3. Infectious/inflammatory disorders…
•
•
Any of the heart’s three layers may be affected by
an infectious process.
The infections are named for the layer of the
heart most involved in the infectious process:
infective endocarditis (endocardium), myocarditis
(myocardium), and pericarditis (pericardium).
Firaol R. (MSc) 367
4. Rheumatic fever
•
•
•
•
Rheumatic fever is a diffuse inflammatory disease
characterized by a delayed response to an infection
by group “A” beta-hemolytic streptococci (GAS) in
the tonsilo-pharyngeal area
Affecting the heart, joints, central nervous system,
skin and subcutaneous tissues.
Rheumatic fever causes chronic progressive damage
to the heart and its valves
Rheumatic fever is principally a disease of
childhood, with a median age of 10 years
Firaol R. (MSc) 368
5. Rheumatic fever…
•
•
The association between sore throat and
rheumatic fever was not made until 1880.
The dramatic decline in the incidence of
rheumatic fever in the developed world is thought
to be largely owing to antibiotic treatment of
streptococcal infection, though it stated to
decline before the era of antibiotic, probably due
improvement of socioeconomic status
Firaol R. (MSc) 369
6. Rheumatic fever
•
•
•
Acute rheumatic fever, which occurs most often in
school-age children, may develop after an
episode of group A betahemolytic streptococcal
pharyngitis
Prompt treatment of strep throat with antibiotics
can prevent the development of rheumatic fever.
The Streptococcus is spread by direct contact with
oral or respiratory secretions.
370
Firaol R. (MSc)
7.
Predisposing factors of rheumatic fever include:
Malnutrition
Overcrowding, and
Lower socioeconomic status
As many as 39% of patients with rheumatic fever
develop various degrees of rheumatic heart
disease associated with:
Valvular insufficiency
Heart failure, and
Death
The disease also affects all bony joints, producing
polyarthritis.
371
Firaol R. (MSc)
8. Pathophysiology …
•
•
Acute rheumatic fever is a sequel of a previous
group A streptococcal infection, usually of the
upper respiratory tract is linked directly to acute
rheumatic fever.
Rheumatic fever follows β-hemolytic streptococcus
pharyngitis within the interval of 2-3 week
Firaol R. (MSc) 372
9. Pathophysiology ……
•
•
•
The mechanism is elusive, but the followings are
proposed ones:
Dysfunction of the immune response
Antigenic Mimicry
Similarity between the carbohydrate moiety of GAS
and glycoprotein of heart valve
Molecular similarity between some Streptococcal
antigens and sarcolema or other moiety of human
myocardial cells.
Firaol R. (MSc) 373
10. Pathophysiology…
•
•
The heart damage and the joint lesions of
rheumatic endocarditis are not infectious or the
tissues are not invaded and directly damaged by
destructive organisms; rather,
Leukocytes accumulate in the affected tissues
and form nodules, which eventually are replaced
by scar tissue.
374
Firaol R. (MSc)
11.
Pathophysiology…
If myocardium is involved in this inflammatory
process, rheumatic Myocarditis is developed,
which temporarily weakens the contractile
power of the heart.
The pericardium also is affected, and
rheumatic Pericarditis occurs during the acute
illness
375
Firaol R. (MSc)
12. Clinical Manifestations
•
•
•
•
Valvular regurgitation: When valves do not close
completely, blood flows backward through the
valve in a process called regurgitation
Valvular stenosis: When valves do not open
completely, a condition called stenosis, the flow of
blood through the valve is reduced.
Intractable heart failure
Serious Dysrhythmia
376
Firaol R. (MSc)
13. Assessment and Diagnostic Findings
•
•
The mitral valve is most often affected, producing
symptoms of left-sided heart failure.
SOB with crackles and wheezes in the lungs.
When a new murmur is detected in a patient with a
systemic infection, infectious endocarditis should
be suspected
377
Firaol R. (MSc)
15. Diagnosis of RF
•
•
Diagnosis of acute rheumatic fever requires a
high index of suspicion.
Jones criteria developed by the American Heart
Association is used to make the diagnosis.
