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. 2016 Jul 1;19(1):51–57. doi: 10.1111/jch.12871

Severity of Alopecia Predicts Coronary Changes and Arterial Stiffness in Untreated Hypertensive Men

Helen Triantafyllidi 1,✉, Agis Grafakos 1, Ignatios Ikonomidis 1, George Pavlidis 1, Paraskevi Trivilou 1, Antonis Schoinas 1, John Lekakis 1
PMCID: PMC8030774  PMID: 27365213

Abstract

An association between androgenic alopecia (AGA), coronary artery disease, and hypertension has been reported in previous epidemiological studies. The authors evaluated the relationship of target organ damage caused by hypertension with AGA in 101 newly diagnosed and untreated hypertension men with mild to moderate AGA (AGA m), severe AGA (AGA s), and non‐AGA. Pulse wave velocity (PWV), office and 24‐hour pulse pressure (PP), carotid intima‐media thickness (IMT), left ventricular hypertrophy (LVH), coronary flow reserve (CFR d), and AGA severity by Hamilton‐Norwood scale were estimated. CFR d was significantly impaired in AGA s patients compared with AGA m (P=.007) and non‐AGA patients (P=.02). No differences were found within groups regarding PWV, PP, IMT, and LVH. AGA severity was related to CFR d (independently) and PP while AGA duration and age of onset were related to CFR d and PP, respectively. The authors conclude that impaired coronary microcirculation and aortic stiffness might precede the appearance of significant stenotic coronary lesions in hypertensive patients with severe AGA. In addition, hypertensive patients with severe and early AGA onset seem to be exposed to an augmented cardiovascular risk.

Androgenic or androgenetic alopecia (AGA), or male pattern baldness, the most common cause of hair loss, is the hereditary thinning of hair induced by androgens in genetically susceptible individuals that occurs after puberty.1 AGA affects approximately 40% and 50% of men at the ages 40 and 50 years, respectively.2 However, it has been suggested that early‐onset AGA (before age 36 years) is genetically different from late‐onset alopecia.3

An association between AGA and severe coronary heart disease has been reported in many epidemiological studies, including the Framingham Heart Study, without any obvious explanation. Many pathophysiological mechanisms have been proposed including insulin resistance, atherosclerotic processes, increased androgen levels, and adverse effects of lipid‐lowering or antihypertensive drugs.4, 5, 6, 7 Early‐onset severe AGA (vertex pattern alopecia) has been associated with increased incidence of hyperinsulinemia and its associated disorders obesity, hypertension, and dyslipidemia and it is suggested as a marker of early‐onset severe coronary artery disease (CAD).5, 8

Arterial hypertension is a major risk factor for cardiovascular (CV) disease (CVD) leading to subclinical organ involvement, otherwise called target organ damage (TOD), an intermediate stage in the continuum of vascular disease as well as an important determinant of CV risk.9 Signs of TOD (left ventricular mass index [LVMI], reduced coronary flow reserve [CFRD], increased carotid intima‐media thickness [cIMT], elevated levels of microalbuminuria [MAU], and impaired aortic stiffness [PWV]) should be investigated thoroughly in hypertensive patients.9

A number of studies have shown that arterial hypertension is strongly associated with AGA, perhaps as a result of hyperaldosteronism, independently of age and sex.10, 11, 12 An association between AGA and arterial stiffness has also been revealed.13 No other studies have ever explored any associations between TOD caused by hypertensive disease and the severity and/or duration of AGA in young men. The purpose of this study is to explore any existing associations between TOD caused by arterial hypertension and the presence, duration, and severity of AGA in first diagnosed and untreated adult hypertensive men.

Patients and Methods

Study Population

We studied 101 consecutive hypertensive men 55 years and younger who visited our outpatient clinic from October 2009 until May 2014 with recently diagnosed and never‐treated stage I or II essential hypertension according to the 2007, 2009, and 2013 guidelines of the European Society of Hypertension.9, 14, 15 All patients underwent the following examinations within 2 weeks: (1) three office blood pressure (BP) measurements in each one of the three subsequent visits in the hypertension outpatient clinic, (2) blood and urine sampling for routine blood chemistry and urine examination, (3) standard 12‐lead electrocardiography, (4) 24‐hour ambulatory BP monitoring (ABPM) to confirm hypertension diagnosis based in clinic repeated BP measurements, (5) transthoracic echocardiography, (6) carotid ultrasonography, and (7) carotid‐femoral PWV. Finally, all hypertensive patients were examined regarding AGA by an experienced dermatologist.

