Pathology of coronary artery disease (coronary failure)

2021-01-28 12:00 AM

Coronary currents typically max out diastolic periods. Because the ability to dilate the endocardial blood vessels is very weak, so when there is a decrease in coronary flow, perfusion occurs mainly in the endothelium.

Outline

Coronary artery disease is a very common disease among heart diseases in developed countries. Usually, the pathogenesis of coronary failure is due to deposition of fat in the lower endothelium of the coronary arteries. Progressive atherosclerosis gradually forms blood clots, causing embolism in the lumen. The main complications of coronary artery disease are angina, myocardial infarction, and sudden death.

Epidemiology of coronary artery disease: includes angina and myocardial infarction in approximately 6% of men> 50 years of age. In Europe every year about 0.3-0.6% more people get sick. In terms of death rate, each year, it accounts for about 120-250 deaths per 100,000 people in industrialized countries. This rate increases with the age: 800 - 1000 deaths / 100,000 deaths in the age group 65 - 74 for men, 300 / 100,000 for women of the same age (Vademecum clinique 1988).

In Vietnam, there is no universal population statistics, but statistics at major hospitals show that most patients with coronary artery disease are at the age of 50 and older. In 1996, in Hanoi City, there were about 200 coronary heart disease patients hospitalized, while in Ho Chi Minh City there were about 400 patients.

Reason

Coronary artery disease: is the main cause.

Most of it is due to coronary atherosclerosis.

Not caused by atherosclerosis: Coronary constriction, vasculitis (inflammation of multiple nodules, lupus erythematosus, congenital abnormality)

Heart valve disease: Aortic valve disease: stenosis, aortic valve, syphilis.

Hypertrophic cardiomyopathy: Two groups of causes can later cause functional coronary failure in which the coronary artery is not narrow.

Mechanism of pathogenesis

Cardiomyopathy and oxygen

Myocardial oxygen consumption: depends on:

Heart rate frequency.

Myocardial contractility (inotropism).

Tension in the heart wall.

This tension is dependent on the intraventricular pressure and ventricular volume.

An increase in one of the above factors will increase myocardial oxygen consumption. In other words, this consumption is proportional to:

Heart rate x systolic artery pressure.

Or heart rate x systolic artery pressure x ejection time.

Reserve rim

Reserve coronaries (Reserve coronaries): Reserve coronary is done by taking oxygen of the heart muscle, almost maximally in the ground state. The rim flow reserve is capable of increasing to 300 - 400% of the base value. Adaptation and increase in oxygen demand are often accompanied by a parallel increase in coronary flow. Coronary flow depends on: perfusion pressure and coronary resistance due to sub-pericardial vasodilation.

The flux coronaries usually maximize the diastolic period. Because the ability to dilate the endocardial blood vessels is very weak, so when there is a decrease in coronary flow, perfusion occurs mainly in the endothelium.

The vasomotor capacity of the coronary arteries

Vascular spasm factor:

Health systolic squeeze: Q is also important for the left ventricle than right ventricle.

The muscle bridge passes through an endocardial coronary artery.

Alpha-receptor stimulation, noradrenaline-mediated dose of beta-receptor inhibition with Dopamine above 15mg / kg / ph, cold test, angiosperm derivatives - thromboxane A2 - prostaglandin F - Neuropeptide Y.

Factors between Denmark:

Metabolites due to TMCT: A denoside, lactate, H + ions, CO2, bradykinin.

Alpha-receptor blockers - beta-receptor stimulation with dopamine doses less than 5mg / kg / ph - sympathomimetic receptors that stimulate the parasympathomimetic mediated by acetylcholine, inhibitors of calcium, nitrite derivatives - prostacyclin - prostaglandin E, EDRF (endothelial factor) - VIP (dilated intestinal peptide: vasodilatation intestinal peptide) substance P.

Myocardial anaemia (TMCT):

Occurs when there is an imbalance between oxygen supply and myocardial oxygen demand.

Mechanism:

Increased oxygen demand (secondary anaemia) during exercise an increase in myocardial oxygen consumption is achieved through an increase in heart rate, systolic BP, and myocardial contractility. In the case of stenosis of a significant coronary artery that means over 70% of coronary artery diameter, coronary flow cannot increase adaptively and in parallel with the increase in oxygen demand should lead to CT.

A sudden decrease in coronary flow (primary anaemia) corresponds to coronary constriction without vascular damage, however, can also occur in a previously narrowed coronary artery.

