CARDIOLOGY CONFERENCE

VALDEZ, Christel
VALENZUELA, Erlyn Joy
VERALLO, Sean Fergie
VERGARA, Tyrone
YOUNG, Julia

VENTRICULAR SEPTAL DEFECT
INTRODUCTION
INTRODUCTION
Henri Roger was the first
man to describe a
ventricular septal defect,
in 1879 he wrote:
A developmental defect of
the heart occurs from which
cyanosis does not ensue in
spite of the fact that a
communication exists between
the cavities of the two
ventricles and in spite of the
fact that the admixture of
venous blood and arterial
blood occurs. This congenital
defect, which is even
compatible with long life, is a
simple one. It comprises a
defect in the interventricular
septum

EPIDEMIOLOGY
Most common CHD in children (25%)
Isolated VSD found in only 10% of adults
with CHD
75-80% of small VSDs close spontaneously by
late childhood
10-15% of large VSDs close spontaneously
60% of defects close before age 3,
90% close before age 8
ANATOMY
A VSD is a
developmental
defect of the
interventricular
septum, wherein
communication
between the
cavities of the 2
ventricles is
observed.
TYPES
PERIMEMBRANOUS VSD: (70-80%) located in the left
ventricle outflow tract beneath the aortic valve; most
common, highest rate of spontaneous closure

MUSCULAR VSD: (5-20%) second most common type of VSD,
occurring in 5-20% of most cases. High rates of spontaneous
closure unless multiple

AV-CANAL TYPE VSD: (5-8%) rarely close spontaneously;
commonly seen in Trisomy 21

SUPRACRISTAL VSD: (5-7%) lie beneath the pulmonic valve
and communicate with the RV outflow tract; least common.



PATHOPHYSIOLOGY
Patent communication between systemic and pulmonary
circulations: Left-to-right shunt
Blood flow through the defect results in
oxygenated blood entering the pulmonary artery
Increased blood flow to the lungs
Increased pulmonary venous return to the LA,
then subsequently to the LV
Increased LV volume LV dilatation and then
hypertrophy
PATHOPHYSIOLOGY
Increased pulmonary blood flow
Increased pulmonary capillary
pressure
Increased pulmonary interstitial
fluid: PULMONARY EDEMA
PATHOPHYSIOLOGY
Blood shunted by VSD away
from aorta
Cardiac output decreases
Compensatory mechanisms
stimulated to maintain adequate
organ perfusion (e.g. catecholamine
release, RAAS)
LEFT-TO-RIGHT SHUNT
PATHOPHYSIOLOGY
During systole, blood leaks from left to right, passes
through the lungs, and re-enters the LV via PV and LA:
2 net effects:
Circuitous refluxing of blood causes volume overload
of LV
Because LV normally has higher pressure (120mmHg)
than RV (20mmHg), leakage of blood elevates RV
pressure and volume: PULMONARY HYPERTESNSION
When PAP reaches levels equal to or higher than systemic
pressure, there is reversal of shunt: EISENMENGER
SYNDROME
EISENMENGER SYNDROME
PAP equal to or higher than the systemic
pressure, there is reversal of shunt from left-to
right, it becomes right-to left
Blood flows from RV to LV causing cyanosis, as
the blood is by-passing the lungs for
oxygenation.
Too late to surgically repair: irreversible damage to
the lung arteries has occurred.
LEFT-TO-RIGHT SHUNT
Pulmonary Flow (Qp) and Systemic Flow
(Qs)ratio is normally equal to 1
The amount of blood that is pumped to the
lungs is equal to the blood that goes to the
body

GRADING
Qp:Qs ratio <1.5 SMALL
Qp:Qs ratio 1.5-2 MODERATE
Qp:Qs ratio >2LARGE

SIGNS AND SYMPTOMS
Initially cyanotic. Presence of shunt reversal eventually
leads to cyanosis.

Pansystolic/Holosystolic murmur along LLSB
+/- palpable thrill
Heart sounds normal
LARGE VSDs: parasternal heave, displaced apex beat

On PE:
Failure to thrive, sweating, tachypnea
DIAGNOSIS
Cardiac auscultation
Considered as sufficient for detection
Echocardiography
May be used to determine the size and location of
VSD; may also provide semi-quantitative information
about shunt volume
MRI
Useful adjunct tool, but infrequently required for the
diagnosis of VSD
ECG
Ventricular hypertrophy
Chest Radiography


VSD REPAIR
Repair is in the first two years of life:
asymptomatic adult survival
normal growth and development

Repair in older children:
late post operative increase in LV chamber size
decreased systolic function is seen

