10. 256
Bangladesh J Cardiol, 2010; 2(2): 256-9Patwary MSR
Intracardiac Echocardiography: An Overview
MSR PatwaryMSR Patwary
National Institute of Cardiovascular Disease (NICVD), Dhaka, Bangladesh
Correspondence : Dr. Mohammad Shafiqur Rahman Patwary, FCPS
Assistant Professor Cardiology, Department of Cardiology
National Institute of Cardiovascular Disease (NICVD)
Dhaka, Bangladesh
Email: dr_md_shafiqur_rahman @ yahoo.com
shafiqur.p@gmail.com, Mobile: 01711675845
FIGURE-1 AcuNav intracardiac Echocardiography Probe
Abstract
Intracardiac echocardiography is now a alternative to
transoesophageal echocardiography for imaging during a
number of interventional procedures. Intracardiac
echocardiography is increasingly being used to guide
percutaneous interventional procedures, principally the
closure of interatrial septal abnormalities, and to support
electrophysiological procedures. Clear views of intracardiac
structures can help a number of other procedures, such as
myocardial biopsy and paravalvular leak closure. The main
advantage of intracardiac echocardiography are clearer
image quality, shorter procedure times, eliminate
chance of esophageal injury during trasoesophageal
echocardiography, reduced need for fluoroscopy and
reduced radiation doses during interventional procedure
and eliminates the need for a general anesthetic during
closure of atrial septal defects.
Introduction
The technology to perform intravascular ultrasound was
developed in the early 1970s but it has taken nearly 30
years to overcome the limitations of poor tissue
penetration, difficult manipulation and size of the probes
to see intracardiac echocardiography emerge into full-time
clinical use1
. Intracardiac echocardiography is now a viable
alternative to transoesophageal echocardiography for
imaging a number of interventional procedures and has
proved particularly successful for guiding the closure of
interatrial septal abnormalities.
Intracardiac echocardiography systems currently available
include the AcuNav catheter (Biosense Webster, California,
USA), the ViewFlexcatheter (EP Medsystems, New Jersey,
USA) and the Ultra intracardiac echocardiography catheter
(Boston Scientific, Boston, USA). The AcuNav ICE catheter
is an 8F or 10F single-use, multifrequency (5-10 MHz), 64-
element, linear phased array, ultrasound catheter that can
perform pulsed and colour doppler imaging (fig 1). It is
capable of tissue penetration of up to 10 cm and has four-
way head articulation to allow multiple angle imaging2
.
Procedure
To perform intracardiac echocardiography, venous access is
usually gained via the right femoral vein under local
anaesthesia and the catheter is gently advanced to the mid-
right atrium. The catheter sometimes needs to be screened
up to avoid catching on venous branches with gentle
anteroposterior steering for tortuous vessels. Advancing a
guidewire through an adjacent sheath can help guide the
catheter to the right heart. The following suggestions will
help image orientation but, as with all imaging modalities,
adjustments need to be made to allow for varying cardiac
anatomy and size. Once in position, the catheters usually
afford an extremely stable position to guide interventional
procedures with only minute per-procedural adjustments
required for image optimization2
.
Visualisation Of Structures With Intracardiac
Echocardiography:
Standard view
The "standard view" is achieved with the intracardiac
echocardiography probe sited in the mid-right atrium and
with the scan plane facing anteriorly. This gives excellent
views of the right atrium, right ventricle and tricuspid valve
(fig 2). From the "standard view" withdrawing the catheter
to the inferior right atrium brings the eustachian ridge, the

36. Rahman M, Taimur SDM, Nazneen S et al.
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Bangladesh J Cardiol, 2010; 2(2): 279-86
people; 50% of 70-year-old Japanese with BMI of 28.0
kg/m2 have diabetes mellitus17,35.
A study31 in newly diagnosed mild type 2 diabetic patients
demonstrated that for any degree of obesity and
abdominal fat distribution, type 2 diabetic patients are
more insulin-resistant than matched non-diabetic
subjects31. Other variables like genetic predisposition,
leading to ß-cell dysfunction, also play a significant role in
the development of the severe insulin resistance of
diabetic patients31. Excessive insulin resistance even with
mild accumulation of body fat may increase the risk of ß-
cell dysfunction, an essential component for the onset of
clinical diabetes31,36. An increase in type 2 diabetes may
have significant impact on public health and could reverse
in the future, the trend toward decreasing CVD mortality31.
