BLOOD TEST PREDICTS SOME RISK OF HEART FAILURE

Two blood markers are strongly linked with the development of heart failure in individuals with mild to severe kidney disease, according to a study appearing in an upcoming issue of the Journal of the American Society of Nephrology (JASN). Elevations in these markers may indicate subclinical cardiovascular changes that subsequently contribute to the development of heart failure.

Patients with chronic kidney disease (CKD) are at increased risk of developing heart failure and other cardiovascular diseases. Nisha Bansal, MD, MAS (University of Washington) Amanda Anderson, PhD, MPH (University of Pennsylvania), and their colleagues conducted a study to see if certain blood tests might help identify patients at especially high risk. These tests -- which measure proteins called high-sensitivity troponin T (hsTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) -- strongly predict heart failure in the general population, but their predictive utility in patients with CKD is unknown. The researchers studied 3483 patients with CKD in the Chronic Renal Insufficiency Cohort (CRIC) Study who were recruited from June 2003 to August 2008 and were free of heart failure when they enrolled. Patients were followed for a median of nearly 6 years.

Compared with participants with the lowest levels of hsTnT at the start of the study, those with the highest hsTnT levels had a nearly 5-fold higher risk of developing heart failure. Those with the highest NT-proBNP levels had a nearly 10-fold higher risk of developing heart failure compared with those with the lowest levels.

"This research is important in that it may advance the application of widely available cardiac biomarkers to identify CKD patients at the highest risk of developing heart failure, the most common cardiovascular complication in this patient population," said Dr. Bansal. "These findings suggest that hsTnT and NT-proBNP may represent distinct biological pathways that likely involve subclinical changes in the structure and function of the heart," said Dr. Anderson.

CLUE TO GENETICS OF CONGENITAL HEART DEFECTS EMERGE FROM DOWN SYNDROME

Down syndrome is the most common chromosomal abnormality in humans, involving a third copy of all or part of chromosome 21. In addition to intellectual disability, individuals with Down syndrome have a high risk of congenital heart defects. However, not all people with Down syndrome have them -- about half have structurally normal hearts.

 Geneticists have been learning about the causes of congenital heart defects by studying people with Down syndrome. The high risk for congenital heart defects in this group provides a tool to identify changes in genes, both on and off chromosome 21, which are involved in abnormal heart development.

Researchers at Emory University School of Medicine, with colleagues at Johns Hopkins University, Oregon Health Science University, and University of Pittsburgh, report results from the largest genetic study of congenital heart defects in individuals with Down syndrome in the journal Genetics in Medicine.

The team found that infants with congenital heart defects, in the context of Down syndrome, were more likely to have rare, large genetic deletions. Those deletions tended to involve genes that affect cilia, cellular structures that are important for signaling and patterning in embryonic development.

These new findings, along with other recent studies, suggest that the risk for congenital heart defects in Down syndrome can come from several genes and environmental factors, in addition to the substantial risk from the extra chromosome 21.

"In Down syndrome, there's a 50-fold increase in risk for heart defects, which is enormous," says senior author Michael Zwick, PhD, associate professor of human genetics and pediatrics at Emory. "Studying congenital heart defects in the 'at risk' Down syndrome population can make it possible to reveal genes that impact the risk of heart defects in all children, including those with typical number of chromosomes."

"Understanding the origin of heart disorders in individuals with Down syndrome may reveal aspects of biology that would allow better personalization of their health care, since genetic alterations that affect the heart may also affect other organs, such as the lungs or gut," Zwick says.

"Our partnership with families who have a child with Down syndrome and our investment in a comprehensive clinical data and biorepository will continue to provide resources to study not only heart defects, but also other Down-syndrome associated medical conditions such as cognitive function, leukemia, and dementia," says co-author Stephanie Sherman, PhD, professor of human genetics at Emory University School of Medicine.

Sherman says the study was a collaborative effort involving participants with Down syndrome, their families and assessment sites across the United States, including those mentioned above along with Kennedy Krieger Institute, Children's National Medical Center and Ohio Nationwide Children's Hospital.

