Pathophysiology of Atherosclerosis-Types-Stages

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Hello friends, in todays post we are going to learn about What is the Pathophysiology of Atherosclerosis and exactly What is Pathophysiology? reffered to in detail.

Pathophysiology Meaning – What is Pathophysiology?

Pathophysiology is one of the most important branches of human physiology and its study represents an enormous advance in the world of medicine.

The study of physiology is closely related to the study of pathophysiology , which is the analysis of diseases that take place in living beings while they perform their vital functions. When studying the diseases of living beings, this branch also studies animals so it has direct application in the field of veterinary medicine.

This branch of medicine makes it possible to explain why diseases occur, how they occur and what their symptoms are. The pathophysiology describes the “history” of the disease and once it has reached the living being.

It is divided into three phases: initial, clinical and resolution.

Initial Phase: The initial phase includes the first changes that the body undergoes from the moment the disease begins until the first symptoms occur.

In this phase the patient does not undergo substantial changes since the disease develops without the subject noticing; Depending on the disease, this stage has different durations.

Clinical Phase: The clinical phase begins when the disease begins to show its characteristic symptoms. These symptoms can appear repeatedly, by episodes and even in severe attacks.

They can also be repeated for years: once the six-month barrier is exceeded, the disease will become chronic.

It is in this phase when the appropriate treatment for each ailment must be applied: remedy must be applied as soon as possible and the disease should not be prolonged any longer in order to ensure a full recovery without sequelae in the subject.

Resolution Phase: The resolution phase has several aspects: it can end the disease, it can become chronic or it can be terminal. Premature diagnosis and knowledge of the disease is key so that the subject does not die.

The pathophysiology is one of the branches of medicine most demanded today because medical research to end disease is a global necessity. One of the ailments on which more studies are being carried out today is Atherosclerosis.

Knowing the pathophysiology of this disease is key to knowing when it begins to develop and being able to achieve an early diagnosis that saves the subject from suffering from this disease.

The pathophysiology of Atherosclerosis, It has a multitude of studies to date thanks to which it has been possible to know that the disease can be detected up to twenty years before.

The investigation of this condition has numerous resources both public and private and is in the focus of most of the pharmaceutical companies that want to start distributing drugs to treat this disease.

The study of pathophysiology has great value in medicine and is one of the branches most in demand today because disease control is a global slogan .

Researchers in this area today play a crucial role since any progress they make can help save thousands of lives: there are still many diseases that are unknown and despite the fact that this science has advanced enormously in the last two centuries, it still has a long way to go. travel.

What is Atherosclerosis / Arteriosclerosis?

Atherosclerosis in general terms is a type of disorder that causes the arterial walls to lose its of elasticity and thicking them which blocks the artery and causes different cardiac attacks.

Atherosclerosis is the chronic disease which is caused by the deposition/accumulation of cholesterol, fats, calcium, and other materials in the innermost layer of large and medium size arteries.

Atherosclerosis is the leading cause of most deaths in united states and other developed countries.

First we will see Types of Sclerosis and What is meaning of Artherosclerosis,

  1. MONCKEBERG’S SCLEROSIS: Calcification of the middle layer of the muscular arteries.

2. ARTERIOLOSCLEROSIS: Proliferative and fibro-muscular or endothelial thickening of the walls of small-caliber arteries and arterioles.

3. ATHEROSCLEROSIS: From the Greek Atheros = dough or puree and from Sklleros = hard. Characterized by the focal formation of atheromas (lipid deposits), in the arterial tunica intima.

According to this classification, Atherosclerosis is part of Arteriosclerosis, because it produces hardening and loss of elasticity of the arteries, but has as its own characteristics, the focal formation of atheromas in the arterial intima.

The most pathophysiological definition of Atherosclerosis is the one made by Digirolamo scientist;

“Pathological alteration of the coronary arteries characterized by the abnormal deposit of lipids and fibrous tissue in the arterial wall , which disorganizes the architecture, the function of the vessels and reduces in a variable way, the blood flow to the myocardium.”

