Gaurav Kapoor
Association of Physical, Psychological and Psychosocial Attributes With Arterial Stiffness in Cardiovascular Disorders: A Systematic Literature Review
Behavioral Psychology,Cardiovascular disease,Obesity,Physical activity,Sedentary behavior
The prevalence of cardiovascular diseases is increasing exponentially in the industrialized world. According to the World Health Organization, 17.8 million people died in 2019 as a result of cardiovascular diseases (CVD), accounting for 31.0% of all fatalities worldwide. Even though CVD is more common in low and middle-income countries, it is responsible for three-quarters of all cardiovascular-related deaths worldwide. The most common attributes for the occurrence of CVD are the physical, psychological, and psychosocial factors. Arterial stiffness, which is a precursor of CVD, is most commonly affected by said factors and serves as a predictor for CVD diagnosis, treatment, and prevention. The purpose of this article is to learn more about the relationship between arterial stiffness and the physical, psychological, and psychosocial characteristics of cardiovascular diseases. In addition to proposed ways to lower the co-morbidities following CVD. PubMed, Medline, and Web of Science were used for the present review. Only articles published between 1988 and 2022 that discussed physical, psychological, and psychosocial characteristics were considered. A narrative discussion is used to extract and review the information from the selected articles. Several factors related to arterial stiffness and cardiovascular illness have been reviewed, and data has been compiled. This review proposed recommendations and a list of linked factors for prevention and to lower morbidity of cardiovascular illness.
Association of Physical, Psychological and Psychosocial Attributes With Arterial Stiffness in Cardiovascular Disorders: A Systematic Literature Review

The prevalence of cardiovascular diseases is increasing exponentially in the industrialized world. According to the World Health Organization, 17.8 million people died in 2019 as a result of cardiovascular diseases (CVD), accounting for 31.0% of all fatalities worldwide. Even though CVD is more common in low and middle-income countries, it is responsible for three-quarters of all cardiovascular-related deaths worldwide. The most common attributes for the occurrence of CVD are the physical, psychological, and psychosocial factors. Arterial stiffness, which is a precursor of CVD, is most commonly affected by said factors and serves as a predictor for CVD diagnosis, treatment, and prevention. The purpose of this article is to learn more about the relationship between arterial stiffness and the physical, psychological, and psychosocial characteristics of cardiovascular diseases. In addition to proposed ways to lower the co-morbidities following CVD. PubMed, Medline, and Web of Science were used for the present review. Only articles published between 1988 and 2022 that discussed physical, psychological, and psychosocial characteristics were considered. A narrative discussion is used to extract and review the information from the selected articles. Several factors related to arterial stiffness and cardiovascular illness have been reviewed, and data has been compiled. This review proposed recommendations and a list of linked factors for prevention and to lower morbidity of cardiovascular illness.

Cardiovascular disorders (CVD) likewise heart diseases and stroke are paramount for annual deaths across the world with also a higher incidence in India [1]. In 2019, World Health Organization (WHO) reported 17.8 million people died with CVD accounting for 31.0% of all deaths worldwide [2]. Thus, CVD was responsible for 38.0% of the 17.0 million premature fatalities. The burden of CVD is higher in poor and middle income nations accounting for three-fourth of all CVD fatalities worldwide. WHO estimates by 2030 India will have a CVD death rate of more than 35.0% [1] as CVD strikes 6-10 years early in Indian population and with proceed higher mortality rate in comparison to western population [1]. In the last four decades, the incidence of Coronary Artery Disease has surged by 300.0% and further rising at an alarming rate of 5%-6% per year in the Indian population [1]. Prevalence of CVD in the rural and urban India population has surged from 1.6% to 7.4% and 1.0% to 13.2% respectively [2]. The exponential economy explosion and urbanization emerging as substantial lifestyle transformer is a incorporating sink in physical activity and energy disbursement; shoot-up in the pro-atherogenic diet and tobacco use [3]. In addition, hazardous lifestyle danger among Indian population with 15.0% population smoking tobacco, 4.3 liters of pure alcohol consumed per capita, more than one fifth (21.0%) population suffering from hypertensive disorder, cardinal determinant of heart attack/failure, kidney disease and/or stroke make the condition worse [4].

