Clinical biochemistry of cardiovascular

Clinical biochemistry of cardiovascular, definition, mechamism, biological function, type of cardiovascular disease, blood vessels, Intermediatedensity lipoprotein (IDL) and LDL, Cardiovascular disease, Atherosclerosis, Congenital heart disease, Heart failure, Heart failure, The therapy of heart illness is determined by the source and type of heart injury. Healthy lifestyle behaviors, such as eating a lowfat, lowsalt diet, obtaining regular exercise and adequate sleep, and not smoking, are critical components of treatment. Medications: If lifestyle changes alone are ineffective in controlling heart disease symptoms and preventing complications, medicines may be required. The drug utilized is determined by the type of heart disease. Surgery or other medical treatments: Some persons suffering from heart disease may require a treatment or surgery. The sort of operation or surgery will be determined by the type of heart disease and the extent of heart damage.

CLINICAL OF BIOCHEMISTRY Assignment: CARDIOVASCULAR DISEASE Student’s name : Dang Quynh Nhu Student’s ID : BTBCIU19059 Instructor : Dr Hoang Le Son I INTRODUCTION The cardiovascular system, also known as the circulatory system, is made up of the heart and blood vessels (arteries, arterioles, capillaries, venules and veins) When it works properly, blood circulation maintains tissue perfusion, supplying substrates for cellular metabolism and removing excretory products It also allows hormones to be transferred from their origin organs to their target tissues, protects against infection by facilitating the flow of white cells and cytokines, and supports haemostasis by delivering platelets and clotting factors to injured tissue, among other critical activities The human circulatory system is an organ system that distributes blood to and from every region of the body via vessels, giving nutrients and oxygen while removing waste products such as carbon dioxide The blood is pumped through a closed tubular system by a muscular heart The pulmonary and systemic circuits are made up of arterial, capillary, and venous components The self-activating characteristic of specific cardiac cells, which ordinarily generate an orderly contraction of the heart chambers, is critical in this function Smooth muscle cells in blood arteries are regulated by a number of signal molecules and play a vital role in blood pressure regulation and oxygen/nutrient distribution Diseases of these blood vessels, particularly hypertension and atherosclerosis, are responsible for much of the illness and death in the developed world Heart The average adult human heart is around 13 by by cm (5 by 3.5 by 2.5 inches), weighs approximately 10.5 ounces, and is somewhat larger than a clenched fist (300 grams) It has a conelike shape, with the wide base pointing upward and right and the tip pointing downward and left It is located above the diaphragm in the thoracic cavity of the chest, behind the sternum of the breastbone, in front of the esophagus, descending aorta, trachea, and lungs (the muscular partition between the chest and abdominal cavities) The heart is roughly two-thirds of the way to the left of the midline II CARDIAC MUSCLE STRUCTURE AND FUNCTION Cardiac muscle is distinct from skeletal and smooth muscle in various ways: More mitochondria enable for ongoing high-level adenosine triphosphate (ATP) generation, allowing for continued operation without tiredness Anaerobic respiration can give enough energy for contraction to persist during periods of low oxygen The primary energy source is lipids [fatty acids and triglycerides (60%)], followed by carbs (35%), amino acids, and ketone bodies (5%) Has fewer but larger T tubules and intercalated discs, which allow for the rapid and synchronized propagation of action potentials between adjacent cells, allowing for coordinated cardiac muscle contraction The electrical signal of the action potential is converted into mechanical work of contraction by the fast release and re-uptake of intracellular calcium reserves III BLOOD FLOW OF THE HUMAN HEART Anemic blood that has been evacuated from the body returns to the right atrium (upper right chamber) via the inferior and superior vena cava veins The tricuspid valve (lower right chamber) allows blood to enter the right ventricle Blood is pushed from the right ventricle out the major pulmonary artery via the pulmonary valve The blood is subsequently pumped into the lungs via the left and right pulmonary arteries Breathing causes the body to absorb oxygen while expelling carbon dioxide As a result, the blood now contains an abundance of oxygen The blood is returned to the heart via four pulmonary veins, where it enters the left atrium (upper left chamber) The mitral valve (lower left chamber) allows blood to enter the left ventricle Through the aortic valve, blood is pushed from the left ventricle into the "aorta," a major artery IV BLOOD VESSELS Blood vessels, which include arteries, veins, and capillaries, serve as a conduit for blood to be delivered to and from every tissue in the human body, delivering oxygen and nutrition while removing carbon dioxide and waste Arteries and veins are made up of three layers of cells and/or polysaccharide matrix, connective and elastic