Dedication

*Mr Charles Benjamin Flint 20th March 1936 – 17th April 2020*

*One of the many victims of the COVID-19 Pandemic DCG*

**VI**

geographic arrangement from artery to the myocardium with particular emphasis on novel treatments offering continuous myocardial protection, again to preserve tissue and improve overall prognosis. Chapter 14 turns attention to coronary artery bypass grafting (CABG) and the management of ascending aorta calcification which is an independent risk factor for cerebrovascular events post-off-pump CABG procedures. Chapter 15 deals with the surgical methodologies available for reconstructing distal aortic dissection. Chapter 16 identifies the complexities of mitral valve repair and focuses on a novel non-resectional repair technique. The penultimate chapter, chapter 17 discusses the complications of minimally invasive left ventricular assistance devices in patients with advanced cardiac failure. Last but by no means least, Chapter 18 discusses the radical approach of Sanal flow choking and its risk association to asymptomatic cardiovascular disease as demonstrated

The eighteen chapters above offer insight into the current state of the art with respect to risk of developing cardiovascular diseases, maintenance of patent vascular access in patients with cardiorenal syndrome, and a plethora of novel interventional technologies all aimed at salvaging damaged tissue and improving

At the inception of this book, the World was a very different place. With the rapid emergence of coronavirus diseases, the value of the content of this book is now more important than ever; especially through the open-access platform allowing

The editors wish to thank the authors of each chapter for providing their expert insight into the chapter content and responding rapidly to our revision requests. Our gratitude is also extended most humbly to those authors and co-authors who

**Dr. David C. Gaze**

**Dr. Aleksandar Kibel** Osijek University Hospital,

Osijek, Croatia

University of Westminster, London, United Kingdom

such knowledge to be freely available to those in less fortunate situations.

have turned any clinical responsibilities to the fight against COVID-19.

We also wish to extend our thanks to the publishing management team at IntechOpen Publishing, notably to Sandra Maljavac and Dolores Kuzelj.

through a review of *In Vitro* and *In Silico* studies.

prognosis and reducing mortality.

**1**

Section 1

Cardiac Risk

Section 1 Cardiac Risk

**3**

**Chapter 1**

**Abstract**

**1. Introduction**

dysfunction.

myocardial infarction, and stroke [1].

Infarction

Correlations between

*Andrei Bojan and Manuela Ciocoiu*

Inflammation and Thrombosis

in the Pathogeny of Myocardial

*Iris Bararu Bojan, Oana-Viola Badulescu, Maria Vladeanu,* 

Atherosclerosis is the main cause of myocardial infarction. This process involves a complex interplay between metabolic pathways governing lipid deposition, inflammatory and immune responses to oxidized lipids, and endothelial dysfunction. Myocardial infarction appears when these processes culminate with a thrombotic event. Markers of inflammation, such as C-reactive protein (CRP), myeloperoxidase (MPO) and leukocyte levels are strong predictors of cardiovascular death, myocardial infarction, and stroke. This process involves a complex interplay between metabolic pathways governing lipid deposition, inflammatory and immune responses to oxidized lipids, and endothelial dysfunction. Myocardial infarction appears when these processes culminate with a thrombotic event. Markers of inflammation, such as C-reactive protein (CRP), myeloperoxidase (MPO) and leukocyte levels are strong predictors of cardiovascular death, myocardial infarction, and stroke. This review will summarize the molecular and cellular links between inflammation and thrombosis in the context of myocardial infarction, which support the concept of a thrombo inflammatory state leading to the

Myocardial infarction is a form of coronary artery disease, in which the occlu-

Myocardial infarction appears when these processes culminate with a thrombotic event. Markers of inflammation, such as C-reactive protein (CRP), myeloperoxidase (MPO) and leukocyte levels are strong predictors of cardiovascular death,

sion of the coronary artery induces ischemia of the subsequent territory and

Atherosclerosis is the main cause of myocardial infarction. This process involves a complex interplay between metabolic pathways governing lipid deposition, inflammatory and immune responses to oxidized lipids, and endothelial

eventually leads to the destruction of up to a billion myocardic cells.

vessel obstruction and to the subsequent myocardial necrosis.

**Keywords:** thrombosis, inflammation, atherosclerosis
