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Calcium emboli to the retinal artery in calcific aortic stenosis
Calcium emboli aortic stenosis
to the retinal
it is not generally appreciated in the cardiovascular literature that calcium emboli to a central retinal artery or its branches may be the presenting feature of otherwise uncomplicated calcific aortic stenosis. The ophthalmologic literature provides good evidence for this point. Over a 7-month period, four such cases have come to our attention. Other potential sources of emboli were excluded by standard noninvasive and invasive diagnostic techniques, and two patients underwent successful aortic valve replacement. Previous studies of calcific aortic stenosis have demonstrated postmortem histologic evidence of calcium emboli to various organs, for example, heart, kidney, or brain. Since these emboli are small, their occurrence is clinically silent. The retinal circulation is unique in that its occlusion by a calcium microembolus results in loss of vision, and this symptom may be a clue to the presence of catcific aortic stenosis. (AM HEART J 101:32, 1931.)
Louis B. Brockmeier, M.D., Robert J. Adolph, M.D., Byron John C. Holmes, M.D., and Joel G. Sacks, M.D., Cirtcinnati,
Abrupt occlusion of the central retinal artery by embolus, thrombus, or spasm is a clinical entity well known to ophthalmologists and well documented in the ophthalmologic literature.‘-” Typically, patients with this syndrome present with abrupt loss of all or part of the visual field in one eye. The funduscopic findings in such cases are well documented and quite specific.‘-j If the visual loss is fleeting, the term ‘“amaurosis fugax” is applied to the syndrome.G If the visual deficit persists beyond a day, retinal infarction is presumed to have occurred. The usual conditions associated with occlusion of the central retinal artery include hypertension, diabetes mellitus, diffuse arteriosclerosis, arteritis, and localized extracranial cerebrovascular atherosclerotic disease. However, the association of retinal artery occlusion with valvular heart disease is well documented; in several reported series, 0.5% to 33% of cases of retinal artery occlusion were associated with valvular heart disease.le7 Emboli from the heart to the systemic circulation have been shown to arise from the left atrium, mitral valve apparatus, left ventricular mural thrombus, cardiac myxoma, or vegetations associated with infective or marantic endocarditis. The From the Division of Cardiology, the Department of Ophthalmology, Cincinnati. Received Reprint College 45267.
32
for publication
July
Department College 3, 1980;
of Internal of Medicine,
accepted
Sept.
requests: Robert J. Adolph, M.D., University of Medicine, MSB 3354, 231 Bethesda Ave.,
Medicine, University 16, 1980.
of Cincinnati Cincinnati, OH
and of
W. Gustin, Ohio
M.D.,
uncomplicated calcified aortic valve is not usually considered by cardiologists to be a source of spontaneous systemic emboli.“-” During aortic valve surgery, calcific emboli can be a problem,“. I3 but spontaneous, clinically important calcific embolization from the aortic valve is probably a rare event. In reviewing the clinical and routine postmortem findings of 1500 cases of typical calcific aortic stenosis, we could find no mention of this problem.‘“, II. 14-26 However, in 1961, Hollenhorst”’ described finding “an irregular, extremely white body unaccompanied by orange-yellow plaques” in the retinas of three patients with radiologically proved calcification of the aortic valve. Van Graefe,Z” in 1859, had previously described a case of retinal artery occlusion associated with calcific aortic valve disease. Holley et al.‘y and Soulie et al.:‘O both applied special radiologic techniques to study postmortem cases of calcific aortic stenosis and found calcific emboli in 19% and 28% of their cases, respectively. These emboli were found most frequently in the heart, kidney, or brain, and all had been clinically silent. In only one of these 230 cases (0.4%) was a calcific microembolus found in a retinal artery. In 1970, Baghdassarian et a1.31reported a case with autopsy-proved occlusion of the retinal artery by a calcific mass in a patient with rheumatic mitral valve disease. In 1968, Catelli”’ briefly described two patients with retinal emboli associated only with calcific aortic stenosis, but angiographic and echocardiographic studies were not performed. Penner and Font,3” in 1969, presented
0002-8703/81/010032
+ 06$00.60/O
0 1981
The
C. V. MO&
co.
Volume Number
Calcium
101 1
emboli
in aortic
stenosis
33
convincing postmortem evidence that a calcific embolism can arise from a calcified aortic valve. Thus, although the association between calcific microemboli to thee retina and valvular heart disease is secure, there has been no careful documentation of clinical and laboratory cardiac findings to show that a calcified aortic valve can be the sou.rce of retinal emboli in the absence off coexistent mitral valve disease and where diagnosis and trea.tment have been undertaken before death. Over a ‘i-month period, four such cases have come to our attention from the practices of three cardiologists. The emboli had occurred over a 4-year period in these patients. They were all examined by at least one of us and studied with standard M-mode echocardiographic niques. Two
and
cardiac
catheterization
tech-
had/ surgical confirmation that their sudden loss of vision was associated only with disease of the aortic valve. MATERIALS
AND RESULTS
