Rangkuman PVC

PVC
Sering ditemukan pada pasien dengan atau tanpa penyakit jantung
struktural.
Frekuensi PVC tidak menentukan simtomatik atau asimtomatik.
Patients without clinically apparent SHD + frequent PVC = increased
adverse events
Patients with SHD + PVC = Not clear prognostic importance
Congestive heart failure (LVEF < 35%) + PVC = cannot predict sudden
death or other outcome.
PVC induced PVCs with short coupling interval (< 300 ms)  only

cardiomyopathy
minority  short QT syndrome, VAs.
Presence of SHD:
1. Myocardial scar (Q-waves or fractionated QRS
complexes)
2. QT interval
3. Ventricular hypertrophy
4. Other evidences of SHD.

Rekomendasi untuk ekokardiografi:

• Majority of patients with frequent PVCs will not go on to
develop cardiomyopathy  no accurate risk prediction.
• Frequent PVCs + no SHD  no adverse cardiac events and
no decline in overall LV ejection fraction.
5. Patients with symptomatic PVCs, a high frequency
of PVCs (>10% burden)
6. When the presence of SHD is suspected
Penilaian ekokardiografi:
7. RV and LV structure and function

Diagnostic
8. Valvular abnormalities
9. PA systolic pressure
ECG, ambulatory monitoring
• Conclusions that PVCs are related to symptoms requires
careful correlation.
• Pts with no SHD + PVCs = benign prognosis.
• 12 lead resting ECG  coupling interval, presence of SHD
Diagnostic
Ambulatory monitoring
Diagnostic
ECG, ambulatory monitoring
Exercise testing
Indikasi: Suggestion of symptoms associated w/ exercise
Tujuan:
1. PVCs are potentiated or suppressed by exercise
2. Provocation of longer duration VAs
Interpretasi:
3. Negative exercise test  decrease the probability
that catecholaminergic polymorphic VT is the cause
4. Oositive exercise test  PVCs worsen with exercise
further investigation  more likely to require
treatment.
Imaging investigations
Contrast enhanced MRI
In most of pts 12-lead ECG & echocardiography = enough
Indikasi:
Presence or absence of SHD remains in doubt
Several forms of SHD associated with PVCs  DCM,
HCM, sarcoidosis, amyloidosis, ARVC  myocardial scar
(delayed gadolinium enhancement ) prognostis
Treatment
(Indications for pts w/o SHD)
The presence of symptoms that are not improved by
explanation of their benign nature and reassurance
In frequent asymptomatic PVCs  decline in LV systolic
function or an increase in chamber volume
PVC > 10 000/ 24 h  serial echocardiography and
Holter monitoring
Fewer PVCs  further investigation if only symptoms
increase
Treatment
(Indications for pts w SHD)
• Symptoms are the form the primary grounds for tx.
• High burden PVCs (> 10%) + impaired LV function to
improve LV function (despite significant scarring +)
• Frequent PVCs + interfere with cardiac
resynchronization therapy
Management
Medical therapy
Catheter ablation
Pts SHD Symptoms Treatment Seleksi pasien:
A No + Mild = Education of benign 1. Should only be considered for patients who are markedly
nature, reassurance (1st) symptomatic with very frequent PVCs
Bila simtom tidak 2. Recommended for patients who remain very symptomatic
membaik  BB, CCB despite conservative treatment
non-dihidropiridime 3. Recommended for patients with very high PVC burdens
(2nd)
associated with a decline in LV systolic function.
Notes: No large RCT for pts A Target:
B No + Marked = Membrane-active AADs 4. Complete elimination
5. Partial success  still be associated with significant
Notes: Risk –benefit ratio has not been carefully
evaluated in patients without SHD improvement in LV systolic function.

C Yes + Marked = Membrane-active AADs Lower efficacy:

6. Multiple PVCs morphologies
Notes: Cautious when use membrane-active AADs to
7. Clinical PVC morphology cannot be induced at the time of
suppress PVCs in pts w/ SHD  increased mortality
the procedure
risk; except amiodarone
8. PVCs origin coronary venous and epicardial foci
Bila lead I negative dari septal/posterior, bila positive dari ……..