Assessment of progression and compensatory mechanism of congestive heart failure in cardiomyopathic hamster

For an assessment of progression and compensatory mechanism congestive heart failure in cardiomyopathic Syrian hamster (UM-X7.1), I examined left ventricular (LV) function with echocardiography, LV peak systolic pressure (PSP), plasma renin activity (PRA) and LV myosin heavy chain isozyme in every week of UM-X7.1 (10-35 weeks, n＝53) and age matched control hamsters (n＝15). A transthoracic echcardiography with 7.5MHz transducer for an assessment of LV function of small animals was developped. LV end-diastolic dimention (LVDd) of UM-X7.1 was proportionally increased with aging until approximately 22 weeks, associated with progressively decreased LV fractional shortening (FS). In UM-X7.1, progressive enlargement of LV dimension and impairment of LV contractility with aging were demonstrated. However, progressive increase in LVDd reached plateau after 22 weeks, suggesting limitation of LV preload reserve at this time. PSP of UM-X7.1 tended to decline from the same week. It was considered that the compensatory mechanism of heart in UM-X7.1 reached limitation at approximately 22 weeks. In metabolic state of myocardium of UM-X7.1, predominant LV myosin isozyme (VM-1) was proportionally decreased with aging and shifted to VM-3 until the late stage. It may be a metabolic compensatory mechanism for improvement of the myocardial efficiency. Furthermore, PRA of UM-X7.1 rised abruptly at approximately the same week as the time of LVDd reaching plateau. The date suggested that the PRA rises after the limitation of compensatory machanism of heart. Therefore the rise of PRA may cause to fall into a vicious cycle of the decompensation of heart failure. The UM-X7.1 is useful model of end-stage of congestive heart failure with some resemblance to human cardiac dysfynction.