Cardiac cycle-dependent changes in aortic area and distensibility are reduced in older patients with isolated diastolic heart failure and correlate with exercise intolerance

Hundley, W. Gregory; Kitzman, Dalane W.; Morgan, Timothy M.; Hamilton, Craig; Darty, Stephen; Stewart, Kathryn P.; Herrington, David M.; Link, Kerry M.; Little, William C.

doi:10.1016/s0735-1097(01)01447-4

Cited by 356 publications

(319 citation statements)

References 26 publications

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“…Recent studies have demonstrated that increased ventricular vascular stiffening 3,11,42 characterized by upward and leftward shifted ESPVR and EDPVR (eg, at the 12-week time period in the HS rats) can result in increased load lability 11 and is closely correlated with exercise duration and peak oxygen consumption. 51 Thus, whereas the 12-week HS rats did not manifest with increased EDP nor increased lung/body weight ratios indicating pulmonary edema, the pathophysiological characteristics at this time point are similar to those described in other animal models 42 and human 11 observations and are potential pathophysiological explanations for the reduced exercise capacity that is characteristic of HFPEF subjects. However, our focus was on the pathophysiological explanation for an elevated EDP at rest and resultant pulmonary edema, which has been observed in several investigations.…”

Section: Discussionsupporting

confidence: 77%

Development of Heart Failure in Chronic Hypertensive Dahl Rats

et al. 2006

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Abstract-The impact of hypertension on left ventricular (LV) structure, pump function, and heart failure in Dahl salt-sensitive rats is poorly characterized but hypothesized to yield insights into the pathophysiology of heart failure with normal or preserved ejection fraction. Eighty Dahl salt-sensitive rats were fed either a high-salt (HS) or low-salt (LS, controls) diet starting at age 7 weeks. Ventricular properties were measured by echocardiography, hemodynamics and end-systolic and end-diastolic pressure-volume relationships (ESPVR and EDPVR, respectively). Compared with LS controls, HS rats developed severe hypertension and LV hypertrophy. At week 12, HS rats developed passive diastolic dysfunction (leftward/upward shifted EDPVR, increased chamber stiffness) with reductions in end-diastolic volume. However, the ESPVR also shifted upward (enhanced end-systolic function) so that overall pump function was enhanced compared with LS, and there was no change in end-diastolic pressure (EDP). At 16 and 20 weeks, HS hearts enlarged so that end-diastolic volumes and EDPVRs became similar to the respective age-matched LS controls. Concomitantly, the ESPVRs and overall pump function curves also moved toward controls, and ejection fraction declined. Despite normal or enhanced overall pump function at these times, EDP and wet lung weight increased, indicative of development of heart failure. In the Dahl salt-sensitive rat, which pathophysiologically retains salt and water, the development of heart failure (increased EDP and wet lung weight) is dissociated from changes in passive diastolic and active systolic properties. These observations suggest that a volume overload sate plays an important pathophysiological role in development of heart failure despite preserved overall ventricular pump function in this model of chronic hypertension. Key Words: remodeling Ⅲ heart failure Ⅲ diastole Ⅲ hypertrophy Ⅲ renal disease H eart failure commonly occurs in patients with a normal or preserved ejection fraction (HFPEF). 1-3 It was advocated previously that HFPEF is primarily because of diastolic dysfunction and, thus, termed "diastolic heart failure" (DHF). 4,5 However, data from our recent clinical and animal studies suggest that HFPEF can occur without diastolic dysfunction. 6 -10 We found that HFPEF in the setting of idiopathic hypertrophic cardiomyopathy and infiltrative cardiac diseases is indeed because of diastolic dysfunction, defined by a reduced chamber capacitance in the absence of systolic dysfunction. 10 However, in the setting of long standing hypertension, HFPEF may not always be because of diastolic dysfunction. 10 We proposed other, extracardiac factors leading to a volume-overloaded state as the underlying pathology, such as might occur with salt and water handling impairments encountered in the setting of renal dysfunction.Two potential limitations of prior studies contribute to the controversy. First, barring a few notable exceptions, 7,11-13 studies of HFPEF have evaluated diastolic properties without any ser...

