Symptoms And Treatment 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]

Dr. Arantza Manzanal explains how takotsubo was initially described “as a syndrome of reversible LV dysfunction with wall-motion abnormalities that involve the apical and midventricular segments” (57). Dr. Paolo Angelini rationalizes that “only during the last 2 decades have Japanese authors specifically categorized transient takotsubo cardiomyopathy (TTC) as an entity in itself. Before that time, TTC was often called “acute myocardial infarction with normal coronary arteries” (312). We will

Coronary artery disease (CAD) is the commonest heart disease in the United States1. Approximately, 29% of patients with Myocardial Infarction ( MI ) present with ST- elevation Myocardial Infarction ( STEMI )2. STEMI is the result of complete occlusion of a major epicardial coronary artery due to thrombus formation. STEMI from a small coronary artery presenting as substantial EKG abnormalities similar to occlusion of a major artery and hemodynamic instability is a rare entity. The epidemiology, typical clinical presentation, outcomes, and optimal management in this group of patients are not sufficiently known.

Ms Chasten was correctly diagnosed and treated for an acute MI complicated by a V Fib cardiac arrest. Her CAD was treated with PTCA and her post MI EF by echo was 20%. She received a LifeVest to protect her while his physicians treated her with beta blockers and

For this myocardial infarction, the right coronary artery was blocked. The parts of the heart that were affected by this blockage was the right atrium, the right ventricle, the interventricular septum, the Sinoatrial node and the AV node, and some parts of the left atrium and ventricle. These parts were affected because the right coronary artery supplies blood to these parts of the heart; since there was a blockage the blood was not able to continue through the right coronary arteries into its branches, which are the sinoatrial nodal artery, the right marginal branch, the posterior interventricular branch, and the atrioventricular nodal artery (Gest).

Anomalous coronary arteries currently affect approximately 1% of the population. And due to the lack of frequency in which coronary anomalies occur, interest and ability to research these anomalies is lacking. The issue is that athletes, specifically young healthy athletes, are at large risk of death from coronary anomalies. In fact, anomalies cause 11.8% of deaths in amateur athletes. This has lead to a current increase in research of these anomalies. Coronary anomalies are typically present at birth, but due to their lack of symptoms they are rarely diagnosed. Encompassing a wide spectrum, these anomalies include but are not limited by: separation of the LAD and LC from the valsalva, absent left circumflex, ectopic origin of the RCA, small

Next we have Cardiac tamponade [which is caused by blunt or penetrating trauma or a few medical conditions such as cancer or autoimmune dieses] which is a serious condition where the blood accumulates in the pericardial sac [the sack around the heart]. While there is no definitive treatment on a basic level and ALS provider can relieve fluid with a needle in a risky but necessary procedure the last form of cardiogenic shock is a pulmonary embolism. A pulmonary embolism is when there is a blood clot blocking the flow of the pulmonary veins leading to obstructive shock and causing heart failure. Interesting enough to mention is the fact that one of the more common causes to cardiogenic shock is damage to the heart muscle however just because you have a heart attack does not necessarily mean you have had caridogenic

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

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.

Despite the absence of a cure or preventative measures for Hypertrophic Cardiomyopathy, there have been notable advances in both diagnostic techniques and successful treatments available.

Our case illustrates that TCM mimicks AMI. Although causality cannot be concluded if there is association. Takotsubo cardiomyopathy represents an estimated 1% to 2% of patients who present with an AMI, but low estimate may be because of under recognition. Advanced age and female are the most common known risk factors for developing TCM. The pathophysiology of TCM is unknown but it is believed to be caused by elevated cathecolamines secondary to acute somatic and emotional stressors.(6,7) Other associated risk factors includes intracranial events, severe infection, surgical trauma and respiratory diseases. Among the physical stressors known to be related with TCM are intracranial occasions, infection, surgical injury and respiratory disease.8 For our situation, the respiratory disease may have contributed to the development of TCM

Cardiopulmonary diseases can include an enormous variety of diseases. It covers all the diseases of the heart and the lungs. Respirations and blood pressure go hand in hand which is why this category is included together. The following paper is on Hypertrophic Cardiomyopathy, specifically focusing on the pediatric population, and even more narrowing on athletes. This is a growing area of concern in the medical field due to the undetected Hypertrophic Cardiomyopathy in athletes until a Sudden Cardiac Death (SCD). Shockingly many athletes are instantly dying on the soccer field and basketball courts not even aware there is a cardiac issue until it is too late. The following paragraphs will explore what is Hypertrophic Cardiomyopathy, who is affected, how it can be detected and what can be done to lower the SCD incidents in young athletes.

Right ventricular infarction may occur with occlusion of the right coronary artery. With infarct affect the posterior wall of the left ventricle and the posterior interventricular septum, they extend to the right ventricular wall in 15 to 30% of cases. The central venous pressure may be elevated markedly if acute right ventricular failure develops. Low right ventricular output causing shock often responds well to vigorous fluid therapy but poorly to vasodilators. Infusions raise both right and left ventricular filling pressures. The diagnosis of right ventricular infarction is difficult but may be established by right sided ECG leads and echocardiographic studies (Bullock, 1996).

The overall character of isolated MB usually shows a benign condition. In asymptomatic patients, therapeutic intervention is not warranted, but in symptomatic patient’s therapy may be initiated to improve quality of life, particularly if there is objective evidence of myocardial ischemia. The main treatment strategy can be divided into three groups: medical therapy, PCI and surgical therapy. Obviously, medical therapy should be the first and principal strategy, and interventions should be limited to patients with refractory angina despite medical therapy.

Takotsubo cardiomyopathy (Broken heart syndrome, Stress cardiomyopathy) is a cardiac condition which usually is described by transient left ventricular dysfunction in the absence of obstructive coronary artery disease where the heart will take the shape of a Japanese Octopus fish trap called Tako-tsubo. Wall motion abnormality of the left ventricle apex is generally transient and resolves within a few days to several weeks. It is often triggered by physical or emotional stressors inclusive of sudden death of a loved person, acute medical illness, perioperative risk while undergoing noncardiac surgery.