The first author was Emory postdoctoral fellow Dhanya Ramachandran, PhD, working with Zwick. Emory co-authors included assistant professors Lori Bean, PhD, Tracie Rosser, PhD and David Cutler, PhD, in the Department of Human Genetics, and Jennifer Mulle, PhD, assistant professor of epidemiology in the Rollins School of Public Health. Ken Dooley, MD, associate professor of pediatrics at Emory and pediatric cardiologist at Children's Healthcare of Atlanta, reviewed medical records and made definitive diagnoses for all study participants.

The study included 452 individuals with Down syndrome. 210 had complete atrioventricular septal defects (AVSDs), a serious heart defect that is relatively common among those with Down syndrome (about 20 percent). The remaining 242 had structurally normal hearts. The Emory team used high density microarrays to probe more than 900,000 sites across the human genome to detect structural variation, including deletions or duplications of DNA.

An atrioventricular septal defect means that the central region of the heart separating the atria from the ventricles has failed to form properly. Such defects increase the workload on the heart, and a complete AVSD leads to heart failure: fluid buildup in the lungs and difficulty breathing, requiring surgery in the first year of life.

The team's results add to evidence for a connection between AVSDs and cilia. Ciliopathies are a class of genetic disorders that include kidney, eye, and neurodevelopmental disorders. Cells in the airways have mobile cilia which sweep mucus and dirt out of the lungs, but almost every cell in the body has a primary (sensory) cilium.

"The finding that ciliome genes may be disrupted in children with Down syndrome and AVSD may indicate differences in life-time care for these individuals," Zwick says. "This is a suggestive result that needs replication in a larger group."

To confirm and strengthen the findings, Zwick and his team are currently performing an independent study of individuals with Down syndrome, using whole genome sequencing to further delineate alterations in genes that perturb heart development in children.

SEVERE PNEUMONIA MAY PERMANENTLY DAMAGE HEART

Severe pneumonia may permanently damage your heart as pneumonia bacterium leaves tiny lesions in the heart, a study suggests.

The researchers found proof that Streptococcus pneumoniae, the leading cause of community-acquired pneumonia, actually physically damages the heart.

The researchers detected tiny lesions that the bacterium leaves in mouse, rhesus macaque and human autopsy tissue samples.

"If you have had severe pneumonia, this finding suggests your heart might be permanently scarred," said study senior author Carlos Orihuela, associate professor of microbiology and immunology at The University of Texas Health Science Center at San Antonio, US.

Streptococcus pneumoniae in the blood invaded the heart and formed lesions in the myocardium, the muscular middle layer of the heart wall, the researchers showed.

The team identified mechanisms by which the bacterium is able to spread across endothelial cells in cardiac blood vessels to travel to and infect the heart.

"Fortunately, we have a candidate vaccine that can protect against this," Orihuela noted.

The candidate vaccine acts to stop both the movement of the infection into the heart and the toxin that kills heart muscle cells called cardiomyocytes.

The vaccine protected immunized animals against cardiac lesion formation, the study showed.

The study appeared in the journal PLoS Pathogen

HOMOEOPATHIC REMEDIES FOR RHEUMATIC HEART DISEASE

Rheumatic heart disease describes a group of short-term (acute) and long-term (chronic) heart disorders that can occur as a result of rheumatic fever. One common result of rheumatic fever is heart valve damage. This damage to the heart valves may lead to a valve disorder.

Rheumatic fever

Rheumatic fever is an inflammatory disease that may affect many connective tissues of the body, especially those of the heart, joints, brain or skin. It usually starts out as a strep throat (streptococcal) infection. Anyone can get acute rheumatic fever, but it usually occurs in children between the ages of 5 and 15 years. About 60% of people with rheumatic fever develop some degree of subsequent heart disease.

Every part of the heart, including the outer sac (the pericardium), the inner lining (the endocardium) and the valves may be damaged by inflammation caused by acute rheumatic fever. However, the most common form of rheumatic heart disease affects the heart valves, particularly the mitral valve. It may take several years after an episode of rheumatic fever for valve damage to develop or symptoms to appear.

