The natural history of aortic regurgitation

Goldschlager, Nora; Pfeifer, James F.; Cohn, Keith; Popper, Robert W.; Selzer, Arthur

doi:10.1016/0002-9343(73)90115-0

Cited by 134 publications

(20 citation statements)

References 16 publications

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“…In addition, we have shown previously that the rate and extent of LV dilatation and hypertrophy during the first 6 months following induction of moderate-to-severe AR is similar among those animals which subsequently develop CHF and those which remain compensated during 3 years of observation [7]. The discordance between the severity of regurgitation and wall stress and associated clinical and cardiac functional status in our animals parallels the common clinical observation in humans that patients with similarly severe AR do not manifest uniform functional or clinical characteristics [11,40]. The differences in response which we have observed might be caused by regional, qualitative or temporal variations in loading conditions not assessed in this study.…”

Section: Discussionsupporting

confidence: 81%

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: Discussionsupporting

confidence: 81%

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

Liu¹,

Magid

Fox³

et al. 1998

Cardiology

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“…Because we did not collect information on duration of atrial fibrillation before the echocardiographic diagnosis of valve disease, we cannot determine whether the greater impact on the risk of stroke attributable to valvular atrial fibrillation at younger ages is due to an increased risk primarily among patients with new-onset atrial fibrillation, as suggested by Szekely,19 or whether atrial fibrillation simply becomes a relatively less important mechanism of stroke in older patients with valve disease as other stroke risk factors become more prevalent, despite the increase in atrial fibrillation prevalence with age in the general population. 47 Our study also provides new quantitative evidence on the relative importance of cardiovascular comorbidities that influence survival in patients with valve disease 7,8,[11][12][13]48 : age, ischemic heart disease, and congestive heart failure. Our multivariate survival model (Table 6) demonstrates that congestive heart failure is a far more important determinant of death among patients with newly diagnosed valvular heart disease than ischemic heart disease.…”

Section: Discussionmentioning

confidence: 80%

“…Moreover, earlier longitudinal studies did not use multivariate analyses to identify independent determinants of morbidity and mortality and were derived largely from observations made on patients referred to tertiary care centers, an important source of bias. [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] We undertook a large population-based historical cohort study of all residents of Olmsted County, Minnesota, who had a first 2-dimensional color Doppler echocardiographic diagnosis of hemodynamically significant mitral or aortic stenosis or regurgitation made between 1985 and 1992 to estimate rates and model determinants of the development of cerebrovascular events and to quantify the influence of cerebrovascular events on survival among these patients.…”

mentioning

confidence: 99%

Predictors of Cerebrovascular Events and Death Among Patients With Valvular Heart Disease

Petty¹,

Khandheria²,

Whisnant³

et al. 2000

Stroke

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Background and Purpose-There is little population-based information on cerebrovascular events and survival among valvular heart disease patients. We used the Kaplan-Meier product-limit method and the Cox proportional hazards model to determine rates and predictors of cerebrovascular events and death among valve disease patients. Methods-This population-based historical cohort study in Olmsted County, Minnesota, reviewed residents with a first echocardiographic diagnosis of mitral stenosis (nϭ19), mitral regurgitation (nϭ528), aortic stenosis (nϭ140), and aortic regurgitation (nϭ106) between 1985 and 1992. Results-During 2694 person-years of follow-up, 98 patients developed cerebrovascular events and 356 died. Compared with expected numbers, these observations are significantly elevated, with standardized morbidity ratio of 3.2 (95% CI, 2.6 to 3.8) and 2.5 (95% CI, 2.2 to 2.7), respectively. Independent predictors of cerebrovascular events were age, atrial fibrillation, and severe aortic stenosis. The risk ratio of severe aortic stenosis was 3.5 (95% CI, 1.4 to 8.6), with atrial fibrillation conferring greater risk at younger age. Predictors of death were age, sex, cerebrovascular events, ischemic heart disease, and congestive heart failure, the greatest risk being among those with both congestive heart failure and cerebrovascular events (risk ratioϭ8.8; 95% CI, 5.8 to 13.4). Valve disease type and severity were not independent determinants of death. Conclusions-The risk of cerebrovascular events and death among patients with valve disease remains high. Age, atrial fibrillation, and severe aortic stenosis are independent predictors of cerebrovascular events, and age, sex, cerebrovascular events, congestive heart failure, and ischemic heart disease are independent predictors of death in these patients.

