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Cardiology

Acute coronary syndromes.

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Epidemiology MI

• Atherothrombosis with complications are

the leading course of death in the world.

• Each year more than 7 mil.of people dye

for atherothrombosis =12,8% of all deaths.

• Each sixth man and each seventh woman

dyes in Europe on myocardial infarction.

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Acute MI

ACS

Acute coronary syndrome is the collection of clinical sym-

ptoms, originating from sudden myocardial ischaemia, on

the basis of atherothrombosis.

It is development of clinical symptoms of coronary heart

disease. Pathophysiologic substrate is unstable AS plaque

in the coronary bed.

Clinical status and examining methods are helpful for the

diagnosis of myocardial infarction, unstable angina and

other non coronary causes.

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On the basis of ECG:

a) with typical acute chest pain lasting (> 20 min) and ST segment elevations. It is acute coronary syndrome with ST elevations (STEMI). It originates on the basis of complete closing of coronary artery and the basic principle of therapy is reperfusion using percutaneous coronary intervention (PCI).

In majority of cases there is acute myocardial infarction with ST segment elevations. If no necrosis is diagnosed, there is the variant of angina pectoris –Prinzmetal´s type (elevation of ST segment is only transient), or unstable angina pectoris, or so called abortive (uncompleted) myocardial infarction.

On basis of ECG:

b) with typical acute chest pain, without ST segment elevations - acute coronary syndrome without ST segment elevations (NSTEMI). On ECG are depressions of ST segments, inversions, narowing, pseudonormaliation of T waves, or ECG may be also normal. On basis of measured troponins diagnosis is - acute myocardial infarction without ST segment elevations, or unstable angina pectoris.Sometimes also noncoronary causes of chest pain are present after excluding of CHD.

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AP (50%), UAP (90%), ACS

(100%)

Angina pectoris

Nestabilná angina

Akútny koronárny syndróm

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Unstable a.pectoris

Unstable angina pectoris (UAP) is defined as acute focal ischemia of the

heart muscle,not leading to the damage and increase of heart troponins in the

blood. On basis of clinical manifestations three basic types of unstable angina

pectoris are:

resting angina, de novo appeared angina pectoris and accelerated angina pectoris.

Most severe are patients with present resting unstable angina pectoris.

• Resting unstable angina pectoris. It appears at rest and lasts > 20 min.

• De novo unstable angina pectoris.

• Worsened (accelerated) unstable angina pectoris. Already diagnosed unstable angina pectoris, that is more often, lasts longer, or it appears with small exercise (worsening is at least of one class of NYHA).

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UAP

• Unstable angina pectoris may be devided after causes:

• secondary - extracardiac influences, worsening the myocardial ischemia (anaemias, febrilities, thyreotoxicosis, tachyarrythmias, respiratory insufficiency);

• primary – manifestation of angina pectoris is without presence of extracardiac influences (coronary cause);

• postinfarct - angina pectoris up to 2 weeks after acute myocardial infarction.

Ethiopathogenesis UAP

Unequality between supply and utilization of oxygen in myocardium.

Morfological substrate is usually unstable atheromatous plaque in the

large epicardial artery. On plaque sits for thrombi rich (white) thrombus,

Transitory fully obstructing the lumen for short time (10 – 15 min).

Also repeated embolization of thrombotic material into the peripheral

coronary bed may be also the cause.

In one thirds of cases there is an increased consumption of oxygen.

To the contrary to stable AP symptomatology is „unstable“, there is

tendency to rapid changes in clinical state of patients. These are often

prone to the progression to acute myocardial infarction with large

irreversible myocardial damage. Clinical manifestation, diagnosis and

treatment is similar to acute myocardial infarction without ST elevation.

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Acute myocardial infarction

• Pathological definition: characteristic is the death of myocardial cells caused by prolonged myocardial ischemia.

• Clinical definition: increased and/or biomarcers at least of one value over 99. percentile of reference value and plus it has to be present at least one of the criterias:

• clinical ischemic symptoms;

• ECG signs of new myocardial ischemia (new ST segment elevation, or new appearance of left bundle branch block, or pathologic Q);

• new appearance of kinetic disturbance, or new loss of viabile myocard with depicting methods.