Case 1. A 40-yiear-old white man suddenly lost the ability to see objects in the upper haIf of the visual field of the left eye. He gave a questionable history of rheumatic fever at age 14 and had been aware of a heart murmur since age 22. He had no cardiac symptoms and was neither hypertensive nor diabetic. Blood pressure was 120/90 and the pulse was regular. When he was seen by one of us, the left ocular fundus showed a large, irregular, white retinal infarct (Fig. l), with adjacent small flame hemorrhages. The carotid upstroke was slightly delayed. A systolic thrill was palpable at the base of the heart and over both carotids. Typical t,o-and-fro murmurs of aortic stenosis and insufficiency were present at the cardiac base. No mitral murmurs were heard. The electrocardiogram showed left ventricular hypertrophy and sinus rhythm. The heart size was normal on a standard chest roentgenogram. The M-mode echocardiogram showed thickened aortic valve, normal mitral valve, and concentric left ventricular hypertrophy. Bilateral selective carotid arteriograms were normal. Cardiac catheterization and angiocardiography revealed a peak systolic gradient of 50 mm Hg across the aortic valve, minimal aortic insufficiency, and normal left ventricular functi’on. No akinetic segments or filling defects were present on the left ventriculogram. At operation, the aortic valve was bicuspid and fibrotic with moderate calcification (Fig. 2). It was replaced with a porcine heterograft. The mitral valve and annulus were grossly normal at operation. Microscopic sections of the excised aortic valve showed fibrin and calcium with no organisms. During a l7-month follow-up, the vision in the left eye improved to normal, and no further embolic episodes occurred. Case 2. A 56-year-old white woman lost vision in her right eye. An ophthalmologist diagnosed occlusion of the
Fig. 1. Photograph of the left fundus in case 1, taken 7 days after the onset of visual symptoms, showing a wedge-shaped infarction of the nerve fiber layer of the retina (arrow). The arteriolar occlusion is probably at the
disc margin, obscuredby edema. central retinal artery, but no fundus photographs were taken and no cardiac evaluation was performed. She had known of a heart murmur since a bout of rheumatic fever at the age of 9 years. At age 60 she underwent cardiac evaluation because of exertional dyspnea. There had been no further embolic episodes. She was not hypertensive or diabetic. Blood pressure was 130/85. The carotid upstroke was delayed. A loud, harsh murmur typical of aortic stenosis was maximal along the left sternal border and radiated equally to both carotid arteries. There was no separate carotid bruit. An atria1 gallop was felt and heard. Neither aortic insufficiency nor mitral murmurs were present. A chest roentgenogram revealed generalized cardiac enlargement. The electrocardiogram showed sinus rhythm and left ventricular hypertrophy. An M-mode echocardiogram showed thickened aortic valve leaflets but a normal mitral valve. Cardiac catheterization and angiocardiography revealed mild resting pulmonary hypertension but no transmitral diastolic gradient. The left ventricular end diastolic pressure was 21 mm Hg. The peak systolic gradient across the aortic valve was 130 mm Hg. Three-plus aortic insufficiency was seen on aortogram. The cardiac index was 2.26 L/min/m’. The left ventriculogram showed no akinetic areas or filling defects. At surgery the aortic valve was bicuspid and heavily calcified, with no gross evidence of active infection. The mitral valve and annulus were grossly normal. The aortic valve was replaced with a Bjork-Shiley prosthesis. During a 5-month follow-up there have been no embolic episodes. The patient is being maintained on warfarin anticoagulation. Case 3. A heart murmur was discovered in a 60-year-old
Brockmeier
et al.
Excised aortic valve from case 1 showing moderately heavy deposits of calcium, one was extremely friable and had a vegetative appearance. Microscopic sections of this excrescence showed no evidence of infection. Lower panel: Roentgenogram of the specimen shown in the upper panel showing the calcific nature of the deposits seen in the upper panel, especially the friable excrescence (arrow) thought to be the source of the calcium embolus. Fig. 2. Upperpanel: of which (arrow)
white woman. At age 64, she suddenly lost sight of objects in the superior visual field of the right eye. An ophthalmologist diagnosed embohc occlusion of a branch of the central retinal artery; a white calcific embolus was seen. No fundus photographs were taken. Bilateral selective carotid arteriograms were normal. She denied all cardiac symptoms. There was no history of rheumatic fever, hypertension, or diabetes mellitus. Blood pressure was 134/70. The carotid upstroke was slightly delayed with an anacrotic shoulder. A left ventricular heave was present with an audible and palpable atriai gallop. A long, barsh, ejection systolic murmur was maximal in the aortic area. A soft murmur of aortic insufficiency was present. There were no carotid bruits. Chest roentgenograms showed a normal-sized heart with poststenotic aortic dilatation. The electrocardiogram showed sinus rhythm and left ventricular hypertrophy. An M-mode echocardiogram showed thickened aortic cusps but a normal mitral valve. No mitral annular calcification, valvular vegetations, or left atria1 myxoma were noted. Cardiac fluoroscopy revealed moderate aortic valvular calcification. Cardiac catheterization revealed normal right heart pressures with a peak transaortic systolic gradient of 45 mm Hg. There was no transmitral diastolic gradient. The left ventriculogram showed no akinetic areas, filling defects, or mitral insufficiency. Surgery was not performed and over a 7-month follow-up there have been no further embolic episodes She is receiving no medical therapy. She still cannot see objects in the upper visual field of her right eye.
