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 Tgαq*44 mice. Doppler- and MRI-based assessments of blood velocity and cardiac performance, respectively, were performed in Tgαq*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 Tgαq*44 mice displayed elongated early diastolic phase with fully preserved cardiac function that, however, progressively deteriorated in older Tgαq*44 mice. As early as in 2-month-old Tgαq*44 mice, the filling rate (FR), max. radial strain and end-systolic volume increased; in 4-month-old Tgαq*44 mice, the ejection fraction, max. circ. strain and ventriculo-arterial coupling decreased, and the ejection time was prolonged; in 6 - 8-month-old Tgαq*44 mice, the stroke volume, max. (both) strains decreased, end-systolic volume, FR and end-diastolic volume increased, and finally, in 12-month-old Tgαq*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 Tgαq*44 mice versus FVB mice regarding systolic LV flow pattern, but indices of mitral diastolic flow were considerably increased in 1-month-old Tgαq*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 Tgαq*44 mice up to the age of 8 months. Systolic peak velocity and mean acceleration time deteriorated only in 12-month-old Tgαq*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 Tgαq*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 Tgαq*44 mice.