Alya Putri Khairani / 13010110220 / B2

Cardiomyopathies
Cardiomyopathies are a group of heart disorders in which the major structural abnormality is limited to the
myocardium. These conditions often result in symptoms of heart failure, and although the underlying cause of
myocardial dysfunction can sometimes be identified, the etiology frequently remains unknown. Excluded from the
classification of this group of diseases is heart muscle impairment resulting from other defined cardiovascular
conditions, such as Hypertension, Valvular Disorders, or Coronary Artery Disease
Cardiomyopathies can be classifi ed into three types based on the anatomic appearance and abnormal physiology
of the left ventricle (LV):
1. Dilated Cardiomyopathy
Ventricular chamber enlargement with impaired systolic contractile function
2. Hypertrophic Cardiomypathy
Abnormally thickened ventricular wall with abnormal diastolic relaxation but usually intact systolic function
3. Restrictive Cardiomyopathy
Abnormally stiffened myocardium (because of fibrosis or an infiltrative process) leading to impaired diastolic
relaxation, but systolic contractile function is normal or near normal

Dilated Cardiomyopathy
Etiology
Myocyte damage and cardiac enlargement in Dilated Cardiomyopathy (DCM) result from a wide spectrum of
genetic, inflammatory, toxic, and metabolic causes:
Idiopathic
Familial (Genetic)
Autosomal dominant, autosomal recessive, X-linked, and mitochondrial patterns of inheritance have been
described, leading to defects in contractile force generation, force transmission, energy production, and
myocyte viability. Identified mutations occur in genes that code for Cardiac Cytoskeletal, Myofibrillar, and
Nuclear membrane proteins
Inflammatory

Infectious (especially viral)

Common responsible infecting organisms include Coxsackievirus group B, Parvovirus B19, and
Adenovirus, among many others. It is hypothesized that myocardial destruction and fibrosis result
from immune-mediated injury triggered by viral
constituents

Noninfectious

Connective tissue disease

Peripartum Cardiomyopathy
Form of DCM that presents with heart failure symptoms between the last month of pregnancy
and up to 6 months postpartum. Risk factors include older maternal age, being African American,
and having multiple pregnancies.

Sarcoidosis
Toxic

Chronic alcohol ingestion

Develops in a small number of people who consume alcoholic beverages excessively and chronically.
Although the pathophysiology of the condition is unknown, Ethanol is thought to impair cellular
function by inhibiting mitochondrial oxidative phosphorylation and fatty acid oxidation

Chemotherapeutic agents (ex/: Doxorubicin)

Metabolic

Hypothyroidsm

Chronic hypocalcemia or Hypophosphatemia

Neuromuscular
Muscular or Myotonic dystrophy

Alya Putri Khairani / 13010110220 / B2

Pathology
Marked enlargement of all four cardiac chambers is typical of DCM, although sometimes the disease is limited to
the left or right side of the heart. The thickness of the ventricular walls may be increased, but chamber dilatation is
out of proportion to any concentric hypertrophy. Microscopically, there is evidence of myocyte degeneration with
irregular hypertrophy and atrophy of myofibers. Interstitial and perivascular fibrosis is often extensive
Pathophysiology
The hallmark of DCM is ventricular dilatation with decreased contractile function. Most often in DCM, both
ventricles are impaired, but sometimes dysfunction is limited to the LV and even less commonly to the right
ventricle (RV)
As ventricular stroke volume and cardiac output decline because of impaired myocyte contractility, two
compensatory effects are activated:
1. The FrankStarling mechanism
Elevated ventricular diastolic volume increases the stretch of the myofibers, thereby increasing the subsequent
stroke
2. Neurohormonal activation
Initially mediated by the sympathetic nervous system. This activation of the Renin-Angiotensin-Aldosterone
(RAA) axis increases peripheral vascular resistance (mediated through Angiotensin II) and intravascular volume
(because of increased Aldosterone).
These compensations may render the patient asymptomatic during the early stages of ventricular dysfunction;
however, as progressive myocyte degeneration and volume overload ensue, clinical symptoms of heart failure
develop. In addition, chronically elevated levels of Angiotensin II and Aldosterone directly contribute to pathological
myocardial remodeling and fibrosis.
As the cardiomyopathic process causes the ventricles to enlarge over time, the mitral and tricuspid valves may fail
to coapt properly in systole, and valvular regurgitation ensues

