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ECG Quiz Answer

Acute Dyspnea and a New Murmur in a Team Physician

John D. Cantwell, MD; David T. Watson, MD; William A. Blincoe, MD; James R. Kauten, MD



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The patient's decrescendo diastolic murmur was consistent with aortic valvular regurgitation (AR). Acute AR, as seen in our patient, is usually caused by infectious endocarditis, aortic dissection, or blunt trauma to the chest (1,2). Our patient however, had no history of chest pain, chest trauma, recent dental work, or a febrile illness. Acute changes in a congenitally deformed valve (bicuspid, myxomatous) are possible. Infectious endocarditis can occur in the absence of a fever; however, this patient had no other stigmata to suggest this diagnosis.

His ECG was unremarkable except for left atrial enlargement (figure 3). The chest x-ray showed pulmonary congestion and pleural effusions consistent with congestive heart failure and a relatively normal-sized heart.


A transesophageal echocardiogram revealed severe AR without vegetations. The left coronary cusp seemed to prolapse. Right and left heart catheterization revealed a normal pulmonary capillary wedge pressure, normal coronary arteries, severe AR, and possible prolapse of the left coronary cusp of the aortic valve. The aortic root was not significantly enlarged.

After discussion among multiple consultants, the patient underwent aortic valve replacement with a mechanical valve (St Jude Medical, Inc, Little Canada, Minnesota) rather than a pulmonary allograft (Ross procedure) (3) or a homograft.

The surgeon found a congenitally bicuspid aortic valve with fusion of the left and right coronary cusps. A fibrous band of supportive structure had apparently torn, perhaps during basketball, causing prolapse of the fused left and right cusps with valvular insufficiency. Valve cultures were negative.


Causes of aortic regurgitation are shown in table 1. The physical findings in acute AR typically differ from those in chronic AR (4,5). The pulse pressure (the difference between the systolic and diastolic blood pressures) usually isn't as wide in acute AR as it is in chronic AR because the diastolic blood pressure can't fall below the relatively high left ventricular (LV) filling pressure in this condition. The rise in resting arterial pulse contour associated with acute AR is not particularly brisk because the acutely depressed LV doesn't eject blood rapidly. The diastolic murmur is shorter in acute AR than in chronic AR, again because LV end-diastolic pressure is higher. The LV becomes more compliant in chronic AR than in acute AR, so an S3 gallop is uncommon in the former and common in the latter.

Table 1. Causes of Aortic Regurgitation in Two Case Series

Cause% of Patients

Mayo Clinic Series (1) (n=225)
Postinflammatory *46
Aortic root dilation21
Bicuspid aortic valve20
Infectious endocarditis9
Associated with a ventricular septal defect2
Massachusetts General
Hospital Series (2) (n=100)
Rheumatic heart disease29
Prior endocarditis18
Active endocarditis8
Marfan syndrome4
Rheumatoid arthritis3
Myxomatous degeneration3
Annuloaortic ectasia **3
Aortic aneurysm2
Old aortic dissection1
Acute aortic dissection1

*Ninety-seven percent of the postinflammatory patients had findings consistent with past rheumatic fever, though only 2% had a clinical history.

**Involves degenerative changes in the aortic wall, usually cystic medial necrosis similar to that found in Marfan syndrome.

The predominant waveforms in the neck are venous pulsations in acute AR and bounding arterial pulses in chronic AR. A patient who has acute AR may appear stable and comfortable at rest but will usually have little cardiac reserve when he or she gets out of bed, even just to use the restroom. Our patient was somewhat atypical in that his pulse pressure was a little wider than one would expect, he did not have an S3 gallop, and the venous and arterial pulses in his neck were not prominent.

Prompt surgery is indicated for patients who have severe acute AR. More than a year after surgery, our patient was asymptomatic, working full-time, and walking briskly. Basketball was discouraged to minimize the risk of anticoagulant-related bleeding. His only limitation is inability to play hide-and-seek with his grandchildren, who can detect the sound of his prosthetic valve.


  1. Olson LJ, Subramanian R, Edwards WD: Surgical pathology of pure aortic insufficiency: a study of 225 cases. Mayo Clin Proc 1984;59(12):835-841
  2. Samuels DA, Curfman GD, Friedlich AL, et al: Valve replacement for aortic regurgitation: long-term follow-up with factors influencing the results. Circulation 1979;60(3):647-654
  3. Chambers JC, Somerville J, Stone S, et al: Pulmonary autograft procedures for aortic valve disease: long-term results of the pioneer series. Circulation 1997;96(7):2206-2214
  4. Perloff JK: Acute severe aortic regurgitation: recognition and management. J Cardiovasc Med 1983;8(2):209-218
  5. Liebson PR: Aortic regurgitation. Cardiol in Practice 1985;2:53-70

Dr Cantwell and Dr Blincoe are cardiologists at Cardiology of Georgia, PC, and Dr Cantwell is a clinical professor of medicine at Morehouse School of Medicine, both in Atlanta. Dr Watson is an internist at the Piedmont Physicians Group in Atlanta. Dr Kauten is a cardiothoracic surgeon at Peachtree Cardiovascular and Thoracic Surgeons and chairman of cardiothoracic surgery at Piedmont Hospital, both in Atlanta. Dr Cantwell is an editorial board member of The Physician and Sportsmedicine. Address correspondence to John D. Cantwell, MD, Cardiology of Georgia, PC, 95 Collier Rd NW, Suite 2075, Atlanta, GA 30309.



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