Atherosclerosis is a disorder in which arterial wall stiffens and loses its elasticity caused by the formation of thickening (atherosclerotic plaque) in its inner layers, which can reduce or obstruct blood flow. Although it is more common in the male population, its prevalence increases in women after the menopause and equalizes with the prevalence of the men of the same age.
Atherosclerosis affects heart, brain, kidneys and other vital organs and extremities and thus represents the leading cause of illness and mortality in the US and most Western countries. Mortality due to coronary heart disease among white males between the age of 55 and 65 is 1 in 100.
How
does it happen?
An
atherosclerotic plaque is forming after the large amount of “bad
cholesterol” LDL-c accumulates
in arteries where they get oxidized, causing inflammation. In order
to defend itself, the organism sends macrophages, a form of white
blood cells to capture the cholesterol.
They
transform the oxidized cholesterol into large foam cells which cause
even more inflammation. As a consequence of
that, arterial smooth muscle cells activate, migrate and proliferate
forming a “cap” above the
inflamed
area.
This doesn’t represent good protection because lipid part beneath can be dangerous if it gets torn out, potentially causing a heart attack or stroke. Over time the organism forms a thick layer thus narrowing the space for blood flow even more.
Signs
and symptoms
Since the atherosclerosis is a slowly developing disorder, at first it shows no symptoms that will warn you about it. The first symptoms are seen when the artery gets obstructed. Signs and symptoms depend on the body part where an arterial obstruction occurred.
Atherosclerosis in heart arteries will be expressed via chest pain, feeling a pressure or discomfort (angina) which may progress into arms, legs or neck.
Atherosclerosis in brain arteries can cause difficulty speaking, blurred vision, loss of coordination or balance, numbness, weakness or paralysis in one side of the face, arm or leg, etc (TIA signs and symptoms).
Atherosclerosis in leg arteries will manifest itself in leg pain, difficulty walking or intermittent claudication.
Atherosclerosis in kidney arteries can cause hypertension or kidney failure.
Some of the most dangerous consequences of atherosclerosis are a heart attack and stroke as it could cause both these health emergencies.
Risk
factors for atherosclerosis
There are some risk factors for atherosclerosis on which we can’t influence such as family history, genetic abnormalities, advanced age, and male gender but many other risk factors are modifiable. You can find some of them in the text below.
Unhealthy diet – It is known that nutrition rich in saturated animal fats and carbohydrates is correlated to atherosclerosis development. Moreover, people who have a diet poor with vitamins, minerals, amino acids, and essential fatty acids have an even larger chance of atherosclerosis.
Obesity – Obesity is associated with high cholesterol levels, hypertension, diabetes, poor physical activity which all may potentially lead to various cardiovascular diseases, as well as atherosclerosis.
Lack of physical activity – People who are physically inactive have a greater chance to develop atherosclerosis.
Dyslipidemia – High concentrations of LDL-c and low concentrations of “good cholesterol” HDL-c favors atherosclerosis.
Diabetes – Diabetes can cause many metabolic disorders which can affect change on arteries which supply different organs.
Hypertension – High blood pressure increases atherosclerotic changes significantly.
Smoking – Nicotine from tobacco smoke cause constriction of blood vessels increasing the atherosclerotic changes.
Prevention
Primary prevention involves fighting risk factors in people who have no expressed symptoms and signs. First of all, it is necessary to carry out proper nutrition, reduce body weight and exercise adequately.
If the patient’s health condition is good but he/she has elevated cholesterol or triglycerides in the blood, stated preventive measures are recommended for 3 – 6 months. There is evidence that people with these conditions may benefit from Omega 3 unsaturated fatty acids.
Pharmacological treatment
If primary prevention does not help the usage of medications is needed. Here are some of the most used drug classes.