Informed consent was obtained during the initial visit of the study, which was approved by the ethical committee of our hospital.

Patients with secondary hypertension, congestive heart failure, previous myocardial infarction, stroke, cardiac valve diseases, history of coronary artery bypass grafting, atrial fibrillation, renal insufficiency, overt proteinuria, or diabetes mellitus, as well as patients taking medication for CVD (ie, statins for hyperlipidemia treatment) or non‐CVDs or hormonal replacement for any reason were excluded from the study.

Diagnostic Workup

The diagnostic workup has been described in detail in a previous study by our research group.16 In summary, each patient underwent the medical examinations listed below:

  • Office BP measurement: Morning office BP was measured in the hospital outpatient clinic, approximately at the same morning hour, by the same cardiologist using a mercury sphygmomanometer after the patients had rested for 5 to 10 minutes in the sitting position. Three measurements were taken at 1‐minute intervals, and the average was used as the office systolic BP (SBP) and diastolic BP (DBP). Office pulse pressure (PP) was calculated as SBP minus DBP while mean BP was defined as DBP plus one third of the PP. Hypertension was diagnosed as SBP ≥140 mm Hg and/or DBP ≥90 mm Hg. Patients were advised to avoid smoking or drinking coffee for at least 2 hours before examination.

  • ABPM measurement: ABPM was carried out on the nondominant arm using a validated Spacelab 90207 recorder (Spacelab, Redmontd, CA). The ABPM device was set to obtain BP readings at 15΄ intervals during the day (7 am–11 pm) and 20′ intervals during the night (11 pm–7 am). All patients had ≥75% successful readings.

  • Transthoracic echocardiogram (TTE): Studies were performed using a Vivid 7 (GE Medical Systems, Horten, Norway) system. Left ventricular (LV) mass index (LVMI) was measured in all patients using the Devereux formula according to the Penn Convention Protocol. LV hypertrophy was defined as LVMI >134 g/m2 in men and >110 g/m2 in women. In addition, left atrial diameter from left parasternal view was estimated.17

  • Coronary flow reserve (CFR) estimation from TTE: Coronary flow velocity profile in the left anterior descending artery was obtained using color‐guided pulse wave Doppler from long‐axis apical projections using a 7‐MHz transducer. We measured resting peak diastolic coronary flow velocity at rest and after adenosine infusion (140 μg/kg/min) for 3 minutes. CFRD was calculated as the ratio of hyperemic to resting diastolic velocity. CFRD <2 has been considered abnormal, 2 to 2.5 as borderline, and >2.5 as normal.9, 18

  • Carotid ultrasonography for cIMT measurement: cIMT was measured in three paired segments of both carotid arteries from a fixed lateral transducer angle using B‐mode ultrasound imaging (7.0–10 MHz, linear array transducer). Measurements were made at the level of the common carotid artery, the carotid bulb, and the internal carotid artery while cIMT <0.9 mm was considered normal.9, 18

  • Carotid‐femoral PWV: Arterial stiffness was estimated by a carotid‐femoral PWV measurement using a Complior SP (Alam Medical, Vincennes, France). Patients were advised to avoid smoking or drinking coffee for at least 2 hours before examination. A PWV <10 m/s was considered normal.9, 19

  • AGA: The Hamilton‐Norwood scale (classes I–VII) is a widely used, standard classification system with good reliability and reproducibility for hair loss in men, evaluating the presence and the severity of alopecia. Hamilton‐Norwood type IV represents the starting grade of severe frontal and vertex AGA.20

In our study, we evaluated alopecia severity based on Hamilton‐Norwood scale classes I to VII, respectively, and we created two AGA categories: AGAm with mild to moderate AGA (equivalent to Hamilton‐Norwood scale classes II–III) and AGAs with moderate to severe AGA (equivalent to Hamilton‐Norwood scale classes IV–VII). In the control group (non‐AGA), hypertensive patients had no AGA (equivalent to Hamilton‐Norwood scale class I).

