Dr M Arman Nasution SpPD

Introduction
 WHO in 1995 defined Cardiomyopathies as diseases of
myocardium associated with cardiac dysfunction
 Types
Dilated Cardiomyopathy(DCM)
Hypertrophic Cardiomyopathy(HCM)
Restrictive Cardiomyopathy(RCM)
Arrythmogenic RVCardiomyopathy(ARVC)
Dilated Cardiomyopathy(DCM)
 DCM is most common of all CMs(60%)
 Aetiology
-Idiopathic (50%)
-Myocarditis (9%)
-Ischemic (7%)
-Others-Viral, Peripartum, Substance abuse etc
 Morphologically
Enlargement of RV & LV cavities without an increase in
ventricular septal or free wall thickness → spherical shape
& dilatation of heart → Displacement of papillary muscles
→ Regurgitant lesions despite valve leaflets being normal
 Dilated CM

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Pathophysiology
 Microscopically –Patchy & diffuse loss of tissue with
interstistial fibrosis & scarring
 Systolic Dysfunction>>> Diastolic dysfunction
 SV is initially maintained by ↑↑ EDV
 With disease progression→Marked LV dilatation with
normal or thin wall →↑ Wall stress + Valvular
Regurgitation →Overt Circulatory Failure
Clinical Features
 Symptoms
-Typically pts c/o months of fatigue, weakness,
reduced exercise tolerance due to CHF
-May also present as a Stroke, Arrythmia or Sudden
Death
 Physical Signs
-Tachycardia
-pulsus alternans
-Jugular venous distension
-Murmurs of AV valve regurgitation
-Gallop heart sounds
Diagnosis
 CXR- Cardiomegaly , Pulmonary venous congestion
 ECG- Normal or low QRS voltage , abn axis, non specific ST
seg abnormalities, LV hypertrophy, conduction defects, AF,
Non sustained VT
 2D Echo
 Coronary Angiography
-usually normal coronaries
-coronary vasodilatation is impaired by ↑ LV filling
pressures
-distinguishes b/w Ischemic & Idiopathic DCM
 Endomyocardial Biopsy
rarely valuable to identify the aetiology
2D Echo
Management
 Aim of treatment
-Manage the symptoms
-Reduce the progression of disease
-Prevent Complications
 Mainstay of Therapy
Vasodilators
+
Digoxin
+
Diuretics
  ACE Inhibitors
Vasodilators (afterload reducing drugs)
-Indicated for all patients
- Reduce symptoms & improve effort tolerance
- Suppress ventricular remodelling & endothelial
dysfunction
-Reduce CV mortality
 Milrinone
-Selective PDE-3 inhibitor
-may improve quality of life but doesn’t affect
mortality
-rarely adm in chronic situations
 Spironolactone
used along with ACE Inhibitors has shown to reduce
mortality by 30% in a large double blind randomized trial
 Digoxin
clinically beneficial as reaffirmed by two large trials in
adults
 β Blockers
untill recently contraindicated but recent studies show that
they not only provide symptomatic improvement but
substantial reduction in sudden death in NYHA class II &
III HF pts
 Amiodarone
-High grade ventricular arrythmias (Sustained VT or VF)
are common in DCM→↑ risk of SCD
-Preferred antiarrythmic agent as it has least negative
inotropic effect & proarrythmogenic potential
-Implantable Defibrillators are used for refractory
arrythmias
 Anticoagulants
-indicated for pts with moderate ventricular
dilatation+mod-severe systolic dysfunction
-H/O stroke , AF or evidence of Intracardiac thrombus
Pts refractory to Pharmacological therapy for
CHF