State after MI

• State after myocardial infarction should

have at least one criterium:

• - appearance of new pathologic Q;

• - evidence of viabile myocardium loss,

is weakened and has worse contractility;

• - evidence of healed, or healing Mi with

section.

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Classification. On basis of clinickal course and

results several forms of MI are recognized.

• Pathologic-anatomical:

• - after the size: microskopic (focal necrosis), small (< 10 % of left ventricle), middle (10 -30 % of left ventricle), large (> 30 % of left ventricle);

• - after the necrosis area: transmural, nontransmural (does not response to Q and non-Q type);

• - after localisation: anterior, inferior, posterior, septal or their combinations;

• - after infarct stages: acute, or developing (6 hours - 7 days); presence of polymorfonuclear leucocytes in the infarcted area; in the most earlier stage up to 6 hours from the beginning polymorfonuclears may not be present and infarction is not possible to discover with microscopy), healing (7 - 28 days); presence of mononuclears and fibroblasts, polymorfonuclears are missing) and healed (> 28 days); scar tissue without cell infiltration).

Classification II

After coronarography: myocardial infarction with closure, or critical

stenosis of RIA, RC, ACD and their beds.

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Classification III

• After ECG:

• - after localization: infarction of anterior wall (ECG changes in leads V1-4; supply RIA), inferior wall (ECG changes in leads II, III, aVF; 85 % supply ACD, 15 % RC), lateral (I, aVL, V5-6; supply RD, RMS, RPLD), posterior (R in V1-2,Q V7-9; supply ACD, RC), right ventricle (V3R,V4R;supply ACD), unclear localization(without ECG changes);

• - after Q: infarction Q type and non-Q type;

• - after presence of ST elevations: myocardial infarction with ST elevations(with total closure of coronary artery),myocardial infarction without ST elevations (often are ST segment depressions, T wave changes; with critical unstable stenosis of coronary artery),

• - after ECG of stages: superacute (big positíve T waves), acute (Pardee waves), subacute (Q oscillations, decreased R oscillations over the infarct area, ST returns to izoelectric line, T wave inverts), chronic stage (rudimentar Q oscillations).

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Clinical picture and diagnosis.

Subjective symptoms.Basic clinical symptom of acute coronary symptoms and myocardial in-

farction is chest pain. It is caused by nerve ending stimulation in ische-

mic (no necrotic) myocardial regions. For angina pain is typical its appea-

rance at rest, or with small exercise (difference to chronic angina pecto

ris!), has high intensity, longer duration and lack of response to nitrolyce-

rine. Agonizing pain is lasting 20 min or more to several hours (no more

than 12 hours), propagating to the left arm, neck, mandibula, back or epi-

gastrium, not releasing after administration of nitroglyceríne. Intensity of

pain depends on the level of obstruction of coronary artery. Stenocardia

may be accompanied by other symptoms (as seen on the next picture),

dyspnea, nausea and vomiting (inferior infarcts), weakness or with palpi-

tations. Myocardial infarction may be also asymptomatic, or with only

small symptoms present. This may be in older persons,with diabetes mel-

litus, hypertension, or after aorto-coronary bypass surgery. Sometimes

Myocardial infarction may be present only with complications as heart

failure, syncope, or peripheral embolization.

Wide scale of symptoms and complications

may be also asymptomatic

vertigopalpitations

dyspnea

chest pain

death

syncope

fatigue

thromboembolism

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Noncoronary causes

• a) aortal dissection,

• b) acute pericarditis.

• c) pleural pain.

• d) pulmonary embolisation.

• e) costochondritis (Tietz´e syndrome).

• f) herpes zooster.

• g) pneumothorax.

• h) reflux ezofagitis.

• i) ulcer of gastroduodenum.

• j) depression.

Physical foundings

Physical founding in acute coronary syndromes and in myocardial infarction may

be also normal, therefore differential diagnosis of chest pain is of importance.

Pathological physical founding may be then only in complications. Often are pre-

sent signs of sympathetic stimulation, increased blood pressure and tachycardia.

In lower infarcts may be present hypotension and bradycardia (Bezold-Jarisch re-

flex). Therapy: volumexpansion and atropine. If systolic BP <90 mm Hg, together

with signs of organ hypoperfusion in acute MI, it shows for the progression to car-

diogenic shock, with poor prognosis.

