Materiały źródłowe

• #1 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9405799/

  Cardiovascular diseases (CVDs) are disorders associated with the heart and circulatory system. Atherosclerosis is its major underlying cause. […] Mechanisms such as dysfunction of the endothelium and inflammation, which have been identified as critical pathways for development of coronary artery disease, have become easier to diagnose in recent years. […] Atherosclerosis is the main cause of cardiovascular-related death worldwide. […] CAD is caused primarily by plaque formation within the intima of the vessel wall, with plaque being defined as a fatty material growing inside intima along with a severe inflammation, especially if the inflammation is chronic. […] Endothelial dysfunction in modern cardiovascular medicine is described as changes in the production and availability of endothelial-derived NO, prostacyclin, and endothelin, as well as their impact on vascular reactivity.

• #2 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  Cardiovascular diseases (CVDs) are disorders associated with the heart and circulatory system. Atherosclerosis is its major underlying cause. CVDs are chronic and can remain hidden for a long time. Moreover, CVDs are the leading cause of global morbidity and mortality, thus creating a major public health concern. This review summarizes the available information on the pathophysiological implications of CVDs, focusing on coronary artery disease along with atherosclerosis as its major cause and arterial hypertension. We discuss the endothelium dysfunction, inflammatory factors, and oxidation associated with atherosclerosis. Mechanisms such as dysfunction of the endothelium and inflammation, which have been identified as critical pathways for development of coronary artery disease, have become easier to diagnose in recent years. Relatively recently, evidence has been found indicating that interactions of the molecular and cellular elements such as matrix metalloproteinases, elements of the immune system, and oxidative stress are involved in the pathophysiology of arterial hypertension. Many studies have revealed several important inflammatory and genetic risk factors associated with CVDs. However, further investigation is crucial to improve our knowledge of CVDs progression and, more importantly, accelerate basic research to improve our understanding of the mechanism of pathophysiology.

• #3 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  Atherosclerosis is the main cause of cardiovascular-related death worldwide. It is a thickening and hardening of the arterial wall, accompanies aging, and is related to major adverse impact on the cardiovascular system and various other diseases. Elevated plasma cholesterol level (>150 mg/dL) is a major cause of the development of atherosclerosis. […] CAD is a common heart condition in which we can observe the narrowing or blockage of major blood vessels—coronary arteries. CAD is caused primarily by plaque formation within the intima of the vessel wall, with plaque being defined as a fatty material growing inside intima along with a severe inflammation, especially if the inflammation is chronic. This in turn causes difficulties in supplying the cardiomyocytes with enough blood, oxygen, and nutrients. As a result, atherosclerotic plaque may erode or rupture, initially resulting in thrombosis and then a closure of the vessel, leading to myocardial infarction, stroke, limb ischemia, and death. The other factors causing this condition are a diseased endothelium, low-grade inflammation, and lipid accumulation.

• #4 Cardiovascular Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535419/

  Atherosclerosis is the pathogenic process in the arteries and the aorta that can potentially cause disease as a consequence of decreased or absent blood flow from stenosis of the blood vessels. […] It involves multiple factors dyslipidemia, immunologic phenomena, inflammation, and endothelial dysfunction. These factors are believed to trigger the formation of fatty streak, which is the hallmark in the development of the atherosclerotic plaque; a progressive process that may occur as early as in the childhood. […] This process comprises intimal thickening with subsequent accumulation of lipid-laden macrophages (foam cells) and extracellular matrix, followed by aggregation and proliferation of smooth muscle cells constituting the formation of the atheroma plaque. […] As this lesions continue to expand, apoptosis of the deep layers can occur, precipitating further macrophage recruitment that can become calcified and transition to atherosclerotic plaques. […] Other mechanisms like arterial remodeling and intra-plaque hemorrhage play an important role in the delay and accelerated the progression of atherosclerotic CVD but are beyond the purpose of this article.

• #5 Cardiovascular Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535419/

  Atherosclerosis is the pathogenic process in the arteries and the aorta that can potentially cause disease as a consequence of decreased or absent blood flow from stenosis of the blood vessels. […] It involves multiple factors dyslipidemia, immunologic phenomena, inflammation, and endothelial dysfunction. These factors are believed to trigger the formation of fatty streak, which is the hallmark in the development of the atherosclerotic plaque; a progressive process that may occur as early as in the childhood. […] This process comprises intimal thickening with subsequent accumulation of lipid-laden macrophages (foam cells) and extracellular matrix, followed by aggregation and proliferation of smooth muscle cells constituting the formation of the atheroma plaque. […] As this lesions continue to expand, apoptosis of the deep layers can occur, precipitating further macrophage recruitment that can become calcified and transition to atherosclerotic plaques. […] Other mechanisms like arterial remodeling and intra-plaque hemorrhage play an important role in the delay and accelerated the progression of atherosclerotic CVD but are beyond the purpose of this article.

• #6 Cardiovascular Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535419/

  Atherosclerosis is the pathogenic process in the arteries and the aorta that can potentially cause disease as a consequence of decreased or absent blood flow from stenosis of the blood vessels. […] It involves multiple factors dyslipidemia, immunologic phenomena, inflammation, and endothelial dysfunction. These factors are believed to trigger the formation of fatty streak, which is the hallmark in the development of the atherosclerotic plaque; a progressive process that may occur as early as in the childhood. […] This process comprises intimal thickening with subsequent accumulation of lipid-laden macrophages (foam cells) and extracellular matrix, followed by aggregation and proliferation of smooth muscle cells constituting the formation of the atheroma plaque. […] As this lesions continue to expand, apoptosis of the deep layers can occur, precipitating further macrophage recruitment that can become calcified and transition to atherosclerotic plaques. […] Other mechanisms like arterial remodeling and intra-plaque hemorrhage play an important role in the delay and accelerated the progression of atherosclerotic CVD but are beyond the purpose of this article.

• #7 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9405799/

  Atherosclerosis occurs in these regions as a result of differences in flow, which is present at sites of low shear stress, turbulence, and oscillating flow. […] Atherosclerosis is characterized by the retention of lipids and inflammatory cells such as macrophages, T lymphocytes, and mast cells in damaged arterial wall, the intima. […] The vascular endothelium is the layer of cells lying under the epithelium lining the inside of the vessel and the muscular layer, which is a boundary between the circulating blood and the vascular wall. […] Its dysfunction is considered to be the earliest marker of atherosclerosis and, in effect, CAD. […] The expression of the nicotinamide adenine dinucleotide phosphate oxidase in the vessel wall with the consequent overproduction of NO has been proposed as an initial step in the chronic dysregulation of normal NO production by eNOS, which is characteristic of the monomeric forms of eNOS. […] Taking this into account, the endothelial dysfunction is directly related to a decreased production and sensitivity of cells to NO. […] Inflammation, ROS, and BP elevation are significant in the pathophysiology of AH.

