 in a phosphorylation-site dependent manner, and suggests that Ac-FTT-2 mediates activation of L3 by binding Ac-DAF-16 during hookworm infection.