Risk of SBE persists and requires prophylaxis



VSD REPAIR
Development of late postoperative PHTN is
largely determined by the age at surgery and
preoperative PVR

Prognosis: degree of pulmonary vascular
resistance elevation before the operation
< or = 1/3 of systemic: pulmonary disease progression
unusual

MANAGEMENT
Medical
Increased caloric density of feedings
Diuretics
ACE Inhibitors
Digoxin



MANAGEMENT
Surgical Closure

At present, direct surgical repair using
cardiopulmonary bypass is the preferred surgical
therapy in most centers.
Most perimembranous and inlet VSDs are
repaired via a transatrial surgical approach.
Transcatheter Closure

Muscular VSDs have been closed with transcatheter
devices for the past 15 years.
The Amplatzer membranous VSD occluder (AGA Medical
Corporation; Golden Valley, Minnesota), has undergone
phase I trials in the United States
Current recommendations are to use this device in older
patients who weigh more than 8 kg and who have a
subaortic rim of more than 2 mm.
Transcatheter Versus Surgical Closure of
Perimembranous Ventricular Septal
Defects in Children
JOURNAL PRESENTATION
Clinical Question
Is a transcatheter approach safer and more
efficient than a surgical approach in the closure
of perimembranous ventricular septal defect in
children ages 3-12 years old?
P: children ages 3-12 years old with perimembranous
ventricular septal defect
I: open heart surgery versus transcatheter closure
O: safe and efficient closure of perimembranous
ventricular septal defect
M: prospective, randomized, controlled clinical trial

Population
January 2009 - July 2010: 465 children age 3 to 12 years
with pmVSD from 3 major medical centers in northwest
China.
After clinical and transthoracic echocardiographic (TTE)
assessment for eligibility:
236: excluded from the study.
229: randomly allocated to either the surgical or
transcatheter group.


Methodology
ECG. Performed prior to operation or intervention and at each
follow-up visit.

Catheterization. Each patient underwent catheterizaion
before surgery or transcatheter intervention.

Occluding Device. The Shanghai pmVSD occluder was used.
Transcatheter device implantation.
Methodology
Surgical Procedure.
Follow-up protocol. All patients were followed up for 2 years.
Each patient underwent serial follow-up at 3 days, 3 months, 6
months, 1 year, and 2 years following intervention or surgery.
Laboratory tests
Results
Patients
- followed-up until June 2012
- median follow-up of 2 years (2 to 40 months).
29 patients withdrew from the study.
Patients who completed follow-up:
101 patients in the transcatheter group
99 patients in the surgery group

Safety and efficacy are considered in terms of success of the
procedure, complications, cost, hospital stay, and time to
return to normal activities.


Conclusion
Transcatheter device closure and surgical repair are both
effective treatments.

Transcatheter device closure is more practical with fewer
complications.

Transcatheter device closure is the treatment of choice
for pmVSD.
Application in Clinical Setting
Preference of transcatheter approach due to
financial considerations.
Less stressful to patients and staff.
Repetitive Delay in Diagnosis
of Ventricular Septal Defect
JOURNAL PRESENTATION

P: patients with ventricular septal defect
I: color doppler echocardiogram, cardiac
catheterization, angiography
O: diagnosis of ventricular septal defect
M: cross-sectional study
PIOM
CLINICAL QUESTION
Does early diagnosis of ventricular septal defect
(VSD) using color doppler echocardiogram,
cardiac catheterization, angiography will lead to
better outcome?

POPULATION
The study included 145 patients with VSD identified through
clinical findings, color Doppler echocardiogram, cardiac
catheterization, and angiography.

METHODOLOGY
This study was across-sectional study done on 145 patients
with VSD during 54 months in Isfahan. The disease was
identified through color Doppler echocardiogram, cardiac
catheterization and angiography. The required data were
collected at the time of definite diagnosis.
RESULTS
Studying 145 cases of VSD indicated that although
the mean age at initial diagnosis was 17months
(16.7713.70), the mean age at definite diagnosis
was 4months(43.5829.06).

Heart murmur led to the initial diagnosis
in123(85%)cases.
CONCLUSION
Diagnosis of VSD at the age of 44 months is too
late and this might lead to irreparable
complications. It would be appropriate that 88%
and 96% of the patients be diagnosed during the
first and fourth year of life, respectively.
Will the results of the study change our approach in the
management of the patient?

ANSWER: YES because early diagnosis will lead to early
management and avoidance of irreparable complications.

ANSWER: We recommend that as early as 17 months,
with clinical findings of VSD, diagnostic exam should be
done for confirmation of the disease. (our setting here in
UST, we can do ECHOCARDIOGRAM around 2,600
pesos)


CLINICAL APPLICATION