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Section: Discussionsupporting

confidence: 77%

Development of Heart Failure in Chronic Hypertensive Dahl Rats

et al. 2006

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“…Evidence that such pathophysiology likely contributes to exertional intolerance was reported by Hundley et al ( Figure 2B). 12 There is a direct relation between arterial distensibility (ie, compliance) and peak oxygen consumption during exercise testing. Patients with cardiac failure symptoms and preserved ejection fraction (EF) are shown by the white triangles and have the stiffest arteries.…”

Section: Ventricular-arterial Stiffeningmentioning

confidence: 99%

Ventricular Arterial Stiffening

2005

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Abstract-Vascular stiffening of the large arteries is a common feature of aging and is exacerbated by many common disorders such as hypertension, diabetes, and renal disease. This change influences the phasic mechanical stresses imposed on the blood vessels that in turn is important to regulating smooth muscle tone, endothelial function, and vascular health. In addition, the heart typically adapts to confront higher and later systolic loads by both hypertrophy and ventricular systolic stiffening. This creates altered coupling between heart and vessel that importantly affects cardiovascular reserve function. In this overview, I discuss the notion of a coupling disease in which stiffness of both heart and arteries interact to limit performance and generate clinical symptoms. This involves changes in the mechanical interaction of both systems, changes in signaling within the arteries themselves, and alterations in coronary flow regulation. Lastly, I briefly review recent development in de-stiffening strategies that may pave the way to treat this syndrome and its clinical manifestations.

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“…The proximal aorta directly receives the blood ejected from the left ventricle and efficiently transports it to peripheral organs. Structural and qualitative changes of the proximal aorta directly affect aortic hemodynamics and LV afterload 5, 6. The diameter of the proximal aorta (AoD) is known to increase as people age 1.…”

Section: Introductionmentioning

confidence: 99%

Increased Proximal Aortic Diameter is Associated With Risk of Cardiovascular Events and All‐Cause Mortality in Blacks The Jackson Heart Study

Kamimura

Suzuki

Musani

et al. 2017

JAHA

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BackgroundEnlargement of the proximal aorta is associated with aortic wall tissue remodeling, including fragmentation of the elastin fibers, increased synthesis of collagen, and calcification, all of which are associated with aortic wall stiffening. We hypothesized that the proximal aortic diameter (AoD) is associated with cardiovascular events in a community‐based cohort of blacks.Methods and ResultsWe investigated the associations between AoD and cardiovascular events among 3018 black participants (mean age, 55.9 years; 69% women) without past history of cardiovascular disease in the Jackson Heart Study. AoD was measured using echocardiography at the level of the sinuses of Valsalva at end diastole. Cardiovascular event was defined as incident myocardial infarction, fatal coronary artery disease, stroke, or heart failure hospitalization. Cox proportional hazards regression models were used to evaluate the association between baseline AoD and cardiovascular events. Over a median follow‐up of 8.3 years, there were 258 cardiovascular events (incident rate, 10.5 per 1000 person‐years). After adjustment for traditional risk factors, increased AoD was significantly associated with cardiovascular events (hazard ratio per 1‐cm increase, 1.72; 95% CI, 1.10–2.69; P<0.05). Participants in the top AoD quintile had a higher incidence of cardiovascular events compared to those not in the top quintile (hazard ratio, 1.47; 95% CI, 1.11–1.94; P<0.005) after adjustment for risk factors.ConclusionsGreater AoD was associated with an increased risk of cardiovascular events in a community‐based cohort of blacks. AoD may be useful as a predictor of incident cardiovascular events and further investigation is warranted.

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Cardiac cycle-dependent changes in aortic area and distensibility are reduced in older patients with isolated diastolic heart failure and correlate with exercise intolerance

Abstract: Older patients with isolated DHF have reduced cardiac cycle-dependent changes in proximal thoracic aortic area and distensibility (beyond that which occurs with normal aging), and this correlates with and may contribute to their severe exercise intolerance.

Cited by 356 publications

References 26 publications

Development of Heart Failure in Chronic Hypertensive Dahl Rats

Development of Heart Failure in Chronic Hypertensive Dahl Rats

Ventricular Arterial Stiffening

Increased Proximal Aortic Diameter is Associated With Risk of Cardiovascular Events and All‐Cause Mortality in Blacks The Jackson Heart Study

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