 Dual Chamber Pacing

 Cardiomyoplasty
 LV Assist Devices
improved pts sufficiently to avoid transplant or enable
later transplant
 Cardiac Transplantation
has substantially prolonged survival in DCM pts with 5
yr survival rate of 78%
Anaesthetic Considerations
 Cardiac procedures which DCM pts undergo
-Correction of AV valve insufficiency
-Placement of ICD device
-LV Assist device placement
-Allograft Transplantation
 Goals of Anaesthetic Mx
- Reduction of afterload
-Optimizing preload
-Minimize myocardial depression
 DCM pts are extremely sensitive to cardiac
depressant anaesthetic drugs
 Anaesthetic Agents
 Fentanyl-(30u/kg )provides excellent anaesthesia &
hemodynamics in pts with EF<0.3
 Remifentanyl- assoc with severe hypotension &
bradycardia ,therefore unsuitable in low EF pts
 Etomidate-least effect on cardiac contractility in pts
undergoing cardiac transplant
 Ketamine-excellent choice in combination with fentanyl
for induction in pts with severe myocardial depression
 Propofol-causes CV depression due to inhibition of
sympathomimetic activity & vasodilatation
 Volatile agents-Desflurane with lowest BG partition
coefficient may allow some benefit for rapid induction,
rapid recovery from anaesthesia & early extubation
 Invasive hemodynamic monitoring
-Mandatory in pts with DCM undergoing surgery
-Physical s/s may not accurately reflect physiological
parameters
-Pts with Implanted defibrillators have severely
depressed cardiac function but are routinely managed
without a PAC
 Hemodynamic Instability
-managed by low dose of inotrope & vasodilator
 Afterload reduction
-improves regional & global indices of ventricular
relaxation & EF during anaesthesia when myocardial
depression may be significant
-it also reduces valvular regurgitation & volumes
 Patients on Amiodarone on long term basis
can interact with anaesthetic agents & further reduce
contractility & conduction-requires careful titration
 Arrythmogenic factors –Hypokalemia,
Hypomagnesemia, & Sympathatic activation should be
monitored & corrected
Hypertrophic Cardiomyopathy (HCM)
 Hypertrophic Obstructive Cardiomyopathy(HOCM)
Idiopathic Hypertrophic subaortic stenosis(IHSS)
Assymetric Septal Hypertrophy
 M/c genetic cardiac disease
Prevalance in adults-0.2%
 Primary myocardial abnormality with sarcomeric disarray
& assymetric LV hypertrophy
Massive left ventricular
hypertrophy, mainly
confined to the septum

Histopathology showing
significant myofiber
disarray and interstitial
fibrosis
 Genetic Basis
 Causes: Inherited,
of HCM
acquired, unknown
 Autosomal dominant
inheritance pattern
 >450 mutations in 13
cardiac sarcomere &
myofilament-related
genes identified
 ?? Role for
environmental
factors
Hypertrophic cardiomyopathy: variants
Hypertrophic cardiomyopathy morphology exhibits heterogeneity. The
mostcommon variant is assymetric septal hypertrophy involving the
entire septum
Pathophysiology
 Subaortic Obstruction
 Diastolic Dysfunction
 Myocardial Ischemia
 Mitral Regurgitation
 Arrythmias
Pathophysiology
Subaortic Obstruction

 Cause -Assymetrical Septal Myocardial Hypertrophy

 Unlike Aortic stenosis hypertrophy begets pressure gradient , not
the other way around
 Wide spectrum of severity of obstruction ch by
Variability- absent to critically severe
Dynamic nature - depends on contractility & loading conditions
Timing - begins early & peaks variably
Location -subaortic
Pathophysiology
 Subaortic Obstruction
Cause-Hypertrophic septum encroaching on the systolic
outflow tract
Bounded-Anteriorly by IVS & Posteriorly by AML
Effect-Systolic anterior motion(SAM) of AML →
accentuating obstruction
Mechanism of SAM
Thickened IVS→Restricted LVOT → ejection of blood at a
higher velocity closer to the AML → Drawing of AML
closure towards the hypertrophied septum due to the
venturi effect during LV systole→ Dynamic LVOT
obstruction
 Factors aggravating SAM & producing Dynamic
Obstruction-
-↑ Contractility
-↓ Afterload (Aortic outflow resistance)
-↓ Preload (End diastolic volume)
 Therapeutically Myocardial depression, Vasoconstriction &
Volume overloading should minimize obstruction &
augment forward flow
 LVOT gradient ≥ 30mmHg assoc with physiologic &
prognostic importance
 LVOTO is assoc with ↑ wall stress, myocardial ischemia,
cell death & eventually fibrosis→VT /VF
 Dynamic LVOTO may also occur in Cardiac tamponade or
Acute MI
Pathophysiology
Diastolic Dysfunction
Hypertrophied & disorganized myocytes with ↑CoT