Indeed, Atherosclerosis is characterized by the presence of lipid deposits in the intimal layer of the arteries, whether of large, medium or small caliber, producing over time, the so-called atherosclerosing plaque that partially or totally obstructs the arterial lumen, leading to myocardial ischemia.

Heart muscle disease derived from myocardial ischemia, secondary to the coronary atherosclerosis process, has received different names over the years, such as: atherosclerotic heart disease, coronary heart disease, heart disease, ischemic disease, etc.

We believe that the most correct, because it includes all pathophysiological entities, is CORONARY ISCHEMIC ATEROSCLEROSA CARDIOPATHY. “

Atherosclerosis Vascular Calcification

Atherosclerosis is a focal pathological phenomenon that affects the great arteries, mainly the aorta and the coronary, carotid, iliac and femoral arteries.

The development of the vascular condition is characterized by an early onset called a fatty streak.or fatty streak.

Over the years this process, which is considered reversible, increases its lipid accumulation and in adolescence the first fibrous lesions appear.

In the following years, these plaques enlarge and modify, and in most cases all these processes are asymptomatic: the ulceration of the plaque, its rupture and thrombosis are what precipitate the clinical event.

Finally, there is currently a controversy regarding the classification, standardization and clinical correlation of plaques.

We hope that the concepts in this article provide the reader with the knowledge and objective definitions that allow a better understanding of the implication of risk factors, the development of arteriosclerosis and its clinical manifestations.

The objective of this article is to provide the knowledge and definitions and explain the different current classifications of human atherosclerosis lesions based on their composition, histology and structure.

The definition of normal intima, fatty streak ( fatty streak ), intermediate lesions and, finally, advanced lesions implies the definition of a succession of events with their histological characteristics and clinical manifestations

The development of atherosclerosis begins in childhood (fatty streak) and is considered a reversible process.

In adolescence, the lesions increase with lipid accumulation and the first fibrous plaques are formed. In the following years, the fibrous plaques enlarge, calcify, hemorrhage, ulcerate or rupture, and thrombosis. Thrombotic occlusion is the one that precipitates the clinical event.

The arteries undergo a natural process throughout life that is characterized by an increase in the thickness of the intimal area, loss of elasticity, increased calcium content and changes in its diameter; These changes occur in the main arterial system and are known by the generic name of Arteriosclerosis.

In contrast to this natural process, atherosclerosis is a focal pathological phenomenon that affects the great arteries, mainly the aorta and the coronary, carotid, iliac and femoral arteries.

In 1958, a study carried out by the WHO defined atherosclerosis as a variable combination of changes in the intima of the arteries consisting of a focal accumulation of lipids, complex carbohydrates, blood and blood products, fibrous tissue and calcium deposit.

One of the latest theories considers that atherosclerosis is an excessive inflammatory and fibroproliferative response, which becomes chronic and does not exert a protective effect against a series of attacks on the arterial intima that favor the deposition of lipids, which influences the progression of plaque.

Arteriosclerotic lesions result from a variety of pathogenic processes including the formation of foamy macrophages and death and accumulation of extracellular lipid, displacement and reduction of the structural intercellular matrix and smooth muscle cells, the generation of mineral deposits, chronic inflammation, neovascularization , rupture of the lesion surface and formation or transformation of hematoma or thrombus in fibromuscular tissue.

called Arteriosclerosis, the hardening and loss of elasticity of the arteries. Later Arteriosclerosis is classified as follows:

Anatomohistology of the arterial wall The atherosclerosis process basically develops in the arterial wall, producing loss of elasticity, abnormal deposit of lipids (atheromas) and obstructive processes, which finally causes ischemia in the affected regions. It is therefore important to know the anatomohistology of the arterial wall, as well as review some physiological concepts of circulation, to understand the pathophysiology of this disease.

The blood vessels constitute a closed vascular system that conducts oxygenated blood from the heart to the tissues to donate oxygen and once desaturated it conducts it from the tissues to the lung and the heart, to saturate it again with oxygen and thus continuously repeat the cycle.

The vascular system is made up of a series of conduits of different anatomohistological constitution, which are adapted for the hemodynamic function they have to perform and are namely:

Pathophysiology of Atherosclerosis

Arteries (Largest) to arterioles to capillaries to venules to veins (smallest) and vice versa.

