Correspondence

Clinical Problem-Solving: Mitral Stenosis — Silent?

N Engl J Med 1996; 334:57-58January 4, 1996

Article

To the Editor:

In his excellent commentary (Clinical Problem-Solving, Sept. 7 issue),1 Dr. Thibault is rightfully surprised that the “mitral stenosis [was] masquerading as pneumonia!” A diagnosis of mitral stenosis could have been made in the emergency room on admission if the physicians had paid more attention to the chest film, because it shows a typical mitral configuration of the heart. There are typical signs of mitralization of the left heart border: the main pulmonary-artery segment is prominent, and the left atrial appendage is bulging. There are also other characteristic signs, including enlargement of the left atrium, a small aortic knob, an enlarged right ventricle, and a normal-sized left ventricle. The superior pulmonary veins are distended, and the inferior pulmonary veins are not easily noticed. Thickened pulmonary septa and Kerley's B lines are visible. The electrocardiogram showing a right-axis deviation is consistent with mitral stenosis in this case. It is understandable that in the noisy atmosphere of an emergency room one might not have been able to hear a diastolic rumble or an accentuated second heart sound, and there was also a marked tachycardia that aggravated the auscultatory interpretation. Always study the classics.

Dushan J. Babich, M.D.
P.O. Box 2577, Southampton, NY 11969

1 References

1. 1

   Thibault GE. Studying the classics. N Engl J Med 1995;333:648-652
   Full Text | Web of Science | Medline

To the Editor:

I greatly enjoyed Dr. Thibault's revisiting the diagnostic problems of mitral stenosis in “Studying the Classics.” The scenario presented is still commonly seen by physicians who care for immigrant populations in which rheumatic fever and its cardiac sequelae remain common. Because these patients have often had poor access to medical care in their native countries as well as in our own, they often present with pulmonary edema in the emergency room rather than with a murmur in a doctor's office. Thus, it is important to be aware of the emergency treatment these patients may require.

Dr. Thibault states that mechanical intervention is the only effective way to improve hemodynamic function in a patient with severe symptoms. Although mechanical intervention is the only definitive therapy, patients in extremis require immediate medical treatment. Beta-blockade may be beneficial and even lifesaving in this situation. As a patient's condition deteriorates and tachycardia ensues, the time for diastole shortens disproportionately more than the time for systole. This means there is less time for blood to flow through the stenotic mitral valve, and the left atrial pressure rises. This causes more distress, greater tachycardia, less time for diastole, and higher left atrial pressure. A vicious circle ensues. If the left ventricular systolic function is normal, then a beta-adrenergic blocking drug can be administered and the circle can be reversed.1 This therapy is effective regardless of whether the patient is in sinus rhythm or has atrial fibrillation. I have seen several patients respond dramatically to this treatment, and this allowed them to be stabilized before mitral-valve replacement.

David W. Baker, M.D., M.P.H.
Emory University School of Medicine, Atlanta, GA 30303

1 References

1. 1

   Gaasch WH, Rourke RA, Cohn LH, Rackley CE. Mitral valve disease. In: Schlant RC, Alexander RW, eds. The heart: arteries and veins. 8th ed. New York: McGraw-Hill, 1994:1489.
   

To the Editor:

We were surprised to read Dr. Thibault's assertion that the patient's fever might have been due to pulmonary edema. Among the 50 patients with congestive heart failure described by Elster et al. in 1956,1 fever was a common finding in the initial stage, with 14 patients having temperatures as high as 101°F and 11 patients as high as 102°F. More than 30 years later, however, Braunwald stated that a low-grade temperature (<38°C) resulting from cutaneous vasoconstriction may occur in severe heart failure but that greater elevations of temperature usually signify the presence of infection, pulmonary infarction, or infective endocarditis.2 Haber et al.3 were able to evaluate 242 afebrile patients with chronic heart failure seen during a period of 12 months at a single hospital, and 50 percent of them had normal erythrocyte sedimentation rates with a mean pulmonary wedge pressure of 26 mm Hg.

In our clinical experience, we have not found cardiogenic pulmonary edema in itself to be a plausible cause of fever, and we do not envision a pathophysiologic mechanism for it. Fever in a patient with heart failure demands a search for a reason other than pulmonary edema.

Basilio J. Anía, M.D.
Juan Morales, M.D.
Hospital Nuestra Señora del Pino

María-Teresa Martínez, M.D.
Centro de Salud de San Gregorio, Las Palmas, Canary Islands, Spain

3 References

1. 1

   Elster SK, Braunwald E, Wood HF. A study of C-reactive protein in the serum of patients with congestive heart failure. Am Heart J 1956;51:533-541
   CrossRef | Web of Science | Medline

2. 2

   Clinical manifestations of heart failure. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine. 3rd ed. Vol. 1. Philadelphia: W.B. Saunders, 1988:471-84.
   

3. 3

   Haber HL, Leavy JA, Kessler PD, Kukin ML, Gottlieb SS, Packer M. The erythrocyte sedimentation rate in congestive heart failure. N Engl J Med 1991;324:353-358
   Full Text | Web of Science | Medline

Author/Editor Response

Dr. Thibault replies:

To the Editor: Dr. Babich correctly points out that there were a number of diagnostic clues in this case (particularly the chest film and electrocardiogram) that should have suggested mitral stenosis to the clinicians even if they did not hear a murmur. Dr. Baker quite appropriately stresses the therapeutic benefits of beta-blockade in treating patients with mitral stenosis if their rising left atrial pressure is related to tachyarrhythmias. In the face of critical mitral stenosis, however, beta-blockade is only a temporizing measure; mechanical intervention is still necessary to improve cardiac output and definitively lower left atrial pressure. Some patients with less critical mitral stenosis who are only symptomatic during tachyarrhythmias may have the need for mechanical intervention postponed by the appropriate use of beta-blockade. Anía et al. raise a long-standing clinical question about whether cardiogenic pulmonary edema may be the cause of fever. I agree with their conclusion that anything other than a very low grade fever (<38°C) should not be attributed to cardiogenic pulmonary edema, and an infection or inflammatory cause must be sought. This case demonstrated the other side of that coin: just because a patient has fever and possible infection does not mean that that explains the whole clinical picture.

George E. Thibault, M.D.
Brigham and Women's Hospital, Boston, MA 02115

Citing Articles (1)

Citing Articles

1. 1

   Gatzoulis, Michael A., Freeman, Marc A.Siu, Samuel C., Webb, Gary D., Harris, Louise, . (1999) Atrial Arrhythmia after Surgical Closure of Atrial Septal Defects in Adults. New England Journal of Medicine 340:11, 839-846
   Full Text