Clinical Findings
Low forward cardiac output
Fatigue and Lightheadedness
Exertional dyspnea associated with decreased tissue perfusion
Pulmonary congestion results in dyspnea, orthopnea, and paroxysmal nocturnal dyspnea
Chronic systemic venous congestion causes ascites and peripheral edema
Recent weight gain (because of interstitial edema)
Physical Examination
1. Signs of decreased cardiac output
Cool Extremities (owing to peripheral vasoconstriction)
Low arterial pressure
Tachycardia
2. Pulmonary venous congestion
Auscultatory rackles (Rales)
Basillar chest dullness to percussion due to pleural effusion
3. Cardiac examination: enlarged heart with leftward displacement of diffuse apical impulse
4. Cardiac auscultation:
S3 as common sign of poor systolic function
Murmur of mitral regurgitation as result of significant left ventricular dilatation

Alya Putri Khairani / 13010110220 / B2

Diagnostic Studies
Chest Radiography
An enlarged cardiac silhouette. If heart failure has developed, then pulmonary vascular redistribution,
interstitial and alveolar edema, and pleural effusions are evident
Severe congestive heart failure. Increased pulmonary vascular
markings are present throughout the lung fields, along with
peribronchiolar cuffing (black arrow) and pleural effusion, which is
indicated by blunting of the costodiaphragmatic angle and tracking
up the right lateral hemithorax (black arrowheads). The presence
of interstitial and alveolar edema produces perihilar haziness and
air bronchograms (open arrows), which occur when the radiolucent
bronchial tree is contrasted with opaque edematous lung tissue

Electrocardiogram
Demonstrates Atrial and Ventricular enlargement. Patchy fibrosis of the myofibers results in a wide array of
arrhythmias, most importantly atrial fibrillation and ventricular tachycardia. Conduction defects (left or right
bundle branch block) occur in most cases. Diffuse repolarization (ST segment and T wave) abnormalities are
common

Echocardiography
It typically demonstrates four-chamber
cardiac enlargement with little
hypertrophy and global reduction of
systolic contractile function. Mitral
and/or tricuspid regurgitation is also
frequently visualized
A globular shape to the ventricle and wall
motion is uniformly reduced. Note that
there is little change in ventricular diameter
from diastole to systole, a sign that overall

Cardiac Catheterization
Often performed to determine whether coexistent coronary artery disease is contributing to the impaired
ventricular function. Typically, hemodynamic measurements show elevated right- and leftsided diastolic
pressures and diminished cardiac output
Cardiac Magnetic Resonance Imaging
Particularly for the diagnosis of myocardial inflammation (Myocarditis)

Treatment
MEDICAL TREATMENT OF HEART FAILURE

Alya Putri Khairani / 13010110220 / B2

Initial Therapy
Salt restriction and Diuretics, Vasodilator therapy with an Angiotensinconverting Enzyme (ACE) inhibitor or
Angiotensin II Receptor Blocker (ARB), and a -blocker.
Patient with advance HF
Treat with Potassium-sparing diuretic Spironolactone

PREVENTION AND TREATMENT OF ARRYTHMIAS

Maintain serum electrolytes (notably, K+ and Mg2+) within their normal ranges, especially during diuretic
therapy, to avoid provoking serious Arrhythmias
Placement of an Implantable Cardioverter-Defibrillator (ICD)
Amiodarone is the contemporary antiarrhythmic studied most extensively in patients with DCM
Electronic Pacemaker for DCM patient with electrical conduction abnormalities that contribute to
dyssynchronous ventricular contraction and reduced cardiac output
PREVENTION OF THROMBOEMBOLIC EVENTS
Chronic Oral Anticoagulation therapy (ex/: Warfarin) is often administered to DCM patients who have severe
depression of ventricular function (e.g., LV ejection fraction <30%) to prevent Thromboembolism
CARDIAC TRANSPLANTATION
In suitable patients, cardiac transplantation offers a substantially better 5-year prognosis than the standard
therapies for DCM previously described. The current 5- and 10-year survival rates after transplantation are 74%
and 55%
Prognosis
Up to one third of patients will experience spontaneous improvement of heart function after the diagnosis of DCM
is made. However, the prognosis for patients with persistent DCM who do not undergo cardiac transplantation is
poorthe average 5-year survival rate is <50%

