2. Acute myocardial infarction
commonly known as a heart attack, is ischemic myocardial necrosis usually resulting
from abrupt reduction in coronary blood flow to a segment of myocardium.
Causes and pathogenesis. In >90% of patients with acute myocardial infarction, an acute
thrombus, often associated with plaque rupture, occludes the artery (previously partially
obstructed by an atherosclerotic plaque) that supplies the damaged area. Altered platelet
function induced by endothelial change in the atherosclerotic plaque presumably
contributes to thrombogenesis. Myocardial infarction is rarely caused by arterial
embolization (in mitral or aortic stenosis, infective endocarditis, and marantic
endocarditis). Myocardial infarction has been reported in patients with coronary spasm
and otherwise normal coronary arteries.Contributory factors for development of
myocardial infarction are psychological stress, physical exertion or overwork, high rise of
arterial blood pressure, alcohol abuse, increased blood coagulation.
3. Pathogenesis
Myocardial ischemia
• Diminished coronary blood flow e.g. in
coronary artery disease, shock.
• Increased myocardial demand e.g.
exercise, emotions
• Hypertrophy of heart without simultaneous
increase of coronary blood
Flow, HT,
valvular heart diseases.
2.) Role of platelets
3.) Acute plaque rupture
4.) Non-atheromatous causes (10%)
• vasospasm
• Emboli, vegetative endocarditis, vasculitis,
hematologic abnormalities
RISK FACTORS…….
• In industrialized countries MI
accounts for 10-25% of all
Deaths.
• Frequency rises with age
• Risk factors to atherosclerosis:
diabetes, hypertension, smoking,
hyperlipidemia
• M>F, incidence rises after menop
4. Classification of MI
*According to size of necrotized area.
Transmural(Q wave) and
subendocardial(non-Q wave)
*According to clinical forms
Anginous
Asthmatic
Abdominal
Arrythmatic
Cerebral
Asymptomatic
*Non ST elevated and ST elevated MI.
5. Clinical features
About 2/3 of patients experience prodromal symptoms for days to weeks before
the event, including unstable angina, shortness of breath, or fatigue
The first symptom of acute myocardial infarction usually is deep. substernal pain
described as heavy, squeezing, and crushing, although occasionally it is described
as stabbing or burning, often with radiation to the back, jaw, or left arm. The pain is
similar to that in angina pectoris but is usually more severe, long-lasting (more
than 30 minutes), and relieved little, or only temporarily, by rest or nitroglycerin.
Pain is accompanied by weakness, excessive sweating. In severe episodes, the
patient becomes apprehensive and may fear of impending death.At times,
discomfort may be very mild, and perhaps 20% of acute myocardial infarctions are
silent or unrecognized as illness by the patient. Women may have atypical chest
discomfort. Older patients may complain of dyspnea more than ischemic-type
chest pain. Nausea and vomiting may occur, especially in inferior myocardial
infarction. Symptoms of left ventricular failure, pulmonary edema, shock or
significant arrhythmia may dominate.
6. Skin is pale, cool, diaphoretic. Peripheral or central cyanosis may be apparent.
Auscultation of lungs may give us wheezes, small-bubble rhonchi in lower parts of lungs.
The pulse is small and fast and may be thready. The blood pressure is variable. Patient
may have increased heart and breathing rate. P The apical impulse is weak. It may be
difficult to palpate it. Auscultation of the heart. Heart sounds are usually diminished; the
presence of a S4 is almost universal. The gallop rhythm is often auscultated. A soft
systolic blowing apical murmur (a reflection of papillary muscle dysfunction) may be
heard. Acute myocardial infarction can provoke changes of rhythm (extrasystoles,
paroxysmal ventricular tachycardia, atrial fibrillation). In 1-3 days following the onset of
the disease, the necrotized focus begins resolving and the patient's temperature rises
Myocardial infarction progresses through the following temporal stages:
1) initial stage - from 20 minutes to first 2 hours,
2) acute stage- first few hours to 7-10 days,
3) subacute stage (healing) - 7 to 28 days,
4) stage of scarring (healing)-29 days to 8 weeks and beyond.
