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ISCHEMIC CARDIAC DISEASE

The most frequent cause of invalidity and


cardiovascular mortality

With a global report 4:1 of men versus women,


although for those under 40 years old the report is
8:1(hormonal protection of women), and after 70
years old is 1:1.

The maximum incidence of clinical manifestations


in men is at the age of 50-60 years, and in women at
60-70 years.
DEFINITION
the result of an imbalance between oxygen
demands and oxygen supply to myocardium
because of some coronary circulation disorders

It can result in ANGINA PECTORIS strokes or


in some major emergencies such as
MYOCARDIAL INFARCTION or
SUDDEN DEATH
The etiopathology of ischemic
cardiopathy :
1. Coronary factors: 2. Extracoronary factors:

- coronary ASC 95% - an increase of myocardial


- coronary arteries energetic needs
abnormalities - hyperthyroidism
- coronary embolisms(AF-atrial - heart rhythm disorders
fibrillation) - febrile conditions
- vasculitis - HTA
- Thromboses - diminution of coronary flow
- Disorders of small coronaries - mitral stenosis
(DM,hypertrophic
cardiomiopathy, coronary - aortic deficiency
spasm Prinzmetal angina - HTP
and coronary sdr X)
The etiopathology of ischemic cardiopathy :
Cardiac pain (angina) is the last modification
produced by the ischemic cascade, that's why
there can be many cases of silent ischemia which
can advance, without precordial pains, to sudden
cardiac events such as myocardial infarction or
sudden death.
Over 95% cases IC is provoked by the coronary
atherosclerosis, its evolution is the same with the
evolution of the atherosclerosis process which
begins in childhood with lipid striae and evolves
gradually to some atheroma plaques:
LDL has an atherogenic role, HDL has an
antiatherogenic role, taking the free cholesterol
and carrying it to the liver where it will be
metabolized, and reducing the LDL oxidation and
its toxicity
Risk factors of coronary
desease
positive family antecedents :
(genetic factors)
age
male
dyslipidemia : total cholesterol rise associated with LDL
cholesterol increase and HDL cholesterol decrease,
represent the main factor of the coronary ischemic
disease
AHT and pulse pressure (> 66 mmHg)
obesity
diabetes mellitus: doubles the risk of coronaropathy.
sedentariness
smoking
excessive use of alcohol
chronic infections
Rise of serum homocistein and hypoestrogenemia
levels in women
CLASSIFICATION
Classification of ischemic cardiopathy
depending on pain:

A. Painful ischemic B. Painless ischemic


cardiopathy cardiopathy
Stable pectoral angina Sudden coronary
death
Unstable pectoral Ischemic rhythm
angina disorders
Ischemic cardiac
Acute myocardial deficiency
infarction accidental EKG
detection
CLASSIFICATION
Classification of ischemic cardiopathy
according to the International Society of
Cardiology
A. Primary cardiac stop
B. Angina pectoris
- at effort
- at novo
- aggravated
- stable
- sudden
C. Myocardiac infraction
- acute MI
- old MI
D. Ischemic cardiac deficiency
E. Ischemic cardiac arrhythmias
CLASSIFICATION
Classification of angina severity according
to the Canadian Cardiovascular Society
CLASS I: Usual activity doesn't cause angina
angina only during strenuous or prolonged
physical activity
CLASS II: Slight limitation of common activity
with angina only during walking or climbing
stairs, heal, postprandial physical effort, in the
cold, under emotional stress or just in the
morning
CLASS III: Marked limitation of ordinary
activities- angina during walking on a 100-200 m
flat field or climbing stairs one floor with a normal
rhythm, under normal circumstances
CLASS IV: Inability to perform any activity
without angina or angina at rest
CLINICAL MANIFESTATIONS
SIGNS AND SYMPTOMS
Pain pectoris is the specific clinical
manifestation of IC;
Appears after physical effort, stress, rich
alimentation or after exposure to cold
(triggering factors);
It is localised retrosternal, irradiates on
shoulder, from the inner part of the forearm,
to the last two fingers of the left hand;
CI pain has a constrictive character, of claw,
retrosternal pressure.
CLINICAL MANIFESTATIONS
SIGNS AND SYMPTOMS

The pain of angina pectoris usually disappear


when the effort stops or when coronarodilating
agents (nitrates) are administrated

The pain of myocardial infarction is usually more


intense, lasts over 20-30 minutes , doesn't stop
neither when the effort stop, nor when nitrates
are administrated and is usually accompanied by
nervous symptoms psychomotor nervousness,
pallor, cold sweats ,variations of arterial tension
cardiac rhythm disorders.