First line drugs are statins, lipid-lowering medications which can stop, reduce, or even reverse the atherosclerotic plaque (other lipid-lowering medications may be used). Likewise, a good antiplatelet drug that may prevent thrombotic complications of atherosclerosis is aspirin (100 mg) or some other medication from this class. Various other cardiovascular medication such as beta blockers, calcium channel blockers, ACE inhibitors or diureticsmay also be introduced into therapy. Furthermore, control and treatment of hypertension and diabetes are part of the recommendations for the prevention of cardiovascular diseases.
Platelets (Thrombocytes) represent the fragments of the cell named megakaryocyte, which is a type of bone marrow cells sent into the circulation. Thrombocytes are small and oval plates with a diameter of only 2 – 4 mm. Normal platelet count range from 150.000 – 450.000 per μL of blood.
Platelet
development
Megakaryocyte comes from hematopoietic stem cell precursors from the bone marrow like all other blood cells. Its transformation into a defined stem is the beginning of the thrombocytopoiesis process. Megakaryoblast is formed from the myeloid stem cell after which it becomes a megakaryocyte. Due to its large size, a megakaryocyte can‘t leave the bone marrow, but it adheres to the walls of the sinus capillary, partially participating in the formation of its wall. As the cell consists of segments, its parts are separated and put into circulation as platelets. Several thousand platelets can be made from one megakaryocyte. Thrombocytes do not come from the normal cell division, as they have no core, and in the true sense of the word, they are not cells. Therefore, the more adequate name is platelet. However, the name thrombocyte is still used sometimes.
Platelet maturation is regulated by factors of colony growth that controls the production of megakaryocytes. In addition to that, a plasma protein which facilitates the maturation of megakaryocytes and their fragmentation called thrombopoietin is constantly being generated in the liver and kidneys.
Structure of platelets
Membrane
Platelets have a very complex structure. Their membrane consists of three layers including
• The outer shell – which is responsible for platelet adhesion and aggregation
• Middle layer – which represents a source of platelet phospholipids involved in the blood clotting process
• The inner layer – which is responsible for the platelet shape
Cytoplasm
Platelet cytoplasm also has a very complex structure. It contains an open channel system responsible for the discharge of the platelet granules’ content into the outer environment. Moreover, the cytoplasm contains a powerful contractile system that allows an easy change in the platelet‘s shape.
Role
in the organism
The main role of platelets is in hemostasis, a process of bleeding stopping in an injured blood vessel. Hemostasis is a process that reduces or prevents blood loss in times of blood vessel injuries. As the blood in the blood vessels is under pressure, cutting or spraying the blood vessel results in blood leakage, and this phenomenon is called bleeding (hemorrhage). If a small blood vessel is injured, bleeding is usually spontaneously stopped by the hemostasis process. However, in the case of injuries of large arteries and veins, hemostasis is not as effective and the injuries must be surgically sanitized. After the damage to the wall of the blood vessel, blood clots accumulate at the site of the injury where they
1.
Liberate the substances that cause the blood vessel to contract,
which reduces the blood loss
2.
Form an aggregate, a platelet plug at the site of
the injury
3.
Participate
in the process of blood clotting, due to coagulation factors that
contain
4. Take part in the healing of the injury.
Aggregation
Platelets begin to adhere to collagen fibers within a few seconds after the occurrence of the damage to the inner part of a blood vessel, and that process is called platelet adhesion. Adhered platelets are activated and they alter their shape while emptying their granules that stimulate further aggregation. The interconnection of a large number of platelets at the site of a blood vessel injury is called platelet aggregation.
Platelet
life span
Circulating platelets have a lifespan of 1 to 2 weeks. Older blood platelets, which are not used during blood clotting, are destroyed by macrophages from liver and spleen. A spleen is not just a place which destroys old platelets, as it is also an important reservoir of these blood elements. It releases a large number of stored platelets into the circulation under the influence of the nervous system in certain occurrences including bleeding or burns.
