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• W2612946871 abstract "Case ReportsMitral Valve Prolapse with Systemic Embolism: Report of Three Cases Akhtar Husain, MB, BS, FACC Huxley Knox-Macaulay, FRCP, FRCPE Mohammad Fakhry, and MB, BCh, DM, MSc Ahmed AmmarMD Akhtar Husain Address reprint requests and correspondence to Dr. Husain: P.O. Box 40033, Al-Khobar 31952, Saudi Arabia. From the Department of Internal Medicine, College of Medicine and Medical Sciences, King Faisal University, Dammam Search for more papers by this author , Huxley Knox-Macaulay From the Department of Internal Medicine, College of Medicine and Medical Sciences, King Faisal University, Dammam Search for more papers by this author , Mohammad Fakhry From the Department of Internal Medicine, College of Medicine and Medical Sciences, King Faisal University, Dammam Search for more papers by this author , and Ahmed Ammar From the Department of Neurosurgery, College of Medicine and Medical Sciences, King Faisal University, Dammam Search for more papers by this author Published Online::1 Sep 1989https://doi.org/10.5144/0256-4947.1989.489SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutIntroductionMitral valve prolapse (MVP) is a common condition in the developed countries and apparently is the most frequently diagnosed valvular heart disease in the United States, with an overall prevalence of 5% and as high as 17% in young females.1 Several clinical studies have suggested that MVP is associated with certain serious complications such as progressive mitral regurgitation, bacterial endocarditis, arrhythmias, and sudden death.2 Moreover, cerebral and ophthalmic ischemic episodes, presumably secondary to embolism, have been reported recently as additional complications of MVP.3–13It is generally believed that rheumatic fever is still a major problem in the developing countries.14 Thus, it is assumed that the commonest form of valvular heart disease in these areas is rheumatic in origin. A recent study has shown that the prevalence rate for MVP in Saudi Arabia is comparable to that reported from the Western countries.15 There should be an awareness of its occurrence and possible complications in the developing countries.We, therefore, present case reports of three young Saudis with MVP complicated by cerebral and retinal embolism and review the relevant literature. Similar complications have been reported previously only from Canada,3–5 England,6 South Africa,7 France,8 and the United States,9–13 but to our knowledge, these are the first cases reported from the Middle East and Asia of cerebral and retinal embolic phenomena associated with MVP.CASE REPORTSCase 1A 16-year-old Saudi girl was referred to the University Hospital because of sudden blindness in the right eye which developed about 12 hours prior to presentation. There was no history of acute rheumatic fever, heart disease, dyspnea, chest pain, palpitations, dizziness, or previous visual symptoms. Ophthalmic examination revealed blindness of the right eye with only perception to light. Features of right central retinal artery occlusion were seen on funduscopy. Carotid pulses were normal, and there was no carotid artery bruit. She was afebrile, and the cardiac apex was in the normal location with no thrill or heaves. First and second heart sounds were normal. There was a grade 3/6 late systolic murmur at the apex, which was accentuated by hand grip. No click, gallop, or opening snap was heard. Results of all hematologic and biochemical investigations were normal. Blood culture showed no growths. Electrocardiograms and chest roentgenogram were normal. No arrhythmia was observed on a 24-hour Holter monitor recording. Echocardiogram showed holosystolic MVP with normal left atrial and left ventricular size.Case 2For a month prior to his referral, a 23-year-old Saudi man experienced recurrent attacks of blurred vision lasting a few minutes at a time. Four days before his visit to the University Hospital, he suddenly developed partial blindness in the mid-zone of the visual field of the left eye. At presentation, he denied any history of rheumatic fever, palpitation, dizziness, chest pain, or dyspnea. Ophthalmic evaluation showed a visual acuity of 0.8 in the left eye and 1.0 in the right eye. Retinal examination revealed obstruction of the left cilioretinal artery with an ischemic area in the retina involving the inferior part of the macula. The carotid pulses were normal with no bruits, while the apical cardiac impulse was in the normal location with no thrills or heaves. First and second heart sounds were normal. There was no click, but an S3 gallop was noted. A grade 1/6 late systolic murmur, which increased to grade 3/6 in the squatting position with a change to musical character, was heard at the mitral area. Results of all hematologic and biochemical investigations were normal. Electrocardiogram and chest roentgenogram were unremarkable. M-mode echocardiography showed thickened posterior leaflet but no evidence of prolapse of the mitral valve. However, the apical four-chamber view on two-dimensional echocardiography showed definite MVP (Figure 1). The left atrial and left ventricular chamber sizes were normal.Figure 1. Two-dimensional echocardiogram (four-chamber apical view) clearly shows both leaflets of the mitral valve prolapsing well into the left atrium during systole. The dotted line defines the mitral annular plane. LV indicates left ventricle; LA, left atrium; RV, right ventricle; and RA, right atrium.Download FigureCase 3This 21-year-old Saudi man was admitted to the neurosurgical unit of the University Hospital with the chief complaint of frontal headache, loss