• #8 Cardiovascular Disease – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK535419/

  Atherosclerosis is the pathogenic process in the arteries and the aorta that can potentially cause disease as a consequence of decreased or absent blood flow from stenosis of the blood vessels. […] It involves multiple factors dyslipidemia, immunologic phenomena, inflammation, and endothelial dysfunction. These factors are believed to trigger the formation of fatty streak, which is the hallmark in the development of the atherosclerotic plaque; a progressive process that may occur as early as in the childhood. […] This process comprises intimal thickening with subsequent accumulation of lipid-laden macrophages (foam cells) and extracellular matrix, followed by aggregation and proliferation of smooth muscle cells constituting the formation of the atheroma plaque. […] As this lesions continue to expand, apoptosis of the deep layers can occur, precipitating further macrophage recruitment that can become calcified and transition to atherosclerotic plaques. […] Other mechanisms like arterial remodeling and intra-plaque hemorrhage play an important role in the delay and accelerated the progression of atherosclerotic CVD but are beyond the purpose of this article.

• #9 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  The vascular endothelium is the layer of cells lying under the epithelium lining the inside of the vessel and the muscular layer, which is a boundary between the circulating blood and the vascular wall. Its cells are specialized in maintaining vascular homeostasis, which is crucial for the proper functioning of organs, especially the heart. Through its role in signal transduction and as a source of many vasoactive substances, it is their key regulator. The vascular endothelium reacts to physical and chemical stimuli through the release of autocrine and paracrine vasoactive agents. Factors of endothelial origin regulate surface tension and cell adhesion, including platelet activation and leukocyte adhesion, smooth muscle cell proliferation, and vascular wall inflammation. The endothelium is considered to be a strong indicator of cardiovascular function and fitness. Its dysfunction is considered to be the earliest marker of atherosclerosis and, in effect, CAD.

• #10 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  The vascular endothelium is the layer of cells lying under the epithelium lining the inside of the vessel and the muscular layer, which is a boundary between the circulating blood and the vascular wall. Its cells are specialized in maintaining vascular homeostasis, which is crucial for the proper functioning of organs, especially the heart. Through its role in signal transduction and as a source of many vasoactive substances, it is their key regulator. The vascular endothelium reacts to physical and chemical stimuli through the release of autocrine and paracrine vasoactive agents. Factors of endothelial origin regulate surface tension and cell adhesion, including platelet activation and leukocyte adhesion, smooth muscle cell proliferation, and vascular wall inflammation. The endothelium is considered to be a strong indicator of cardiovascular function and fitness. Its dysfunction is considered to be the earliest marker of atherosclerosis and, in effect, CAD.

• #11 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  In our review, we focus on endothelial dysfunction as one of the first and most important causes of the processes leading to CAD and atherosclerosis. In the case of both diseases, these processes constitute a starting point for further research and implications in the course of the disease development. […] Endothelial dysfunction in modern cardiovascular medicine is described as changes in the production and availability of endothelial-derived NO, prostacyclin, and endothelin, as well as their impact on vascular reactivity. In this case, reactive oxygen species (ROS) such as H2O2 reach the regulatory molecules, which leads to the activation of the cells. […] The endothelial dysfunction is directly related to a decreased production and sensitivity of cells to NO. As a result, we have an effective disturbance in the functioning of the entire vessel and its homeostasis, which leads to an observation of prothrombotic and proinflammatory phenomena, along with lower susceptibility of the blood vessel wall.

• #12 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9405799/

  Atherosclerosis occurs in these regions as a result of differences in flow, which is present at sites of low shear stress, turbulence, and oscillating flow. […] Atherosclerosis is characterized by the retention of lipids and inflammatory cells such as macrophages, T lymphocytes, and mast cells in damaged arterial wall, the intima. […] The vascular endothelium is the layer of cells lying under the epithelium lining the inside of the vessel and the muscular layer, which is a boundary between the circulating blood and the vascular wall. […] Its dysfunction is considered to be the earliest marker of atherosclerosis and, in effect, CAD. […] The expression of the nicotinamide adenine dinucleotide phosphate oxidase in the vessel wall with the consequent overproduction of NO has been proposed as an initial step in the chronic dysregulation of normal NO production by eNOS, which is characteristic of the monomeric forms of eNOS. […] Taking this into account, the endothelial dysfunction is directly related to a decreased production and sensitivity of cells to NO. […] Inflammation, ROS, and BP elevation are significant in the pathophysiology of AH.

• #13 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  In our review, we focus on endothelial dysfunction as one of the first and most important causes of the processes leading to CAD and atherosclerosis. In the case of both diseases, these processes constitute a starting point for further research and implications in the course of the disease development. […] Endothelial dysfunction in modern cardiovascular medicine is described as changes in the production and availability of endothelial-derived NO, prostacyclin, and endothelin, as well as their impact on vascular reactivity. In this case, reactive oxygen species (ROS) such as H2O2 reach the regulatory molecules, which leads to the activation of the cells. […] The endothelial dysfunction is directly related to a decreased production and sensitivity of cells to NO. As a result, we have an effective disturbance in the functioning of the entire vessel and its homeostasis, which leads to an observation of prothrombotic and proinflammatory phenomena, along with lower susceptibility of the blood vessel wall.

• #14 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  The vascular endothelium is the layer of cells lying under the epithelium lining the inside of the vessel and the muscular layer, which is a boundary between the circulating blood and the vascular wall. Its cells are specialized in maintaining vascular homeostasis, which is crucial for the proper functioning of organs, especially the heart. Through its role in signal transduction and as a source of many vasoactive substances, it is their key regulator. The vascular endothelium reacts to physical and chemical stimuli through the release of autocrine and paracrine vasoactive agents. Factors of endothelial origin regulate surface tension and cell adhesion, including platelet activation and leukocyte adhesion, smooth muscle cell proliferation, and vascular wall inflammation. The endothelium is considered to be a strong indicator of cardiovascular function and fitness. Its dysfunction is considered to be the earliest marker of atherosclerosis and, in effect, CAD.

• #15 Pathophysiology of Cardiovascular Diseases: New Insights into Molecular Mechanisms of Atherosclerosis, Arterial Hypertension, and Coronary Artery Disease

  https://www.mdpi.com/2227-9059/10/8/1938

  Atherosclerosis is the main cause of cardiovascular-related death worldwide. It is a thickening and hardening of the arterial wall, accompanies aging, and is related to major adverse impact on the cardiovascular system and various other diseases. Elevated plasma cholesterol level (>150 mg/dL) is a major cause of the development of atherosclerosis. […] CAD is a common heart condition in which we can observe the narrowing or blockage of major blood vessels—coronary arteries. CAD is caused primarily by plaque formation within the intima of the vessel wall, with plaque being defined as a fatty material growing inside intima along with a severe inflammation, especially if the inflammation is chronic. This in turn causes difficulties in supplying the cardiomyocytes with enough blood, oxygen, and nutrients. As a result, atherosclerotic plaque may erode or rupture, initially resulting in thrombosis and then a closure of the vessel, leading to myocardial infarction, stroke, limb ischemia, and death. The other factors causing this condition are a diseased endothelium, low-grade inflammation, and lipid accumulation.