Hyperthropic Cardiomyopathy
HCM is characterized by asymmetric (or sometimes global) left ventricular hypertrophy that is not caused by
chronic pressure overload (i.e., not the result of systemic hypertension or aortic stenosis). Other terms frequently
used to describe this disease are Hypertrophic Obstructive Cardiomyopathy and Idiopathic Hypertrophic
Subaortic Stenosis. In this condition, systolic LV contractile function is vigorous but the thickened muscle is stiff,
resulting in impaired ventricular relaxation and high diastolic pressures
Etiology
HCM is a familial disease in which inheritance follows an autosomal dominant pattern with variable penetrance,
and hundreds of mutations in several different genes have been implicated. The pathophysiology and natural
history of familial HCM are quite variable and appear related to particular mutations within the disease-causing
gene, rather than the actual gene involved
Pathology
Although hypertrophy in HCM may
involve any portion of the ventricles,
Asymmetric Hypertrophy of the
Ventricular Septum is most
common. The histology of HCM is
unusual. The myocardial fibers are in
a pattern of extensive disarray. Short,
wide, hypertrophied fibers are
oriented in chaotic directions and are
surrounded by numerous cardiac
fibroblasts and extracellular matrix.
This myocyte disarray and fibrosis are
characteristic of HCM and play a role

Pathophysiology
The predominant feature of HCM is marked ventricular hypertrophy that reduces the compliance and diastolic
relaxation of the chamber, such that filling becomes impaired. It is useful to consider the pathophysiology of HCM
based on whether such systolic outflow tract obstruction is present:
HCM WITHOUT OUTFLOW TRACT OBSTRUCTION

Alya Putri Khairani / 13010110220 / B2

Although systolic contraction of the LV is usually vigorous in HCM, hypertrophy of the walls results in increased
stiffness and impaired relaxation of the chamber. The reduced ventricular compliance alters the normal pressure
volume relationship, causing the passive diastolic fi lling curve to shift upward. Dyspnea, especially during
exertion, is thus a common symptom in this disorder
HCM WITH OUTFLOW TRACT OBSTRUCTION
Approximately one third of patients with HCM manifest systolic outflow tract obstruction. The mechanism of
systolic obstruction is thought to involve abnormal motion of the anterior mitral valve leaflet toward the LV outflow
tract where the thickened septum protrudes. The process is explained as:
1. During ventricular contraction, ejection of blood toward the aortic valve is more rapid than usual, because it
must flow through an outflow tract that is narrowed by the thickened septum
2. This rapid flow creates Venturi forces that abnormally draw the anterior mitral leaflet toward the septum during
contraction
3. The anterior mitral leaflet approaches and abuts the hypertrophied septum, causing transient obstruction of
blood flow into the aorta

Causing:
(1) During systolic obstruction, a pressure gradient develops between the main body of the LV and the outflow
tract distal to the obstruction
(2) The elevated ventricular systolic pressure increases wall stress and myocardial oxygen consumption, which
can result in Angina
(3) Because obstruction is caused by abnormal motion of the anterior mitral leaflet toward the septum, the
mitral valve does not close properly during systole, and Mitral Regurgitation may result
(4) Such regurgitation further elevates left atrial and pulmonary venous pressures and may worsen
symptoms of Dyspnea and develop Atrial Fibrilation

Clinical Findings

Ventricular Fibrillation, resulting in sudden cardiac death, particularly in young adults with HCM during
strenuous physical exertion

Dyspnea owing to elevated diastolic LV (and therefore pulmonary capillary) pressure

Angina

Myocardial ischemia may be contributed

Syncope in HCM may result from cardiac arrhythmias that develop because of the structurally abnormal
myofibers

Alya Putri Khairani / 13010110220 / B2

Orthostatic lightheadedness occurs because venous return to the heart is reduced on standing by the
gravitational pooling of blood in the lower extremities

Physical Examination

Presence of S4 generated by left atrial contraction into the stiffened LV

Systolic murmur of LV outflow obstruction is rough and crescendodecrescendo in shape, heard best at the
left lower sternal border
As the stethoscope is moved toward the apex, the Holosystolic blowing murmur of the accompanying mitral
regurgitation may be auscultated
Valsava Maneuver

Diagnostic Studies
The ECG typically shows left ventricular hypertrophy and left atrial enlargement
Echocardiography is very helpful in the evaluation of HCM. The degree of LV hypertrophy can be measured
and regions of asymmetrical wall thickness readily identified
Cardiac Catheterizations major feature in patients with obstruction is the finding of a pressure gradient
within the outflow portion of the LV, either at rest or during maneuvers that transiently reduce LV size and
promote outflow tract obstruction
Genetic testing
Treatment

