Prevalence and Clinical Outcome of Mitral-Valve Prolapse
Lisa A. Freed, M.D., Daniel Levy, M.D., Robert A. Levine, M.D., Martin G. Larson, Sc.D., Jane C. Evans, D.Sc., M.P.H., Deborah L. Fuller, R.D.C.S., Birgitta Lehman, R.D.C.S., and Emelia J. Benjamin, M.D.
Background Mitral-valve prolapse has been described as a commondisease with frequent complications. To determine the prevalenceof mitral-valve prolapse in the general population, as diagnosedwith the use of current two-dimensional echocardiographic criteria,we examined the echocardiograms of 1845 women and 1646 men (mean[±SD] age, 54.7±10.0 years) who participated inthe fifth examination of the offspring cohort of the FraminghamHeart Study.
Methods Classic mitral-valve prolapse was defined as superiordisplacement of the mitral leaflets of more than 2 mm duringsystole and as a maximal leaflet thickness of at least 5 mmduring diastasis, and nonclassic prolapse was defined as displacementof more than 2 mm, with a maximal thickness of less than 5 mm.
Results A total of 84 subjects (2.4 percent) had mitral-valveprolapse: 47 (1.3 percent) had classic prolapse, and 37 (1.1percent) had nonclassic prolapse. Their age and sex distributionswere similar to those of the subjects without prolapse. Noneof the subjects with prolapse had a history of heart failure,one (1.2 percent) had atrial fibrillation, one (1.2 percent)had cerebrovascular disease, and three (3.6 percent) had syncope,as compared with unadjusted prevalences of these findings inthe subjects without prolapse of 0.7, 1.7, 1.5, and 3.0 percent,respectively. The frequencies of chest pain, dyspnea, and electrocardiographicabnormalities were similar among subjects with prolapse andthose without prolapse. The subjects with prolapse were leaner(P<0.001) and had a greater degree of mitral regurgitationthan those without prolapse, but on average the regurgitationwas classified as trace or mild.
Conclusions In a community-based sample of the population, theprevalence of mitral-valve prolapse was lower than previouslyreported. The prevalence of adverse sequelae commonly associatedwith mitral-valve prolapse in studies of patients referred forthat diagnosis was also low.
Mitral-valve prolapse has been described as a common disorder,with prevalence estimates generally ranging from 5 to 15 percentand up to 35 percent in some studies.1,2,3,4,5,6,7 In addition,mitral-valve prolapse has often been portrayed as a diseasewith frequent and serious complications, including stroke, atrialfibrillation, heart failure, and mitral regurgitation requiringsurgery.8,9,10,11,12,13 However, previous studies examiningthe prevalence and epidemiology of prolapse have been limitedby the use of hospital-based samples or highly selected patientsreferred because of mitral-valve prolapse, who are more likelyto have clinical complications.14,15 They have also relied onM-mode or two-dimensional echocardiographic views that are notspecific for the diagnosis of mitral-valve prolapse.2,7,16,17The frequent diagnosis of prolapse and the emphasis on potentialcomplications may have marked effects on young, otherwise healthypersons, including anxiety about the possibility of adverseevents, ineligibility for insurance or increased insurance rates,and the need for antibiotic prophylaxis.18,19
Studies describing the three-dimensional shape of the mitralannulus20,21 have allowed the two-dimensional echocardiographiccharacterization of prolapse to be refined, thus minimizingfalse positive diagnoses.22,23,24 To our knowledge, however,no investigators have evaluated a community-based sample ofsubjects using current two-dimensional echocardiographic criteriato determine the prevalence and potential complications of mitral-valveprolapse. Therefore, in a study designed to be free of referralbias, we examined the prevalence of mitral-valve prolapse andits clinical associations in an unselected sample of outpatients.
Methods
Subjects
The Framingham Heart Study was established in 1948 as a prospectiveepidemiologic investigation of a large cohort of men and women.25The offspring of the original subjects and the spouses of theoffspring were enrolled in a prospective study in 1971.26 Subjectswho participated in the fifth examination of the offspring cohort,which began in January 1991 and was completed in January 1995,were the focus of this study. The examination protocol was approvedby the institutional review board of Boston Medical Center,and all subjects gave informed consent.