Case 4. A 56-year-old white woman suddenly lost sight in her left eye. She had known of a heart murmur since age 20 but had never had rheumatic fever. After several days, her vision improved until she was left with permanent loss of the upper visual field in the left eye. Retinal photographs showed a pure white body in a branch of the central retinal artery (Fig. 3). Bilateral selective carotid arteriograms were normal. She was not hypertensive or diabetic and had no cardiac symptoms. Blood pressure was 118/76. The carotid upstroke was normal. A loud harsh ejection systolic murmur was maximal in the aortic area and radiated widely to the carotid arteries. There was no diastolic murmur. The electrocardiogram and chest roentgenograms were normal. Cardiac fluoroscopy showed moderate calcification of the aortic valve leaflets but none in the mitral valve or annulus. An M-mode echocardiogram showed thickened aortic vaive cusps with a normal mitral valve. No evidence of atria1 myxoma, valvular vegetations, or mitral annular calcification was seen. Cardiac catheterization and surgery were not performed. Through a 4-year follow-up there have been no further embohc episodes and no cardiac symptoms. Direct anatomic confirmation that the visual symptoms of these patients were caused by calcific microemboli is impossible because the involved eye was not available for pathologic examination. However, because of previous isolated case reports describing the historic and ophthalmoscopic findings in cases where anatomic analysis was possible,“‘. ” we feel confident that these cases do represent true calcific microemboli to the retina from calcified
Volume
101
Number
1
Calcium
emboli
in aortic
stenosis
35
aortic valves. The nlormal carotid arteriograms in three of
the casesserve to exclude the carotid artery asthe source of the emboli. DISCUSSION
Calcification of the aortic valve occurs in a variety of congenital and acquired cardiac diseases. Ordinarily, this calcification assumesclinical importance only by restricting the motion of the valve cusps, reducing the valve orifice area, and causing progressive aortic stenosi;s.The obstruction to left ventricular outflow eventually leads to hypertrophy of the left ventricle and failure to increase cardiac output adequately during exercise. This latter phenomenon, ventricular arrhythmias, reflex vasodilatation, and hypersensitive carotid sinus have been hypothesized to explain the occurrence of effort-related syncope and near-syncope in patients with aortic stenosis.1”.I*. 31In younger patients with noncalcific aortic stenosis (which is usually congenital), these mechanisms may well be operative. However, in older patients the heavy deposits of calcium on the aortic valve leaflets deformed by rheumatic valvulitis, infective endocarditis, or congenital anomalies of the cusps can acquire a vegetative appearance. At times these sterile calcific vegetations can be quite friable and small flecks of calcium can be released into the systemic circulation spontaneously or as a result of cardiac catheterization o,r aortic valvotomy or replacement.‘“, 28.35 Traditional teaching has held .that the three cardinal symptoms of calcific aortic stenosis are angina pectoris, syncope, or congestive heart failure.‘“, ‘I The occurrence of any of these symptoms in a patient with a typical basal systolic murmur and an aortic valve area of 1.0 cm’ or less would prompt most physicians to recommend replacement of the aortic valve in otherwise suitable candidates. Prevalence. We would like to suggest that there is another mode of presentation in calcific aortic stenosis-one that is usually independent of the hemodynamic severity of the lesion but which is seen only with moderate or heavy calcification of the aortic valve cusps. The spontaneous embolization of a fleck of calcific debris to a central retinal artery leading to abrupt, loss of vision in either eye and a white spot visible on ophthalmoscopic examination can be the initial presentation of calcific aortic stenosis in a middle-aged or elderly patient. The loss of vision may be partial or complete, temporary or permanent. In our experience it is certainly not a rare complication, and its significance is not generally appreciated in the cardiologic literature. It probably occurs relatively infrequently, but it can be a
Fig. 3. Photograph of the left fundus in case4, taken a
few days after the onset of visual symptoms, showing an embolus(small arrow) in the inferior temporal artery. A collateral vessel(large arrow) suppliesthe arteriole distal to the obstruction.
most disturbing symptom. Perhaps calcific microemboli lodging in arteries elsewhere in the central nervous system play a role in producing the episodes of dizziness or transient focal neurologic deficits that occur so commonly in patients with aortic stenosis.“-” The available literature on this subject is scanty, and further clinical observations on this point would be of value. Mechanism. Calcific microemboli have been shown rather conclusively to be the cause of focal retinal ischemia and infarction.“‘, ” What is not so clear from the available literature is whether larger calcific emboli can cause significant cerebral cortical or brainstem ischemia or infarction and result in significant disabling stroke. Our literature review and our two cases in which no operation was performed suggest that this is not a likely occurrence, at least during our short period of follow-up in four patients. We could find no reports of significant hemispheric or brainstem strokes attributed to calcific emboli from the aortic valve. Presumably, this is because the emboli found at postmortem examination in these patients are small, ranging from 0.1 to 6 mm in size.‘9 Since the size of the central retinal artery is small (approximately 0.28 mm in diameter),“” it is clear why such a small embolus can produce such a dramatic clinical picture only if it lodges in this particular artery. Diagnosis. A calcium microembolus to the retinal artery can only be proved by anatomic confirma-
6
Bmckmeier
et al. merican
tlon,
that
is, after
enucleation
sf the
eye
or
at
postmortem examination.“’ However, if a typical calcium embolus (Fig. 3) is seen in the affected eye and the aortic valve is calcified, a presumptive diagnosis can be made. If a calcium embolus is seen on ophthalmoscopic examination and if the carotid arteries show atheromas by physical examination, angiography, or postmortem examination, it is difficult to be certain whether the retinal embolus originated from the calcified aortic valve or from the atheromatous carotid artery. The diagnostic distinction between the ophthalmoscopic appearance of a calcium embolus and a cholesterol embolus may be possible if the symptomatic patient first presents to an ophthalmologist.“’ The ophthalmoscopic differentiation may be more difficult for the internist or cardiologist. Therapy. Management of tbis syndrome must remain speculative. The paucity of natural history data may make it seem more benign than it is. The calcific retinal arterial emboli may be recurrent and bilateral”‘; if so, valve replacement must surely be warranted because therapy with anticoagulants or antiplatelet drugs would have no known rational basis. If the emboli are composed in part of platelets or fibrin, either class of agent could be useful, however. Our two patients who did not undergo surgery and two from the literature’ have not had recurrent emboli during follow-ups of 3 months to 13 years. During this time, they have received no medical therapy. Conclusions. Our current approach to patients with embolic visual problems and aortic valvular calcification by fluoroscopy is to perform carotid arteriography first to exclude carotid atheromas as a source of retinal emboh6 If a typical carotid lesion is seen, we could recommend carotid endarterectomy. We have not yet encountered such a case. If the carotid arteries appear normal, and echocardiography shows no evidence of intracardiac masses or vegetations, cardiac catheterization is carried out even in the absence of cardiac symptoms. It is our policy to recommend valve replacement if the calculated aortic valve area is 1.0 cm’ or less,if there is no mitral valve involvement, and if left ventriculography shows no source of emboli. If the stenosis is not that severe and cardiac symptoms are absent, careful observation, supplemented perhaps with antiplatelet drugs, seemsthe more prudent course, with valve replacement recommended only for recurrent or bilateral symptomatic retinal emboli.
Buerk Fowler
who performed the who examined the Poon and Kenneth
cases 2 and 3, respectively, the manuscript.
Jowmai
and Dr. Noble
0.
