Blood Fat; Blood Lipids (or blood fats) are lipids in the blood, either free or bound to other molecules. They are mostly transported in a protein capsule, and the density of the lipids and type of protein determines the fate of the particle and its influence on metabolism. The concentration of blood lipids depends on intake and excretion from the intestine, and uptake and secretion from cells. Blood lipids are mainly fatty acids and cholesterol. Hyperlipidemia is the presence of elevated or abnormal levels of lipids and /or lipoproteins in the blood, and is a major risk factor for cardiovascular disease.
Blood Viscosity; Blood viscosity is the thickness and stickiness of blood. It is a direct measure of the ability of blood to flow through the vessels. It is also a key screening test that measures how much friction the blood causes against the vessels, how hard the heart has to work to pump blood, and how much oxygen is delivered to organs and tissues. Importantly, high blood viscosity is easily modifiable with safe lifestyle-based interventions.
Brain Tissue Blood Supply Status; Brain Blood Supply; Blood transports oxygen and other nutrients necessary for the health of neurons, so a constant flow of blood to the brain must be maintained. According to Love and Webb, 1992, the brain uses approximately twenty percent of the body’s blood and needs twenty-five percent of the body’s oxygen supply to function optimally. Blood flow in a healthy person is 54 milliliters per 1000 grams of brain weight per minute. There are 740 milliliters of blood circulating in the brain every minute. 3.3 milliliters of oxygen are used per minute by every 1000 grams of brain tissue. This means that approximately 46 milliliters of oxygen are used by the entire brain in one minute. During sleep, blood flow to the brain is increased, but the rate of oxygen consumption remains the same.
Cerebral Blood Vessel Elasticity; Cerebral Blood Vessel Elasticity; Like a steel cylindrical pipe, an artery is comprised of an inner space (the “lumen”, filled with blood) enclosed by a wall. The wall is made up of a number of layers, two of which are muscle tissue and elastic tissue. When a region of the blood vessel wall weakens, it can balloon out to form a sac-like structure. This structure is called an aneurysm (a word derived from the Greek, aneurysma – widening), and the major problem associated with aneurysms is that they can rupture, an event, which may be fatal.
Cerebral Blood Vessel Resistance;
Cerebrovascular Blood Oxygen Pressure (PaO2); In the alveoli, the partial pressure of oxygen is around 100 mm Hg and that of carbon dioxide is around 40 mm Hg. In the cells of the body, the PaO2 is closer to 40. The range of normal for Pa02 is 75 – 100 mm Hg. If your Pa02 is less than this, it means you are not getting enough oxygen. It is the differences in partial pressure between the capillaries and alveoli that drive oxygen from the alveoli into the capillaries in the lungs, and it is the difference between partial pressures of oxygen in the blood and that in the cells that drives the flow of oxygen from the tissue capillaries into cells. PaO2 is a measure of all the oxygen in the blood – both that which is attached to hemoglobin, and that which is dissolved in the plasma. The majority of oxygen is carried in the blood attached to hemoglobin and only around 1.5% is dissolved in plasma. A low-level of oxygen in the blood is referred to as hypoxemia. When hypoxemia results in a low level of oxygen in tissues it is then referred to as hypoxia. Tissue hypoxia results in tissue damage, and if not corrected, eventually cell death.
Cerebrovascular Blood Oxygen Saturation (Sa); SaO2 is a measure of how much hemoglobin is occupied by oxygen.
Cerebrovascular Blood Oxygen Volume (CaCO2); Measuring oxygen levels in three different systems of Caco-2 cell culture.
Cholesterol Crystal; Cholesterol Crystals, as cholesterol builds up along the wall of an artery, it crystallizes from a liquid to a solid state and then expands. When the cholesterol crystallizes, two things can happen. If it’s a big pool of cholesterol, it will expand, causing the “cap’ of the deposit to tear off in the arterial wall. Or the crystals, which are sharp needle-like structures, pole their way through the cap covering the cholesterol deposit. The crystals then work their way into the bloodstream. It is the presence of this material, as well as damage to an artery, that disrupts plaque and puts the body’s natural defense mechanism – clotting – into action, which can lead to dangerous, if not fatal clots. Cholesterol in moderation is healthy and necessary for life.
Coronary Artery Elasticity; Coronary Artery Elasticity is also referred to as arteriosclerosis, which is a group of diseases characterized by thickening and loss of elasticity of the arterial walls which progressively blocks the coronary arteries and their branches. Arteriosclerosis is the most common cause of cardiovascular disability and death. Other forms of arteriosclerosis include arteriolosclerosis and medialcalcific stenosis, both of which are uncommon in the coronary vasculature.