Firaol R. (MSc) 379
16. Jones criteria of RF
Major criteria Minor criteria
Carditis
Migratory poly arthritis
Sydenham’s Chorea
Subcutaneous nodules
Erythema marginatum
Clinical
-Fever
-Arthralgia
Laboratory
- Elevated acute phase
reactants : ESR, CRP
Prolonged PR interval
Plus- Supportive evidence of recent Group A streptococcal infection ( e.g.
positive throat culture or rapid antigen detection test ; and/or elevated or
increasing streptococcal antibody test : ASO titer , Anti DNAase , Anti NADase
etc )
Firaol R. (MSc) 380
17. Jones criteria of RF…
• In a ddition to evidence of a previous
streptococcal infection, the diagnosis of acute
rheumatic fever requires 2 major Jones criteria
or 1 major plus 2 minor Jones criteria
Firaol R. (MSc) 381
18. Dx of RF…
d)
e)
1) Carditis, (pancarditis here), occurs in as many as 40- 60%
of patients and may manifest as:
a) New murmur
b) Cardiomegaly
c) Congestive heart failure
Pericarditis with or without a pericardial rub
Valvular disease: mitral and aortic valves are commonly
affected.
Firaol R. (MSc) 382
20. Dx of RF…
2) Migratory polyarthritis- occurs in 75% of cases and
involves many joints at a time.
The larger joints are mainly affected.
Firaol R. (MSc) 384
21. Dx of RF…
3) Subcutaneous nodules: occur in 10% of patients
and are edematous fragmented collagen fi
bers. They
are fi
rm painless nodules on the extensor surfaces of
wrists, elbows, and knees.
Firaol R. (MSc) 385
22. Dx of RF…
•
4) Erythema marginatum - occurs in about 5% of cases.
The rash is serpiginous and long lasting.
Firaol R. (MSc) 386
23. Dx of RF…
5) Sydenham’s chorea (i.e., St Vitus’ dance)- is a
characteristic movement disorder that occurs in 5-10%
of cases.
Sydenham’s chorea consists of rapid purposeless
movements of the face and upper extremities. Onset may
be delayed for several months to years and may cease
when the patient is asleep
Firaol R. (MSc) 387
24. Dx of RF…
•
•
•
Laboratory Studies:
No specific confirmatory laboratory tests exist.
However, several laboratory findings indicate
continuing rheumatic inflammation.
Some are part of the Jones minor criteria.
Firaol R. (MSc) 388
25. Dx of RF…
•
•
•
•
Laboratory minor criteria
Acute phase reactants (e.g. raised ESR and C-
reactive protein [CRP])
Leukocytosis may be seen.
Anemia usually is caused by suppression of
erythropoiesis.
ECG: PR interval prolongation is seen in 25% of all
cases but is neither specific to nor diagnostic
Firaol R. (MSc) 389
26. Treatment of RF
1) Treat group A streptococcal infection regardless of
organism detection.
All patients with acute rheumatic fever should be given
appropriate antibiotic.
Ampicillin 500 mg PO QID or Amoxicillin 500 mg PO TID
for 10 days or
Benzathin penicillin 1.2 million IU IM single dose or
Erythromycin 500 mg PO QID for 10 days ( for
penicillin allergic patient)
Firaol R. (MSc) 390
27. Treatment of RF…
•
2) Therapy for manifestation of acute rheumatic
fever
Arthritis:
ASA is given at dose 2 gm four times per day
for 4-6 weeks, no indication for steroids.
Firaol R. (MSc) 391
28. Treatment of RF…
•
•
•
•
Carditis
Severe Carditis with congestive heart failure should be
treated with;
Prednisolone 60 to 80 mg /day, to be tapered as patient
improves
Start ASA during tapering phase to be given for 4-6weeks
But both have no influence on the future development of
valvular heart disease (VHD).
Firaol R. (MSc) 392
29. Treatment of RF…
•
•
Sydenham’s chorea: In majority of the cases it
is self-limiting.
But in symptomatic patients benzodiazepines
(diazepam) or phenothiazines (haloperidol)
may be helpful in controlling symptoms.
Firaol R. (MSc) 393
30. Treatment of RF…
•
•
3. Administer secondary prophylaxis: is indicated for all
patients with rheumatic fever.
Taking benzathin penicillin is the first choice for better
compliance and longer prevention.
Benzathin penicillin 1.2 million IU IM every 4 weeks ,
but if the there is high risk of recurrence, it can be
given every 3weeks
Alternative antibiotics
Oral penicillin V (250mg twice/day)
Oral sulfadiazine (1g/day)
N.B. In a patient with an established RHD, it is advisable
to get the prophylaxis lifelong.
