Austin Flint Murmur

Etiology

As others had previously suggested, an echocardiogram-based study found the Austin Flint murmur was not associated with rapid mitral inflow.[2] The authors concluded that the murmur resulted from the regurgitant aortic jet alone.[2] Another study of echocardiogram findings found that the auscultated sound resulted from the abutment of the aortic regurgitant jet against the left ventricular epicardium.[3] A prior study had suggested that the Austin Flint murmur arose from a regurgitant aortic jet directed at the anterior mitral leaflet resulting in shuddering of the leaflet.[4] The authors hypothesized that this shuddering resulted in vibrations and shock waves that ultimately distorted the regurgitant aortic jet and caused the familiar sound heard in the Austin Flint murmur. Ultimately, there is no consensus about the cause of the sound auscultated as the Austin Flint murmur.

Epidemiology

One would expect the prevalence of the Austin Flint murmur to correlate with that of severe aortic regurgitation. In the Framingham study, the incidence of moderate to severe aortic regurgitation was less than 1% in age groups under 70 years old.[5] In the 70 to 83-year-old age group, the incidence was 2.2% for men and 2.3% for women.[5] However, not all patients with severe aortic regurgitation will have an Austin Flint murmur; therefore, the true prevalence of the murmur is currently unknown.

Pathophysiology

In developing countries, the most common cause of aortic regurgitation remains rheumatic heart disease.[6] In developed countries, aortic regurgitation occurs most often in young patients with a bicuspid aortic valve and in patients with advanced age when the burden of calcific aortic disease is highest.[5]

History and Physical

The Austin Flint murmur is a rumbling diastolic murmur best heard at the apex of the heart that is associated with severe aortic regurgitation and is usually heard best in the fifth intercostal space at the midclavicular line. Younger patients are more likely to have a history of a bicuspid aortic valve or rheumatic heart disease, while older patients are more likely to suffer from calcific valvular disease. A blood pressure reading on the patient will show an increased pulse pressure due to the backflow of blood through the aortic valve during diastole. An astute clinician may be able to palpate a "water hammer" pulse, which is also known as "Corrigan's pulse." This finding demonstrates arterial swelling followed by a brisk diastolic fall. Patients may endorse a history of syncope or lightheadedness associated with an inability to maintain forward flow through the aortic valve and the significant difference between systolic and diastolic pressure. Decreasing exercise tolerance and the inability to perform activities of daily living should prompt screening for this condition. 

Evaluation

The most appropriate test to order in a patient with an Austin Flint murmur is a transthoracic Doppler echocardiogram.[7] A cardiac magnetic resonance imaging (MRI) scan is indicated if the echocardiogram images are suboptimal due to body habitus.[7] In severe asymptomatic aortic regurgitation, the American College of Cardiology (ACC) and the American Heart Association (AHA) recommend yearly monitoring with a transthoracic echocardiogram.[7] This monitoring interval should be shortened in patients that develop left ventricular (LV) dilation despite being asymptomatic.

Treatment / Management

Treatment and management of a patient with an Austin Flint murmur are the same as other patients with severe aortic regurgitation regardless of whether an Austin Flint murmur is present. Medical management consists of treating hypertension with afterload reducing agents such as dihydropyridine calcium channel blockers or angiotensin-converting enzyme inhibitors/angiotensin receptor blockers.[7] Definitive management is with aortic valve replacement.[7] Metallic prosthetic valves are a preferred choice in younger patients who can tolerate anticoagulation due to increased longevity compared to bioprosthetic valves.[7] Elderly patients and patients with contraindications to anticoagulation should undergo implantation of bioprosthetic valves, which do not require the same lifelong anticoagulation therapy as a metallic valve.[7] Patients who are poor surgical candidates, as determined by the Society of Thoracic Surgeons' cardiac risk score (STS score), can be evaluated for the implantation of a transcatheter aortic valve replacement.[7](A1)

Differential Diagnosis

The differential diagnosis for patients presenting with a cardiac murmur and a widened pulse pressure includes conditions associated with hyperdynamic circulation. These include: 

• Thyrotoxicosis
• Severe anemia
• Wet beriberi or Thiamine deficiency
• Presence of arteriovenous fistulae 
• Pregnancy

Other intracardiac causes of similar physical presentation include:

• Infective endocarditis
• Mitral stenosis
• Tricuspid stenosis
• Mitral regurgitation
• Pulmonic regurgitation

As originally described by Flint in 1862, the murmur was "presystolic in timing and indistinguishable from that of mitral stenosis."[1] The Austin Flint murmur can be differentiated from organic mitral stenosis by the presence of an opening snap in mitral stenosis. Further differentiation is achievable with amyl nitrate inhalation, which will decrease the intensity of the Austin Flint murmur due to a decrease in afterload. The murmur of mitral stenosis will increase in both duration and intensity with amyl nitrate inhalation.

Prognosis

The prognosis of patients with severe aortic regurgitation associated with the Austin Flint murmur depends on a variety of factors. Within ten years of diagnosis of severe aortic regurgitation, 75% of patients will either pass away or require valve replacement.[8] Predictors of survival include: age, functional class, comorbidities, atrial fibrillation, and left ventricular end-systolic diameter corrected for body surface area.[8] Those with severe left ventricular dysfunction have a survival rate of 62% compared to 96% in patients with preserved left ventricular function.[9]

Complications

Complications of severe chronic aortic regurgitation include progressive LV dysfunction and dilation that can lead to progressive, symptomatic congestive heart failure, myocardial infarction, arrhythmias, and sudden cardiac death. The presence of symptomatic aortic regurgitation portends a higher risk of complications, as well as the presence of echocardiographic findings of reduced LV ejection fraction and worsening LV end-systolic dimension. This highlights the importance of monitoring patients with aortic regurgitation to prevent adverse outcomes.