Modulation of Thin Filament Activity in Long and Short Term Regulation of Cardiac Function

Author(s):  
R. John Solaro ◽  
Beata M. Wolska ◽  
Grace Arteaga ◽  
Anne F. Martin ◽  
Peter Buttrick ◽  
...  
Lupus ◽  
2018 ◽  
Vol 27 (14) ◽  
pp. 2206-2214 ◽  
Author(s):  
C Li ◽  
J Zhao ◽  
S Liu ◽  
W Song ◽  
J Zhu ◽  
...  

Background Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare and life-threatening condition with poor prognosis in patients with antiphospholipid syndrome (APS). Pulmonary thromboendarterectomy (PTE) is the optimal surgical option for CTEPH. Objectives This retrospective cohort study aimed to evaluate the efficacy and risk of PTE in patients with APS-associated CTEPH. Methods Consecutive patients with APS-associated CTEPH diagnosed between January 2012 and September 2017 at Peking Union Medical College Hospital were retrospectively evaluated. Demographics, clinical manifestations, antiphospholipid antibody (aPL) profiles, and pulmonary arterial hypertension–targeted medications were collected. Deterioration of cardiac function and death were chosen as the endpoints, in order to assess the effect of PTE on short-term and long-term prognoses (evaluated by the change of cardiac function after treatment and cardiac deterioration or death in the follow-up, respectively). Results A total of 20 patients with APS-associated CTEPH were enrolled, and eight patients underwent PTE. Chi-square test ( p = 0.01) and Kaplan–Meier curves (log rank test, p = 0.04) showed that there were statistically significant differences in both short-term and long-term prognoses between patients with and without PTE. Conclusion These results provide strong evidence that PTE is a curative resolution in patients with APS-associated CTEPH. Following a full specialized and multidisciplinary risk-benefit evaluation to limit the risk of thrombosis or bleeding and to manage possible thrombocytopenia, PTE is at least a temporal curative resolution for CTEPH complicated with APS.


PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0222334
Author(s):  
Rafael Aguiar Marschner ◽  
Patrícia Banda ◽  
Simone Magagnin Wajner ◽  
Melissa Medeiros Markoski ◽  
Maximiliano Schaun ◽  
...  

Author(s):  
D. Beitzke ◽  
F. Gremmel ◽  
D. Senn ◽  
R. Laggner ◽  
A. Kammerlander ◽  
...  

Abstract Levosimendan improves cardiac function in heart failure populations; however, its exact mechanism is not well defined. We analysed the short-term impact of levosimendan in heart failure patients with ischemic and non-ischemic cardiomyopathy (CMP) using multiparametric cardiac magnetic resonance (CMR). We identified 33 patients with ischemic or non-ischemic CMP who received two consecutive CMR scans prior to and within one week after levosimendan administration. Changes in LV ejection fraction (LVEF) and LV volumes, as well as changes in strain rates, were measured prior to and within one week after levosimendan infusion. LV scarring, based on late gadolinium enhancement (LGE), was correlated to changes in LV size and strain rates. Both LV endiastolic (EDV) and endsystolic volumes (ESV) significantly decreased (EDV: p=0,001; ESV: p=0,002) after levosimendan administration, with no significant impact on LVEF (p=0.41), cardiac output (p=0.61), and strain rates. Subgroup analyses of ischemic or non-ischemic CMP showed no significant differences between the groups in terms of short-term LV reverse remodeling. The presence and extent of scarring in LGE did not correlate with changes in LV size and strain rates. CMR is able to monitor cardiac effects of levosimendan infusion. Short-term follow-up of a single levosimendan infusion using CMR shows a significant decrease in LV size, but no impact on LVEF or strain measurements. There was no difference between patients with ischemic or non-ischemic CMP. Quantification of LV scarring in CMR is not able to predict changes in LV size and strain rates in response to levosimendan.


Circulation ◽  
1984 ◽  
Vol 69 (1) ◽  
pp. 113-119 ◽  
Author(s):  
C S Liang ◽  
L G Sherman ◽  
J U Doherty ◽  
K Wellington ◽  
V W Lee ◽  
...  

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