Sedentary behavior/Physical inactivity are recognized element for CVD costing $53.8 billion in 2013 worldwide with an estimated 13.4 million disability-adjusted life year lost [5]. Low levels of physical exercise and sedentary behaviour have both been linked to arterial stiffness. Studies suggest arterial stiffness to increase with age in both sedentary as well as physically active people. But, in physically active people the rate of change is much slower than sedentary individuals. Fernberg et al. [6], 2021 and Horta et al. [7], 2015 conducted self-report studies on younger populations in Sweden and Brazil, finding reduced arterial stiffness to be inversely related to moderate and vigorous physical activity while sedentary behaviour to be positively related. Ahmadi-Abhari et al. [8], 2017 found avoiding sedentary lifestyle and engaging in high levels of moderate to vigorous physical activity substantially link to a slowing of the age-related progression of aortic stiffness. Funck et al. [9], 2016 documented insufficient physical activity to be associated with increased arterial stiffness in both type II diabetes and healthy patients. Stamatelopoulos et al. [10], 2020 discovered mean Pulse Wave Velocity (PWV) values to drop linearly with increasing intensity of physical exercise in normal weight postmenopausal women. In addition, physical exercise was also linked to lower Body Mass Index (BMI), Low Density Lipoproteins (LDL), cholesterol, and triglyceride levels and insulin resistance. Nosova et al. [11], 2014 found inactivity to cause vascular “deconditioning” state defined by decreased endothelial function leading to arterial stiffness and increased arterial tone.

Smoking has long been recognized as a significant risk factor in development and progression of CVD. The pathophysiological process of vascular injuries following smoking is anticipated to be changes in hemostatic components of endothelial function and blood lipid profile. Even minor changes in the dynamic/elastic vessel-wall characteristics act as a powerful mechanism [12]. Studies in the healthy smokers show smoking to cause changes in functional variables such arterial dispensability and blood pressure. Smoking in hypertensive patient increases risk of CVD with acute increases in arterial stiffness, blood pressure, and heart rate in response to smoking may increase the strain on the arterial and left-ventricular walls as well as alter the distribution of circumferential and tensile stress [13]. Smoking causes plaque rupture and an acute ischemic event by causing an increase in the load on the plaque. Studies also confirm the link between arterial stiffness and smoking habits in both normotensive and hypertensive young and old people (Fig. 1). Rehill et al. [14], 2006 found long-term tobacco smoking to be linked to endothelial dysfunction and an elevated Augmented Index (Alx). Furthermore after 4 weeks of quitting smoking there may be partial reversibility of the Alx in long-term smokers. The effect on endothelial dysfunction in long-term smokers, particularly young smokers has also been supported by Binder et al. [15], 2008. According to Vlachopoulos et al. [16], 2004, smoking cigar increases acute stiffness of major arteries and wave reflection and thus, is not a safe alternative to cigarette. Furthermore, in 2007, Rhee et al. [17], confirmed long-term smoking among male smokers with hypertension to acquire increased aortic stiffness and blood pressure significantly. In comparison to smokers with no history of hypertension, these effects last longer. In the same year, Jatoi et al. [18], discovered significant linear link between smoking status and arterial stiffness utilising Pulse wave velocity (PWV) and enhanced index with age, sex, BMI, heart rate, and mean arterial pressure. According to Kim et al. [19], 2005, cigarette smoking raises systolic and diastolic blood pressure, heart rate and Brachial ankle PWV significantly at 5 minutes in both chronic smokers and non smokers before returning to normal at 15 and 30 minutes respectively. Furthermore, this study also found that chronic smokers reflect higher systolic blood pressure and brachial ankle PWV than non-smokers. In addition to smoking alcohol consumption has well established link with hypertension, the most common cause of cardiovascular illness. Physiological activation of the endothelium to discharge endothelin or suppression of endothelium-dependent nitric oxide generation are two prominent mechanisms that raise blood pressure with consumption of alcohol [20]. Observational studies support light to moderate alcohol having a cardiac preventive impact in adults over the age of 40 years and predict J-shaped association between alcohol and arterial stiffness lowering the risk of CVD. In contrast, a study found moderate alcohol consumption to lower risk of CVD and ischemic stroke but increased the risk of subarachnoid haemorrhage in middle-aged women [21]. But, van den Elzen et al. [22], 2005 found moderate alcohol consumption to affect vascular stiffness particularly in younger women. Similarly, Oda et al. [23], 2017 found that even moderate alcohol consumption (140 gram per week) impaired endothelial and vascular functions in men. But Oda et al. [24], 2020 documented that little amount of alcohol had no deadly effect on women but excessive alcohol use impaired the endothelium function in women. On the flipside, heavy and long-term alcohol consumption not only negates the benefits, but also puts the aortic stiffness at risk. van Trijp [25] study on younger males with average age of 28 years found heavy drinkers to pose significantly higher Alx, a precursor of arterial stiffness. Charakida et al. [26], supported the same with their study in 2019 which found that drinking methods having a significant impact on arterial stiffness with excessive intensity in contrast to frequency of drinking, resulting in negative effects on PWV. Furthermore, Tanaka [27], 2016 found Japanese men consuming more than 46 grams of alcohol per day were well associated with a lower mean value of percentage of endothelium dependent flow mediated vasodilation compared to those who had never drunk. Furthermore there was no discernible link between the beneficial effects of light alcohol consumption on endothelial function in this study. In today’s world obesity has emerged as an independent risk factor for CVD, chronic kidney disease and cognitive decline. It is caused by a diet high in saturated fat, highly processed carbohydrates and incorporation of a sedentary lifestyle [28]. The loss of cushioning effect is inextricably connected to an increase in female susceptibility to vascular stiffness [29]. In obese adults, endothelium and vascular smooth muscle cell hardening, immune cell dysfunction, perivascular adipose tissue inflammation, and extracellular matrix remodelling enhance the arterial rigidity [30]. This has been backed up by studies. Logan et al. [31], 2020 found a significant link between waist hip ratio and augmented index and elasticity of smaller arteries in adults below the age of 55 years. Furthermore, researchers discovered no link between BMI and AIx, as well as the elasticity of smaller arteries. Zebekakis et al. [32], 2005 discovered flexibility of muscle arteries decreases and diameter increases in both genders over a wide range of age groups with a higher BMI. Safar et al. [33], 2006 discovered metabolic syndrome including BMI, dyslipidemia, hyperglycemia and hypertension to be is closely linked to increased aortic rigidity as people get older in age. Strasser et al. [34], 2015 found central obesity and visceral fat index to be strongly linked to PWV and arterial stiffness in the middle-aged population. To substantiate the preceding correlation, in a meta-analysis, Li et al. [35], 2017 discovered arterial stiffness to be recognised as a cardiovascular danger which increases in patients with obesity who have no symptoms of heart disease. Dyslipidemia such as elevated LDL cholesterol and triglycerides or low levels of High‐Density Lipoprotein (HDL) (cholesterol, and/or total cholesterol are an established risk factor which play a crucial role in the development and progression of vascular disease such as CVD and ischemic stroke. Even among animals, hypercholesterolaemia induced by a cholesterol-rich diet leads to an initial reduction in arterial stiffness followed by a progressive increase over time which can be reversed by lowering serum cholesterol [36]. Studies have noted that large quantity of small dense low-density lipoprotein-cholestrol-C and disproportion of triglycerides and HDL-C may be an instigating factor for the progression of arterial stiffness in healthy population. Further it has been documented that cholesterol particularly oxidised LDL cholesterol has a range of non-atheromatous direct actions on the artery wall that can cause arterial stiffness. Peroxynitrite production and a generalised condition of exaggerated oxidative stress are also caused by oxidised LDL cholesterol, both of which can damage elastin directly [37]. Ferrier et al. [38], 2002 noticed a rigorous decline in cholesterol to be favorable in the treatment of ischemic cardiac disease population and normal lipid levels with depletion in arterial stiffness in larger arteries. To add to the evidence, a review published by Wilkinson and Cockcroft [39], 2007 found link between plasma cholesterol and the stiffness of the major arteries. To back this another study published by Li et al. [40], 2018 found ratio of small dense low density lipoprotein-cholesterol to triglycerides or high density lipoprotein-cholesterol to predict arterial stiffness progression in normotensive subjects and that a higher ratio was directly linked to a higher risk of arterial stiffness.