Disorders
An increased platelet count called thrombocytosis increases the tendency of a pathological blood clot (thrombus) formation. That blood clot can induce life-threatening complications such as heart attack and ischemic stroke. A decrease in blood platelet count is called thrombocytopenia. Physiological thrombocytopenia occurs normally in the women immediately prior to menstrual bleeding. Female sex hormones reduce the formation and maturation of blood platelets. Severe thrombocytopenia causes spontaneous bleeding, especially in the gums and digestive tract.
Frank’s sign is a diagonal crease in the ear lobe which is considered as a predictive sign of heart disease. It was named after the American pulmonologist, Dr. Sanders T. Frank, who first noticed the connection between heart diseases and creases on one or both ear lobes. The crease is usually spread almost across the entire ear lobe, and in some cases, it looks as if it starts just from the hole through which the earring is placed.
The presence of Frank’s sign is associated with a decrease in telomere size, an accelerated aging marker, which may lead to atherosclerosis. It is thought to happen due to chronic local ischemia, leading to disruption and displacement of elastic fibers, associated with thickening of the intima of arterioles.
The first research of Frank’s sign
The first studies regarding Frank’s sign date back to 1973. the year in which Dr. S. Frank published a research article in which a possible correlation was hypothesized between the presence of this cutaneous marker and the development of cardiovascular diseases, especially coronary heart disease and diabetes. The article was published in the New England Journal of Medicine (NEJM) under the name “Aural sign of coronary-artery disease”. Many studies were conducted since then, showing a correlation between Frank’s sign and heart disease, exceptionally in people under the age of 60.
Frank’s sign classification
Classification of Frank’s sign was based on descriptive evaluation which includes:
Grade
1 – a
small amount of wrinkling on the earlobe
Grade
2a – a
superficial crease on the earlobe
Grade
2b – a
crease that surpasses more than halfway across the earlobe
Grade
3 – a
deep crease that affects the entire earlobe
Other
indicators of heart diseases
Cardiovascular diseases are the leading cause of death, and commonly, the first sign of problems with heart may be a suffered heart attack, which is fatal in 30% of cases. Although it is impossible to detect all the warnings indicating that you have problems with your heart, there are some visible external signs that may predict a future cardiac event. Some of them include:
Nail
clubbing
An occurrence recognized as nail clubbing can also represent a sign that there is something wrong with your heart. The nails are becoming thicker and wider, changing their shape. Such changes are often present in both hands, and they do not cause pain. The reason for nail clubbing is the insufficient supply of oxygenated blood to fingers, which they try to overcome with the increased production of growth factors.
Xanthomas
Large, yellow fatty bumps (Xanthomas) that can appear on your knees, elbows, or eyelids do not represent a danger on themselves, but their presence can indicate other problems. These fatty bumps are generally seen in people with familial hypercholesterolemia, a genetic disorder that causes exceptionally high levels of low-density lipoprotein cholesterol (LDL-c) that are making fat deposits on the skin. In addition to that, fat deposits can accumulate in the arteries that supply the heart, causing various cardiovascular problems.
Arcus
senilis
Arcus senilis represents fat deposits manifested via the white, grey or blue ring located around the cornea. It is caused by lipid deposits in the edge of the cornea. Although it doesn’t affect the vision, arcus senilis is correlated with heart diseases
Iker Casillas, 5 times World’s Best Goalkeeper, achieved the greatest victory of his life. On the opposite side was a heart attack, a ruthless enemy who takes millions of lives a year, but once again, “San Iker” shows us that he is a true champion, he survived that fight and took the biggest victory of his astonishing career.
How did all start?
The day was May 20, 1981. On lazy, sunny, Wednesday afternoon, in the second-largest city in population belonging to the autonomous community of Madrid, 18 kilometers southwest from central, in Mostoles, the legend was born.
Just 16 years later, he was first called up to the senior team squad to face Rosenborg in the UEFA Champions League. In starting the 1999-2000 UEFA Champions League group stage fixture against Olympiakos on 15 September 1999, he became the youngest goalkeeper ever to feature in the competition at the time, aged 18 years and 177 days. Casillas had made his La Liga debut in a 2–2 draw against Athletic Bilbao at San Memes Stadium. In May 2000, he became the youngest ever goalkeeper to play in and win a Champions League final when Real Madrid defeated Valencia 3-0, just four days after his 19th birthday.