tissues, and smooth muscle cells, as well as their own system of blood vessels (vasa vasorum) and nerves that feed and regulate their structure and, thus, activity Capillaries, which are responsible for the actual transfer of molecules between the blood and the cells, are typically composed of a single layer of cells joined by connective tissue Vasoconstriction is generally caused by peptide hormones like vasopressin, angiotensin II, and endothelin, or by neurological transmitter molecules like epinephrine Epinephrine can also elicit vasodilatation and/or vasoconstriction via a2- and b2-receptors, respectively, and increased heart rate and contractile force via b1-receptors, all via the Gi or Gs, adenylyl cyclase/cAMP messenger system Vasodilation is caused by chemicals like nitric oxide (NO), which diffuses across the plasma membrane of blood vessel cells and binds to a soluble guanylate cyclase This enzyme generates cGMP, which activates protein kinase G, resulting in the dephosphorylation and inactivation of smooth muscle myosin molecules via MLCK inactivation Despite the fact that the average lifetime of NO in the body is only a few seconds, its pharmacological effects are seen in medications such as sublingual nitroglycerin for chest pain via decreased cardiac workload, treatment of neonatal patients with pulmonary hypertension in an intensive care setting, and even modern erectile disorder drugs (e.g., sildenafil/ Viagra), which prolong the lifetime of cGMP and, thus, vasodilation of vessels in the penis V Intermediate-density lipoprotein (IDL) and LDL Following multiple rounds of LPL action, apo C and apo E (not shown) are transported back to HDL from the diminishing VLDL This leads in the development of an IDL including apo B100 and some of the remaining apo E IDL, like HDL and chylomicron remnants, can be removed from the liver via the apo E receptor (genetic defects in the apo E ligand or its receptor elicit type III hyperlipidemia, in which IDL, chylomicron remnants, and HDL are elevated) LDL is formed using cholesteryl esters from either the liver (endogenous) or chylomicron leftovers after further hydrolysis of triacylglycerol in IDL by LPL and transfer of the remaining apo E to HDL (exogenous) VLDLs lose surface area as their triacylglycerols are digested, eventually reducing them to cholesteryl ester-enriched LDL LDL's principal role is to transport cholesterol to peripheral tissues LDL receptors, which are responsible for this absorption, are coupled with clathrin-coated pits on these cells' plasma membranes and identify apo B100 (Figure 16-8) LDL particles and receptors are then endocytosed into numerous tissues, including the liver The receptors and clathrin mostly recycle back to the plasma membrane Most of the LDL (70%) binds to receptors on liver hepatocytes The remainder of the LDL associates with receptors on peripheral cells Lipoprotein disorders in which LDL receptors, or their capacity to bind the apo B100 ligand, are defective, result in an increased level of cholesterol in LDL remaining in circulation, causing hypercholesterolemia and atherosclerosis HDL HDL, a discoidal particle generated in the liver and secreted into plasma, aids in this function by acting as a cholesterol scavenger and promoting the transfer of cholesterol from the periphery to the liver for conversion to bile acids and eventual elimination (Figure 16-8) This cholesterolremoving ability is what earns HDL the title of "good" cholesterol carrier Lecithin, cholesterol ester, lecithin cholesterol acyl transferase (LCAT), apo A1, apo C, and apo E are all found in mature HDL particles Cholesterol efflux regulatory protein (CERP), an ATP-binding protein transporter, facilitates the acquisition of cholesterol by circulating HDL from peripheral cells CERP is activated by apo A1 and flips unesterified cholesterol and lecithin to the cell membrane's outer layer CERP then distributes free cholesterol and lecithin to HDL as substrates for LCAT Apo A1 also activates LCAT in developing HDL and acts as a ligand for a cell surface receptor on peripheral cells LCAT catalysis produces cholesterol esters, which migrate to the core of nascent HDL for eventual transport back to the liver "Reverse cholesterol transport" refers to the complete process of LCAT extraction of cell cholesterol and incorporation into HDL for liver clearance Another important role of HDL is to act as a storage site for apo A1, apo C, and apo E Transfer of apo C is necessary for chylomicron and VLDL metabolism, whereas transfer of apo E is required for clearance of chylomicron remnants, IDLs, and HDLs As a result, HDL contributes to both external and endogenous lipid transport mechanisms VI CARDIOVASCULAR DISORDER Cardiovascular disease Cardiovascular disease (CVD) is defined as disease of the heart and blood vessels (usually always arteries) supplying any organ The heart (coronary artery disease), the brain (cerebrovascular disease), and the limbs are the most usually affected organs by arterial disease (peripheral arterial disease) Renovascular disease is a major contributor to chronic renal disease and hypertension Because atherosclerosis is by far the most common cause of cardiovascular disease in developed countries, the term 'cardiovascular disease' is