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The goal of this study was to assess the alterations in left ventricle (LV) blood flow velocity patterns in relation to progressive impairment of cardiac function in the course of heart failure (HF) in a unique murine model of chronic HF in Tgaq*44 mice. Doppler- and MRI-based assessments of blood velocity and cardiac performance, respectively, were performed in Tgaq*44 mice at the age of 1, 2, 4, 6, 8 and 12 months as compared with age-matched FVB control mice. One-month-old Tgaq*44 mice displayed elongated early diastolic phase with fully preserved cardiac function that, however, progressively deteriorated in older Tgaq*44 mice. As early as in 2-month-old Tgaq*44 mice, the filling rate (FR), max. radial strain and end-systolic volume increased; in 4-month-old Tgaq*44 mice, the ejection fraction, max. circ. strain and ventriculo-arterial coupling decreased, and the ejection time was prolonged; in 6 – 8-month-old Tgaq*44 mice, the stroke volume, max. (both) strains decreased, end-systolic volume, FR and end-diastolic volume increased, and finally, in 12-month-old Tgaq*44 mice, the ejection fraction, cardiac output and stroke volume were all severely impaired. In the early phase of HF development, no differences were observed in Tgaq*44 mice versus FVB mice regarding systolic LV flow pattern, but indices of mitral diastolic flow were considerably increased in 1-month-old Tgaq*44 mice versus FVB mice. In the late phase of HF, despite progressive deterioration of cardiac function, LV pulse flow blood velocity was not altered in Tgaq*44 mice up to the age of 8 months. Systolic peak velocity and mean acceleration time deteriorated only in 12-month-old Tgaq*44 mice, with peak acceleration and mean velocity values still preserved. We demonstrated that the cardiac mitral diastolic flow pattern displayed adaptive changes in the very early phase of HF development in Tgaq*44 mice and that these changes preceded early alterations in LV haemodynamics. Then, despite the progressive deterioration of cardiac haemodynamics, peak and mean in- and out-flow velocities remained unchanged for a relatively long time and deteriorated only at the end-stage HF. Altogether, we revealed that in addition to cardiac performance, adaptive vascular performance represents an important factor determining LV mitral inflow and ejection flow phenotype during the progression of chronic HF in Tgaq*44 mice [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the effect of lead (Pb)-contaminated drinking water on magnetic resonance imaging (MRI)-estimated cardiac function, vascular reactivity, and serum lipids in rats. For 3 months, male Wistar rats, aged 4–6 weeks, were given drinking water with the addition of lead acetate at a concentration of 100 ppm Pb (10 rats) or water free from Pb (8 control rats). The cardiac MRI was performed at rest and under β-adrenergic stimulation on a 4.7 T scanner using electrocardiogram-triggered gradient echo (FLASH) cine sequence. After 1–2 weeks of the MRI test, experiments were performed ex vivo. After stabilization of perfusion pressure (PP), norepinephrine at doses from 0.01 to 5.0 μg was dissolved in Krebs solution, injected in a volume of 100 μl, and next infused at a concentration of 0.5 μg/ml into the isolated mesenteric artery. In this manner, preconstricted mesenteric bed was used to determine PP changes induced by acetylcholine, given at doses from 0.05 to 5.0 μg, before and during the infusion of nitric oxide synthase inhibitor (1.0 μg/ml). At the end, dobutamine (5 mg), followed by potassium chloride (10.5 mg), was injected. Lipid levels were determined enzymatically, blood Pb level was measured by the atomic absorption spectrophotometer. This study showed that Pb impairs the left ventricular systolic and diastolic function. Pb-induced changes in response to resistance of vessels to vasoactive agents may be secondary to the reduced left ventricular ejection fraction. The high-density lipoprotein subfraction 2 (HDL2) is involved in the cardiovascular effect of Pb. [ABSTRACT FROM AUTHOR]

Main funding source(s): 1) National Science Centre, Poland (UMO 2016/23/B/ST4/00795) 2) the Innovation Incubator 4.0 project funded by the Ministry of Science and Higher Education, Poland (POIR 2014-2020) Main funding source(s): 1) National Science Centre, Poland 2) the Innovation Incubator 4.0 project funded by the Ministry of Science and Higher Education, Poland This has now been updated as follows: Type of funding sources: Public grant(s) - National budget only. I Eur Heart J i 2021; https://doi.org/10.1093/eurheartj/ehab724.3400 In the originally published version of this abstract, the Funding Acknowledgement was incomplete and read: Type of funding sources: Public grant(s) - National budget only. [Extracted from the article]