of recent memory, and olfactory hallucination (strange odors) for 1 day prior to admission. At that time, his mother, while riding with him in the car, noticed that his behavior was abnormal and that he lost his way while driving to a familiar place. She also observed that his conversation did not make sense. On the morning of admission, he woke up complaining of frontal headache and smelling strange odors. Later that day, the rest of his family realized that he could not remember most of the events of the previous 2 weeks. There was no history of trauma or any other illness in the past. General examination revealed a slightly drowsy but fit-looking young man. Neurologic examination was unremarkable except for evidence of loss of recent memory. Carotid pulses felt equal on palpation, and no bruits were heard. The apical cardiac impulse was not displaced. First and second heart sounds were normal. A midsystolic click and a grade 3/6 late systolic murmur were heard at the apex. These signs were interpreted as indicative of MVP. Results of all hematologic and biochemical investigations were normal.Computed tomographic scan of the brain showed an area of low density in the right temporal region with no enhancement with contrast (Figure 2). The EEG showed irregular slow and sharp waves in the right hemisphere with the maximum voltage in the anterior to mid-temporal region, suggesting an irritative lesion which may have caused a focal seizure. No arrhythmia was recorded in 24-hour Holter monitoring. Echocardiogram showed holosystolic MVP with normal left atrial and left ventricular size.Figure 2. Skull CT scan shows the low-density area (arrow) in the right temporal lobe.Download FigureDISCUSSIONIn 1966 Barlow and Bosman described a 23-year-old woman with MVP who experienced transient left arm weakness, but they did not relate the neurologic disorder to her cardiac lesion.16 In 1976 Barnett et al were the first to suggest an association between cerebral ischemic events and MVP and proposed that the ischemic episodes were thromboembolic in origin.3 On the other hand, the earliest report of retinal vascular lesions in MVP was presented by Woldoff et al.11 Since then, there have been numerous communications suggesting a causal relationship between MVP and ischemia of the eye and brain.3–13 None of our three patients with MVP suffered from hypertension, diabetes mellitus, rheumatic heart disease, vasculitis, hematologic disorders, or any other predisposing factor for strokes. Therefore, it is very likely that the ischemic attacks in these young Saudis were due to thrombotic emboli originating in a prolapsed mitral valve.In case 2, only the apical four-chamber view showed the MVP without evidence of prolapse on the M-mode or the parasternal long axis view, though the mitral valve leaflets, especially the posterior, were thickened. Recently, the reliability of the apical four-chamber view for the diagnosis of MVP has been questioned.17 However, in this patient, both the anterior and posterior leaflets showed marked superior displacement with their coaptation distinctly superior to the mitral annular plane (3+ displacement). This pattern is very unusual in a normal subject.17,18 Abbasi et al have shown that the four-chamber view was significantly more sensitive than M-mode and long axis for the diagnosis of MVP.19 If one applies the diagnostic criteria suggested by Perloff et al, this patient has two major (apical systolic murmur and marked superior systolic displacement of the mitral leaflets and their coaptation) and one minor criteria (focal neurologic attack). They believe that one or more major criteria establish the probability of pathologic MVP beyond reasonable doubt.The observed association of MVP and thromboembolism has generated considerable interest and controversy. The possibility of a coincidental occurrence of two common clinical conditions cannot be entirely ruled out. It is, however, extremely important to determine the relationship between MVP and thromboembolic phenomena so that appropriate preventive action can be taken if the association turns out to be causal in nature. Since arrhythmias are a relatively common complication of this valvular disorder, thromboembolism in MVP may be secondary to atrial fibrillation. Alternatively, embolization may be due to infective endocarditis. Nevertheless, in most cases of MVP, emboli probably arise from either noninfective thrombotic vegetations formed over ulcerative lesions on a valve with myxomatous degeneration5,7,10,20 or from a thrombus formed in a small cul-de-sac between the left atrial wall and the atrial side of the ballooning mitral leaflet.4Interestingly, Steele and colleagues have suggested that the decreased platelet survival time in their MVP patients was due to the deposition of platelets with formation of platelet thrombi on an abnormal prolapsed mitral valve.21 Barnett et al, in their original paper, reported 12 cases of MVP with cerebral ischemic events.3 Three of them suffered from atrial fibrillation. Ten had abnormal physical findings in the form of a click, a murmur, or both. Four had normal echocardiogram although all of them had proved MVP by angiocardiography. Subsequently in another study, this same group of workers found MVP in a significantly higher percentages of subjects among young persons (below 45 years) presenting with strokes compared to age-matched controls.5 Despite these and other reports, the role of MVP in cerebral ischemia remains controversial for several reasons.First, there is lack of direct pathologic proof. Because of the relatively young age of the patients and the nonlethal nature of the ischemic brain