Patients were interviewed regarding the age of alopecia onset (early onset was defined as age ≤25 years while late onset was defined as age >25 years); the duration of hair loss, which, in turn, was classified into classes 1 to 3 (<5, 5–20, >20 years); and the paternal and maternal family history of AGA.

Statistical Analysis

The Kolmogorov‐Smirnov test was used to assess the normality of distribution. Since almost all variables (body mass index [BMI], triglycerides, MAU, IMT, LVMI, Hamilton‐Norwood scale, and AGA duration were excluded) were normally distributed and are expressed as mean±standard deviation. BMI, triglycerides, MAU, IMT, LVMI, Hamilton‐Norwood scale, and AGA duration are expressed as median value plus 25% to 75% interquartile range. Unpaired Student t test was used to compare numeric differences within groups. Pearson's analysis was used to identify any relationships between AGA indices and target organ damages as well as other variables. Multiple linear stepwise regression analysis was performed to explore the independent relationship of Hamilton‐Norwood scale with age, BMI, smoking habit, cholesterol levels, office and ambulatory SBP and PP, and CFRD, which were included in the regression analysis model as independent variables. Because of the collinearity between office and ambulatory parameters, we examined them in separate regression models. Similarly, because of the collinearity of SBP and PP, each covariate was entered in the model separately. Level of statistical significance was defined as a two‐sided P<.05. Statistical analysis was performed with SPSS version 21 (SPSS Inc, Chicago, IL).

Results

Demographic and clinical characteristics as well as TOD and AGA indices regarding the two hypertensive AGA groups, AGAm and AGAs as well as the control hypertensive group (non‐AGA) are listed in Table 1. All three groups had similar results regarding demographic, clinical, blood pressure and echocardiographic findings. No significant differences were revealed regarding PWV, IMT, La and LVMI. Interestingly, we found that CFRD was significantly impaired in AGAs patients compared to AGAm (P=.007) and non‐AGA patients (P=.02) (Figure 1).

Table 1.

Demographic and Clinical Characteristics, Target Organ Damage, and Alopecia Indices of the Study Groups

Men With Mild to Moderate Androgenic Alopecia (n=34) Men With Severe Androgenic Alopecia (n=28) Men Without Androgenic Alopecia (n=39) P P 1 P 2
Demographic and clinical characteristics
Age, y 45±5 44±8 43±8 .34 .15 .68
Weight, kg 91±13 94±18 91±13 .54 .84 .42
Body mass index, kg/m2 a 28 (26–31) 28 (26–33) 29 (27–31) .43 .50 .66
Current smokers, No. (%) 16 (47) 11 (39) 14 (40) .41 .42 .96
Total cholesterol, mg/dL 221±35 218±35 218±39 .73 .71 .99
Triglycerides, mg/dLa 133 (110–163) 109 (85–161) 135 (89–164) .21 .21 .86
LDL, mg/dL 147±32 148±30 143±34 .95 .63 .60
HDL, mg/dL 45±7 47±11 47±10 .29 .32 .91
Creatinine, mg/dL 1.03±0.1 0.96±0.2 0.9±0.2 .20 .13 .97
Office SBP, mm Hg 141±15 147±18 147±12 .18 .10 .89
Office DBP, mm Hg 90±9 90±12 93±8 .97 .30 .38
Office PP, mm Hg 49±15 55±16 51±16 .17 .61 .38
24‐h SBP, mm Hg 140±12 140±10 139±10 .98 .66 .63
24‐h DBP, mm Hg 91±8 91±8 90±9 .88 .58 .50
24‐h PP, mm Hg 49±7 48±6 49±6 .88 .99 .87
24‐h Heart rate, beats per min 79±7 78±9 76±8 .44 .12 .54
Target organ damage indices
PWV, m/s 10.6±2 10.3±1.6 10.5±1.5 .56 .89 .58
IMT, mma 0.9 (0.8–1.2) 0.9 (0.8–1.1) 0.9 (0.7–1.3) .73 .37 .35
CFRDIASTOLE 3.01±0.9 2.4±0.6 2.8±0.7 .007 .29 .02
Left atrium diameter, mm 38±4 37±4 37±4 .33 .31 .99
LVMI, g/m2 86±30 78±20 88±21 .23 .71 .08
Androgenic alopecia indices
Age of alopecia onset, y 35±8 28±8 – .001 – –
Duration of alopecia (class 1/2/3), % 27/59/14 0/54/46 – <.001 – –
Paternal alopecia history, % 62 82 10 .07 <.001 <.001
Maternal alopecia history, % 38 50 31 .35 .54 .22
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Abbreviations: CFR, coronary flow reserve; DBP, diastolic blood pressure; HDL, high‐density lipoprotein; IMT, carotid intima‐media thickness; LDL, low‐density lipoprotein; LVMI, left ventricular mass index; PP, pulse pressure; PWV, pulse wave velocity; SBP, systolic blood pressure. Duration of alopecia: class 1=<5 years, class 2=5 to 20 years, class 3=>20 years. Data are expressed as mean±standard deviation or as median and 25 to 75 interquartile range.a P refers to differences between men with mild to moderate androgenic alopecia (AGA) and men with severe AGA, P 1 refers to differences between men with mild to moderate AGA and non‐AGA men, and P 2 refers to differences between men with severe AGA and non‐AGA men. Italics highlight the statistical significance of the result regarding P <0.05

