Diabetes, Heart and Cardiovascular Diseases News Chronicle.  Diabetes, Cardiovascular and Heart Diseases
 Article 216
    Published on July 26, 2017

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Broken heart or Takotsubo syndrome causes lasting damage to the heart muscle

In United Kingdom, more than 3,000 people are affected every year with "broken heart syndrome" (also known as Takotsubo syndrome or Takotsubo cardiomyopathy) and these symptoms are similar to heart attack and syndrome. Studies shows women were affected mostly with "broken heart syndrome". Till now, healthcare professionals thought that the heart would recover fully after "broken heart syndrome" without a medical intervention. A current study by researchers at the Aberdeen University, Aberdeen, United Kingdom shows long-lasting damages to heart and a temporary heart failure condition with "broken heart syndrome" condition. The "broken heart syndrome" may be triggered due emotional distress (due to a sudden rush of hormones). The life expectancy of an individual with "broken heart syndrome" is similar to a heart attack patient.


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Statistics shows between three percent and 17 percent of the people die due to "broken heart syndrome" within five years of diagnosis. About 90 percent of the suffers were female individuals and a stressful trigger condition was identified in about 70 percent of them. Researchers studied heart functioning of 52 patients with "broken heart syndrome" using cardiac MRI scans and ultrasound. The study results shows heart muscle's pumping motion and squeezing motion actions during heartbeat were affected with "broken heart syndrome". They also observed fine scars in some parts of the heart muscle causing reduction in the elasticity of the heart. Reduction in the elasticity prevents proper contraction of the heart.


Broken heart or Takotsubo syndrome causes lasting damage to the heart muscle.
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Authors of the study say their study shows need to find out effective treatment for "broken heart syndrome". Lead author of the study was Dr. Dana Dawson, Reader in Cardiovascular Medicine, Aberdeen University, Aberdeen, United Kingdom. The study findings were published in the Journal of the American Society of Echocardiography (JASE), under the title "Alterations in Cardiac Deformation, Timing of Contraction and Relaxation, and Early Myocardial Fibrosis Accompany the Apparent Recovery of Acute Stress-Induced (Takotsubo) Cardiomyopathy An End to the Concept of Transience". The British Heart Foundation (BHF) has funded this project.


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AT04A vaccine reduces LDL cholesterol and atherosclerosis to prevent heart disease

Scientists at the AFFiRis, Austria have done a successful therapy with AT04A vaccine on mice models to protect them against the build-up of cholesterol in the arteries. This therapy uses immune system to stop low-density lipoprotein cholesterol (LDL) or bad cholesterol in our arteries, a risk factor to atherosclerosis (fat or fatty material) and cardiovascular diseases (CVD). The AT04A vaccine guides our immune system to fight with an enzyme, PCSK9 (Proprotein convertase subtilisin/Kexin type 9) which stops the process of natural cleaning of LDL or bad cholesterol from our arteries. The therapy results with AT04A vaccine on mice models compared with unvaccinated mice shows


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  • Reduction in the total amount of cholesterol by 53 percent
  • Damage to blood vessels with atherosclerosis (fatty material) reduced by 64 percent
  • Blood vessel inflammation biological markers reduced by 21 to 28 percent
  • Reduced arterial wall inflammation

AT04A vaccine reduces LDL cholesterol and atherosclerosis to prevent heart disease.

Now to find out the safety on humans with AT04A vaccine, scientists are conducting Phase I trial with 72 people and the findings are expected by the end of 2017. Co-author of the study was Dr. Gnther Staffler, chief technology officer at AFFiRis, Austria. The study findings were published in the Oxford Academic Journals, under the title "The AT04A vaccine against proprotein convertase subtilisin/kexin type 9 reduces total cholesterol, vascular inflammation, and atherosclerosis in APOE*3Leiden.CETP mice".


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