Other manifestations: cardiac rhythm disorders,


signs of cardiac deficiency
INVESTIGATIONS

Laboratory
EKG at rest and at effort
Pulmonary Rx
Echocardiography
Coronaroangiography
INVESTIGATIONS
Laboratory investigations

Complete haemoleucograme
Creatinine
Glycaemia a jeun
Lipidic profile (Cholesterol, HDL, LDL,
Triglyceride)
PCR
Homocistein
EKG
INVESTIGATIONS
BETWEEN CRISIS DURING CRISIS
ST subdenivelation
( subendocardiac
lesions) Normal aspect in 1/3
Normal aspect in over cases
1/3 cases ST subdenivelation
Negative T wave Negative or Flat T
( subepicardiac wave negative
lesions) Intraventricular
HighT wave (idem) blocks
QT lengthening
EKG at
effort
The Possibility of diagnosis in
primary medicine.
Anamnesis
EKG signs of ischemia ; EKG at rest ; EKG at effort
( EKG manifestations)
Laboratory investigations (CK si CKMB detemination
excludes the possibility of an AMI)
sudden reduction of arterial pressure during the effort
test denotes a severe ischemia
Associated diseases
Risk factors
Precocious diagnosis of ischemic cardiopathy
TREATMENT
1. Unpharmacological treatment: identifying and controlling risk
factors
2. Pharmacological treatment
a). Acute attack - medium - sublingual nitoglycerine or
spray
- severe - nitroglycerine i.v.
b). chronic -among the prolonged prophylactic medicines
reccomended in angina pectoris are indicated :
1.Betablokers (propanolol, athenol, metroprolol);
2.Nitrates (nitroglycerine, isosorbide dinitrate);
3.Calcium channels blockers.
4.Reducing the atherosclerosis process:
- hipolipemiante medication- statins,
fenofibrats
- metabolic trimetazidina
- antiagregants - aspirin , clopidogrel)
- antioxidants
MEDICINES USED IN THE CHRONIC
TREATMENT OF ANGINA PECTORIS
GROUP ACTIVE COMERCIAL DOSE
SUBSTANCE NAME
NITRATES Nitroglycerine- Nitroretard 6,25 mg 2-3x/
retard Pentacard 20 mg 2x /d
Isosorbid Maycor, Isodinit 20 mg 2 x / d
mononitrate Nitropector 20 mg 2 x / d
Isosorbid dinitrate
Pentaerithrityl Inderal 20 mg 2-3 x /d
Tetranitrate
BETA- Propanolol
Propanolol Inderal 20 mg 3-4/d
BLOCKERS Metroprolol Betaloc zok 50 mg 2 x /d
Bisoprolol Concor 5 mg 2 x/d
Atenolol Atenolol 50-100mg 1x/d
Betaxolol Lokren 20 mg 1x/d
Carvedilol Dilatrend 12,5-25 mg
2x/d
DRUGS USED IN CHRONIC TREATMENT OF
ANGINA PECTORIS

GROUP ACTIVE COMERCIAL DOSE


SUBSTANCE NAME
CALCIUM Nifedipine Corinfar 20 mg 3x/day
CHANNELS Amlodipine Tenox 5 mg x2/day
BLOCKERS Felodipine Plendil 5 mg 1x/day
Verapamil Cardamil 40-80 mg 4x/d
Diltiazem Diacord 30-60 mg 4x/d

METABOLIC Trimetazidine Preductal 20 mg 3x/day


SELECTIVE Ivrabadine Corlentor 7.5 mg x2/d
INHIBITOR AL
It
ANTIAGGREGA Aspirin Aspirina 75-150 mg/d
NTS Ticlopidine Ticlid 250 mg 2x/d
clopidogrel Plavix 75 mg 1x/d
SPECIFICATIONS-ASSOCIATIONS

the most frequently used association is the


one between nitrates and beta-
blockers (for example nitrates + long-
acting beta-blockers- atenolol, metropolol);
-other association : nitrates + calcium
blockers;
-or beta-blockers+calcium blockers.
In addition antiagregant medication
hipolipemiant medication
The surgical treatment of angina
pectoris

1). Percutan coronaries angioplasty (PTCA), with


ballon is indicated for patients with only one
affected vessel.

