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Association between Pulse Pressure and Impaired Pulmonary Function in Non-Smoking Adults
Korean J Clin Lab Sci 2020;52:119-127  
Published on June 30, 2020
Copyright © 2020 Korean Society for Clinical Laboratory Science.

Hyun Yoon

Department of Clinical Laboratory Science, Wonkwang Health Science University, Iksan, Korea
Correspondence to: Hyun Yoon
Department of Clinical Laboratory Science, Wonkwang Health Science University, 514 Iksan-daero, Iksan 54538, Korea
E-mail: yh9074@yahoo.co.kr
ORCID: https://orcid.org/0000-0002-4741-9664
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
According to previous studies, an impaired pulmonary function is associated with arterial stiffness (AS). The pulse pressure (PP) is an important predictor of AS, but the association of an impaired pulmonary function with the PP is unclear. Therefore, this study assessed the associations between the PP and the predicted forced vital capacity (predicted FVC) and predicted forced expiratory volume in one second (predicted FEV1) in Korean non-smoking adults. The data obtained from 6,857 adults during the 2013∼2015 Korean National Health and Nutrition Examination Survey were analyzed. After adjusting for the related variables, the ORs of restrictive pulmonary disease (RPD, the predicted FVC<80.0% with FEV1/FVC≥70.0%) using the normal PP group (PP≤60 mmHg) as a reference group was significant for the high PP group (PP>60 mmHg; 1.337 [95% confidence interval (CI), 1.049∼1.703]). In addition, the ORs of obstructive pulmonary disease (OPD, FEV1/FVC<70.0%) using the normal PP group as a reference group were significant for the high PP group (1.339 [95% CI, 1.093∼1.642]). In conclusion, a high PP is positively associated with both RPD and OPD in Korean non-smoking adults.
Keywords : Non-smoker, Obstructive pulmonary diseases, Pulse pressure, Restrictive pulmonary diseases
INTRODUCTION

Chronic obstructive pulmonary disease (COPD) is the leading cause of mortality in high- (5.0%) and middle-income countries (6.9%) [1]. Impaired lung function, which is indicated by reduced forced expiratory volume in forced vital capacity (FVC) and first second of exhalation (FEV1), contributes significantly to cardio- and cerebrovascular events and mortality [2, 3]. Impaired lung function occurs due to smoking, hypertension, chronic kidney disease, and type 2 diabetes mellitus [4, 5]. Some previous studies reported that arterial stiffness (AS) is increased in COPD [6-8]. It has been suggested that a link between vascular and pulmonary disease may explain a proportion of the excess cardiovascular mortality in COPD.

Pulse pressure (PP), which is the difference between systolic blood pressure (SBP) and diastolic blood pressure (DBP), is known to be a strong risk factor for cardiovascular events and mortality or all-cause mortality [9, 10]. In addition, PP is an important predictor of AS and pulse wave velocity (PWV) because PP is determined by the elastic of the large arteries and the magnitude of wave reflections [11, 12]. However, little research exists regarding the relationship between PP and impaired pulmonary function. Therefore, this study aimed to investigate the association between PP and impaired pulmonary function in Korean non-smoking adults aged ≥20 years using the data obtained in 2013∼2015 from the sixth Korean National Health and Nutrition Examination Survey (KNHANES-VI).

MATERIALS AND METHODS

1. Subjects

This study was based on most recent data from the KNHANES VI (2013∼2015). The KNHANES is a cross-sectional survey conducted nationwide by the Division of Korean National Health and Welfare. KNHANES comprises a health interview survey, a health behavior survey, a health examination survey, and a nutrition survey. Households as sampling units were stratified and collected through a multistage, probability-based sampling design based on sex, age, and geographic area, using household registries. At the time each survey was done, participants provided written informed consent for use of their data in further analyses and were given the right to refuse to participate, in accordance with the National Health Enhancement Act. In the KNHANES VI, 22,948 individuals over age 1 were sampled for the survey. We excluded 13,524 subjects who were missing for pulmonary function test, and those (592 subjects) for whom data were missing for important analytic variables, such as various blood chemistry tests. In addition, we excluded the current-smoker (1,975 subjects who smoked more than one cigarette a day). Finally, 6,857 subjects were included in the statistical analysis. The KNHANES VI study has been conducted according to the principles expressed in the Declaration of Helsinki (2013-07CON-03-4C, 2013-12EXP-03-5C, 2015-01-02-6C). All survey participants agreed with the use of epidemiological research to identify risk factors and death causes of chronic diseases. Participants’ records and information in the KNHANES were anonymous and de-identified prior to analysis. Further information can be found in “The KNHANES V Sample,” which is available on the KNHANES website. The official website of KNHANES (http://knhanes.cdc.go.kr) is currently operating an English-language information homepage. The data of the respective year are available to everyone free of charge. If the applicant completes a simple subscription process and provides his/her email address on the official website of KNHANES, the data of the respective year can be downloaded free of charge. If additional information is required, the readers may contact the department responsible for the storage of data directly (Su Yeon Park, sun4070@korea.kr).

