Oxidized LDL, which attracts macrophages and forms foam cells Why is unstable plaque more dangerous than stable plaque? Unlike stable plaque, unstable plaque is associated with thrombus formation that can block blood flow and tissue oxygenation.
Is your plaque stable or unstable?
If the plaque is loaded with calcium on its outer border and is low in fat, it is likely to be a stable plaque and the person is not at high risk for a heart attack. On the other hand, if the plaque is full of fat and has very little calcium, it is an unstable plaque and the person is at significant risk for a heart attack.
What happens when a plaque ruptures?
Once a plaque ruptures, it can trigger an acute thrombosis (clot) by activating platelets and the clotting cascade. Illustration from from Libby P: Inflammation in Atherosclerosis. Nature 202;420:868 What makes an unstable plaque much more dangerous than a stable plaque? a.
Is plaque harmful to Your Heart?
However, such plaque isn’t harmful… until it gets inflamed. As mentioned in the “Cardiovascular Inflammation” section, CV inflammation (usually from prediabetes) produces these soft plaques. As discussed in the “How Does Arterial Plaque Form?” section, the body’s immune system attacks plaque, leaving fluid and inflammatory cells.
How can I tell if my Heart plaque is stable?
A regular X ray or calcium scan can tell if your plaques are likely to break off to cause a heart attack ( J Thorac Dis, Apr 2018;10 (4):2365–2376). If the plaque is loaded with calcium on its outer border and is low in fat, it is likely to be a stable plaque and the person is not at high risk for a heart attack.
Why is an unstable plaque more dangerous quizlet?
Why is unstable plaque more dangerous than stable plaque? Unlike stable plaque, unstable plaque is associated with thrombus formation that can block blood flow and tissue oxygenation.
What is the first line of defense when treating hyperlipidemia?
Lifestyle changes such as exercising and eating a healthy diet are the first line of defense against high cholesterol.
Which of the following substances inhibits platelet aggregation at plaque sites?
Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered Aspirin) Inhibits prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis.
What is the difference in composition between Ldls and Hdls?
The main structural difference between LDL and HDL is their compositions. Approximately 50 percent of the weight of an LDL particle is cholesterol and only 25 percent is protein. High-density lipoprotein particles, on the other hand, consist of 20 percent cholesterol by weight and 50 percent protein.
What can I take instead of statins to lower cholesterol?
7 cholesterol-lowering alternatives to statinsFibrates. Mostly used for lowering triglyceride levels in patients whose levels are very high and could cause pancreatitis. ... Plant stanols and sterols. ... Cholestyramine and other bile acid-binding resins. ... Niacin. ... Policosanol. ... Red yeast rice extract (RYRE) ... Natural products.
What is the most popular medication for high cholesterol?
Statins. Statins are the most common medicine for high cholesterol. They reduce the amount of cholesterol your body makes. You take a tablet once a day.
Which medications prevent platelet aggregation?
Platelet aggregation inhibitors such as; Aspirin and related cyclooxygenase inhibitors. Oral thienopyridines such as clopidogrel, ticagrelor, ticlopidine, and prasugrel.
Can statins affect platelets?
Statins interfere with platelet aggregation and have anti-inflammatory, anti-oxidative, and anti-apoptotic properties [26–29]. Previous studies have demonstrated that platelet aggregation and leukocyte activity are significantly increased after ischemic stroke and contribute to the severity of brain damage [4, 30].
Does aspirin prevent platelet aggregation?
Aspirin is effective in the prevention of cardiovascular events in high-risk patients. The primary established effect of aspirin on hemostasis is to impair platelet aggregation via inhibition of platelet thromboxane A2 synthesis, thus reducing thrombus formation on the surface of the damaged arterial wall.
Why is LDL considered bad cholesterol?
LDL stands for low-density lipoproteins. It is sometimes called the "bad" cholesterol because a high LDL level leads to a buildup of cholesterol in your arteries.
What does it mean when your HDL and LDL are both high?