During the initial stage of the acute phase of Q-wave myocardialinfarction within a few
minutes the T wave becomes tall, pointed, and upright and ST-segment elevation follows
rapidly. In acute stage necrotic focus forms. R wave voltage diminishes and pathological
Q wave develops during this stage. Later T wave becomes negative. New-onset left
bundle branch block may be a sign of recent myocardial infarction
7. , too. In subacute stage the ST segment
usually returns to normal within few weeks,
but the pathological Q wave persists as a
marker of previous infarction. T wave may
become less negative, smoothed or even
positive in last stage of myocardial
infarction. The depth of Q wave may
become less and size of R wave may
increase in the stage of
scarring.Subendocardial myocardial
infarction (non-Q wave) may be presentif
the ECG shows only transient ST-segment
and T-wave changes. Localization of the
myocardial infarction
8. According to localization.
Anterior myocardial infarction
*anterior lateral-changes in I,II,Avl,V5,V6
leads.
*anterior septal-V1-V3 leads.
*anterior apical-V3 and V4 leads.
*widespread anterior-I,II,aVL ,V1-V6
leads
Posterior myocardial infarction
*posterior diaphragmatic(inferior)-
III,II,aVF leads
*posterior lateral-III,II,Avf,V5-V6 leads.
10. Creatine kinase (CK) rises within 4 to 8 h and generally returns to normal by 48 to 72 h.
An important drawback of total CK measurement is its lack of specificity for acute
myocardial infarction, as CK may be elevated with skeletal muscle trauma. Then it was
found that disproportional elevation of the MB isoenzyme of the creatine kinase (CK-MB)
was very specific for myocardial injury. The CK-MB has the advantage over total CK that
it is not present in significant concentrations in extracardiac tissue and therefore is
considerably morespecific. Normal CK-MB for 24 h virtually rules out myocardial
infarction.
Myoglobin is released into the blood within only a few hours after the onset of acute
myocardial infarction. Although myoglobin is one of the first serum cardiac markers that
rise above the normal range after acute myocardial infarction, it lacks cardiac specificity,
and it is rapidly excreted in the urine, so that blood levels return to the normal range
within 24 h of the onset of infarction. Myoglobin and the contractile proteins troponin-T
and troponin-I are also released by infarcted myocardium.
Cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI) have amino acid
sequences different from those of the skeletal muscle forms of these proteins. These
differences have permitted the development of quantitative assays for cTnT and cTnI
with highly specific monoclonal antibodies. Since cTnT and cTnI are not normally
detectable in the blood of healthy individuals but may increase after acute myocardial
infarction to levels over 20 times higher than the
11. cutoff value (usually set only slightly above the noise level of the assay), the
measurement of cTnT or cTnI is of considerable diagnostic use, and they are now the
preferred biochemical markers for myocardial infarction. The cardiac troponins are
particularly valuable when there is clinical suspicion of either skeletal muscle injury or a
small myocardial infarction. Levels of cTnl may remain elevated for 7 to 10 days after
AMI, and cTnT levels may remain elevated for up to 10 to 14 days
Echocardiography. Echocardiography may be useful in evaluating wall motion, presence
of ventricular thrombus, papillary muscle rupture,
Treatments
cutoff value (usually set only slightly above the noise level of the assay), the
measurement of cTnT or cTnI is of considerable diagnostic use, and they are now the
preferred biochemical markers for myocardial infarction. The cardiac troponins are
particularly valuable when there is clinical suspicion of either skeletal muscle injury or a
small myocardial infarction. Levels of cTnl may remain elevated for 7 to 10 days after
AMI, and cTnT levels may remain elevated for up to 10 to 14 days.Echocardiography.
Echocardiography may be useful in evaluating wall motion, presence of ventricular
thrombus, papillary muscle rupture,
12. MYOCARDITIS
Myocarditis is collection of diseases of
infectious, toxic, and autoimmune etiologies
characterized by inflammation of the heart.
Subsequent myocardial destruction can lead
to dilated cardiomyopathy.
14. Dallas Classification (1987)
Initial Biopsy
Myocarditis: Myocardial necrosis, degeneration, or both, in the absence of
significant coronary artery disease with adjacent inflammatory infiltrate with or
without fibrosis.