REFERENCES
1. 2.
3.
4. 5. 6.
7. 8.
9. 10. 11. 12.
13.
14.
15. 16.
Appen RE, Wray SH, Cogan DG: Central retina1 artery occlusion. Am J Ophthalmol79:374, 1975. Liversedae LA. Smith VH: Neuromedical and onhthah~ic aspects of central retinal artery occlusions. Trans Qphthalmol Sot UK 82:571, 1962. Karjalainen K: Occlusion of the central retinal artery and retinal branch arterioles. Acta Ophthalmol (suppl) 109:9, 197:. Ellis CJ, Hamer DB, Hunt RW, et al: Medical investigations of retinal vascular occlusion. Br Med J 2:1093, 1964. Russell R: The source of retinal emboli. Lancet 2:789, 1968. Hooshmand H, Vines FS, Lee HM, Grindal A: Amaurosis fugax: Diagnostic and therapeutic aspects. Stroke 5:643, 1974. Coates G: Obstruction of the central artery of the retina. Royal Lond Ophthalmol Hosp l&262, 1905: Dalev R. Mattinelv TW. Holt CL. Bland EF. White PD: Systemic arterialembolism in rheumatic heart disease. A~x HEART J 42:566, 1951. Hutchinson EC, Stock JPP: Paroxysmal cerebral &hernia in rheumatic heart disease. Lancet 2:653, 1963. McGinn S, White PD: Clinical observations on-aortic stenosis. Am J Med Sci 188:1, 1934. Wood P: Aortic stenosis. Am J Cardiol 1:553, 1958. Larmi TKI, Karkola P, Kairaluoma MI, Sutinen S, Partanen-Talsta A: Calcium microemboli and microfilters in valve operations. Ann Thorac Surg 24:34, 1977. Hollev KE. Bahn RC. McGoon DC. Mankin HT: Calcific embohzation associated with valvotomy for calcific aortic stenosis. Circulation 28:175, 1963. Kumpe CW, Bean WB: Aortic stenosis: A study of the clinical and pathologic aspects of 107 proved cases. Medicine 27339, 1948. Roberts WC: The structure of the aortic vaive in clinically isolated aortic stenosis. Circulation 42:91, 1970. Contratto AW, Levine SA: Aortic stenosis with special reference to angina pectoris and syncope. Ann Intern Med 10:1636,
17. 18.
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20. 21. 22. 23. 24. 25. 26. 27. 28.
We are grateful to Dr. John B. Flege surgery in case 1, Johanna van der Bel-Kahn pathologic specimen in case 1, Drs. James
who examined who reviewed
t4earl
29.
1937.
Dry TJ, Willius FA: Calcareous disease of the aortic valve. AM HEART J 17:138, 1939. Marvin HM, Sullivan AG: Clinical observations upon syncope and sudden death in relation to aortic stenosis. AM HEART J l&705, 1934. Roberts WC, Perloff JK, Constantino T: Severe valvuiar aortic stenosis in patients over 65 years of age. Am J Cardiol 27:497, 1971. Friedberg CK, Sohval AR: Nonrheumatic calcific aortic stenosis. AM HEART J 17:452, 1939. Clawson BJ, Noble JF, Lufkin NH: The calcified nodular deformity of the aortic valve. AM HEART J 15:58, 1938. Sophian LH: Calcific aortic valvular stenosis. Am J Med Sci 210:644, 1945. Reich NE: Calcitlc aortic valve stenosis: A ciinicopathologic correlation of 22 cases. Ann Intern Med 22:234, 1945. Margolis HM, Ziellessen FO, Barnes AR: Calcareous aortic valvular disease. AM HEART J 6:349, 1931. Christian HA: Aortic stenosis with calcification of the cusps. JAMA 97:158, 1931. Campbell M: The natural history of congenital aortic stenosis. Br Heart J 30:514, 1968. Hollenhorst RW: Significance of bright plaques in the retinal arteries. JAMA 178:23, 1961. Von Graefe A: Veber embolie der arteria centralis retinal als ursache plotzlicher erblindung. Von Graefe’s Arch Ophthalmol 5:136, 1859. Holley KE, Bahn RC, McGoon DC, Mankin HT: Sponta-
Cakium
Volume101 Number1
30.
31.
32.
neous calcific embolization associated with calcific aortic stenosis. Circulation 27:197, 1963. Souli P, Caramanian M, Souli J, Bader JC, Colcher E: Les embolies calcaires des orificielles calcifees du coeur gauche. Arch Ma1 Coeur 162:1657, 1969. Baghdassarian SA, Crawford JB, Rathbun JE: Calcific emboli of the retinal and ciliary arteries. Am J Ophthalmol 69:372, 1970. Catelli P: Stenosi aortica valvolare calcifica ed embolie retiniche. Cardiol Prat 19:303, 1968.
33. 34. 35.
36.
emboli
in aortic
stenosis
37
Penner R, Font RL: Retinal embolism from calcified vegetations of aortic valve. Arch Ophthalmol81:565, 1969. Hammarsten J: Syncope in aortic stenosis. Arch Intern Med 87:274, 1951. Yacoub MH, Lise M, Balcon R: Total occlusion of the left femoral artery by a calcium embolus from a heavily calcified aortic valve. Am J Cardiol 25:359, 1970. Henle, J., cited in Warwick R: Eugene Wolfe’s anatomy of the eye and orbit, ed 7. Philadelphia, 1976, WB Saunders Co, p 145.