A total of 3736 subjects who participated in the fifth examinationwere evaluated; 245 were excluded because of technically inadequateechocardiograms. Thus, the study group consisted of 3491 subjects(1845 women and 1646 men; mean [±SD] age, 54.7±10.0years) for whom two-dimensional echocardiograms were availablethat were adequate for evaluating the mitral valve. Five ofthese subjects had a history of mitral-valve repair or replacement,only one of whom had undergone surgery for mitral-valve prolapse.The other four had undergone surgery for other abnormalities,such as mitral stenosis and ischemic regurgitation. These fivesubjects were included in the calculation of the prevalenceof mitral-valve prolapse and associated clinical conditions,but they were excluded from all other analyses of the mitralvalve and clinical characteristics because of the surgical intervention.
To ensure that no cases of mitral-valve prolapse were missed,we examined the echocardiograms of all subjects who had previouslybeen identified as possibly having leaflet displacement suggestingprolapse in any two-dimensional view or on M-mode echocardiographyat any examination of the offspring cohort. This broad approachidentified 518 subjects. First, we assessed the echocardiogramsobtained at the fifth examination of these subjects to identifythose in whom qualitative superior displacement of the mitralleaflets during systole warranted a quantitative evaluationto determine whether prolapse was actually present. The 151case subjects identified in this way were paired with controlsmatched for age and sex who were drawn from the fifth examinationand who were initially coded as having no evidence of prolapse.The echocardiograms of these two subgroups were then examinedfor mitral-valve prolapse by cardiologists who were unawareof the subjects' status.
Echocardiographic Methods
All subjects underwent standard two-dimensional echocardiographywith a commercially available system (Sonos 1000, HewlettPackard,Andover, Mass.) that used a 2.5-MHz transducer. Images wererecorded on videotape, including complete parasternal, apical,and subcostal views and color Doppler assessment of valvularregurgitation. All measurements were performed with a Sony Off-lineCardiac Analysis System (Sum 1010, Sony, Park Ridge, N.J.).
We used current two-dimensional echocardiographic criteria basedon the three-dimensional shape of the annulus and clinical correlations12,20,21,22,23,24to diagnose mitral-valve prolapse according to the maximal superiordisplacement of the mitral leaflets during systole relativeto the line connecting the annular-hinge points. We measuredthe displacement of the anterior and posterior mitral leafletsin the parasternal and apical long-axis views, which were scannedby tilting the transducer to visualize all three scallops ofthe posterior leaflet.12,20,21,22,23 Because the lateral scallopof the posterior leaflet is most difficult to evaluate fromthese views, we also measured the displacement of this leafletin the apical four-chamber view22,27; however, the degree ofdisplacement was always confirmed by examination of the long-axisscans. The thickness of the mitral leaflets during diastasiswas measured from the leading to the trailing edge of the thickestarea of the mid-portion of the leaflet, excluding focal areasof thickness and chordae.12,22,24,28,29,30 Each leaflet wasmeasured and categorized according to the maximal thickness.
On the basis of prior clinical and prognostic studies, subjectswere classified as having classic prolapse if displacement exceeded2 mm and maximal thickness was at least 5 mm (Figure 1 and Figure 2)and as having nonclassic prolapse if displacement exceeded2 mm but the maximal thickness was less than 5 mm.8,12,22,23,24,28Borderline degrees of displacement (2 mm) are not associatedwith increased leaflet thickness, mitral regurgitation, leftatrial enlargement, valve-related complications, or progressionover a period of 10 years and were not included in the definitionof prolapse.22,24,31 The degree of mitral regurgitation wasassessed as the ratio of the maximal regurgitant jet area tothe area of the left atrium in the parasternal and apical long-axisand apical four-chamber views.32 The degree of regurgitationwas considered to be trace, mild, moderate, or severe on thebasis of ratios of >0 to 10, >10 to 20, >20 to 40,and >40 percent, respectively.32
Figure 1. Classic Mitral-Valve Prolapse during Systole.
The parasternal long-axis view shows the mitral leaflets prolapsing (>2 mm), as indicated by the dotted line, into the left atrium during systole. LA denotes left atrium, and LV left ventricle.
Figure 2. Classic Mitral-Valve Prolapse with Leaflet Thickening (Arrows) during Diastole.
The parasternal long-axis view demonstrates mitral-leaflet thickening (5 mm) during diastole. LA denotes left atrium, and LV left ventricle.