• #16 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  Coronary artery disease is due to coronary artery atherosclerosis: Subintimal deposition of atheromas in large and medium-sized coronary arteries. […] Vascular endothelial dysfunction can promote atherosclerosis and contribute to coronary artery spasm. Endothelial dysfunction is also recognized as a cause of angina in the absence of epicardial coronary artery stenosis or spasm. […] Coronary atherosclerosis is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing angina pectoris). The degree of stenosis required to cause ischemia varies with oxygen demand. […] Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.

• #17 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  Coronary artery disease is due to coronary artery atherosclerosis: Subintimal deposition of atheromas in large and medium-sized coronary arteries. […] Vascular endothelial dysfunction can promote atherosclerosis and contribute to coronary artery spasm. Endothelial dysfunction is also recognized as a cause of angina in the absence of epicardial coronary artery stenosis or spasm. […] Coronary atherosclerosis is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing angina pectoris). The degree of stenosis required to cause ischemia varies with oxygen demand. […] Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.

• #18 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  Coronary artery disease is due to coronary artery atherosclerosis: Subintimal deposition of atheromas in large and medium-sized coronary arteries. […] Vascular endothelial dysfunction can promote atherosclerosis and contribute to coronary artery spasm. Endothelial dysfunction is also recognized as a cause of angina in the absence of epicardial coronary artery stenosis or spasm. […] Coronary atherosclerosis is often irregularly distributed in different vessels but typically occurs at points of turbulence (eg, vessel bifurcations). As the atheromatous plaque grows, the arterial lumen progressively narrows, resulting in ischemia (often causing angina pectoris). The degree of stenosis required to cause ischemia varies with oxygen demand. […] Occasionally, an atheromatous plaque ruptures or splits. Reasons are unclear but probably relate to plaque morphology, plaque calcium content, and plaque softening due to an inflammatory process. Rupture exposes collagen and other thrombogenic material, which activate platelets and the coagulation cascade, resulting in an acute thrombus, which interrupts coronary blood flow and causes some degree of myocardial ischemia.

• #19 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  The consequences of acute ischemia, collectively referred to as acute coronary syndromes (ACS), depend on the location and degree of obstruction and range from unstable angina, nonST-segment elevation myocardial infarction (NSTEMI), to ST-segment elevation myocardial infarction (STEMI), which can result in transmural infarction, and other complications including malignant ventricular arrhythmias, conduction defects, heart failure, and sudden death. […] Coronary artery spasm is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow; symptomatic ischemia (vasospastic angina) may result. […] In arteries with atheroma, the atheroma causes endothelial dysfunction, possibly resulting in local hypercontractility. Proposed mechanisms include loss of sensitivity to intrinsic vasodilators (eg, acetylcholine) and increased production of vasoconstrictors (eg, angiotensin II, endothelin, leukotrienes, serotonin, thromboxane) in the area of the atheroma. […] Coronary artery dissection is a rare, non-traumatic tear in the coronary intima with creation of a false lumen. Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen sometimes causing coronary ischemia or infarction.

• #20 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  The consequences of acute ischemia, collectively referred to as acute coronary syndromes (ACS), depend on the location and degree of obstruction and range from unstable angina, nonST-segment elevation myocardial infarction (NSTEMI), to ST-segment elevation myocardial infarction (STEMI), which can result in transmural infarction, and other complications including malignant ventricular arrhythmias, conduction defects, heart failure, and sudden death. […] Coronary artery spasm is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow; symptomatic ischemia (vasospastic angina) may result. […] In arteries with atheroma, the atheroma causes endothelial dysfunction, possibly resulting in local hypercontractility. Proposed mechanisms include loss of sensitivity to intrinsic vasodilators (eg, acetylcholine) and increased production of vasoconstrictors (eg, angiotensin II, endothelin, leukotrienes, serotonin, thromboxane) in the area of the atheroma. […] Coronary artery dissection is a rare, non-traumatic tear in the coronary intima with creation of a false lumen. Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen sometimes causing coronary ischemia or infarction.

• #21 Overview of Coronary Artery Disease – Cardiovascular Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/cardiovascular-disorders/coronary-artery-disease/overview-of-coronary-artery-disease

  The consequences of acute ischemia, collectively referred to as acute coronary syndromes (ACS), depend on the location and degree of obstruction and range from unstable angina, nonST-segment elevation myocardial infarction (NSTEMI), to ST-segment elevation myocardial infarction (STEMI), which can result in transmural infarction, and other complications including malignant ventricular arrhythmias, conduction defects, heart failure, and sudden death. […] Coronary artery spasm is a transient, focal increase in vascular tone, markedly narrowing the lumen and reducing blood flow; symptomatic ischemia (vasospastic angina) may result. […] In arteries with atheroma, the atheroma causes endothelial dysfunction, possibly resulting in local hypercontractility. Proposed mechanisms include loss of sensitivity to intrinsic vasodilators (eg, acetylcholine) and increased production of vasoconstrictors (eg, angiotensin II, endothelin, leukotrienes, serotonin, thromboxane) in the area of the atheroma. […] Coronary artery dissection is a rare, non-traumatic tear in the coronary intima with creation of a false lumen. Blood flowing through the false lumen expands it, which restricts blood flow through the true lumen sometimes causing coronary ischemia or infarction.

• #22 The Role of Pro-Inflammatory Cytokines in the Pathogenesis of Cardiovascular Disease

  https://www.mdpi.com/1422-0067/25/2/1082

  With cardiovascular disease (CVD) being a primary source of global morbidity and mortality, it is crucial that we understand the molecular pathophysiological mechanisms at play. Recently, numerous pro-inflammatory cytokines have been linked to several different CVDs, which are now often considered an adversely pro-inflammatory state. […] In this regard, pre-clinical and clinical evidence has clearly demonstrated the involvement and dynamic nature of pro-inflammatory cytokines in many heart conditions; however, the clinical utility of the findings so far remains unclear. […] Although there is a diverse array of heart disease etiologies, the involvement of aberrant inflammatory processes seems to be a common link between different types of CVDs. […] In view of the opposing effects of different cytokines in the pathogenesis as well as therapeutics of CVD, it is becoming evident that a balance of pro-inflammatory and anti-inflammatory cytokines is essential for maintaining cardiovascular health.

