atherosclerosis
TRANSCRIPT
TABLE OF CONTENTS1 • CORONARY HEART DISEASES: A
GENERAL VIEW
2 • ATHEROSCLEROSIS : GENERAL VIEW
3 • PATHOPHYSIOLOGY OF ATHEROSCLEROSIS
4 • RISK FACTORS ASSOCIATED WITH ATHEROSCLEROSIS
5 • CLINICAL MANIFESTATIONS
6 • CARDIAC REMODELING
7 • DIAGNOSIS/ MEDICAL TESTS
8• PREVENTION AND TREATMENT
OF ATHEROSCLEROSIS (OBJECTIVES)
9 • DRUGS AND MEDICINES RECOMMENDED
10 • NUTRITIONAL MANAGEMENT AND DIETARY GUIDELINES
11 • CONCLUSION
12 • REFERENCES
• Lifestyles of populations across the world
have changed dramatically in the 20th
century. These changes (collectively
termed as epidemiological transition)
have been brought about by a number of
developments in science and technology
that now affect every facet of human
existence.
• Most human societies have moved from
agrarian diets and active lives to fast
foods and sedentary habits. Combined
with increasing tobacco use, these changes
have fuelled the epidemic of obesity,
diabetes, hypertension, dyslipidemia and
cardiovascular diseases (CVD).
Source: Non-communicable Diseases Country Profiles 2014 by World health Organization(WHO)
Figure 1:
• Coronary heart disease (CHD) is the most
common form of Cardiovascular diseases
(CVD) and caused by atherosclerosis in the
large and medium sized arteries that supply
the heart muscle with oxygen and nutrients.
• Also called as coronary artery disease (CAD)
• In developed nations the rise in the burden of
CVD occurred over several decades due to a
long period of epidemiological transition.
• In India, perhaps because of the rapid pace of
economic development, epidemiological
changes have spanned a much shorter time. As
a consequence, cardiovascular disease (CVD)
has emerged as the leading cause of death all
over India, with coronary heart disease (CHD)
affecting Indians at least 5-6 years earlier than
their western counterparts.
Figure 2: The proportions of cardiovascular deaths caused by ischaemic heart disease, cerebrovascular disease, inflammatory heart disease, rheumatic heart disease, hypertensive heart disease, and other cardiovascular diseases in 2011. From- Epidemiological studies of Coronary Heart Disease and the evolution of preventive cardiology Nathan D. Wong Nature Reviews Cardiology 11, 276–289 (2014)
Men Women
ATHEROSCLEROSIS : GENERAL VIEW
• Atherosclerosis (also known as arteriosclerotic vascular disease or ASVD) is a special form of arteriosclerosis in which an artery wall thickens as a result of invasion and accumulation of WBCs.
• Atherosclerosis is a syndrome affecting arterial blood vessels due to a chronic inflammatory response of WBCs in the walls of arteries. This is promoted by low-density lipoproteins (LDL, plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high-density lipoproteins (HDL). It is commonly referred to as a "hardening" or furring of the arteries. It is caused by the formation of multiple atheromatous plaques within the arteries.
• Atherosclerosis is a chronic disease that remains asymptomatic for decades.
• The incidence of atherosclerosis is difficult to determine since it mainly an asymptomatic condition. The pathological process begins in childhood and continues throughout the life. In the United Kingdom, the frequency of clinical manifestations of atherosclerosis is high, especially in the West of Scotland.
PATHOPHYSIOLOGY FOR ATHEROSCLEROSIS
RISK FACTORS ASSOCIATED WITH ATHEROSCLEROSIS
Age
Family history
A. Unmodifible risk factors
B. Modifiable risk factorsHyperlipidemia
Hypertension
Diabetes mellitus
Cigarette smoking
Metabolic syndrome
High- saturated fat, high cholesterol diet
Physical inactivity
Elevated low-densitylipoprotein cholesterol
Hormonal factors
High altitude and cold
Acute-life event stress
Work- related stress
Alcohol
Oral Contraceptive pill
C. Newer novel risk factorsElevated
homocysteine levels
Elevated lipoprotein (a)
levels
Elevated triglycerides
levels
Oxidative stress
Fibrinogen
High sensitive C-reactive
protein
CLINICAL MANIFESTATIONS
• Angina pectoris
• Myocardial infarction
• Calcification of the artery walls
• Ulceration and rupture
• Superimposed thrombosis
• Hemorrhage into the plaque
• Aneurysmal dilation
• Transient ischaemic attack
• Permanent neurological damage.
