The Characteristics of Takotsubo Cardiomyopathy

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]

Cardiomyopathies can be caused by genetic disorders/defects, viral illness, some endocrine conditions, autoimmune diseases, and excessive use of alcohol and drugs. Pharmacology treatment of diagnosed LVSD is predominately the same, although it is recognised

Through more research, dilated cardiomyopathy has been found to have a genetic component (MacRae, 2010). Though there have been families who have volunteered to be screened, there are still some 40 chromosomal loci and potential disease genes discovered so far. The reason for the wide range of variants of potential loci is due to how prevalent the disease is in families. For example, the more individuals who have been diagnosed with the disease, researchers were then able to find similar loci among the affected; whereas, the families who had fewer affected individuals laid a wider range of

The coronary artery that was occluded in M.T.’s coronary circulation were the right coronary artery. When coronary blood flow is interrupted for an extended period, myocyte necrosis occurs. This results in MI. In the majority of MI, the decrease in coronary flow is the result of atherosclerotic CAD (McCance & Huether, 2014). M.T. is experiencing transmural MI. According to H. Michael Bolooki (2010), a transmural MI is characterized by ischemic necrosis of the full thickness of the affected muscle segment(s), extending from the endocardium through the myocardium to the epicardium. M.T. was exhibiting crushing substernal chest pain radiating down his left arm. He was complaining of dizziness and nausea. During M.T.’s physical exam, he

The heart cannot help but break for the suffering of children who are marked by the cruelty of congenital diseases. One such disease is tetralogy of tallot which as a congenital ailment occurs at birth and involves four different kinds of cardial defects (Mayo Clinic, 2015). The incidents of tetralogy of fallot is actually quite rare with only five out of every 10,000 developing it at birth (National Heart, Lung, and Blood Institute, 2011). It is still important to be familiar with. One reason for the need of understanding the disease is that of all congenital heart disorders it is the one most frequently seen, and the mortality rate is another consideration as 50% will not survive past the age of six should tetralogy of fallot be left untreated (Bhimji & Mancini, 2015). Finally, while vast improvements have been made in intervention of the disease improving survivability the condition will have an effect upon a patients throughout their lifetimes. It is because of these that it is important for early recognition, diagnosis, treatment and care of the disease be enacted to ensure not only a positive health outcome but also a good quality of life.

Supraventricular tachycardia is increase in heart rate over 150 bpm due to do the over firing or redirected firing of the SA Node conduction above the ventricles. With supraventricular tachycardia the patient can have an abrupt onset and termination of rhythm, flattened or retrograde conduction P waves and narrow QRS waves specifically less than 0.08 second (Kyle, 2012).

Myocarditis is a very difficult disease to treat and to properly diagnose. The disease is symptomatic in some patients and asymptomatic in others. Myocarditis is one of the proposed mechanisms of sudden athlete death (SAD). Cardiovascular diseases are the number one cause of morbidity and mortality in western societies. Myocarditis is an inflammatory heart disease that may be caused by different pathogens and triggers; it is gaining increasing importance because of its links to sudden death syndrome in young athlete, and to dilated cardiomyopathy (Yilmaz et al., 2012). There are many proposed causes of sudden athlete death; one of the primary causes is hypertrophic cardiomyopathy (HCM). As with any disease we should investigate all factors influencing its pathology including but not limited to: genetic, cultural, and environmental factors. Hypertrophic cardiomyopathy is a heritable disease that is typically passed down as an autosomal dominant trait; only one copy of the dominant allele is required to display the effected phenotype.

This condition may be caused by ischemia, hypertension, heart valve abnormalities, alcoholism, as well as hemochromatosis, diabetes and amyloidosis. Idiopathic cardiomyopathies are put in to classes that include arrhythmogenic right ventricular cardiomyopathy, hypertrophic, dilated and restrictive according to gross, minute and clinical features. Spongiform or noncompaction cardiomyopathy is considered a characteristic common to different types of cardiomyopathies.[William, Coleman and Gregory. 2009, Harvey and Leinwand,

Hypertrophic cardiomyopathy (walls of ventricles become thick) with thickening of the walls also come stiffness resulting in the heart being unable to fill adequately also reducing the stroke volume