Impaired relaxation+ ↑ Chamber stiffness

Diastolic Dysfunction→↓ rate of rapid ventricular filling

↑ atrial systolic filling

↑ Filling pressures & pulmonary congestion

Pathophysiology of HCM
 Myocardial Ischemia
 Often occurs without atherosclerotic coronary artery
disease
 Postulated mechanisms
 Abnormally small and partially obliterated intramural
coronary arteries as a result of hypertrophy
 Inadequate number of capillaries for the degree of LV mass
Clinical Presentation
 Dyspnea on exertion (90%)
 Angina (70-80%)
 Syncope (20%)
 Sudden cardiac death
Diagnosis
 ECG-↑ QRS voltage, ST-T changes, Axis deviation, LV
Hypertrophy +strain pattern
 CXR-Lt atrial enlargement or normal
 Echo
 Invasive Cardiac Cath- indicated for suspected CAD
or Severe mitral valve disease
- shows LV pressure gradient,↓ ventricular volume, ↑
LVEDP
(A)Dynamic LVOTO with SAM are shown in this parasternal long-axis (PLAX)
view
(B)Suboptimal mitral leaflet coaptation accompanies SAM and is typically
accompanied by a posteriorly directed MR jet. Note the turbulence created in within the
LVOT
Management
 Pharmacological
 Surgical
 Non Surgical Alternatives
 Implantable Cardioverter Defibrillator(ICD)
 Cardiac Transplantation
 Pharmacological
 β Blockers- mainstay of therapy
relieves symptoms of exercise intolerance & dyspnoea assoc with CHF
by- negative inotropic effect
-HR reduction
-lower myocardial O2 demand
- longer diastolic filling times
 CCB-Verapamil is indicated if β Blockers not tolerated or ineffective
-it improves diastolc function & ventricular relaxation causing
improved filling decreased obstructive features in 50% pts
-CCBs with strong vasodilatory effect are C/I in pts with obstructive
symptoms
 Disopyramide- has negative inotropic & vasoconstrictive effects
-most effective agent to reduce LVOTO , gradient & relieving the
symptoms
 Surgical Correction
 Indications
Subaortic gradients≥ 50mmHg frequently assoc with
CHF & are refractory to medication
 Septal Myotomy +Partial Mymectomy thru a transaortic
approach relieves the obstruction, reduces the LVOTO
gradient, SAM & MR
 Complications –CHB or septal perforation (0-2%)
 Mortality rate-1to 3%
 Intraop guidance & Evaluation of surgical result by an
experienced echocardiographer are essential for the
success of the procedure
Surgical Septal Myectomy

Nishimura RA et al. NEJM. 2004. 350(13):1320.

 Non Sugical alternatives
 Septal Ablation with Ethanol
-Non surgical septal reduction therapy
-2-5 ml of Ethanol is adm thru an angioplasty balloon catheter lumen
to the first major septal perforator of the LAD
- reduce LVOT grad in 85-90% pts immediately
-Further ↓in grad & sympt improvement seen over next 3-6mths
- Permanent heart blocks ( 5-10%)
 Dual Chamber or AV Sequential Pacing(DDD)
-Exact mechanism unkn
-Possible mech: Excitation of the septum of LV contracts it away from
apposing wall which may reduce the LVOT gradient
-now rarely recommended since symptoms actually worsen despite
gradient reductions
 Alcohol Septal Ablation