2. General characteristics and blood chemistry

Research subjects were classified by gender and by age into less than 50 years, 50∼59 years, 60∼69 years, and 70 years or older. Research subjects were classified by sex (men and women), alcohol drinking (yes or no), and regular exercise (yes or no). Alcohol drinking was indicated as “yes” for participants who had consumed at least one glass of alcohol every month over the last year. Regular exercise was indicated as “yes” for participants who had exercised on a regular basis regardless of indoor or outdoor exercise. Regular exercise was defined as 30 min at a time and 5 times/wk in the case of moderate exercise, such as swimming slowly, doubles tennis, volleyball, badminton, table tennis, and carrying light objects; and for 20 min at a time and 3 times/wk in the case of vigorous exercise, such as running, climbing, cycling fast, swimming fast, football, basketball, jump rope, squash, singles tennis, and carrying heavy objects. Anthropometric measurements included body mass index (BMI), waist measurement (WM), SBP, and DBP. Blood chemistry included measurement of triglycerides (TGs), high-density lipoprotein cholesterol (HDL-C), fasting blood glucose (FBG), predicted forced vital capacity (predicted FVC), predicted forced expiratory volume in 1 second (predicted FEV1), and FEV1/FVC.

3. Definitions of PP, RPD, OPD

PP was calculated as the difference between SBP and DBP. High PP was classified when the PP was >60 mmHg [13] because the cutoff for the high PP was not yet clear. The obstructive pulmonary disease (OPD) was defined FEV1/FVC<70.0% and restrictive pulmonary disease (RPD) was defined the predicted FVC<80.0% with FEV1/FVC≥70.0% [14, 15].

4. Statistical analysis

The collected data were statistically analyzed using SPSS WIN version 18.0 (SPSS Inc., Chicago, IL, USA). The distributions of the participant characteristics were converted into percentages, and the successive data were presented as averages with standard deviations. The distribution and average difference in clinical characteristics and iron related indices according to normal PP and high PP were calculated using chi-squared and an independent t test. Multiple linear regression analysis models were constructed for the predicted FVC and FEV1 and FEV1/FVC: model 2) were adjusted for age, gender, drinking alcohol, regular exercise, TGs, HDL-C, FBG, BMI, WM, and either SBP and DBP or PP. In the case of logistic regression for odds ratio of OPD and RPD, the 4 models constructed were: 1) non-adjusted; 2) adjusted for age, gender, drinking, and regular exercising; 3) further adjusted for TGs, HDL-C, and FBG; 4) further adjusted for BMI and WM. The significance level for all of the statistical data was set as P<0.05.

RESULTS

1. Clinical characteristics of research subjects

The clinical characteristics of the research subjects are shown in Table 1. The prevalence rates of high PP in men and women were 346 (14.3%) and 617 (13.6%), respectively. The prevalence rates of RPD and OPD were 569 (8.3%) and 828 (12.1%), respectively. The following parameters were significantly higher (P< 0.001) in men than in women: alcohol intake, regular exercise, SBP, DBP, BMI, WM, TGs, FBG, OPD, and RPD. However, the following were significantly lower (P< 0.001) in men than in women: HDL, predicted FVC, predicted FEV1, and FEV1/FVC.

General characteristics of research subjectsN (%), Mean±SD, (N=6,857)