Clinical Variables
Clinical variables were derived from assessments of the subjects'histories and physical examinations performed by FraminghamHeart Study physicians. Diagnoses of cardiovascular end pointswere made by a committee of three physicians who evaluated recordsfrom the Framingham Heart Study clinic examinations, interimhospitalizations, and visits to personal physicians in accordancewith published criteria.33,34 The clinical variables that wecompared in subjects with mitral-valve prolapse and those withoutprolapse were age, sex, symptoms of chest pain or dyspnea, historyof hypertension (defined as a systolic blood pressure of atleast 140 mm Hg or a diastolic blood pressure of at least 90mm Hg on each of two successive readings obtained by the clinicphysician or as current use of antihypertensive medication),presence of coronary heart disease (defined as angina pectoris,coronary insufficiency, or myocardial infarction), presenceof diabetes mellitus (glucose level of at least 140 mg per deciliter[7.7 mmol per liter] after a 12-hour fast or the use of insulinor an oral hypoglycemic agent), current cigarette smoking, andpresence of hypercholesterolemia (defined as a serum total cholesterollevel of at least 240 mg per deciliter [6.21 mmol per liter]).33,34The two groups were also compared with respect to history ofheart failure, atrial fibrillation, cerebrovascular disease(defined as stroke or transient ischemic attack), and syncope.33,34
The physical examination included measurements of body-massindex (the weight in kilograms divided by the square of theheight in meters), waist-to-hip ratio, and systolic and diastolicblood pressures and assessments for mitral systolic murmur andmid-systolic click. Electrocardiographic variables assessedincluded the presence of atrial and ventricular ectopy, leftatrial enlargement (defined as a terminal P-wave force of 1mm by 1 mm in lead V1), and left ventricular hypertrophy (definedby the presence of increased voltage with a pattern indicatingstrain).35
Statistical Analysis
For the dichotomous clinical variables, the differences betweensubjects with mitral-valve prolapse and those without prolapsewere tested with use of the Wald chi-square test for logistic-regressionanalysis, after adjustment for age, sex, and body-mass index.Continuous variables were evaluated by means of analysis ofcovariance. The evaluation of the difference in age was adjustedfor sex. Body-mass index and waist-to-hip ratio were adjustedfor sex and age. All other comparisons were adjusted for age,sex, and body-mass index. Systolic and diastolic blood pressureswere also adjusted for treatment with antihypertensive medications.Values are given as least-squares means and standard errors.All comparisons were made by comparing all the subjects withprolapse with those without prolapse. This was an a priori decisionmade because of the relatively small number of subjects withprolapse. All P values were two-sided. Correlation coefficientswere used to express intraobserver and interobserver variability.SAS statistical software (version 6.11, SAS Institute, Cary,N.C.) was used for all calculations.
Results
Prevalence of Mitral-Valve Prolapse
Quantitative evaluation revealed that 47 subjects (1.3 percent)had classic mitral-valve prolapse and 37 (1.1 percent) had nonclassicmitral-valve prolapse (Table 1). The remainder of the subjectsdid not meet quantitative criteria for prolapse, including all151 subjects whose initial qualitative evaluation had not suggestedprolapse. Among subjects with classic prolapse, the mean (±SD)maximal leaflet displacement was 3.8±1.0 mm, the meanthickness of the anterior leaflet was 5.0±0.6 mm, andthe mean thickness of the posterior leaflet was 5.6±0.5mm. The corresponding values in the subjects with nonclassicprolapse were 3.1±0.6 mm, 3.9±0.5 mm, and 4.1±0.6 mm. Among subjects without prolapse, the maximal leafletdisplacement was 0.5±2.0 mm, the mean thicknessof the anterior leaflet was 3.3±0.7 mm, and the meanthickness of the posterior leaflet was 3.4±0.8 mm.
The age and sex distributions of the subjects with prolapsewere similar to those of the subjects without prolapse. Thesex-adjusted mean (±SE) age of the patients with classicprolapse was 56.7±1.5 years, as compared with a meanage of 55.4±1.6 years for those with nonclassic prolapseand of 54.7±0.2 years for those without prolapse (P=0.19).The range of ages for the group as a whole was 26 to 84 years;mitral-valve prolapse had no predilection for young subjectsand a fairly even distribution (2 to 3 percent) among subjectsin each decade of age from 30 to 80 years. With respect to sex,59.5 percent of the subjects with mitral-valve prolapse werewomen, as compared with 52.7 percent of those without prolapse(P=0.21) (Table 1).
