Takotsubo Cardiomyopathy (TTC)

Takotsubo cardiomyopathy was first acknowledged in Japan in 1990 by Sato et al (Djuric 512). The United States did not have any report of Takotsubo until 1998 (Sharkey e460). Since 1998, scientific interest in Takotsubo has steadily increased. Dr. Scott Sharkey validates the increase in scientific interest: “In 2000, only 2 publications were recorded, compared with nearly 300 in 2010. Now, takotsubo is widely recognized, with reports form 6 continents and diverse countries” (e460).

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The most common manifestation is chest pain (70% to 90%). Less common symptoms includes; dyspnea (20%) and pulmonary edema may be present. Acute heart failure, cardiogenic shock, and cardiac arrhythmias are uncommon.(9,10) About one third of patients with TCM have ECG

Mr S is tachycardic (Awtry, Jeon, & Ware, 2006), which means that there is disruption of the normal electrical impulse. The presence of atrial fibrillation would suggest that the disruption in electrical activity is occurring in the left atrium rather than the sinus node. If the heart rate has been elevated for a prolonged period it could lead to tachycardia induced cardiomyopathy (TIC) which can lead to HF (Patel & Whittaker, 2007). The increase in resting bpm is a compensatory mechanism used to maintain cardiac output when there is a loss in pumping capacity (Watson, Gibbs, & Lip, 2000). The potential diagnosis of heart disease or failure is further evidenced by no palpable apex beat. This displacement of the apex beat usually indicates cardiomegaly; cardiomegaly is a sign that the heart cannot keep up with its workload and so enlarges to compensate (Madhok et al., 2008). This enlarged heart starts to retain fluid, causing the lungs to become congested and can potentially result in the irregular pulse found on investigation (Kruijt & Turin, 2012). This excessive fluid in the airways can also be the cause of inspiratory crackles. If on examination there appeared to be transudate, this can help to add to the clinical suspicion of chronic heart failure. The character of the crackle can also help in diagnosis; a moist late inspiratory crackle suggests restrictive (alveolar)

The third defect is Right Ventricular Hypertrophy, which causes a thicker than normal right ventricle. Right ventricular hypertrophy occurs because the heart pumping action becomes harder creating an increase in the hearts work load. Subsequently, this causes a thicker and more muscular heart muscle. This defect causes also causes a reduction in oxygen flowing to the body. The left side of the heart may be underdeveloped from increased work load on the right side of the heart.

Apical hypertrophic cardiomyopathy is a disease that mainly affects the apex of the heart and does not cause any obstruction. [1] These abnormalities in the heart muscle can cause a wide variety of symptoms. As the heart becomes stiff it increases the pressure in the left ventricle which can push blood back into the lungs, causing shortness of breath in exercise. Chest pain can occur as there is not enough oxygen available to the cardiac muscle due to insufficient blood supply. Palpitations and lightheadedness, along with other conditions can occur as a result of HCM. In addition to these discomforting symptoms, the patient may develop an arrhythmias that often goes unnoticed. An arrhythmia takes place as the electrical conduction of the heart is disturbed by the abnormal scattering of myocytes. The two most common arrhythmias are atrial fibrillation causing palpitations, and ventricular tachycardia that can be life threatening causing sudden death. Both conditions can be controlled with medication. [4]

Takotsubo cardiomyopathy also called as Stress-induced transient cardiomyopathy, apical ballooning syndrome, and broken heart syndrome was first reported in 1991 [1 in Japan, and accounts for 1.2% of acute coronary syndromes (ACS) that present with elevated cardiac biomarkers [1,2,3. The condition is often associated with acute medical illnesses, catastrophic life events, and intense physical or emotional stress [2, 3. Although the pathogenesis of stress-induced cardiomyopathy is not fully understood, the hypothesis includes catecholamine excess [16, coronary vasospasm, micro vascular dysfunction and dynamic mid cavity or left ventricular outflow tract obstruction. Postmenopausal women appear to be at a higher risk for developing the disease as about 80% of Takotsubo cardiomyopathy occurs in postmenopausal women [3].

Takotsubo cardiomyopathy (TC) was originally described in Japan in early 1990s and has been recognized as an increasingly prevalent transient cardiomyopathy triggered by emotional or physical stress. In the past two decades, several variations of this ballooning syndrome have been described including the classic apical ballooning type, a biventricular type , a mid-ventricular type, and finally a basal type [1].

