Atrial fibrillation 50 years after acute rheumatic fever as the first manifestation of rheumatic mitral stenosis D. Luke Glancy, MD
Figure. Electrocardiogram in a dyspneic patient with a history of polyarthritis due to acute rheumatic fever 50 years earlier. See text for explication.
A
56-year-old woman had a history of acute rheumatic fever with polyarthritis at age 6 years. She had been seen intermittently as an outpatient at our hospital over the past 6 years with systemic arterial hypertension, obesity, adult-onset diabetes mellitus, and peptic ulcer disease. All of her electrocardiograms over that period showed left atrial enlargement, and many had large QRS voltage consistent with left ventricular enlargement. She was never told of rheumatic heart disease. On the day of admission, she came to the emergency department with the new onset of palpitations, diaphoresis, and dyspnea. An electrocardiogram showed atrial flutter/fibrillation with an irregular ventricular response at 156 beats/minute, Ashman’s phenomenon, and nonspecific ST-T changes (Figure). 232
The couplet of wide QRSs with right bundle branch block configurations just past the middle of the tracing could have been a couplet of left ventricular premature complexes, but was not followed by a pause and was more likely an example of Ashman’s phenomenon. The first wide QRS followed a short R-R interval that followed a longer R-R interval. The longer interval caused the refractory period after the last narrow QRS to lengthen, and when the next impulse from the atria entered the atrioventricular conduction system early, it was blocked From the Section of Cardiology, Department of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana. Corresponding author: D. Luke Glancy, MD, 1203 West Cherry Hill Loop, Folsom, LA 70437 (e-mail: [email protected]). Proc (Bayl Univ Med Cent) 2017;30(2):232–233
in the right bundle branch, the part of the atrioventricular conduction system with the longest refractory period. The distal part of the right bundle branch was depolarized late, probably by transseptal conduction, and thus was refractory when the next impulse arrived. Even longer runs of aberrant ventricular conduction due to persistent functional refractoriness of the right bundle branch have been misdiagnosed as ventricular tachycardia, an error recognized by Ashman and his colleagues (1). An hour after she arrived in the emergency department, the patient spontaneously reverted to sinus rhythm. With her lying on her left side, a soft opening snap and a low-pitched diastolic murmur of mitral stenosis were heard, as well as a soft murmur of mitral regurgitation. On chest radiograph, the pulmonary arteries and the left atrial appendage were large and produced a straight left heart border. A transthoracic echo-Doppler study demonstrated a dilated left atrium with an anteroposterior diameter of 5.6 cm (reference,
April 2017
1.9–4.0). The other chamber sizes were normal. The thicknesses of the ventricular septum and left ventricular posterior wall (1.2 cm) were just above the upper limit of normal. The mitral valvular leaflets were thick, calcified, and noncompliant. The peak diastolic pressure gradient across the mitral valve was 20 mm Hg with a mean gradient of 9 mm Hg. The mitral valvular orifice area was 0.8 cm2 both by measurement of the two-dimensional image and by the pressure halftime. Left and right ventricular systolic function were normal. Mild mitral and tricuspid regurgitation were noted, and pulmonary arterial systolic pressure was 60 mm Hg (reference, 15–30). Cardiac catheterization confirmed the echocardiographic findings, and coronary arteriography was normal. Mitral valve replacement with a 33 mm St. Jude mechanical prosthesis and the postoperative course were uneventful. 1.
Gouaux JL, Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am Heart J 1947;34(3):366–373.
Atrial fibrillation 50 years after acute rheumatic fever as the first manifestation of rheumatic mitral stenosis
233
Figure. Electrocardiogram in a dyspneic patient with a history of polyarthritis due to acute rheumatic fever 50 years earlier. See text for explication.
A
56-year-old woman had a history of acute rheumatic fever with polyarthritis at age 6 years. She had been seen intermittently as an outpatient at our hospital over the past 6 years with systemic arterial hypertension, obesity, adult-onset diabetes mellitus, and peptic ulcer disease. All of her electrocardiograms over that period showed left atrial enlargement, and many had large QRS voltage consistent with left ventricular enlargement. She was never told of rheumatic heart disease. On the day of admission, she came to the emergency department with the new onset of palpitations, diaphoresis, and dyspnea. An electrocardiogram showed atrial flutter/fibrillation with an irregular ventricular response at 156 beats/minute, Ashman’s phenomenon, and nonspecific ST-T changes (Figure). 232
The couplet of wide QRSs with right bundle branch block configurations just past the middle of the tracing could have been a couplet of left ventricular premature complexes, but was not followed by a pause and was more likely an example of Ashman’s phenomenon. The first wide QRS followed a short R-R interval that followed a longer R-R interval. The longer interval caused the refractory period after the last narrow QRS to lengthen, and when the next impulse from the atria entered the atrioventricular conduction system early, it was blocked From the Section of Cardiology, Department of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana. Corresponding author: D. Luke Glancy, MD, 1203 West Cherry Hill Loop, Folsom, LA 70437 (e-mail: [email protected]). Proc (Bayl Univ Med Cent) 2017;30(2):232–233
in the right bundle branch, the part of the atrioventricular conduction system with the longest refractory period. The distal part of the right bundle branch was depolarized late, probably by transseptal conduction, and thus was refractory when the next impulse arrived. Even longer runs of aberrant ventricular conduction due to persistent functional refractoriness of the right bundle branch have been misdiagnosed as ventricular tachycardia, an error recognized by Ashman and his colleagues (1). An hour after she arrived in the emergency department, the patient spontaneously reverted to sinus rhythm. With her lying on her left side, a soft opening snap and a low-pitched diastolic murmur of mitral stenosis were heard, as well as a soft murmur of mitral regurgitation. On chest radiograph, the pulmonary arteries and the left atrial appendage were large and produced a straight left heart border. A transthoracic echo-Doppler study demonstrated a dilated left atrium with an anteroposterior diameter of 5.6 cm (reference,
April 2017
1.9–4.0). The other chamber sizes were normal. The thicknesses of the ventricular septum and left ventricular posterior wall (1.2 cm) were just above the upper limit of normal. The mitral valvular leaflets were thick, calcified, and noncompliant. The peak diastolic pressure gradient across the mitral valve was 20 mm Hg with a mean gradient of 9 mm Hg. The mitral valvular orifice area was 0.8 cm2 both by measurement of the two-dimensional image and by the pressure halftime. Left and right ventricular systolic function were normal. Mild mitral and tricuspid regurgitation were noted, and pulmonary arterial systolic pressure was 60 mm Hg (reference, 15–30). Cardiac catheterization confirmed the echocardiographic findings, and coronary arteriography was normal. Mitral valve replacement with a 33 mm St. Jude mechanical prosthesis and the postoperative course were uneventful. 1.
Gouaux JL, Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am Heart J 1947;34(3):366–373.
Atrial fibrillation 50 years after acute rheumatic fever as the first manifestation of rheumatic mitral stenosis
233
