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Show /. Clin. Neuro-ophth'l/mol. 1: 153-100, 19~ I. Mitral Valve Prolapse and Amaurosis Fugax ROBERT L. LESSER, M.D. MURK-HEIN HEINEMANN, M.D. HENRY BORKOWSKI, JR., M.D. LAWRENCE S. COHEN, M.D. Abstract Because there have been reports of ocular and/or cerebral ischemic events associated with mitral valve prolapse, we reviewed a series of patients with mitral valve prolapse to determine the frequency of amaurosis fugax. Among 59 patients, 13 (22%) had symptoms while among 75 controls, only one had amaurosis fugax. We conclude that patients with mitral valve prolapse have an increased risk of ocular and/or cerebral ischemia. Introduction Mitral valve prolapse is a common cardiac abnormality which is characterized by a mid-systolic click followed by a late systolic murmur. Recently there have been reports of ocular and/or cerebral ischemic events associated with mitral valve prolapse. These reports have been either sporadic cases or reviews of patients with either cerebral or ocular ischemia in whom mitral valve prolapse has been found. The purpose of our report is to determine the frequency of ocular ischemic events among a series of patients with mitral valve prolapse. We have attempted to answer the following questions: 1. How frequently do these events occur compared to a control population? 2. What patterns of ischemia do they follow? 3. Can a high-risk patient be identified? 4. What are the long-term implications for a patient with mitral valve prolapse? Materials and Methods (see Table 1) Patients with echocardiographically documented prolapse of the mitral valve were selected to be From the Departments of Ophthalmology & Visual Science (RLL, M-HH) and Internal Medicine (LSC), Yale University School of Medicine, New Haven; and the Cardiovascular laboratories (HB), Saint Mary's Hospital, Waterbury, Connecticut. June 1981 interviewed (see Figs. 1 and 2). In addition to fundamental information such as the patient's sex and age, a complete medical history was taken. The circumstances that led up to and the method of diagnosis of mitral valve prolapse were recorded. Patients who experienced their first cardiac or noncardiac symptoms after the age of 45 years were excluded from the study in order to exclude patients with arteriosclerotic ischemic heart disease. Similarly, patients who had a history of indirect chest trauma, rheumatic heart disease, myocardial infarction, or mitral valve surgery were excluded. Patients were questioned whether or not they had experienced chest pain, palpitations, dyspnea, or transient weakness of the arms or legs. They were asked if they had noted any partial or complete 1055 of vision in one or both eyes. A complete ocular history was taken. In order to rule out coexisting eye disease in those patients reporting visual symptoms of transient visual loss, subjects were questioned as to the use of medications such TABLE 1. Telephone Interview I. Age 2. Sex 3. Method of diagnosis 4. Onset of symptoms (if ,my) 5. Presence of cardiac symptoms 6. History of rheumatic heart disease. myocardial infarction. indirect chest trauma or mitral valve surgery 7. Noncardiac symptoms Partial or complete loss of vision in one or both eyes Loss of consciousness Headache Transient weakness of arms and/or legs 8. Ocular history 9. Family history Mitral valve prolapse Cardiovascular disease Cerebrovascular disease Migraine 10. Medications Oral contraceptives, steroids, coumadin, aspirin, and persantinI' 153 Mitral V.llve Prolapse - - .- Chr.-', loJJ .11 I, ~ .-.I l - -"' _ •.=- ,.,-~ _-T......-. "'" ,. ~ - Figure 1. Echocardiogram of a normal mitral valve ALMV = anterior leaflet of mitral valve. PLMV = posterior leaflet of mitral valve. D = opening of mitral valve at onset of diastole, E to F = partial closure of valve after early rapid diastolic filling. A = opening motion of ALMV due to atrial contraction. C = complete closure of MV at onset of systole. RE = right ventricle, IV = interventricular septum; LV = left ventricle. PWLV = posterior wall of LV. Figure 2. [,ho,,udiogram showing mitr.ll v.llve prol.lpse. Line indicat"s I.lte syslolic pc'st.-rim motion of both th.