Angina occurs when the heart muscle's oxygen demand exceeds the capacity of the coronary system to supply. Pain is a direct manifestation of myocardial ischaemia and accumulation of metabolites due to lack of oxygen. Once the ischemic heart muscle pH decreases in the coronary sinuses, loss of cellular potassium, increases in lactate production, the appearance of ECG abnormalities, deterioration of ventricular function. Factors that determine myocardial oxygen consumption are heart rate, myocardial contractility, and systolic pressure. An increase in one or more of the above factors plus decreased coronary blood flow will create angina.

Consequences of TMCT:

Metabolism: lactate secretion.

Hemodynamic: disturbed relaxation, decreased ventricular elasticity and subsequently decreased contractility.

About ECG: repolarization disorder appears.

Clinically: the appearance of angina.

Pathology

One or more coronary arteries are narrowed by plaque. There are areas of necrosis and fibrosis in the myocardium, usually localized in the lower endocardium. The left ventricle may be enlarged.

Symptom

Mechanical symptoms

Angina pain with the following characteristics:

Location: Behind the sternum.

Direction: Down face in left finger arm, however, it can spread to shoulder to back, to jaw, teeth, up to the neck.

Painful nature: Maybe vague as if something is blocking the chest, spasm, or as if something is pressing on the chest. Whether or not the person feels pain. Note that patients who describe the exact pain point in the heart, transient hot throbbing pain is usually not angina due to coronary failure.

Duration: Pain is short and lasts no more than a few minutes.

The pain usually begins after exertion, decreases and goes away with rest or with a coronary dilator. Cold is also a trigger for pain.

Physical symptoms

During an attack, there may be nothing but there may be an increase in heart rate and blood pressure values, the hearing may be mid and end-systolic blowing due to papillary muscle dysfunction due to ischemia.

ECG symptoms:

It is most useful to record in chest pain by allowing changes to occur in coronary failure: ST depression is typical, in addition, ST elevation is sometimes seen, arrhythmias especially ventricular extrasystole. . Out of attack when the patient is at rest, the ECG is normal in 30% of patients with typical angina.

Diagnose

Implementing the quadrants

Clinical diagnosis: Based on the characteristic chest pain as described above that occurs with exertion and subsides after rest. The diagnosis can be confirmed by ECG monitoring showing reversibility of ischemic changes or by using a test therapy with sublingual nitro-glycerine that the pain disappears within 1.5-3 minutes. Failure to see a rapid analgesic response can rule out a suspicion of angina (ie not angina due to coronary failure or vice versa, the most severe form of coronary failure, myocardial infarction).

Subclinical diagnosis:

EKG heart: Helps early diagnosis, prognosis and treatment monitoring.

Technique: Use a dynamometer or a roller mat, incrementally increments every 30 watts for a bike or use a Bruce chart for a rolling mat. A specialist is required to continuously monitor the ECG and BP during the procedure. Method sensitivity: 60% and 80% specificity in coronary detection. Mortality rate is less than 0.01%.

Point:

Diagnose stable angina or atypical chest pain.

Bilan in young people is more at risk of bilan with stable coronary artery disease with or without treatment.

Evaluate the effectiveness of CT treatment:

Evaluate the results of coronary artery surgery or after coronary artery, bilan after myocardial infarction on days 10-15.

Functional assessment of some heart valve diseases (except aortic stenosis).

Evaluate the function of compensated heart failure.

Criteria: Based on many factors such as: ST depression and horizontal depression over 1mm or down above 0.08 mm after the QRS complex; ST elevation (rare); time exertion; maximum work achieved; typical diabetes attack occurs; The ECG changes during or after the exercise test; blood pressure and heart rate; theoretical heart rate attainment level; Arrhythmia appeared on the test and/or sign of left heart failure.

The stress test results are associated with the age and sex of the patient (difficult to conclude in women <55 years old, false positives> 20% in people <40 years old while decreasing to <10% in people> 60 years)

Holter ECG in 24 hours: Helps diagnose silent coronary disease, diagnose and monitor Prinz metal’s EKG attack, or increase ventricular stimulation.

Radioisotope:

Principle: Investigation of regional myocardial perfusion by comparing the distribution of radioactive isotope Thallium 201 into the myocardium during exercise and after a period of reperfusion at rest.

Benefits and drawbacks: More sensitive than stress test (80%), more specific (90%) allows identifying anaemic areas, assessing myocardial function. Limit of method: false positive if left branch block, high cost.