In LV failure 3. heart sound and inspiratory rales are present. If systolic murmur on

apex is present, it may show for dysfunction, or rupture of papillary muscle with

subsequent mitral regurgitation. Friction pericardial murmur is present with peri-

carditis.

Prognostic classification after Killip is present after the physical foundings.

Pacients in class I have good prognosis and in class IV triede more than the half of

them dyes.

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Class I rales in lungs and 3. heart

sound are not present

Class II rales < 50 % in lungs and/or

3. heart sound

Class III rales > 50 % in lungs – signs

of pulmonary edema

Class IV cardiogenic shock

Angina pectoris NYHA

– Class 0: Asymptomatic

– Class 1: Angina with strenuous Exercise

– Class 2: Angina with moderate exertion

– Class 3: Angina with mild exertion

• Walking 1-2 level blocks at normal pace

• Climbing 1 flight of stairs at normal pace

– Class 4: Angina at any level of physical

exertion

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Lab.diagnosisLaboratory methods have for diagnosis of ACS basic significance. The most im-

porimportant biomarkers of myocardial damage are heart troponine T (cTnT) and

heart troponine I (cTnI); myocardial izoenzyme creatinkinase (CK-MB) and myoglo-

bine are just of helpful. Heart troponins are highly specific for myokard and nor-

mally are not present in blood examinations. Their estimation in blood is therefore

the definitive sign for the myocardial damage. For acute myokardial infarction is

typical at least one increase of troponine for more than 99. percentile of the refe-

rence values of healthy people. Myocardial damage may be caused also of nonco-

ronary causes. For the diagnosis of AMI there are also other criteria from the defi-

nition needed. Increased troponine levels may have also other reasons. Mild in-

crease may be present in patients with myopathies and with chronic kidney disea-

se. Values have negative prognostic significance. Between troponins T and I there

is not significant difference and it is possible to evaluate just one of them. Positive

troponin finding in the peripheral blood is after 3 - 4 hours from the beginning of

AMI, maximum are reached after 12 - 36 hours. Higher troponine values may last

to 2 weeks. With small infarcts troponins in blood may be only within 2 – 3 days.

Normal troponine value after 12 hours after the last chest pain excludes the diag-

nosis of myocardial infarction. Isoenzyme of creatininkinase (CK-MB) had its diag-

stic usefullness before using troponins. Myoglobin was used for early diagnosis of

MI, nowadays its estimation is not recommended.

Dg NSTEMILaboratory diagnosis of ACS without ST segment elevations has the ba-

sic significance and influence the therapy of these patients. Increased

troponins show for AMI, worse prognosis and is indication for early coro-

narography. (To the contrary estimation of signs of necrosis with STEMI

did not influence therapy and brings just the information about the size of

infarct).

In ACS there are also other changes of biochemical and hematological

values. Often is hyperglycaemia, increased FW, leucocytosis. Increased

hsCRP shows for poor prognosis. Estimation of BNP, or its prohormone

fragment (nT-proBNP) helps to discriminate cardial from noncardial dys-

pnea. Repeated estimations after several days brings also prognostic in-

formation. Besides glycaemia estimation it is necessary to evaluate also

lipid profile (up to 24-48 hours) after beginning of ACS. Later it comes to

lowering of cholesterol and HDL-cholesterol. Next control is then only

after 8 weeks. Prognosis of patients with acute MI is influenced also with

renal function parameters. Recommended is to evaluate creatinin, creati-

nine clearance, and microalbuminuria (i.e. simple ratio of albumine/creati-

nine in urine). The new and exact biomarker is cystatine C.

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Biomarkers

• Myoglobin reaches double of normal values up to 2

hours with peak to 4 hours from the beginning of MI

symptoms

• TnT, Tn I

• CK, elevation CK-MB between 4 - 6 hours after

beginning of acute MI and lasts 24 - 48 hours

• hs CRP, NT pro BNP

• Fatty acid binding proteins (FABPs) - free fatty acid

unbound to albumin (FFAu), ischaemia modified

albumin (IMA)