• #23 The Role of Pro-Inflammatory Cytokines in the Pathogenesis of Cardiovascular Disease

  https://www.mdpi.com/1422-0067/25/2/1082

  With cardiovascular disease (CVD) being a primary source of global morbidity and mortality, it is crucial that we understand the molecular pathophysiological mechanisms at play. Recently, numerous pro-inflammatory cytokines have been linked to several different CVDs, which are now often considered an adversely pro-inflammatory state. […] In this regard, pre-clinical and clinical evidence has clearly demonstrated the involvement and dynamic nature of pro-inflammatory cytokines in many heart conditions; however, the clinical utility of the findings so far remains unclear. […] Although there is a diverse array of heart disease etiologies, the involvement of aberrant inflammatory processes seems to be a common link between different types of CVDs. […] In view of the opposing effects of different cytokines in the pathogenesis as well as therapeutics of CVD, it is becoming evident that a balance of pro-inflammatory and anti-inflammatory cytokines is essential for maintaining cardiovascular health.

• #24 The Role of Pro-Inflammatory Cytokines in the Pathogenesis of Cardiovascular Disease

  https://www.mdpi.com/1422-0067/25/2/1082

  The participation of pro-inflammatory cytokines in the development of cardiac fibrosis and apoptosis, as well as their relationship with other pathogenic factors, such as oxidative stress and intracellular calcium overload, will be described. […] In the context of myocardial tissue, TNFα induces cell apoptosis in both myocytes and endothelial cells. […] Inhibition of TGF-β in mice with aortic constriction was found to result in less fibroblast activation and myocardial fibrosis without any change in cardiac hypertrophy. […] Overall, pro-inflammatory cytokines are considered to inhibit fibrotic remodeling of the heart. […] The result of several diseases and pathogenic mechanisms discussed so far culminate in heart failure, at which point the heart cannot meet the demands of the body.

• #25 The Role of Pro-Inflammatory Cytokines in the Pathogenesis of Cardiovascular Disease

  https://www.mdpi.com/1422-0067/25/2/1082

  The participation of pro-inflammatory cytokines in the development of cardiac fibrosis and apoptosis, as well as their relationship with other pathogenic factors, such as oxidative stress and intracellular calcium overload, will be described. […] In the context of myocardial tissue, TNFα induces cell apoptosis in both myocytes and endothelial cells. […] Inhibition of TGF-β in mice with aortic constriction was found to result in less fibroblast activation and myocardial fibrosis without any change in cardiac hypertrophy. […] Overall, pro-inflammatory cytokines are considered to inhibit fibrotic remodeling of the heart. […] The result of several diseases and pathogenic mechanisms discussed so far culminate in heart failure, at which point the heart cannot meet the demands of the body.

• #26 Azthena logo with the word Azthena

  https://www.news-medical.net/news/20250115/The-role-of-inflammation-in-the-pathogenesis-of-heart-failure.aspx

  Inflammation is a key player in the development of HF, and its role in the pathogenesis of HF has been extensively studied. […] Inflammation is associated with elevated HF risk and adverse prognosis. […] Targeting cardiac inflammation has been suggested as a promising treatment strategy for HF. […] The summary of inflammatory mechanisms contributing to the pathogenesis of different HF types, current anti-inflammation therapies for HF, and the results of clinical trials could provide new perspectives for understanding and targeting the role of inflammation in HF through the development of effective clinical therapeutic strategies.

• #27 CV Physiology | Pathophysiology of Heart Failure

  https://cvphysiology.com/heart-failure/hf003

  Cardiac dysfunction precipitates changes in vascular function, blood volume, and neurohumoral status. […] There is also evidence that other factors such as nitric oxide and endothelin (both of which are increased in heart failure) may play a role in the pathogenesis of heart failure. […] Therefore, it is essential to understand the pathophysiology of heart failure because it serves as the rationale for therapeutic intervention.

• #28 Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-022-01055-2

  Epigenetics is closely related to cardiovascular diseases. Genome-wide linkage and association analyses and candidate gene approaches illustrate the multigenic complexity of cardiovascular disease. Several epigenetic mechanisms, such as DNA methylation, histone modification, and noncoding RNA, which are of importance for cardiovascular disease development and regression. […] Recent studies have found that epigenetic modification plays an important role in the occurrence and development of cardiovascular diseases. Epigenetics mainly regulates cardiovascular disease-related genes function and expression level through DNA methylation, histone modification, and noncoding RNA regulation, thus affecting cardiovascular disease progression. […] Most importantly, it can be used as cardiovascular disease biomarkers for cardiovascular disease diagnosis, treatment response prediction and evaluation.

• #29 Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-022-01055-2

  Epigenetics is closely related to cardiovascular diseases. Genome-wide linkage and association analyses and candidate gene approaches illustrate the multigenic complexity of cardiovascular disease. Several epigenetic mechanisms, such as DNA methylation, histone modification, and noncoding RNA, which are of importance for cardiovascular disease development and regression. […] Recent studies have found that epigenetic modification plays an important role in the occurrence and development of cardiovascular diseases. Epigenetics mainly regulates cardiovascular disease-related genes function and expression level through DNA methylation, histone modification, and noncoding RNA regulation, thus affecting cardiovascular disease progression. […] Most importantly, it can be used as cardiovascular disease biomarkers for cardiovascular disease diagnosis, treatment response prediction and evaluation.

• #30 Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-022-01055-2

  Epigenetics is closely related to cardiovascular diseases. Genome-wide linkage and association analyses and candidate gene approaches illustrate the multigenic complexity of cardiovascular disease. Several epigenetic mechanisms, such as DNA methylation, histone modification, and noncoding RNA, which are of importance for cardiovascular disease development and regression. […] Recent studies have found that epigenetic modification plays an important role in the occurrence and development of cardiovascular diseases. Epigenetics mainly regulates cardiovascular disease-related genes function and expression level through DNA methylation, histone modification, and noncoding RNA regulation, thus affecting cardiovascular disease progression. […] Most importantly, it can be used as cardiovascular disease biomarkers for cardiovascular disease diagnosis, treatment response prediction and evaluation.

• #31 Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-022-01055-2

  Interestingly, because of the reversibility of epigenetic modifications, genes and proteins that control these changes have become new targets for cardiovascular disease treatment. […] The correlation of epigenetics with cardiovascular diseases has primarily been identified in the function and expression of epigenetic-related enzymes found in cardiovascular diseases. […] Several studies have shown that DNA methylation plays important roles in cardiovascular diseases. […] The abnormal methylation status of candidate genes is involved in the mechanism and development of cardiovascular disease and can be used as a marker to assess cardiovascular disease progression. […] Recently, the regulatory role of DNA methylation in cardiac hypertrophy and heart failure has attracted much attention.

