By N. Ghista Dhanjoo, Eddie Yin-kwee Ng
For the 1st time, this priceless e-book exhibits how cardiac perfusion and pumping should be quantified and correlated. Self-contained and unified in presentation, the reasons within the compendium are exact sufficient to seize the reader s interest and whole adequate to supply the heritage fabric to discover extra into the topic. Mathematically rigorous and clinically orientated, the e-book is an enormous source for biomedical engineers, cardiologists, cardiac surgeons and clinicians. for college students, it really is an excellent textbook for senior-level classes in cardiovascular engineering.
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Additional resources for Cardiac perfusion and pumping engineering
14. 35 Dependence of the LV scale ﬁbrosis factor (SFF) on FC of angina pectoris. that the decrease of LV contractility reserve accompanied by decrease in inhomogeneity. Thus, the contractility reserve decrease due to IHD impairs LV performance, and involves LV structural transformation toward lower inhomogeneity. Generally, the transition from the normal structure of LV to the pathologic one is called myocardial or cardiac remodeling. This is the point of the next section. 5. 62 The adaptation process is associated with changes in genetic expression.
In fact, the performance of LV is the result of interaction between LV architecture, with its attendant peculiarities, and myocardial properties. In the pathologic state, disease impairs structure and function dynamically and unequally. Hence, the consequences are diﬃcult to interpret. Meanwhile in the normal heart, the LV function must strongly correspond to LV structure. At the microscopic level, myocardial function is based on muscular contractility. Commonly, contractility is taken as the ability to generate mechanical tension and the ability to shorten.
The higher value of FC implies the decrease of patients’ tolerance to physical load; that is, degradation of LV functional reserve. Figures 8 and 9 present the relationships between the patients’ FC and the CV s-EF, and the mean value of LV diastolic elasticity, respectively. The obtained data show that a CV s-EF increase results in an FC increase, and a ∆H decrease also leads to an FC increase. In other words, the decrease of myocardial contractility that arose from the increase of LV wall nonuniformity and stiﬀness resulted in the decrease of patient tolerance to physical load.