Variables Category Total (N=6,857) Men (N=2,427) Women (N=4,430) P
Age (years) 57.63±10.58 59.08±10.84 56.83±10.35 <0.001
<50 1,799 (26.3) 556 (22.9) 1,243 (28.1) <0.001
50∼59 2,119 (30.9) 680 (28.1) 1,439 (32.5)
60∼69 1,793 (26.1) 702 (28.9) 1,091 (24.6)
≥70 1,146 (16.7) 489 (20.1) 657 (14.8)
Alcohol drinking Yes 3,049 (44.5) 1,553 (64.0) 1,496 (33.8) <0.001
Regular exercising Yes 1,619 (23.6) 882 (36.3) 737 (16.6) <0.001
SBP (mmHg) 120.79±16.78 122.91±15.76 119.63±17.21 <0.001
DBP (mmHg) 75.87±10.02 78.00±10.25 74.70±9.69 <0.001
PP (mmHg) 44.92±13.41 44.91±13.31 44.93±13.47 0.946
High PP 963 (14.0) 346 (14.3) 617 (13.6) 0.708
BMI (kg/m2) 24.15±3.07 24.46±2.89 23.98±3.14 <0.001
WM (cm) 82.27±9.03 86.11±8.23 80.17±8.75 <0.001
TGs (mg/dL) 134.86±94.34 154.57±117.12 124.07±77.03 <0.001
HDL-C (mg/dL) 80.78±11.99 47.25±11.19 52.71±11.98 <0.001
FBG (mg/dL) 102.04±22.46 106.33±24.82 99.70±20.69 <0.001
Predicted FVC (%) 93.31±11.83 91.31±11.94 94.41±11.62 <0.001
Predicted FEV1 (%) 93.29±13.41 91.01±14.20 94.54±12.80 <0.001
FEV1/FVC (%) 77.69±7.26 74.70±8.38 79.33±5.96 <0.001
RPD 569 (8.3) 229 (9.4) 340 (7.7) <0.001
OPD 828 (12.1) 543 (22.4) 285 (6.4) <0.001

Abbreviations: SBP, systolic blood pressure; DBP, diastolic blood pressure; PP, pulse pressure; High PP, PP>60 mmHg; WM, waist measurement; BMI, body mass index; TGs, triglycerides; HDL-C, high density lipoprotein cholesterol; FBG, fasting blood glucose; Predicted FVC, predicted forced vital capacity; Predicted FEV1, predicted forced expiratory volume in 1 second; RPD, restrictive pulmonary diseases, predicted FVC<80.0% with FEV1/FVC≥70.0%; OPD, obstructive pulmonary diseases, FEV1/FVC<70.0%.



2. Clinical characteristics of subjects according to normal and high pulse pressure

The clinical characteristics of subjects according to normal and high PP are shown in Table 2. Age (P< 0.001), BMI (P<0.001), WM (P<0.001), SBP (P<0.001), DBP (P=0.005), PP (P<0.001), TGs (P<0.001), and FBG (P<0.001) were higher in the high PP group than in the normal PP group. HDL-C (P<0.001), predicted FVC (P<0.001), and FEV1/FVC (P<0.001) were lower in the high PP group than in the normal PP group, but predicted FEV1 (P=0.223) was not significant.

Clinical characteristics of subjects according to normal and high pulse pressure N (%), Mean±SD, (N=6,857)

Variables Normal PP (N=5,894) High PP (N=963) P
Age (years) 56.00±10.04 67.63±7.95 <0.001
Women 3,813 (64.7) 617 (64.1) 0.708
Alcohol drinker 2,718 (46.1) 331 (34.4) <0.001
Regular exerciser 1,407 (23.9) 212 (22.0) 0.208
BMI (kg/m2) 24.10±3.09 24.51±2.95 <0.001
WM (cm) 81.88±9.07 84.66±8.37 <0.001
SBP (mmHg) 116.86±13.70 144.83±13.58 <0.001
DBP (mmHg) 76.00±9.73 75.02±11.57 0.005
PP (mmHg) 40.86±8.73 69.81±9.67 <0.001
TGs (mg/dL) 133.11±92.96 145.62±101.73 <0.001
HDL-C (mg/dL) 50.98±12.01 49.50±11.83 <0.001
FBG (mg/dL) 101.12±21.87 107.71±25.06 <0.001
Predicted FVC (%) 93.81±11.58 90.28±12.82 <0.001
Predicted FEV1 (%) 93.37±12.96 92.80±15.92 0.223
FEV1/FVC (%) 78.09±7.03 75.24±8.13 <0.001
Restrictive pulmonary diseases 456 (7.7) 113 (11.7) <0.001
Obstructive pulmonary diseases 629 (10.7) 199 (20.7) <0.001

Abbreviations: See Table 1; Normal PP, PP≤60 mmHg; High PP, PP>60 mmHg.



3. Multiple linear regression analyses for the independent factors determining predicted FVC and FEV1

The multiple linear regression analyses for the independent factors that determine predicted FVC and FEV1 are shown in Tables 3 and 4. We used a multivariate model adjusted for confounders that may be significantly associated with the dependent variables (predicted FVC and FEV1). Predicted FVC was inversely associated with SBP (P<0.001) and PP (P<0.001) but positively associated with DBP (P=0.005). Predicted FEV1 was inversely associated with SBP (P=0.031) and PP (P=0.029) but not associated with DBP (P=0.221).