M-mode echocardiographic observations during and after healing of active bacterial endocarditis limited to the mitral valve Analysis of 99 M-mode echocardiograms recorded during and up to 144 months after healing of active bacterial endocarditis limited to the mitral valve in 27 patients disclosed the following: (1) Little to no change occurred in the echocardiographic size of the vegetations during the first 6 weeks after diagnosis and institution of appropriate antibiotic therapy unless a major systemic embolus occurred. (2) The echocardiographic size of the vegetations did not determine the amount of cardiac damage or dysfunction produced by the valvular infection. (3) The larger the vegetations by echocardiogram, the greater was the likelihood of a clinical event compatible with a systemic embolus. (4) The gravest prognostic sign yielded by the echocardiogram was evidence of rupture of chordae tendineae. (5) Although a useful adjjunct to diagnosis before appropriate antibiotic therapy was instituted, once bacter.iologic cure was achieved, the echocardiogram was of limited value in delineating an active from a healed vegetation. l(6) The echocardiographic appearance of the vegetations was not determined by the type of infecting Ibacterium. (AM HEART J 101:37, 1981.)
Mazhar U. Sheikh, M.D., Edgar A. Covarrubias, M.D., Nayab Ali, M.D., Won Ro Lee, M.D., Nasreen M. Sheikh, M.D., and William C. Roberts, M.D. Bethesda, Md., and Washington, D.C.
Since 1972, many reports have described echocardiographic features of vegetations in one or more cardiac valves.‘-3 Most reports have described the echocardiographic features during the period of active infection, and few studies, are available describing long-term follow-up by serial echocardiograms in patients with active infective endocarditis. Recently, Stafforld et al.” described serial echocardiographic observations up to 10 months in two
METHODS Patients. Satisfactory echocardiogramswere performed
From the Section of Cardiology, Medical Divisions, Columbia General Branch, National of Health, Bethesda. Received
Georgetown and Howard University and the Department of Pathology, District of Hospital, Washington, D.C., and the Pathology Heart, Lung, and Blood Institute, National Institutes
for publication
Reprint requests: Medical Division, DC 20003.
0002-8703/81/010037
Mazhar District
Sept.
3, 1980;
accepted
Sept.
U. Sheikh, of Columbia
M.D., Georgetown General Hospital,
+ 09$00.90/O
0 1981 The
in 68 patients hospitalized at the DC. General Hospital from 1975through 1979with active infective endocarditis; 27 (40%)had evidenceof bacterial endocarditis limited to the mitral valve. Clinical findings in these 27 patients are listed in Table I. Among the 27 patients, 31 episodesof active infective endocarditis were documented. During eachactive episode,each patient had a precordial murmur
17, 1980. University Washington,
C. V. Mosby
patients, and Stewart et a1.j reported similar observations in 12 patients up to 30 months, both groups with active infective endocarditis limited to the mitral valve. Because of the sparsity of serial echocardiographic information in patients with active infective endocarditis limited to the mitral valve, echocardiographic findings were analyzed in 27 such patients.
Co.
to the retinal
it is not generally appreciated in the cardiovascular literature that calcium emboli to a central retinal artery or its branches may be the presenting feature of otherwise uncomplicated calcific aortic stenosis. The ophthalmologic literature provides good evidence for this point. Over a 7-month period, four such cases have come to our attention. Other potential sources of emboli were excluded by standard noninvasive and invasive diagnostic techniques, and two patients underwent successful aortic valve replacement. Previous studies of calcific aortic stenosis have demonstrated postmortem histologic evidence of calcium emboli to various organs, for example, heart, kidney, or brain. Since these emboli are small, their occurrence is clinically silent. The retinal circulation is unique in that its occlusion by a calcium microembolus results in loss of vision, and this symptom may be a clue to the presence of catcific aortic stenosis. (AM HEART J 101:32, 1931.)
Louis B. Brockmeier, M.D., Robert J. Adolph, M.D., Byron John C. Holmes, M.D., and Joel G. Sacks, M.D., Cirtcinnati,
Abrupt occlusion of the central retinal artery by embolus, thrombus, or spasm is a clinical entity well known to ophthalmologists and well documented in the ophthalmologic literature.‘-” Typically, patients with this syndrome present with abrupt loss of all or part of the visual field in one eye. The funduscopic findings in such cases are well documented and quite specific.‘-j If the visual loss is fleeting, the term ‘“amaurosis fugax” is applied to the syndrome.G If the visual deficit persists beyond a day, retinal infarction is presumed to have occurred. The usual conditions associated with occlusion of the central retinal artery include hypertension, diabetes mellitus, diffuse arteriosclerosis, arteritis, and localized extracranial cerebrovascular atherosclerotic disease. However, the association of retinal artery occlusion with valvular heart disease is well documented; in several reported series, 0.5% to 33% of cases of retinal artery occlusion were associated with valvular heart disease.le7 Emboli from the heart to the systemic circulation have been shown to arise from the left atrium, mitral valve apparatus, left ventricular mural thrombus, cardiac myxoma, or vegetations associated with infective or marantic endocarditis. The From the Division of Cardiology, the Department of Ophthalmology, Cincinnati. Received Reprint College 45267.
32
for publication
July
Department College 3, 1980;
of Internal of Medicine,
accepted
Sept.
requests: Robert J. Adolph, M.D., University of Medicine, MSB 3354, 231 Bethesda Ave.,
Medicine, University 16, 1980.
of Cincinnati Cincinnati, OH
and of
W. Gustin, Ohio
M.D.,
uncomplicated calcified aortic valve is not usually considered by cardiologists to be a source of spontaneous systemic emboli.“-” During aortic valve surgery, calcific emboli can be a problem,“. I3 but spontaneous, clinically important calcific embolization from the aortic valve is probably a rare event. In reviewing the clinical and routine postmortem findings of 1500 cases of typical calcific aortic stenosis, we could find no mention of this problem.‘“, II. 14-26 However, in 1961, Hollenhorst”’ described finding “an irregular, extremely white body unaccompanied by orange-yellow plaques” in the retinas of three patients with radiologically proved calcification of the aortic valve. Van Graefe,Z” in 1859, had previously described a case of retinal artery occlusion associated with calcific aortic valve disease. Holley et al.‘y and Soulie et al.:‘O both applied special radiologic techniques to study postmortem cases of calcific aortic stenosis and found calcific emboli in 19% and 28% of their cases, respectively. These emboli were found most frequently in the heart, kidney, or brain, and all had been clinically silent. In only one of these 230 cases (0.4%) was a calcific microembolus found in a retinal artery. In 1970, Baghdassarian et a1.31reported a case with autopsy-proved occlusion of the retinal artery by a calcific mass in a patient with rheumatic mitral valve disease. In 1968, Catelli”’ briefly described two patients with retinal emboli associated only with calcific aortic stenosis, but angiographic and echocardiographic studies were not performed. Penner and Font,3” in 1969, presented
0002-8703/81/010032
+ 06$00.60/O
0 1981
The
C. V. MO&
co.