- .lnterior .lnd pc,.,h·rinr il'Jflt'h. Chesl wall • ..,t....... ... ....... ~."'" s:- ~ ~1~." .~ .... - '" • as oral contraceptives, steroids, coumadin, aspirin, and/or persantine. A family history was taken with particular attention to a history of prolapsed mitral Results (see Tables 2 and 3) Fifty-seven patients with mitral valve prolapse were included in this study. Thirteen had eye symptoms. Among 75 controls only one had symptoms. The one control patient was a 26-year-old male with several episodes of intermittent monocular amaurosis without systemic symptoms or any positive findings on ophthalmologic, cardiologic, or echocardiographic exams. Of the mitral valve prolapse patients with symptoms, 12 had valve, cardiovascular and cerebrovascular disease. Those patients who had visual symptoms had a complete ophthalmic examination, including corrected visual acuity, motility exam, slit lamp exam, central and peripheral visual fields and dilated fundus examination. Patients for this study were obtained from the following sources: 1) Echocardiography laboratory, Yale-New Haven Hospital. New Haven, Ct.; 2) Echocardiography laboratory, St. Mary's Hospital. Waterbury, Ct.; 3) Echocardiography laboratory, Cardiology Associates of New Haven, New Haven, Ct. Control patients were selected from a series of patients presenting for routine eye examination. We attempted to match these patients by age and sex to the group of patients with known mitral valve prolapse. After we obtained permission from the cardiologist to interview the patients, we sent a letter to the patient stating that we would telephone them. We then c.llled and interviewed the patients. Only one patient refused to participate. RV ....... . . ~ ..., , - I Journal of Clinical Neuro-ophthalmology Mitr.ll V,llve l'rol.lpse Summary. A 32-year-old woman had multiple episodes of bilateral dimming of vision lasting from 10-20 seconds. Patient 2. A 47-y('ar-old whit(' mall' (RS) sought medic.ll help 5 Y('Jrs (,Jrlier aft('r ('xpNi('ncing s('ver.ll ('pisod('s of transi('nt light-h('ad('dness precipitated by rising from a r('cumb('nt position. On physical ('xamination a murmur was noted, and subsequ('nt echocardiographic evaluation documented the presence of mitral valve prolapse. The patient's antecedent medical history was negative. Since the initial symptoms were noted, the patient has had multiple episodes of palpitations, usually occurring in the sitting position, which were accompanied by a momentary lapse of attention followed by bilateral dimming of vision lasting from 15 to 30 seconds. The patient also noted that his perception of color changed and that everything assumed an orange-yellow hue. Often these symptoms were accompanied by tingling of the extremities usually on the left side. Ophthalmic examination was normal. The patient is presently maintained on Inderal, 80 mg daily. Summary. A 47-year-old patient with a history of light-headedness and palpitations had bilateral dimming of vision lasting from 15 to 30 seconds associated with left-sided paresthesias. Patient 3. E.P., 29-year-old white female, underwent thorough physical examination 2 years previously after experiencing a syncopal episode. A heart murmur was noted, and echocardiographic examinations confirmed the presence of mitral valve prolapse. The patient reported that she had experienced several episodes of bilateral gray-outs which were especially severe upon rising. These episodes all lasted less than 30 seconds and were not accompanied by palpitations, chest pain, or extremity weakness. Eleven months after her syncopal episode the patient had a seizure. She ~as told that the seizure was characterized by loss of consciousness, rigidity, and clonic movements of her extremities. She denied experiencing an aura, nor was she incontinent. The patient has been maintained subsequently on Dilantin, 400 mg daily. She has had no additional seizures although she has continued to have intermittent gray-outs precipitated by changes in posture. Summary. A 29-year-old female with mitral valve prolapse had bilateral gray-outs lasting about 30 seconds, and associated with syncope and sei-zures. Patient 