commonly used and perceived to mean 'atherosclerotic disease,' the term 'coronary artery disease' or 'coronary heart disease' to mean atherosclerosis of the coronary arteries, and 'cerebrovascular disease' to mean atherosclerosis of the cerebral vasculature Coronary artery atherosclerosis causes a reduction in blood supply to the myocardium, often known as ischaemia When this reaches a critical point, the heart muscles die, resulting in a'myocardial infarction' (MI), which is frequently, but not always, accompanied by diagnostic abnormalities on the electrocardiogram (ECG) Atherosclerosis Chronic atherosclerosis leads to hardening of the plaque by calcium as well as thickening and stiffening (arteriosclerosis) of the affected arterial walls The exact mechanism of the formation of a plaque is still under investigation, but current opinion is that the initial step involves oxidation of LDL, probably by the enzymatic action of lipoproteinassociated phospholipase A2 These oxidized LDL particles are more readily taken up by macrophages that can invade endothelial cells in the wall of an artery that are themselves damaged by oxidation The injury initiates an immune response by macrophages, which bind to the area via the protein vascular cell adhesion molecule-1 and vainly attempt to remove the oxidized LDL molecules Platelets are also recruited to the site of injury and attempt to cover the area The accumulation of oxidized LDL and the monocytes/ macrophages attempting to ingest it is known as a fatty streak— continued inflammation and growth of the fatty streak leads to an atheroma of the arterial wall As the immune response continues the monocytes/ macrophages die, releasing inflammatory factors such as IL-1 and tumor necrosis factor-a More white blood cells, including T-lymphocytes and mast cells, are recruited with continued inflammation of the arterial wall The continued inflammation also impacts smooth muscle cells, both leading to increased numbers and movement toward the growing plaque, adding to its size and composition Congenital heart disease Congenital (present at birth) heart disease is caused by faulty cardiac development A septal defect is a hole in the septum, the wall that separates the left and right sides of the heart The hole could be in the interatrial septum or the interventricular septum These flaws allow blood to flow from one side of the heart to the other, reducing the heart's pumping function significantly When a blood channel termed the ductus arteriosus, which is present in the fetus, fails to close after birth, the condition is known as patent ductus arteriosus The ductus arteriosus connects the pulmonary trunk to the aorta It permits blood to bypass the lungs by traveling from the pulmonary trunk to the aorta Because the lungs not function before birth, this is natural If the ductus arteriosus fails to shut after birth, blood flows from the aorta to the pulmonary trunk in the opposite way As a result, blood flows through the lungs at a higher pressure, damaging them Furthermore, the amount of work required by the left ventricle to maintain normal systemic blood pressure rises Heart failure Heart failure (HF) is characterized by the inability of the heart to fill with (diastolic HF) or eject (systolic HF) blood, or both Congestive heart failure refers to pulmonary congestion produced by back pressure generated by the left ventricle's failure to move blood around the body Ischaemic heart disease is by far the most prevalent cause, however it can also be caused by any structural or functional cardiac pathology, such as valvular heart disease, hypertension, or viral cardiomyopathy Although chronic heart failure might be relatively asymptomatic, dyspnea is the most common symptom In its early phases Acute life-threatening pulmonary oedema may also occur as a medical emergency There is a wide range of severity Between these two extremes, symptomatic heart failure is a rather typical reason for emergency room visits Heart failure has an overall frequency of about 2%, but it is significantly greater in the elderly, affecting up to 15% of people over the age of 85 Its incidence is expected to rise as the population ages It affects men more than women at all ages The illness worsens over time, and people with heart failure have a lower life expectancy and a lower quality of life In the United Kingdom, more than 40% of patients die within 18 months of being diagnosed VII DIAGNOSTIC TESTS FOR CARDIOVASCULAR DESEASE Electrocardiogram (ECG or EKG) (ECG or EKG) An electrocardiogram (ECG) is a rapid and painless examination that records electrical signals in the heart It can detect whether the heart is beating too quickly or too slowly Holter recording A Holter monitor is a portable ECG device that is worn for a day or more to record the activity of the heart during daily activities This test can detect irregular heartbeats that a standard ECG cannot Echocardiogram This noninvasive scan creates detailed images of the heart in action using sound waves It depicts how blood flows through the heart and its valves An echocardiography can assist in determining whether a valve is constricted or leaking Stress testing or exercise tests These tests frequently entail walking on a treadmill or riding a stationary