Thyroid hormones help your body make and break down cholesterol. People whose thyroid gland is underactive, a condition called hypothyroidism, have higher levels of both HDL and LDL cholesterol.
Why is HDL called the good cholesterol?
For HDL cholesterol, or "good" cholesterol, higher levels are better. High-density lipoprotein (HDL) cholesterol is known as the "good" cholesterol because it helps remove other forms of cholesterol from your bloodstream. Higher levels of HDL cholesterol are associated with a lower risk of heart disease.
What is the main goal of treatment in patients with hyperlipidemia?
The goal of therapy is to decrease cardiovascular morbidity and mortality by lowering cholesterol to a target level. The target LDL cholesterol is determined by the number of patient risk factors. The goal is achieved through diet, lifestyle modification, and drug therapy.
What causes upregulation of LDL receptors?
Up-regulation of low-density lipoprotein receptor in human hepatocytes is induced by sequestration of free cholesterol in the endosomal/lysosomal compartment. Biochem Pharmacol.
What pharmacotherapeutic options are available for the management of Hyperlipidaemias?
Statins, fibrates, cholesterol absorption inhibitors, nicotinic acid, and bile acid sequestrants can all be used to achieve patient-specific lipid goals.
What is mild hyperlipidemia?
Hyperlipidemia means your blood has too many lipids (or fats), such as cholesterol and triglycerides. One type of hyperlipidemia, hypercholesterolemia, means you have too much non-HDL cholesterol and LDL (bad) cholesterol in your blood. This condition increases fatty deposits in arteries and the risk of blockages.
What is unstable plaque?
A. Unlike stable plaque, unstable plaque is associated with an increased likelihood of hemorrhage that can lead to shock.
Why is bad cholesterol called bad cholesterol?
A. It is called bad cholesterol because it is atherogenic.
Can immunoglobulin cause renal failure?
A. immunoglobulin molecules can disrupt blood flow and cause renal failure.
Can unstable plaque cause hypertension?
C. Unlike stable plaque, uns table plaque is associated with thrombus formation that can cause hypertension.
Why do plaques grow slowly?
Slowly growing plaques expand gradually due to accumulation of lipid in foam cells and migration and proliferation of smooth muscle cells. These plaques tend to stabilize and are not prone to rupture. The so-called fibrin cap on the lesion matures.
Which side of the artery is the atherosclerotic plaque?
The right side of the artery has a fairly normal appearance, but an atherosclerotic plaque has evolved on the left side. The mass of the "atheroma" is composed of a mixture of lipid and subintimal smooth muscle cells. Note that much of the lumen of the artery is occupied by this growing lesion.
How does fatty streak evolve?
The cartoon below summarizes the steps by which a fatty streak evolves. Injury to the endothelium triggers monocyte adhesion, a loosening of endothelial cell junctions, and migration of monocytes beneath the endolthelium where they differentiate into macrophages. The more permeable endothelium also permits LDL to enter the intima of the artery, and macrophages begin engulfing the LDL by phagocytosis. After macrophages become laden with lipid from ingesting LDL, they are referred to as "foam cells," and collections of these create fatty streaks.
What happens to LDL in the arterial wall?
Oxidation of LDL in the arterial wall occurs as a result of its exposure to nitric oxide, macrophages, and some enzymes such as lipoxygen ase.
Can unstable plaques release lipids?
c. Unstable plaques can release their lipid content into the blood stream.
What is unstable plaque?
A. Unlike stable plaque, unstable plaque is associated with an increased likelihood of hemorrhage that can lead to shock.
Why is bad cholesterol called bad cholesterol?
A. It is called bad cholesterol because it is atherogenic.
Can immunoglobulin cause renal failure?
A. immunoglobulin molecules can disrupt blood flow and cause renal failure.
Can unstable plaque cause hypertension?
C. Unlike stable plaque, uns table plaque is associated with thrombus formation that can cause hypertension.
How Does Arterial Plaque Form?
I agree with Dr. Cannon and Harvard Health that plaque forms when LDL cholesterol gets stuck inside the artery wall. However, I think Dr. Cannon and Harvard Health skipped some critical parts.