4. A 32-year-old white male (p.G.) had an I8-month history of intermittent light-headedness and bilateral graying of vision precipitated by qUickly sIttIng up, before physical examination and ('chocardiography documented mitral valve proI. lpse. The patient's antecedent medical history was negative. He has had no additional symptoms nor has any progression been noted. Ophthalmologic examination was normal. The patient described his visual symptoms as gray-outs lasting from a few seconds to 3 minutes not accompanied by palpitations, chest pain, or extremity weakness. By more gradually changing position, the patient has been able to minimize the frequency of his symptoms and he is not presently medicated. Summary. A 32-year-old man had Iight-headedness and gray-outs associated with postural change. Patient 5. A 29-year-old female (S.L.) underwent echocardiography after an 8-month history of intermittent palpitations, left arm pain, Iight-headedness, and transient partial binocular visual loss. Often the symptoms would be postexertional and lasted up to 20 minutes. Usually palpitations would precede the onset of the other symptoms. Visual loss was always bilateral and partial, and rarely lasted at least 20 minutes. Ophthalmologic examination was normal. Antecedent medical history was negative. Summary. A 29-year-old patient had transient bilateral visual loss lasting for about 30 seconds. Patient 6. P.F., 22-year-old white female, underwent echocardiographic examination after experiencing several episodes of chest pain and palpitations. These symptoms were often accompanied by weakness and tingling of the right arm. She also noted several episodes of bilateral gray-outs, usually accompanied by palpitations which lasted several minutes. She also reported one episode in which all vision in the right eye was lost for roughly 10 mInutes. The patient had a history of left-sided migraines, often preceded bv an au~a. She denied visual loss, scotoma, or chro~atopsiaduring these attacks, however. The episodes of monocular visual loss, moreover, were not accompanied by headache. Ophthalmologic examination was normal except for low myopic refractive error. She is presently asymptomatic on Inderal, 80 mg daily. Summary. A 22-year-old female had bilateral gray-outs and one episode of a monocular grayout. Patient 7. J.e., a white 46-year-old male, suddenly lost consciousness while at the wheel of a tractor trailer truck 10 years earlier. He emerged unscathed from the accident, although subsequent phySical examination uncovered mitral valve prolapse. Antecedent medical history was negative. Ov~r the past 4 years the patient has had three addItIOnal episodes of loss of consciousness while driving. In addition, he has had numerous palpitatIOns which were often accompanied by binocular gray-outs lasting from 30 seconds to 5 minutes. He denied experiencing chest pain or extremity weakness. Journal of Clinical Neura-ophthalmology Ophthalmologic examination W,lS norm,ll. Recently the p,ltient has been medic,lted with quinidine which has controlled his p,llpit,ltions, but the gray-outs still occur. Summary. A 4o-ye,H-old white m,lle had syncope and bil,lteral gr,ly-outS. Patient 8. R.M.. ,1 27-year-old white m,lle. presented to his internist 2 years earlier with chest pain and p,llpit,ltions. Subsequent ev,llu,ltion including echocardiogr,lphy demonstrated prolapse of the mitr,ll v,llve. The p,ltient reported th,lt often he experienced p,llpit,ltions which usu,llly occurred following strenuous physical activity. He also noted brief binlKular gray-outs lasting several minutes. Ophthalmologic evaluation was normal. Antecedent medical history was negative. Summary. A 27-year-old man with chest pain and postexertional palpitations had intermittent, associated binocular gray-outs. Patient 9. CM.. 36-year-old white female, was found to have prolapse of the mitral valve 3 years previously after presenting with a complaint of experiencing frequent episodes of Iight-headedness and binocular gray-outs lasting 5 seconds. Symptoms were related to postural changes primarily. She denied chest pain or extremity weakness. Ophthalmologic examination was