Clinical Findings and Symptoms
None of the 84 subjects with mitral-valve prolapse had a historyof heart failure, 1 (1.2 percent) had atrial fibrillation, 1(1.2 percent) had cerebrovascular disease (stroke or transientischemic attack), and 3 (3.6 percent) had syncope, as comparedwith unadjusted prevalences of these findings in the group withoutprolapse of 0.7, 1.7, 1.5, and 3.0 percent, respectively (Table 2).One subject with classic prolapse had undergone mitral-valverepair before the examination; he was also the one subject withprolapse who had atrial fibrillation. Subjects with prolapsehad a greater degree of mitral regurgitation than those withoutprolapse. The mean (±SE) ratio of the jet area to theleft atrial area was 15.1±1.3 percent among subjectswith classic mitral-valve prolapse, 8.9±1.5 percent amongsubjects with nonclassic prolapse, and 2.4± 0.6 percentamong 218 control subjects without prolapse (P<0.001). However,on average, subjects with classic prolapse had mild regurgitationand those with nonclassic or no prolapse had trace regurgitation.Severe regurgitation, with the area of the regurgitant jet beinggreater than 40 percent of the area of the left atrium, occurredin 7 percent of the subjects with classic prolapse, as comparedwith none of the subjects who had nonclassic prolapse and 0.5percent of those without prolapse. One subject with classicprolapse had a remote history of infective endocarditis.
Table 2. Prevalence of Various Clinical Findings According to the Presence or Absence of Mitral-Valve Prolapse.
The prevalences of chest pain and dyspnea were similar in thepatients with prolapse and those without it (Table 3). The prevalenceof coronary heart disease was marginally lower among the subjectswith prolapse (P=0.06). The prevalences of risk factors forcoronary heart disease, including smoking, hypertension, diabetes,and hypercholesterolemia, are summarized in Table 3.
Table 3. Prevalence of Various Clinical Characteristics.
Physical and Electrocardiographic Findings
Physical and electrocardiographic findings are shown in Table 4.Subjects with prolapse were significantly leaner on the basisof body-mass index and waist-to-hip ratio and were more likelyto have systolic murmurs and mid-systolic clicks than thosewithout prolapse. There were no significant differences betweenthe two groups in systolic or diastolic blood pressure or inthe prevalence of electrocardiographic abnormalities.
Table 4. Physical and Electrocardiographic Findings.
Reproducibility of Echocardiographic Findings
The intraobserver and interobserver correlations for mitral-leafletdisplacement, leaflet thickness, and the degree of mitral regurgitationin 20 subjects exceeded 0.97.
Discussion
The prevalence of mitral-valve prolapse in this unselected groupof ambulatory subjects was substantially lower than that previouslyreported (classic prolapse, 1.3 percent; nonclassic prolapse,1.1 percent).1,2,3,4,5,6,7 In contrast to previous reports,we found that the rates of heart failure, atrial fibrillation,cerebrovascular disease, and syncope were no higher among subjectswith mitral-valve prolapse than among those without prolapse.Chest pain and dyspnea were present in 11 to 15 percent of thosewith prolapse, a range that was lower than the value in subjectswithout prolapse and that is consistent with previous reports.36In addition, as reported previously,1,4,5,37,38 we found thatsubjects with prolapse were leaner (lower body-mass index andwaist-to-hip ratio) than those without prolapse. Subjects withprolapse were more likely to have mitral regurgitation (P<0.001),but the degree of regurgitation in those with prolapse was,on average, mild.
The numerous referral-based studies have increased our understandingof the pathophysiology and management of prolapse in its mostsevere forms. Our findings, however, imply that a small proportionof persons in an outpatient setting have mitral-valve prolapseand that the clinical profile of these subjects is more benignthan previously indicated by the available literature.
Mitral-valve prolapse has been described as the most commoncardiac valvular abnormality in industrialized countries.39In previous studies with higher prevalences, the subjects havelargely been volunteers,2,3,6 some self-referred and some "self-selected."In two studies,3,6 subjects were selected from large clinicor hospital practices. Such studies are subject to selectionbias: volunteers who respond to advertisements and randomlyselected volunteers who agree to participate in a study may,in fact, be concerned about their cardiac status because theyhave affected relatives or a remote history of a heart murmur.As a result, the reported prevalences may not reflect thosein the general community.
Prolapse is an abnormal displacement of the mitral leafletsrelative to their surrounding structures. Previous studies usedM-mode echocardiography or less specific two-dimensional criteria(including displacement of the anterior leaflet in the apicalfour-chamber view) to diagnose mitral-valve prolapse. M-modeechocardiography fails to display the leaflets in relation totheir surrounding annular attachments,16 and the results varywidely depending on the orientation of the transducer.17 Two-dimensionalviews display the leaflets and annulus, but the results mustbe interpreted in the context of the three-dimensional saddle-likeshape of the valve.20,21 A side-to-side (four-chamber) viewthrough such a structure can normally show leaflets apparentlybulging upward relative to the low points of the annular saddlein the absence of any leaflet disease or distortion.20,21,22Eliminating the use of such views reduces the frequency of diagnosiswithout excluding persons with thickening of the leaflets, regurgitation,or valve-related complications characteristic of the myxomatousprocess.22,24 Prior reports have in fact shown that estimatesof the prevalence of prolapse are lower when more specific criteriaare used.7
In addition to ensuring a low false positive rate through theuse of newer diagnostic criteria, our study design minimizedfalse negative rates as well. All subjects suspected of havingprolapse at any prior examination with the use of older, lessspecific criteria were screened with use of the newer, highlyspecific criteria, and the results were then assessed in a blindedfashion. The low false negative rate was confirmed by the findingof no cases of mitral-valve prolapse among our control subjects.