2). Stentation

3). coronary bypass graft (CABG) represents


the treatment chosen for the complex
coronaropathy (3 or more affected vessels)
The treatment of asymptomatic
ischemia
It must be individualized depending on the
following:
a) the positivity degree of effort testing;
b) The age, the job, the general medical condition;
The execution of coronary angioplasty associated
with coronary bypass is recommended to these
patients (it is recommended to patients with
severe ischemia, previously evaluated with non-
invasive methods);
The general measures of treatment include beta-
blockers and aspirin
The management of coronary
patient

education
Treatment aspects
Periodic evaluation aspects
complications- approach
The determination of associated clinical
conditions - associated diseases dyslipidemia,
diabetes, obesity, arteriopathies, AHT
The patients cardiovascular risk factors
determination :
The modification of the way of living
The fully qualified medical officers
attitude towards a patient with angina
pectoris
1.The patients information about the main risk factors for
angina pectoris
2. Modifying the way of living and the patients instruction
for his own disease nursing.
3. The determination of a chronic treatment for the angina
together with the specialized doctor.
4. The monitorisation of the compliance to the treatment
and of its efficiency through periodical examinations and
investigations.
5. The recommendations for patients with unstable angina
or for non responsive patients concerning the importance of
the invasive investigations for the surgical treatment
opportunity appreciation.
6. The cooperation with specialists both in the evaluation
stage of the diagnosis and of the treatment and the future
appreciation of the evolution under treatment.
DYSLIPIDEMIA
Dyslipidemia has no symptom but it
is a very important risk factor for the
systematic vascular disease and
especially for coronation and for
cerebral circulation
It represents the total cholesterol
increase (TC) associated with the LDL
increase and the HDL decrease (and
the VLDL increase)
TC represents the sum of the seric
lipoprotein fraction (LDL, HDL, VLDL)
NORMAL VALUES
TC= LDL+HDL+VLDL
VLDL= TGL/5
TC<190 mg/dl and LDL< 115 mg/dl
CT<175 mg/dl and LDL< 100 mg/dl for
diabetical patients or patients with
manifest cardiovascular disease
HDL>40 mg/dl for men
HDL>46 mg/dl for women
TGL<150 mg/dl
The risk factors for coronary disease
include according to their
importation:
1.An LDL increase
2.A HDL decrease
3.A TC increase
4.A TGL increase (the studies proved
that a higher level of the TGL
announces the appearance of the
diabetes long time before)
THE DYSLIPIDEMIA CAUSES

Dyslipidemia can be primary or genetically


secondary:
- obesity, sedentariness
- DM
- alcohol consumption
- Hipotiroidism
- CRD
- Oral contraceptives
- Diuretics
- Beta-blocker
LIST OF FOODS HIGH IN CHOLESTEROL
CONTENT
Pork
Lard
Salami and sausages
Butter, margarine, sour cream, cream
Eggs
Ewe-cheese
Pig liver, brains
Nuts, hazelnut, pistachio nut
Chocolate, concentrated sweets
Treatment
It has as objective the TC, LDL, TGL
level reduction and the HDL increase
but also the other risk factors
elimination (smoking, the excessive
alcohol consumption, HTA, obesity)
1. The dietetic treatment- diet
indication(6 months) but also the
modification of the way of living
2. Medicines treatment
MEDCINES TREATMENT

1. HMG Co-A Reductase Inhibitors (the enzyme


that intervenes in the cholesterol synthesis in
liver) STATINS
- decrease LDL with 25-60%
-stabilize the aterom plate
-has a less influence on the HDL and the TGL
- monitorize transaminases and CK
a) Simvastatinum ( Simvacard, Simvor, Vasilip, Zeplan,
Zocor)
b) Lovastatinum (Lovastatin, Medostatin)
c) Pravastatinum (Pravator, Lipostat)
d) Fluvastatinum (Lescol)
e) Atorvastatinum (Sortis)
f) Rosuvastatinum ( Crestor)
MEDCINE TREATMENT
2. Fibrations
decrease TGL and increase HDL

- influence less TC and LDL


a) Bezafibratum (Regardin)
b) Fenofibratum ( Lipanthyl 160 mg, Lipofib)
3. Nicotinic acid and derivatives
a) Acipimoxum (Olbetam)
b) Acidum nicotinicum (Niaspan- from the B group)
- decrease TGL, less LD
4. Other hipolipemiants
a) Omega 3 acid (Omacor)
b) Ezetimibum (Ezetrol)
The fully qualified medical
officers attitude
1. the periodical determination of the TC for
middle age men, for women after the
menopause and for old persons.
2. recommendations about the modification
of the way of living
3. the adjacent risk factors control
4. diet indications
5. the drug treatment initiation
6. the monitorisation of the adverse effect
on liver and on muscles
7. prophylactic treatment with aspirin
God didnt destroyed the death for
my sake and I consider this as being
inadmisible.

Eugen Ionescu Testament -


Figaro Litteraire Paris

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