Volume Number
Calcium
101 1
emboli
in aortic
stenosis
33
convincing postmortem evidence that a calcific embolism can arise from a calcified aortic valve. Thus, although the association between calcific microemboli to thee retina and valvular heart disease is secure, there has been no careful documentation of clinical and laboratory cardiac findings to show that a calcified aortic valve can be the sou.rce of retinal emboli in the absence off coexistent mitral valve disease and where diagnosis and trea.tment have been undertaken before death. Over a ‘i-month period, four such cases have come to our attention from the practices of three cardiologists. The emboli had occurred over a 4-year period in these patients. They were all examined by at least one of us and studied with standard M-mode echocardiographic niques. Two
and
cardiac
catheterization
tech-
had/ surgical confirmation that their sudden loss of vision was associated only with disease of the aortic valve. MATERIALS
AND RESULTS
Case 1. A 40-yiear-old white man suddenly lost the ability to see objects in the upper haIf of the visual field of the left eye. He gave a questionable history of rheumatic fever at age 14 and had been aware of a heart murmur since age 22. He had no cardiac symptoms and was neither hypertensive nor diabetic. Blood pressure was 120/90 and the pulse was regular. When he was seen by one of us, the left ocular fundus showed a large, irregular, white retinal infarct (Fig. l), with adjacent small flame hemorrhages. The carotid upstroke was slightly delayed. A systolic thrill was palpable at the base of the heart and over both carotids. Typical t,o-and-fro murmurs of aortic stenosis and insufficiency were present at the cardiac base. No mitral murmurs were heard. The electrocardiogram showed left ventricular hypertrophy and sinus rhythm. The heart size was normal on a standard chest roentgenogram. The M-mode echocardiogram showed thickened aortic valve, normal mitral valve, and concentric left ventricular hypertrophy. Bilateral selective carotid arteriograms were normal. Cardiac catheterization and angiocardiography revealed a peak systolic gradient of 50 mm Hg across the aortic valve, minimal aortic insufficiency, and normal left ventricular functi’on. No akinetic segments or filling defects were present on the left ventriculogram. At operation, the aortic valve was bicuspid and fibrotic with moderate calcification (Fig. 2). It was replaced with a porcine heterograft. The mitral valve and annulus were grossly normal at operation. Microscopic sections of the excised aortic valve showed fibrin and calcium with no organisms. During a l7-month follow-up, the vision in the left eye improved to normal, and no further embolic episodes occurred. Case 2. A 56-year-old white woman lost vision in her right eye. An ophthalmologist diagnosed occlusion of the
Fig. 1. Photograph of the left fundus in case 1, taken 7 days after the onset of visual symptoms, showing a wedge-shaped infarction of the nerve fiber layer of the retina (arrow). The arteriolar occlusion is probably at the
disc margin, obscuredby edema. central retinal artery, but no fundus photographs were taken and no cardiac evaluation was performed. She had known of a heart murmur since a bout of rheumatic fever at the age of 9 years. At age 60 she underwent cardiac evaluation because of exertional dyspnea. There had been no further embolic episodes. She was not hypertensive or diabetic. Blood pressure was 130/85. The carotid upstroke was delayed. A loud, harsh murmur typical of aortic stenosis was maximal along the left sternal border and radiated equally to both carotid arteries. There was no separate carotid bruit. An atria1 gallop was felt and heard. Neither aortic insufficiency nor mitral murmurs were present. A chest roentgenogram revealed generalized cardiac enlargement. The electrocardiogram showed sinus rhythm and left ventricular hypertrophy. An M-mode echocardiogram showed thickened aortic valve leaflets but a normal mitral valve. Cardiac catheterization and angiocardiography revealed mild resting pulmonary hypertension but no transmitral diastolic gradient. The left ventricular end diastolic pressure was 21 mm Hg. The peak systolic gradient across the aortic valve was 130 mm Hg. Three-plus aortic insufficiency was seen on aortogram. The cardiac index was 2.26 L/min/m’. The left ventriculogram showed no akinetic areas or filling defects. At surgery the aortic valve was bicuspid and heavily calcified, with no gross evidence of active infection. The mitral valve and annulus were grossly normal. The aortic valve was replaced with a Bjork-Shiley prosthesis. During a 5-month follow-up there have been no embolic episodes. The patient is being maintained on warfarin anticoagulation. Case 3. A heart murmur was discovered in a 60-year-old
Brockmeier
et al.
Excised aortic valve from case 1 showing moderately heavy deposits of calcium, one was extremely friable and had a vegetative appearance. Microscopic sections of this excrescence showed no evidence of infection. Lower panel: Roentgenogram of the specimen shown in the upper panel showing the calcific nature of the deposits seen in the upper panel, especially the friable excrescence (arrow) thought to be the source of the calcium embolus. Fig. 2. Upperpanel: of which (arrow)
white woman. At age 64, she suddenly lost sight of objects in the superior visual field of the right eye. An ophthalmologist diagnosed embohc occlusion of a branch of the central retinal artery; a white calcific embolus was seen. No fundus photographs were taken. Bilateral selective carotid arteriograms were normal. She denied all cardiac symptoms. There was no history of rheumatic fever, hypertension, or diabetes mellitus. Blood pressure was 134/70. The carotid upstroke was slightly delayed with an anacrotic shoulder. A left ventricular heave was present with an audible and palpable atriai gallop. A long, barsh, ejection systolic murmur was maximal in the aortic area. A soft murmur of aortic insufficiency was present. There were no carotid bruits. Chest roentgenograms showed a normal-sized heart with poststenotic aortic dilatation. The electrocardiogram showed sinus rhythm and left ventricular hypertrophy. An M-mode echocardiogram showed thickened aortic cusps but a normal mitral valve. No mitral annular calcification, valvular vegetations, or left atria1 myxoma were noted. Cardiac fluoroscopy revealed moderate aortic valvular calcification. Cardiac catheterization revealed normal right heart pressures with a peak transaortic systolic gradient of 45 mm Hg. There was no transmitral diastolic gradient. The left ventriculogram showed no akinetic areas, filling defects, or mitral insufficiency. Surgery was not performed and over a 7-month follow-up there have been no further embolic episodes She is receiving no medical therapy. She still cannot see objects in the upper visual field of her right eye.