As the arterial system is the most frequently attacked by atherosclerosis, we are going to refer mainly to its characteristics.

The arterial walls are thick and compact which allows them to withstand the high pressures generated within the circulatory system.

They are composed of concentric cylinders arranged one inside the other, in which there are cellular and extracellular components.

There are three layers that, arranged as cylinders, form the arterial structure and are called the arterial lumen towards the periphery as follows:

1.- Intima arterial.

2.- Middle or muscle-elastic layer.

3.- External or adventitial layer.

Intimate layer

The endothelium is the innermost area o the arterial intima, precisely the one that is in the closest contact with the circulatory stream. This topographic situation of the endothelium gives it the characteristic of a biological interface of capital importance in vascular homeostasis and in blood flow-arterial wall relationships.

The arterial intima is constituted in turn by several areas: the most internal and in contact with the blood as we have indicated is the endothelial layer, composed of a continuous monolayer of metabolically very active cells, which extends through the entire system vascular, which is why it is the largest organ in the human body.

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Its weight is calculated at 3.5 kg and its extension ranges from 400 to 1000 m2, according to various researchers.

In recent years, knowledge in the pathogenesis of cardiovascular disease has deepened due to the demonstration of the involvement of the endothelium in vascular homeostasis.

Not so long ago, the endothelial membrane was only described as a simple semi-permeable double-path membrane in relation to the circulatory stream and the arterial wall; today, on the other hand, it is considered as a true organ with multiple and delicate functions of the endocrine type, paracrine autocrinologicas

Endothelial cells vary their morphology according to the site of the arterial tree where they must perform their function.

The areas with greater predisposition to the development of atherosclerosis plaques are found in curvatures, arterial branches, ostiums, presenting an octagonal or cobblestone-like morphology, while in the areas more resistant to atherosclerosis, these cells have a shape oriented in the direction of flow circulatory.

The biochemical and biological implication of the octagonal arrangement is an increase in the permeability of the wall to the passage of lipoprotein and other molecules, which predisposes to a greater tendency to atherosclerosis damage.

The junction between endothelial cells varies from simple contact between cell membranes to true junction bridges, called desmosomes.

Endothelial cell junctions vary according to the characteristics and topography of each vessel, which is why we can say that no endothelial cell is exactly the same as the other.

The Endothelium, therefore, is not a uniform layer, it is a specialized tissue that changes its cell morphology according to its location or function in the human body.

Each endothelial cell has its own characteristics, attributes, configuration, microdomains, types of selectins, chemotactic substances, immunoglobulins and receptors, which confer individuality and a number of functions. The endothelial cell layer rests on a basement membrane below which,

It is important to discuss the constitution of the arterial intima because it is relatively common that when describing the pathophysiology of atherosclerosis, the details of its anatomohistology are not adequately defined.

Biochemists and physiologists consider that the intima and endothelium are synonymous, while pathologists describe the intima as composed of several structures, namely:

1. Endothelial layer or endothelium.

2. Basal membrane.

3. Subendothelium.

Some groups of researchers even consider that the arterial internal elastic layer is part of the arterial intima. We believe that the description of pathologists is correct to describe the structure of this arterial zone.

Under the basement membrane that supports the vascular endothelium, as we have indicated, is the Subendothelium made up of collagen, fibronectin, microfibrils, proteoglycans and elastin.

The proportion of each of these components of the subendothelium is variable, depending on the level of the vascular tree considered.

Among the most outstanding functions of the vascular endothelium, the following stand out:

1. It acts as a semi-impermeable barrier between the blood and the vascular wall.

2. It is in charge of the vascular vasomotor function, maintaining the balance between vasodilator and vasoconstrictor substances, with a slight predominance of vasodilation.

3. Maintains the balance of physiological thromboresistance, through the balance between procoagulant and anticoagulant substances.

4. It regulates the proliferation and cell migration of smooth muscle, macrophages and fibroblasts.

Stages of Atherosclerosis

1. Type I injury

It consists of initial and minimal changes that do not increase the thickness of the arterial wall beyond what is normal for this area. The term initial injury has also been used to define this type of injury.