Multiple linear regression analysis for the independent factors determining predicted FVC (N=6,857)

Variables Predicted FVC (%)

β 95% CI P β 95% CI P
Age (years) −0.068 −0.108 to −0.043 <0.001 −0.066 −0.106 to −0.042 <0.001
Women 0.058 0.750 to 2.121 <0.001 0.059 0.787 to 2.146 <0.001
Current drinker −0.005 −0.710 to 0.452 0.663 −0.006 −0.714 to 0.447 0.652
Regular exerciser −0.012 −0.994 to 0.306 0.299 −0.012 −0.998 to 0.302 0.294
BMI (kg/m2) −0.087 −0.501 to −0.170 <0.001 −0.089 −0.507 to −0.178 <0.001
WM (cm) −0.096 −0.186 to −0.065 <0.001 −0.096 −0.186 to −0.065 <0.001
TGs (mg/dL) 0.003 −0.003 to 0.004 0.810 0.002 −0.003 to 0.003 0.868
HDL-C (mg/dL) 0.047 0.020 to 0.072 <0.001 0.046 0.020 to 0.071 <0.001
FBG (mg/dL) −0.062 −0.045 to −0.020 <0.001 −0.062 −0.045 to −0.020 <0.001
SBP (mmHg) −0.092 −0.089 to −0.041 <0.001 None
DBP (mmHg) 0.047 0.017 to 0.095 0.005 None
PP (mmHg) None −0.075 −0.090 to −0.041 <0.001

Abbreviations: See Table 1.


Multiple linear regression analysis for the independent factors determining predicted FEV1 (N=6,857)

Variables Predicted FEV1 (%)

β 95% CI P β 95% CI P
Age (years) 0.064 0.043 to 0.119 <0.001 0.064 0.044 to 0.119 <0.001
Women 0.067 1.083 to 2.685 <0.001 0.068 1.100 to 2.687 <0.001
Current drinker −0.005 −0.809 to 0.549 0.707 −0.005 −0.810 to 0.547 0.704
Regular exerciser −0.018 −1.318 to 0.201 0.150 −0.018 −1.319 to 0.200 0.149
BMI (kg/m2) 0.112 0.295 to 0.682 <0.001 0.111 0.295 to 0.678 <0.001
WM (cm) −0.162 −0.311 to −0.170 <0.001 −0.162 −0.311 to −0.170 <0.001
TGs (mg/dL) −0.002 −0.004 to 0.003 0.861 −0.003 −0.004 to 0.003 0.844
HDL-C (mg/dL) 0.048 0.024 to 0.084 <0.001 0.048 0.024 to 0.083 <0.001
FBG (mg/dL) −0.043 −0.040 to −0.011 0.001 −0.043 −0.040 to −0.011 0.001
SBP (mmHg) −0.039 −0.060 to −0.003 0.031 None
DBP (mmHg) 0.021 −0.017 to 0.074 0.221 None
PP (mmHg) None −0.032 −0.060 to −0.003 0.029

Abbreviations: See Table 1.



4.Comparisons of the odds ratio of high pulse pressure according obstructive and restrictive pulmonary diseases

The comparisons of RPD and OPD for high PP are shown in Table 5. After adjustment for related variables (age, gender, alcohol drinking, regular exercise, TGs, HDL-C, FBG, BMI, and WM), the odds ratios (ORs) of a high PP with the normal group as a reference were significantly higher in the RPD group (1.337 [95% CI, 1.049∼1.703]) and OPD group (1.339 [95% CI, 1.093∼1.642]).

Comparisons of the odds ratio of high pulse pressure according obstructive and restrictive pulmonary diseases (N=6,857)

Variables High PP (PP>60 mmHg)

Model 1 Model 2 Model 3 Model 4
Normal 1 1 1 1
Restrictive pulmonary diseases 1.872 (1.499∼2.338) 1.404 (1.107∼1.781) 1.365 (1.074∼1.735) 1.337 (1.049∼1.703)
Obstructive pulmonary diseases 2.390 (1.996∼2.862) 1.333 (1.090∼1.631) 1.363 (1.113∼1.669) 1.339 (1.093∼1.642)

Abbreviations: See Table 1; Model 1 [ORs (95% CI)], Non-adjusted; Model 2 [ORs (95% CI)], Model 1 adjusted for age, gender, alcohol drinking, and regular exercising; Model 3 [ORs (95% CI)], Model 2 further adjusted for TGs, HDL-C, and FBG; Model 4 [ORs (95% CI)], Model 3 further adjusted for BMI and WM.


DISCUSSION

This study investigated the association between PP and impaired pulmonary function in Korean non-smoking adults using data from the KNHANES-VI, which was conducted in 2013∼2015. After adjusting for related variables, PP was found to be inversely associated with predicted FVC and FEV1 and positively associated with both RPD and OPD.