normal. Antecedent medical history was negative. The patient is presently asymptomatic and off all medications. Summary. A 36-year-old woman had a history of light-headedness and orthostatic binocular grayouts lasting about 5 seconds. Patient 10. A 25-year-old female (N.K.) was well until 1 year before when she began experiencing chest pain and palpitations. Echocardiograms documented the presence of mitral valve prolapse. Associated episodes included light-headedness and binocular gray-outs usually lasting several minutes. Gray-outs were invariably accompanied by palpitations. Antecedent medical history was negative. The patient is presently maintained on Inderal. Summary. A 25-year-old female had binocular gray-outs lasting several minutes. Patient 11. A 44-year-old female (M.J.) who first noted the onset of chest pain and postexertional gray-outs at age 32 had documented mitral valve prolapse. She has been treated with lnderal and has been asymptomatic. Her eye examination has been negative. Summary. A 44-year-old female had binocular postexertional gray-outs accompanied by chest pain, lasting 3-4 minutes. Patient 12. A 22-year-old female (K.r.l. the daughter of patient 11, had chest pain and palpitations at age 19. Physical exam and echocardiography documented mitral valve prolapse. The pa- June 1981 Lesser, Heinem;mn, Borkowski, Cohen tient has had multiple episodes of binocular gray outs lasting from 30 seconds up to a few minutes associated with palpitations, usually postexertional. The patient is asymptomatic now on lnderal, 40 mg d,lily. Her eye examination is negative. Summary. A 22-year-old female had binocular gr,ly-outs, usu.llly postexertion.ll, and associated p,llpitations. Patient 13. A 37-year-old female (J.M.) first noted binocular gray-outs at age 37. She has had associated chest pain, usually postexertional. Her eye examination has been negative. Summary. A 37-year-old female had binocular gray-outs which were usually postexertional with associated chest pain. Discussion Although the click-murmur syndrome was described in the late 1800s, it was not until the 1960s that this complex of sounds was attributed to an abnormality of the mitral valve leaflets (see Fig. 3). Although mitral valve prolapse can occur in association with coronary artery disease, rheumatic heart disease, the Marfan syndrome, or hypertrophic cardiomyopathy, in the majority of patients no specific etiology can be found. Mitral valve prolapse is found in about 0.5% of men and in 6% of women. About one-third to one-half of the patients have a history of chest pain, but unlike angina pectoris, the pain is not usually related to physical exertion and does not usually respond to nitroglycerin. About 50% of the patients will have arrhythmias on ambulatory electrocardiogram monitoring. Other symptoms include light-headedness and syncope. Many patients will have no symptoms at all. Some patients with mitral valve prolapse have thoracic skeletal abnormalities such as scoliosis, pectus excavatum, and a straight thoracic spine. The characteristic ausculatory findings in mitral valve prolapse are single or multiple systolic clicks which usually occur in mid- to late systole in combination with a systolic murmur which is usually confined to late systole. Quite commonly, the murmur begins immediately after the systolic click. The timing of the click and duration of the murmur are related to left ventricular volume and therefore can be modified by position change, physiologic maneuvers, and pharmacologic intervention. With standing, or during the straining phase of the valsalva maneuver, or after amyl nitrate inhalation, the click will occur earlier in systole and the murmur will usually increase in duration and therefore become more holosystolic. Although mitral valve prolapse is generally thought to be harmless, reports of complications such as clinically significant cardiac rhythm disturbances, infective endocarditis, and sudden death 157 Mitr.!1 ValvE' ProlapsE' Jr--;H~- Chordae PapdlarY~r~--Tmuscles Figure J. Proldpsed mitrdl vdlve. have appeared. I-III The first eye complications were reported in 1975. One patient had a branch artery occlusion and