Real Madrid – the biggest chapter
Casillas began his career in Real Madrid’s youth system, during 1990 – 91 season. For the next 16 years he was the central part of the team. During his time in Real, Iker has won literally everything that football goalkeeper can win.
4x Spanish Super Cup winner (01/02, 03/04, 08/09, 12/13)
2x FIFA Club World Cup winner (2014, 2015)
3x Intercontinental Cup winner (1998, 2002, 2003)
2x Uefa Supercup winner (02/03, 14/15)
Honestly, I don’t have to use up many words to say how good he is, the results are there for all to see. He has won everything there is to win and has been on the same great level for so many years now, which is possibly hardest of all for a goalkeeper. Spain almost never concede goals and Casillas is the main reason for that.
Gianluigi Buffon on Casillas prior to the UEFA EURO 2012 Final
International career
Casillas debuted for Spain at the under-17 level. At age 16, he was the youngest player in the Spanish squad that placed third at the 1997 FIFA U-17 World Championship in Egypt. Two years later, he went on to win the FIFA World Youth Championship and the UEFA-CAF Meridian Cup that same year. As a senior, he debuts for Spain national team on EURO 2000.
Casillas is currently the most capped player in the history of the Spain national team. Following his full international debut at the senior level on 3 June 2000 against Sweden (at 19 years and 14 days), Casillas was an unused substitute at UEFA Euro 2000. He was part of the roster for the 2002 FIFA World Cup, initially as the understudy to Santiago Cañizares. Coincidentally, he became first-choice when Cañizares had to withdraw from the tournament due to injury from a freak accident. At 21, Casillas was one of the youngest first-choice goalkeepers in the tournament. He played an instrumental role in Spanish progression when he saved two penalties in the shoot-out during the round of 16 match against the Republic of Ireland, earning him the nickname “The Saint”. One of his saves during the quarter-final against South Korea during the 2002 World Cup was rated by Fifa as one of the top ten saves of all time.
Unfortunatlly for Iker and Spain, on Euro 2004 and World Cup 2006, they did not well. They lost their matches in the Round of 16. After that, the beast has been awakened. From 2008. to 2012. Iker Casillas was the best goalkeeper in the world. He won that title 5 years in a row and in that period, Spain has won 2008 European Championship, 2010 FIFA World Cup and 2012 EURO. In June 2014, Casillas was selected to represent Spain in his fourth World Cup. On 5 September 2015, Casillas kept a clean sheet in his 100th game as Spain’s captain. On 31 May, Casillas was named to Vicente del Bosque’s final 23-man Spain squad for Euro 2016. The following day, he became the most-capped European player by earning his 167th cap in a 6–1 friendly win over South Korea.
After finishing his career in Real Madrid, in 2015, Iker moved to FC Porto and won Portuguese champion in 2017/18 and 2 times Portuguese Super Cup in 2018. and 2019. 1
But on the first may we were all witnesses of a terrible event.
The 37-year-old goalkeeper suffered the heart attack during training on Wednesday morning and he was immediately escorted to a local hospital.
Iker Casillas suffered an acute heart attack during Wednesday morning’s training session,” Porto said in a statement.
“The training session was promptly interrupted to provide assistance to the Porto goalkeeper, who is currently at the Hospital CUF Porto.
“Casillas is doing well, he’s stable and his heart problem has been resolved.”
Let’s take closer look what actually happened.
Sudden death in people younger than 35, often due to undiscovered heart defects or overlooked heart abnormalities, is rare. When these sudden deaths occur, it’s often during physical activity, such as playing a sport, and more often occurs in males than in females.1
Millions of elementary, high school and college athletes compete yearly without incident. If you or your child is at risk of sudden death, talk to your doctor about precautions you can take.