Borderline myocarditis: Inflammatory infiltrate too sparse or myocyte damage not
apparent.
No myocarditis
Subsequent Biopsies
Ongoing (persistent) myocarditis with or without fibrosis.
Resolving (healing) myocarditis with or without fibrosis.
Resolved (healed) myocarditis with or without fibrosis.
15.
16.
17. Patients(59%) frequently present days to weeks after an acute febrile illness,
particularly a flu-like syndrome
Myocarditis is most commonly asymptomatic, with no evidence of left ventricular
dysfunction - fever, malaise, fatigue, arthralgias, myalgias, and skin rash.
Cardiac symptoms may result from systolic or diastolic left ventricular dysfunction
or from tachyarrhythmias or bradyarrhythmias (dyspnea, fatigue, decreased
exercise tolerance, palpitations )
In cases where a dilated cardiomyopathy has developed, signs of peripheral or
pulmonary thromboembolism may be found.
Diffuse inflammation may develop leading to pericardial effusion, without
tamponade, and pericardial and pleural friction rub as the inflammatory process
involves surrounding structures
SIGNS AND SYMPTOMS
18. Clinical Findings
Physical Examination -Tachycardia,
hypotension, fever and tachycardia may be
disproportionate to the degree of fever
Bradycardia is seen rarely, and a narrow pulse
pressure is occasionally detected
Murmurs of mitral or tricuspid regurgitation are
common , S3 and S4 gallops may also be
heard.
Distended neck veins, pulmonary rales,
wheezes, gallops, and peripheral edema may be
detected
19. Diagnostic Studies
Electrocardiography
The most common abnormality is sinus tachycardia.
may show ventricular arrhythmias or heart block, or it may mimic the findings in
acute myocardial infarction or pericarditis with ST segment elevation, ST segment
depression, PR segment depression, and pathological Q-waves
Relations between these clinical and laboratory findings
Echocardiography
to exclude other causes of heart failure and identify ventricular thrombi.
There are no specific echocardiographic features of myocarditis.
Segmental or global wall motion abnormalities can mimic myocardial infarction.
Patients with fulminant myocarditis tend to present with more normal cardiac
chamber dimensions and thickened walls, compared with patients with less acute
myocarditis who have greater left ventricular dilation and normal wall thickness.
Right ventricular dysfunction is an uncommon but important predictor of death or
cardiac transplantation
20. Bood test.
Leukocytosis is present in 25% of cases. Erythrocyte sedimentation rate (ESR) is
elevated in 60% of patients with acute myocarditis. C-reactive protein (CRP) is
usually elevated but non-specific.
Biochemical blood test.
Cardiac enzyme levels are only elevated in aminority of patients. Creatine kinase MB
subunits are elevated in only 5.7% of patients with biopsy-proven myocarditis.
Cardiac troponin I or T are elevated in at least 50% of patients with biopsy-proven
myocarditis. They may also help to identify those with resolution of viral myocarditis.
Serum viral antibody titers for viral myocarditis. Common viral antibody titers
available for clinical evaluation include coxsackie virus group B, HIV,
cytomegalovirus, Epstein-Barr virus, hepatitis virus family, and influenza viruses.
Titers increase 4-fold or more with gradual fall during recovery period (nonspecific),
hence requiring serial testing.
21. ECG. Sinus tachycardia is the most frequent finding. ST-segment elevation
without reciprocal depression, particularly when diffuse, is helpful in differentiating
myocarditis from acute myocardial infarction. Decreased QRS amplitude and
transitory Q-wave development is very suggestive of myocarditis. As many as 20%
of patients will have a conduction delay, including Mobitz I, Mobitz II, or complete
heart block. Left or right bundle-branch block is observed in approximately 20% of
abnormal ECG findings and may persist for months. Ventricular exstrasystole,
paroxysmal ventricular tachycardia are most common arrhythmias in myocarditis.
Chest radiography. A chest radiograph often reveals a normal cardiac silhouette,
but pericarditis or clinical congestive heart failure is associated with cardiomegaly.