Mitral-valve prolapse has been reported to be the leading causeof isolated mitral regurgitation39 and regurgitation requiringsurgery.40 Duren et al., for example, found complications suchas the need for mitral-valve surgery, stroke, infectious endocarditis,and sudden death in one third of patients with mitral-valveprolapse (100 of 300) who were followed for an average of 6.1years, with an average complication rate of 5.4 percent peryear.10 Marks et al. reported complications in 27 percent ofpatients with classic mitral-valve prolapse (86 of 319).12 Astrong association with complications is generally reportedin hospital-based samples, in which patients are commonly referredfor the complications under investigation. Some authors havedocumented this referral bias by showing that the rate of complicationswas lower among affected family members of referred study patients.13
The design of the Framingham Heart Study effectively minimizesselection bias. Consequently, we found a low prevalence of conditionsreported by others as complications attributable to prolapse.This low prevalence is also consistent with the relatively lowrisks of serious complications reported in some previous studies.11,13The low prevalence of serious complications among subjects withprolapse in the community is similar to the findings in studiesof hypertrophic cardiomyopathy. Studies at major referral institutionssuggested that this disease was frequently symptomatic and hada high rate of severe complications, including sudden death.Eliminating such patient-referral and selection biases throughthe use of outpatient samples has dramatically changed the perceptionof hypertrophic cardiomyopathy and its natural history.14,15
Referral bias or patterns of seeking medical attention for symptomsmay also help explain the previous perception of prolapse asa disease heavily affecting young women, which is not what wefound. The relatively low sensitivity of clicks and murmursfor prolapse in our study may also reflect the relatively mildnature of prolapse in the general population as compared withreferral-based series, as does the absence of a significantdifference in the prevalence of ventricular ectopy between thosewith prolapse and those without prolapse. This finding is consistentwith previous findings that serious ventricular arrhythmiasand sudden death are more likely in patients with prolapse whohave severe mitral regurgitation and left ventricular dysfunction.39Long-term follow-up will be necessary for the fullest determinationof complication rates and natural history in this sample.
Although the number of subjects in the study was large 3491 the number of subjects with prolapse was moderate(84), and there was a low prevalence of potential complications.The low prevalence of prolapse and potential complications resultedin wide 95 percent confidence intervals. In addition, as withany cross-sectional study, the prevalence of prolapse and theseverity of complications were affected by survival bias. Infact, those who had the most serious complications of prolapse,such as sudden death, may not have been included in our studybecause they were not among the members of the cohort who participatedin the fifth study examination. Finally, the subjects were predominantlywhite, and it is possible that the results may not be generalizableto other ethnic and racial groups.
Quantification of the prevalence of mitral-valve prolapse inthe general population is important for several reasons. Itdefines the magnitude of the condition and provides a basisfor determining the validity of proposed associations. It alsoallows researchers to address whether prolapse occurs more frequentlyamong patients with presumed complications, such as stroke,than in the general population. In addition, both prevalenceand complication rates are important factors in balancing thepotential risks and benefits of antibiotic prophylaxis againstendocarditis.19 The low frequency of complications in our studymay alter the perception of the severity of the disease andallay anxiety for those in whom mitral-valve prolapse is diagnosedin a general outpatient setting.
Supported in part by a contract (N01-HC-38038) with the NationalHeart, Lung, and Blood Institute; by grants from the NationalInstitute of Neurological Disorders and Stroke (5-R01-NS-17950-16),the National Heart, Lung, and Blood Institute (2-R01-HL-38176-06),and the HewlettPackard Foundation; and by the Roman W.DeSanctis Clinical Scholar Fund.
Source Information
From the National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, Mass. (L.A.F., D.L., M.G.L., J.C.E., D.L.F., B.L., E.J.B.); the Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston (L.A.F., R.A.L.); Harvard Medical School, Boston (L.A.F., D.L., R.A.L.); the National Heart, Lung, and Blood Institute, Bethesda, Md. (D.L.); the Divisions of Cardiology and Clinical Epidemiology, Beth Israel Deaconess Medical Center, Boston (D.L.); and the Divisions of Cardiology (D.L., E.J.B.) and Epidemiology and Preventive Medicine (D.L., M.G.L., J.C.E., E.J.B.), Boston University School of Medicine, Boston.