• #32 Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-022-01055-2

  Therefore, regulating the abnormal DNA methylation process is of great significance for further understanding heart failure pathogenesis. […] These differentially expressed methylated genes in heart failure may be a new markers for the detection and diagnosis of heart failure. […] Histone modification is one of the important regulatory mechanisms in epigenetics. Abnormal histone modification results in an imbalance in the expression of genes associated with cardiovascular disease, resulting in changes in cellular phenotypes and cardiac function. […] Cardiovascular disease can also be regulated by histone methylation. […] The role of HAT and HDACs-mediated epigenetic processes in vascular homeostasis and cardiovascular disease has received extensive attention. […] In recent years, increasing evidence has accumulated for noncoding RNAs function in gene regulation and cardiovascular disease pathogenesis. Noncoding RNAs are attractive targets for potential clinical interventions.

• #33 Interplay of Reactive Oxygen Species (ROS) and Epigenetic Remodelling in Cardiovascular Diseases Pathogenesis: A Contemporary Perspective

  https://www.imrpress.com/journal/FBL/29/11/10.31083/j.fbl2911398

  Cardiovascular diseases (CVDs) continue to be the leading cause of mortality worldwide, necessitating the development of novel therapies. […] Despite therapeutic advancements, the underlying mechanisms remain elusive. Reactive oxygen species (ROS) show detrimental effects at high concentrations but act as essential signalling molecules at physiological levels, playing a critical role in the pathophysiology of CVD. […] However, the link between pathologically elevated ROS and CVDs pathogenesis remains poorly understood. Recent research has highlighted the remodelling of the epigenetic landscape as a crucial factor in CVD pathologies. […] Unravelling the intricate link between ROS and epigenetic changes in CVD is challenging due to the complexity of epigenetic signals in gene regulation.

• #34 Radiation-induced heart disease: a review of classification, mechanism and prevention

  https://www.ijbs.com/v15p2128.htm

  However, glutathione and other antioxidants are also consumed during their activity, and the cell’s ability to maintain redox balance is ultimately impaired. […] When the amount of endogenous and/or exogenous ROS exceeds the scavenging capacity of antioxidants, ROS begins to dominate and cause damage to cardiac myocytes. […] Cell apoptosis and necrosis occur in various types of cells in the heart after exposure to radiation, among which mitochondrial dysfunction and irreversible damage are the key links of cell apoptosis and necrosis, and the occurrence of mitochondrial dysfunction is closely related to endoplasmic reticulum (ER) stress. […] With the development of research, several studies have indicated that micro-RNAs (miRNAs) play an important role in the occurrence and progression of RIHD.

• #35 Radiation-induced heart disease: a review of classification, mechanism and prevention

  https://www.ijbs.com/v15p2128.htm

  However, glutathione and other antioxidants are also consumed during their activity, and the cell’s ability to maintain redox balance is ultimately impaired. […] When the amount of endogenous and/or exogenous ROS exceeds the scavenging capacity of antioxidants, ROS begins to dominate and cause damage to cardiac myocytes. […] Cell apoptosis and necrosis occur in various types of cells in the heart after exposure to radiation, among which mitochondrial dysfunction and irreversible damage are the key links of cell apoptosis and necrosis, and the occurrence of mitochondrial dysfunction is closely related to endoplasmic reticulum (ER) stress. […] With the development of research, several studies have indicated that micro-RNAs (miRNAs) play an important role in the occurrence and progression of RIHD.

• #36 Ferroptosis in cardiovascular diseases: role and mechanism | Cell & Bioscience | Full Text

  https://cellandbioscience.biomedcentral.com/articles/10.1186/s13578-023-01169-2

  In multicellular organisms, regulatory cell death is a crucial aspect of growth and development. Ferroptosis, which was postulated roughly ten years ago, is a mode of cell death that differs from apoptosis, autophagy, and pyrodeath. This distinct pattern of cell death is triggered by an imbalance between oxidants and antioxidants and strongly associated with the metabolism of iron, lipids, amino acids, and glutathione. A growing body of research has implicated ferroptosis in the incidence and progression of many organ traumas and degenerative diseases. […] Recently, ferroptosis has gained attention as a crucial regulatory mechanism underlying the initiation and development of a variety of cardiovascular diseases, including myocardial ischemia/reperfusion injury, cardiomyopathy, arrhythmia, chemotherapy, and Corona Virus-2-induced cardiac injury.

• #37 Ferroptosis in cardiovascular diseases: role and mechanism | Cell & Bioscience | Full Text

  https://cellandbioscience.biomedcentral.com/articles/10.1186/s13578-023-01169-2

  In multicellular organisms, regulatory cell death is a crucial aspect of growth and development. Ferroptosis, which was postulated roughly ten years ago, is a mode of cell death that differs from apoptosis, autophagy, and pyrodeath. This distinct pattern of cell death is triggered by an imbalance between oxidants and antioxidants and strongly associated with the metabolism of iron, lipids, amino acids, and glutathione. A growing body of research has implicated ferroptosis in the incidence and progression of many organ traumas and degenerative diseases. […] Recently, ferroptosis has gained attention as a crucial regulatory mechanism underlying the initiation and development of a variety of cardiovascular diseases, including myocardial ischemia/reperfusion injury, cardiomyopathy, arrhythmia, chemotherapy, and Corona Virus-2-induced cardiac injury.

• #38 Ferroptosis in cardiovascular diseases: role and mechanism | Cell & Bioscience | Full Text

  https://cellandbioscience.biomedcentral.com/articles/10.1186/s13578-023-01169-2

  Ferroptosis has a pro-inflammatory impact in macrophages and this process can be blocked by RAS-selective lethal 3. […] Ferroptosis occurs in the early stages of I/R injury and represents the dominant form of cell death during prolonged reperfusion. […] Therefore, ferroptosis plays an important role in I/R injury. […] In I/R, bone marrow stromal cell exo-culture demonstrated increased cell proliferation and GSH content and decreased iron concentration, ROS levels, and iron death marker protein levels. […] Thus, the above findings indicate that ferroptosis is a potential therapeutic target for myocardial I/R injury. […] Ferroptosis may contribute to the development of AF. […] Ferroptosis has been suggested as a possible therapeutic target for the treatment of COVID-19. […] In diabetic cardiomyopathy, non-coding RNA may be involved in disease progression by inducing ferroptosis. […] These findings suggest a potential strategy for treating and preventing diabetic cardiomyopathy by targeting lncRNA-ZFAS1. […] Puerarin can inhibit cardiac ferroptosis and protect cardiac function in HF mice with over-afterload.