bike while having the heart rate monitored Exercise testing can indicate how the heart responds to physical activity and whether or not symptoms of heart disease arise during exercise If you are unable to exercise, you may be prescribed medication Catheterization of the heart This test can detect cardiac artery blockages A catheter is a long, thin, flexible tube that is placed into a blood artery, typically in the groin or wrist, and guided to the heart Dye is delivered to arteries in the heart via the catheter The dye makes the arteries more visible on X-ray images acquired during the exam CT scan of the heart (cardiac) You recline on a table within a doughnut-shaped machine for a heart CT scan Inside the machine, an X-ray tube spins around your body, collecting images of your heart and chest Magnetic resonance imaging (MRI) of the heart (cardiac) A cardiac MRI creates comprehensive images of the heart by using a magnetic field and computer-generated radio waves VIII TREATMENT The therapy of heart illness is determined by the source and type of heart injury Healthy lifestyle behaviors, such as eating a low-fat, low-salt diet, obtaining regular exercise and adequate sleep, and not smoking, are critical components of treatment Medications: If lifestyle changes alone are ineffective in controlling heart disease symptoms and preventing complications, medicines may be required The drug utilized is determined by the type of heart disease Surgery or other medical treatments: Some persons suffering from heart disease may require a treatment or surgery The sort of operation or surgery will be determined by the type of heart disease and the extent of heart damage IX LIFESTYLE AND HOME REMERDIES Heart complaint can be bettered — or indeed averted — by making certain life changes The following changes are recommended to ameliorate heart health Do not bomb Smoking is a major threat factor for heart complaint, especially atherosclerosis Quitting is the stylish way to reduce the threat of heart complaint and itscomplications However, talk to your provider, If you need help quitting Eat healthy foods Eat plenitude of fruits, vegetables and whole grains Limit sugar, swab and impregnated fats Control blood pressure unbridled high blood pressure increases the threat of serious health problems Get your blood pressure checked at least every two times if you are 18 andolder.However, you may need more-frequent checks, If you have threat factors for heart complaint or are over age 40 Ask your health care provider what blood pressure reading is stylish for you Get a cholesterol test Ask your provider for a birth cholesterol test when you are in your 20s and also at least every to times You may need to start testing earlier if high cholesterol is in your family You may need more-frequent checks if your test results are not in a desirable range or you have threat factors for heart complaint Managediabetes However, tight blood sugar control can help reduce the threat of heart complaint, If you have diabetes Exercise Physical exertion helps you achieve and maintain a healthy weight Regular exercise helps control diabetes, high cholesterol and high blood pressure all threat factors for heart complaint With your provider's OK, aim for 30 to 60 twinkles of physical exertion most days of the week Talk to your health care provider about the quantum and type of exercise that is stylish for you Maintain a healthy weight Being fat increases the threat of heart complaint Talk with your care provider to set realistic pretensions for body mass indicator( BMI) and weight Manage stress Find ways to help reduce emotional stress Getting further exercise, rehearsing awareness and connecting with others in support groups are some ways to reduce and managestress However, talk to your provider about strategies to help, If you have anxiety or depression Exercise good hygiene Regularly wash your hands and encounter and floss your teeth to keep yourself healthy Exercise good sleep habits Poor sleep may increase the threat of heart complaint and other habitual conditions Grown-ups should aim to get to hours of sleep daily kiddies frequently need further Go to bed and wake at the same time every day, including onweekends.However, talk to your provider about strategies that might help, If you have trouble sleeping X REFERENCES Oliver, M Francis , Jacob, Stanley W and Entman, Mark L (2020, February 13) human cardiovascular system Encyclopedia Britannica https://www.britannica.com/science/human-cardiovascular-system Diethrich, E Bronson , Godman, Michael James , Entman, Mark L , Prout, W.G , DeBakey, Michael E , Oliver, Michael Francis and Warren, James V (2022, July 7) cardiovascular disease Encyclopedia Britannica https://www.britannica.com/science/cardiovascular-disease Saba, A., & Oridupa, O (2012) Lipoproteins and Cardiovascular Diseases In S Frank, & G Kostner (Eds.), Lipoproteins - Role in Health and Diseases IntechOpen https://doi.org/10.5772/48132 Tests to Diagnose Heart Problems - Health Encyclopedia - University of Rochester Medical Center (2022) Retrieved 30 July 2022, from Https://www.urmc.rochester.edu/encyclopedia/content.aspx?contenttypeid=85&contentid= P00208 https://www.mayoclinic.org/diseases-conditions/heart-disease/diagnosis-treatment/drc20353124