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Review |

Baldness and Coronary Artery Disease:  The Dermatologic Point of View of a Controversial Issue FREE

Alfredo Rebora, MD
[+] Author Affiliations

From the Department of Dermatology, University of Genoa, Genoa, Italy.Dr Rebora is now with the Department of Endocrinologic and Metabolic Diseases,Section of Dermatology, University of Genoa.


Arch Dermatol. 2001;137(7):943-947. doi:10-1001/pubs.Arch Dermatol.-ISSN-0003-987x-137-7-dre0006.
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Published online

Objective  Several articles, most of them written by nondermatologists, have stressedthat bald men have a higher risk for coronary artery disease than men whoare not bald. This study was performed to evaluate the validity of such conclusionsfrom a dermatologic point of view.

Design  A review of the 24 articles in literature from 1954 to 1999 as providedby MEDLINE and a previous review.

Results  Five articles contained simple comments; 1 was a review of the previousliterature; and 3 dealt only with the lipid profile. The remaining 15 articlesdealt with coronary artery disease and baldness, and 9 of these concludedthat there is a relationship between the 2 conditions, especially in youngersubjects with severe early-onset androgenetic alopecia.

Conclusions  Baldness did not coincide with androgenetic alopecia in some of thearticles examined, which makes it difficult to settle the issue. Subjectswho develop baldness before their 30s may have a higher risk for coronaryartery disease than other men, and they may be individuals with early-onsetandrogenetic alopecia who also present with particularly elevated dihydrotestosterone-testosteroneratios. The baldness theory should be included as a secondary hypothesis inlarge epidemiological studies of coronary artery disease. Such studies shouldinclude dermatologic expertise for accurate, cost-effective evaluation ofbaldness.

IN THE LAST decade, several articles have indicated that bald men havea higher-than-normal risk for coronary artery disease (CAD) and that early-onsetandrogenetic alopecia (AGA), in particular, is somehow related to CAD. Suchconclusions cannot be underestimated by dermatologists who treat with patientswith AGA and who may prescribe systemic drugs. On the other hand, most ofthese articles have been written by nondermatologists, without confirmationby specialists in dermatology. Since AGA affects about 90% of the generalpopulation, epidemiological studies may rely only on disease severity. Thediagnosis of AGA is only apparently easy, and other forms of nonscarring alopeciasmay be incorrectly included in studies conducted by nondermatologists. Therefore,I screened the literature to evaluate the validity of the conclusions froma dermatologic point of view.

Medical literature published in any language since 1954 on baldnessand CAD was identified through a MEDLINE search using the key words coronary and baldness. Additionalreferences were identified from the reference lists of a published review.1

The articles reviewed involved studies of patients with baldness whowere recruited to evaluate other risk factors for CAD, and observational studies(case-control and cohort studies) concerning the possible association of baldnesswith CAD. Each study was evaluated according to the following criteria: howit was conducted; presence of possible flaws; number of patients examined;accuracy of the diagnosis of baldness; measure of the severity of baldness;cardiac outcome of the patients, adjustment for other risk factors (eg, smoking,history of hypertension, diabetes, high cholesterol level, alcohol intake,and physical activity), if any; and statistical analysis to assess the significanceof the association. Additional statistical tests (χ2 test)were performed whenever necessary.

Twenty-four articles met the criteria. Five articles26contained simple comments; 1 was a survey of the previous literature1; and 3 dealt only with the lipid profile.79The remaining 15 articles were therefore analyzed.

Gertler and White10 studied men who hada myocardial infarction before 40 years of age. The subjects entered the studyup to 10 years after the infarction occurred. Baldness was defined accordingto the Hamilton scale. Other risk factors for CAD were not studied. Therewas no difference between bald patients and controls. Only patients who survivedmyocardial infarction entered the study, and there was no information aboutthose who died.

Buechner et al11 compared 40 "heart patients"with 153 controls. No better definition of heart patients was provided. Thesubjects were defined as bald when they presented with extensive frontal andcoronal hair loss. The number of persons in each group was not given. Onlysmoking was considered among CAD risk factors. Statistical analysis was donewith the rank test. There was no statistical significance, possibly becauseof the small size of the sample.