How common is sudden cardiac death in young athletes?
Most deaths due to cardiac arrest are in older adults, particularly those with coronary artery disease. Cardiac arrest is the leading cause of death in young athletes, but the incidence of it is unclear. Perhaps 1 in every 50,000 sudden cardiac deaths a year occurs in young athletes.
What can cause sudden cardiac death in young people?
The causes of sudden cardiac death in young people vary. Most often, death is due to a heart abnormality.
For a variety of reasons, something causes the heart to beat out of control. This abnormal heart rhythm is known as ventricular fibrillation.
Some specific causes of sudden cardiac death in young people include:
Hypertrophic cardiomyopathy (HCM). In this usually inherited condition, the walls of the heart muscle thicken. The thickened muscle can disrupt the heart’s electrical system, leading to fast or irregular heartbeats (arrhythmias), which can lead to sudden cardiac death.Hypertrophic cardiomyopathy, although not usually fatal, is the most common cause of heart-related sudden death in people under 30. It’s the most common identifiable cause of sudden death in athletes. HCM often goes undetected.
Coronary artery abnormalities. Sometimes people are born with heart arteries (coronary arteries) that are connected abnormally. The arteries can become compressed during exercise and not provide proper blood flow to the heart.
Long QT syndrome. This inherited heart rhythm disorder can cause fast, chaotic heartbeats, often leading to fainting. Young people with long QT syndrome have an increased risk of sudden death.
1
Other causes of sudden cardiac death in young people include structural abnormalities of the heart, such as undetected heart disease that was present at birth (congenital) and heart muscle abnormalities.
Other causes include inflammation of the heart muscle, which can be caused by viruses and other illnesses. Besides long QT syndrome, other abnormalities of the heart’s electrical system, such as Brugada syndrome, can cause sudden death.
Commotio cordis, another rare cause of sudden cardiac death that can occur in anyone, occurs as the result of a blunt blow to the chest, such as being hit by a hockey puck or another player. The blow to the chest can trigger ventricular fibrillation if the blow strikes at exactly the wrong time in the heart’s electrical cycle.
Are there symptoms or red flags parents, coaches and others should be on the lookout for that signal a young person is at high risk of sudden cardiac death?
Many times these deaths occur with no warning, indications to watch for include:
Unexplained fainting (syncope). If this occurs during physical activity, it could be a sign that there’s a problem with your heart.
Family history of sudden cardiac death. The other major warning sign is a family history of unexplained deaths before the age of 50. If this has occurred in your family, talk with your doctor about screening options.
Shortness of breath or chest pain could indicate that you’re at risk of sudden cardiac death. They could also indicate other health problems in young people, such as asthma.
Can sudden death in young people be prevented?
Sometimes. If you’re at high risk of sudden cardiac death, your doctor will usually suggest that you avoid competitive sports. Depending on your underlying condition, medical or surgical treatments might be appropriate to reduce your risk of sudden death.
Another option for some, such as those with hypertrophic cardiomyopathy, is an implantable cardioverter-defibrillator (ICD). This pager-sized device implanted in your chest like a pacemaker continuously monitors your heartbeat. If a life-threatening arrhythmia occurs, the ICD delivers electrical shocks to restore a normal heart rhythm.
Who should be screened for sudden death risk factors?
There’s debate in the medical community about screening young athletes to attempt to identify those at high risk of sudden death.
Some countries such as Italy screen young people with an electrocardiogram (ECG or EKG), which records the electrical signals in the heart. However, this type of screening is expensive and can produce false-positive results — indications that an abnormality or disease is present when it isn’t — which can cause unnecessary worry and additional tests.
It’s not clear that routine exams given before athletes are cleared to play competitive sports can prevent sudden cardiac death. However, they might help identify some who are at increased risk.Paragraph
For anyone with a family history or risk factors for conditions that cause sudden cardiac death, further screening is recommended. Repeat screening of family members is recommended over time, even if the first heart evaluation was normal.
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