Figure 1.

Figure 1

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CFRD levels in hypertensive patients without androgenic alopecia (non‐AGA), with mild to moderate androgenic alopecia (AGAm), and with severe androgenic alopecia (AGAs). *P refers to significant difference between AGA s and AGA m groups and **P between AGA s and non‐AGA groups.

In AGAs patients, AGA started earlier in life (P=.001) and lasted longer (P<.001) compared to AGAm patients. As for the family AGA history, both AGAs and AGAm groups had an increased incidence of paternal AGA history compared with non‐AGA patients (P<.001). On contrary, no differences were found regarding maternal AGA history.

The following Pearson and Spearman univariate relationships were revealed.

  • In the whole AGA population, the severity of alopecia, estimated by Hamilton‐Norwood scale, was negatively related with CFRD (r=−0.31, P=.02) and positively related with office PP (ρ=0.24, P=.04). In addition, the duration of alopecia was related with CFRD (r=−0.26, P=.03), office PP (ρ=0.26, P=.04), and 24‐hour PP (r=0.24, P=.04), and the age of alopecia onset was negatively related with office PP (r=−0.23, P=.04).

  • In the AGA group and subgroup, PWV was positively related with Hamilton‐Norwood scale (r=0.39, P=.04) and negatively with CFRD (ρ=−0.36, P=.01) in AGAs patients. In the subgroup of AGA patients with age of alopecia onset 25 years or younger (n=18), the age of alopecia onset was negatively related with cIMT (ρ=−0.52, P<.02).

Finally, when we combined two parameters of alopecia, severity and early onset, we found that the subgroup of AGAs patients with alopecia onset 25 years and younger (n=13) were younger (41±7 vs 46±6 years, P=.03), with decreased CFRD (2.3±0.7 vs 2.8±0.8, P=.04) and increased PP (59±13 vs 50±16, P=.04) compared with the rest of the AGA patients (n=49) (Figure 2).

Figure 2.

Figure 2

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CFRD levels in hypertensive patients with severe androgenic alopecia (AGAs) with AGA onset ≤25 years old and mild to moderate androgenic alopecia (AGAm) plus hypertensive patients with AGAs with AGA onset >25 years old.

We performed multivariate stepwise regression analysis, where the following baseline parameters were inserted as independent variables: age, BMI, smoking habit, cholesterol levels, and CFRD. Office SBP and PP, 24‐hour SBP, and PP were also inserted as independent variables (each one inserted separately in a different model due to collinearity of office and ambulatory parameters as well as between SBP and PP). We found that Hamilton‐Norwood scale independently related with predicted CFRD level in the whole AGA population (Table 2).

Table 2.