Cotton et al12 compared 91 men with myocardialinfarction or angina with 98 blood donors. The subjects were classified into4 groups: no baldness, receding frontal hairline, a critical bald area, andtotal or subtotal hair loss. The cardiac group had higher scores for baldness,as well as for blood pressure and smoking habit. Nevertheless, multivariateanalysis showed that baldness was highly significantly associated with CAD(P≤.001).

Hamby et al13 prospectively evaluated710 men. Baldness was merely defined as frontoparietal hair loss. A significantlyhigher proportion of bald men had CAD than did nonbald men. Eighty-one percentof the bald men with CAD were bald before the clinical onset of CAD, and 65%were bald before 35 years of age.

Ben Halim et al14 interviewed 48 men whowere in the hospital for myocardial infarction and compared them with 48 menwith benign conditions. Hypertension and diabetes were exclusion criteria.Baldness was classified according to the Hamilton scale. No statistical differenceswere found between the 2 groups.

Cooke15 examined 478 hospitalized menin London, England. Baldness was defined as Hamilton class III or worse. Menwith diabetes were excluded. Cooke concluded that there was little relationshipbetween baldness and CAD. When Cooke's data were reanalyzed, however,1 a possible stronger relationship was revealed. The50- to 59-year-old group had an odds ratio (OR) of 2.77 (95% confidence interval[CI], 1.19-6.47). The data were insufficient to adjust baldness for otherrisk factors. My reanalysis of Cooke's data revealed that his bald subjectshad smoked significantly more than his nonbald subjects (52% vs 35%; OR, 1.57;95% CI, 1.05-2.35); therefore, smoking may account for the differences observedin CAD. Actually, smokers did not have CAD more often than nonsmokers (OR,0.69; 95% CI, 0.45-1.07); however, only individuals who smoked 10 or morecigarettes daily were defined as smokers, a factor that could underscore thevariable.

Persson and Johansson16 studied 464 menfor 22 years for CAD. Baldness was defined as "baldness or tonsure," and nostatistical analysis was performed. Nevertheless, baldness was suggested tobe "a new risk factor" for CAD. In their review, Herrera and Lynch1 reanalyzed the data and suggested that the percentageof bald men with CAD was not significantly higher than that of nonbald men(25% vs 19%; P = .16).

Emidy et al17 evaluated 1594 men who were40 to 59 years old at entry for 25-year mortality from CAD. Baldness was notdefined. Only 40- to 49-year-old bald men were found to be more susceptibleto CAD. Other CAD risk factors were considered in the statistical analysis.The original data were not available to me.

The case-control study of Lesko et al18involved 665 men younger than 55 years who had survived a first myocardialinfarction. The controls were 772 men admitted for noncardiac diagnoses. Menwith history of rheumatic heart disease, cardiomyopathy, or prior cardiacsurgery were excluded from both groups. Baldness was scored using the 12-pointmodified Hamilton scale. Other risk variables, such as blood pressure level,lipid levels, glucose intolerance, and cigarette smoking, were evaluated ininterviews and self-reports. After adjusting for age, the OR estimate forbaldness involving the vertex area of the scalp was 1.4 (95% CI, 1.20-1-90).The risk of myocardial infarction increased with the severity of baldness(P<.01), and the OR was 3.4 (95% CI, 1.70-7.00)for severe vertex baldness.

Herrera et al19 assessed the relationshipbetween the extent and progression of baldness and CAD in a cohort study of2017 men from the Framingham Study who were 35 to 74 years old. Baldness wasassessed twice 6 years apart on the front, sides, or back areas of the scalp.The subjects were classified as having no bald areas (n = 153), 1 bald area(n = 420), 2 bald areas (n = 587), and 3 bald areas (n = 857). A cohort of403 men was divided into 3 groups: rapid progression (34 men whose conditionprogressed from no hair loss to hair loss in all areas); moderate progression(145 men who had no hair loss initially and 2 bald areas 6 years later or1 initial bald area that progressed to all bald areas); and mild or no progression(224 men who had no change in their baldness, whose baldness progressed from1 to 2 bald areas, or whose baldness had decreased). The cohort was followedup for up to 24 years for new occurrences of CAD. The results were analyzedwith the Cox proportional hazards regression model, and all regressions wereadjusted for age and CAD risk factors. The extent of baldness was not associatedwith any of the outcomes, but progression demonstrated a 2.4 OR for CAD (95%CI, 1.30-4.40), a 3.8 OR for CAD mortality (95% CI, 1.90-7.70), and a 2.4OR for all-cause mortality (95% CI, 1.50-3.80).