the other had a central vein occlusion. No systemic abnormalities except for mitral valve prolapse were found. II In 1977, Kimball and Hedges l2 reported a 28-year-old white man who had a history of black-outs involving either eye lasting from about 1 to 3 minutes for a total of 12 to 15 episodes over 2 years. Again, no other abnormalities were noted except for mitral valve prolapse. [n 1977, Wilson et al. 1:1 reported 10 patients with mitral valve prolapse with visual changes: four with homonymous field loss; four with amaurosis fugax; two with retinal artery disease and no other significant vascular abnormalities. Recently, Caltrider et al. 14 reported six patients with retinal occlusive disease and mitral valve prolapse. Three of the patients had branch artery occlusions: one patient had a central retinal artery occlusion, one patient had an episode of amaurosis fuga x involving the carotid system, and one patient had "ischemic fundi with thready arteries and massive retinitis proliferans involving the disc of both eyes." The latter patient's findings were felt to be compatible with "atypical Eales' disease." The one patient with central retinal artery occlusion was 76 years old, but all other patients were age 50 or under. The patient with atypical Eales' disease was 14 yec1rs old. [n all cases no other vascular abnormalities were found except mitral valve prolapse. The first neurologic complication was reported by Barlow and Bosmiln" in 1966, when they described a woman with mitral valve prolapse who had transient parasthesias of the left arm. Ten years later, Barnett et aLI" described 12 patients with mitral valve prolapse with either transient or ,\)mpl('t('d strokes. Ages ranged from 10 to 67 with an average of 38. Most of the patients had hemiplegia; some had homonymous field loss. Two patients had vertigo, dizziness, and decreased hearing associated with vertebrobasilar disease. Seven of the patients had previous cardiac symptoms. Since that report, other instances of mitral valve prolapse and transient ischemic attacks have also been reported. l Ii--2:1 Barnett et al. 24 reported the influence of age on the incidence of cerebral ischemic events in patients with mitral valve prolapse. [n the group over age 45, only 5.7% of the prolapse patients and 7.1% of the controls had cerebral ischemic events. In the group under age 45, however, 40% of the patients with cerebral ischemic events had prolapse while only 6.8% of the controls had them. In this younger group, six of the 24 patients with prolapse were excluded because of other underlying causes. In the other 18, however, no other risk factors such as polycythamia, platelet abnormalities, collagen vascular disease, prosthetic valves, or oral contraceptive ingestion were noted. Barnett et al. concluded that there was about a 4.5 times risk of patients under age 45 having strokes if they had mitral valve prolapse. Recently there has been a report of familial mitral valve prolapse in which eight of 27 family members had mitral valve prolapse and four of those eight had strokes before age 40. 2 " The main findings in our study were that 22% of p.ltients with mitral valve prolapse had episodes of transient amaurosis compared to 1.33% of the controls. Most episodes were in the vertebral-basilar system; some of these episodes were related to postural change. In all patients, no associated diseases were found. All patients with symptoms had a thorough eye exam, and none had other ocular causes which could mimic the transient ischemia Journal of Clinical Neuro-ophthalmology that they described. We could not identify .1 highrisk patient, nor could we predict wh.1t the longterm implic.ltions will be. The mech.mism f'H tr.msient .1m.1Ufl1sis in mitr.11 valve prol.lpse is thought hl be emblllic Miuoscopic ex.lln of .lffected mitr.ll Il'.lflets h.1S shown repl.lCement l)f norm.11 le.1fll't tissue by myxom.ltous tissue. In .1 review llf 35 C.1Sl'S l)f mVXl)m.1tous mitral valves. 10 h.ld .1dhl'rent fibrin .ll1t1 red blood cells. This n1.lY le.ld tl) thrllmbus fllrm.ltilll1 with subsequent emboli. Steele et .11. h.lVe drnllll1str.lted shl)rtened pl.1telet sur"iv.1l times in p.1tienls with mitr.ll v.llve pr,'l.lpse.