Firaol R. (MSc) 394
31. Medical Management…
•
*
*
Prophylactic antibiotics are prescribed:
For 5 years (or until age 21) if the patient did
not experience carditis, or
For 10 years (or until age 40,) if the patient
had carditis or develops valvular heart disease.
395
Firaol R. (MSc)
32.
Patients with RF are at risk for:
Embolic phenomena of the lung (e.g, recurrent
pneumonia, pulmonary abscesses)
Kidney (e.g, hematuria, renal failure)
Heart (e.g, myocardial infarction)
Brain (e.g, stroke)
396
Firaol R. (MSc)
33. Infective Endocarditis
•
•
•
Infective endocarditis is an infection of the valves
and endothelial surface of the heart.
Endocarditis usually develops in people with
cardiac structural defects (e.g, valve disorders)
Infective endocarditis is more common in older
people.
397
Firaol R. (MSc)
34. •
•
Infective Endocarditis…
There is a high incidence of staphylococcal
endocarditis among IV injection drug users who
most commonly have infections of the right heart
valves.
Invasive procedures, particularly those involving
mucosal surfaces, can cause a bacteremia.
398
Firaol R. (MSc)
35. Risk Factors for Infective Endocarditis
•
•
•
•
High Risk
Prosthetic cardiac valves
History of bacterial endocarditis (even without
heart disease)
Complex cyanotic congenital malformations
Surgically constructed systemic or pulmonary
shunts or conduits
399
Firaol R. (MSc)
36. •
•
•
•
Moderate Risk
Mitral valve prolapse with valvular regurgitation or
thickened leaflets.
Hypertrophic cardiomyopathy
Acquired valvular dysfunction
Most congenital cardiac malformations and
surgical repair of atrial and ventricular septal
defect, or patent ductus arteriosus as well.
400
Firaol R. (MSc)
37. Pathophysiology
•
•
Infective endocarditis is most often caused by
direct invasion of the endocardium by a microbe :
Streptococci
Enterococcus,
Pneumococcal
Staphylococci
The infection usually causes deformity of the valve
leaflets, but it may affect other cardiac structures.
401
Firaol R. (MSc)
39. Clinical Manifestations
•
•
•
•
•
Fever and a heart murmur
Clusters of petechiae may be found on the body.
Small, painful nodules may be present in the
pads of fingers or toes.
Irregular, red or purple, painless, flat macules
may be present on the palms, fi
ngers, hands,
soles, and toes.
Headache; temporary or transient cerebral
ischemia; and strokes
Firaol R. (MSc) 403
40.
Diagnosis
Blood cultures.
An echocardiogram may assist in the diagnosis by
Demonstrating a moving mass on the valve,
Identification of vegetations, abscesses,
New prosthetic valve dehiscence, or new
regurgitation
Development of heart failure
404
Firaol R. (MSc)
41. Prevention
•
•
A key strategy is primary prevention in high-risk
patients is antibiotic prophylaxis.
Antibiotic prophylaxis is recommended for high risk
patients immediately before and after the
following procedures:
Dental procedures that induce gingival or
mucosal bleeding.
Tonsillectomy or adenoidectomy.
405
Firaol R. (MSc)
42. Management
•
•
•
Appropriate IV antibiotic chosen on the base of
sensitivity study.
Complete eradication takes two weeks
Subsequent blood cultures may be performed to
evaluate the effectiveness of antibiotics
406
Firaol R. (MSc)
43. Myocarditis
•
•
Myocarditis, an inflammatory process involving the
myocardium, can cause heart dilation, thrombi on
the heart wall (mural thrombi), and degeneration
of the muscle fibers themselves.
Most patients with mild symptoms recover
c o m p l e t e l y, b u t s o m e p a t ie n t s d ev e l o p
cardiomyopathy and heart failure.
Firaol R. (MSc) 407
44. Pathophysiology
•
•
Myocarditis usually results from viral (eg. human
immunodef i
ciency virus [HIV], influenza A),
bacterial, rickettsial, fungal, parasitic and
protozoal disease
It also may be immune related, occurring after
acute systemic infections such as rheumatic fever.
Firaol R. (MSc) 408
45. Pathophysiology…
• Myocarditis may result from an inflammatory reaction to
toxins such as pharmacologic agents used in the treatment
of other diseases (Immune suppressive therapy) (eg,
anthracyclines for cancer therapy), ethanol, or radiation
(especially to the left chest or upper back).