• Peripheral Arterial disease
• Tendon xanthomas
• Premature xanthelasma
• Hypertension
• Abnormal heart sounds
• Increased heart rate
• Central abdominal pain following a meal (post
prandial mesentric angina)
Peripheral arterial disease (affects the legs)
Tendon xanthomas affecting hands, eye, face, back and buttocks.
ANGINA PECTORIS
MYOCARDIAL INFARCTION
CARDIAC REMODELING
• Cardiac remodeling may be defined as genome expression, molecular, cellular and interstitial changes that are manifested clinically as changes in size, shape and function of the heart after cardiac injury.
• It occurs after myocardial infarction, pressure overload (aortic stenosis, hypertension), inflammatory heart muscle (myocarditis), idiopathic dilated cardiomyopathy or volume overload (valvular regurgitation).
• The process of cardiac modeling is mainly influenced by hemodynamic load and neurohormonal activation.
• The myocyte is the major cardiac cell involved in the remodeling process. Other components involved include the interstitium, fibroblasts, collagen and coronary vasculture; relevant processes also include ischemia, cell necrosis and apoptosis.
CLINICAL TESTS/ DIAGNOSIS FOR ATHEROSCLEROSIS
• Blood tests• Electrocardiogram• Chest X-ray• Ankle/ Brachial Index• Echocardiography• Magnetic Resonance
imaging (MRI)• Position emission
tomography (PET)
PREVENTION AND TREATMENT OF ATHEROSCLEROSIS
The most important measures to protect against the development of atherosclerosis and its progression to serious vascular disease are:
DRUGS TO PREVENT ATHEROSCLEROSIS
• HMG-CoA Reductase inhibitors
• Fibric acid derivatives• Niacin• Bile acid sequestrants• Cholesterol Absorption
inhibitors• Combination therapies.• Nitrates, beta-blockers
and calcium antagonists
NUTRITIONAL MANAGEMENT AND DIETARY GUIDELINES
FOR ATHEROSCLEROSIS
AIMS AND OBJECTIVES OF THE DIET
1 •Maintenance of good nutrition
2 •Acceptability of the program
3 •Proper rest to the heart
Cardiac prudent diet Diet should be low in saturated fats, Trans fats as well as cholesterol. 20kcal/kg body weight is recommended for obese patients in bed and 25kcal/kg body
weight for those near ideal body weight. Fats should be 15-20% of total calories Carbohydrate intake should be limited to 60 per cent of total energy in patients with
metabolic syndrome. Normal allowances of protein are recommended (1gram/kg body weight). Mega doses of niacin have been known to be an effective treatment of dyslipdemia Diet should be rich in dietary fibre, MUFA and PUFA. Vitamin B6, B12, and folic acid supplementation decreases the risk of cardiovascular
disease related to homocysteine risk factor. 200-300mg of Vitamin C reduces cholesterol A restriction of sodium of 1600-2300 mg is satisfactory among patients with
atherosclerosis Potassium helps to maintain cell fluid balance and plays a role in muscle contraction.
Low levels of this mineral have been associated with high blood pressure. Magnesium helps muscles relax, affects the muscle tone of blood vessels and keeps
heart rhythm steady. Low glycaemic index diets may preserve HDL cholesterol and thus have a potentially
positive effect in reducing CHD risk.
• A functional food is any food that has a
positive effect on a person’s health,
physical performance or state of mind.
• Reduces the risk of chronic diseases and
physiological benefits when eaten on a
regular basis in adequate amounts.
• Foods rich in antioxidants,
hypocholesterolemic agents and
phytochemicals protect from Coronary
Heart diseases.
• Antioxidants including Vitamin C, E β-
carotene have potential health benefits of
reducing cardiovascular diseases.
FUNCTIONAL FOODS FOR CORONARY HEART DISEASE AND ATHEROSCLEROSIS
FUNCTIONAL FOODS IDEAL FOR ATHEROSCLEROSIS AND CORONARY HEART DISEASE
Atherosclerosis is the cause of more than 50% mortality in industrial countries.
Atherosclerosis is a disease in which plaque builds up inside your arteries. Over
time, plaque hardens and narrows your arteries, limiting the flow of oxygen-rich
blood. This can lead to serious problems. Atherosclerosis is a disease in which
plaque builds up inside your arteries. Over time, plaque hardens and narrows
your arteries, limiting the flow of oxygen-rich blood. This can lead to serious
problems Atherosclerosis usually doesn't cause symptoms until it severely narrows
or totally blocks an artery. Many people don't know they have the disease until
they have a medical emergency. When symptoms do happen, they are specific to
the arteries affected by atherosclerosis. A physical examination, imaging, and other
diagnostic tests can tell if the patient have this disease. Treatments include
medicines, and medical procedures or surgery. Lifestyle changes can also help.