The major causes of diastolic heart failure are hypertension-induced myocardial hypertrophy and myocardial ischemia-induced ventricular transformation (coronary artery disease). Hypertrophy and ischemia cause a decreased ability of the myocytes to actively pump calcium from the cytosol, resulting in impaired relaxation. Some of the other causes are aortic valvular disease and cardiomyopathies. Diabetes can also lead to diastolic heart failure (Huether and McCune 2012). Other risk factors for this disease are chronic kidney disease, obstructive sleep apnea, and older age. There are two types of the heart failure: systolic heart failure and diastolic heart failure. In systolic heart failure, the left ventricle has difficulty contracting and ejecting blood into the circulation, which causes reduced left ventricular fraction. On the other hand, diastolic heart failure has a slow and delayed relaxation and increased chamber rigidity, which then causes inadequate filling of blood and

Hypertrophic cardiomyopathy is characterized by interventricular septal hypertrophy (in absence of other cardiovascular conditions), causing decrease of left ventricle cavity and potentially leading to outflow obstruction. (1) (6) As a consequence of mutations in several genes encoding for thick and thin filaments which build the cardiac muscle, morphological changes occur leading to tangled, thickened myocardial fibers. It is an important cause of morbidity and mortality. Symptomatology varies a lot, from asymptomatic patients to those with severe cardiac function impairment. Some of the most common symptoms of HCM, which are not specific to this disorder may be: shortness of breath at rest or with exertion, fatigue, chest pain, arrhythmias, dizziness, but not only.

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These separate forms of the condition come with distinct traits that vary from one to the next. Dilated cardiomyopathy, “The most common form, this occurs when the muscle fibers of one or both pumping chambers are weak and unable to contract normally” (“Understand Pediatric” 1). Which means that the heart beats abnormally due to lack of blood flow. Often with DCM the heart is weak and fails because it cannot sufficiently pump blood throughout the body (“Understanding Pediatric” 1). The article on “Understanding Pediatric Cardiomyopathy” states that hypertrophic cardiomyopathy is the second most common form. HCM has a few characteristics that can be mistaken for dilated cardiomyopathy. Thick and stiff muscles may stop the heart from contracting properly, which may narrow the passageways for blood to move out of the heart (“Understanding Pediatric” 1). So, the muscles within the heart thicken to try and help blood flow. In an advanced form of hypertrophic cardiomyopathy, there is a chance that the muscles may thin to try to help the poor pumping action (“Understanding Pediatric” 1). When HCM tries to help the body it, in itself, can cause failure. A

Akashi, K. Nakazawa, M. Sakakibara, F. Miyake, H. Koike, K. Sasaka 2003). Echocardiography with left ventricle pathognomonic wall motion abnormalities such as the base contracting normally but the remaining walls being severely hypokinetic is a key diagnostic feature in takotsubo cardiomyopathy. ECG findings are often confused with those found during an acute anterior wall myocardial infarction because they mimic classic ST-segment elevation, T-wave inversion or QT-interval prolongation (Azzarelli S, Galassi AR, Amico F, Giacoppo M, Argentino V, Tomasello SD, Tamburino C, Fiscella A., 2006), making it difficult to diagnose upon presentation. A coronary angiogram, typically used to evaluate individuals with left ventricular dysfunction, will not reveal any significant blockages. Myocardial enzymes rise only moderately at worst, which may be easily overlooked during diagnosis. Blood tests will show increased white blood cell count, to believe bacterial infections are present although the results will usually be negative.

The aim of this case presentation is to improve the nursing knowledge base and to gain a better understanding of the aetiology, diagnosis, nursing management, and medical therapy used in the treatment of peripartum cardiomyopathy.

Cardiomyopathy is an uncommon presentation in hyperthyroid patients. There are very few case reports of Throtoxic cardiomyopathy. The mechanism due to which cardiomyopathy occurs in hyperthyroid patients is not very well understood. After extensive literature search, it was found that some of the mechanisms which are described include genomic and non-genomic and direct action of Thyroid hormone on the cardiac muscle may cause cardiomyopathy. In this case report, a case of Multinodular goitre with dilated cardiomyopathy is described.