-blockers

Calcium channel antagonists

Antiarrythmic drug

ICD

Dual-chamber permanent pacemaker

Surgical therapy (Myomectomy) is considered for patients whose symptoms do not respond adequately to
pharmacologic therapy or doing Percutaneous Septal Ablation

Genetic counseling should be provided to all patients with HCM

Prognosis
The incidence of sudden death in HCM is 2% to 4% per year in adults and 4% to 6% in children and adolescents

Restrictive Cardiomyopathy
Characterized by abnormally rigid (but not necessarily thickened) ventricles with impaired diastolic filling but
usually normal, or nearnormal, systolic function. This condition results from either (1) Fibrosis or scarring of the
Endomyocardium or (2) Infiltration of the myocardium by an abnormal substance
Examples of Restrictive Cardiomyopathies:
Noninfiltrative

Idiopathic

Scleroderma
Infiltrative

Amyloidosis
The most common recognized cause of restrictive cardiomyopathy in nontropical countries. In this
systemic disease, insoluble misfolded amyloid fi brils deposit within tissues, including the heart, causing
organ dysfunction. Amyloid fi brils can pathologically develop from a host of different proteins that
distinguish the categories of disease

Primary Amyloidosis: caused by deposition of immunoglobulin light chain AL fragments secreted by

a plasma cell tumor

Secondary Amyloidosis: characterized by the presence of AA amyloid (derived from the

inflammatory marker serum amyloid A) in a variety of chronic inflamatory conditions, such as
Rheumatoid Arthritis

Hereditary Amyloidosis: autosomal dominant condition in which amyloid fibrils form from point
mutations in the protein transthyretin

Senile Amyloidosis: condition in the elderly, in which amyloid deposits, derived from Transthyretin or
other proteins, are found scattered throughout the vascular system, muscles, kidney, and lung
In each form of amyloidosis, cardiac involvement is marked by deposition of extracellular amyloid
between myocardial fibers in the atria and ventricles, in the coronary arteries and veins, and in the
heart valves

Sarcoidosis
Storage disease

Hemochromatosis

Glycogen storage disease

Endomyocardial disease

Alya Putri Khairani / 13010110220 / B2

Endomyocardialfibrosis
Hypereosinophilic syndrome
Metastatic tumors
Radiation therapy

Pathophysiology
Reduced compliance of the ventricles in restrictive cardiomyopathy result in abnormally high diastolic pressures.
This condition has two major consequences:
(1) Elevated systemic and pulmonary venous pressures, with signs of right- and left-sided vascular congestion
(2) Reduced ventricular cavity size with decreased stroke volume and cardiac output

Physical Examination
Signs of congestive heart failure are often present, including pulmonary rales, distended neck veins, ascites, and
peripheral edema. Jugular venous distention may paradoxically worsen with inspiration (the Kussmaul sign)
because the stiffened RV cannot accommodate the
increased venous return
Diagnostic Studies
Chest radiograph usually shows a normal sized heart with signs of pulmonary congestion
ECG often displays nonspecific ST and T wave abnormalities; conduction disturbances such as atrioventricular
block or abundle branch block may be present
Transvenous endomyocardial biopsy demonstrates the presence of infiltrative matter such as amyloid, iron
deposits (hemochromatosis), or metastatic tumors
Computed tomography (CT) and Magnetic resonance imaging (MRI)
Useful to identify the thickened pericardium of constrictive pericarditis, a finding that is not expected in
restrictive cardiomyopathy
Treatment
Symptomatic therapy for all etiologies includes salt restriction and cautious use of diuretics to improve symptoms
of systemic and pulmonary congestion. Maintenance of sinus rhythm (e.g., converting atrial fibrillation if it occurs)
is important to maximize diastolic fi lling and forward cardiac output. In the case of Primary (AL) Amyloidosis,
chemotherapy followed by autologous bone marrow stem cell transplantation has proved effective in selected
patients with early cardiac involvement

Sumarry!