Radiography of ventricular chamber: Intravenous injection of Technium. It is possible to evaluate individual and total left ventricular contraction as well as left heart function.

Echocardiography and Doppler :

2-way ultrasound:

Analysis of partial activity such as contractility reduction, non-contractility, even local contractile disorders, cardiac abnormalities in the common body of the coronary arteries such as calcification.

Calculate the index of left ventricular contraction to assess total left ventricular function.

With Doppler helps diagnose mitral regurgitation due to myocardial ischemia, pulmonary vascular pressure. Variations in the ventricular filling, assessment of arterial flow during exercise and rest.

Effort echocardiography is diagnosed through visual disturbance of cardiac wall movement for a diagnostic sensitivity of> 90% if the imaging is good.

Angiography: Contrast pump to scan the entire coronary and ventricular system. For the coronary system worth assessing the degree, location of coronary damage as well as perfusion status, vascular distribution and calcification, congenital abnormalities, for the ventricular chamber to analyse the contraction. partial squeeze, left ventricular function, ejection index and mitral regurgitation due to myocardial anaemia. Coronary angiography is the decisive tool used to assess the severity of coronary artery disease as well as for diagnosis when other probes do not allow the determination of coronary failure. It can be said that coronary angiography is an indispensable test for coronary artery disease, especially when it is necessary to have a surgical intervention, but this is an expensive technique and requires specialists.

Myocardial flicker with Thallium 201 or Technetium 99m: Sensitivity 70-90% and specificity 60-90% but expensive.

Differential diagnosis

Pre-cardiac pain due to neurobiological disorders: Is common in practice especially in the young. Pain is usually in the apex of the heart, not exertion but resting. The pain can last for hours every day. In addition, other symptoms of plant neurological disorders may also be included.

Pain caused by spinal - rib disease: Arthritis, intercostal neuritis. Examination of local pain, pain does not spread.

Pain caused by gastrointestinal disease:

Pain caused by spasm of the oesophagus is also behind the sternum, accompanied by difficulty swallowing, belching. Sometimes it spreads to the arms and also lessens after taking nitro-glycerine. Taking cine of the oesophagus allows for an accurate diagnosis.

Gastroesophageal reflux syndrome: Causes hot feeling behind the sternum, worsens when lying on your back, eases after using antacids.

Clinical manifestations of angina

Stable angina

Pain occurs associated with exertion.

Unstable angina

New onset of severe angina (<2 months) and / or attacks = 3 attacks / day.

Pain at rest or only with very mild activity.

Progressive angina: stable but more recently, more persistent, more common and occurs with milder exertion.

Patients with one of the three criteria above are referred to as having unstable angina (Harríson 2005).

Coronary constriction

Also known as Prinz metal’s angina. Occurs on a completely normal coronary artery or is a narrowing of atheroma near the site of the spasm. Angina is similar but more severe and typically occurs at rest with a very high elevation of ST-segment on the ECG. Note that coronary spasm can cause a heart attack as well as malignant arrhythmias. Diagnosis is confirmed based on IV coronary angiography with IV injection of Methergine (ergonovine).

Silent myocardial ischemia

Detected by Holter recording or exercise ECG test mainly occurs in people with symptomatic myocardial ischemia. ST-T change is noted but asymptomatic despite coronary artery disease.

Heart attack

Occurs when one or more branches of a coronary artery are blocked. Myocardial infarction (MI) is severe ischemic necrosis and the myocardial system with a damaged charge equal to or greater than 2 cm2.

Clinical symptoms: Chest pain is similar to angina but is much more intense and lasts longer (> 30 minutes), less remission at rest and after nitro-glycerine. However, 25% of myocardial infarction is clinically silent.

Subclinical symptoms:

ECG:

Infarction has Q: ST wave elevation, T inversion, Q wave necrosis.

Infarction without Q wave: ST depression, persistent ST-T variation without Q wave appearance.

Men: Increase CPK, CPK-MB, GOT, LDH, Troponin T.

Diagnosis:

According to the World Health Organization, MI is diagnosed when there are two of the following three signs: variable angina, ECG changes according to the progression of the disease and the increase in cardiac enzymes.