.
Alcohol Septal Ablation

Before After
Implanatable Cardioverter Defibrillator (ICD)
 HCM is the most common cause of SCD in otherwise
healthy young individuals
 VT /VF is primarily responsible for SCD
 Identification of High Risk Individuals is very important
-Pts < 30yrs at the time of diagnosis
-Prior cardiac arrest
-Symptomatic VT on Holter monitor
-Family H/O SCD or Syncope
 The only effective modality to prevent SCD in HCM pts
is an ICD
 Pharmacological therapy for prevention of SCD in these pts
has been abandoned
 Anaesthetic Considerations
 Aim of Anaesthetic management - Avoid aggravating the subaortic
gradient
 Anaesthetic goals for a patient with HCM are same for cardiac or non
cardiac surgery :
Preload- Increased
Afterload-Increased
Contractility-Depressed
Avoid tachycardia, Inotropes, Vasodilators
 To achieve these,
-Maintain adequate volume status
-Avoid direct or reflex increase in HR or contractility by heavy
premedication & maintaining adequate anaesthesia & analgesia
-Continuation of β blockers or CCBs upto the day of sx & restart
immediately after sx
-Use of vasoconstrictors to maintain MAP or CPP instead of
Inotropes
Anaesthetic Considerations
 Induction- IV Narcotics/
Propofol in carefully titrated doses can be used
 Maintenance-Halothane is advantageous because of its negative
inotropic & chronotropic effect
 Intraop Hypotension- Trendelenburg position, Volume replacement,
& Vasoconstrictors
 Arrythmia management
-Asymptomatic Nonsustained VT-benign
-Pts with ICD device needs to be suspended in presence of
Electrocautery
-Chronic AF :B Blocker+Verapamil
-Amiodarone is effectve in restoring NSR in pts with HCM
 Monitoring
ECG-closely monitor for arrythmias
CVP/PAC/TEE- for volume status, Hemodynamic monitoring
 Avoid Inotropes, B agonists & Calcium
 HCM vs. Athletic Heart
HCM Athletic heart
 Can be asymmetric  Concentric & regresses with deconditioning
 Wall thickness: > 15 mm  < 15 mm
 LA: > 40 mm  < 40 mm
 LVEDD : < 45 mm  > 45 mm
 Diastolic function: always abnormal  Normal
 Occurs in about 2% of elite althetes – typical
sports, rowing, cycling, canoeing

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Restrictive Cardiomyopathy
 WHO in 1995 defined RCM as restrictive filling & reduced
diastolic volume of either or both ventricles with normal or
near normal systolic function & wall thickness
 Classification of RCM
 Myocardial
Nonifiltrative – Idiopathic, Familial, HCM, Diabetic
Infiltrative- Amyloidosis, Sarcoidosis
Storage diseases- Haemochromatosis, Glycogen storage diseases
 Endomyocardial
Endomyocardial fibrosis
Carcinoid
Radiation
Drug Induced –Serotonin, Methysergide, Busulfan, Ergotamine
 Pathophysiology

 Hallmark –Abnormal Diastolic Dysfunction

 Impaired ventricular relaxation & abnormal Compliance causes rapid
filling in early diastole & impeded filling during rest of diastole
 Characteristic
-Ventricular diast waveform of Dip & Plateau (Square root sign)
-RA pressure waveform-M or W shaped due to rapid y descent
 Pressure in the ventricle rises precipitously in response to small volume
 Both ventricles appear thick with small cavities in contrast to
corresponding dilated atria
 Lt sided Pulmonary venous pressure >Rt sided venous pressure by
5mmHg
 PASP↑↑ upto 50mmHg
 Either RVF or LVF or BVF
 Restrictive Pattern
“Square-Root Sign” or “Dip-and-Plateau”
Clinical Features/Diagnosis
 Symptoms of Rt &/or Lt heart failure
 Kussmaul’s sign- ↑ JVP during inspiration
 Pulsus paradoxus- infrquent
 CXR- pulmonary congestion, small heart size
 ECG- BBBs, low voltage, QR or QS complexes
 2D Echo
2D ECHO
Characteristi RCM Constrictive Pericarditis
c
Jugular venous ↑ with more rapid y descent ↑ with less rapid y descent
waveform
Paradoxical Pulse Rare Frequent
Auscultation Late S3, low pitched, S4 occ Early S3,highpitched, No S4
Heart size N to ↑ N to ↑
MR/TR Frequently present Frequently absent
CXR Pericardial calcification rare common
ECG Conduction abn common rare
ECHO Major enlargmt of Atria Slight enlargmt of Atria
LAP>RAP Always Absent
RVP waveform Square root pattern, Dip & Square root pattern
Plateau less prominent
RVEDP/LVEDP
LVEDP>RVEDP by 5mmHg ↑ ↑ & Equal