Case 4. A 56-year-old white woman suddenly lost sight in her left eye. She had known of a heart murmur since age 20 but had never had rheumatic fever. After several days, her vision improved until she was left with permanent loss of the upper visual field in the left eye. Retinal photographs showed a pure white body in a branch of the central retinal artery (Fig. 3). Bilateral selective carotid arteriograms were normal. She was not hypertensive or diabetic and had no cardiac symptoms. Blood pressure was 118/76. The carotid upstroke was normal. A loud harsh ejection systolic murmur was maximal in the aortic area and radiated widely to the carotid arteries. There was no diastolic murmur. The electrocardiogram and chest roentgenograms were normal. Cardiac fluoroscopy showed moderate calcification of the aortic valve leaflets but none in the mitral valve or annulus. An M-mode echocardiogram showed thickened aortic vaive cusps with a normal mitral valve. No evidence of atria1 myxoma, valvular vegetations, or mitral annular calcification was seen. Cardiac catheterization and surgery were not performed. Through a 4-year follow-up there have been no further embohc episodes and no cardiac symptoms. Direct anatomic confirmation that the visual symptoms of these patients were caused by calcific microemboli is impossible because the involved eye was not available for pathologic examination. However, because of previous isolated case reports describing the historic and ophthalmoscopic findings in cases where anatomic analysis was possible,“‘. ” we feel confident that these cases do represent true calcific microemboli to the retina from calcified
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aortic valves. The nlormal carotid arteriograms in three of
the casesserve to exclude the carotid artery asthe source of the emboli. DISCUSSION
Calcification of the aortic valve occurs in a variety of congenital and acquired cardiac diseases. Ordinarily, this calcification assumesclinical importance only by restricting the motion of the valve cusps, reducing the valve orifice area, and causing progressive aortic stenosi;s.The obstruction to left ventricular outflow eventually leads to hypertrophy of the left ventricle and failure to increase cardiac output adequately during exercise. This latter phenomenon, ventricular arrhythmias, reflex vasodilatation, and hypersensitive carotid sinus have been hypothesized to explain the occurrence of effort-related syncope and near-syncope in patients with aortic stenosis.1”.I*. 31In younger patients with noncalcific aortic stenosis (which is usually congenital), these mechanisms may well be operative. However, in older patients the heavy deposits of calcium on the aortic valve leaflets deformed by rheumatic valvulitis, infective endocarditis, or congenital anomalies of the cusps can acquire a vegetative appearance. At times these sterile calcific vegetations can be quite friable and small flecks of calcium can be released into the systemic circulation spontaneously or as a result of cardiac catheterization o,r aortic valvotomy or replacement.‘“, 28.35 Traditional teaching has held .that the three cardinal symptoms of calcific aortic stenosis are angina pectoris, syncope, or congestive heart failure.‘“, ‘I The occurrence of any of these symptoms in a patient with a typical basal systolic murmur and an aortic valve area of 1.0 cm’ or less would prompt most physicians to recommend replacement of the aortic valve in otherwise suitable candidates. Prevalence. We would like to suggest that there is another mode of presentation in calcific aortic stenosis-one that is usually independent of the hemodynamic severity of the lesion but which is seen only with moderate or heavy calcification of the aortic valve cusps. The spontaneous embolization of a fleck of calcific debris to a central retinal artery leading to abrupt, loss of vision in either eye and a white spot visible on ophthalmoscopic examination can be the initial presentation of calcific aortic stenosis in a middle-aged or elderly patient. The loss of vision may be partial or complete, temporary or permanent. In our experience it is certainly not a rare complication, and its significance is not generally appreciated in the cardiologic literature. It probably occurs relatively infrequently, but it can be a
Fig. 3. Photograph of the left fundus in case4, taken a
few days after the onset of visual symptoms, showing an embolus(small arrow) in the inferior temporal artery. A collateral vessel(large arrow) suppliesthe arteriole distal to the obstruction.
