dacsx

1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
CORONARY
ATHEROSCLEROSIS
STUDENTS
William Cruz
Kevin Herrera
Jorge Pacheco
Angie Chamba
Sonia Quijilema
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018

2. CORONARY ATHEROSCLEROSIS
DEFINITION
Artery disease that affects the intimal layer of the medium and large caliber arteries, is
characterized by the accumulation of lipid material, and cellular elements, especially
macrophages and smooth muscle cells (CML) in the inner layer of the arteries.
PATHOPHYSIOLOGICAL BASES.
a) Lipoproteins.- Certain irrigation factors, such as hypertension or
hypercholesterolemia, favor the penetration and retention of LDL in the intima.
The aggregated LDL is captured by CML and macrophages, whereas the oxidized
LDL is captured mainly by macrophages that are converted to foam cells.
b) Endothelial dysfunction.- This can produce increased permeability, which
facilitates the accumulation of LDL in the intima; an overproduction of adhesion
molecules and chemotactic substances, which facilitates the binding and
migration of monocytes, and a disturbance of the balance between vasoactive
agents or between their pro- and anti-thrombogenic functions, with the consequent
increase in platelet adhesion.

3. c) Accumulation of monocytes and T-lymphocytes: The first cellular episode
morphologically detectable in atherogenesis, after infiltration by lipids, is the
focal adhesion of circulating monocytes to the endothelium and its migration to
the intima.
Macrophages possess the ability to phagocytose and eliminate harmful
substances, particularly LDLm. The uptake of these LDLm is produced by the
scavenger receptors.
Macrophages, T lymphocytes and immunomodulation are attributed an active role
in the processes that contribute to the progression and rupture of atherosclerotic
plaques. These cells weaken the fibrous capsule of the plaques because they
secrete factors that inhibit the synthesis of proteins. of matrix, such as IFN-γ
produced by T lymphocytes, and enzymes that actively degrade connective tissue,
such as metalloproteinases (interstitial collagenase, gelatinases, stromelysin)
produced by macrophages.
d) Smooth muscle cells in the atherosclerotic lesion: The CML constitute the
major cellular component of the atherosclerotic lesions in development and of the
restenosed plaques after revascularization.
e) Thrombotic complication.- The formation of coronary thrombi, frequently
secondary to the rupture and erosion of atherosclerotic plaques, plays a
fundamental role in the development of acute coronary syndromes.
RISK FACTOR'S
 Vascular risk factors.- Vascular risk factors and concomitant diseases
(vasculocerebral stroke, ischemic heart disease, renal failure or peripheral
vascular disease) represent the first challenge of Western medicine, ahead of
cancer, infections and traffic accidents.
 Coronary risk factors.- The factors are divided into non-modifiable (sex, age,
family history, menopause) and modifiable (hypercholesterolemia, dyslipidemia,
hypertension, smoking, diabetes, obesity, psychosocial factors and alcoholism,
among others).

4.  Main risk factors.- According to the JNC VII report are the following: HBP,
smoking, obesity (BMI equal to or greater than 30) (BMI: weight in kg / height in
m2), physical inactivity, dyslipidemia, DM, microalbuminuria, filtering
glomerular tumor less than 60 mL / min and age (more than 55 years in men and
65 in women) and a family history of premature cardiovascular disease (men
under 55 years of age and women under 65 years of age).
SECONDARY PREVENTION.
 Concept.- Secondary prevention refers to the set of measures aimed at reducing
mortality and the risk of new clinical episodes in patients who have already
suffered coronary heart disease.
 Modification of lifestyle.- The caloric intake of the diet should be adequate to
avoid overweight.
It is essential to reduce the caloric intake of saturated fats (less than 10% or even
7% of total calories), limit the intake of polyunsaturated fats (up to 10% of total
calories) and, on the other hand, give preference to the monounsaturated ones (that
must contribute 15% or 20% of the total calories).
Dietary cholesterol should be reduced to less than 300 mg / day and even to less
than 200 mg / day.
The recommendation to avoid smoking is even more important than in primary
prevention, since the risk of death or a new infarction is reduced by 50% after one
year for those who stop smoking.
CONTROL OF CARDIOVASCULAR RISK FACTORS.
 LDL-cholesterol.- The latest revision of the National Cholesterol Education
Program (NCEP) regarding the treatment of hypercholesterolemia in adults
establishes less than 100 mg / dL (2.6 mmol / L) the desirable concentration of
LDL cholesterol.
 HDL-cholesterol.- Low HDL-cholesterol (less than 40 mg / dL, 1 mmol / L) is a
risk of new coronary episodes and should, therefore, be the subject of attention.

5.  Hypertriglyceridemia.- If the concentration of triglycerides reaches figures
between 200 and 499, the non-HDL cholesterol (total cholesterol-HDL
cholesterol) should be at concentrations lower than 130 mg / dL and even try to
reduce it to less than 100mg / dL. In the case of a triglyceride figure equal to or
higher than 500 mg / dL, the objective is to try to reduce these figures first with
fibrates and then lower the LDL-cholesterol to the indicated targets.
 Diabetes mellitus.- HbA1c must be maintained below 7%, but intense decreases
(6-6.5 increase the incidence of side effects).
 Obesity.- Frequently, obesity is associated with coronary disease and can also
coexist with accompanying risk factors.
 Hypertension.- The current recommendation is to reduce PA in coronary patients
to figures below 140/90 mm Hg and close to 130/80 mm Hg, since lower values
do not seem to provide a greater benefit and could even be dangerous.
PHARMACOTHERAPY
 Beta-blockers.- All beta-blockers, except those with intrinsic sympathomimetic
action, provide cardiovascular protection.
 Platelet antiaggregants.- Acetylsalicylic acid, clopidogrel.
 Anticoagulants.- In the case of patients with a history of systemic embolism, with
atrial fibrillation, ventricular aneurysm, extensive area of dyskinetic or
hypokinetic myocardium.
 Inhibition of the renin-angiotensin-aldosterone system.- These drugs reduce
mortality, probably by decreasing the proliferation of vascular smooth muscle
cells and left ventricular hypertrophy, improving endothelial function and
protecting the atheromatous plaque from rupture.
 Nitrates.- It does not seem that nitrates, administered orally or transdermally,
decrease the mortality of patients with infarction, for which reason their use is not
well-founded in a generalized way.
 Calcioantagonistas.- The reduction in mortality and reinfarction that verapamil
and diltiazem can provide in myocardial infarction without Q wave; they can be
used in case beta-blockers are contraindicated.

6.  Antiarrhythmics. The beneficial effect is due in part to its antiarrhythmic
properties, since supraventricular and ventricular arrhythmias are frequent in
ischemic heart disease. You can use amiodarone.
 Hormone replacement.- During the last years, the administration of estrogens in
postmenopausal women has been studied throughout different trials, but for now
there is the impression that there is no benefit and that even cardiovascular
episodes increased during the first 2 years.
BIBLIOGRAPHY
 Badimon.I, Marrugat.J, Gil.B, Cía.P. "Coronary atherosclerosis". In Farreas.V;
Rozman.C. Internal medicine, 18th edition, Barcelona: Elsevier, 2016 .p.464-47.