CT/MRI Rarely thickened Thickened pericardium>3mm

pericardium
Endomycardial Non specific abn Normal
 Management
Depends on the Aetiology

 Idiopathic
Diuretics-To relieve congestion
B-blockers, Amiodarne, CCBs- Control of HR
Long term anticoagulation
CCBs, ACEI- To enhance myocardial relaxation
Dual Chamber Pacing- AV block
Cardiac Transplantation- Refractory Heart Failure
 Amyloidosis- Melphelan, prednisone, H+L transplant
 Haemochromatosis- Phlebotomy, Desferrioxamine
 Carcinoid- Somatostatin analogs, Valvuloplasty/Valve
replacement
 Sarcoidosis –Steroids , Pacing, ICD, Transplantation
 EMF with eosinophilic cardiomyopathy:
Endocardiectomy +TV/MV replacement
Anaesthetic Considerations
 Adults with RCM present for CT or MVR/TVR
 Diastolic dysfunction + filling abn- Poor CO & systemic perfusion
 Aggresive preop diuretic tharapy- Severe hypovolemia
 Pulmonary Congestion leads to ↑ Airway pressures
 Induction-Avoid drugs causing ↓ venous return, bradycardia &
myocardial depression
Fentanyl (30u/kg), Sufentanyl, Etomidate , Ketamine provide stable
hemodynamics for induction
Remifentanil, Propofol –unsuitable
 Invasive hemodynamic monitoring & TEE
 Inotropic support to maintain CO
 Diuretics / Vasodilators may be deleterious because higher filling
pressures are needed to maintain the CO
Arrythmogenic RV Cardiomyopathy (ARVC)
 Progressive replacement of RV myocardium with fat & fibrous
tissue creating an excellent envt of fatal arrythmias
 Typical involves regional RV→Global RV→Partial LV
involvement with sparing of septum
 Familial Inheritance, adolescents
 Presentation
-Onset of Arrythmias from RV range fromVPCs-VF
-SCD 75% due to VT/VF in sports related exercise
-CHF 25%
-Progressive RV & LV Dysfunction
 Diagnosis- Genetics, ECG, Serial Echo, EM Biopsy
ECG-Inverted T waves (Rt precordial leads)
QRS >110ms
Extrasystoles +LBBB
 Anaesthetic Considerations
 Any Family H/O SCD or syncope at an early age must alert
the anaesthesiologist
 Arrythmias are more likely in the periop period
 Intraop /Postop Avoid any noxious stimuli
Light anaesthesia
Inadequate analgesia
Hypercarbia
Hypovolemia
Acidosis-detrimental due to its effect on arrythmia
generation & myocardial function
 GA perse doesn’t appear to be arrythmogenic
 Propofol , Midazolam, fentanyl-successfully used
 Amiodarone- Antiarrythmic of choice during Anaesthesia
 disease of the heart muscle in which the heart loses its ability to
pump blood effectively
 the heart muscle becomes enlarged or abnormally thick or rigid.
 In rare cases, the muscle tissue in the heart is replaced with scar
tissue.
 As cardiomyopathy progresses  the heart becomes weaker and
less able to pump blood through the body  to heart failure,
arrhythmias, systemic and pulmonary edema and, more rarely,
endocarditis
The 3 main types of cardiomyopathy are:
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
 most common form of cardiomyopathy
generally occurs in adults aged 20 to 60 years
more common in men