• #39 Study reveals mechanism linking heart disease to cancer development | EurekAlert!

  https://www.eurekalert.org/news-releases/1040595

  Previous studies have shown that heart disease and cancer may be connected through shared risk factors, such as smoking, diabetes, and obesity. However, a newly released study has shed light on the potential connection between extracellular bubbles released after a heart attack and an increased risk of developing cancer. […] Researchers at Tel Aviv University (TAU) and the Leviev Cardiothoracic and Vascular Center at the Sheba Medical Center have found a mechanism which is responsible for increasing the risk of developing cancer among patients with heart disease: those small extracellular bubbles, or vesicles (sEVs), that are secreted from the sick heart to heal itself are released into the bloodstream and promote the growth of cancer cells throughout the body. […] Caller explains: In 2013, the Israeli cardiologist Tal Hasin showed for the first time that there is a connection between heart failure and cancer. Patients with heart disease are at a higher risk of developing cancer, and since heart disease is already a leading cause of deathfirst place in the US and second place in Israel that means that many people are at risk. Our research revealed that the diseased heart secrete a cancer-promoting factors, which we identified as small extracellular vesicles (sEVs).

• #40 Study reveals mechanism linking heart disease to cancer development | EurekAlert!

  https://www.eurekalert.org/news-releases/1040595

  Prof. Jonathan Leor: Many theories have been proposed to explain the increased risk of cancer in heart patients. They started with shared risk factors such as smoking, diabetes, and obesity and ended with a single protein or molecule. We showed for the first time that the diseased heart secretes sEVs that contain thousands of different growth factors. These bubbles directly promote the growth of certain tumors and also modulate the immune system, making the body more vulnerable to tumor growth. […] To test their hypothesis, the researchers at TAU inhibited the formation of sEVs in animal models with heart disease and found that the risk of cancer decreases along with the inhibition of vesicle production. […] Prof. Leor: When you systemically inhibit the formation of sEVs, you get less cancer but you cause collateral damage along the way.

• #41 Researchers discover mechanism linking stress to heart disease – Cardiovascular News

  https://cardiovascularnews.com/researchers-discover-mechanism-linking-stress-to-heart-disease/

  Heightened activity in the amygdala has been associated with a greater risk of heart disease and stroke, according to a study published in The Lancet that provides new insights into the possible mechanism by which stress can lead to cardiovascular disease in humans. […] The researchers also found that the heightened activity in the amygdala was linked to increased bone marrow activity and inflammation in the arteries, and suggest that this may cause the increased cardiovascular risk. The authors suggest a possible biological mechanism, whereby the amygdala signals to the bone marrow to produce extra white blood cells, which in turn act on the arteries causing them to develop plaques and become inflamed, which can cause heart attack and stroke. […] The researchers note that the activity seen in the amygdala may contribute to heart disease through additional mechanisms, since the extra white blood cell production and inflammation in the arteries do not account for the full link.

• #42 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  The common pathophysiologic state that perpetuates the progression of heart failure is extremely complex, regardless of the precipitating event. Compensatory mechanisms exist on every level of organization, from the subcellular all the way through to organ-to-organ interactions. Only when this network of adaptations becomes overwhelmed does heart failure ensue. […] Most important among the adaptations are the following: The Frank-Starling mechanism, in which an increased preload helps to sustain cardiac performance; alterations in myocyte regeneration and death; myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented; activation of neurohumoral systems. […] The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and regeneration. This process eventually leads to remodeling, usually the eccentric type. Eccentric remodeling further worsens the loading conditions on the remaining myocytes and perpetuates the deleterious cycle.

• #43 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  The common pathophysiologic state that perpetuates the progression of heart failure is extremely complex, regardless of the precipitating event. Compensatory mechanisms exist on every level of organization, from the subcellular all the way through to organ-to-organ interactions. Only when this network of adaptations becomes overwhelmed does heart failure ensue. […] Most important among the adaptations are the following: The Frank-Starling mechanism, in which an increased preload helps to sustain cardiac performance; alterations in myocyte regeneration and death; myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented; activation of neurohumoral systems. […] The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and regeneration. This process eventually leads to remodeling, usually the eccentric type. Eccentric remodeling further worsens the loading conditions on the remaining myocytes and perpetuates the deleterious cycle.

• #44 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  The common pathophysiologic state that perpetuates the progression of heart failure is extremely complex, regardless of the precipitating event. Compensatory mechanisms exist on every level of organization, from the subcellular all the way through to organ-to-organ interactions. Only when this network of adaptations becomes overwhelmed does heart failure ensue. […] Most important among the adaptations are the following: The Frank-Starling mechanism, in which an increased preload helps to sustain cardiac performance; alterations in myocyte regeneration and death; myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented; activation of neurohumoral systems. […] The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and regeneration. This process eventually leads to remodeling, usually the eccentric type. Eccentric remodeling further worsens the loading conditions on the remaining myocytes and perpetuates the deleterious cycle.

• #45 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of neuroendocrine systems, most notably the above-mentioned adrenergic systems and RAAS. […] The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which increases calcium afterload and, via an increase in cyclic adenosine monophosphate (cAMP), causes an increase in cytosolic calcium entry. […] The increased calcium entry into the myocytes augments myocardial contractility and impairs myocardial relaxation (lusitropy). […] The increase in afterload and myocardial contractility (known as inotropy) and the impairment in myocardial lusitropy lead to an increase in myocardial energy expenditure and a further decrease in cardiac output.

• #46 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of neuroendocrine systems, most notably the above-mentioned adrenergic systems and RAAS. […] The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which increases calcium afterload and, via an increase in cyclic adenosine monophosphate (cAMP), causes an increase in cytosolic calcium entry. […] The increased calcium entry into the myocytes augments myocardial contractility and impairs myocardial relaxation (lusitropy). […] The increase in afterload and myocardial contractility (known as inotropy) and the impairment in myocardial lusitropy lead to an increase in myocardial energy expenditure and a further decrease in cardiac output.

• #47 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  The increase in myocardial energy expenditure leads to myocardial cell death/apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a cycle of further increased neurohumoral stimulation and further adverse hemodynamic and myocardial responses. […] In addition, the activation of the RAAS leads to salt and water retention, resulting in increased preload and further increases in myocardial energy expenditure. […] The concept of the heart as a self-renewing organ is a relatively recent development. This paradigm for myocyte biology created an entire field of research aimed directly at augmenting myocardial regeneration. […] In heart failure, this mechanism for replacement becomes overwhelmed by an even faster increase in the rate of myocyte loss. This imbalance of hypertrophy and death over regeneration is the final common pathway at the cellular level for the progression of remodeling and heart failure.

• #48 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  The increase in myocardial energy expenditure leads to myocardial cell death/apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a cycle of further increased neurohumoral stimulation and further adverse hemodynamic and myocardial responses. […] In addition, the activation of the RAAS leads to salt and water retention, resulting in increased preload and further increases in myocardial energy expenditure. […] The concept of the heart as a self-renewing organ is a relatively recent development. This paradigm for myocyte biology created an entire field of research aimed directly at augmenting myocardial regeneration. […] In heart failure, this mechanism for replacement becomes overwhelmed by an even faster increase in the rate of myocyte loss. This imbalance of hypertrophy and death over regeneration is the final common pathway at the cellular level for the progression of remodeling and heart failure.