~';-·~·' It is Ill)t c1e.H why episl, des ,)f .lm.1url)sis shl)uld IMve lKcurred more frequently in the vertebr.ll-b.lsil.H svstem in our study. Whether this is rel.lted in ;0011.' W.1Y to hypotensive episodes or to embl)li is unknown. VVe cl'l1clude th.lt transient ischemic events do occur ml)re frequently in patients with mitral valve prolapse. In l)ur series they were more frequent in the vertebral-basilar system. Classically, attacks in the vertebral-basilar system occur in both eyes without complete loss of vision, usually lasting less than 1 minute. occasionally associated with flickering or flashing sensations. ~9 This study adds further support to the concept that patients with mitral valve prolapse are at a greater risk for ocular and cerebral ischemic episodes. We feel that any patient under age 45 with amaurosis fugax involving either the carotid or vertebral-basilar system should have echocardiography to look for mitral valve prolapse. References 1. Hurst, S.W., and Logue, R.B.: Disease of the Heart and Pericardium. The Heart. McGraw-HilI. New York, 1978, pp. 1014-1023. 2. Devereux, R.B., Perloff, I.K., Reichek, N., and 10sephson, ME.: Mitral valve prolapse: Special article. Circulation 54: 3-14, 1970 3. Barlow, I. B.. Pocock, WA, Marchand, 1'., and Denny, M: The significance of latl' ,y,tolic murmurs. Am. Heart]. 37: 443-452, 1903. 4. Barlow, I.B, and Pocock, W.A.. The problem of nonejection systolic clicks and associated mitral systolic murmurs: Emphasis on thl' bilillwing mitral leaflet syndrome. Am. Heart /. 90: 030-b55, 1975. 5. Marshall, CE., and 5hdppell, SD: Suddl'n death dnd the ballooning posterior Il'afll't ,yndroml': Detailed andtomic dnd histochemicdl inve,tigation. Arch. Pathol. 98: 134-138, 1974. 6. BdrlOW, I.B., and Bosmdn, C.K.: Aneury,mal protrusion of the posterior leaflet of the mitral valve: An auscultatory-electocardioWdphic ,yndrome. Am. Heart]. 71: 166-178, 1960. 7. Hancock, E. W., and Cohn, K.: The ,yndrc'ml' .1"0cidted with mid-systolic click .1I1d I.lte sy,tolic murmur. Am.]. Med. 41: 183-196, 1%0. 8. Femex, M., and Fernex, C: La degenerc",ceI1lT mucoide des valvules mitrales: ses n'pereus,ions fonetionnelles. Helv. Med. ActJ 25: 094-705, 19511. June 1981 Lesser, Heinemann, Borkowski, Cohen 0. Brown, a.R., Kloster, F.E., and De Mors, H.: Incidence of mitral vdlve proldpse in the asymptomatic norm.11. (Abstract.) 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Pomerance, A., and Davies, M.j.: Strokes: A complication of mitral v.llve prtllapse. Lancet 2: t 180, 1977. 23 Malcolm, AD., Boughner, D.R., Barnett, H.I.M.. and Silver, MD.: Clinical features and investig.ltive findings in the presence of mitral leaflet prolapse. A study of 85 consecutive patients. 8r. HeJrt]. 38: 244-250, 1070. 24. Barnett, H.I.M., Boughner, D.R., Cooper, P.F., Taylor, D.W., Kostuk, W.)., and Nichol, P.M.: Further evidence rel.lting mitr.11 v.llve prol.lpse to cerebral ischemil- events. N. Engl. 1. Med. 302: 13Q -I.t4, 1980. 25. Ricl', C.P.A., Boughner, D.R" Stiller, C, and Ebers, C.C: F.lmilial stwke syndrtlme associated with mitral valve prtll.lpse. Ann. Neuwl. 7: 130-134, 1980. 20. Pomerance, A.: B.lllooning deformity (mucoid degeneration) of .ltrioventricul.H valves. 8r. Heart /. 31: 343-349, 1969. 27. Davis, R.H., Schuster, B., Knobel, S.F., and Fisch, C: Myxomatous degeneration of the mitral valve. Am. /. Clrdhl/. 28: 449, 1071. 159 Mitral Valve Prolapse 28. Steele, P., Weily, H., Rainwater, j., and Vogel, R.: Platelet survival time and thromboembolism in patients with mitrdl valve prolapse. Circulation 60; 434b, 1070. 20. Hoyt, W.F.: Ocular symptoms and signs. Extraudni. 11 Occlusive Cerebrovascular Disease: Didgnosis .lI1d M.l1ldgement, Lj. Wylie dnd W.K. Ehrenfield, Eds. W.B. 5.lUnders, Philddelphia, 1070, vol. 31, pp. t,4- Q 5. Acknowledgments The authors thank Karen Meister for her technical assistance, and Dr. Stephen Wolfson for contributing patients to this study. Write for reprints to: Robert L. Lesser, M.D., Department of Ophthalmology & Visual Science, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06510. journal of Clinical Neuro-ophthalmology |