 the heart muscle begins to dilate or stretch and become thinner


 Ventricular chamber size

over time, the heart becomes weaker  heart failure
 symptoms of heart failure: fatigue, edema, and SOB
 can also lead to heart valve problems (regurgitation),
arrhythmias, and blood clots in the heart (poor blood flow),
emboli formation
 a common reason for needing a heart transplant.
Ischemic cardiomyopathy - caused by CAD & MI , w/c leave scars in the
heart muscle
Idiopathic cardiomyopathy - the cause is unknown.
Hypertensive cardiomyopathy - seen in people who have high BP for a
long time, particuarly when it has gone untreated for years.
Infectious cardiomyopathy - HIV, viral myocarditis
Alcoholic cardiomyopathy - usually begins about 10 years after sustained,
heavy alcohol consumption.
Toxic cardiomyopathy – due to cocaine, amphetamines, and some
chemotherapy drugs (doxorubicin, daunorubicin)
Peripartum cardiomyopathy: This type appears in women during the last
trimester of pregnancy or after childbirth.
Radiotherapy (cobalt)
diabetes and thyroid disease
 occurs when the heart muscle thickens abnormally (left ventricle)
 1.) obstructive type - the septum thickens and bulges into the
left ventricle blocks the flow of blood into the aorta  the
ventricle must work much harder to pump blood past the
blockage and out to the body
- symptoms can include chest pain, dizziness, shortness of
breath, or fainting.
- can also affect the mitral valve, causing blood to leak
backward through the valve.
2.) non-obstructive type - the entire ventricle may become
thicker (symmetric ventricular hypertrophy) or it may
happen only at the bottom of the heart (apical hypertrophy).
The right ventricle also may be affected.
Pathophysiology:
 Left ventricular hypertrophy (thick ventricular wall)  
ventricular chamber size  hold less blood   CO
  pressure in the ventricles and lungs
 changes in the cardiac muscles  interfere with the heart's electrical
signals, leading to arrhythmias  sudden cardiac arrest

Causes:
inherited because of a gene mutation
develop over time because of high blood pressure or aging
often, the cause is unknown.
 tends to mostly affect older adults
the ventricles become stiff and rigid due to replacement of the
normal heart muscle with abnormal tissue, such as scar tissue.
As a result, the ventricles cannot relax normally and expand to fill
with blood, which causes the atria to become enlarged.
Eventually, blood flow in the heart is reduced, and complications
such as heart failure or arrhythmias occur.
Causes:
radiation treatments, infections, or scarring after surgery
Hemochromatosis - a condition in which too much iron is deposited
into tissues, including heart tissue
Amyloidosis, a disease in which abnormal proteins are deposited into
heart tissue
Sarcoidosis, a disease in which inflammation produces tiny lumps of
cells in various organs in the body, including the heart
Having a family history of cardiomyopathy, heart failure, or sudden cardiac
death
Having a disease or condition that can lead to cardiomyopathy, such as:
Coronary artery disease
A previous heart attack
Myocarditis
Diseases that can damage the heart (for example, hemochromatosis,
sarcoidosis, or amyloidosis)
Long-term alcoholism
Long-term high blood pressure
Diabetes and other metabolic diseases
 some have no symptoms in the early stages of the disease
as cardiomyopathy progresses and the heart weakens, signs and
symptoms of heart failure usually appear.
These signs and symptoms include:
Tiredness
Weakness
Shortness of breath after exercise or even at rest
Swelling of the abdomen, legs, ankles, and feet
Other signs and symptoms: dizziness, lightheadedness, fainting during
exercise, abnormal heart rhythms, murmurs
The main goals of treating cardiomyopathy are to:
Manage any conditions that cause or contribute to the
cardiomyopathy
Control symptoms so that the person can live as normally as possible
Stop the disease from getting worse
Reduce complications and the chance of sudden cardiac death
Medications:
Diuretics, which remove excess fluid and sodium from the body.
Angiotensin-converting enzyme (ACE) inhibitors, which lower blood
pressure and reduce stress on the heart.
Beta-blockers, which slow the heart rate by reducing the speed of
the heart's contractions. These medicines also lower BP
Calcium channel blockers, which slow a rapid heartbeat by reducing
the force and rate of heart contractions, decrease BP
 Digoxin - increases the force of heart contractions and slows the
heartbeat.
Anticoagulants, which prevent blood clots from forming. Anticoagulants
are often used in the treatment of dilated cardiomyopathy.
Antiarrhythmia medicines, which keep the heart beating in a normal
rhythm.
Antibiotics, which are used before dental or surgical procedures.
Antibiotics help to prevent endocarditis, an infection of the heart walls,
valves, and vessels.
Corticosteroids, which reduce inflammation.
 Septal myectomy
- also called septal myomectomy
- is open-heart surgery for hypertrophic obstructive
cardiomyopathy
- generally used in younger patients and when medicines aren't
working well.
Procedure:
1. a surgeon removes part of the thickened septum that is bulging
into the left ventricle  this widens the pathway in the
ventricle that leads to the aortic valve and improves blood flow
through the heart and out to the body
2. If necessary, the mitral valve can be repaired or replaced at the same
time. This surgery is often successful, and the person can return to a
normal life with no symptoms.
 Surgically implanted devices.
- Surgeons can place several different types of devices in the
heart to help it beat more effectively.
1. A left ventricular assist device (LVAD)
- helps the heart pump blood to the body
- LVAD can be used as a long-term therapy or as a short-term
treatment for people who are waiting for a heart transplant.
2. An implantable cardioverter defibrillator (ICD)
- is used in people who are at risk of life-threatening arrhythmia
or sudden cardiac death.
- This small device is implanted in the chest and connected to
the heart with wires. If the ICD senses a dangerous change in
heart rhythm, it will send an electric shock to the heart to
restore a normal heartbeat.
Heart Transplant
Left Ventricular
Assist Device
(LVAD)
The doctor may recommend lifestyle changes to manage a condition that is
causing the cardiomyopathy. These changes may help reduce symptoms.
Lifestyle changes may include:

Quitting smoking
Losing excess weight
Eating a low-salt diet
Getting moderate exercise, such as walking, and avoiding strenuous exercise
Avoiding the use of alcohol and illegal drugs
Getting enough sleep and rest
Reducing stress
Treating underlying conditions, such as diabetes and high blood pressure
an operation in which the diseased heart in a person is replaced with
a healthy heart from a deceased donor.
90% of heart transplants are performed on patients with end-stage
heart failure --- condition has become so severe that all
treatments, other than heart transplant, have failed.

Survival rates:
88 % of patients survive the first year after transplant
72 % survive for 5 years
50 % survive for 10 yrs.
16 % survive 20 years.
Patients who might not be candidates for heart transplant
surgery, because the procedure is less likely to be successful.

Advanced age - most transplant surgery isn't performed on

patients older than 70 years.
Poor blood circulation throughout the body, including the brain.
Diseases of the kidney, lungs, or liver that can't be reversed.
History of cancer or malignant tumors.
Inability or unwillingness to follow lifelong medical instructions
after a transplant.
Pulmonary arterial hypertension (high blood pressure in the
lungs) that can't be reversed.
Active infection throughout the body.
Organs are matched for blood type and size of donor and recipient.

The Donor Heart

Guidelines on how a donor heart is selected :
 the donor meet the legal requirement for brain death
 consent forms are signed
 younger than 65 years of age
 have little or no history of heart disease or trauma to the chest
 not exposed to hepatitis or HIV
 donor heart must be transplanted w/in 4 hrs. after removal from
the donor
Heart Transplant (cont.)
 A bypass machine is hooked up to the arteries and veins of the heart. The
machine pumps blood through the patient's lungs and body while the
diseased heart is removed and the donor heart is sewn into place.
Preventing Rejection
Immunosuppressants used: cyclosporine, tacrolimus, MMF (mycophenolate
mofetil), and steroids such as prednisone.
Watching for Signs of Rejection
Shortness of breath
Fever
Fatigue
Weight gain
Reduced amounts of urine
Preventing Infection
Failure of the donor heart
Primary Graft Dysfunction
Rejection of the Donor Heart
Cardiac Allograft Vasculopathy - the walls of the new heart's coronary
arteries become thick, hard, and lose their elasticity. - can cause heart
attack, heart failure, dangerous arrhythmias,
and sudden cardiac arrest
Complications from medicines - risk of infection, diabetes,
osteoporosis , high blood pressure, kidney damage, and cancer
Infection
Cancer – lymphoma and skin cancer (due to suppression of the
immune system)
Ass Wr WB