Firaol R. (MSc) 409
46. Pathophysiology…
•
•
•
It may begin in one small area of the myocardium
and then spread throughout the myocardium.
The degree of myocardial inflammation and necrosis
determines the effects
The greater the destruction, the greater the
hemodynamic effect and resulting signs and
symptoms
Firaol R. (MSc) 410
47. Clinical Manifestations
•
•
•
•
•
The symptoms of acute myocarditis depend on the degree
of myocardial damage.
Patients may be asymptomatic, with an infection that
resolves on its own.
However, they may develop mild to moderate symptoms and
seek medical attention, often reporting fatigue and
dyspnea, palpitations, and occasional discomfort in the
chest and upper abdomen.
The most common symptoms are flulike.
Patients may also sustain sudden cardiac death or quickly
develop severe congestive heart failure
Firaol R. (MSc) 411
48. Assessment and Diagnostic Findings
•
•
•
Assessment of the patient may reveal no detectable
abnormalities; as a result, the entire illness can go
undiagnosed.
Patients may be tachycardic or may report chest pain
Cardiac MRI with contrast may be diagnostic and can
guide clinicians to sites for endocardial biopsies, which
may be diagnostic for an organism or its genome
Firaol R. (MSc) 412
49. Assessment and Diagnostic Findings
•
•
•
Patients without any abnormal heart structure (at
least initially) may suddenly develop dysrhythmias or
ST–T-wave changes.
If the patient has structural heart abnormalities
(cardiac enlargement, faint heart sounds (especially
S1), a gallop rhythm, or a systolic murmur.
The WBC count and ESR may be elevated
Firaol R. (MSc) 413
50. Management
•
•
•
Patients are given specif ic treatment for the
underlying cause if it is known (eg, penicillin for
hemolytic streptococci) and are placed on bed rest to
decrease cardiac workload.
Bed rest also helps decrease myocardial damage and
the complications of myocarditis.
In young patients with myocarditis, activities,
especially athletics, should be limited for a 6-month
period or at least until heart size and function have
returned to normal
Firaol R. (MSc) 414
51. Management…
• If heart failure or dysrhythmia develops,
management is essentially the same as for all
causes of heart failure and dysrhythmias, except
that beta-blockers are avoided because they
decrease the strength of ventricular contraction
(have a negative inotropic effect)
Firaol R. (MSc) 415
53. Valvular heart diseases
• The valves of the heart control the flow of blood
through the heart into the pulmonary artery and
aorta by opening and closing in response to the blood
pressure changes as the heart contracts and relaxes
through the cardiac cycle.
Firaol R. (MSc) 417
54. Valvular heart diseases…
•
•
•
When any of the heart valves do not close or open
properly, blood flow is affected.
When valves do not close completely, blood flows
backward through the valve, a condition called
regurgitation.
When valves do not open completely, a condition
called stenosis, the flow of blood through the valve is
reduced.
Firaol R. (MSc) 418
55. Mitral disorders
•
Disorders of the mitral valve fall into the following
categories:
Mitral regurgitation
Mitral stenosis
Firaol R. (MSc) 419
56. Mitral regurgitation
•
•
•
Mitral regurgitation involves blood flowing back
from the left ventricle into the left atrium during
systole.
Often the edges of the mitral valve leaflets do not
close during systole.
The leaflets cannot close completely because the
leaflets and chordae tendineae have thickened
and fibrosed
Firaol R. (MSc) 420
57. Mitral regurgitation …
•
•
The most common causes in developing countries
are rheumatic heart disease
Other conditions that lead to mitral regurgitation
include;
Collagen-vascular diseases (eg, systemic lupus
erythematous),
Cardiomyopathy, and
Ischemic heart disease may also result in changes in the
left ventricle
Firaol R. (MSc) 421
58. Pathophysiology
•
•
•
Mitral regurgitation may result from problems with
one or more of the leaflets, the chordae tendineae,
the annulus, or the papillary muscles.
A mitral valve leaflet may shorten or tear.
T he a n n u l u s m a y be s t re t c h e d by he a r t
enlargement or deformed by calcification.
Firaol R. (MSc) 422
59. Pathophysiology…
•
•
•
•
•
Regardless of the cause, blood regurgitates into the atrium
during systole
With each beat of the left ventricle, some of the blood is forced
back into the left atrium, adding to the blood flowing in from the
lungs.