Address reprint requests to Dr. Benjamin at the Framingham Heart Study, Boston University School of Medicine, 5 Thurber St., Framingham, MA 01702-6334, or at emelia{at}fram.nhlbi. nih.gov.
References
Levy D, Savage D. Prevalence and clinical features of mitral valve prolapse. Am Heart J 1987;113:1281-1290. [CrossRef][Medline]
Markiewicz W, Stoner J, London E, Hunt SA, Popp RL. Mitral valve prolapse in one hundred presumably healthy young females. Circulation 1976;53:464-473. [Free Full Text]
Procacci PM, Savran SV, Schreiter SL, Bryson AL. Prevalence of clinical mitral-valve prolapse in 1169 young women. N Engl J Med 1976;294:1086-1088. [Abstract]
Savage DD, Garrison RJ, Devereux RB, et al. Mitral valve prolapse in the general population. 1. Epidemiologic features: the Framingham Study. Am Heart J 1983;106:571-576. [CrossRef][Medline]
Savage DD, Devereux RB, Garrison RJ, et al. Mitral valve prolapse in the general population. 2. Clinical features: the Framingham Study. Am Heart J 1983;106:577-581. [CrossRef][Medline]
Bryhn M, Persson S. The prevalence of mitral valve prolapse in healthy men and women in Sweden. Acta Med Scand 1984;215:157-160. [Medline]
Warth DC, King ME, Cohen JM, Tesoriero VL, Marcus E, Weyman AE. Prevalence of mitral valve prolapse in normal children. J Am Coll Cardiol 1985;5:1173-1177. [Abstract]
Nishimura RA, McGoon MD, Shub C, Miller FA Jr, Ilstrup DM, Tajik AJ. Echocardiographically documented mitral-valve prolapse: long-term follow-up of 237 patients. N Engl J Med 1985;313:1305-1309. [Abstract]
Devereux RB, Hawkins I, Kramer-Fox R, et al. Complications of mitral valve prolapse: disproportionate occurrence in men and older patients. Am J Med 1986;81:751-758. [CrossRef][Medline]
Duren DR, Becker AE, Dunning AJ. Long-term follow-up of idiopathic mitral valve prolapse in 300 patients: a prospective study. J Am Coll Cardiol 1988;11:42-47. [Abstract]
Wilcken DEL, Hickey AJ. Lifetime risk for patients with mitral valve prolapse of developing severe valve regurgitation requiring surgery. Circulation 1988;78:10-14. [Free Full Text]
Marks AR, Choong CY, Sanfilippo AJ, Ferré M, Weyman AE. Identification of high-risk and low-risk subgroups of patients with mitral-valve prolapse. N Engl J Med 1989;320:1031-1036. [Abstract]
Zuppiroli A, Rinaldi M, Kramer-Fox R, Favilli S, Roman MJ, Devereux RB. Natural history of mitral valve prolapse. Am J Cardiol 1995;75:1028-1032. [CrossRef][Medline]
Spirito P, Chiarella F, Carratino L, Berisso MZ, Bellotti P, Vecchio C. Clinical course and prognosis of hypertrophic cardiomyopathy in an outpatient population. N Engl J Med 1989;320:749-755. [Abstract]
Maron BJ, Casey SA, Poliac LC, Gohman TE, Almquist AK, Aeppli DM. Clinical course of hypertrophic cardiomyopathy in a regional United States cohort. JAMA 1999;281:650-655. [Free Full Text]
Sahn DJ, Wood J, Allen HD, Peoples W, Goldberg SJ. Echocardiographic spectrum of mitral valve motion in children with and without prolapse: the nature of the false positive diagnosis. Am J Cardiol 1977;39:422-431. [CrossRef][Medline]
Markiewicz W, London E, Popp RL. Effect of transducer placement on echocardiographic mitral valve motion. Am Heart J 1978;96:555-556. [CrossRef][Medline]
Leatham A, Brigden W. Mild mitral regurgitation and the mitral prolapse fiasco. Am Heart J 1980;99:659-664. [CrossRef][Medline]
Devereux RB, Frary CJ, Kramer-Fox R, Roberts RB, Ruchlin HS. Cost-effectiveness of infective endocarditis prophylaxis for mitral valve prolapse with or without a mitral regurgitant murmur. Am J Cardiol 1994;74:1024-1029. [CrossRef][Medline]
Levine RA, Triulzi MO, Harrigan P, Weyman AE. The relationship of mitral annular shape to the diagnosis of mitral valve prolapse. Circulation 1987;75:756-767. [Free Full Text]
Levine RA, Handschumacher MD, Sanfilippo AJ, et al. Three-dimensional echocardiographic reconstruction of the mitral valve, with implications for the diagnosis of mitral valve prolapse. Circulation 1989;80:589-598. [Free Full Text]