Multiple Regression Analysis of Independent Associations Between CFR and Androgenic Alopecia Severity in Hypertensive Men

Model A (Office SBP) Model B (Office PP) Model C (24‐h SBP) Model D (24‐h PP)
CFRD CFRD CFRD CFRD
β P Value β P Value β P β P
Hamilton‐Norwood scale −0.28 .02 −0.34 .01 −0.33 .01 −0.35 .01
Age 0.11 .43 0.10 .48 0.10 .48 0.33 .81
BMI −0.19 .18 −0.15 .28 −0.15 .28 −0.18 .19
Smoking habit 0.10 .47 0.12 .42 0.12 .42 0.04 .79
Cholesterol −0.19 .19 −0.21 .13 −0.21 .13 −0.21 .13
Office SBP −0.26 .07 – – – – – –
Office PP – – −0.005 .97 – – – –
24‐h SBP – – – – 0.001 .99 – –
24‐h PP – – – – – – −0.10 .45
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Abbreviations: BMI, body mass index; CFRD, coronary flow reserve in diastole; SBP, systolic blood pressure. Because of the collinearity between office and ambulatory blood pressure (BP) parameters as well as between systolic BP and pulse pressure, we examined four separate regression models. In each model, office systolic BP, office pulse pressure (PP), 24‐hour systolic BP, and 24‐hour PP were inserted separately. Significant β and P values are indicated in italics.

Discussion

An existing relationship between AGA and atheromatosis as well as CAD in hypertensive populations has been revealed in several epidemiological studies10, 11, 12. This is the first study, to our knowledge, that provides data regarding the possible pathophysiologic mechanisms that might underline the relationship between AGA and CAD. The main finding of our study is that coronary microcirculation (CFRD) is significantly decreased in hypertensive patients with AGAs compared with either hypertensive patients with AGAm or hypertensive non‐AGA patients and is independently related with AGA severity and duration.

AGA is the most common cause of hair loss and affects approximately half of men aged 50 years and older.2 It appears that there is higher incidence of AGA in the fathers of bald men compared with the fathers of nonbald men.21 We confirm those results, since we found a positive history of alopecia in fathers in two thirds of our AGA patients.

CVD is the leading cause of death worldwide and its prevention and early detection are the major goals of health care. Since the study by Cotton and colleagues,22 who first suggested in 1972 that male AGA could be a risk factor for CVD, a number of epidemiological studies (Framingham Study,4 Copenhagen City Heart Study,23 Physicians’ Health Study15) concluded that AGA is linked with premature atherosclerosis, CAD, and myocardial infarction,5, 8 especially if AGA appears and rapidly progresses during adulthood as well as if arterial hypertension and hyperlipidemia are present. However, the exact association between AGA and CAD remains controversial as the exact mechanism of the predisposition to CAD in AGA patients has not been explained satisfactory.24 Androgens that have been implicated in early‐onset AGA‐related CAD could promote coronary atherosclerosis and vasoconstriction either by directly stimulating the proliferation of vascular smooth muscle cells or by modulating risk factors associated with atherosclerosis (lipid profile, hypertension, insulin resistance).16, 17

Fewer studies have discussed the association between AGA and arterial hypertension. Hypertension is strongly associated with AGA, independently of age,10 while AGA might be an indicator of increased arterial stiffness.13 Androgens, especially testosterone, seem to favor a BP increase and its consequences.25, 26 On the other hand, increased serum aldosterone levels directly participate in the development of alopecia as well as to a hypertensive response caused by its pleiotropic effects since it potentiates angiotensin II, impairs endothelial function, reduces vascular compliance, and promotes hypertension through central nervous system mechanisms.11, 27, 28

In the absence of significant epicardial coronary or myocardial pathology, CFR is an indicator of early functional and structural alterations in coronary microcirculation caused by endothelial dysfunction, structural remodeling of intramyocardial arterioles, and accumulation of fibrillar collagen.29 Disturbed coronary microcirculation, expressed as impaired CFR, has been shown to have an independent prognostic value in hypertension.9, 30 In our study, we noticed that CFRD was reduced in the AGAs group compared with the AGAm and non‐AGA groups. Interestingly, the relationship between CFRD and Hamilton‐Norwood scale (AGA severity) was independent and corrected for factors that might influence coronary microcirculation such as age, weight, SBP and PP, aortic stiffness, smoking habit, and cholesterol levels. Those results suggest that impaired coronary microcirculation might be considered as a subclinical pathophysiological link between AGA and CAD in hypertensive patients.

