dilated cardiomyopathy

Gene Identified That Plays a Role in People Who Recover from Dilated Cardiomyopathy

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human heart

Researchers at the Mayo Clinic investigating factors related to recovery from dilated cardiomyopathy have identified a variant in a specific gene that plays a role in people who recover from the condition and those who don’t. Results of the genome-wide association study (GWAS), published in Circulation Research, is expected to spur future research to target the gene for future dilated cardiomyopathy treatments.

“We found genetic variation in the CDCP1 gene, a gene that no one has heard of in cardiology, and its link to improvement in heart function in these patients,” says lead author Naveen Pereira, MD, a Mayo Clinic cardiologist.

Cardiomyopathy is characterized by its effect on the heart’s left ventricle, making it more difficult to pump blood throughout the rest of the body.

According to the investigators, CDCP1 genetic variation leads to differences in the protein’s structure which may influence a person’s susceptibility to disease or response to specific drugs. Once the gene was associated with improving function in the left ventricle, the team examined why this occurs. A key finding was that the CDCP1 gene is often variably expressed in fibroblasts of people with dilated cardiomyopathy, and fibrosis—an excess of fibrous connective tissue in the heart—plays a central role in prognosis of patients with the condition. Further, Pereira noted that genetic variation in or near CDCP1 has a significant association with heart failure death.

Strengthening the case for CDCP1 as a drug target, the Mayo Clinic researchers observed that decreasing the expression of the gene in cardiac connective tissue decreased fibroblast proliferation in the heart. It also downregulated the IL1RL1 gene, which encodes a prominent heart failure biomarker aST2, which when found in high levels is associated with fibrosis and death. This suggests the importance of developing a better understanding of the relationship between CDCP1 and aST2, as researchers search for ways to treat heart failure.

This finding now comes as heart failure rates are expected to rise significantly over the rest of the decade. The American Heart Association forecasts that heart failure will affect eight million people in the U.S. by 2030, a 46% increase over current rates. Of those cases, between 30% and 40% are caused by dilated cardiomyopathy.

Building in this research, the Mayo Clinic team is continuing studies in animal models to better understand the role CDCP1 plays in heart failure, and they are developing molecules to assess their potential as treatments for dilated cardiomyopathy.

“By continuing with this research that started with a human population that we took to the molecular and now animal laboratory, we hope to find new avenues for treatments to take back to the human population we studied, to improve patients’ survival and quality of life ultimately,” says Pereira.

Methamphetamine Abuse Exacts Heavy Toll on the Heart

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A new study sheds light on two poorly understood cardiac complications of methamphetamine (MA) abuse: pulmonary arterial hypertension (PAH) and dilated cardiomyopathy (CMP).

In what is believed to be the largest case series to date, investigators found that the clinical features of patients with MA-PAH and MA-CMP are distinct from each other, but both carry significant disease burden and mortality risk.

There is also a “striking sex imbalance between these two pathologies,” Susan X Zhao, MD, Santa Clara Valley Medical Center, San Jose, California, told theheart.org | Medscape Cardiology.

“Methamphetamine abuse is like a silent tsunami, sweeping upwards of 33 million people worldwide along its deadly path,” said Zhao. “Unlike opioid abuse, which can lead to overdose-related death, the detrimental effects of methamphetamine are more long-term and less well known.”

Their results are published in the March issue of JACC: Heart Failure.

MA abuse exerts its cardiotoxic effects by stimulating release of catecholaminergic neurotransmitters in both the central and peripheral nervous system, which modulates heart rate and blood pressure. MA abuse is known to cause PAH and CMP, but until now no study has compared the clinical characteristics and overall impact on survival of these two distinct pathologies.

“Silent Tsunami”

Zhao and colleagues retrospectively studied the clinical characteristics and outcomes of 50 patients with MA-PAH, 296 with MA-CMP, and 356 control patients with a documented history of MA abuse but without overt cardiac pathology (MA-CTL).

They found a strong female predominance in the MA-PAH group (58%) and a strong male predominance in the MA-CMP group (86%). Alcoholism and hypertension were more common in the MA-CMP group.

Both the MA-CMP and the MA-PAH groups had advanced disease with significant morbidity and mortality. The mean left ventricular ejection fraction in the MA-CMP group was 25.2% with dilated left and right ventricles, whereas the MA-PAH group had a median right ventricular (RV) systolic pressure of 75 mm Hg with dilated right heart and significantly reduced RV systolic function.