The anatomical substrate consists of small clusters of macrophages containing cytoplasmic lipid droplets (foamy macrophages) observable in the intima.

These changes are sometimes so subtle that differentiating type I injuries from type 0 injuries (normality) is quite a subjective task, and when interpreting the results of numerous studies (taking into account that they are carried out after one year of life) it has to be assumed that It starts from a type I lesion, since there is always a minimal degree of macrophages in the intima.

2. Type II injury

It includes what is macroscopically defined as fatty streak, which consists of yellowish plaques deposited on the arterial intimal surface. With the Sudan III or IV technique, these plaques acquire a reddish hue, visible on macroscopic examination, which is why some studies have defined them as Sudanophilic lesions.

The microscopic characteristics of type II lesions are more evident than type I lesions, and they contain a greater number of foamy macrophages (this is what has been called intracellular lipid accumulation).

Microscopic studies have determined that although all fibrous streaks correspond to type II lesions, not all of them manifest macroscopically in the form of fatty streaks (Figs. 4 and 5).

3. Type III injury

Also known as intermediate lesion, transitional lesion or pre-atheroma, and it applies to those lesions that morphologically and chemically are between type II and type IV lesions (or atheroma), and that are constituted by abundant accumulations of foamy macrophages, some of them which discharge this material to the outside, giving rise to accumulations of extracellular lipids, generally in a small proportion.

4. Type IV lesion

Known as atheroma, this type of injury is considered an advanced injury due to the disorganization of the intima. It is defined by the massive presence of abundant accumulations of extracellular lipids that are observed as lipid masses (lipid nuclei) under the light microscope and are usually located in the musculoskeletal layer.

These lesions may include the presence of cholesterol crystals, and in some cases this lipid center is large enough to be seen with the naked eye when the artery is cut; however, in some cases they do not determine vascular lumen narrowing.

Type IV lesions begin to appear in the second half of the second decade of life, they can narrow the arterial lumen only minimally and are not angiographically visible, but they are symptomatic producers (clinically relevant) due to the development of fissures on their surface, hematomas or thrombus.

This type of lesion usually appears in the areas of eccentric adaptive intimal thickening: then the atheroma is, at least initially, an eccentric lesion. It is the equivalent of what other authors describe as plaque, fibrolipid plaque, or fibrous plaque.18 .

When the plaque is enriched in collagen and then in fibrous tissue, the lesion is labeled type V. The potential importance of type IV can be very important, although it does not narrow the lumen, since this type of lesion is considered vulnerable to rupture due to the abundance of macrophages.

5. Type V injury

Type V, VI, VII and VIII lesions are more advanced atherosclerotic lesions 1,14,15,19,20 . The biological measure used to designate these lesions is the destructuring and deformity of a part of the intima, which includes, among other changes, the presence of deposits of

calcium. They are given from the fourth decade of life. They are not necessarily visible angiographically, nor must they be clinically manifest lesions.

They have a high prevalence of fibrous connective tissue; when the new tissue is part of a lesion with a lipid center (type IV) this type of morphology is called fibroatheroma or Va lesion.

If it presents areas of calcification, it is called type Vb and, finally, if the lipid center does not exist or is generally minimal, it is called Vc. These lesions, as a rule, narrow the arteries more than type IV ones and develop clefts, bruises, and thrombosis with important clinical consequences.

The most prominent clinical aspect of these lesions is that they cause 20% of sudden coronary deaths and myocardial infarctions that generally occur in the absence of luminal thrombus. On the other hand, injuries of more than 75% motivate the majority of clinical vascular accidents.

Lastly, in patients with stable angina they have a reduction of the lumen of more than 50% with a frequency of presence of thrombus of 20%. In conclusion, these serious lesions narrow the lumen of the vessel and present a significant reduction in arterial blood flow.

The morbidity and mortality of the plaques occurs mainly in types IV and V, in which there is frequent rupture of the surface of the lesion with hematoma or hemorrhage and deposit of thrombus 19.

6. Type VI lesions

They are complicated lesions that have visible thrombotic deposits and bleeding in addition to lipid and collagen (complicated fibroatheroma or complicated lesions).