Impaired lung function, as assessed by a reduction in the forced expiratory volume measured in the FEV1 and FVC, contributes significantly to several major health issues, such as cardiovascular events and mortality, as well as all-cause mortality [16]. PP was an independent predictor of total mortality and was a more potent predictor of total mortality than SBP or DBP [17, 18]. PP is known to be a strong risk factor for arterial and peripheral vascular disease because PP is an important predictor of AS [19-21]. AS increases left ventricular pulsatile work and is associated with left ventricular hypertrophy (LVH) and alteration of cardiac function [22, 23]. PP was associated with LVH [24, 25], heart failure [26, 27], cardiac mass [28], and cardiac hypertrophy [29]. In particular, when PP and SBP increased in parallel, they have an adverse effect on cardiac hypertrophy [29].

We were investigated the association of PP and RPD and OPD in Korean non-smoking adults, using data from the KNHANES VI, and the ORs of RPD and OPD from the normal PP group as a reference group and found significant values for the high PP group (RPD, 1.337 [95% CI, 1.049∼1.703]; OPD, 1.339 [95% CI, 1.093∼1.642]). Currently, research on the association of PP with pulmonary disease is rare, and the mechanism behind the relationship between PP and pulmonary disease remains ambiguous. However, there are potential mechanisms that link PP with pulmonary disease. First, the association between cardiac dysfunction and abnormal pulmonary function has been previously reported [30-34]. Pelà et al [31] reported that patients with COPD exhibit significant changes in their left ventricular geometry, resulting in concentric remodeling. Olson et al [32] reported that an increase in cardiac size could place significant constraints on the pulmonary function and likely plays a major role in the restrictive patterns often reported in heart failure patients. In addition, Kolb et al [33] suggested that right ventricular dysfunction is associated with hypoxic pulmonary vasoconstriction, pulmonary vascular remodeling, and disruption of pulmonary vascular beds due to the underlying lung disease. Second, PP can be associated with impaired pulmonary function because an increase in PP causes vascular injury to systemic and pulmonary arteries. Guntheroth suggested that increased PP produces injury in the pulmonary arteries due to the exaggerated distension of the arterial wall with each heartbeat [34]. Pulmonary artery stiffening may contribute to the progression of pulmonary hypertension by contributing to chronic microvascular damage in lungs [35]. Third, previous studies have reported that AS is associated with decreased pulmonary function. Jankowich et al reported that FEV1 is inversely associated with AS measured by peripheral pulse pressure (r=−0.37, P<0.001) in the general population [36]. Zureik et al [37] reported that PWV was inversely associated with both FVC (P<0.006) and FEV1 (P<0.001). They suggested that increased AS can also occur in parallel with increased pulmonary vascular resistance and vessel stiffness. In addition, patients with pulmonary arterial hypertension may show altered vascular function in systemic arteries [38].

We investigated the association between pulmonary function (predicted FVC and FEV1) and blood pressure (SBP and DBP) and PP. Predicted FVC was inversely associated with SBP (P<0.001) but positively associated with DBP (P=0.005). Predicted FEV1 was inversely associated with SBP (P=0.031) but not associated with DBP (P=0.221). Both predicted FVC (P<0.001) and FEV1 (P=0.029) were inversely associated with PP. These results may be a result of the PP calculation method (the difference between SBP and DBP). An increase in PP may occur in the following cases: when SBP increases and DBP decreases; when SBP increases even if DBP does not; and when DBP decreases even if SBP does not. An increase in PP corresponds to the first and second cases in our results.

In fact, smoking is the most important factor in impaired pulmonary function and is associated with AS and PP [39, 40]. Therefore, we excluded current smokers in our study for further clarification of the link between impaired pulmonary function and PP. The results of our study conducted on non-smokers showed that high PP was positively associated with both RPD and OPD. One of the reasons for this is that SBP increased with a decrease in predicted FVC and FEV1, but DBP decreased with a reduction in predicted FVC (although not predicted FEV1). Our results may also provide the fundamental data that link impaired pulmonary function with AS. The limitation of the present study was that because this study was cross-sectional, the ability to establish a causal relationship between the impaired pulmonary function and PP was limited. However, despite this limitation, this is the first study to report on the relationship between impaired pulmonary function and high PP in Korean non-smoking adults. Therefore, more accurate results may be obtained by performing a cohort study.

In conclusions, this study investigated the association of PP and impaired pulmonary function in Korean non-smoking adults using data from KNHANES-VI, which was conducted in 2013∼2015. PP was inversely associated with the predicted FVC and FEV1 levels. Increased PP was positively associated with both RPD and OPD.