This causes the left atrium to stretch and eventually hypertrophy
and dilate.
The backward flow of blood from the ventricle diminishes the
volume of blood flowing into the atrium from the lungs.
As a result, the lungs become congested, eventually adding extra
strain on the right ventricle
Firaol R. (MSc) 423
60. Clinical Manifestations
•
•
•
Chronic mitral regurgitation is often asymptomatic,
but acute mitral regurgitation (eg, that resulting from
a myocardial infarction) usually manifests as severe
congestive heart failure.
Dyspnea, fatigue, and weakness are the most common
symptoms.
Palpitations, shortness of breath on exertion, and
cough from pulmonary congestion also occur.
Firaol R. (MSc) 424
61. Assessment
A systolic murmur is heard as a high-pitched, blowing
sound at the apex.
The pulse may be irregular as a result of extra systolic
beats or atrial fibrillation.
Doppler echocardiography is used to diagnose and
monitor the progression of mitral regurgitation.
Trans esophageal echocardiography (TEE) provides the
best images of the mitral valve.
Firaol R. (MSc) 425
62. Medical Management
•
•
Patients with mitral regurgitation and heart failure
benefi
t from afterload reduction (arterial dilation) by
treatment with;
Angiotensin-converting enzyme (ACE) inhibitors, such
as captopril (Capoten), enalapril (Vasotec), lisinopril
(Prinivil, Zestril), ramipril (Altace), or hydralazine
(Apresoline);
Firaol R. (MSc) 426
63. Medical Management…
•
•
•
Angiotensin receptor blockers (ARBs), such as
losartan (Cozar) or valsartan (Diovan); and beta-
blockers, such as carvedilol (Coreg).
Once symptoms of heart failure develop, the patient
needs to restrict activity level to minimize symptoms.
Surgical intervention consists of mitral valvuloplasty
(ie, surgical repair of the valve) or valve replacement
Firaol R. (MSc) 427
64. Mitral stenosis
•
•
•
•
Mitral stenosis is an obstruction of blood flowing
from the left atrium into the left ventricle.
It is most often caused by rheumatic endocarditis,
which progressively thickens the mitral valve
leaflets and chordae tendineae.
The leaflets often fuse together.
Eventually, the mitral valve orifi
ce narrows and
progressively obstructs blood flow into the ventricle.
Firaol R. (MSc) 428
65. Clinical Manifestations
•
•
•
•
The fi
rst symptom of mitral stenosis is often dyspnea on
exertion as a result of pulmonary venous hypertension.
Patients are likely to show progressive fatigue as a result of
low cardiac output.
The enlarged left atrium may create pressure on the left
bronchial tree, resulting in a dry cough or wheezing.
Patients may expectorate blood (ie, hemoptysis) or
experience palpitations, orthopnea, paroxysmal nocturnal
dyspnea (PND), and repeated respiratory infections
Firaol R. (MSc) 429
66. Assessment and Diagnostic Findings
•
•
•
•
The pulse is weak and often irregular because of atrial
fibrillation (caused by the strain on the atrium).
A low pitched, rumbling, diastolic murmur is heard at the
apex.
Doppler echocardiography is used to diagnose mitral stenosis.
Electrocardiography (ECG) and cardiac catheterization with
angiography may be used to determine the severity of the
mitral stenosis. Firaol R. (MSc) 430
67. Medical Management
•
•
Patients with mitral stenosis may benefi
t from
anticoagulants to decrease the risk for developing
atrial thrombus
Patients with mitral stenosis are advised to avoid
strenuous activities and competitive sports, both
of which increase the heart rate.
Firaol R. (MSc) 431
68. Medical Management…
•
•
Surgical intervention consists of valvuloplasty,
usually a commissurotomy to open or rupture the
fused commissures of the mitral valve.
Percutaneous trans luminal valvuloplasty or
mitral valve replacement may be performed
Firaol R. (MSc) 432
70. Aortic regurgitation
•
•
Aortic regurgitation is the flow of blood back into
the left ventricle from the aorta during diastole.
It may be caused by inflammatory lesions that
deform the leaflets of the aortic valve, preventing
them from completely closing the aortic valve orifice.
Firaol R. (MSc) 434
71. Aortic regurgitation…
•
•
•
•
This valvular defect also may result from;
Infective or rheumatic endocarditis
Congenital abnormalities
Diseases such as syphilis, a dissecting aneurysm that
causes dilation or tearing of the ascending aorta,
blunt chest trauma.