In some cases, it is not possible to definitively diagnose MI, but only can say that there may be MI. Often there is a very suggestive typical clinical symptom, but lack of objective evidence on ECGs and enzymes. If clinical suspicion is much, it may be small MI. Before a patient, a man> 35 years old, a woman> 50 years old, has chest pain, it is necessary to consider investigating whether an MI or not. Must be differentially diagnosed with pneumonia pain, pulmonary artery obstruction, pericarditis, rib fracture, oesophageal spasm, aortic aneurysm, and situations that cause acute abdominal pain due to intra-lumen disease stomach.

Symptoms:

Arrhythmia: extrasystole, ventricular fibrillation, ventricular tachycardia, atrioventricular block ...

HF: C ó stunned or not.

Cardiac bulging.

Treatment

The principles of treatment

Improved risk factors:

This is a top measure of value because it is inexpensive, applicable to the rich/poor but requires the determination and cooperation of the patient. Specifically, living hygiene and diet to lose fat, exercise walking, swimming, cycling, avoiding stress, monitoring, examining, regular lipid testing, daily stress test. year.

Treatment of the aetiology:

If you know it. Although it has the ability to improve clearly, it only applies to individuals and units with high economic conditions. Examples: treatment of atherosclerosis with lipolytic, surgical treatment for congenital or acquired heart valve damage.

Specific treatment

Internally medical treatment:

With drugs such as: nitrés derivatives, molsidomine, beta-blockers, calcium inhibitors, other molecules, maleate de perhexiline (Pexid), anti-agglutination.

Percutaneous coronary angioplasty (Angioplasties coronaries transluminal percutanée) (PTCA)

Using a catheter inserted into the percutaneous coronary artery to determine the degree of coronary stenosis, then using a small balloon, 2-4 mm in diameter pumped up in the narrow position, see results when shallow. 50% of the previous aperture, the success rate usually reaches 90-95% in the first stage.

Pontage aorto-coronaire (Pontage aorto-coronaire).

The method is performed by transplanting the internally visible vein and especially the inner breast artery into the damaged coronary artery. Surgical mortality is about 1-4%, this method has improved the outlook and symptoms of myocardial infarction.

Specific treatment of exertion angina pain

Treatment of relieving exertional angina:

Should be applied immediately before admission and applied as soon as possible will work to prevent worse complications from occurring.

Rest, avoid exertion.

Using sublingual Nitrés derivatives (Natirose 0.75mg tablets) can be repeated after 5 minutes or repeated 0.4mg Natispray after 5 minutes if necessary, if not reduced after 15 minutes need to question whether unstable angina or myocardial infarction.

Long-term treatment of exertional angina:

Types of beta-blockers:

Unless there are contraindications, this drug is the treatment of choice for exertion angina, effective treatment when the resting heart rate is between 50-60 / min and during exercise less than 100 / min. Start with a low dose, gradually increase the dose in the absence of complications. Specifically:

Propranolol (Avlocardyl 40mg tablet) is non-selective, has no intrinsic sympathomimetic activity, a dose of 2-4 tablets divided into 2 times daily.

Atenolol (Tenormine) 50-100mg tablet, selective on the heart but has intrinsic sympathomimetic activity, dose of 50-100mg, once a day.

Metoprolol (Lopressor) 100mg tablet or Seloken 100-200mg tablet, selective heart, no intrinsic sympathetic activity, dose 50-100mg / day 1 time.

Acebutolol (Sectral) 200-400mg tablet, selected heart locü, has intrinsic sympathomimetic activity, dose of 400 mg/day is used only once or twice (starting 200 mg/day in 2 divided doses).

If there is no response to see if there is a mechanism of coronary artery spasm during an episode, it is important to never stop abruptly from beta-blocker therapy as there is a risk of arrhythmia, myocardial infarction, and sudden death.

Nitrate derivatives:

Often used first and in combination with other drugs (such as beta-blockers and calcium blockers) include:

Nitro-glycerine (pills or aerosol) has very few contraindications (except for obstructive cardiomyopathy) and few side effects (most commonly hypotension, headache).

Single, Double Nitrate or Nitrate derivatives in tablet or tape form.

Tolerance to Nitrés derivatives often occurs in high, prolonged doses. The diminishing phenomenon, if the Nitrate gap is respected, means not taking Nitrés after 18 hrs and not pasting between 20 hrs and 8 am, which explains the importance of the combination with beta-blockers or calcium inhibitors, especially in the disease. people have night pain.

Specifically:

Oral:

Trinitrine (Lénitral) capsule 2.5 mg and 7.5 mg dose: 2 capsules / day in 2 divided doses.