most disturbing symptom. Perhaps calcific microemboli lodging in arteries elsewhere in the central nervous system play a role in producing the episodes of dizziness or transient focal neurologic deficits that occur so commonly in patients with aortic stenosis.“-” The available literature on this subject is scanty, and further clinical observations on this point would be of value. Mechanism. Calcific microemboli have been shown rather conclusively to be the cause of focal retinal ischemia and infarction.“‘, ” What is not so clear from the available literature is whether larger calcific emboli can cause significant cerebral cortical or brainstem ischemia or infarction and result in significant disabling stroke. Our literature review and our two cases in which no operation was performed suggest that this is not a likely occurrence, at least during our short period of follow-up in four patients. We could find no reports of significant hemispheric or brainstem strokes attributed to calcific emboli from the aortic valve. Presumably, this is because the emboli found at postmortem examination in these patients are small, ranging from 0.1 to 6 mm in size.‘9 Since the size of the central retinal artery is small (approximately 0.28 mm in diameter),“” it is clear why such a small embolus can produce such a dramatic clinical picture only if it lodges in this particular artery. Diagnosis. A calcium microembolus to the retinal artery can only be proved by anatomic confirma-
6
Bmckmeier
et al. merican
tlon,
that
is, after
enucleation
sf the
eye
or
at
postmortem examination.“’ However, if a typical calcium embolus (Fig. 3) is seen in the affected eye and the aortic valve is calcified, a presumptive diagnosis can be made. If a calcium embolus is seen on ophthalmoscopic examination and if the carotid arteries show atheromas by physical examination, angiography, or postmortem examination, it is difficult to be certain whether the retinal embolus originated from the calcified aortic valve or from the atheromatous carotid artery. The diagnostic distinction between the ophthalmoscopic appearance of a calcium embolus and a cholesterol embolus may be possible if the symptomatic patient first presents to an ophthalmologist.“’ The ophthalmoscopic differentiation may be more difficult for the internist or cardiologist. Therapy. Management of tbis syndrome must remain speculative. The paucity of natural history data may make it seem more benign than it is. The calcific retinal arterial emboli may be recurrent and bilateral”‘; if so, valve replacement must surely be warranted because therapy with anticoagulants or antiplatelet drugs would have no known rational basis. If the emboli are composed in part of platelets or fibrin, either class of agent could be useful, however. Our two patients who did not undergo surgery and two from the literature’ have not had recurrent emboli during follow-ups of 3 months to 13 years. During this time, they have received no medical therapy. Conclusions. Our current approach to patients with embolic visual problems and aortic valvular calcification by fluoroscopy is to perform carotid arteriography first to exclude carotid atheromas as a source of retinal emboh6 If a typical carotid lesion is seen, we could recommend carotid endarterectomy. We have not yet encountered such a case. If the carotid arteries appear normal, and echocardiography shows no evidence of intracardiac masses or vegetations, cardiac catheterization is carried out even in the absence of cardiac symptoms. It is our policy to recommend valve replacement if the calculated aortic valve area is 1.0 cm’ or less,if there is no mitral valve involvement, and if left ventriculography shows no source of emboli. If the stenosis is not that severe and cardiac symptoms are absent, careful observation, supplemented perhaps with antiplatelet drugs, seemsthe more prudent course, with valve replacement recommended only for recurrent or bilateral symptomatic retinal emboli.
Buerk Fowler
who performed the who examined the Poon and Kenneth
cases 2 and 3, respectively, the manuscript.
Jowmai
and Dr. Noble
0.
REFERENCES
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Penner R, Font RL: Retinal embolism from calcified vegetations of aortic valve. Arch Ophthalmol81:565, 1969. Hammarsten J: Syncope in aortic stenosis. Arch Intern Med 87:274, 1951. Yacoub MH, Lise M, Balcon R: Total occlusion of the left femoral artery by a calcium embolus from a heavily calcified aortic valve. Am J Cardiol 25:359, 1970. Henle, J., cited in Warwick R: Eugene Wolfe’s anatomy of the eye and orbit, ed 7. Philadelphia, 1976, WB Saunders Co, p 145.
M-mode echocardiographic observations during and after healing of active bacterial endocarditis limited to the mitral valve Analysis of 99 M-mode echocardiograms recorded during and up to 144 months after healing of active bacterial endocarditis limited to the mitral valve in 27 patients disclosed the following: (1) Little to no change occurred in the echocardiographic size of the vegetations during the first 6 weeks after diagnosis and institution of appropriate antibiotic therapy unless a major systemic embolus occurred. (2) The echocardiographic size of the vegetations did not determine the amount of cardiac damage or dysfunction produced by the valvular infection. (3) The larger the vegetations by echocardiogram, the greater was the likelihood of a clinical event compatible with a systemic embolus. (4) The gravest prognostic sign yielded by the echocardiogram was evidence of rupture of chordae tendineae. (5) Although a useful adjjunct to diagnosis before appropriate antibiotic therapy was instituted, once bacter.iologic cure was achieved, the echocardiogram was of limited value in delineating an active from a healed vegetation. l(6) The echocardiographic appearance of the vegetations was not determined by the type of infecting Ibacterium. (AM HEART J 101:37, 1981.)
Mazhar U. Sheikh, M.D., Edgar A. Covarrubias, M.D., Nayab Ali, M.D., Won Ro Lee, M.D., Nasreen M. Sheikh, M.D., and William C. Roberts, M.D. Bethesda, Md., and Washington, D.C.
Since 1972, many reports have described echocardiographic features of vegetations in one or more cardiac valves.‘-3 Most reports have described the echocardiographic features during the period of active infection, and few studies, are available describing long-term follow-up by serial echocardiograms in patients with active infective endocarditis. Recently, Stafforld et al.” described serial echocardiographic observations up to 10 months in two
METHODS Patients. Satisfactory echocardiogramswere performed
From the Section of Cardiology, Medical Divisions, Columbia General Branch, National of Health, Bethesda. Received
Georgetown and Howard University and the Department of Pathology, District of Hospital, Washington, D.C., and the Pathology Heart, Lung, and Blood Institute, National Institutes
for publication
Reprint requests: Medical Division, DC 20003.
0002-8703/81/010037
Mazhar District
Sept.
3, 1980;
accepted
Sept.
U. Sheikh, of Columbia
M.D., Georgetown General Hospital,
+ 09$00.90/O
0 1981 The
in 68 patients hospitalized at the DC. General Hospital from 1975through 1979with active infective endocarditis; 27 (40%)had evidenceof bacterial endocarditis limited to the mitral valve. Clinical findings in these 27 patients are listed in Table I. Among the 27 patients, 31 episodesof active infective endocarditis were documented. During eachactive episode,each patient had a precordial murmur
17, 1980. University Washington,
C. V. Mosby
patients, and Stewart et a1.j reported similar observations in 12 patients up to 30 months, both groups with active infective endocarditis limited to the mitral valve. Because of the sparsity of serial echocardiographic information in patients with active infective endocarditis limited to the mitral valve, echocardiographic findings were analyzed in 27 such patients.
Co.