In many cases, the cause is unknown and is
classified as idiopathic
Firaol R. (MSc) 435
72. Clinical Manifestations
•
•
Aortic insuffi
ciency develops without symptoms in
most patients. Some patients are aware of a forceful
heartbeat, especially in the head or neck.
Exertional dyspnea and fatigue follow. Signs and
symptoms of progressive left ventricular failure
include breathing difficulties (eg, orthopnea, PND).
Firaol R. (MSc) 436
73. Assessment and Diagnostic Findings
•
•
A diastolic murmur is heard as a high-pitched,
blowing sound at the third or fourth intercostal space
at the left sternal border.
The pulse pressure (i.e, difference between systolic
and diastolic pressures) is considerably widened in
patients with aortic regurgitation.
Firaol R. (MSc) 437
74. Assessment and Diagnostic Findings
•
•
One characteristic sign of the disease is the water-hammer
(Corrigan’s) pulse, in which the pulse strikes the palpating
finger with a quick, sharp stroke and then suddenly collapses.
The diagnosis may be confi
rmed by Doppler echocardiography
(preferably trans esophageal), radionuclide imaging, ECG,
magnetic resonance imaging (MRI), and cardiac
catheterization.
Firaol R. (MSc) 438
75. Management
•
•
•
The patient is advised to avoid physical exertion and
competitive sports.
The medications usually prescribed fi
rst for patients
with symptoms of aortic regurgitation are vasodilators
such as calcium channel blockers (eg, nifedipine and
ACE inhibitors (eg, captopril, enalapril, lisinopril,
ramipril), or hydralazine.
Surgery is recommended for any patient with left
ventricular hypertrophy, regardless of the presence
or absence of symptoms
Firaol R. (MSc) 439
76. Aortic Stenosis
•
•
•
Aortic valve stenosis is narrowing of the orifi
ce
between the left ventricle and the aorta.
In adults, the stenosis is often a result of
degenerative calcifications.
Calcif i
cations may be caused by inflammatory
changes.
Firaol R. (MSc) 440
77. Aortic Stenosis…
•
•
•
Diabetes mellitus, hypercholesterolemia,
hypertension, and low levels of high density
lipoprotein cholesterol may be risk factors for
degenerative changes of the valve.
Congenital leaflet malformations or an abnormal
number of leaflets may be involved.
Rarely rheumatic endocarditis may cause adhesions or
fusion of the commissures and valve ring.
Firaol R. (MSc) 441
78. Clinical Manifestations
•
•
•
Many patients with aortic stenosis are asymptomatic.
When symptoms develop, patients usually fi
rst have
exertional dyspnea, caused by increased pulmonary
venous pressure due to left ventricular failure.
Orthopnea, PND, and pulmonary edema may also
occur, along with dizziness and syncope because of
reduced blood flow to the brain.
Firaol R. (MSc) 442
79. Clinical Manifestations…
•
•
•
Angina pectoris is a frequent symptom; it results
from the increased oxygen demands of the
hypertrophied left ventricle.
Blood pressure is usually normal but may be low.
Pulse pressure may be low (30 mm Hg or less) because
of diminished blood flow
Firaol R. (MSc) 443
80. Assessment and Diagnostic Findings
•
•
On physical examination, a loud, rough systolic
murmur may be heard over the aortic area.
The sound to listen for is a systolic crescendo–
decrescendo murmur, which may radiate into the
carotid arteries and to the apex of the left
ventricle.
Firaol R. (MSc) 444
81. Assessment and Diagnostic Findings…
•
•
•
Doppler echocardiography is used to diagnose
and monitor the progression of aortic stenosis.
P a t i e n t s w i t h s y m p t o m s u s u a l l y h a ve
echocardiograms every 6 to 12 months, and those
without symptoms have echocardiograms every 2
to 5 years.
Evidence of left ventricular hypertrophy may be
seen on a 12-lead ECG and an echocardiogram.
Firaol R. (MSc) 445
82. Medical Management
•
•
•
Medications are prescribed to treat dysrhythmia or
left ventricular failure.
Defi
nitive treatment for aortic stenosis is surgical
replacement of the aortic valve.
Patients who are symptomatic and are not surgical
candidates may benefi
t from one-balloon or two-
balloon percutaneous valvuloplasty procedures.
Firaol R. (MSc) 446