Isosorbide dinitrate such as: Langoran capsule 20-40mg or 80mg LP dose 40 - 80mg / day. Risordan 10-20mg tablets, 40mg dose / day, divided 2.3 times per day. Risordan LP tablet 20-40mg dose of 40mg / day. Or 5- isosorbide mononitrate such as: Monicor LP 20mg a day orally 2 capsules.

Molsidomine (Corvasal) is not a nitrate derivative but has similar effects in addition to antiplatelet aggregation. Brand name: Corvasal tablets 2-4mg, dose 1/2 - 1 tablet. The benefit of this group is that there is no tolerance.

Sugar paste: Trinitrine as Cordipath 5mg dose, paste in the morning and on the chest, should be pasted intermittently, only during the day.

Calcium inhibitors:

If beta-blockers are contraindicated (such as decompensated heart failure, atrioventricular conduction disturbances, Raynaud's bronchial asthma), in addition to nitrate derivatives and molsidomine, the use of calcium inhibitors is the drug of choice. are in mixed angina or major spasm.

Specifically:

Diltiazem (Tildiem) 60mg or Bi-Tildiem 90-120mg tablet, dose of 2 60mg tablets / day before eating or 90mg tablet 2 times / day.

In severe form: 180 mg/day in 3-4 divided doses, contraindicated: sinus node failure, degree 2 atrioventricular block, degree 3 without a pacemaker, left heart failure, pregnancy. Side effects: sinus bradycardia, atrioventricular block, oedema of the lower extremities, weakness, drowsiness, digestive disorders.

Nifedipine (Adalate) 10mg tablet. Dose 2 capsules per day with meals, for heavy forms can be used 3-4 capsules a day. Contraindications: pregnancy, side effects, facial swelling, headache, leg oedema, abdominal pain, hypotension, tachycardia.

It is possible to combine both types in severe or inoperable coronary angioplasty such as:

Tenormine 80-100mg / day + Adalate 3 capsules / day or Monicor LP 1 capsule / day. When combining beta-blockers with Diltazem, heart rate and sinus arrhythmia should be monitored.

Or Seloken 100-200mg / day + Corvasal 4mg 3 times / day + Adalate 1 capsule 4 times / day. Nitriderm TTS. 5mg paste from 20 hours to 8 hours.

Or the exception in the resistant form: Pexid 100mg tablet 1 tablet/day for 3 days + then 2 tablets/day need to be monitored closely because of side effects such as: mediocre, liver damage, nerve.

Other drugs:

Potassium channel activator (Nicorandil) acts to dilate and dilate the coronary and peripheral veins. There is no decrease in cardiac contractility and no resistance to treatment.

Amiodarone has antiarrhythmic and anti-ischemic effects. Watch for side effects.

Trimetazidine.

Pain relief and sedation.

Intervention method:

-Nong and stent (brackets): based on angiogram results and demonstrated anaemia by a thallium exercise test. Contraindications are not much except for the general stenosis of the left coronary artery or calcified coronary artery.

Aortic-coronary bridging: when the patient has clinical symptoms, failed dilatation with recurrent stenosis, the most branched injury is the left coronary trunk with severe cardiomyopathy.

Treatment of Prinz metal’s MS

During an attack: Nitro-glycerine or 1 capsule of Adalate slowly swallowed while lying down.

Next, it is necessary to treat with calcium inhibitors, heparin, high dose nitrate derivatives, not with beta inhibitors.

Note: Contraindicated to combine Tildiem with Cordium or Tildiem with Isoptin.

Treatment of angina is not stable

Need to stay in the heart resuscitation centre.

Due to spasm (night, rest) required for nitrate and calcium inhibition.

Due to exacerbation or worsening of exercise exertion: For beta-blocker, nitrate and/or calcium inhibitor.

Specifically:

Rest, monitoring, oxygen.

Clinical monitoring, electrocardiogram and biochemistry (CPK).

Sedation: Tranxene 15-30mg / day.

Anti-pain: Morphine 1/2 -1ctg subcutaneously or intravenously, if not responding to Nitrés derivatives.

Nitrate derivatives: continuous transmission by the electric pump as Risordan dose 2-5 mg/hour or

Lenitral dose 1 mg/hour or Corvasal, should not exceed 48 hours.

Calcium inhibitors: Tildiem 3-4 tablets / day.

Beta-blockers: N If no mechanism by spasms. Acebutolol 200-400mg / day

Tenormine 80-100ng / day.

Heparine 400-800v / kg continuous infusion or low molecular weight heparin (Enoxaparin 1mg / kg subcutaneous injection 2 times / day).