• #49 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  The increase in myocardial energy expenditure leads to myocardial cell death/apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a cycle of further increased neurohumoral stimulation and further adverse hemodynamic and myocardial responses. […] In addition, the activation of the RAAS leads to salt and water retention, resulting in increased preload and further increases in myocardial energy expenditure. […] The concept of the heart as a self-renewing organ is a relatively recent development. This paradigm for myocyte biology created an entire field of research aimed directly at augmenting myocardial regeneration. […] In heart failure, this mechanism for replacement becomes overwhelmed by an even faster increase in the rate of myocyte loss. This imbalance of hypertrophy and death over regeneration is the final common pathway at the cellular level for the progression of remodeling and heart failure.

• #50 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  Research indicates that local cardiac Ang II production (which decreases lusitropy, increases inotropy, and increases afterload) leads to increased myocardial energy expenditure. […] Ang II has also been shown in vitro and in vivo to increase the rate of myocyte apoptosis. In this fashion, Ang II has similar actions to norepinephrine in heart failure. […] Ang II also mediates myocardial cellular hypertrophy and may promote progressive loss of myocardial function. […] The neurohumoral factors above lead to myocyte hypertrophy and interstitial fibrosis, resulting in increased myocardial volume and increased myocardial mass, as well as myocyte loss. […] In the failing heart, increased myocardial volume is characterized by larger myocytes approaching the end of their life cycle. […] As more myocytes drop out, an increased load is placed on the remaining myocardium, and this unfavorable environment is transmitted to the progenitor cells responsible for replacing lost myocytes.

• #51 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  Research indicates that local cardiac Ang II production (which decreases lusitropy, increases inotropy, and increases afterload) leads to increased myocardial energy expenditure. […] Ang II has also been shown in vitro and in vivo to increase the rate of myocyte apoptosis. In this fashion, Ang II has similar actions to norepinephrine in heart failure. […] Ang II also mediates myocardial cellular hypertrophy and may promote progressive loss of myocardial function. […] The neurohumoral factors above lead to myocyte hypertrophy and interstitial fibrosis, resulting in increased myocardial volume and increased myocardial mass, as well as myocyte loss. […] In the failing heart, increased myocardial volume is characterized by larger myocytes approaching the end of their life cycle. […] As more myocytes drop out, an increased load is placed on the remaining myocardium, and this unfavorable environment is transmitted to the progenitor cells responsible for replacing lost myocytes.

• #52 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  These features, namely, the increased myocardial volume and mass, along with a net loss of myocytes, are the hallmark of myocardial remodeling. […] As heart failure advances, there is a relative decline in the counterregulatory effects of endogenous vasodilators, including nitric oxide (NO), prostaglandins (PGs), bradykinin (BK), atrial natriuretic peptide (ANP), and B-type natriuretic peptide (BNP). […] This decline occurs simultaneously with the increase in vasoconstrictor substances from the RAAS and the adrenergic system, which fosters further increases in vasoconstriction and thus preload and afterload. […] This results in cellular proliferation, adverse myocardial remodeling, and antinatriuresis, with total body fluid excess and worsening of heart failure symptoms. […] Systolic and diastolic heart failure each result in a decrease in stroke volume.

• #53 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  These features, namely, the increased myocardial volume and mass, along with a net loss of myocytes, are the hallmark of myocardial remodeling. […] As heart failure advances, there is a relative decline in the counterregulatory effects of endogenous vasodilators, including nitric oxide (NO), prostaglandins (PGs), bradykinin (BK), atrial natriuretic peptide (ANP), and B-type natriuretic peptide (BNP). […] This decline occurs simultaneously with the increase in vasoconstrictor substances from the RAAS and the adrenergic system, which fosters further increases in vasoconstriction and thus preload and afterload. […] This results in cellular proliferation, adverse myocardial remodeling, and antinatriuresis, with total body fluid excess and worsening of heart failure symptoms. […] Systolic and diastolic heart failure each result in a decrease in stroke volume.

• #54 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  Although there are commonalities in the neurohormonal responses to decreased stroke volume, the neurohormone-mediated events that follow have been most clearly elucidated for individuals with systolic heart failure. […] The ensuing elevation in plasma norepinephrine directly correlates with the degree of cardiac dysfunction and has significant prognostic implications. […] Norepinephrine, while directly toxic to cardiac myocytes, is also responsible for a variety of signal-transduction abnormalities, such as downregulation of beta1-adrenergic receptors, uncoupling of beta2-adrenergic receptors, and increased activity of inhibitory G-protein. […] Changes in beta1-adrenergic receptors result in overexpression and promote myocardial hypertrophy. […] ANP and BNP are endogenously generated peptides activated in response to atrial and ventricular volume/pressure expansion.

• #55 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  Although there are commonalities in the neurohormonal responses to decreased stroke volume, the neurohormone-mediated events that follow have been most clearly elucidated for individuals with systolic heart failure. […] The ensuing elevation in plasma norepinephrine directly correlates with the degree of cardiac dysfunction and has significant prognostic implications. […] Norepinephrine, while directly toxic to cardiac myocytes, is also responsible for a variety of signal-transduction abnormalities, such as downregulation of beta1-adrenergic receptors, uncoupling of beta2-adrenergic receptors, and increased activity of inhibitory G-protein. […] Changes in beta1-adrenergic receptors result in overexpression and promote myocardial hypertrophy. […] ANP and BNP are endogenously generated peptides activated in response to atrial and ventricular volume/pressure expansion.

• #56 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  ANP and BNP are released from the atria and ventricles, respectively, and both promote vasodilation and natriuresis. […] Their hemodynamic effects are mediated by decreases in ventricular filling pressures, owing to reductions in cardiac preload and afterload. […] BNP, in particular, produces selective afferent arteriolar vasodilation and inhibits sodium reabsorption in the proximal convoluted tubule. […] It also inhibits renin and aldosterone release and, therefore, adrenergic activation. […] ANP and BNP are elevated in chronic heart failure. […] Other vasoactive systems that play a role in the pathogenesis of heart failure include the ET receptor system, the adenosine receptor system, vasopressin, and tumor necrosis factor-alpha (TNF-alpha). […] Elevated levels of ET-1 closely correlate with the severity of heart failure.

• #57 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  ANP and BNP are released from the atria and ventricles, respectively, and both promote vasodilation and natriuresis. […] Their hemodynamic effects are mediated by decreases in ventricular filling pressures, owing to reductions in cardiac preload and afterload. […] BNP, in particular, produces selective afferent arteriolar vasodilation and inhibits sodium reabsorption in the proximal convoluted tubule. […] It also inhibits renin and aldosterone release and, therefore, adrenergic activation. […] ANP and BNP are elevated in chronic heart failure. […] Other vasoactive systems that play a role in the pathogenesis of heart failure include the ET receptor system, the adenosine receptor system, vasopressin, and tumor necrosis factor-alpha (TNF-alpha). […] Elevated levels of ET-1 closely correlate with the severity of heart failure.