The cohort study of Schnohr et al20 involved13 000 men and women, 30 to 79 years of age, who did not have ischemicheart disease at entry. During the 12-year follow-up period, 750 first myocardialinfarctions were diagnosed. Baldness was scored in the frontoparietal regionas "no bald triangle, bald triangle but >3 cm in front of ear, bald trianglebut ≤3 cm in front of ear." In the crown-top region, baldness was describedas "thick hair, partly thin hair, bald spot or bald spot and front." The Coxproportional hazards model was used to control for various myocardial infarctionrisk factors. Separate models were used for men and women. In the analysis,the frontoparietal baldness variable was included in the model as no baldnessor bald triangle. The "crown-top baldness" variable was included as no baldnessor bald spot. Schnohr and colleagues found that "men lose their hair, butwomen keep it." There was a significant correlation (P<.05)between the small or large triangle of frontoparietal baldness and myocardialinfarction in men (relative risk [RR], 1.6; 95% CI, 1.10-2.30). The relationshipbetween crown-top baldness and myocardial infarction was borderline (P<.06), with a 1.2 RR (95% CI, 1.00-1.50) for men witha bald spot or bald top/front compared with men with thick hair/partly thinhair. The combined variable for baldness was significantly associated witha higher risk (RR, 1.7; P<.02; 95% CI, 1.10-2.50)for myocardial infarction in men but not in women.

Ford et al21 studied 3932 men aged 26to 76 years at entry. Baldness was scored as none, minimum, moderate, andsevere. Scoring details have been published elsewhere, but were unavailableto me. Dermatologic examination was performed by a third-year dermatologyresident. A proportional hazards regression model was used that included ageand several risk factors for CAD. In a 14-year follow up, 378 men (9.6%) diedof myocardial infarction and 939 (23.9%) had incident CAD events. There were61 deaths (3%) and 239 CAD events (11.8%) in 2019 men younger than 55 years.Baldness was not associated with an increased rate of CAD incidence or mortality.For men younger than 55 years, however, the OR for severe baldness was 2.51(95% CI,1.01-6.24) for CAD mortality and 1.72 (95% CI, 0.96-3.08) for CADincidence.

In 1998, Schnohr et al22 published anotherreport on their series of 13 000 men and women and found no correlationbetween all-cause mortality and baldness.

Mirić et al23 conducted a case-controlstudy of 842 men younger than 60 years who were admitted for a first-timenonfatal myocardial infarction. The controls were 712 patients with acutepeptic ulcer or traffic accident injuries who had normal electrocardiographicfindings at rest and no history of CAD. Baldness was categorized as no baldness,frontal baldness, parietal baldness, and frontoparietal baldness. TraditionalCAD risk factors were taken into account. Men with parietal baldness had a1.90 adjusted OR for myocardial infarction (95% CI, 1.42-2.20), and thosewith frontoparietal baldness 1.68 (95% CI, 1.20-2.50).

Lotufo et al24 examined the associationof baldness and CAD in a retrospective cohort of 22 071 male physicians.Coronary artery disease was defined as nonfatal myocardial infarction, anginapectoris, and/or coronary revascularization. Baldness was not defined butwas measured according to a simplified Hamilton scale. Subjects were askedwhich of the scale sketches mostly approximated their status at 45 years ofage. Compared with men with no hair loss, those with frontal baldness hada relative risk of 1.09 (95% CI, 0.94-1.25), while those with mild, moderate,and severe vertex baldness had a relative risk of 1.23 (95% CI, 1.05-1.43),1.32 (95% CI 1.10-1.59), and 1.36 (95% CI, 1.11-1.67), respectively. The findingsof multivariate analysis, after potential confounders were controlled for,did not alter the results.