Alya Putri Khairani / 13010110220 / B2

Cardiogenic Shock
Cardiogenic shock (CS) is characterized by systemic hypoperfusion due to severe depression of the cardiac index
[<2.2 (L/min)/m2] andsustained systolic arterial hypotension (<90 mmHg), despite an elevated filling pressure
[pulmonary capillary wedge pressure (PCWP) > 18 mmHg]. It is associated with in-hospital mortality rates >50%.
The major causes of CS are:
INCIDENCE
CS is the leading cause of death of patients hospitalized
with MI. Early reperfusion therapy for acute MI
decreases the incidence of CS. The rate of CS
complicating acute MI fell from 20% in the 1960s but
has plateaued at ~8% for >20 years. LV failure
accounts for ~80% of the cases of CS complicating
acute MI
PATHIOPHISIOLOGY
CS is characterized by a vicious circle in which
depression of myocardial contractility, usually due to
ischemia, results in reduced cardiac output and arterial
pressure (BP), which result in hypoperfusion of the
myocardium and further ischemia and depression of the
cardiac output

Systolic myocardial dysfunction reduces stroke volume and,

together with diastolic dysfunction, leads to elevated LV enddiastolic pressure and PCWP as well as to pulmonary
congestion. Reduced coronary perfusion leads to worsening
ischemia and progressive myocardial dysfunction and a rapid
downward spiral, which, if uninterrupted, is often fatal

Alya Putri Khairani / 13010110220 / B2

A systemic inflammatory response syndrome may accompany large infarctions and shock. Inflammatory cytokines,
inducible nitric oxide synthase, and excess nitric oxide and peroxynitrite may contribute to the genesis of CS as
they do to other forms of shock
PATIENT PROFILE
In patients with acute MI, older age, female sex, prior MI, diabetes, and anterior MI location are all associated with
increased risk of CS. Shock associated with a first inferior MI should prompt a search for a mechanical cause.
Reinfarction soon after MI increases the risk of CS. Two-thirds of patients with CS have flow-limiting stenoses in all
three major coronary arteries, and 20% have left main coronary artery stenosis
TIMING
Shock is present on admission in only one-quarter of patients who develop CS complicating MI; one-quarter
develop it rapidly thereafter, within 6 h of MI onset. Another quarter develop shock later on the first day.
Subsequent onset of CS may be due to reinfarction, marked infarct expansion, or a mechanical complication
DIAGNOSIS
Due to the unstable condition of these patients, supportive therapy must be initiated simultaneously with
diagnostic evaluation.
Clinical Findings

Continuing chest pain and dyspnea and appear pale, apprehensive, and diaphoretic
Mentation may be altered, with somnolence, confusion, and agitation
Pulse: weak and rapid, often in the range of 90110 beats/min, or severe bradycardia due to high-grade
heart block may be present
Systolic blood pressure (BP) is reduced (<90 mmHg) with a narrow pulse pressure (<30 mmHg), but
occasionally BP may be maintained by very high systemic vascular resistance
Tachypnea, Cheyne-Stokes respirations, and jugular venous distention may be present
The precordium is typically quiet, with a weak apical pulse
S1 is usually soft, and an S3 gallop may be audible
Acute, severe MR and VSR are usually associated with characteristic systolic murmurs
Rales are audible in most patients with LV failure causing CS
Oliguria (urine output < 30 mL/h) is common

Laboratory Findings

WBC count is typically elevated with a left shift

Blood Urea Nitrogen and Creatinine rise progressively
Hepatic Transaminases may be markedly elevated due to liver hypoperfusion. Poor tissue perfusion may
result in an anion gap acidosis and elevation of lactic acid level
Prior to support with supplemental O2, arterial blood gases usually demonstrate Hypoxemia and metabolic
Acidosis, which may be compensated by Respiratory Alkalosis.
Cardiac markers, Creatine Phosphokinase and its MB fraction, are markedly elevated, as are Troponins I and
T

Electrocardiogram

In CS due to acute MI with LV failure, Q waves and/or >2-mm ST elevation in multiple leads or left bundle branch
block are usually present. More than one-half of all infarcts associated with shock are anterior. Global ischemia due
to severe left main stenosis is usually accompanied by severe (e.g., >3 mm) ST depressions in multiple leads
Chest Roentgenogram

The chest x-ray typically shows pulmonary vascular congestion and often pulmonary edema, but these findings
may be absent in up to a third of patients. The heart size is usually normal when CS results from a first MI but is
enlarged when it occurs in a patient with a previous MI
Echocardiogram

Doppler mapping demonstrates a left-to-right shunt in patients with VSR and the severity of MR when the latter is
present. Proximal aortic dissection with aortic regurgitation or tamponade may be visualized or evidence for
pulmonary embolism obtained
Pulmonary Artery Catheterization

