Does Paroxysmal Atrial Tachycardia Terminate While Taking Hawthorn Berries Supplement? – Publisher and reviewer affiliations are the last provided in your Loop research profiles and may not reflect your status at the time of review.
Cardiovascular disease (CVD) is a major health burden with increasing prevalence. They remain the leading causes of morbidity and mortality worldwide. The use of medicinal herbs continues to be an alternative treatment approach for various diseases, including CVD. Currently, there is an unprecedented push for the use of herbal preparations in modern medicinal systems. This impetus is based on several aspects, not least of which is its promise as a cost-effective therapeutic compared to standard modern therapies and the general belief that they are safe. However, the claimed safety of herbal preparations has yet to be adequately tested. Consequently, public awareness should be raised about herbal medicinal safety, toxicity, life-threatening adverse effects, and potential herb-drug interactions. Over the years, laboratory data have shown that medicinal herbs may have therapeutic value in CVD, as they can interfere with several CVD risk factors. Consequently, there have been many attempts to move herbal medicinal studies from the bench to the bedside, in order to effectively use herbs in CVD treatments. In this review, we introduce CVD and its risk factors. Next, we review the use of herbs for the treatment of disease in general and CVD in particular. In addition, data on the potential ethnopharmacological therapeutics and anti-CVD medicinal properties of four widely used plants, namely Ginseng, Ginkgo biloba, Ganoderma lucidum and Gynostemma pentaphyllum, are collected and reviewed. In particular, the employment of these four plants in the context of CVDs, such as myocardial infarction, hypertension, peripheral vascular diseases, coronary diseases, cardiomyopathies and dyslipemias We also strive to document recent studies aimed at dissecting the cellular and molecular cardioprotective mechanisms of the four plants, using recently reported in vitro and in vivo studies. Finally, we reviewed and reported the results of recent clinical trials that have been conducted with these four medicinal herbs with special emphasis on their efficacy, safety, and toxicity.
Does Paroxysmal Atrial Tachycardia Terminate While Taking Hawthorn Berries Supplement?
Cardiovascular diseases (CVD) are diseases of the heart or blood vessels. CVD accounts for a global annual toll of more than 17 million deaths. As a result, CVD remains the most common cause of death worldwide and is a significant health and economic burden worldwide. The World Health Organization (WHO) reported that CVD accounts for 31% of annual global deaths (World Health Organization, 2017). In Europe, CVDs account for 45% of all deaths according to the European Cardiovascular Disease Statistics 2017 (Martinet et al., 2019). Current statistics from the American Heart Association estimate that about half of the US population has some form of CVD (Benjamin et al., 2019).
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CVDs are a variety of diseases such as peripheral vascular disease, coronary heart disease (CHD), heart failure, heart attack (myocardial infarction), stroke, cardiomyopathies, dyslipidemias and hypertension, among others (Figure 1) (Toth, 2007; Reiner et al. al., 2019). CVD mainly originates from vascular dysfunction, which then causes organ damage. For example, the heart can suffer a heart attack, or the brain can suffer a stroke due to vascular insufficiency. The main culprits of vascular deterioration include atherosclerosis, thrombosis and high blood pressure (BP). Common risk factors for CVD include smoking, an unhealthy diet, diabetes mellitus, hyperlipidemia, elevated levels of low-density lipoprotein (LDL) cholesterol, suppressed levels of high-density lipoprotein (HDL) cholesterol, and hypertension (Figure 1) (World Health Organization). , 2017).
Figure 1 Pathological processes involved in the development and progression of CVD. Several risk factors can predispose to CVD. These may include hypertension, smoking, dyslipidemias resulting from an unhealthy diet, or endocrinopathies such as diabetes mellitus, hypothyroidism, and aging. Risk factors can lead to pathological alterations, most of which may be due to endothelial dysfunction or VSMC alterations. Endothelial dysfunction or VSMC alterations increase the risk of developing atherosclerosis and hypertension. Atherosclerosis and hypertension are themselves risk factors for CVD and enhancers for the development of other CVDs such as myocardial infarction, coronary artery disease or stroke. VSMC, vascular smooth muscle cell; ECM, extracellular matrix; NO, nitric oxide; eNOS, endothelial nitric oxide synthase; iNOS, inducible nitric oxide synthase; Ox-LDL, oxidized low-density lipoprotein.
CVD prevention is favored by a healthy vascular endothelium. A healthy endothelium has vasodilatory, anti-atherogenic and anti-inflammatory properties (Celermajer, 1997). Several CVD risk factors lead to endothelial cell (EC) dysfunction, which has been implicated as a key event in the pathogenesis of atherosclerosis, coronary vasoconstriction, and probably myocardial ischemia. Interestingly, EC dysfunction is a reversible phenomenon, opening the door to CVD therapies based on its reversal (Figure 1) (Celermajer, 1997).