Some of the 15 studies were performed with a sample size that was toosmall to detect a difference; others had substantial biases, possibly yieldingresults in favor of a nonexistent association. The studies of Gertler andWhite10 and Mirić et al23examined only patients who survived myocardial infarction. No informationwas collected about those who did not survive. In the study of Buechner etal,11 cases were not defined and only percentageswere provided. The original data for the studies of Hamby et al13and Emidy et al17 are not available. In thestudies of Ben Halim et al14 and Cooke,15 diabetes was an exclusion criterion, but persons withdiabetes can also be bald. Risk factors for CAD were considered, but datawere insufficient for adjusting, and the definition of "smoker" penalizedthe study. No statistical analysis was performed in Persson and Johansson's16 study, but when it was done later, the findings provedthat the authors' conclusion was unwarranted. Schnohr and colleagues' 1998study dealt only with all-cause mortality. The remaining 6 articles1821,23,24involved many subjects and provided ample methodological information and resultdata (Table 1).

DEFINITION OF BALDNESS

Baldness and hair lossare popular terms. Androgenetic alopecia is the correctmedical designation for the disease that seems to be the topic of the studiesthat were reviewed. But was this the case?

Lesko et al18 and Lotufo et al24 mention male pattern baldness and, by referring tothe Hamilton baldness scale as modified by Norwood, clearly refer to AGA.Also, Herrera et al19 mention baldness and referto the Hamilton baldness scale. Schnohr et al20and Mirić et al23 merely use the term baldness, without referring to any known AGA scale. Fordet al21 use alopeciaand baldness indifferently. None of the authors ofthe 6 articles refers to AGA as the disease they were dealing with.

DIAGNOSIS OF AGA

If it is conceded that by baldness, the authorsmeant AGA, was AGA the real diagnosis? Androgenetic alopecia is only apparentlyeasy to diagnose. Ford et al21 (they were theonly epidemiologists to rely at least on a dermatology resident) defined baldnessas the condition that "corresponded to observable baldness upon the firstencounter with the participant." Actually, AGA deserves a little more attention.In the 1995 study by Herrera et al,19 for example,one wonders if such attention was totally lacking. Thirty-seven of their 420patients who had 1 bald area in 1956 had no bald spots 6 years later. Sinceno active medication was available for AGA at the time, AGA would have spontaneouslyregressed in 12% of the patients. Herrera and colleagues confirmed this findingwhen they included men "who had decreased baldness" in their "no progressiongroup." To the best of my knowledge, there is no evidence that AGA may spontaneouslyrevert to normality. Thus, one would legitimately suspect that some otherconditions (alopecia areata, trichotillomania, acute telogen effluvium?) couldhave been included in the study.

SEVERITY OF AGA

The severity of AGA was assessed in various ways. Lesko et al18 relied on the telephone assessment of the subjectsand the interviewing nurses using the Hamilton/ Norwood scale and a continuous5-point scale. It has been noted that the nurses were aware of the study hypothesis,5 but, more important, the subjects' own scoring couldhave been biased in many ways. Dermatologists are well aware of the peculiaritiesinherent in patients' attitude toward the hair loss problem. Some patientsdramatize their negligible alopecia. Lotufo et al24relied on the patients' memory of a condition that had developed 40 yearsbefore. This typical recall bias jeopardizes theirconclusions, which were otherwise based on very low relative risks.

Herrera et al19 relied on a simple classificationbased on the Hamilton scale. Observing their Figure 1, however, one wondersif in fact there is a difference between "two areas" and "all areas." Also,the finding that 42.5% of all-age individuals are "completely bald," ie, "comparableto Hamilton scale class VIII," is an exceedingly high percentage, and, inany case, is in contrast with prevalences found by other authors. Irrespectiveof myocardial condition, Lesko et al18 foundonly 37 subjects with "severe vertex" baldness, corresponding to a mere 2.6%.None of their subjects belonged to Hamilton scale class VIII. Similarly, only9.2% of the patients of Mirić et al23had "fronto-parietal" baldness, and only 11.6% of the patients of Schnohret al20 had a "bald top and front." Only 6.9%of the subjects of Ford et al21 had "severe"baldness. This latter figure is also the general average obtained by summingall data from the extreme degrees of baldness in the studies of Lesko et al,18 Mirić et al,23Schnohr et al,20 and Ford et al.21Conversely, Mirić and colleagues, Schnohr and colleagues, Ford andcolleagues, and Lesko and colleagues found no baldness in 35.5%, 58.9%, 64.0%,and 38.1%, respectively, of men younger than 55 years. Therefore, the findingof a 6.4% prevalence of "normal" men in Herrera and colleagues' study is toolow to be reliable, at least when simple clinical observation is used as adiagnostic tool. Furthermore, this wide range of figures shows that normality of scalp hairiness is a vague concept.