Their use is generally recommended for measurement of filling pressures and cardiac output to confirm the
diagnosis and optimize use of IV fluids, inotropic agents, and vasopressors
Left Heart Catheterization and Coronary Angiopathy

Measurement of LV pressure, definition of the coronary anatomy, and left ventriculography provide useful
information and are indicated in most patients with CS complicating MI. Because of the procedural risk in this
critically ill population, cardiac catheterization should be performed

Alya Putri Khairani / 13010110220 / B2

THE EMERGENCY MANAGEMENT OF PATIENTS WITH CARDIOGENIC SHOCK
Initial therapy is aimed at maintaining adequate systemic and coronary perfusion by raising systemic BP with
Vasopressors and adjusting volume status to a level that ensures optimum LV filling pressure. There is interpatient variability, but the values that are generally associated with adequate perfusion are systolic BP of ~90
mmHg or mean BP > 60 mmHg and PCWP of ~20 mmHg. Hypoxemia and acidosis must be corrected; most
patients require ventilator support with either Endotracheal Intubation or Bilevel Positive Airway Pressure (BiPAP) to correct these abnormalities and reduce the work of breathing. Negative inotropic agents should be
discontinued and the doses of renally cleared medications adjusted. Hyperglycemia should be corrected with
continuous infusion of Insulin. Bradyarrhythmias may require Transvenous Pacing. Recurrent ventricular
tachycardia or rapid atrial fibrillation may require immediate treatment
Vasopressor

Various IV drugs may be used to augment BP and cardiac output in patients with CS.
(1) Norepinephrine
Increases myocardial O2 consumption; it should be reserved for patients with CS and refractory hypotension, in
particular those without elevated systemic vascular resistance. It should be started at a dosage of 2-4 g/min
and titrated upward as necessary. If systemic perfusion or systolic pressure cannot be maintained at >90
mmHg with a dosage of 15 g/min, it is unlikely that a further increase will be beneficial
(2) Dopamine
At low doses ( 2 g/kg per min), it dilates the renal vascular bed; at moderate doses (210 g/kg per min), it
has positive chronotropic and inotropic effects as a consequence of -adrenergic receptor stimulation. At
higher doses, a vasoconstrictor effect results from -receptor stimulation. It is started at an infusion rate of 25
g/kg per min, and the dosage is increased every 25 min to a maximum of 2050 g/ kg per min
(3) Dobutamine
A synthetic sympathomimetic amine with positive inotropic action and minimal positive chronotropic activity at
low doses (2.5 g/kg per
min), but moderate chronotropic activity at higher doses. Although the usual dosage is up to 10 g/kg per min,
its vasodilating activity precludes its use when a vasoconstrictor effect is required
Aortic Counterpulsation

In CS, mechanical assistance with an Intraaortic Balloon Pumping (IABP) system capable of augmenting both
arterial diastolic pressure and cardiac output is helpful in rapidly stabilizing patients. A sausage-shaped balloon is
introduced percutaneously into the
aorta via the femoral artery; the balloon is automatically inflated during early diastole, augmenting coronary blood
flow. The balloon collapses in early systole, reducing the afterload against which the LV ejects. IABP improves
hemodynamic status temporarily in most patients.
IABP is useful as a stabilizing measure in patients with CS prior to and during Cardiac Catheterization and
Percutaneous Coronary Intervention (PCI) or prior to urgent surgery. IABP is contraindicated if aortic regurgitation is
present or aortic dissection is suspected
Reperfusion Revascularization

The rapid establishment of blood flow in the infarct-related artery is essential in the management of CS and forms
the centerpiece of management. Early revascularization with PCI or CABG is a class I recommendation for patients
age <75 years with ST elevation elevation or left bundle branch block MI who develop CS within 36 h of MI and who
can be revascularized within 18 h of development of CS. When mechanical revascularization is not possible, IABP
and fibrinolytic therapy are recommended. Older patients who are suitable candidates for aggressive care should
also be offered early revascularization

Alya Putri Khairani / 13010110220 / B2

PROGNOSIS
Within this high-risk condition, there is a wide range of expected death rates based on age, severity of
hemodynamic abnormalities, severity of the clinical manifestations of hypoperfusion, and the performance of early
revascularization. Independent risk factors are advanced age; depressed cardiac index, ejection fraction, and BP;
more extensive coronary artery disease; and renal insufficiency