**1. Introduction**

Stress-induced cardiomyopathy is caused by intense emotional or physical stress leading to rapid and severe reversible cardiac dysfunction. This condition can occur following a variety of emotional stressors such as grief, fear, extreme anger, and surprise. On the other hand, many physical stressors (i.e., stroke, seizure or acute asthma) can also trigger the condition. Suspicion of stress cardiomyopathy is based on clinical symptoms, abnormal electrocardiogram (ECG), mildly elevated serum cardiac troponin, significantly elevated serum natriuretic peptide levels (BNP or NT-proBNP), and noninvasive cardiovascular imaging. Stressinduced cardiomyopathy symptoms following severe stress are often indistinguishable from a heart attack and may include: (1) chest pain, dyspnea, or both during stress period (often sudden and intense) [1]; (2) shortness of breath, (3) rapid or irregular heartbeat, (4) sweating and (5) dizziness [2]. The exact pathophysiology of stress-induced cardiomyopathy remains elusive, and several mechanisms may be involved (**Figure 1**).

Considering the causes of stress-induced cardiomyopathy, the exact cause of stress-induced cardiomyopathy is unclear. In patients without coronary heart disease, emotional stress can lead to severe, reversible left ventricular dysfunction. Although the mechanism of stress-induced cardiomyopathy is unclear, excessive sympathetic stimulation may be central to its etiology, perhaps involving excess catecholamines (**Figure 1**), but the link between the two is unclear. One possibility is ischemia due to epicardial coronary spasm; additionally increased sympathetic tone can lead to vasoconstriction in patients without coronary artery disease [3]. Other studies have demonstrated that these patients have reduced coronary flow reserve and regional deficits in cardiac imaging [4]. Another possible mechanism for catecholamine-mediated myocardial stunning is direct muscle cell damage, as the density of adrenergic receptors in the apex is higher than in other areas of the myocardium [1]. Elevated levels of catecholamines lead to a concentration-dependent decrease in muscle cell viability, which can be explained

#### **Figure 1.**

*Schematic diagram of the pathological mechanism of stresses-induced cardiac dysfunction. β-AR, estrogen receptor beta; ROS/RNS, reactive oxygen/nitrogen species; MAPK, mitogen-activated protein kinase; Akt, protein kinase B; mTOR, mammalian target of rapamycin; SERCA2, sarcoplasmic reticulum calcium ATPase 2; RyR, ryanodine receptor; Nrf2, nuclear factor erythroid-derived 2-like 2; ATP, adenosine triphosphate; PDE5A, phosphodiesterase 5A; SIRT1, Sirtuin 1; PGC1-alpha, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; OKG, cGMP-dependent protein kinase or protein kinase G.*

#### *Stress-Induced Cardiomyopathy DOI: http://dx.doi.org/10.5772/intechopen.105584*

by the marked release of creatine kinase in cells and the decreased viability due to calcium overload mediated by circulating AMPs [5]. Animal models suggest that catecholamines are a potential source of free radicals, which in turn may contribute to cardiomyopathy by promoting lipid peroxidation, increasing membrane permeability and muscle cell damage (**Figure 1**) [6]. Myocyte dysfunction may be caused by increased trans-sarcolemmal calcium influx and cellular calcium overload as free radicals interfere with the transport capacity of sodium and calcium transporters (**Figure 1**) [7]. Abnormal coronary blood flow has recently been reported in patients with stress-related myocardial dysfunction in the absence of obstructive disease [8]. Evidence that stress cardiomyopathy may be caused by neurogenic myocardial stunning also revealed a unique pattern of ventricular synergy with meta-iodobenzyl guanidine myocardial scintigraphy, suggesting the presence of cardiac sympathetic hyperactivity and maintaining coronary blood flow [9]. The distribution of primary cardiac injury did not correspond to the perfusion area of a single coronary artery. Plasma levels of catecholamines and stress-related neuropeptides are usually higher than the patient's physiological levels. Unlike polymorphonuclear inflammation in stress cardiomyopathy infarcts, contractile band necrosis is a distinct form of stress-induced cardiomyocyte injury characterized by hypercontraction of sarcomeres, eosinophilic transverse bands, and interstitial mononucleitis, and endomyocardial biopsy shows contractile band necrosis in patients with this syndrome [1]. Research shows that contractile band necrosis is a type of cell death detected as early as 2 min after cell injury, resulting in the release of cardiac enzymes [10]. Excessive circulating catecholamines and focal myocarditis contractile bands were found in the circulatory system of pheochromocytoma, suggesting a circulating catecholamine dependence of focal myocarditis [11], subarachnoid hemorrhage [12, 13], eclampsia [13], and in persons who died from fatal asthma necrosis [14]. All together, these suggest that catecholamines may be the link between emotional stress and heart damage (**Figure 1**).

A surge of stress hormones may temporarily damage the heart, many studies have found. Triggers of stress cardiomyopathy due to stress hormones include: (1) financial stress; (2) surgical stress; (3) bereavement stress; (4) asthma attack stress; (5) chronic disease or diagnostic stress; (6) other. Risk factors for stress cardiomyopathy are also quite different from any physical discomfort, mainly including: (1) age: most cases occur in people over 50; (2) intense physical or emotional events: such as a loved one accidental death, medical diagnosis, sudden economic decline or unemployment, divorce, physical abuse, car accident, major surgery, natural disaster, or intense fear; (3) side effects of certain medications: some are used to treat severe allergic reactions, diabetic neurological problems, depression symptoms or hypothyroidism drugs, etc. may cause a surge in stress hormones, leading to stress cardiomyopathy; (4) gender: this condition affects women much more than men; (5) neurological disorders; (6) previous or current mental illness.

Stress-induced cardiomyopathy is diagnosed by looking for certain markers to distinguish it from other heart conditions. Possible tests should include: (1) blood tests: to check the levels of certain fats, cholesterol, sugars, and proteins in the blood; (2) chest X-ray: common imaging tests of the lungs, heart, and aorta; (3) coronary angiography: this the procedure is usually done in conjunction with cardiac catheterization; (4) echocardiography: this test uses sound waves to take dynamic pictures of the heart's chambers and valves; (5) electrocardiogram (ECG): this test measures the electrical activity of the heart and can help determine whether a part of the heart

is enlarged, overworked, or damaged; (6) Magnetic Resonance Imaging (MRI): uses large magnets, radio waves, and a computer to produce images of the heart and blood vessels.