What is the body's reaction to plaque in the artery walls?
Cardiovascular Inflammation. As I mentioned earlier, the body sometimes sets up an inflammatory reaction to the plaque in the artery walls . This is a dangerous situation. Immune cells (such as neutrophils and macrophages) can release enzymes to digest that plaque.
What happens if LDL is stuck in the artery wall?
When LDL cholesterol leaks through the artery wall and gets stuck, it can form harmful plaque. And this plaque puts us at risk for heart attack and stroke. Heart attack is the most common cause of death (especially in the US), while stroke is the most common cause of long-term disability.
Why do patients come to see me?
Patients will often come to see me because they had a positive calcium score. They forget that soft plaques don’t show up on a calcium score— calcium score is only indicative of stable, hardened, calcified plaque. And it’s the soft plaque which we should be worried about.
Is HDL good or bad cholesterol?
Many still call HDL by that name, but it’s also a misnomer. Recent information shows that calling HDL the “good cholesterol” (and LDL the “bad cholesterol”) is overly simplistic in terms of what is really happening.
When does plaque growth start?
Plaque growth starts when there’s an injury in the inner lining of the artery wall. That endothelial, single-cell layer is what we will call the “intima.”
Does primary care medicine recognize plaque?
Unfortunately, our current culture in primary care medicine doesn’t recognize that fact. The physicians making up our medical community, the medical standards committees, the patients—none of them realize the importance of preventing plaque.
How to prevent heart attacks?
You can help to prevent heart attacks by eating a heart-healthy anti-inflammatory diet and exercising, and your doctor may prescribe statin drugs. Exercise helps to prevent heart attacks by making plaques more stable so they do not break off as easily ( BMJ Open Sport & Exercise Medicine, 2018;4 (1):e000370). A new study shows that statin drugs are associated with increased amounts of calcium in heart arteries that stabilize plaques so they are less likely to break off ( JAMA Cardiology, August 18, 2021).
How do bacteria affect the immune system?
These colon bacteria influence how quickly you form plaques in your arteries. Foods favored by the bacteria that turn on your immune system are classified as pro-inflammatory and increase risk for forming plaques in your arteries to increase risk for heart attacks ( Front Pharmacol, Sept 25, 2018;9:1082). Anti-inflammatory foods are favored by types of bacteria that help to prevent plaques from forming and decrease heart attack risk. A diet that is high in anti-inflammatory foods such as fruits, vegetables, whole grains, legumes and nuts is associated with reduced risk for cardiovascular disease, while pro-inflammatory foods such as sweets, refined grains, juices, meat from mammals and processed meats are associated with plaque formation and increased risk for a heart attack ( J Amer Coll Cardiology, July 2017;70 (4)).
What makes a plaque stable?
34 He noted that the majority of fibrous caps overlying lipid cores from lesions with superficial thrombi contained smooth muscle cells with varying numbers of macrophages . What makes a plaque stable is the intact and thick fibrous cap that is made up of smooth muscle cells in a matrix rich in type I and III collagen. Richardson and coworkers performed mechanical tests on strips of fibrous caps with infiltrating macrophages from human aortic samples with ulcerated or intact plaque caps and showed a good correlation of increase in macrophage density with greater extensibility and decreased maximum stress (force per unit area). 35
What is a vulnerable plaque?
