The bigger view
The bigger view
Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 17.7 million deaths each year.1
According to the European Society of Cardiology, almost 49 million people living with the condition across the region.2 To reduce pressure on healthcare services and the costs associated with treating cardiovascular incidents, maintaining a healthy heart is key. A healthy diet and regular exercise should be adhered to for optimal cardiovascular health, supported by nutritional interventions such as supplements where appropriate. For many people, achieving the necessary levels of micronutrients through diet alone can be difficult. In these cases, supplementation provides a simple and convenient way for individuals to reach the desired intake.
A prevention-led approach may be the solution to improve the health of populations worldwide. The key to a healthy heart is supporting the three pillars of cardiovascular health: cholesterol and triglycerides levels, blood pressure and blood flow. Emerging research has shown certain bioactive compounds can help to address specific areas of heart health.
Five ways to improve the workings of a healthy heart
- Promote healthy heart function
- Promote healthy blood lipids
- Prevent LDL cholesterol oxidation
- Promote healthy blood pressure
- Support healthy circulation and blood vessels
Healthy circulation for healthy hearts
The cardiovascular system supports a variety of functions in the human body, from regulating temperature and pH levels, to removing waste and transporting oxygen and nutrients to the brain and other organs. Previously often overlooked, healthy blood flow, or circulation, is of particular importance as it not only ensures the right amount of oxygen-rich blood is delivered around the body, but also reduces unnecessary strain on the heart. However, there are a range of risk factors that can result in poor blood circulation with the primary cause often being the clumping together of platelets in the blood. Platelets can play an important role in the body following injuries, clotting in an effort to prevent blood loss. Yet, if they become too ‘sticky’ then these activated platelets can aggregate inside blood vessels – making it harder for the blood to flow around the body and increasing the likelihood of unneeded, and potentially dangerous blood clots. Additionally, activated platelets can also produce plaques which may then build up, resulting in the development of atherosclerosis – narrowing the arteries and restricting blood flow. Stress, obesity, pregnancy and both inactivity and extreme exercise all increase the likelihood of platelet aggregation.
What can trigger platelet aggregation? The main causes of blood clots.
Three major factors in cardiovascular disease (CVD): high cholesterol levels, high blood pressure and platelet aggregation are the main cause of blood clots.
Unfortunatelly there are much more factors that can induce platelet activation that may lead to blood clot formation, such as:
- Metabolic diseases are associated with chronic inflammation and platelet activation
- Chronic inflammation associated with infections
- Doing excessive training, heavy sports
- Smoking cigarettes / living in a smoggy, big city with polluted air
Platelets release a plethora of inflammatory mediators with no known role in haemostasis (the mechanism that leads to cessation of bleeding from a blood vessel). Many of these mediators modify leukocyte and endothelial responses to a range of different inflammatory stimuli.3
Platelets have emerged as crucial coordinators of inflammation through their interactions with monocytes, neutrophils, lymphocytes, and the endothelium. As a response to injury or disease, the versatility and reactivity of platelets in recruiting leukocytes and initiating an inflammatory response is highly beneficial. However, the reactivity of platelets also brings disadvantages, sometimes generating and maintaining a raised inflammatory burden which accelerates tissue damage or the progress of a disease, for example, in atherosclerosis, diabetes or inflammatory bowel disease.4, 5, 6
Simply put: chronic inflammation induces platelet activation and activated platelets release pro-inflammatory mediators that amplify the inflammatory response and platelet activation.
All kinds of chronic inflammations might lead to platelet activation whether it is arthritis, inflammation of varicose veins, acute pancreatitis, inflammatory bowel disease, etc.
Another example is the enhanced immunothrombosis that characterizes severe cases of COVID-19 disease caused by the SARS-nCoV-2 virus. Severe infections with SARS-nCoV-2 can result in a cytokine storm, systemic inflammatory response and immunothrombosis, leading to microvascular thrombosis (widespread blood clots in tiny blood vessels).7 Antiplatelet therapy is often used in cases of severe infection and some cases of less severe infection (e.g., use of acetylsalicylic acid in influenza). However, its use has become much more widespread since the advent of the SARS-nCoV-2 virus as targeting platelet hyperactivity may help prevent or delay the progression of illness from mild to severe.
Hyperactive platelets, a cause of platelet aggregation, can also lead to the development of atherosclerosis – which can, in turn, cause myocardial infarctions and cerebrovascular haemorrhages if the atherosclerotic plaques rupture.
Atherosclerosis is thickening or hardening of the arteries caused by a buildup of plaque in the inner lining of an artery. Risk factors may include high cholesterol and triglyceride levels, high blood pressure, smoking, diabetes, obesity, physical activity, and eating saturated fats.