4.3. Obesity and adipose tissue function
Initially, adipose tissue was believed to be a passive depot
for storing excess calories. More recently, however, studies
have revealed that adipocytes synthesize and secrete
biologically active molecules implicated in cardiovascular
pathophysiology, able to modify CVD risk. These mediators
or adipokines include adiponectin, resistin, leptin,
plasminogen activator inhibitor-1 (PAI-1), TNF-a, IL-6 and
other less well-characterized molecules32,37-39. Evidence
suggests that adipokines play a pivotal role in body
metabolism homeostasis but are also actively implicated in
the atherosclerotic process39,40. Proinflammatory
adipokines expression is elevated in obese humans and
animals with excess adiposity40; on the other hand a
reduction in fat mass is strongly correlated with a decrease
in circulating proinflammatory adipokines levels. Indeed
visceral fat depot seems to be more active than other body
fat depots in producing a variety of these adipokines40.
Among these mediators, adiponectin and leptin, two of the
most well-studied adipokines, seem to possess a
prominent role. Leptin, an adipokine implicated in the
regulation of appetite, has been recently shown to enhance
cellular immune responses41, and to increase blood
pressure42,43. Furthermore evidence suggests that leptin
increases sympathetic nerve activity, stimulates generation
of reactive oxygen species, induces platelet aggregation
and promotes arterial thrombosis44. Clinical studies show
that leptin is an independent CHD risk factor and a
potentially useful biomarker in CVD44. Addition ally
adiponectin, the most abundant adipose tissue-derived
peptide, has insulin sensitizing properties and is down
regulated in obesity45. Firm evidence suggests that
adiponectin has many anti-inflammatory and
antiatherogenic effects both on myocardium and vascular
wall6. Interestingly adiponectin plasma levels have been
found to be more closely related to the amount of visceral
than total fat.
Conclusively altered expression of adipokines in obesity
might be partly responsible for the insulin resistance state
and accelerated atherosclerosis in obese individuals.
4.4. Obesity and dyslipidemia
It is well established that obesity and insulin resistance
state are strongly associated with quantitative and
qualitative alterations in plasma lipids. Obesity and
obesity-related insulin resistance state are characterized by
impaired adipocytes trapping of fatty acids and excessive
adipocytes lipolysis46. These alterations lead to high
circulating NEFA levels that result in increased hepatic
lipogenesis. Overwhelming of hepatic secretory capacity
leads to hepatic steatosis by the newly synthesized TG and
increased VLDL ApoB circulating levels47. Further to VLDL
dysregulation, obesity is also associated with low HDL
levels. An impaired lipoprotein lipase activity and enhanced
cholesteryl ester transfer protein (CETP)-mediated lipid
exchanged contribute to the observed HDL-C reduction in
obesity46,47. In addition TG-rich HDL-C constitutes a better
substrate for hepatic lipase, further lowering therefore
HDL-C levels. Down regulation of adiponectin may also be
associated with deregulated HDL metabolism in obesity47.
Atherogenic dyslipidemia is clinically presented as elevated
serum TG levels, increased levels of small dense low-
density lipoprotein (sdLDL) particles, and decreased levels
of HDL-C46. Indeed evidence suggests that as BMI
increases over 21 kg/m2, dyslipidemia is progressively
developed, and sdLDL is raised17,46. These changes are
postulated to increase CHD risk by 3-6 fold17. The use of
WC=90 cm for men in combination with plasma TG
levels=2 mmol/L has shown to be highly discriminatory for
the development of CHD32.
4.5. Obesity and cardiac function
It has been long known that morbidly obese subjects
develop obesity-related cardiomyopathy. Nevertheless it is
becoming more and more clear that mild obesity (BMI 25
kg/m2) is also associated with impaired cardiac function. In
a mean 14-year follow-up of 5881 participants in the
Framingham Heart Study48, a graded increase in the risk of
developing heart failure (HF) was observed across BMI
categories. Compared with subjects with a normal BMI,
obese subjects had a doubling of HF risk48. However it
should be also noted that in HF patients higher BMI is not
an adverse prognostic feature49. Instead patients with low
BMI seem to have poorer prognosis, a fact possibly
dependent on HF-related cachexia49.