요 약

선행 연구에서 동맥경화와 폐기능이상과 연관성이 있었다. 맥압은 동맥경화의중요한 예측이지만 아직까지 폐기능이상과 맥압의 연관성은 불분명하다. 따라서, 본 연구는 대한민국 비흡연 성인을 대상으로 맥압과 폐기능장애(예측 강제 폐활량, 예측 강제 날숨량 1초율)의 관련성을 알아보고자 실시하였다. 본 연구는 2013년부터 2015년까지 3년간의 대한민국 국민건강영양조사자료에서 비흡연 성인(6,857명)을 대상으로 실시하였다. 본 연구의 주요 결과는 맥압과 폐기능장애에 대한 관련 변수를 보정한 후의 결과에서, 정상 맥압(pulse pressure, PP≤60 mmHg)에 비하여 고맥압(PP>60 mmHg; 1.337 [95% confidence interval (CI), 1.049∼1.703)에서 제한성 폐질환(restrictive pulmonary disease, RPD; the predicted FVC<80.0% with FEV1/FVC≥70.0%)의 교차비(odds ratio, OR)가 유의하게 높았다. 추가적으로, 정상맥압에 비하여 고맥압(1.339 [95% CI, 1.093∼1.642])에서 폐쇄성 폐질환(obstructive pulmonary disease, OPD; FEV1/FVC< 70.0%)의 교차비가 유의하게 높았다. 결론적으로, 대한민국 비흡연 성인에서 제한성 폐질환 및 폐쇄성 폐질환은 고맥압과 유의한 관계가 있었다.