The observations of Herrera et al19 differfrom those of the other authors, because Herrera and colleagues also examinedthe progression of AGA in their subjects over a 24-year follow-up period.Individuals whose condition progressed rapidly to complete baldness (7.8%)were reported to have a high risk for developing CAD. The doubts regardingHerrera and colleagues' diagnosis of AGA remain and may also have biased thisconclusion. The concept of the early onset and/or rapid progression of AGAis probably important, however. In the study of Hamby et al,1365% of the subjects with CAD were bald before 35 years of age. In the studyof Lesko et al,18 men at all stages of baldnesswith onset before the age of 25 years had an OR that was significantly higherthan that of men with no hair loss (2.1; 95%CI, 1.20-3.50). Partial reanalysisreveals that subjects younger than 25 years with Hamilton class VI-VII hada nonadjusted OR of 3.26 (95% CI, 1.50-7.25). In the study of Schnohr et al,20 the incidence of myocardial infarction in the 30-to 39-year-old group with the most severe type of AGA (11.1%) was not onlydefinitely higher than in the same age group with less severe AGA but wasalmost comparable to the incidence in the 60- to 69-year-old group, irrespectiveof AGA severity.

Some questions regarding the possibly incorrect diagnosis of AGA andthe lack of a satisfactory definition of the condition in the articles thatwere reviewed do not permit a definitive conclusion of the baldness/CAD issue.In fact, the real problem lies in the striking difference between the accuracyof the diagnosis of myocardial infarction based on clinical, laboratory, andinstrumental approaches and the approximation of the diagnosis of AGA that,instead, relies on simple clinical observation "upon the first encounter withthe participant." In recent years, major advances have been made in our knowledgeof the main pathogenetic factors at work in AGA, but there is still no accuratemethod with which to establish the diagnosis and especially the severity ofthe condition.

Actually, 10 articles concluded that a relationship existed, especiallyin younger subjects with severe early-onset AGA. Therefore, the baldness/CADissue cannot be discarded. The existence of a particular group of subjectswho develop baldness before their 30s was recently recognized.24Such subjects present with an unusually elevated dihydrotestosterone-testosteroneratio compared with men with later-onset AGA, which may account for otherclinical features, including thoracic hairiness25and, perhaps, a higher susceptibility for developing CAD. The baldness theoryshould be included as a secondary hypothesis in large epidemiological studieson CAD risk factors. Such studies should include dermatologic expertise foraccurate, cost-effective evaluation of baldness.

Worry about the issue is currently increasing and should be primarilyaddressed by specialists. An epidemiological study with baldness as the primaryhypothesis could also be undertaken. Progressing baldness can be consideredas a manifest indicator of possible major risk for CAD, and balding youngmen may benefit from early aggressive screening of other better-known riskfactors for CAD. Practicing dermatologists should be cautious, however, inaddressing the problem with younger patients who are already concerned withtheir appearance so as not to aggravate their psychological distress.

Accepted for publication October 25, 2000.

Thanks are due to Cosetta Minelli, MD, for helping me to comply withthe reviewers' requirements and to Diana Sears Panconesi, who kindly correctedmy English.

Corresponding author: Alfredo Rebora, MD, Department of Dermatology,Clinica Dermatologica, Viale Benedetto XV, 7, 16132 Genova, Italy (e-mail: rebdermo@unige.it).