They are usually subdivided into VIa: surface rupture with thrombus and hemorrhage as important components; type VIb: presence of thrombus without bleeding, and type VIc: bleeding without thrombus.

Clinically, complicated lesions with the presence of obstructive but labile thrombus are known as unstable lesions, and would be the morphological equivalent of unstable angina.

There are multiple causes that determine hemorrhage and thrombotic deposition. Erosion or ulceration of the lesion is one of the well-known causes.

The surface fissure would cause massive hemorrhage within the lesion, thrombotic deposition, rapid expansion of the lesion and symptoms. Bleeding within the lesion is sometimes caused by the rupture of newly formed capillaries.

Thrombotic deposition in the lesion can form in the absence of surface defects or hemorrhage due to changes in blood flow secondary to the deformity that an elevated lesion imparts to the surface, facilitating platelet deposition in susceptible individuals.

Elevated plasma fibrinogen levels have been found in people with ischemic episodes.

Many type VI lesions appear after the third or fourth decade of life, after first passing the atheroma phase (type IV); however, massive fissures or hemorrhages have also been found associated with only fatty streak injuries.

In reality, this type of injury is an extreme and more advanced situation than the type IV and V injuries already described.

7. Type VII lesions (calcific lesion)

In the fourth decade, some advanced atherosclerosis lesions mineralize, and the term type VII lesion is applied to them. The calcium deposit replaces the extracellular deposit of dead cells and lipids.

The amount of calcium is variable and, although small crystalline calcium particles can also be seen under the microscope in type IV lesions in young people, type VII is used to describe lesions with significant mineralization, although there is also a deposit of lipids and tissue fibrous.

8. Type VIII lesions (fibrotic lesion)

Some atherosclerotic lesions, frequently in the arteries of the lower extremities, can be formed entirely by collagen scar, with minimal or no lipid component (either because it has disappeared or because there never has been).

They can severely obstruct the lumen of medium-sized arteries or completely occlude them. The term fibrotic is the one that best defines this type of injury.

Intracranial Atherosclerosis and Abdominal Aortic Atherosclerosis

Atherosclerosis or forming of plaque occuring in the cranial of the brain is called intracranial atherosclerosis and the trombosis or plaque formed in the abdominal duct of aorta which causes blockage of aorta is called Abdominal aorta atherosclerosis.

pathophysiology and stages of atherosclerosis for Intracranial and abdominal aorta is similar as mentioned above.

Atherosclerosis is currently considered an epidemic that has become a global Public Health problem. The condition is as old as humanity, with descriptions of atherosclerosis plaques in Egyptian mummies, 500 years before Christ.

Atherosclerosis in developed and industrialized countries is the main cause of morbidity and mortality. Indeed, Finland and the United States of America rank first among young adults and middle-aged men.

According to the US Office of Social Security Administration, coronary atherosclerotic ischemic heart disease is the leading cause of work disability, causing millions of dollars of financial loss. The North American Commission for Research on Heart Disease states, that a healthy male in the US. You have an approximately one in five chance of developing coronary heart disease before age 60, mainly in the form of myocardial infarction.

According to studies carried out, 25% of those who suffer a first premature cardiac ischemic attack, die within the first three hours of the onset of symptoms; Of those who survive, 10% die in the first weeks after the crisis and, middle-aged people who manage to recover from it, have reduced longevity, with five times more likely to die during the following five years, than the people with no history of coronary heart disease.

The reason for the increase in coronary atherosclerosis in the aforementioned countries is unknown, however, it seems linked to the high development and prosperity achieved by them, which exposes their inhabitants to the abundance and risk factors for coronary disease, which have been discovered over the years, such as dyslipidemia, smoking, Arterial Hypertension, Stress, etc.

Another fact that must be taken into account in this explanation is the high life expectancy of the population in these nations, precisely because due to their characteristics, they have overcome infectious diseases, perinatal mortality, malnutrition, etc.

This allows the individuals in them to reach ages where the clinical manifestations of atherosclerosis complications appear (angina pectoris, myocardial infarction, sudden death, etc.). For this reason we believe it convenient to remember the words of Lucretius, expressed 50 years before Christ:

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