Ample evidence suggests that obesity is associated with
altered cardiac hemodynamics50. Obesity is characterized
by a hyperdynamic circulation in order to maintain
metabolic demands in the excess adipose depots and
increased fat-free mass50. Furthermore obesity-related
hypertension imposes an elevated afterload to left
ventricle (LV), while obstructive sleep apnoea disorders
may also augment right ventricular afterload50. This altered
hemodynamic profile may lead to eccentric or even
concentric LV hypertrophy (LVH)50. Indeed several studies
have demonstrated a positive association between heart
and body weight20,51. LVH can lead to LV diastolic
dysfunction and evidence suggests that obesity (increased
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38. Rahman M, Taimur SDM, Nazneen S et al.
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Bangladesh J Cardiol, 2010; 2(2): 279-86
better than measurements of percentage of body fat using
dual-energy X-ray absorptiometry62. The International Day
for Evaluation of Abdominal obesity (IDEA)63, a cross-
sectional, study of more than 168,000 primary care
patients, indicated that routine measurement ofWC in
addition to BMI is a useful clinical marker for CVD risk
assessment even in patients with normal weight63.
Ingelson et al.64 investigated the prevalence of subclinical
disease in obesity (generalized and abdominal) by use of a
panel of 5 common tests (electrocardiography,
echocardiography, carotid ultrasound, ankle-brachial
pressure, and urinary albumin excretion), stratified by BMI
category (normal, overweight, and obese) and WC (normal
or increased). It was demonstrated that overweight and
obesity are associated with a high prevalence of subclinical
disease, which partly contributed to the increased risk of
overt cardiovascular disease64.
Anthropometric measurements are useful indices in clinical
practice, however they do not distinguish abdominal
(visceral) fat from subcutaneous abdominal fat. Therefore
more sophisticated methods for assessing body fat
compartments have been used like magnetic resonance
imaging (MRI), computerized tomography (CT), or even
ultrasound65,66. Even though these imaging techniques are
currently regarded more as research tools, they can add
valuable information on cardiovascular risk
stratification65,66. Nevertheless as these newer methods
have not been fully validated yet, simple anthropometric
measurements remain the golden tool readily available to
any clinician for easily assessing the presence of abdominal
obesity.
Management strategies of major risk factors should be
number one priority in obese patients. Further to target
cholesterol levels as have been put forth by ATP III16, it is
highly recommended to keep WC<102 cm (men) /<88 cm
(women), blood pressure <140 / 90 mmHg (or <130/80
mmHg for patients with diabetes mellitus or chronic
kidney disease), a ratio of total cholesterol/ HDL-C <6 67
and glycemic control with fasting plasma glucose <110
mg/dL (6 mmol/L) and HbA1c <6.5% if feasible68. "Healthy"
lifestyle modifications, like discontinuing smoking,
decreasing fat and cholesterol content in diet, consuming
vegetables and fruits and exercising regularly (at least 30
min of moderate activity a day) should also be encouraged.
In cases of severe obesity drugs for weight loss or even
surgical treatment of obesity can be tested. Nevertheless it
should be noted that both drugs and surgery are often
associated with adverse side-effects and complications.
Conclusively, obesity should always be taken into account
in cardiovascular risk stratification and strategies to
promote optimal body weight should be encouraged. WC
should be evaluated in every patient and kept below the
standardized limits. Finally, vigilance for control of other
modifiable risk factors is crucial, given that obese patients
are at increased cardiovascular risk compared to non-obese
population.
6. Conclusion
"Obesity epidemic" is a major social problem, expanding
rapidly from Western societies to the rest of the world. It is
directly linked to cardiovascular risk, and it is now
considered as a major, independent risk factor for
atherosclerosis. Understanding of the mechanisms leading
to obesity, and those linking obesity with cardiovascular
disease is crucial for the design of therapeutic strategies
targeting obesity in the context of atherosclerosis
prevention. Therefore, obesity should be considered as a
disease requiring treatment and more importantly
prevention in the general population.
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