Coronary Artery Resistance; A conscious, chronically instrumented canine model was used to investigate resistance changes in the distribution of the circumflex coronary artery as the artery was constricted. Several discrete constrictions were studied at two different levels of flow: resting and peak flow reactive hyperaemia. The resistance of the bed downstream from the constriction was calculated by formulae which defined the coronary back pressure as either venous pressure (Pv) or the arterial pressure at which coronary flow ceased (Pc). When Pv was taken as the back pressure, the resistance of the coronary bed during reactive hyperaemia progressively increased as the upstream artery was constricted. When Pc was taken as the back pressure, calculated coronary resistance for reactive hyperaemia showed little change. It is not known if elastic recoil of coronary resistance vessels, consequent to low poststenotic pressure, could occur to the extent required to be the physical basis for the calculated increase in resistance when Pv is taken to be the back pressure. Use of Pc as the back pressure implies that the coronary circulation contains a segment having the hydraulic characteristics of a collapsible tube.
Coronary Perfusion Pressure; Coronary Perfusion Pressure; the heart is an aerobic organ that is dependent for its oxygen supply entirely on coronary perfusion. Under resting condition, the myocardium extracts the maximum amount of oxygen from the blood it receives. The O2 saturation of blood returning from the coronary sinus to the right atrium has the lowest saturation of any body organ (30%). Interruption of coronary blood flow will result in immediate ischemia. Coronary blood flow is directly dependent upon perfusion pressure and inversely proportional to the resistance of the coronary vessel. Coronary perfusion occurs in diastole hence diastolic pressure is more important than systolic pressure in determining coronary perfusion. Coronary vessels are divided into epicardial or conductance vessels (R1), pre capillary (R2) and microvascular vessels (R3). The epicardial vessels, the site most commonly affected by atherosclerosis, offer negligible resistance to coronary flow. Resistance to flow occurs in the pre capillary (R2), and microvascular (R3) vessels which are termed resistance vessels. The increase coronary blood flow in response to increase myocardial oxygen demand (MVO2) is achieved by the dilation of these resistance vessels. Three factors play a key role in modifying vascular tone; the accumulation of local metabolites, endothelial factors and neural tone. The accumulation of adenosine during ischemia is an example of local metabolic factors. The most important endothelial substance mediating vasodilation is nitric oxide (NO). Other important mediators are bradykinin, endothelium derived 2 hyperpolarizing factor, and prostacyclin. On the other hand, endothelin-1 (ET-1) is a well-known vasoconstricting substance. Angiotensin II and thromboxane A2 are other well-known endothelium derived constricting factors. Alpha-receptor adrenergic stimulation results in coronary vasoconstriction whereas beta 1 receptor stimulation leads to vasodilatation.
Galectin-3; This protein has been shown to be involved in the following biological processes: cell adhesion, cell activation and chemoattraction, cell growth and differentiation, cell cycle, and apoptosis. Given galectin-3’s broad biological functionality, it has been demonstrated to be involved in cancer, inflammation and fibrosis, heart disease, and stroke. have also shown that the expression of galectin-3 is implicated in a variety of processes associated with heart failure, including myofibroblast proliferation, fibrogenesis, tissue repair, inflammation, and ventricular remodeling. Galectin-3 associates with the primary cilium and modulates renal cyst growth in congenital polycystic kidney disease.
Total Peripheral Resistance(TPR); Resistance to blood flow through arterioles and capillaries. the total resistance to flow of blood in the systemic circuit; the quotient produced by dividing the mean arterial pressure by the cardiac minute-volume.
Left Ventricular Effective Pump Power;
Left Ventricular Ejection Impedance; reflects the indicators of resistance status of the left ventricular outflow channel.
Influence Factors: (1) The fact whether the outflow channel has lesion. The aortic stenosis and other conditions can make VER increased. (2) The outflow channel has no lesion, while the emptying rate of aortic blood is slow, so VER is increased. (3) The entire vascular resistance is large.
Myocardial Blood Demand; The heart normally receives 4% of cardiac output, or ~ 250 mL/min of blood. Fatty acids and lactate are the predominant sources of energy, although glucose can be utilized. The myocardium cannot compensate for underperfusion by increasing oxygen extraction significantly (maximal ER is 90%), and thus the only compensatory mechanisms available are to increase blood flow by either changing regional vascular resistance or perfusion pressure. There are two settings in which myocardial supply and demand can be mismatched – profoundly low perfusion pressures, and irreversible stenosis. In the latter setting, vasodilation of non-critically stenoses vessels can shunt blood away from fixed-diameter vessels, leading to a decrease in coronary blood flow to a susceptible region, a phenomena know as “coronary steal.”
Myocardial Blood Perfusion Volume; Myocardial Blood Perfusion is the damage to the heart and the risk of future heart damage.