References
  1. WHO. Disease burden and mortality estimates 2000-2016 [Internet]. Geneva: WHO; 2017 cited 2020 May 08.
    Available from: https://www.who.int/healthinfo/global_burden_disease/estimates/en/index1.html.
  2. Hole DJ, Watt GC, Davey-Smith G, Hart CL, Gillis CR, Hawthorne VM. Impaired lung function and mortality risk in men and women: findings from the renfrew and paisley prospective population study. BMJ. 1996;313:711-715. https://doi.org/10.1136/bmj.313.7059.711.
    Pubmed KoreaMed CrossRef
  3. Sin DD, Wu L, Man SF. The relationship between reduced lung function and cardiovascular mortality: a population-based study and a systematic review of the literature. Chest. 2005;127:1952-1959. https://doi.org/10.1378/chest.127.6.1952.
    Pubmed CrossRef
  4. Yokomichi H, Nagai A, Hirata M, Kiyohara Y, Muto K, Ninomiya TNinomiya T, et al. Survival of macrovascular disease, chronic kidney disease, chronic respiratory disease, cancer and smoking in patients with type 2 diabetes: BioBank Japan cohort. J Epidemiol. 2017;27(3S):98-106. https://doi.org/10.1016/j.je.2016.12.012.
    Pubmed KoreaMed CrossRef
  5. Imaizumi Y, Eguchi K, Kario K. Lung disease and hypertension. Pulse. 2014;2:103-112. https://doi.org/10.1159/000381684.
    Pubmed KoreaMed CrossRef
  6. McAllister DA, Maclay JD, Mills NL, Mair G, Miller J, Anderson DAnderson D, et al. Arterial stiffness is independently associated with emphysema severity in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2007;76:1208-1214. https://doi.org/10.1164/rccm.200707-1080OC.
    Pubmed KoreaMed CrossRef
  7. Mills NL, Miller JJ, Anand A, Robinson SD, Frazer GA, Anderson DAnderson D, et al. Increased arterial stiffness in patients with chronic obstructive pulmonary disease: a mechanism for increased cardiovascular risk. Thorax. 2008;63:306-311. https://doi.org/10.1136/thx.2007.083493.
    Pubmed CrossRef
  8. Costanzo L, Pedone C, Battistoni F, Chiurco D, Santangelo S, Antonelli-Incalzi R. Relationship between FEV1 and arterial stiffness in elderly people with chronic obstructive pulmonary disease. Aging Clin Exp Res. 2017;29:157-164. https://doi.org/10.1007/s40520-016-0560-3.
    Pubmed CrossRef
  9. Benetos A, Thomas F, Joly L, Blacher J, Pannier B, Labat CLabat C, et al. Pulse pressure amplification a mechanical biomarker of cardiovascular risk. J Am Coll Cardiol. 2010;55:1032-1037. https://doi.org/10.1016/j.jacc.2009.09.061.
    Pubmed CrossRef
  10. Zhao L, Song Y, Dong P, Li Z, Yang X, Wang S. Brachial pulse pressure and cardiovascular or all-cause mortality in the general population: a meta-analysis of prospective observational studies. J Clin Hypertens. 2014;16:678-685. https://doi.org/10.1111/jch.12375.
    Pubmed CrossRef
  11. Dart AM, Kingwell BA. Pulse pressure-a review of mechanisms and clinical relevance. J Am Coll Cardiol. 2001;37:975-984. https://doi.org/10.1016/s0735-1097(01)01108-1.
    Pubmed CrossRef
  12. Zheng X, Jin C, Liu Y, Zhang J, Zhu Y, Kan SKan S, et al. Arterial stiffness as a predictor of clinical hypertension. J Clin Hypertens. 2015;17:582-591. https://doi.org/10.1111/jch.12556.
    Pubmed CrossRef
  13. Park SY, Oh HJ, Yoon H. Association of metabolic syndrome, metabolic syndrome score and pulse pressure in Korean adults: Korea National Health and Nutrition Survey, 2012. J Korea Acad Industr Coop Soc. 2014;15:5660-5667. http://doi.org/10.5762/KAIS.2014.15.9.5660.
    CrossRef
  14. Swanney MP, Ruppel G, Enright PL, Pedersen OF, Crapo RO, Miller MRMiller MR, et al. Using the lower limit of normal for the FEV1/FVC ratio reduces the misclassification of airway obstruction. Thorax. 2008;63:1046-1051. https://doi.org/10.1136/thx.2008.098483.
    Pubmed CrossRef
  15. Ranu H, Wilde M, Madden B. Pulmonary function tests. Ulster Med J. 2011;80:84-90. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229853/.
    Pubmed CrossRef
  16. Sin DD, Man SF. Chronic obstructive pulmonary disease as a risk factor for cardiovascular morbidity and mortality. Proc Am Thorac Soc. 2005;2:8-11. https://doi.org/10.1513/pats.200404-032MS.
    Pubmed CrossRef
  17. Tozawa M, Iseki K, Iseki C, Takishita S. Pulse pressure and risk of total mortality and cardiovascular events in patients on chronic hemodialysis. Kidney Int. 2002;61:717-726. https://doi.org/10.1046/j.1523-1755.2002.00173.x.
    Pubmed CrossRef
  18. Domanski M, Mitchell G, Pfeffer M, Neaton JD, Norman J, Svendsen KSvendsen K, et al. Pulse pressure and cardiovascular disease-related mortality: follow-up study of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA. 2002;287:2677-2683. https://doi.org/10.1001/jama.287.20.2677.
    Pubmed CrossRef
  19. Assmann G, Cullen P, Evers T, Petzinna D, Schulte H. Importance of arterial pulse pressure as a predictor of coronary heart disease risk in PROCAM. Eur Heart J. 2005;26:2120-2126. https://doi.org/10.1093/eurheartj/ehi467.
    Pubmed CrossRef
  20. Korhonen P, Kautiainen H, Aarnio P. Pulse pressure and subclinical peripheral artery disease. J Hum Hypertens. 2014;28:242-245. https://doi.org/10.1038/jhh.2013.99.
    Pubmed CrossRef
