Key result
Cyclosporine accelerates HF development in HFpEF swine, increasing LVEDP by ~4 mmHg.
Why the study?
Does cyclosporine treatment improve cardiac function in a swine model of heart failure with preserved ejection fraction?
Does cyclosporine treatment improve cardiac function in a swine model of heart failure with preserved ejection fraction?
Cyclosporine treatment accelerated heart failure development in a swine model of HFpEF, indicating it is not a viable therapy, while highlighting the utility of 2D speckle tracking for early detection of diastolic impairment.
Answers are grounded in this paper and cite their sources.
Cyclosporine accelerated HFpEF progression in swine; leaves open human translation and advises against further therapeutic pursuit.
We recently reported that mitochondrial dysfunction, characterized by increased mitochondrial permeability transition (MPT), was present in a translational swine model of heart failure with preserved ejection fraction (HFpEF). Cyclophilin D is a key component of the MPT pore, therefore, the purpose of this study was to test the efficacy of a novel cyclosporine (CsA) dosing scheme as a therapeutic alternative for HFpEF. Computed tomography (CT), two-dimensional speckle tracking two-dimensional speckle tracking (2DST), and invasive hemodynamics were used to evaluate cardiac function. CT imaging showed 14 weeks of CsA treatment caused eccentric myocardial remodeling (contrasting concentric remodeling in untreated HF animals) and elevated systemic pressures. 2DST detected left ventricular (LV) mechanics associated with systolic and diastolic dysfunction prior to the onset of significantly increased LV end diastolic pressure including: (1) decreased systolic apical rotation rate, longitudinal displacement, and longitudinal/radial/circumferential strain; (2) decreased early diastolic untwisting and longitudinal strain rate; and (3) increased late diastolic radial/circumferential mitral strain rate. LV mechanics associated with systolic and diastolic impairment was enhanced to a greater extent than seen in untreated HF animals following CsA treatment. In conclusion, CsA treatment accelerated the development of heart failure, including dilatory LV remodeling and impaired systolic and diastolic mechanics. Although our findings do not support CsA as a viable therapy for HFpEF, 2DST was effective in differentiating between progressive gradations of developing HF and detecting diastolic impairment prior to the development of overt diastolic dysfunction.
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Hiemstra et al. (2013) studied Heart failure with preserved ejection fraction (HFpEF) induced by aortic banding (n=15). Cyclosporine (CsA) vs. Placebo (banded HF sedentary control) and nonsham sedentary control was evaluated on Left ventricular end-diastolic pressure (LV EDP, mmHg) (p=<0.05). Cyclosporine accelerated heart failure development in HFpEF swine, causing eccentric remodeling and increasing LV end-diastolic pressure to 15 vs 11 mmHg in controls.
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