Biomarkers

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Natriuretic peptide values for diagnosis

senzitivity specificity pozit.predict. neg.predict

acute dyspnea

excluding ac.heart failure

BNP <30-50 pg/ml 97% 62% 71% 96%

NT-proBNP <300 pg/ml 99% 68% 62% 99%

confirms ac.heart failure

single values

BNP <100 pg/ml 90% 76% 79% 89%

NT-proBNP <900 pg/ml 90% 85% 76% 94%

several values

BNP to exclude <100 pg/ml 90% 73% 75% 90%

to confirmation >400 pg/ml 63% 91% 86% 74%

NT-proBNP age <50r <450 pg/ml 90% 84% 88% 66%

50-75r <900 pg/ml

>75r <1800 pg/ml

Electrocardiography

• For dg.of ACS isof basic importance! After ECG ACS are devided and treated! For disconery of acute ischaemia important is evaluation of ST segment. If ST elevations are lasting more than 20 min = acute MI STEMI, which needs early reperfusion treatment. Lack of elevations,or ST depressions on entry EKG, if stenocardia ends, diagnosis of ACS does not exclude. Often repeated ECG are helpful, best during AP. Patients with normal ECG at entry had significantly better prognosis.

• From ECG result depends the therapy. ECG informs about the place of ischemia, about its enlargement, about complications, about treatment effectivity and about the prognosis. ECG estimates the stage of myo-

cardial infarction. These criteria are not used with changed QRS com-plex and ST segment changes (Tawara bundle branch blocks, LV hy-pertrophy, WPW syndrome), when evaluation of acute ischaemia is not possible.

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ECG

After myocardial infarction there are typical new

developed pathologic Q oscillations. Pathologic Q

is characterised as any Q in leads V1-3,or Q lon-

ger ≥ 0,03 sek and depth ≥ 0,1 mV at least in 2

adjacent leads (I, II, aVL, aVF, V4-6).

If we have just one ECG, these criteria are not pre-

sent with left and right bundle branch block, left

ventricular hypertrophy and WPW syndrome.

ECG

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STEMI

Lokalization of MI

At present we recognize after ECG

three types of AMI: acute infarction of

anterior, inferior and lateral wall.

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AMI - anteroseptal

AMI - inferior

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AMI - posterolateral

AMI – anteroseptal with ES

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Depicting dg.methods

ECG

ECHOCG

MR (less present and useful)

CT (cine CT – coronary bed,calcium score)

Scintigraphy (viabile/nonviabile myocardium)

Selective coronarography (gold standard)

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Therapy

• Risk of dying on ACS is less the earlier

hospital treatment is available.

• Diagnosis estimation is of importance,

available defibrillator, CPR resuscitation,

and 12-lead ECG.

• Standard care of ACS consists of prehos-

pital, hospital and subsequent ambulatory

care.

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Rapid reperfusion PCI (thrombolysis)

Stabilization and lowering

of thrombus size

IIb/IIIa inhibitors, ASA, clopidogrel,

heparine, LMWH

oxygen demand in

myocardium

Beta-blockers, antihypertensives, pain

release

oxygen supply for

myocardium

oxygen, nitrates, PCI, CABG

Therapy and prevention of

malignant arrythmias

defibrillation, resuscitation, ECG

monitoring

Slowering of LV

remodellation

ACEI

Stabilization of

atherosclerotic plague

Statins

STEMI

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Therapy

Before hospital

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Indicat. therapy

ALL acid acetylsalicylic

NTG

Oxygen

heparin (before direct

PTCA)

Clopidogrel

160 - 325mg p.o.

70 - 100 j/kg i.v.

300 - 600 mg p.o.

Stenokar

dia

nitrates

opiates

NTG s.l., NTG or ISDN i.v.

fentanyl 1 - 2 ml i.v., morfin 2 - 5

mg i.v.

HR >

60/min

beta-blockers metoprolol 5 - 15 mg slowly i.v.

HR <

45/min

atropine atropin 0,5 - 3,0 mg i.v.

HY beta-blockers, nitrates

ACEI

NTG/ISDNi.v,captopril 25mg po

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AS

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PCI - stent

Bare Metal Stents= Restenosis (Scar Tissue);

Drug Eluting Stents = Thrombosis (Blood

Clots).

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Complications

• Heart failure, cardiogenic shock

• Mechanical complications

Rupture of the wall

Rupture of the interventricular septum

Acute mitral regurgitation

• Arrythmias - ventricular tachycardia/ fibril-lation, AV blocks

• Intramural thrombosis

• Pericarditidis

• Aneurysm