Aspirine 250-300mg / day.

If not responding despite combination therapy with nitres + beta-blocker + calcium inhibitors: acute coronary intervention.

Treatment of silent myocardial anaemia

Need to strengthen treatment against angina.

Establish coronary bilan.

Treatment of myocardial infarction

Myocardial infarction is considered a serious complication of coronary failure or myocardial anaemia. Treatment must be done at a cardiological resuscitation center.

The purpose of treatment is to reduce pain, minimize the spread of blood tissue, and prevent /

treatment of arrhythmias and mechanical complications. Specifically:

Hospitalized in a cardiac intensive care centre with continuous heart monitoring.

Keep an emergency intravenous line for arrhythmias.

Early treatment of fibrinolysis with streptokinase, APSAC, or tissue plasminogen activator (tPA) can minimize infarction area and death and limit left ventricular dysfunction. Inappropriate subjects, fibrinolysis should be given as soon as possible in coronary intensive care or intensive care units. Patient was given within 3 hours after onset of better symptoms but allowed to use the drug <12 hours after infarction. Complications include bleeding, arrhythmia due to reperfusion, and in case of streptokinase use, possible allergies. Anticoagulants (aspirin and heparin) are started at the same time as the fibrinolytic. Follow-up coronary angiography is usually reserved for patients with recurrent chest pain or a positive stress test before discharge. In patients with contraindications to fibrinolysis, Initial coronary artery is needed to ensure coronary flow. In centers with coronary intervention often preferred over fibrinolysis

Pain management: Morphine sulfate 2-4 mg IV every 5-10 minutes until pain or side symptoms appear (manage with naloxone 0.4-1.2mg IV); hypotension (if bradycardia is treated with atropine 0.5mg IV, otherwise fluid can be changed with caution).

Nitro-glycerine 0.3 mg sublingual if systolic BP is above 100mmHg; if chest pain persists for IV nitro-glycerine (start with 10 micrograms/min, gradually increase to a maximum of 200 micrograms/min, monitor closely).

Oxygen 2-4 liters/min by nasal inhalation, to maintain O2 saturation> 90%.

Mild sedation (Example: Diazepam 5 mg orally X 4 times / 24h).

Anti-constipation snacks: Use stool pastes eg. docusate sodium 100-200mg / 24h).

Beta-blockers: Reduce myocardial O2 consumption, limit infarction area, reduce mortality. The drug works well in cases of hypertension, tachycardia, persistent angina; Contraindicated in heart failure, systolic BP below 95 mmHg, heart rate <50 l / min, atrioventricular block or history of bronchospasm. Give IV for example metoprolol 5mg / 5-10 min up to a total dose of 15mg then give orally metoprolol 25-100mgX 2 times / day.

Anticoagulants / antiplatelet agents:

Patients following haemolysis are usually followed by aspirin and heparin anticoagulation, the time of initiation depends on the type of fibrinolysis. In the case of not being able to use blood, fibrinolysis can give aspirin 80-325 mg/day and low dose Heparin 5000vv injected subcutaneously or intravenously / 12 hours. An effective heparin dose (PTT time twice the control time) followed by oral anticoagulation is recommended for use in patients with severe heart failure, with ventricular clots diagnosed by ultrasound, or with major motor disturbance areas in the anterior MI.

ACE inhibitors: Reduce mortality in patients with asymptomatic left ventricular dysfunction after MI (ejection index less than 40%) and can be given in patients with hemodynamic stability. For example, captopril 6.25mg first dose then increased to 50mg orally 3 times/day.

Preventive

There are many systematic steps:

Determine the risk

Simultaneous collection of information on combined risk factors allows for a full assessment of the individual risk factor of coronary arteries for specific advice.

Specific advice

For both people who have not yet suffered and for those who have already

Smoking: Quit smoking completely. The risk of smoking is even greater when many factors are combined. Prevention requires special attention if it is a man.

Blood pressure: It is necessary to have a treatment regime to closely monitor the cases even in the early stage or only a limited increase in blood pressure.

Hypercholesterolemia: Be careful when blood cholesterol rises above 220 mg% with the advice of a special diet as well as need special examination and treatment when the increase is over 260mg%.

Increase your training and physical activity more. Weight loss implies a clear reduction in risk factors.

Diabetes: Continuous treatment with close follow-up with a specialist centre is the right choice for the patient.

Oral female contraceptive: minimize the use.