Sex-Related Differences in Dynamic Right Ventricular-Pulmonary Vascular Coupling in Heart Failure With Preserved Ejection Fraction
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Myocardial contractility—often referred to as inotropy—is the inherent capacity of the myocardium to contract independent of loading conditions, that is, preload and afterload (discussed in Chaps. 1 and 2 , respectively). Thus, for a given preload and afterload, contractility is a manifestation of all other factors that influence the interactions between contractile proteins. The incorporation of all these factors makes a simple definition of "contractility" difficult, and it is more easily understood through discussions of changes in contractility. Clinically, a change in left ventricular contractility can be defined as a change in the work performed per beat at a constant end-diastolic volume and aortic pressure.
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An elastance-based control (EBC) algorithm has been developed to produce a Frank-Starling response in a mockloop used for evaluation of ventricular assist devices. In this paper, the EBC has been tested for changes in contractility and afterload in order to evaluate its capabilities of mimicking the natural heart response. The results have shown that the end-systolic pressure-volume relationship remains fixed despite changes in afterload and reduction in end systolic pressure with decreasing contractility changes. The EBC algorithm has shown performance similar to the natural heart in response to afterload and contractility changes.
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In cat papillary muscles contracting physiologically, increasing the afterload caused a biphasic change in contractility. In response to an increase in afterload, contractility (as measured by peak shortening, peak developed force, or peak dF/dt) initially decreased (antihomeometric autoregulation) over the first few beats and then increased slowly with t 1/2 of about 3 min at 30 °C and about 1 min at 37 °C (homeometric autoregulation). The antihomeometric autoregulation is due to decreased active shortening when the afterload is increased, since it also occurs in response to increased afterload in isotonic contractions. The secondary slow increase in contractility is primarily due to the increase in mean diastolic length that occurs as a result of increased afterload. The time course and the magnitude of the biphasic change in contractility are very similar to those observed in response to afterload increase in intact hearts; we suggest that the secondary slow increase in contractility that we observed is a contributory mechanism to homeometric autoregulation (or the Anrep effect), as it is observed in the whole heart.
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Myocardial contractility—often referred to as inotropy—is the inherent capacity of the myocardium to contract independent of preload and afterload (discussed in Chaps. 1 and 2, respectively). Thus for a given preload and afterload, contractility is a manifestation of all other factors that influence the interactions between contractile proteins. The incorporation of all these factors makes a simple definition of "contractility" difficult, and it is more easily understood through discussions of changes in contractility. Clinically, a change in left ventricular contractility can be defined as a change in the work performed per beat at a constant end-diastolic volume and aortic pressure.
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Afterload
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To clarify the importance of pulmonary hypertension in the diagnosis and treatment of heart failure with preserved ejection fraction (HFpEF).Pulmonary hypertension is frequently present in HFpEF because of both elevated pulmonary venous pressure and some element of pulmonary vasoconstriction. HFpEF may be the most common cause of pulmonary hypertension in the elderly. The noninvasive detection of pulmonary hypertension can distinguish patients with HFpEF from those with diastolic dysfunction without heart failure. Pulmonary hypertension may be an important target for treatment of HFpEF. Phosphodiesterase-5 inhibitors are a promising method to treat pulmonary hypertension because of HFpEF.Pulmonary hypertension is an important contributor to the pathophysiology of HFpEF, can be used to recognize HFpEF and may be an important target for therapy.
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The cardiovascular effects of propofol infusions, designed to maintain constant plasma concentrations, were examined in an open-chested pig model. Regional myocardial contractility was measured with the end-systolic pressure-length relationship (Ees) and left ventricular afterload quantified by the effective arterial elastance (Ea). The propofol plasma concentrations in this study varied between 0 and 7.73 (SEM 0.96) micrograms/mL. A significant correlation for the increasing propofol plasma concentration and a decrease in myocardial contractility (P = 0.0056) was demonstrated, and the Ea remained constant. This gave rise to a reduction in stroke volume (P = 0.002) and, combined with a decrease in the heart rate (P = 0.0001), led to a reduction in the cardiac output (P = 0.0001). When the propofol infusion was stopped, myocardial contractility did not recover in parallel with the decrease in plasma propofol concentration.
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