The combination of the VDN aging model and myocardial infarction significantly reduced ejection fraction, stroke volume, and cardiac output compared to all other groups (P<0.05).
p-value: p=<0.05
The vitamin D(3) and nicotine (VDN) model is a model of isolated systolic hypertension (ISH) due to arterial calcification raising arterial stiffness and vascular impedance similar to an aged and stiffened arterial tree. We therefore analyzed the impact of this aging model on normal and diseased hearts with myocardial infarction (MI). Wistar rats were treated with VDN (n = 9), subjected to MI by coronary ligation (n = 10), or subjected to a combination of both MI and VDN treatment (VDN/MI, n = 14). A sham-treated group served as control (Ctrl, n = 10). Transthoracic echocardiography was performed every 2 wk, whereas invasive indexes were obtained at week 8 before death. Calcium, collagen, and protein contents were measured in the heart and the aorta. Systolic blood pressure, pulse pressure, thoracic aortic calcium, and end-systolic elastance as an index of myocardial contractility were highest in the aging model group compared with MI and Ctrl groups (P(VDN) < 0.05, 2-way ANOVA). Left ventricular wall stress and brain natriuretic peptide (P(VDNxMI) = not significant) were highest, while ejection fraction, stroke volume, and cardiac output were lowest in the combined group versus all other groups (P(VDNxMI) < 0.05). The combination of ISH due to this aging model and MI demonstrates significant alterations in cardiac function. This model mimics several clinical phenomena of cardiovascular aging and may thus serve to further study novel therapies.
Jegger et al. (Sat,) conducted a other in Isolated systolic hypertension and myocardial infarction (n=43). Vitamin D(3) and nicotine (VDN) treatment and/or myocardial infarction vs. Sham-treated control was evaluated on Cardiac function and structural alterations (including ejection fraction, stroke volume, and cardiac output) (p=<0.05). The combination of the VDN aging model and myocardial infarction significantly reduced ejection fraction, stroke volume, and cardiac output compared to all other groups (P<0.05).