Bangladesh Journal of Cardiology(Vol. 02,No.02,September 2010) Official Publication of Labaid Cardiac Hospital

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Health & Medicine

Published on March 16, 2014

Author: mominulbd



Bangladesh Journal of Cardiology(Vol. 02,No.02,September 2010) Official Publication of Labaid Cardiac Hospital

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 @, 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

Rahman M, Taimur SDM, Nazneen S et al. 282 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 ReviewArticles

Rahman M, Taimur SDM, Nazneen S et al. 284 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. References 1. Kosti RI, Panagiotakos DB. The epidemic of obesity in children and adolescents in the world. Cent Eur J Public Health 2006;14:151-9. 2. Lazarou C, Panagiotakos DB, Panayiotou G, Matalas AL. Overweight and obesity in preadolescent children and their parents in Cyprus: prevalence and associated socio- demographic factors-the CYKIDS study. Obes Rev 2008 May;9(3):185-93. 3. Yusuf S, Hawken S, Ounpuu S, et al. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case- control study. Lancet 2004;364:937-52. 4. Haslam DW, James WP. Obesity. Lancet 2005;366:1197- 209. 5. Grundy SM. Obesity, metabolic syndrome, and coronary atherosclerosis. Circulation 2002;105:2696-8. 6. Frayn KN. Obesity and metabolic disease: is adipose tissue the culprit? Proc Nutr Soc 2005;64:7-13. 7. McGill Jr HC, McMahan CA, Herderick EE, et al. Obesity accelerates the progression of coronary atherosclerosis in young men. Circulation 2002;105:2712-8. 8. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults-The Evidence Report. National Institutes of Health. Obes Res 1998; 6 Suppl 2: 51S-209S. 9. Prospective Studies C. Body-mass index and cause- specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies. Lancet 2009 Mar 28; 373(9669):1083-96. 10. Franzosi MG. Should we continue to use BMI as a cardiovascular risk factor? Lancet 2006;368:624-5. 11. Sowers JR. Obesity as a cardiovascular risk factor. Am JMed 2003;115(Suppl 8A): 37S-41S. 12. Romero-Corral A, Montori VM, Somers VK, et al. Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies. Lancet 2006;368:666-78. ReviewArticles

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