or eye insult, significant postmortem evidence is lacking. However, there is some indirect evidence in that fibrin and platelet thrombi have been observed at surgery and autopsy on the surface of mitral valve with myxomatous degeneration.10,22 Although there have been four cases of autopsied fatal embolism reported, in one case there was no thrombus seen in the heart.23 Two cases had another predisposing factor (one had atrial fibrillation and one had an adenocarcinoma),24,25 There was only one case with documented thrombus on the atrial surface of the posterior mitral valve leaflet.6 Second, based on their observations in young stroke patients, this causal relationship between cerebral ischemic attacks and MVP has been postulated mainly by neurologists. On the other hand, cardiologists who see a large population of patients with MVP have not recorded an increased risk of strokes among them. In a large cardiac series of 237 patients with echocardiography-documented MVP followed up for a mean period of 6.2 years and maximum of 10.4 years, 10 developed strokes. Of these 10, eight suffered from other disorders that could have caused their stroke (one infective endocarditis, one left ventricular aneurysm with mural thrombus, and six atrial fibrillation). There were, therefore, only two patients of this very large group whose stroke might be explained on the basis of MVP alone.26 These data strongly argue against a causal relationship between MVP and ischemic events. However, it is possible that only a small subset of MVP patients are prone to this complication. If this is true, then this subset needs to be defined. Suggested features of such a subset include multiple valvular prolapse27 and redundancy of mitral leaflets.26 Confirmation of these and evaluation of other possible features is needed.Physicians who are not aware of the probable association between MVP and embolism are likely to misdiagnose the embolism as being secondary to rheumatic mitral valve disease, particularly in the absence of echocardiography. Interestingly, the first patient was referred to us as a case of embolism due to rheumatic mitral valve disease. Another patient (unpublished) was also initially diagnosed several years ago at another hospital as having retinal embolism complicating rheumatic heart disease. Recent further evaluation, including echocardiography at our hospital, revealed that she was suffering from a prolapsed mitral valve. We feel strongly that in young patients (below 45 years) with acute cerebral ischemic events of unexplained etiology, MVP should be excluded by careful clinical examination and further evaluation which must include echocardiography. Mitral valve prolapse should be considered also as a possible source of embolism in transient ischemic attacks or strokes in some older patients. However, a causative role for MVP in this category of patients would be much harder to prove as there are more common etiologic and risk factors operating in this age group.From all the available evidence, it would appear that the risk of thromboembolism in the MVP patient population may be restricted to a small subgroup of individuals that is particularly prone to this complication. Therefore, we do not feel it is justified to warn patients of this risk or to use antiplatelet therapy routinely in MVP. Nevertheless, it would be prudent to treat those patients who have had an ischemic episode with antiplatelet drugs. Moreover, in view of the high incidence of MVP in young females, the use of oral contraceptives should be considered contraindicated in those with documented MVP. Further studies to define the prevalence of MVP and its complications are needed not only in Saudi Arabia but also in other regions of the Middle East. Comparisons can then be made with other areas of the world so that a comprehensive and global picture of this apparently common cardiac disorder and its possible complications may begin to emerge.ARTICLE REFERENCES:1. Savage DD, Garrison RJ, Devereux RB, et al. Mitral valve prolapse in the general population: I. Epidemiologic features: the Framingham study . Am Heart J. 1983; 106 (3): 571–6. Google Scholar2. Retchin SM, Fletcher RH, Earp J, et al. Mitral valve prolapse: disease or illness? Arch Intern Med. 1986; 146 (6): 1081–4. Google Scholar3. 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Watson RT. TIA, stroke, and mitral valve prolapse . Neurology. 1979; 29 (6): 886–9. Google Scholar10. Hanson MR, Conomy JP, Hodgman JR. Brain events associated with mitral valve prolapse . Stroke. 1980; 11 (5): 499–505. Google Scholar11. Woldoff HS, Gerber M, Desser KF, et al. Retinal vascular lesions in two patients with prolapsed mitral valve leaflets . Am J Ophthalmol. 1975; 79 (3): 382–5. Google Scholar12. Wilson LA, Keeling PW, Malcolm AD, et al. Visual complication of mitral leaflet prolapse . Br Med J. 1977; 2 (6079): 86–8. Google Scholar13. Sandok BA, Giuliani ER. Cerebral ischemic events in patients with mitral valve prolapse . Stroke. 1982; 13 (4): 448–50. Google Scholar14. Agarwal BL. Rheumatic heart disease unabated in developing countries . Lancet. 1981; 2 (8252): 910–1. Google Scholar15. Al-Harthi SS, Husain IS, Al-Orainey IO, et al. Prevalence of mitral valve prolapse in presumably healthy young Saudi men . Ann Saudi Med. 1988; 8 (1): 40–2. Google Scholar16. 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Google Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 9, Issue 5September 1989 Metrics History Accepted18 January 1989Published online1 September 1989 InformationCopyright © 1989, Annals of Saudi MedicinePDF download" @default.
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