Afterload reduction therapy with nitroprusside in severe aortic regurgitation: Improved cardiac performance and reduced regurgitant volume

Miller, Richard R.; Vismara, Louis A.; DeMaria, Anthony N.; Salel, Antone F.; Mason, Dean T.

doi:10.1016/s0002-9149(76)80003-3

Cited by 98 publications

(17 citation statements)

References 15 publications

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“…(Circulation 1988;78:92-103) P revious studies have shown that vasodilator drugs acutely reduce the regurgitant volume and improve cardiac performance in aortic insufficiency. [1][2][3][4][5][6][7] Consequently, vasodilator therapy has emerged as an important modality for the shortterm management of patients with this lesion. These findings also raise the possibility that long-term therapy may chronically reduce the volume overload to the left ventricle.…”

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confidence: 99%

Long-term vasodilator therapy of chronic aortic insufficiency. A randomized double-blinded, placebo-controlled clinical trial.

et al. 1988

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Although vasodilator drugs acutely reduce regurgitation and improve cardiac performance in aortic insufficiency, their long-term effects on left ventricular size and function are uncertain. Consequently, we performed a double-blinded, placebo-controlled trial using hydralazine in 80 minimally symptomatic patients who had clinically stable, moderate-to-severe aortic insufficiency. Patients randomized to hydralazine displayed a progressive reduction in left ventricular end-diastolic volume index (LVEDVI) measured by radionuclide angiography, the predetermined end point of the study. At 24 months, mean LVEDVI had been reduced by 30 38 ml/m2, an 18% reduction from baseline. In contrast, LVEDVI changed minimally in patients randomized to placebo, and the intergroup differences over time were statistically significant (p<0.03). The hydralazine group also experienced reductions in left ventricular end-systolic volume index and increases in ejection fraction that were significantly different (both p<0.01) from changes in placebo-treated patients. These findings show that long-term treatment with hydralazine reduces the volume overload in aortic insufficiency and suggest that such therapy may have a beneficial effect on the natural history of the disease. (Circulation 1988;78:92-103) P revious studies have shown that vasodilator drugs acutely reduce the regurgitant volume and improve cardiac performance in aortic insufficiency. 1-7 Consequently, vasodilator therapy has emerged as an important modality for the shortterm management of patients with this lesion. These findings also raise the possibility that long-term therapy may chronically reduce the volume overload to the left ventricle. maintain cardiac performance in or close to the normal range." However, prolonged volume overload often leads to deterioration in left ventricular performance so that later in the course, signs and symptoms of cardiac dysfunction frequently develop.8,'0 An intriguing prospect is that the prophylactic administration of a vasodilator drug during the stable plateau phase of volume overload might be able to reduce either the extent of left ventricular dilation or its progression. The present study was undertaken to test the hypothesis that long-term vasodilator therapy with oral hydralazine reduces the volume overload and, hence, the left ventricular end-diastolic volume in clinically stable, moderate-to-severe aortic insufficiency. It was conducted as a prospective, randomized, placebocontrolled, double-blinded trial with change in left ventricular volume measured by radionuclide angiography as the predetermined end point.

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confidence: 99%

Long-term vasodilator therapy of chronic aortic insufficiency. A randomized double-blinded, placebo-controlled clinical trial.

et al. 1988

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“…Miller and co-workers [56] reported similar results in a mixed group of patients with severe chronic or acute aortic regurgitation. Intravenous nitroprusside, the most commonly used vasodilator therapy for such patients, was observed by Pepine and associates [57] to reverse premature aortic valve closure in a small group of patients with acute aortic regurgitation.…”

Section: Managementmentioning

confidence: 63%

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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“…It has been known for nearly two decades that vasodilating agents (nitroprusside, hydralazine, nifedipine, and angiotensin-converting enzyme [ACE] inhibitors) are effective in reducing the regurgitant volume in patients with AR and, in doing so, reducing LV volumes and increasing LV ejection fraction [6••, [12][13][14][15][16][17][18][19][20][21]. Until recently, however, it was uncertain if this effect was merely "cosmetic" in nature and whether this afterload reduction might mask the development of irreversible LV dysfunction.…”

Section: Medical Therapymentioning

confidence: 99%

Aortic regurgitation

Bonow¹

2000

Curr Treat Options Cardio Med

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Left ventricular (LV) systolic function is an important determinant of long-term prognosis in patients with chronic aortic regurgitation (AR). Impaired LV systolic function identifies a group of patients who are at risk of developing postoperative congestive heart failure and death after aortic valve replacement (AVR). Hence, asymptomatic patients with definite evidence of impaired LV function should undergo operation without waiting for the development of symptoms or more severe LV dysfunction. Among asymptomatic patients with normal LV systolic function (normal ejection fraction), prognosis is excellent, and fewer than 5% per year require surgery because of symptom development or LV dysfunction. Patients likely to require surgery can be identified on the basis of age, severity of LV dilatation, and progressive increase in LV dimensions or decrease in resting ejection fraction during the course of serial follow-up studies. Afterload-reducing therapy in asymptomatic patients with severe AR and normal LV function has beneficial hemodynamic effects; chronic therapy may reduce the likelihood of symptoms or LV systolic dysfunction. Aortic valve replacement should be performed once significant symptoms develop. In the absence of important symptoms, the operation should also be performed in patients with AR who manifest consistent and reproducible evidence of either LV contractile dysfunction at rest or extreme LV dilatation. Noninvasive imaging should play a major role in evaluation. An important clinical decision--such as recommending AVR in the asymptomatic patient--should not be based on a single echocardiographic or radionuclide angiographic measurement. When these data consistently indicate impaired contractile function at rest or extreme LV dilatation on repeat measurement, however, operation is indicated in the asymptomatic patient. This strategy should reduce the likelihood of irreversible LV dysfunction in these patients and enhance long-term postoperative survival.

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Afterload reduction therapy with nitroprusside in severe aortic regurgitation: Improved cardiac performance and reduced regurgitant volume

Cited by 98 publications

References 15 publications

Long-term vasodilator therapy of chronic aortic insufficiency. A randomized double-blinded, placebo-controlled clinical trial.

Long-term vasodilator therapy of chronic aortic insufficiency. A randomized double-blinded, placebo-controlled clinical trial.

Recognition and Treatment of Acute Aortic Regurgitation

Aortic regurgitation

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