Herrera  CRLynch  C Is baldness a risk factor for coronary artery disease? a review ofthe literature. J Clin Epidemiol. 1990;431255- 1260
Link to Article
Not Available, Predicting coronary artery disease [editorial]. BMJ. 1972;8313
Cheng  TO Baldness and coronary disease [letter]. J Clin Epidemiol. 1991;44865
Link to Article
Wilson  PWKannel  WB Is baldness bad for the heart? JAMA. 1993;2691035- 1036
Link to Article
Kleinmuntz  B Baldness and myocardial infarction [letter]. JAMA. 1993;27048
Link to Article
Sheikh  K Baldness and ischemic heart disease in a national sample of men. Am J Epidemiol. 1997;145670- 671
Link to Article
Trevisan  MFarinaro  EKrogh  V  et al.  Baldness and coronary heart disease risk factors. J Clin Epidemiol. 1993;461213- 1218
Link to Article
Guzzo  CAMargolis  DJJohnson  J Lipid profiles, alopecia, and coronary disease: any relationship? Dermatol Surg. 1996;22479- 486
Link to Article
Sasmaz  SSenol  MOzcan  A  et al.  The risk of coronary heart disease in men with androgenetic alopecia. J Eur Acad Dermatol Venereol. 1999;12123- 125
Link to Article
Gertler  MMWhite  PD Findings on masculinity. Coronary Heart Disease in Young Adults. Cambridge, Mass Harvard University Press1954;72- 79
Buechner  HABrown  MTretola  RJ Baldness and emphysema. J La State Med Soc. 1964;116329- 332
Cotton  SGNixon  JMCarpenter  RGEvans  DW Factors discriminating men with coronary heart disease from healthycontrols. Br Heart J. 1972;34458- 464
Link to Article
Hamby  RIAintablian  AHoffman  I  et al.  Is male baldness a coronary risk factor [abstract]? Clin Res. 1977;25226A
Ben Halim  MMMeyrick  GJeans  WDMurphy  DBurton  JL Myocardial infarction, androgen, and the skin. Br J Dermatol. 1978;9863- 68
Link to Article
Cooke  NT Male pattern alopecia and coronary artery disease in men. Br J Dermatol. 1979;101455- 458
Link to Article
Persson  BJohansson  BW The Kockum study: twenty-two-year follow-up. Acta Med Scand. 1984;216485- 493
Link to Article
Emidy  LZhang  HStamler  J  et al.  Does the state of your pate relate to your fate? baldness, coronaryrisk factors, and 25-year mortality in the Peoples Gas Company. J Clin Epidemiol. 1990;431255- 1260 Program and abstracts of the 27th Annual Conference on CardiovascularDisease Epidemiology1987; Charleston, SCAbstract 76. Cited by: Herrera CR, Lynch C. Is baldness a risk factor for coronary artery disease? a review of the literature
Link to Article
Lesko  SMRosenberg  LShapiro  S A case-control study of baldness in relation to myocardial infarctionin men. JAMA. 1993;269998- 1003
Link to Article
Herrera  CRD'Agostino  RBGerstman  BBBosco  LABelanger  AJ Baldness and coronary heart disease rates in men from the FraminghamStudy. Am J Epidemiol. 1995;142828- 833
Schnohr  PLange  PNyboe  JAppleyard  MJensen  G Gray hair, baldness, and wrinkles in relation to myocardial infarction:the Copenhagen City Heart Study. Am Heart J. 1995;1301003- 1010
Link to Article
Ford  ESFreedman  DSByers  T Baldness and ischemic heart disease in a national sample of men. Am J Epidemiol. 1996;143651- 657
Link to Article
Schnohr  PNyboe  JLange  PJensen  G Longevity and gray hair, baldness, facial wrinkles, and arcus senilisin 13,000 men and women: the Copenhagen City Heart Study. J Gerontol A Biol Sci Med Sci. 1998;53M347- M350
Link to Article
Mirić  DFabjianić  DGiunio  L  et al.  Dermatological indicators of coronary risk: a case-control study. Int J Cardiol. 1998;67251- 255
Link to Article
Lotufo  PAChae  CUAjani  UAHennekens  CHManson  JE Male pattern baldness and coronary heart disease: the Physician's HealthStudy. Arch Intern Med. 2000;160165- 171
Link to Article
Sreekumar  GPPardinas  JWong  CQ  et al.  Serum androgens and genetic linkage analysis in early onset androgeneticalopecia. J Invest Dermatol. 1999;113277- 279
Link to Article

