*6.1.7 Cardiac CT coronary angiography*

CT coronary angiography is an alternative for the quantification of calcified or noncalcified plaque. This approach is useful in specific subset of symptomatic patients with obesity or when stress test is equivocal, uninterpretable stress test, or in cases when a discrepancy exists between clinical presentation and stress test results. This technique allows evaluation of luminal stenosis and plaque characterization and quantification [50].

One major challenge with CT coronary angiography is that image quality degrades as BMI increases; this degradation increases in background noise. In patients with overweight can reduce signal-to-noise ratio, and low vessel opacification may occur when contrast is inspected.

#### **6.2 Invasive evaluation of CAD in obesity**

#### *6.2.1 Coronary angiography*

Patients undergoing catheterization have potential difficulties: suboptimal radiographic visualization, vascular access laborious, bleeding, radial access is preferred in obesity patients because it has been associated with three times lower rate of complications than transfemoral access and higher radiation exposure to both patients with obesity and staff [51].

#### *6.2.2 PCI and obesity*

In the Cath PCI Registry after multivariable adjustment obesity was independently associated with a greater mortality rate and lower bleeding rate. Adequate anticoagulation is important in this subpopulation [52, 53]. Another study reported that patients with severe obesity have major risk of contrast-induced nephropathy. Dialysis and vascular complications, gastrointestinal bleeding, and MACE (Major Adverse Cardiovascular Events) are not statistically different [54].

#### *6.2.3 Intravascular ultrasound*

Several intravascular imaging techniques such as intravascular ultrasound, virtual histology intravascular ultrasound, and optical coherence tomography allow in vivo assessment of plaque burden, plaque morphology, and response to therapy.

Abdominal visceral adiposity independently predicted the presence and extent of noncalcified coronary plaque that also contained multiple features of plaque vulnerability [55].

The appropriate choice of test to assess CVD depends on local expertise, the relative strengths and weaknesses of each modality, and individual patient characteristics that contribute to the pretest likelihood of CVD and the risk/benefit ratio of using a given modality.

## **7. Clinical management, treatment, and secondary cardiac disease**

Obesity paradox refers to the fact that although obesity increases the risk of CVD for those who had already an CVD, excess weight is not a risk factor to develop adverse outcomes including death [56].

Although weight loss would be believed to significantly benefit cardiovascular outcomes, this benefit has only been shown in weight loss performed through bariatric surgery in which more than 10–15% of body weight is lost; therefore, that modest weight loss has not been shown to impact cardiovascular outcomes [57, 58].

#### *Obesity and Cardiovascular Risk DOI: http://dx.doi.org/10.5772/intechopen.106877*

To treat obesity requires a multidisciplinary management in which the eating pattern, amount of exercise, stress, sleep pattern are evaluated. So, it is not enough exercise and nutrition to evaluate all the factors related to weight gain together.

Some clinical trials demonstrate the cardiovascular impact of Mediterranean diet in reducing MACE in patients with high cardiovascular risk. However, lifestyle changes in diabetes patients have failed to show a significant reduction in MACE, only those with weight loss greater than 10% had significant results [59, 60].

Pharmacological treatment has impact on weight reduction as well. For example, liraglutide has been shown to reduce death by 13% and 22% from cardiovascular causes in patients with type 2 diabetes in LEADER trial [61].

Recently semaglutide at 2.4 mg dose in obese patients without diabetes has demonstrated a significant body weight reduction (14.9% vs. 2.4% with placebo). In total, 69% of body weight reduction ≥10% at 68 weeks and 50% body weight reduction ≥15% .

Further reduction in waist circumference, systolic blood pressure, and improvement of physical function [62].

Orlistat was approver in 1998 for the treatment of obesity and demonstrated 37% reduction in progression from prediabetes to diabetes and significant reduction of associated disease such as hypertension and blood lipid levels [63].

Naltrexone SR/Bupropion SR is another drug approved in the United States for the treatment of obesity and has cardiovascular security trial (LIGHT trial – Cardiovascular Outcomes Study of Naltrexone SR/Bupropion SR in Overweight and obese subjects with cardiovascular risk factors). Bupropion suppresses appetite transiently due to an endorphin-mediated mechanism of action. Naltrexone blocks the endorphin, which allows a long-term appetite suppression effect [64]. However, because of the early unanticipated termination of the trial, it is not possible to assess non-inferiority to the prespecified upper limit of 1.4. Consequently, the cardiovascular safety of this treatment remains uncertain and will require evaluation in a new adequately powered outcome trial.

Lorcaserine was approved in the obesity treatment but recently was removed for the Food and Drug Administration (FDA), due to a possible increased risk of cancer [65].

Finally, patients with body mass index greater than 35 kg/m2 with comorbidities or greater than 40 kg/m<sup>2</sup> without them get benefit from bariatric surgery. Nonrandomized prospective studies desmonstrated a reduction of cardiovascular death in this group of patients [66].