Psychosocial factors have also been linked to CVD especially with individuals experiencing persistent work stress, social isolation and depression. In today’s environment, mental stress is a novel risk factor for CVD that has been linked to left ventricular dysfunction, myocardial ischemia and infarction, and even sudden cardiac death in otherwise healthy people [41]. The specific nature of its pathways that mediate the link between psychosocial stress and cardiovascular risk is still unknown. Though several explanations have been proposed to explain the process that causes the same, acute psychological stress according to some theories induces transitory endothelial dysfunction which contributes to this risk [42]. In addition, stress-related inflammatory reactions too is likely to play a vital role. Low socioeconomic level has been linked to chronic inflammation and an increased risk of CVD in adults [43]. Vlachopoulos et al. [44], 2006 documented acute mental stress to cause sustained increase in aortic stiffness and wave reflections in nineteen healthy people. Similarly, Ellins et al. [45], 2008 noted inflammatory reactions to acute psychological stress are linked to structural alterations in the artery wall in otherwise healthy people. Looking into anxiety is a substantial and independent driver of arterial stiffness [46]. A brief period of mild to moderate stress not inducing lasting alterations in autonomic function reflect considerable negative effects on arterial stiffness in women [47]. In the year 2020, Kume et al. [48], found mental stress to increase arterial stiffness in a variety of segments in young male adults but this increase was not uniform across all segments. Lipman et al. [49], 2002 documented middle-aged and older individuals, presented with larger arterial pressure responses to mental stress are associated with increased carotid stiffness and poorer arterial baroreflex sensitivity.

Cardiovascular diseases are prevalent in all sections of the society across the globe (Table 1). With modification in lifestyle namely reducing psychosocial factors, cessation from smoking and alcohol consumption, reducing the prevalence of obesity and promotion of healthy eating and physical activity do control morbidity due to cardiovascular illness.