Myocardial Oxygen Consumption; Myocardial Oxygen Balance is determined by the ratio of oxygen supply to oxygen demand. Increasing oxygen supply by increasing either arterial oxygen content or coronary blood flow leads to an increase in tissue oxygen levels (usually measured as the partial pressure of oxygen, pO2). Increasing oxygen demand alone (i.e. myocardial oxygen consumption) decreases tissue oxygen levels. Normally, when oxygen demand increases there is a proportionate increase in coronary blood flow and oxygen supply so that tissue oxygen levels are maintained during times of increased oxygen demand. This increase in blood flow is performed by local regulatory mechanisms. This tight coupling between oxygen demand and coronary blood flow is impaired in coronary artery disease because oxygen supply is limited by vascular stenosis.
NT-proBNP; BNP and NT-proBNP are substances that are produced in the heart and released when the heart is stretched and working hard to pump blood. Heart failure can be confused with other conditions, and it may co-exist with them. BNP and NT-proBNP levels can help doctors differentiate between heart failure and other problems, such as lung disease. An accurate diagnosis is important because the treatments are often different and must be started as soon as possible. Higher-than-normal results suggest that a person has some degree of heart failure, and the level of BNP or NT-proBNP in the blood is related to its severity. Although BNP and NT-proBNP are usually used to recognize heart failure, an increased level in people with acute coronary syndrome (ACS) indicates an increased risk of recurrent events.
Pulse Wave Velocity Coefficient Arterial stiffness can be assessed noninvasively with the use of pulse wave velocity (PWV) measurement, that is, the velocity of the pulse wave to travel a given distance between 2 sites of the arterial system. Aortic PWV determined from a single measurement is strongly associated with the presence and extent of atherosclerosis and that this measurement is highly related to cardiovascular risk as assessed by the standard Framingham equations.
Stroke index; A cardiodynamic measure. Stroke volume is the amount of blood the left ventricle ejects in one beat, measured in milliliters per beat (ml/beat). The stroke volume can be indexed to a patient’s body size by dividing by the body surface area to yield the stroke index.
Stroke Volume (SV) also Cardiac Stroke Volume is the amount of blood pumped by the left ventricle of the heart in one contraction. The stroke volume is not all of the blood contained in the left ventricle. The heart does not pump all the blood out of the ventricle. Normally, only about two-thirds of the blood in the ventricle is put out with each beat. What blood is actually pumped from the left ventricle is the stroke volume and it, together with the heart rate, determines the cardiac output, the output of blood by the heart per minute. Stroke volume is an important determinant of cardiac output, which is the product of stroke volume and heart rate. Because stroke volume decreases in certain conditions and disease states, stroke volume itself correlates with cardiac function. Assessment of the cardiac output is important in determining the work that the heart is actually performing with respect to the rest of the cardiovascular system.
Vascular Elasticity; To understand Blood Vessel Elasticity, we first need to understand the anatomy of the vessels. There are three types of vessels – arteries, veins, and capillaries. Arteries, veins, and capillaries are not anatomically the same. They are not just tubes through which blood flows. Both arteries and veins have layers of smooth muscle surrounding them. Arteries have a much thicker layer, and many more elastic fibers as well. The largest artery, the aorta leaving the heart, also has cardiac muscle fibers in its walls for the first few inches of its length immediately leaving the heart. Arteries have to expand to accept the blood being forced into them from the heart, and then squeeze this blood into the veins when the heart relaxes. Arteries have the property of elasticity, meaning that they can expand to accept a volume of blood, then contract and squeeze back to their original size after the pressure is released. A good way to think of them is like a balloon. When you blow into the balloon, it inflates to hold the air. When you release the opening, the balloon squeezes the air back out. It is the elasticity of the arteries that maintains the pressure on the blood when the heart relaxes, and keeps it flowing forward. If the arteries did not have this property, your blood pressure would be more like 120/0, instead of 120/80 that is more normal. Arteries branch into arterioles as they get smaller. Arterioles eventually become capillaries, which are very thin and branching.
Vascular Resistance; Total Peripheral Resistance (TPR) is the sum of the resistance of all peripheral vasculature in the systemic circulation. This should not be confused with Pulmonary Vascular Resistance, which is the resistance in the pulmonary circulation. Vascular resistance is a term used to define the resistance to flow that must be overcome to push blood through the circulatory system. The resistance offered by the peripheral circulation is known as the systemic vascular resistance (SVR), while the resistance offered by the vasculature of the lungs is known as the pulmonary vascular resistance (PVR). The systemic vascular resistance may also be referred to as the total peripheral resistance. Vasoconstriction (i.e., decrease in blood vessel diameter) increases SVR, whereas vasodilation (increase in diameter) decreases SVR.