Diagnostics
Electrocardiographic manifestations of cardiac infectious-inflammatory disorders

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Abstract

Inflammatory disorders of the heart, although uncommon in the general population, often present initially to the emergency department. Symptoms and clinical manifestations are shared with other more common cardiopulmonary diseases, particularly acute coronary syndrome and congestive heart failure, making prompt diagnosis challenging. This review will highlight some of the clinical and electrocardiographic features that will help early diagnosis and differentiation of inflammatory cardiac disorders from other more common conditions.

Introduction

The tissue of the heart is generally divided into 3 layers: the outer covering, or pericardium; the muscular myocardium; and the inner layer, endocardium. The pericardium, which also covers the proximal ends of blood vessels entering and exiting the heart, is essentially a double-layered sac. The outer layer is the relatively thick and rigid fibrous pericardium, whereas the inner serous pericardium is divided into an outer parietal layer that lines the surface of the fibrous pericardium and an inner visceral layer that adheres to the surface of the heart, more commonly referred to as the epicardium[1]. The pericardial space is formed between the 2 layers of the serous pericardium and, under normal conditions, is filled with approximately 50 mL of plasma ultrafiltrate (Fig. 1A and B).

The pericardium, although not essential for cardiac function, works to limit distention of cardiac chambers and effectively couples the ventricles and atria so that changes in pressure and volume are transmitted throughout the heart. It also helps to protect the heart from inflammation or infection spreading from adjacent structures. The pericardium is composed of collagen (predominately) and elastin; the low ratio of elastin to collagen accounts for its ability to stretch only with gradual, long-term pressure. The myocardium is a relatively thick layer of muscle. The endocardium is significantly thinner and is comparable to the endothelium of the vasculature, consisting of epithelial and connective tissue [1] (Fig. 1A and B).

The inflammatory disorders of the heart are classified according to the anatomic layer, or segment of the heart, affected: pericardium (pericarditis), myocardium (myocarditis), and endocardium (endocarditis); in some cases, 2 segments can be involved, such as with myopericarditis. These various conditions are not infrequently encountered in the emergency department (ED). Their presentations are most often straightforward. Yet at times, the diagnosis is difficult in that subtle findings and nonspecific symptoms can be the early and/or only manifestations. In addition, they can mimic other common diseases such as acute myocardial infarction (AMI), “flu-like” viral illnesses, and chest infections such as bronchitis or pneumonia. Although pericarditis may present with “classic” electrocardiographic (ECG) findings, patients with myocarditis and endocarditis can also present with variable ECG findings depending on the severity and anatomic involvement of the disease process. This review focuses on the ECG findings and presentations of these cardiac inflammatory disorders.

Section snippets

Myocarditis

Myocarditis refers to inflammation of the myocardium resulting from a range of heterogeneous etiologies. These various causes are generally grouped into infectious, autoimmune, or non–immune-mediated insults. In the case of infection, it is believed that immune-mediated processes are responsible for myocardial damage rather than to pathogen-directed cytotoxicity. Fungal, protozoal, parasitic, bacterial, and viral pathogens have all been implicated. Some common viral pathogens are adenovirus,

Endocarditis

Endocarditis has long been recognized as an infection of the endocardial surface of the heart, often involving not only the heart valves but also the mural endocardium or septum. It is seen more often in intravenous drug users, patients with prosthetic heart valves, or those individuals with congenital structural anomalies of the heart. Often these infections are secondary to episodes of bacteremia or fungemia. Implicated pathogens have an increased ability to adhere to surfaces and thus a

Pericarditis

Pericarditis involves inflammation of the pericardium. It often involves the closely opposed superficial epicardium and can readily extend to the adjacent myocardium, thus developing into myopericarditis (Fig. 1A and B). Pericarditis can result from a diverse group of insults including infectious, autoimmune/connective tissue disease, post–myocardial infarction, malignancy, trauma/iatrogenic, or toxins. In many cases, the cause is unknown and is often simply called postviral or, more

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