Ventricular-Arterial and Ventricular-Ventricular Interactions and Their Relevance to Diastolic Filling
Section snippets
Ventricular-Arterial Coupling
The interaction of the heart with the systemic vasculature, termed ventricular-arterial (V-A) coupling, is a key determinant of cardiovascular performance. The capacity of the body to augment cardiac output, regulate systemic blood pressure, and respond appropriately to elevations in heart rate and preload depends on both the properties of the heart and the properties of the vasculature into which the heart ejects blood. Normal physiologic V-A coupling matches these properties so that maximal
Dynamic Changes in Diastolic Function and the Effects of Loading Conditions
Diastolic abnormalities may involve active ventricular relaxation and/or passive ventricular filling. During dynamic exercise in health (and during moderate acute increases in cardiac afterload such as during handgrip exercise) there is an increase in the rate of LV active relaxation via sympathetically mediated activation of sarcoendoplasmic reticulum adenosine triphosphatase and via protein kinase A (PKA)–mediated phosphorylation of troponin I and of phospholamban and titin.38, 39, 40 This
Relevance of V-A Coupling to Diastolic Heart Failure
Many patients with HFpEF are hypertensive, typically with isolated “systolic” hypertension. Systolic hypertension is predominantly due to increased large artery stiffness and results in an increased pulsatile LV afterload (impedance) often leading to LV hypertrophy. A recent study showed that in older patients with “diastolic” heart failure, impaired exercise tolerance correlated with aortic stiffness, which was significantly increased compared with age-matched controls.49 Another study showed
Ventricular Interaction
The term “series ventricular interaction” refers to the phenomenon whereby each ventricle ejects all of the blood that it receives from the other ventricle, and is a consequence of the Frank-Starling mechanism. There are also important direct interactions between the ventricles during diastole and systole. Because the ventricles share a common interventricular septum, the compliance of one ventricle is influenced by changes in the volume, pressure, and/or compliance of the other. This
DVI and HFnEF?
At present, the relevance of ventricular-ventricular interactions is unknown in HFnEF. However, there is some indirect evidence to suggest that on exercise, increased external constraint to LV filling may contribute to impaired use of the Starling mechanism. Kitzman et al64 performed invasive cardiopulmonary exercise testing in 7 patients with CHF and a normal LVEF and no significant coronary artery disease or valvular heart disease, and compared them with 10 age- and sex-matched healthy
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Noninvasive Positive Pressure Ventilation for Acute Decompensated Heart Failure
2020, Heart Failure ClinicsDouble-outlet right ventricle
2018, Critical Heart Disease in Infants and ChildrenPrognostic value of left ventricular-arterial coupling in elderly patients with septic shock
2017, Journal of Critical CareAssociation of Thoracic Aorta Calcium Score With Left Ventricular Hypertrophy and Clinical Outcomes in Patients With Severe Aortic Stenosis After Aortic Valve Replacement
2017, Annals of Thoracic SurgeryCitation Excerpt :Moreover, arterial stiffening adversely affects the LV through increased afterload. This mechanism, termed as ventricular-vascular coupling, has been proposed as one of the important factors in the development of LVH [13]. Arterial stiffening is associated with atherosclerosis, and increased arterial stiffness is a common finding in AS patients who are relatively older and who often present with traditional risk factors for atherosclerosis.
Causes of exercise intolerance in heart failure with preserved ejection fraction: Searching for consensus
2014, Journal of Cardiac FailureCitation Excerpt :Tachycardia would be predicted to unmask these deficits leading to a reduction in exercise preload. Finally, elevated filling pressures due to diastolic dysfunction could compromise left ventricular SV by compromising right ventricular SV or by accentuating ventricular interdependence.54–56 Given the widespread belief that diastolic dysfunction is an important factor compromising exercise tolerance, it is surprising that the exercise studies reviewed here do not demonstrate a consistent deficit in peak exercise SV.
Causes and Pathophysiology of Heart Failure with Preserved Ejection Fraction
2014, Heart Failure ClinicsCitation Excerpt :Patients with HFPEF were reported to have decreased Ea/Ees ratios when compared with those of age-matched controls, but not when compared with hypertensive controls without HF (Fig. 1C).18,20 The main features of LV diastolic dysfunction are: slowed LV relaxation, enhanced LV stiffness,21 reduced ventricular restoring forces,10 impaired diastolic suction,22 and ventricular dyssynchrony.23 From the practical point of view, characterization of diastolic function is more difficult than that of systolic function, and this is also reflected by the many currently used quantitative indices of LV diastolic function obtained by invasive hemodynamic tests and noninvasive investigations.