  21. Chrysant GS. Peripheral vascular disease is associated with increased pulse wave velocity and augmentation index: clinical implications. J Clin Hypertens. 2014;16:788-789. https://doi.org/10.1111/jch.12407.
    Pubmed CrossRef
  22. Nitta K, Akiba T, Uchida K, Otsubo S, Otsubo Y, Takei TTakei T, et al. Left ventricular hypertrophy is associated with arterial stiffness and vascular calcification in hemodialysis patients. Hypertens Res. 2004;27:47-52. https://doi.org/10.1291/hypres.27.47.
    Pubmed CrossRef
  23. Zile MR, Gottdiener JS, Hetzel SJ, McMurray JJ, Komajda M, McKelvie RMcKelvie R, et al. Prevalence and significance of alterations in cardiac structure and function in patients with heart failure and a preserved ejection fraction. Circulation. 2011;124:2491-2501. https://doi.org/10.1161/CIRCULATIONAHA.110.011031.
    Pubmed CrossRef
  24. Palmieri V, Devereux RB, Hollywood J, Bella JN, Liu JE, Lee ETLee ET, et al. Association of pulse pressure with cardiovascular outcome is independent of left ventricular hypertrophy and systolic dysfunction: the strong heart study. Am J Hypertens. 2006;19:601-607. https://doi.org/10.1016/j.amjhyper.2005.12.009.
    Pubmed CrossRef
  25. Toprak A, Reddy J, Chen W, Srinivasan S, Berenson G. Relation of pulse pressure and arterial stiffness to concentric left ventricular hypertrophy in young men (from the Bogalusa Heart Study). Am J Cardiol. 2009;103:978-984. https://doi.org/10.1016/j.amjcard.2008.12.011.
    Pubmed CrossRef
  26. Vaccarino V, Holford TR, Krumholz HM. Pulse pressure and risk for myocardial infarction and heart failure in the elderly. J Am Coll Cardiol. 2000;36:130-138. https://doi.org/10.1016/s0735-1097(00)00687-2.
    CrossRef
  27. Haider AW, Larson MG, Franklin SS, Levy D. Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Framingham Heart Study. Ann Intern Med. 2003;138:10-16. https://doi.org/10.7326/0003-4819-138-1-200301070-00006.
    Pubmed CrossRef
  28. Brahimi M, Dahan M, Dabiré H, Levy BI. Impact of pulse pressure on degree of cardiac hypertrophy in patients with chronic uraemia. J Hypertens. 2000;18:1645-1650. https://doi.org/10.1097/00004872-200018110-00016.
    Pubmed CrossRef
  29. Safar ME, Levy BI, Struijker-Boudier H. Current perspectives on arterial stiffness and pulse pressure in hypertension and cardiovascular diseases. Circulation. 2003;107:2864-2869. https://doi.org/10.1161/01.CIR.0000069826.36125.B4.
    Pubmed CrossRef
  30. Kaushal M, Shah PS, Shah AD, Francis SA, Patel NV, Kothari KK. Chronic obstructive pulmonary disease and cardiac comorbidities: a cross-sectional study. Lung India. 2016;33:404-409. https://doi.org/10.4103/0970-2113.184874.
    Pubmed KoreaMed CrossRef
  31. Pelà G, Li Calzi M, Pinelli S, Andreoli R, Sverzellati N, Bertorelli GBertorelli G, et al. Left ventricular structure and remodeling in patients with COPD. Int J Chron Obstruct Pulmon Dis. 2016;11:1015-1022. https://doi.org/10.2147/COPD.S102831.
    Pubmed KoreaMed CrossRef
  32. Olson TP, Beck KC, Johnson BD. Pulmonary function changes associated with cardiomegaly in chronic heart failure. J Card Fail. 2007;13:100-107. https://doi.org/10.1016/j.cardfail.2006.10.018.
    Pubmed KoreaMed CrossRef
  33. Kolb TM, Hassoun PM. Right ventricular dysfunction in chronic lung disease. Cardiol Clin. 2012;30:243-256. https://doi.org/10.1016/j.ccl.2012.03.005.
    Pubmed KoreaMed CrossRef
  34. Guntheroth WG. Increased pulse pressure causes vascular injury in pulmonary and systemic arteries. Decreasing the pulsatility with banding and vasodilators can stabilize pulmonary hypertension. J Clinic Experiment Cardiol. 2010;1:107. https://doi.org/10.4172/2155-9880.1000107.
    CrossRef
  35. Tan W, Madhavan K, Hunter KS, Park D, Stenmark KR. Vascular stiffening in pulmonary hypertension: cause or consequence? (2013 Grover Conference series). Pulm Circ. 2014;4:560-580. https://doi.org/10.1086/677370.
    Pubmed KoreaMed CrossRef
  36. Jankowich MD, Taveira T, Wu WC. Decreased lung function is associated with increased arterial stiffness as measured by peripheral pulse pressure: data from NHANES III. Am J Hypertens. 2010;23:614-619. https://doi.org/10.1038/ajh.2010.37.
    Pubmed CrossRef
  37. Zureik M, Benetos A, Neukirch C, Courbon D, Bean K, Thomas FThomas F, et al. Reduced pulmonary function is associated with central arterial stiffness in men. Am J Respir Crit Care Med. 2001;164:2181-2185. https://doi.org/10.1164/ajrccm.164.12.2107137.
    Pubmed CrossRef
  38. Peled N, Shitrit D, Fox BD, Shlomi D, Amital A, Bendayan DBendayan D, et al. Peripheral arterial stiffness and endothelial dysfunction in pulmonary arterial hypertension. J Rheumatol. 2009;36:970-975. https://doi.org/10.3899/jrheum.081088.
    Pubmed CrossRef
  39. Nettleton JA, Follis JL, Schabath MB. Coffee intake, smoking, and pulmonary function in the atherosclerosis risk in communities study. Am J Epidemiol. 2009;169:1445-1453. https://doi.org/10.1093/aje/kwp068.
    Pubmed KoreaMed CrossRef
  40. Mahmud A, Feely J. Effect of smoking on arterial stiffness and pulse pressure amplification. Hypertension. 2003;41:183-187. https://doi.org/10.1161/01.hyp.0000047464.66901.60.
    Pubmed CrossRef


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