The rapid degeneration of myocardial fibers and diffuse inflammation lead to ventricular dilation and hypertrophy which cause atrial enlargement and stasis of blood in the left ventricle (Park, 2008). The enlargement of the remaining heart chambers is mainly due to left ventricular failure, but it may also be secondary to the primary cardiomyopathic process. Dilated cardiomyopathy is associated with both systolic and diastolic dysfunctions, with decreased systolic function being the predominant abnormality (Parker, 2008). This dysfunction leads to decreased contractility and general contractile dysfunction (Parker, 2008). Progressive dilation can lead to significant mitral and tricuspid regurgitation, which may further decrease the cardiac output and increase end-systolic volumes and ventricular wall stress. In turn, this leads to further dilation and myocardial dysfunction (Friedberg, 2008). Dilated cardiomyopathy is the most common type of heart muscle disease in pediatrics (Chow, Ateah, Scott, Ricci, & Kyle, 2013). Dilated cardiomyopathy can be a life threatening condition and can decrease life expectancy if severe damage occurs. Currently, the five-year survival rate for children diagnosed with dilated cardiomyopathy is between forty and eighty percent. The survival rate decreases if they child is diagnosed at five years or older (Friedberg, 2008).

Electrocardiographic changes can include left ventricular hypertrophy with repolarisation changes with T wave inversion and deep Q waves. In family members carrying HCM gene mutations, the electrocardiogram may demonstrate only minor abnormalities. The presence of non-sustained ventricular tachycardia, a risk factor for sudden death, should be tested for by means of Holter monitoring (Maron et al., 2003). At present, the diagnosis of HCM relies on echocardiography revealing symmetric or asymmetric hypertrophy. Secondary causes of hypertrophy, including valvular disease or systemic hypertension, should be excluded. 2D imaging of the left ventricle by echocardiography can confirm the diagnosis in affected patients. The ejection fraction, a measure of left ventricular systolic function, is typically preserved but there is usually evidence of diastolic dysfunction. These can be measured by tissue Doppler ultrasonography, which can show diastolic dysfunction before the development of hypertrophy (Maron, 2002). Histologically, HCM is characterized by cardiac myocyte disarray and fibrosis. Myocyte death and myocardial scarring may be present and coronary arteries may have thickened walls. This pathology can promote ventricular tachycardia and ventricular fibrillation (Maron, 2002).

Congenital Heart Defect’s (CHD) affect about 1% of all births in the United States or about 40,000 babies per year (www.CDC.gov). Tetralogy of Fallot (TOF) is a CHD that accounts for an estimated 10% of these births. There are many factors that are involved in the diagnosis, treatment and quality of life for these children. The effects of the CHD vary in severity, therefore the effects it has on a child’s life vary. The etiology of TOF, how specific organs, cells, and tissues are affected, and what organ systems are affected will all be discussed and explained. . The effects vary greatly between patients this paper will focus on the average effects of this condition in order to provide a better understanding of TOF.

Tetralogy of fallot is a complicated and rare congenital heart disease. It happens in 5 out of 10000 babies where males and females are equally affected. Children with Down syndrome or DiGeorge syndrome are more common. It involves four types of heart abnormalities and malformations. The four defects are overriding aorta, pulmonary stenosis, ventricular septal defect and right ventricular hypertrophy. As a result, blood flow is significantly changed where the blood is not fully oxygenated in the lungs and the tissues in the body receive poor oxygenated blood. This causes severe complications and problems to the patients.

The results demonstrated that the extent of LGE was associated with an increased risk of sudden cardiac death events. The estimated risk of SCD events at 5 years increased incrementally with respect to %LGE, ranging from 4.9% in patients with 10% LGE to 6.9% in patients with 20% LGE. It concluded that extensive LGE measured by contrast-enhanced cardiovascular magnetic resonance (CMR) provided additional information for assessing SCD event risk among HCM patients.

In addition, scientists have found that genetics also plays a role in cardiac arrhythmias and that in some cases patients have commented that they had no symptoms before they succumbed to some form of episode of cardiac distress, like a sudden heart attack. This has proven to be standard for many different forms of arrhythmias, whether it’s due to genetics or not. One such case is the long QT syndrome (LQTS) which is estimated to affect one in every 5000 people and is recognized as a family disorder, frequent in children during their childhood years (Wilde, and Bezzina 1352–1358.) Patients with this disorder can have symptoms of a fluttering heartbeat, shortness of breath, and chest pain, while other patients might not experience any symptoms at all (Wilde, and Bezzina 1352–1358.) Another known disorder is cardiac conduction disease, which is mostly due to some form of cardiac injury (Wilde, and Bezzina 1352–1358.) Symptoms for this