Today’s concept of vulnerable plaque has evolved primarily from the early pioneering work uncovering the pivotal role of plaque rupture and coronary thrombosis as the major cause of acute myocardial infarction and sudden cardiac death. Since the first historical description of plaque rupture in 1844, several key studies by leading researchers and clinicians have lead to the current accepted views on lesion instability. Important to the complex paradigm of plaque destabilization and thrombosis are many discoveries beginning with the earliest descriptions of advanced plaques, reminiscent of abscesses encapsulated by fibrous tissue capable of rupture. It was not until the late 1980s that studies of remodeling provided keen insight into the growth of advanced plaques, beyond the simple accumulation of lipid. The emphasis in the next decade, however, was on a focused shift toward the mechanisms of lesion vulnerability based on the contribution of tissue proteolysis by matrix metalloproteinases as an essential factor responsible for thinning and rupture of the fibrous cap. In an attempt to unify the understanding of what constitutes a vulnerable plaque, morphological studies, mostly from autopsy, suggest the importance of necrotic core size, inflammation, and fibrous cap thickness. Definitive proof of the vulnerable plaque, however, remains elusive because animal or human data supporting a cause-and-effect relationship are lacking. Although emerging imagining technologies involving optical coherence tomography, high-resolution MRI, molecular biomarkers, and other techniques have far surpassed the limits of the early days of angiography, advancing the field will require establishing relevant translational animal models that produce vulnerable plaques at risk for rupture and further testing of these modalities in large prospective clinical trials.
How do TCFAs differ from ruptures?
Despite morphological similarities, TCFAs differ from ruptures considering that they generally exhibit smaller necrotic cores, fewer macrophages within the fibrous cap, and less calcification. 28,29 Although the vulnerable plaque was not a recognized entity in the American Heart Association consensus document, it was highlighted in our modified classification scheme published later in 2000. 22 One of the major limitations of the original American Heart Association classification was a lack of understanding that the fibrous cap undergoes thinning before the onset of rupture, a concept forwarded by Dr Peter Libby 30 ( Figure 3) and further defined by our laboratory. 27
What is the importance of identifying vulnerable plaques?
Therefore, it is essential to further identify meaningful surrogates of lesion instability at the highest risk of rupture. Moreover, vulnerable plaques tend to occur at multiple sites, and some have advocated the concept of the vulnerable patient, defined by high atherosclerotic burden, high-risk/vulnerable plaques, or thrombogenic blood. Paradoxically, these patients might be recognized by biomarkers other than those directed toward specifically identifying vulnerable plaques.
Why is the adoption of a common nomenclature important?
As the understanding of the pathophysiology of lesion instability began to expand, there was a necessity for consensus terms regarding vulnerability; the adoption of a common nomenclature would help support the study of acute coronary events. To meet this need, a group of prominent investigators convened in 2003 to resolve issues of terminology surrounding the identification of high-risk and vulnerable coronary artery plaques. 15 A unification of conceptual terms was adopted to provide a fundamental basis for clinicians and researchers whereby diagnostic methods of identifying vulnerable patients and the plaques that contribute to their increased risk can be identified, in addition to defining the critical lesions that may be amenable to treatment.
Why are morphological studies important?
From the view of vulnerable plaque detection, morphological studies should provide valuable insight regarding which criteria are important for localizing high-risk lesions using imaging modalities and assessing the potential risk for rupture. Obvious important cause-and-effect data are missing from the current paradigm because of our inability to accurately detect vulnerable plaques in humans in vivo and because of the lack of an animal model. In this regard, representative lesions in current animal models rarely progress beyond the stage of fibroatheroma; more often, they consist of only masses of lipid-laden intimal macrophages without a well-developed fibrous cap or necrosis. Lesions with this histology rarely become clinically significant except in examples of severe hyperlipidemia, in which the lumen can become obstructed by the sheer plaque burden, a situation that is quite atypical in human disease. 52 Therefore, a major limitation today exists partly because the precise mechanisms of progression from an asymptomatic stable to high-risk plaque (TCFA or vulnerable plaque) that lead to rupture and thrombosis are incompletely understood.
Is plaque rupture a sign of vulnerability?
Remodeling, as mentioned above, can also be an important sign of vulnerability. In this regard, plaque ruptures had the highest remodeling index, followed by lesions with hemorrhage > TCFAs > healed plaque ruptures > fibroatheromas. 46 Conversely, lesions of total occlusion or erosion exhibited negative remodeling. 46 From this study, it becomes evident that all lesions derived from or related to plaque rupture show positive remodeling, which may represent one important surrogate for detecting lesion vulnerability.