Levine RA, Stathogiannis E, Newell JB, Harrigan P, Weyman AE. Reconsideration of echocardiographic standards for mitral valve prolapse: lack of association between leaflet displacement isolated to the apical four chamber view and independent echocardiographic evidence of abnormality. J Am Coll Cardiol 1988;11:1010-1019. [Abstract]
Perloff JK, Child JS. Mitral valve prolapse: evolution and refinement of diagnostic techniques. Circulation 1989;80:710-711. [Free Full Text]
Nidorf SM, Weyman AE, Hennessey R, Newell JB, Levine RA. The relationship between mitral valve morphology and prognosis in patients with mitral valve prolapse: a prospective echocardiographic study of 568 patients. J Am Soc Echocardiogr 1993;6:S8-S8.abstract
Dawber TR, Meadors GF, Moore FE Jr. Epidemiological approaches to heart disease: the Framingham Study. Am J Public Health 1951;41:279-286.
Kannel WB, Feinleib M, McNamara PM, Garrison RJ, Castelli WP. An investigation of coronary heart disease in families: the Framingham Offspring Study. Am J Epidemiol 1979;110:281-290. [Free Full Text]
Shah PM. Echocardiographic diagnosis of mitral valve prolapse. J Am Soc Echocardiogr 1994;7:286-293. [Medline]
Chandraratna PAN, Nimalasuriya A, Kawanishi D, Duncan P, Rosin B, Rahimtoola SH. Identification of the increased frequency of cardiovascular abnormalities associated with mitral valve prolapse by two-dimensional echocardiography. Am J Cardiol 1984;54:1283-1285. [Medline]
Weissman NJ, Pini R, Roman MJ, Kramer-Fox R, Andersen HS, Devereux RB. In vivo mitral valve morphology and motion in mitral valve prolapse. Am J Cardiol 1994;73:1080-1088. [CrossRef][Medline]
Louie EK, Langholz D, Mackin WJ, Wallis DE, Jacobs WR, Scanlon PJ. Transesophageal echocardiographic assessment of the contribution of intrinsic tissue thickness to the appearance of a thick mitral valve in patients with mitral valve prolapse. J Am Coll Cardiol 1996;28:465-471. [Abstract]
Vivaldi MT, Sagie A, Adams MS, et al. 10-Year echocardiographic and clinical follow-up of patients with nonclassic mitral valve prolapse: does it progress? Circulation 1994;90:Suppl I:I-222.abstract
Helmcke F, Nanda NC, Hsiung MC, et al. Color Doppler assessment of mitral regurgitation with orthogonal planes. Circulation 1987;75:175-183. [Free Full Text]
Kannel WB, Wolf PA, Garrison RJ, eds. The Framingham Study: an epidemiological investigation of cardiovascular disease. Section 35. Survival following initial cardiovascular events: 30 year follow-up. Bethesda, Md.: National Heart, Lung, and Blood Institute, 1988. (NIH publication no. 88-2969.)
Kannel WB, Gordon T, eds. The Framingham Study: an epidemiological investigation of cardiovascular disease. Section 30. Some characteristics related to the incidence of cardiovascular disease and death: Framingham Heart Study, 18-year follow-up. Washington, D.C.: Government Printing Office, 1974. (DHEW publication no. NIH-74-599.)
Levy D, Labib SB, Anderson KM, Christiansen JC, Kannel WB, Castelli WP. Determinants of sensitivity and specificity of electrocardiographic criteria for left ventricular hypertrophy. Circulation 1990;81:815-820. [Free Full Text]
Devereux RB, Kramer-Fox R, Brown WT, et al. Relation between clinical features of the mitral prolapse syndrome and echocardiographically documented mitral valve prolapse. J Am Coll Cardiol 1986;8:763-772. [Abstract]
Devereux RB, Brown WT, Lutas EM, Kramer-Fox R, Laragh JH. Association of mitral-valve prolapse with low body-weight and low blood pressure. Lancet 1982;2:792-795. [Medline]
Cohen JL, Austin SM, Segal KR, Millman AE, Kim CS. Echocardiographic mitral valve prolapse in ballet dancers: a function of leanness. Am Heart J 1987;113:341-344. [CrossRef][Medline]
Devereux RB, Kramer-Fox R, Kligfield P. Mitral valve prolapse: causes, clinical manifestations, and management. Ann Intern Med 1989;11:305-317.