Aortic stiffness reflects accelerated changes in arterial structure and function and reliably predicts a fatal and nonfatal CV event in hypertensive patients.9 Arterial stiffness, estimated by cardioankle vascular index, was increased in asymptomatic young adults with AGA.13 In our study, no significant differences regarding PWV were revealed within the groups, maybe because of their relatively young age, similar BP level, the short natural history of hypertension in our patients, or even the small number of patients in each group. Those three parameters (age, BP, and long hypertension history) seem to be important determinants of PWV increase. However, a positive relationship between PWV and AGA severity was found, suggesting a relationship between arteriosclerosis and AGA. There is a close relationship between increased PWV (LV afterload, wall stress, mass and myocardial oxygen demands increase) and impaired CFR (reduction in myocardial perfusion) in newly diagnosed hypertensive patients.31 Since both impaired PWV and CFR were associated with AGA severity in our study, we hypothesized that those pathophysiological mechanisms might lead to future CAD in hypertensive patients with severe AGA.

The Framingham Heart Study proved PP as a strong predictor of coronary events in patients with essential hypertension.32 Indeed, both office and 24‐hour PP represent reliable, available, reproducible, and inexpensive indices of aortic stiffness and subsequently CV risk. In our study, PP (office and 24‐hour) was related to AGA severity, duration, and age of onset, confirming the relationship between arterial stiffness and AGA.

Our hypothesis regarding the link between arterial stiffness, coronary microcirculation, and AGA stands on our results in hypertensive patients with severe AGA and early age of AGA onset. That subgroup of AGA patients had impaired coronary microcirculation and increased aortic stiffness, estimated by PP, compared with the rest of the AGA patients. Office and 24‐hour BP parameters, PWV, and IMT were also impaired but nonsignificant. We believe that, although younger, those hypertensive patients have an increased future CV risk.

In hypertensive patients, increased cIMT usually reflects generalized vascular damage (intimal atherosclerotic process and medial hypertrophy).33, 34 Since common cIMT was found to be significantly higher in patients with severe vertex pattern AGA, the latter might be considered as a noninvasive additional risk factor for subclinical atherosclerosis and possible CAD.35 We found an inverse relationship between impaired cIMT and AGA onset in the subgroup of hypertensive patients with AGA onset 25 years and younger. The latter might confirm the hypothesis that early‐onset AGA is genetically different from late‐onset AGA and is associated with more pronounced CVD.3

Study Limitations

Several limitations should be considered concerning this observational study. Its cross‐sectional nature prevents any cause‐effect relationship between any associations found as well as any prognostic significance of AGA. The relatively small number of patients overall and in each study group might be the reason for the lack of significant differences within groups regarding several TOD indices, PWV, and PP. Since hypertension has a high prevalence in the population, a greater number of patients is necessary in order to generalize the results of this study in both untreated and treated hypertensive patients with different medications or patients with severe hypertension. Another possible limitation of our study is the absence of blood testosterone or aldosterone measurements in our patients and the investigation of any existing correlation of their levels with TOD and alopecia indices.

Clinical Implications

Clinical evaluation of asymptomatic adult men with AGA (especially those with severe AGA), a nonmodifiable possible CAD risk factor, for other modifiable risk factors (ie, arterial hypertension) and subclinical vascular damage (CFR, PWV, PP) might lead to the primary prevention of a fatal disease in an era when resources are scarce and expensive screening tests for CAD are sometimes not easily available.

Conclusions

The severity, early onset, and longevity of AGA are related to subclinical vascular damage (impaired coronary microcirculation and aortic stiffness as well as increased carotid atherosclerosis) in adult untreated men with newly diagnosed essential hypertension. In addition, hypertensive patients with severe and early AGA onset seem to be exposed to an augmented CV risk.

Disclosure

The authors state that there is no conflict of interest.

J Clin Hypertens (Greenwich). 2017;19:51–57. DOI: 10.1111/jch.12871. © 2016 Wiley Periodicals, Inc.

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