Afterload mismatch and preload reserve in chronic aortic regurgitation.

Ricci, Donald R.

doi:10.1161/01.cir.66.4.826

Cited by 58 publications

(22 citation statements)

References 53 publications

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“…Our results indicate that, in an animal model of chronic, pure, isolated AR without confounding nonvalvular cardiac diseases, interstitial fibrosis and myocyte degeneration/necrosis develop in response to a hemodynamic burden comparable in severity to that which can be associated with CHF in humans with chronic AR [11][12][13]. Our histopathologic findings are consistent with results previously reported from similar assessments in patients who have undergone aortic valve replacement for AR [1-4, 14, 15] or who have died with severe AR and CHF [1,16].…”

Section: Discussionmentioning

confidence: 72%

Fibrosis, Myocyte Degeneration and Heart Failure in Chronic Experimental Aortic Regurgitation

Liu¹,

Magid

Fox³

et al. 1998

Cardiology

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Myocardial fibrosis and myocyte degeneration have been reported in patients with chronic aortic regurgitation (AR), and may be related to the pathophysiology of congestive heart failure (CHF) in this disease. To define the relationship between myocardial histopathologic variations and CHF in chronic AR, we performed gross and microscopic evaluations of postmortem tissue from a rabbit model of chronic AR manifesting left ventricular (LV) responses to AR similar to those in humans. Moderate-to-severe chronic AR (echocardiographic regurgitant fraction = 52 ± 13%) was induced by closed-chest aortic valve perforation in 11 New Zealand White rabbits; 5 control rabbits were sham operated. Six of the 11 AR rabbits died 1.5 ± 0.8 years (range 0.6–2.8 years) after AR induction; all 6 had gross and histologic anatomic evidence of CHF at necropsy. The remaining 5 AR rabbits survived until sacrifice at 2.9 ± 0.1 years of AR; none had pathologic evidence of CHF. Cardiac hypertrophy and the extent of LV fibrosis and myocyte necrosis all were greatest among the 6 AR CHF rabbits. No inflammatory response was apparent in any animal. Moderate-to-severe chronic experimental AR frequently results in CHF which is strongly associated with myocardial fibrosis and necrosis, without evidence of inflammation. These histopathologic variations may be pathophysiologically related to CHF development.

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Section: Discussionmentioning

confidence: 72%

Fibrosis, Myocyte Degeneration and Heart Failure in Chronic Experimental Aortic Regurgitation

Liu¹,

Magid

Fox³

et al. 1998

Cardiology

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“…25,26 Eccentric hypertrophy preserves LV diastolic compliance, such that LV filling pressures remain normal or mildly increased despite a large regurgitant volume. In addition, eccentric hypertrophy increases LV mass, such that the LV volume/mass ratio is normal, and LV ejection fraction (LVEF) is maintained by increased preload.…”

Section: Pathophysiologymentioning

confidence: 99%

Valvular Heart Disease

2005

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Abstract-Aortic regurgitation (AR) is characterized by diastolic reflux of blood from the aorta into the left ventricle (LV).Acute AR typically causes severe pulmonary edema and hypotension and is a surgical emergency. Chronic severe AR causes combined LV volume and pressure overload. It is accompanied by systolic hypertension and wide pulse pressure, which account for peripheral physical findings, such as bounding pulses. The afterload excess caused by systolic hypertension leads to progressive LV dilation and systolic dysfunction. The most important diagnostic test for AR is echocardiography. It provides the ability to determine the cause of AR and to assess the severity of AR and its effect on LV size, function, and hemodynamics. Many patients with chronic severe AR may remain clinically compensated for years with normal LV function and no symptoms. These patients do not require surgery but can be followed carefully for the onset of symptoms or LV dilation/dysfunction. Surgery should be considered before the LV ejection fraction falls below 55% or the LV end-diastolic dimension reaches 55 mm. Symptomatic patients should undergo surgery unless there are excessive comorbidities or other contraindications. The primary role of medical therapy with vasodilators is to delay the need for surgery in asymptomatic patients with normal LV function or to treat patients in whom surgery is not an option. The goal of vasodilator therapy is to achieve a significant decrease in systolic arterial pressure. Future therapies may focus on molecular mechanisms to prevent adverse LV remodeling and fibrosis. Key Words: aorta Ⅲ echocardiography Ⅲ valves Ⅲ ventricles A ortic regurgitation (AR) is characterized by diastolic reflux of blood from the aorta into the left ventricle (LV) due to malcoaptation of the aortic cusps. Its clinical presentation is variable and depends on a complex interplay of a number of factors, including acuity of onset, aortic and LV compliance, hemodynamic conditions, and severity of the lesion. Although chronic AR is generally well tolerated for many years, acute AR may lead to rapid cardiac decompensation and, if untreated, to early death. 1 This review focuses on the clinical manifestations of AR, evaluation of its severity and hemodynamic consequences, and its treatment. PrevalenceThe prevalence of chronic AR and incidence of acute AR are not precisely known. Singh et al 2 reported the prevalence of chronic AR detected by color Doppler echocardiography in a large unselected adult population (the Framingham Offspring Study). The overall prevalence AR in men was 13% and in women 8.5%. However, most of the AR in this population was trace or mild in severity; moderate or severe AR was rare (Table 1). Multiple logistic regression analysis revealed age and male gender to be predictors of AR. Interestingly, hypertension did not predict AR on multivariate analysis, confirming results of earlier studies that hypertension is associated with modest increases in aortic root size but not AR when age is included in the...

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“…231 As the disease progresses, recruitment of preload reserve and compensatory hypertrophy permit the ventricle to maintain normal ejection performance despite the elevated afterload. 232,233 The majority of patients remain asymptomatic throughout this compensated phase, which may last for decades. Vasodilator therapy has the potential to reduce the hemodynamic burden in such patients.…”

Section: Pathophysiologymentioning

confidence: 99%