Recently, inflammation has been confirmed as a risk factor for cardiovascular disease, especially during atherosclerosis and coronary artery disease. Elevated levels of high-sensitivity C-reactive protein (hs-CRP) and/or interleukin-6 (IL-6) are associated with higher absolute cardiovascular risk (Ridker et al., 1997; Ridker et al., 2000), where the CANTOS study, for the first time, established reduced rates of cardiovascular events after anti-interleukin-1 beta (IL-1β)-based therapy, independent of cholesterol levels (Ridker et al. , 2017). In addition, common CVD risk factors, such as diabetes or hypertension, may predispose to CVD through inflammation mediation (Dokken, 2008; Aday and Ridker, 2018).
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In the case of atherosclerosis, for example, inflammation can lead to functional impairment of EC. Dysfunctional ECs allow the accumulation of low-density lipoprotein (LDL) particles in the intimal wall of the vessel where they are modified into oxidized LDL. Oxidized LDL can activate dysfunctional ECs to expose cell adhesion molecules (VCAM-1 and ICAM-1) that bind and recruit inflammatory leukocytes (T cells and monocytes) to the subendothelial space (Davies et al ., 1993; Moore and Tabas, 2011). These inflammatory blood cells secrete interleukins and cytokines, produce reactive oxygen species (ROS) and thus form an inflamed microenvironment within the arterial wall. The inflamed microenvironment promotes vascular smooth muscle cell (VSMC) proliferation, matrix accumulation, and lipid deposition, leading to the formation of an atherosclerotic plaque. Monocytes can reach the vessel intima, differentiate into macrophages, and take up oxidized LDL to become foam cells (Tabas et al., 2007; Moore and Tabas, 2011; Douglas and Channon, 2014 ; Saleh Al-Shehabi et al., 2016; Martinet et al., 2019). Gradual thickening of the intima occurs over the years and continues to expand causing total or reduced occlusion of blood flow to organs, ultimately leading to CVD, such as myocardial infarction or stroke (Maguire et al., 2019 ). In addition, VSMC proliferation leads to narrowing of the arterial lumen and dysregulation of vasotone (Douglas and Channon, 2014). In general, multiple atherosclerotic plaques form in the intima and one of them may eventually undergo necrotic rupture, leading to acute luminal thrombosis, blood vessel occlusion, and cardiovascular complications, including myocardial infarction, unstable angina (chest pain caused by ischemia of the heart muscle). sudden cardiac death or stroke (Virmani et al., 2002). As a result, atherosclerosis is not only a risk factor, but also a major contributor to the incidence of CVD. About 50% of all deaths in developed countries are due to atherosclerosis (Tedgui and Mallat, 2006).
Hypertension, also called high BP, is a major risk factor for CVD and contributes to other CVD and other diseases (2017). Hypertension is an independent predisposing factor for heart failure, coronary artery disease, stroke, retinopathy, nephropathy, and peripheral arterial disease (Sawicka et al., 2011; NCD Risk Factor Collaboration, 2017) . Most of these diseases are associated with high mortality and morbidity (Abegaz et al., 2017). Furthermore, hypertension is the most significant risk factor for atherosclerosis and any clinical outcome of atherosclerosis (Sawicka et al., 2011). Hypertension is a “silent killer” as it does not show symptoms until later stages of the disease (Sawicka et al., 2011). Therefore, it is not surprising that hypertension affects 1.4 billion people and accounts for about 9.4 million deaths per year (Cooper et al., 2017; Egan et al., 2019). Finally, the prevalence of hypertension is estimated to increase by 30% worldwide by 2025 (Kearney et al., 2005).
The American Heart Association hypertension guidelines define hypertension as a persistently elevated BP in the arteries [systolic BP (SBP) greater than 130/diastolic BP (DBP) greater than 80 mm Hg] (Muntner et al. , 2018). If high BP is not controlled, it can induce arterial remodeling; the walls of the small vessels thicken, and the vessels lose their elasticity and become narrower. This process is called arteriosclerosis and can lead to “target organ damage” (TOD) (Triantafyllidi et al., 2010; Fan et al., 2017). TOD affects several organs such as the brain, kidney or retina and can lead to death (Mensah, 2016; Abegaz et al., 2017). Arteriosclerosis can be seen in coronary vessels where it can lead to myocardial infarction (Rakugi et al., 1996). In the brain, arteriosclerosis can lead to narrowing of the vessel lumen, hardening of the vessel wall, and the formation of blood clots, which can cause a stroke (Johansson, 1999). Strokes have effects on cognitive and physical behaviors, and can lead to dementia, paralysis or death (Abegaz et al., 2017). Nephrosclerosis of the kidney is also due to arteriosclerosis that hardens the nephron, ultimately affecting renal filtration and causing electrolyte imbalances (Bidani and Griffin, 2004; Lim et al., 2016). In general, EVERYTHING