Although an atherosclerotic plaque may remain clinically silent, it is prone to disruption, leading to local platelet activation and aggregation. Therefore, the major complication of atherosclerosis is thrombosis, with local occlusion or distal embolism - a generalized disease process known as atherothrombosis. The three main clinical manifestations of atherothrombosis are coronary heart disease (myocardial infarction and angina), peripheral arterial disease and cerebral ischaemia.
For those who have already experienced a cardiovascular event or when other CVD risks including high blood pressure have been identified, drugs with an antiplatelet effect are often recommended as secondary prevention for maintaining healthy blood circulation. While these medicines are often linked to negative health consequences – e.g. stomach problems, Cardio Fortis acts as a natural blood thinner and is easy on the stomach. Thanks to its Fruitflow® ingredient, Cardio Fortis gets to work immediately and its benefits are long lasting, making it ideal for primary prevention. With its powerful ingredients Cardio Fortis can have a positive impact on wider cardiovascular health to improve the lives of many across the world.
Excercise induced inflammation
Exercise is associated with good health, and increasing exercise is usually linked to longer life, better mental health, less metabolic problems, stronger bones, and improved cardiovascular health.8 However, strenuous exercise is associated with an increased risk of vascular thrombotic events and sudden death.9 We experience stress related to exercise as lack of breath, muscular fatigue, or even acute pain. On a molecular level, during exercise, we are inducing an inflammatory burst, which is mediated by platelets. Excessive exercise releases adrenalin and serotonin and generates thrombin10, resulting in platelet activation.9
In addition, intense aerobic exercise can reduce the amount of anti-aggregatory nitric oxide (NO) produced by the vascular endothelium, especially in untrained subjects, as the amount of oxygen reaching the NO-producing cells is reduced.11 Hyperaggregability develops, and platelets then coordinate a series of pro-inflammatory events.12
This sequence of events has two major consequences. Firstly, after exercise, the potential for blood to coagulate and form a blood clot increases. This state is termed hypercoagulability, and can last for up to 48 hours after an exercise session.13 The extent of hypercoagulability depends on the duration and intensity of the exercise undertaken as well as training status; it is worse in untrained individuals at lower intensities of exercise but still occurs in well-trained individuals at higher intensities of exercise. This increase in coagulation capacity can be dangerous, especially for those with underlying health conditions such as atherosclerosis or cardiac problems, leading to an increased risk of thrombosis and sometimes even sudden death.14 The second consequence of platelet activation during exercise is increased inflammation.
A small exploratory study using a treadmill test showed that Cardio Fortis component Fruitflow® intake caused reduced exercise-induced platelet microparticle generation and the induced increase in thrombin generation capacity was also reduced. For those who do excessive training once in a while Cardio Fortis intake is recommended.
The majority of the world’s population (92%) currently breathe air that fails to meet World Health Organization guidelines. As reported by the Global Burden of Disease Report, outdoor fine particulate matter (particulate matter with an aerodynamic diameter <2.5 µm) exposure is the fifth leading risk factor for death in the world, accounting for 4.2 million deaths . The World Health Organization attributes 3.8 million additional deaths to indoor air pollution. As such, air pollution is now the largest environmental risk factor for health.
Particulate air pollution is related to natural events - volcanic emissions, dust storms, forest fires - and human activities such as vehicle or machinery emissions and traditional cooking practices. Both types of events result in the suspension of soot, gases and other air particulate matter (PM). PM is usually classified by its size; PM10 denotes particles <10 µm in diameter, PM2.5 particles are <2.5 µm in diameter, and PM0.1 particles are <0.1 µm in diameter. Smaller PM is more toxic than larger PM, as they are easily transported to more tissues in the body. PM2.5 are small enough to penetrate lung alveoli, while PM0.1 pass through the alveolar-capillary membrane and into the bloodstream.15 PM in the bloodstream induces cytotoxic and inflammatory responses.
Particulate matter promotes arterial thrombosis and atherosclerosis through increased platelet activation16, leading to accelerated coronary heart disease and strokes, which are the main causes of death from air pollution.15, 17
Some exploratory tests were conducted to expose platelets to airborne particulate matter, such as diesel emissions, in the presence or absence of Fruitflow®. These in vitro tests showed that Fruitflow® reduces the platelet activation caused by PM2.5 by approximately one third.18
A growing focus on menopause, and changes in women’s cardiovascular health accompanying the reduction in oestrogen levels during menopause has highlighted platelet hyperactivity as a target in this area.
Besides other functions oestrogen provides protection on the cardiovascular system so that women’s risk of CVD is significantly lower than men’s for 50–60 years.19 When natural levels of oestrogen decline during perimenopause, this protective effect is lost. In the space of 5–10 years, women’s CVD risk equals that of men.20 In part, this effect relates to the loss of oestrogen signalling to regulate the elasticity of blood vessels.
During perimenopause, platelet oestrogen receptors reduce in number, and after menopause, they disappear. Alongside reduced nitric oxide, this removes a layer of protection from women’s platelets. Simultaneously, the dropping oestrogen levels cause increased instability from disturbed metabolism, an unhealthy balance of blood fats, and damaged blood vessels. Platelets can become persistently sticky after menopause, both a cause and consequence of women’s increased cardiovascular risk profile.