Vascular redistribution, interstitial and alveolar edema, pleural effusion may also
accompany severe myocarditis. Echocardiography. This is performed to exclude
other causes ofheart failure (valvular, amyloidosis, congenital) and to evaluate the
degree of cardiac dysfunction (usually diffuse hypokinesis and diastolic
dysfunction). It also may allow gross localization of the extent of inflammation (wall
motion abnormalities, wall thickening, pericardial effusion). In addition,
echocardiography may distinguish fulminant from acute myocarditis by identifying
near-normal left ventricular diastolic dimensions and increased septal thickness in
fulminant myocarditis (versus increased left ventricular diastolic dimensions and
normal septal thickness in acute myocarditis), with marked improvement in systolic
function in time.
22.
23. MRI.
This imaging technique is used for assessment of the extent of inflammation and
cellular edema, although it is still nonspecific. Delayed- enhanced MRI has also
been used to quantify the amount of scarring that occurred following acute
myocarditis. PCR identification of a viral infection from myocardial tissue,pericardial
fluid, or other body fluid sites can be helpful. Biopsy. The gold standard is still
biopsy of the myocardium, generally done in the setting of angiography. A small
tissue sample of the endocardium and myocardium is taken, and investigated by a
pathologist by light microscopy and if necessary immunochemistry and special
staining methods. Histopathological features are: myocardial interstitium with
abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages.
Focal destruction of myocytes explains the myocardial pumpfailur
24. IMAGING STUDIES
Chest radiography
MRI is capable of showing abnormal signal intensity in the
affected myocardium
Cardiac catheterization
elevated left ventricular end-diastolic pressure, a depressed
cardiac output, and increased ventricular volumes
Coronary angiogram typically demonstrates normal
coronary arteries.
Endomyocardial biopsy
- gold standard for the diagnosis of myocarditis
Dallas criteria (an inflammatory infiltrate of the myocardium
+injury to the adjacent myocytes)
borderline myocarditis is made when the infiltrate is not
accompanied by myocyte injury
25. LABORATORY STUDIES
Cardiac troponin I may be more sensitive
because it is present for longer periods after
myocardial damage from any cause.
Erythrocyte sedimentation rate (ESR) is
elevated in 60% of patients with acute
myocarditis.
Leukocytosis is present in 25% of cases.
OTHER TESTS
If a systemic disorder (eg, SLE) is suspected,
antinuclear antibody (ANA) and other collagen
vascular disorder laboratory investigations may
be useful
26. Non-pharmacological treatment
• Bed rest
• Reducing salt and liquids intake
• No training for athletes – 6 months
Therapeutic options
• treatment of heart failure
• treatment of arrhythmias
• treatment of conduction abnormalities – heart
blocks
27. Therapeutic options
• Intravenous gamma - globulin in children
• Antibiotics in bacterial myocarditis
• Anti-lymphocyte monoclonal antibodies
• Alfa and beta interferon (positive viral PCR reaction)
• Immunosupresion in giant cell myocarditis and autoimmune
myocarditis
• Glucocorticoids and azathioprine – debatable (negative viral
PCR reaction)
• NSAIDs are contraindicated in the ACUTE PHASE (increase
cardiomyocyte lesion and necrosis)
28. Treatment of heart failure
Vasodilators (nitroglycerin, sodium nitroprusside)
Angiotensin II converting enzyme inhibitors ( enalapril, lisinopril,
ramipril) or angiotensin II receptor blockers ( valsartan, losartan,
candesartan)
Loop diuretics ( furosemide, torasemide)
Mineralocorticoid receptor antagonists (spironolactone, eplerenone)
Beta-blockers (metoprolol succinate, bisoprolol, nebivolol, carvedilol)
Drugs with positive inotropic effect (dobutamine, milrinone)
Surgical treatment in Myocarditis
Implantation of pacemaker in patients with complete heart block
Cardiac transplantation
Left ventricular assist device
29. Sudden death
Heart failure
Arrhythmias
Progression to dilative cardiomyopathy
PROPHYLAXIS
Prevention of infectious diseases by means of
appropriate immunizations and early treatment appears to
be important in decreasing the incidence of myocarditis.
