PENYAKIT JANTUNG KATUP

NON-RHEUMATIK
Until the mid-20th century the predominant
etiology of acquired valvular heart disease
world wide was rheumatic
In developed countries  incidence of rheumatic
disease declined after the second half of the 20th
century as a result of improvements in living and
health care conditions

These improvements increased longevity so

that valve conditions characteristic of old age
predominante (age-related valvular heart
disease)
AORTA STENOSIS
AORTA STENOSIS
Aortic valve : maintains the
anterograde flow of blood to the
aorta
Consists of 3 thin, mobile, fibrous
cusps attached to the aortic wall
in a crescentic or semilunar
manner.
• Normal aortic valve area is 2-4 cm2
• A gradient between LV and aorta
appears if valve area < 1.5 cm2
• Considered severe < 1 cm2
AORTA STENOSIS
Narrowed aortic valve commonly
due to calcium build up causing
obstruction to left ventricle
outflow during systolic

The morphologic hallmark of non-

rheumatic  heaped-up calcified
masses within the aortic cusps
that protrude through the outflow
into the sinuses of Valsalva,
preventing the opening of the
cusps.
ETIOLOGI
 AORTIC
REGURGITATION
ETIOLOGY
ANATOMI
MITRAL

 Subvalvular apparatus
(papillary muscles with
their supporting left
ventricular walls and
chordae tendineae)
 Mitral annulus
 Mitral valve leaflets
 ISCHEMIC
MITRAL REGURGITATION
2 different mechanisms :
1. Acute or subacute ischemic MR
• Papillary muscle rupture
• Papillary muscle infarction (lack of
contractility)

2. Chronic ischemic MR
• Alteration in LV size, shape, pappilary
muscle gemometry, annular dilatation,
depressed LV systolic function
 Precordial palpation

• Location, amplitudo, duration, and reffereal of impuls  tip of the

fingers
• Normal impuls on apex = ICS V MCL sinistra
• LVH  exaggeration of the amplitude, duration and often size of the
normal left ventricular thrust.
The impulse may be displaced laterally and downward into the sixth or
seventh intercostal space.
• RVH  often results in a sustained systolic lift at the lower left
parasternal area

Swanton 2003 ; Loscalzo 2010

 Precordial palpation

• Abnormal precordial pulsations occur during systole (left

ventricular dyssynergy due to ischemic heart disease or diffuse
myocardial disease)  left midprecordium, one or two
interspaces above the left ventricular apex
• Thrills are palpable, low frequency vibrations associated with
heart murmurs (≥ 4 grade murmur)
• Percussion should be performed to identify normal or abnormal
position of the heart, stomach, and liver

Swanton 2003 ; Loscalzo 2010

 Cardiac auscultation – Heart Sound
• The first heart sound (S1)  mitral (M1) & tricuspid (T1) valve closure

• Splitting of S1 by 10–30 ms is a normal phenomenon

• The first component of S1 is usually mitral valve closure, and the second to
tricuspid valve closure
• Widening of the S1 is due most often to complete RBBB

• S1 is louder  shortened (tachycardia), increased AV flow (high cardiac

output or prolonged because of mitral stenosis
• A soft S1  poor conduction of sound through the chest wall, a slow rise of
the left ventricular pressure pulse, immobile anterior mitral leaflet (rigidity
and calcification)

Loscalzo 2010 ; Lily 2011 ; Bonow 2012

 Cardiac auscultation – Heart Sound

• The second heart sound (S2)  aortic (A2) and pulmonic (P2) valve closure

• This sound (S2) normally splits into audibly distinct aortic (A2) and pulmonic
(P2) components during inspiration, when the augmented inflow into the
right ventricle and thus delays closure of the pulmonic valve
• A2 usually louder than P2, in pulmonary hypertension P2 is louder

• Fixed splitting S2, independent of respiration  ASD

• Paradoxical splitting  a delay in aortic valve closure causing P2 to precede

A2  LBBB, aortic valve disease

Loscalzo 2010 ; Lily 2011 ; Bonow 2012