• #58 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  ANP and BNP are released from the atria and ventricles, respectively, and both promote vasodilation and natriuresis. […] Their hemodynamic effects are mediated by decreases in ventricular filling pressures, owing to reductions in cardiac preload and afterload. […] BNP, in particular, produces selective afferent arteriolar vasodilation and inhibits sodium reabsorption in the proximal convoluted tubule. […] It also inhibits renin and aldosterone release and, therefore, adrenergic activation. […] ANP and BNP are elevated in chronic heart failure. […] Other vasoactive systems that play a role in the pathogenesis of heart failure include the ET receptor system, the adenosine receptor system, vasopressin, and tumor necrosis factor-alpha (TNF-alpha). […] Elevated levels of ET-1 closely correlate with the severity of heart failure.

• #59 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  TNF-alpha has been implicated in response to various infectious and inflammatory conditions. […] Elevations in TNF-alpha levels have been consistently observed in heart failure and seem to correlate with the degree of myocardial dysfunction. […] In individuals with systolic dysfunction, therefore, the neurohormonal responses to decreased stroke volume result in temporary improvement in systolic blood pressure and tissue perfusion. […] However, in all circumstances, the existing data support the notion that these neurohormonal responses contribute to the progression of myocardial dysfunction in the long term. […] In diastolic heart failure (heart failure with preserved ejection fraction [HFpEF]), the same pathophysiologic processes occur that lead to decreased cardiac output in systolic heart failure, but they do so in response to a different set of hemodynamic and circulatory environmental factors that depress cardiac output.

• #60 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  TNF-alpha has been implicated in response to various infectious and inflammatory conditions. […] Elevations in TNF-alpha levels have been consistently observed in heart failure and seem to correlate with the degree of myocardial dysfunction. […] In individuals with systolic dysfunction, therefore, the neurohormonal responses to decreased stroke volume result in temporary improvement in systolic blood pressure and tissue perfusion. […] However, in all circumstances, the existing data support the notion that these neurohormonal responses contribute to the progression of myocardial dysfunction in the long term. […] In diastolic heart failure (heart failure with preserved ejection fraction [HFpEF]), the same pathophysiologic processes occur that lead to decreased cardiac output in systolic heart failure, but they do so in response to a different set of hemodynamic and circulatory environmental factors that depress cardiac output.

• #61 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  TNF-alpha has been implicated in response to various infectious and inflammatory conditions. […] Elevations in TNF-alpha levels have been consistently observed in heart failure and seem to correlate with the degree of myocardial dysfunction. […] In individuals with systolic dysfunction, therefore, the neurohormonal responses to decreased stroke volume result in temporary improvement in systolic blood pressure and tissue perfusion. […] However, in all circumstances, the existing data support the notion that these neurohormonal responses contribute to the progression of myocardial dysfunction in the long term. […] In diastolic heart failure (heart failure with preserved ejection fraction [HFpEF]), the same pathophysiologic processes occur that lead to decreased cardiac output in systolic heart failure, but they do so in response to a different set of hemodynamic and circulatory environmental factors that depress cardiac output.

• #62 Heart Failure: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/163062-overview

  In HFpEF, altered relaxation and increased stiffness of the ventricle (due to delayed calcium uptake by the myocyte sarcoplasmic reticulum and delayed calcium efflux from the myocyte) occur in response to an increase in ventricular afterload (pressure overload). […] The impaired relaxation of the ventricle then leads to impaired diastolic filling of the left ventricle (LV).

• #63 COVID-19 and cardiovascular disease: from basic mechanisms to clinical perspectives | Nature Reviews Cardiology

  https://www.nature.com/articles/s41569-020-0413-9

  COVID-19 can cause cardiovascular disorders, including myocardial injury, arrhythmias, acute coronary syndrome and venous thromboembolism. […] The presence of underlying cardiovascular comorbidities in patients with COVID-19 is associated with high mortality. […] Understanding the biological features of the virus will contribute to the development of diagnostic tests, vaccines and pharmacological therapies and can further our knowledge of tissue tropism. […] The high burden of systemic inflammation associated with COVID-19 has been proposed to accelerate the development of subclinical disorders or cause de novo cardiovascular damage. […] Myocardial injury during the course of COVID-19 is independently associated with high mortality. […] COVID-19 can trigger acute coronary syndrome. […] The mechanisms underlying the development of COVID-19-related cardiovascular injury are not known. […] The interaction between the S protein and ACE2 is likely to have a central role in disease pathogenesis, especially in cardiovascular manifestations of this disease.

• #64 COVID-19 and cardiovascular disease: from basic mechanisms to clinical perspectives | Nature Reviews Cardiology

  https://www.nature.com/articles/s41569-020-0413-9

  COVID-19 can cause cardiovascular disorders, including myocardial injury, arrhythmias, acute coronary syndrome and venous thromboembolism. […] The presence of underlying cardiovascular comorbidities in patients with COVID-19 is associated with high mortality. […] Understanding the biological features of the virus will contribute to the development of diagnostic tests, vaccines and pharmacological therapies and can further our knowledge of tissue tropism. […] The high burden of systemic inflammation associated with COVID-19 has been proposed to accelerate the development of subclinical disorders or cause de novo cardiovascular damage. […] Myocardial injury during the course of COVID-19 is independently associated with high mortality. […] COVID-19 can trigger acute coronary syndrome. […] The mechanisms underlying the development of COVID-19-related cardiovascular injury are not known. […] The interaction between the S protein and ACE2 is likely to have a central role in disease pathogenesis, especially in cardiovascular manifestations of this disease.

• #65 Open Access Macedonian Journal of Medical Sciences (OAMJMS).

  https://oamjms.eu/index.php/mjms/article/view/8848

  BACKGROUND: Coronavirus disease 2019 (COVID-19) causes a hypercoagulable state with a high incidence of thrombotic complications. Patients with a history of myocardial revascularization have more severe complications due to COVID-19. Coronary stent thrombosis has become significantly more common during the COVID-19 pandemic. […] RESULTS: Coronavirus infection has contributed to the change in the course of myocardial infarction in patients undergoing myocardial revascularization. The incidence of stent thrombosis has a positive correlation with the severity of the coronavirus infection. The previous myocardial revascularization procedures significantly increase the risk of mortality in patients with coronavirus infection. This is especially actual for elderly patients. […] CONCLUSION: One of the most vulnerable groups is elderly patients who have undergone myocardial revascularization after myocardial infarction in the past and have concomitant diseases. An analysis of scientific publications has shown that further larger-scale clinical studies are needed to confirm the hypothesis about the negative impact of coronavirus infection on stent thrombosis in patients who have undergone COVID-19.

Zobacz więcej