Waller BF, Morrow AG, Maron BJ, et al. Etiology of clinically isolated, severe, chronic, pure mitral regurgitation: analysis of 97 patients over 30 years of age having mitral valve replacement. Am Heart J 1982;104:276-288. [CrossRef][Medline]
Mitral-Valve Prolapse
Jeresaty R. M., Cheng T. O., Freed L. A., Levy D., Levine R. A., Evans J. C., Benjamin E. J.
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Full Text
N Engl J Med 1999;
341:1471-1472, Nov 4, 1999.
Correspondence
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[Abstract][Full Text]
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[Abstract][Full Text]
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[Abstract][Full Text]
Lau, E.W, Prasad, N
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5: 82-85
[Abstract][Full Text]
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[Abstract][Full Text]
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[Abstract][Full Text]
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34: 1345-1345
[Full Text]
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[Abstract]
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[Abstract][Full Text]
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156: 1021-1027
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88: iv11-19
[Full Text]
Pellerin, D, Brecker, S, Veyrat, C
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88: iv20-28
[Full Text]
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22: e6-e6
[Abstract][Full Text]
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40: 1298-1304
[Abstract][Full Text]
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106: 1305-1307
[Full Text]
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106: 1355-1361
[Abstract][Full Text]
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33: 1950-1955
[Abstract][Full Text]
Hoffman, J. I. E., Kaplan, S.
(2002). The incidence of congenital heart disease. J Am Coll Cardiol
39: 1890-1900
[Abstract][Full Text]
Atalar, E., Aqil, T., Aytemir, K., Haznedarolu, I., Ozer, N., Kiliq, H., Kuru, G., Aksdyek, S., Ovtinq, K., Kes, S., Kirazli, e., Ozmen, F.
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8: 41-44
[Abstract]
Jouven, X., Ducimetiere, P.
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22: 1759-1761
Smolens, I. A., Pagani, F. D., Deeb, G. M., Prager, R. L., Sonnad, S. S., Bolling, S. F.
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72: 1210-1216
[Abstract][Full Text]
Mohty, D., Orszulak, T. A., Schaff, H. V., Avierinos, J.-F., Tajik, J. A., Enriquez-Sarano, M.
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104
: I-1-I-7
[Abstract][Full Text]
Priori, S.G., Aliot, E., Blomstrom-Lundqvist, C., Bossaert, L., Breithardt, G., Brugada, P., Camm, A.J., Cappato, R., Cobbe, S.M., Di Mario, C., Maron, B.J., McKenna, W.J., Pedersen, A.K., Ravens, U., Schwartz, P.J., Trusz-Gluza, M., Vardas, P., Wellens, H.J.J., Zipes, D.P.
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22: 1374-1450
Aessopos, A., Farmakis, D., Karagiorga, M., Voskaridou, E., Loutradi, A., Hatziliami, A., Joussef, J., Rombos, J., Loukopoulos, D.
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[Abstract][Full Text]
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107: 1237-1237
[Full Text]
Zouridakis, E. G., Parthenakis, F. I., Kochiadakis, G. E., Kanoupakis, E. M., Vardas, P. E.
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3: 292-298
[Abstract]
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: 300S-320S
[Full Text]
Enriquez-Sarano, M.
(2000). Reply. J Am Coll Cardiol
36: 2014-2015
[Full Text]
Jouven, X., Zureik, M., Desnos, M., Courbon, D., Ducimetiere, P.
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343: 826-833
[Abstract][Full Text]
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21: 255-258
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(1999). Mitral-Valve Prolapse. NEJM
341: 1471-1472
[Full Text]
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1999: 14-14
[Full Text]
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1999: 16-16
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1999: 1-1
[Full Text]
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1999: 1-1
[Full Text]
Gilon, D., Buonanno, F. S., Joffe, M. M., Leavitt, M., Marshall, J. E., Kistler, J. P., Levine, R. A.
(1999). Lack of Evidence of an Association between Mitral-Valve Prolapse and Stroke in Young Patients. NEJM
341: 8-13
[Abstract][Full Text]
Nishimura, R. A., McGoon, M. D.
(1999). Perspectives on Mitral-Valve Prolapse. NEJM
341: 48-50
[Full Text]