Symptoms

Symptoms of heart valve problems, which are often the result of rheumatic heart disease, can include: chest pain, excessive fatigue, heart palpitations (when the heart flutters or misses beats), a thumping sensation in the chest, shortness of breath, and swollen ankles, wrists or stomach

HOMOEOPATHIC REMEDIS

ARSENICUM ALBUM 30-- Palpitation , pain and dyspnea. Rheumatic heart of cigarette smokers and tobacco chewers

AURUM MET 30-  Pain in the heart and a feeling as if the heart stopped beating for two or three seconds. Rheumatism with hypertension

CACTUS GRANDIFLORUS 3X- Pain in the heart with feeling of construction in it. Vertigo  and low blood pressure

KALI NITRICUM 30- Violent stitch in the heart with steady with steady but weak pulse

KALMIA LAT 30- Heartrheumatism of tobacco smokers and chewers . Pains are so sharp as if he will not be able to take the next breath. Pain travels to shoulder blades

LACHESIS 200- Rheumatic pains of heart specially during menopause. Constricted feeling around the heart

NATRIUM IOD 30- Incipient rheumatic endocarditis. Vertigo and dyspnea

RANUNCULUS BULBOSUS Q- 10-15 drops a dose relieves various kinds of pains and rheumatic pains in the chest walls , in the ribs, sternum, heart, muscular tissue and shoulder blades when these are worse in cold air and atmospheric changes

SPIGELIA 30- Rheumatic carditis with trembling pulse

SPONGIA 30- Rheumatism with asthmatic symptoms

SUMBUL 30- Aching and numbness of the left arm with pain in the heart  and hypochondrial regions

STOMACH IS THE WAY TO A WOMANS HEART

You've heard that romance starts in the kitchen and not in the bedroom. Well, researchers at Drexel University finally have the science to support that saying -- but not the way you might think.

In a new study published online in the journal Appetite, researchers found that women's brains respond more to romantic cues on a full stomach than an empty one. The study explored brain circuitry in hungry versus satiated states among women who were past-dieters and those who had never dieted.

The study's first author Alice Ely, PhD, completed the research while pursuing a doctoral degree at Drexel, and is now a postdoctoral research fellow at the Eating Disorders Center for Treatment and Research, part of the UC San Diego School of Medicine. Michael R. Lowe, PhD, a professor in the College of Arts and Sciences at Drexel University, was senior author.

"We found that young women both with and without a history of dieting had greater brain activation in response to romantic pictures in reward-related neural regions after having eaten than when hungry," said Ely.

Ely said the results are contrary to several previous studies, which showed that people typically demonstrate greater sensitivity to rewarding stimuli when hungry. Such stimuli may include things like food, money and drugs.

"In this case, they were more responsive when fed," she said. "This data suggests that eating may prime or sensitize young women to rewards beyond food. It also supports a shared neurocircuitry for food and sex."

The latest finding, based on a small pilot study, grew from Ely and her Drexel colleagues' earlier work investigating how the brain changes in response to food cues. Specifically, the researchers looked at whether the brain's reward response to food differed significantly in women at risk for future obesity (historical dieters) versus those who had never dieted. All of the study participants were young, college-age women of normal weight.

In that study, published in Obesity in 2014, the researchers found that the brains of women with a history of dieting responded more dramatically to positive food cues when fed as compared to women who had never dieted or who were currently dieting.

"In the fed state, historical dieters had a greater reaction in the reward regions than the other two groups to highly palatable food cues versus neutral or moderately palatable cues," she said. Highly palatable cues included foods like chocolate cake; neutral cues were things like carrots.

Ely said the data suggests historical dieters, who longitudinal studies have shown are more at risk for weight gain, may be predisposed by their brain reward circuitry to desire food more than people who have not dieted.

"Based on this study, we hypothesized that historical dieters are differentially sensitive -- after eating -- to rewards in general, so we tested this perception by comparing the same groups' brain activation when viewing romantic pictures compared to neutral stimuli in a fasted and fed state," she said. Testing was done using MRI imaging.

While both groups' reward centers responded more to romantic cues when fed, the historical dieters' neural activity noticeably differed from the non-dieters in one brain region that had also turned up in the earlier food studies.

"The pattern of response was similar to historical dieter's activation when viewing highly palatable food cues, and is consistent with research showing overlapping brain-based responses to sex, drugs and food," said Ely.