Beetroot for treating heart failure

Beetroot juice supplements may enhance exercise capacity in patients with heart failure, according to a new proof-of-concept study. The study examined the impact of dietary nitrate in the form of beetroot juice supplements on the exercise capacity of eight heart failure patients with reduced ejection fraction, a condition in which the heart muscle doesn't contract effectively and can't get enough oxygenated blood to the body.

Researchers found that the beetroot supplement resulted in significant increases in exercise duration, peak power and peak oxygen uptake while exercising. The improvements were not accompanied by any changes in the breathing responses of the patients, and there was no change in their exercise efficiency, a measure of how much external work a person gets for a certain input of energy.

Abnormalities in aerobic exercise responses play a major role in the disability, loss of independence and reduced quality of life that accompany heart failure, elevations in ventilatory demand and decreases in peak oxygen uptake are highly predictive of mortality in patients with heart failure. Dietary supplementation may be a valuable addition to treatment for exercise intolerance among heart failure patients with reduced ejection fraction.
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Links between protein and heart failure

Study on two specially bred strains of mice showed how abnormal addition of the phosphate to a specific heart muscle protein may sabotage the way the protein behaves in a cell, and may damage the way the heart pumps blood around the body. Different people may have more or less altered phosphorylation that might help patients who may benefit from targeted therapies.

A form of heart disease known as heart failure with preserved ejection fraction-the amount of blood squeezed out when the heart contracts impairs the heart's ability to quickly and efficiently relax between the heart beats and overworking the organ. Common symptoms of heart failure include shortness of breath, but those with the form in which the ejection fraction is preserved at baseline have particular difficulty when they try to increase their activity or exercise.

Heart failure with preserved
ejection fraction does not respond well to common heart failure medications. The condition is common in adults, though some children with genetic disorders of heart muscle proteins share features of this condition. Heart failure was associated with changes in heart muscle cells through altered phosphorylation in the heart muscle protein cardiac troponin I cTnI, which regulates heart contraction.

Researchers examined the function of the mouse hearts through echocardiography as well as measurements with tiny catheters placed in the heart compared to mice without this altered phosphorylation. At baseline the mice with hyperphosphorylation on this specific site experienced a longer time to heart relaxation and lower left ventricular peak filling rate (depressed diastolic function), but the amount of blood ejected during contraction was normal.

The researchers then stimulated both strains of mouse hearts with adrenaline to assess the impact of increased demand on the hearts. The mice with hyperphosphorylation had very limited ability to increase the ejection of blood from the heart compared to the controls in response to adrenaline. However, the mice with hyperphosphorylation did show some improvement in relaxation, though relaxation remained slower than controls at peak drug effect.

Researchers then subject both sets of mice to brief periods of reduced oxygen flow to the heart and then restored the flow of oxygen, they discovered that the hearts of mice with hyperphosphorylation were protected from this form of stress.
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Blood cancer gene could prevents heart failure

Coronary heart disease is the leading cause of death across the globe. Most of these deaths are caused by a heart attack-myocardial infarction where the blood flow to the heart is acutely blocked causing irreversible damage to the heart muscle.

People may survive a heart attack, but the damage that has occurred to the heart muscle can develop to heart failure – a debilitating condition in which the heart cannot pump blood around the body.

The gene Runx1 increases in damaged heart muscle after a heart attack. Mice with a limited capacity to increase Runx1 gene activation were protected against the adverse changes that lead to heart failure.

The Runx1 gene has been extensively studied in the context of its role in leukaemia and normal blood cell development, however until now its role in the heart was unknown.
Now researchers believe that the increased expression of the Runx1 gene, which happens after a heart attack, contributes to adverse changes in the shape and pumping action of the heart.
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Nicotine in e-cigarette causes high blood pressure

Nicotine is a nitrogen-containing chemical, which is made by different types of plants, including the tobacco plant. E-cigarettes contain nicotine, increase blood pressure and cause heart disease.

Arterial stiffness is associated with       e-cigarette because of nicotine. Regular vaping with nicotine liquids or being exposed to other people’s vapours could cause damage to blood circulation.

Stiffer arteries make it harder for the heart to pump blood round the body, this increases strain on the heart and increases the risk of damage to the heart muscle.

The condition is associated with high blood pressure, coronary artery disease, stroke, heart failure and atrial fibrillation. Exposure to active and passive cigarette smoking causes a permanent increase in arterial stiffness.
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