**Angelos Tsipis, MD, PhD, MSc**

Department of Cardiology, Onassis Cardiac Surgery Centre, Athens, Greece

Department of Pathology, Medical School, National and Kapodistrian University of Athens, Athens, Greece

**IV**

cular risk in obese individuals."

cardiac patients.

The authors of the second chapter investigate the molecular adaptation of right ventricular (RV) in response to left ventricular (LV) infarction. RV failure is common in patients with acute ST-segment elevated myocardial infarction and animal models of remodeling post-myocardial infarction. However, a systematic analysis of chamber-specific changes in the expression of genes linked to cardiac function, apoptosis, fibrosis, receptor responsiveness, and inflammation is lacking. The underlying reason for biventricular failure due to myocardial infarction and/ or transient ischemic events is not clear but may be a consequence of hemodynamic changes during infarction and ischemic events in the RV as well. Nevertheless, RV failure is a severe complication during the subsequent post-infarct period and a

Human physiological activity and condition during illness are under the control of the circadian rhythm. It is well known that many cardiovascular processes show daily variations depending on the circadian rhythm (blood pressure, heart rate), and the gene expression of the cardiomyocyte circadian clock influences myocardial contractile function, metabolism, and other gene expressions. The authors present a review of the latest knowledge on the impact of circadian rhythm and circadian

The authors of the next chapter discuss the importance of human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) to investigate the mutationspecific mechanism. While animal models fail to recapitulate human cardiac disease phenotype properly, hiPSC-CMs have been successful in recapitulating crucial phenotypes of many genetic cardiac diseases in terms of morphology, contractility, Ca2+ handling, ion channel biophysics, cell signaling, and metabolism. Most strikingly, hiPSC-CMs provide the patient-specific platform to study the disease mechanism and drug response individually, which the traditional disease modeling technique would never offer. In addition, cardiac subtype-specific arrhythmias and drug screening could be performed with the help of an unlimited supply of hiPSC-CMs, thus chamber-specific treatment modalities could be identified. Certainly, by improving the current weaknesses of hiPSC-CMs, and incorporating with new gene-editing techniques, complex cardiac disease mechanisms could be deciphered and novel effective treatment therapies could be identified to improve the life of

In the last decades, major advances have been made in the understanding of molecular and genetic issues, as well as in the pathophysiology and clinical assessment of cardiomyopathies. Especially, understanding the genetic basis of dilated cardiomyopathy (DCM) has improved considerably with the availability of genetic analysis. To further improve the prognosis of patients, it is important to regularly gather knowledge about the current state of DCM and adapt the appropriate diagnostic workups. Therefore, this chapter provides the reader with a comprehensive overview of the current state of DCM from definition over etiology, including the

The following chapter is a review of myocardial changes associated with obesity. It is recognized that obesity contributes to cardiovascular and metabolic disorders through alterations in the levels of adipocyte-derived cytokines called adipokines. The authors conclude that, "our understanding of adipokine biology and obesityinduced adiposopathy increases, and the major challenge will reside in translating this information into new prognostic and therapeutic approaches to limit cardiovas-

genetic aspects to management for cardiovascular specialists.

limitation to further prognosis.

rhythm genes on myocardial infarction.

**1**

Section 1

Myocardial Ischemia

Section 1 Myocardial Ischemia

**3**

**Chapter 1**

*Angelos Tsipis*

**1. Introduction**

and cellular biology of cardiology.

the rate and the rhythm of the heart.

**2. Cardiomyocyte: structure and function**

Introductory Chapter:

Cardiomyocyte - Fundamental

In the field of cardiology, some of the most dramatic advances in recent years have come from understanding the molecular and cellular basis of cardiovascular disease. The knowledge of the pathological basis of disease in some cases allows the development of new strategies for prevention and treatment. This book was planned not only to convey the new facts of cardiovascular diseases but also to boost the excitement and challenges of research in the dynamic area of modern molecular

Cells are the fundamental unit of life, and the large number of them reflects the diversity of their function. The myocardium is composed principally of specialized muscle cells called cardiomyocytes. The major components of cardiac myocytes, cell membrane (sarcolemma) and T-tubules, necessary in excitationcontraction coupling, thereby facilitate a fast and synchronous contraction across the entire cell volume, sarcoplasmic reticulum, nucleus, and contractile elements. Cardiomyocytes contain many more mitochondria than skeletal muscle cells reflecting the dependence of cardiac muscle cell on aerobic metabolism. The functional intracellular contractile unit of cardiac muscle is the sarcomere that contains the contractile proteins myosin and actin. Sarcomeres also contain the regulatory proteins troponin and tropomyosin. Functional integration of myocytes is mediated by intercalated disks, which join individual cells and within which specialized intercellular junctions permit mechanical and electrical coupling. Intercalated disk contains various junctional complexes including the zonula adherens, desmosomes, and gap junctions. One of the most important types of adhesive interactions required for the formation and maintenance of tissues is that mediated by the cadherin family. The expression and distribution of many of these junctional components are often perturbed in cardiovascular disease [1–4]. One of the components of intercalated disks is gap junctions which facilitate synchronous myocyte contraction by providing electrical coupling. Deregulation of gap junction in cardiovascular disease may contribute to electromechanical dysfunction and arrhythmias. In addition, the cardiac conduction system consists of specialized myocardial fibers that conduct electrical impulses more readily than surrounding myocardial fibers and regulate

Unit of Heart Life and Disease