Reducing platelet hyperactivity during and after menopause may go some way towards compensating for the loss of the protective effects of oestrogen on the cardiovascular system. Alongside diet and exercise advice, dietary antiplatelets can be potentially useful adjunct therapy suitable for long term use.
- World Health Organization, ‘Cardiovascular diseases (CVDs) fact sheet’, Accessed on: 17th October 2017 [WHO]
- European Society of Cardiology, ‘About Cardiovascular Disease in Europe 2017 Statistics’, 2017 [Escardio]
- Storey, R.; Thomas, M.R. The role of platelets in inflammation. Haemost. 2015, 114, 449–458. [CrossRef]
- Matowicka-Karna, J. Markers of inflammation, activation of blood platelets and coagulation disorders in inflammatory bowel diseases. Postepy Hig. Med. Dosw. 2016, 70, 305–312. [CrossRef]
- Von Hundelshausen, P.; Lievens, D. Platelets in atherosclerosis. Haemost. 2011, 106, 827–838. [CrossRef] [PubMed]
- Pretorius, E. Platelets as Potent Signaling Entities in Type 2 Diabetes Mellitus. Trends Endocrinol. Metab. 2019, 30, 532–545. [CrossRef]
- Connors, J.M.; Levy, J.H. Thromboinflammation and the hypercoagulability of COVID-19. Thromb. Haemost. 2020, 18, 1559–1561. [CrossRef] [PubMed]
- Konings, J.; Kremers, R.; Bloemen, S.; Schurgers, E.; Selmeczi, A.; Kelchtermans, H.; Van Meel, R.; Meex, S.J.; Kleinegris, M.-C.; De Groot, P.G.; et al. Strenuous exercise induces a hyperreactive rebalanced haemostatic state that is more pronounced in men. Haemost. 2016, 115, 1109–1119. [CrossRef] [PubMed]
- Galloza, J.; Castillo, B.; Micheo, W. Benefits of Exercise in the Older Population. Med. Rehabil. Clin. N. Am. 2017, 28, 659–669. [CrossRef]
- Sedgwick, M.J.; Thompson, M.; Garnham, J.; Thackray, A.E.; Barrett, L.A.; Powis, M.; Stensel, D.J. Acute high-intensity interval rowing increases thrombin generation in healthy men. J. Appl. Physiol. 2016, 116, 1139–1148. [CrossRef]
- Nosarev, A.V.; Smagliy, L.V.; Eanfinogenova, Y.; Popov, S.; Kapilevich, L.V. Exercise and NO production: Relevance and implications in the cardiopulmonary system. Cell Dev. Biol. 2015, 2, 73. [CrossRef]
- Hilberg, T.; Menzel, K.; Gläser, D.; Zimmermann, S.; Gabriel, H.H.W. Exercise intensity: Platelet function and platelet-leukocyte conjugate formation in untrained subjects. Res. 2008, 122, 77–84. [CrossRef] [PubMed]
- Smith, J.E. Effects of strenuous exercise on haemostasis. J. Sports Med. 2003, 37, 433–435. [CrossRef]
- Montagnana, M.; Lippi, G.; Franchini, M.; Banfi, G.; Guidi, G.C. Sudden Cardiac Death in Young Athletes. Med. 2008, 47, 1373–1378. [CrossRef] [PubMed]
- Cohen, A.J.; Brauer, M.; Burnett, R.; Anderson, H.R.; Frostad, J.; Estep, K.; Balakrishnan, K.; Brunekreef, B.; Dandona, L.; Dandona, R.; et al. Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: An analysis of data from the Global Burden of Diseases Study 2015. Lancet 2017, 389, 1907–1918. [CrossRef]
- Robertson, S.; Miller, M.R. Ambient air pollution and thrombosis. Fibre Toxicol. 2018, 15, 1. [CrossRef]
- Bourdrel, T.; Bind, M.-A.; Bejot, Y.; Morel, O.; Argacha, J.-F. Cardiovascular effects of air pollution. Cardiovasc. Dis. 2017, 110, 634–642. [CrossRef] [PubMed]
- Mussler, B.; Raederstorff, D.; Richard, N. Water Soluble Tomato Extract Protects against Adverse Effects of Air Pollution. International Patent Application published as WO 2018/083137 A1, 11 May 2018.
- Iorga, A.; Cunningham, C.M.; Moazeni, S.; Ruffenach, G.; Umar, S.; Eghbali, M. The protective role of estrogen and estrogen receptors in cardiovascular disease and the controversial use of estrogen therapy. Sex Differ. 2017, 8, 33. [CrossRef]
- Newson, L. Menopause and cardiovascular disease. Post Reprod. Health 2018, 24, 44–49. [CrossRef]