Figures

Tables

References

Herrera  CRLynch  C Is baldness a risk factor for coronary artery disease? a review ofthe literature. J Clin Epidemiol. 1990;431255- 1260
Link to Article
Not Available, Predicting coronary artery disease [editorial]. BMJ. 1972;8313
Cheng  TO Baldness and coronary disease [letter]. J Clin Epidemiol. 1991;44865
Link to Article
Wilson  PWKannel  WB Is baldness bad for the heart? JAMA. 1993;2691035- 1036
Link to Article
Kleinmuntz  B Baldness and myocardial infarction [letter]. JAMA. 1993;27048
Link to Article
Sheikh  K Baldness and ischemic heart disease in a national sample of men. Am J Epidemiol. 1997;145670- 671
Link to Article
Trevisan  MFarinaro  EKrogh  V  et al.  Baldness and coronary heart disease risk factors. J Clin Epidemiol. 1993;461213- 1218
Link to Article
Guzzo  CAMargolis  DJJohnson  J Lipid profiles, alopecia, and coronary disease: any relationship? Dermatol Surg. 1996;22479- 486
Link to Article
Sasmaz  SSenol  MOzcan  A  et al.  The risk of coronary heart disease in men with androgenetic alopecia. J Eur Acad Dermatol Venereol. 1999;12123- 125
Link to Article
Gertler  MMWhite  PD Findings on masculinity. Coronary Heart Disease in Young Adults. Cambridge, Mass Harvard University Press1954;72- 79
Buechner  HABrown  MTretola  RJ Baldness and emphysema. J La State Med Soc. 1964;116329- 332
Cotton  SGNixon  JMCarpenter  RGEvans  DW Factors discriminating men with coronary heart disease from healthycontrols. Br Heart J. 1972;34458- 464
Link to Article
Hamby  RIAintablian  AHoffman  I  et al.  Is male baldness a coronary risk factor [abstract]? Clin Res. 1977;25226A
Ben Halim  MMMeyrick  GJeans  WDMurphy  DBurton  JL Myocardial infarction, androgen, and the skin. Br J Dermatol. 1978;9863- 68
Link to Article
Cooke  NT Male pattern alopecia and coronary artery disease in men. Br J Dermatol. 1979;101455- 458
Link to Article
Persson  BJohansson  BW The Kockum study: twenty-two-year follow-up. Acta Med Scand. 1984;216485- 493
Link to Article
Emidy  LZhang  HStamler  J  et al.  Does the state of your pate relate to your fate? baldness, coronaryrisk factors, and 25-year mortality in the Peoples Gas Company. J Clin Epidemiol. 1990;431255- 1260 Program and abstracts of the 27th Annual Conference on CardiovascularDisease Epidemiology1987; Charleston, SCAbstract 76. Cited by: Herrera CR, Lynch C. Is baldness a risk factor for coronary artery disease? a review of the literature
Link to Article
Lesko  SMRosenberg  LShapiro  S A case-control study of baldness in relation to myocardial infarctionin men. JAMA. 1993;269998- 1003
Link to Article
Herrera  CRD'Agostino  RBGerstman  BBBosco  LABelanger  AJ Baldness and coronary heart disease rates in men from the FraminghamStudy. Am J Epidemiol. 1995;142828- 833
Schnohr  PLange  PNyboe  JAppleyard  MJensen  G Gray hair, baldness, and wrinkles in relation to myocardial infarction:the Copenhagen City Heart Study. Am Heart J. 1995;1301003- 1010
Link to Article
Ford  ESFreedman  DSByers  T Baldness and ischemic heart disease in a national sample of men. Am J Epidemiol. 1996;143651- 657
Link to Article
Schnohr  PNyboe  JLange  PJensen  G Longevity and gray hair, baldness, facial wrinkles, and arcus senilisin 13,000 men and women: the Copenhagen City Heart Study. J Gerontol A Biol Sci Med Sci. 1998;53M347- M350
Link to Article
Mirić  DFabjianić  DGiunio  L  et al.  Dermatological indicators of coronary risk: a case-control study. Int J Cardiol. 1998;67251- 255
Link to Article
Lotufo  PAChae  CUAjani  UAHennekens  CHManson  JE Male pattern baldness and coronary heart disease: the Physician's HealthStudy. Arch Intern Med. 2000;160165- 171
Link to Article
Sreekumar  GPPardinas  JWong  CQ  et al.  Serum androgens and genetic linkage analysis in early onset androgeneticalopecia. J Invest Dermatol. 1999;113277- 279
Link to Article

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Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
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For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
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