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“…In the minority of patients, who have mild to moderate acute aortic regurgitation, medical therapy is successful, and the findings of chronic aortic regurgitation will eventually develop. In most patients, who have severe acute aortic regurgitation, the natural history depends on whether or not heart failure is present [4,54]. Patients with moderate or severe congestive heart failure due to acute aortic regurgitation have a oneyear mortality rate of up to 80%; the prognosis is particularly poor for patients who have acute aortic regurgitation due to infective endocarditis [3].…”

Section: Natural Historymentioning

confidence: 99%

Recognition and Treatment of Acute Aortic Regurgitation

O’Rourke

Walsh

1986

J Intensive Care Med

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Address reprint requests to Dr O'Rourke. Acute aortic regurgitation usually results from infective endocarditis, but is also caused by aortic dissection and trauma to the heart. Most of the left ventricular stroke volume is regurgitated back into the left ventricle; thus, the forward stroke volume to the body and the cardiac output may be severely compromised. An acute increase in left ventricular end-diastolic volume results in a marked increase in left ventricular end-diastolic pressure, and the mitral valve usually closes prematurely. Compensatory tachycardia is the rule and helps to shorten diastole; thus, the time available for aortic regurgitation to occur is reduced, and the cardiac output is often maintained.On physical examination, there is tachycardia; the peripheral arterial pulse shows a rapid rise, but the systolic pressure is normal; the diastolic pressure is normal or even reduced; and the pulse pressure is often normal. The electrocardiogram (ECG) may be normal except for sinus tachycardia and often for nonspecific ST-T changes. The chest roentgenogram usually shows signs of pulmonary venous hypertension or even pulmonary edema. Echocardiography may show vegetations on the aortic valve, prolapse of an aortic leaflet into the left ventricle, and premature mitral valve closure. Doppler echocardiography is useful in detecting the presence of aortic regurgitation.In cases of infective endocarditis, the appropriate antibiotic therapy must be given. Aortic regurgitation due to dissection of the aorta is usually an indication for surgery. In patients with severe aortic regurgitation, available medical therapy includes digitalis, diuretics, and vasodilators. When patients respond dramatically to the use of digitalis, diuretics, and arterial dilators, surgical therapy can be delayed until heart failure and infection are controlled and the patient is more stable. If the patient does not respond immediately and dramatically to therapy, then valve replacement should not be delayed, even if the infection is uncontrolled or the patient has had little antibiotic therapy.Acute aortic regurgitation is a potentially lethal disorder that frequently results in severe left ventricular decompensation and secondary right-heart failure; it often is associated with important arrhythmias, particularly atrioventricular or bundle branch due to involvement of the conduction system by the underlying pathologic process [1,2]. Acute aortic regurgitation and its complications are usually responsive to medical or surgical treatment [1-3].However, successful treatment of acute aortic regurgitation depends on the early diagnosis of acute left ventricular volume overload, an understanding of the pathophysiology, and an aggressive therapeutic approach. Early aortic valve replacement is often necessary because most patients with acute severe aortic regurgitation die within one year unless the incompetent aortic valve is replaced surgically [4]. However, perioperative morbidity and mortality are reduced, and the results of operation are...

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The natural history of aortic regurgitation

Cited by 134 publications

References 16 publications

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

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

Predictors of Cerebrovascular Events and Death Among Patients With Valvular Heart Disease

Recognition and Treatment of Acute Aortic Regurgitation

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