More than half (57%) of patients with MA-CMP had New York Heart Association functional class III/IV heart failure during follow-up, but only 14% of them received an implantable cardioverter-defibrillator to prevent sudden arrhythmic death. This is likely due to a combination of reasons, including ongoing substance abuse, poor functional status/prognosis, and/or issues with adherence, the researchers say.

After a median follow-up of 20 months, both MA-CMP and MA-PAH were associated with significantly increased mortality (18.0% and 15.2%, respectively), above and beyond that seen in the MA-CTL group (4.5%).

On logistic regression analyses, male sex, concurrent alcohol abuse, and the presence of systemic hypertension were independent factors associated with MA-CMP. The combination of MA and alcohol increases heart rate and blood pressure beyond those seen in MA users alone. This pharmacologic interaction may explain the significantly higher prevalence of systemic hypertension in the MA-CMP group, the investigators say.

In contrast with MA-CMP, the only clinical factor shown to be associated with MA-PAH was female sex. Women made up 58% of the MA-PAH group, compared with 14% of the MA-CMP group.

These results, say the researchers, suggest that the scale is tipped toward the MA-CMP phenotype when the MA user is male, with concomitant alcohol abuse and presence of systemic hypertension, whereas female sex and some other unknown factors, which may be clinical and/or genetic, predispose to the development of MA-PAH.

Limitations of the study include its retrospective design, as well as incomplete information on the duration and route of MA administration, which may play a key role in determining susceptibility in a given patient to a particular cardiovascular complication subtype.

Going forward, the investigators say future research is needed to establish a mechanistic relationship between MA use and these distinct forms of cardiac pathology, as well as the interaction of MA with other concurrent risk factors (such as alcohol abuse) or pre-existing cardiac conditions (such as hypertension).

The authors of an accompanying editorial say this study focuses “much-needed attention on the importance of MA in cardiovascular disease. Unfortunately, there are currently no approved pharmacologic therapies for MA and relapse rates after cognitive therapy as high as 88% have been documented,” note Ori Ben-Yehuda, Columbia University, New York City, and Neil Siecke, Swedish Vascular and Heart Institute, Seattle, Washington.

“The opioid epidemic has contributed to a documented decline in life expectancy in the United States in 2016. Although less immediate in its effect on mortality, the cardiovascular effects of methamphetamine may have an appreciable effect on the life expectancy and quality of life of abusers of the drug. MA research and treatment should be a priority, not just of addiction medicine, but of cardiovascular medicine as well,” the editorial writers conclude.

George Michael death: What is dilated cardiomyopathy and how does it affect the body.

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The heart problem involves the left ventricle becomes stretched, thin and weaker, which affects how blood is able to pump around the body.

Goerge Michael died from problems with his heart and also suffered a build-up of fat in his liver.

The heart condition singer George Michael died from, dilated cardiomyopathy, is a disease of the heart muscle.

The star died from problems with his heart and also suffered a build-up of fat in his liver, a coroner has revealed.

The heart problem involves the left ventricle becoming stretched, thin and weaker, which affects how blood is able to pump around the body.

In some cases it is an inherited condition and people who have the inherited form have a 50% chance of passing it on to their children.

The disease explained 

Otherwise, it is caused by things such as viral infections, uncontrolled high blood pressure and problems with the heart valves.

A lack of vitamins and minerals in the diet, heavy drinking and recreational drug use can also lead to the condition.

Due to the heart not pumping effectively, fluid can build up in the lungs, ankles, abdomen and other organs of the body – causing heart failure.

George Michael 

Most symptoms come on slowly but include shortness of breath, swelling of the ankles and stomach and excessive tiredness.

Myocarditis is inflammation in or around the heart and is usually caused by a viral, bacterial or fungal infection.

Symptoms include pain or tightness in the chest which can spread to other parts of the body.
Other symptoms are shortness of breath and tiredness.

Myocarditis is potentially fatal, although it sometimes exhibits no symptoms at all.

It is notoriously hard to detect and can lead to heart failure in severe cases.

People can sometimes have a high temperature, suffer headaches and have aching muscles and joints.

Non-alcoholic fatty liver disease is caused by a build-up of fat in the liver and is usually seen in people who are oveAround one in three people in the UK are thought to be in the early stages of non-alcoholic fatty liver disease.

While it usually causes no harm, it can lead to serious liver damage and increases the risk of diabetes, heart attacks and strokes.