These include following a healthy diet, getting regular exercise, maintaining a
healthy weight, and quitting smoking.
CONCLUSION
1. Bhandari U, Sharma J, Zafar R. “The protective action of ethanolic ginger extract in cholesterol fed rabbits.” Journal of Ethnopharmacology 1998; 61(2):167-171.
2. Bordia A, Verma S, Srivatava K. “Effect of ginger and fenugreek on blood lipids, blood sugar and platelet aggregation in patients with coronary artery disease.” Prostaglandins Leukot Essent Fatty Acids 1997; 56(5):379-384.
3. Dietetics, 7th Multicolour Edition, B. Srilakshmi, New Age International Publishers, pp-257-2864. Ferrari Roberto, Sharpe Norman et al., “Cardiac remodelling- Concepts and clinical Implications:
A Consensus Paper From an International Forum on Cardiac remodelling”, Journal of the American College of Cardiology :2000-35(3): 569-582
5. Fuhrman B, Rosenblat M, Hayek T, et al. “Ginger extract consumption reduces plasma cholesterol, inhibits LDL oxidation and attenuates development of atherosclerosis in atherosclerotic, apolipoprotein E deficient mice.” Journal of Nutrition 2000; 130 (5):1124-1131.
6. http://www.diabetes-guide.org/glycaemic index of common foods (Copyright 2011 by T McDonald)7. Kaixun Huang, Huibi Xu ,” Selenoproteins and Atherosclerosis”, Selenoproteins and Mimics
Advanced Topics in Science and Technology in China 2012, pp 141-160. 8. Kurowska Elizabeth, Spence David, et. al, “ HDL- Cholesterol- raising effect of orange juice in
subjects with hypercholesterolemia”, American Journal of Clinical Nutrition, 2000; 72: 1095-1100.9. Latif R, “Chocolate/Cocoa and human health: a review”, Netherlands Journal of Medicine; 2013:
71(2); 63-6810. Lumb A. “Effect of dried ginger on human platelet function.” Thrombosis Haemostastis
1994;71(1):110-11111. Orekhov N Alexander, “ Anti-Atherosclerotic Drugs from Natural products”, Natural products
Chemistry Research, 2013, (1-4)12. Prabhakaran Dorairaj & Yusuf Salim, “Cardiovascular disease in India: Lessons learnt &
challenges ahead”, Indian journal of Medical Research, 2010, (529-530)13. Puri Nidhi, Gupta Kumar Prem, Sharma Jaishree, Puri Deepak, “Prevalence of atherosclerosis in
coronary artery and internal thoracic artery and its co-relation to North- West Indians”, Indian Association of Cardiovascular-Thoracic Surgeon, 2010; 26: 243-246.
JOU
RN
AL
RE
FER
EN
CE
S
14. Shoji N, Iwasa A, Takemoto T, et al. “Cardiotonic principles of ginger.” Journal of Pharmaceutical Sciences 1982; 71 (10):1174-1175.
15. Srinivasan K. Black pepper and its pungent principle - piperine, a review of diverse physiological effects. Critics Review for Food Science and Nutrition 2007; 47: 735–748.
16. Sung Heungsup, Min Won-Ki, et. al. , “The effect of green tea ingestion over four weeks on atherosclerotic markers”, Association of Clinical Biochemists 2005; 42: 292-297
17. Synopsis of Causation: Atherosclerosis, Ministry of Defence , Dr Rajeev Srivastava, Ninewells Hospital and Medical School, Dundee , Professor Richard Sutton, Chelsea and Westminster Hospitals, London September 2008.
18. Textbook of Medical Physiology, 11th edition, Guyton & Hall, Elseveir Publications, pp- 848-85119. Thomson M, Al Qattan K, Al Sawan S, et al. “The use of ginger as a potential anti-inflammatory and
antithrombotic agent.” Prostaglandins Leukot Essential Fatty Acids 2002; 67(6):475-478.20. Verma S, Singh J, Khamesra R, et al. “Effect of ginger on platelet aggregation in man.” Indian
Journal of Medical Research 1993; 98:240-242.21. Zavoshy Rosa, Noroozi Mostafa, Jahanihashemi Hassan, “ Effect of low calorie diet with rice ran oil
on cardiovascular risk factors in hyperlipidemic patients”, Journal of Medical Sciences, 2012; 626-631
JOU
RN
AL
RE
FER
EN
CE
S
