Artificial Heart

The need to mend broken hearts has never been greater. In the USA alone, around 610,000 people die of heart disease each year. A significant number of those deaths could potentially have been prevented with a heart transplant but, unfortunately, there are simply too few hearts available.

In 1967 the South African surgeon Christiaan Barnard performed the world’s first human heart transplant in Cape Town. It seemed like a starting gun had gone off; soon doctors all around the world were transplanting hearts.

The problem was that every single recipient died within a year of the operation. The patients’ immune systems were rejecting the foreign tissue. To overcome this, patients were given drugs to suppress their immune system. But, in a way, these early immunosuppressants were too effective: they weakened the immune system so much that the patients would eventually die of an infection. It seemed like medicine was back to square one.

Early Mechanisms

One solution that researchers have pursued since the late 1960s is an artificial heart. Perhaps the most influential device was kick-started by Willem Kolff, the physician-inventor who produced the first kidney dialysis machine. Kolff invited a fellow medical engineer, one Robert Jarvik, to work with him at the University of Utah, and the result was the Jarvik-7. Made up of two pumps, two air hoses and four valves, the Jarvik-7 was more than twice as big as a normal human heart and could only be implanted in the biggest patients – mainly adult men. It had wheels, was as big and heavy (although not as tall) as a standard household refrigerator, and was normally connected to sources of compressed air, vacuum and electricity.

In 1982, Jarvik and Kolff won approval from the US Food and Drug Administration to use it in human patients and implanted it that same year. Their first patient was a 61-year-old dentist called Barney Clark, who lived on the Jarvik-7 for 112 days. A second patient was implanted in 1984 and died after 620 days. History records a total of five patients implanted with the Jarvik-7 for permanent use, all of whom died within 18 months of the surgery from infections or strokes.

The device has been tweaked and renamed many times; at the time of writing, it was the world’s only FDA-approved total-replacement artificial heart device used as a bridge-to-transplant for patients. Another widely used artificial heart, a direct descendent of the Jarvik-7, is the SynCardia. And in the early 2000s, Massachusetts-based company Abiomed unveiled a new heart that (unlike the SynCardia) was designed to be permanent – a total replacement heart for end-stage heart failure patients who were not candidates for transplant and couldn’t be helped by any other available treatment.

But all these versions of artificial heart devices, whether they are meant to support the heart or replace it completely, are trying to copy the functions of the heart, mimicking the natural blood flow. The result is what’s called a pulsatile pump, the flow of blood going into the body like a native heart, at the average of 80 spurts a minute needed to sustain life. That’s the cause of the gentle movement you feel when you put your fingers to your wrist or your chest – your pulse, which corresponds with the beating of your heart.

Today, scientists are working on a new wave of artificial hearts with one crucial difference: they don’t beat.

Pulseless Hearts

The Archimedes’ screw was an ancient apparatus used to raise water against gravity. Essentially, it is a screw in a hollow pipe; by placing the lower end in water and turning it, water is raised to the top. In 1976, during voluntary medical mission work in Egypt, cardiologist Dr. Richard K. Wampler saw men using one such device to pump water up a river bank. He was inspired. Perhaps, he thought, this principle could be applied to pumping blood.

The result was the Hemopump, a device as big as a pencil eraser. When the screw inside the pump spun, blood was pumped from the heart to the rest of the body. It was the world’s first ‘continuous flow’ pump: Rapidly spinning turbines create a flow like water running through a garden hose, meaning the blood flow is continuous from moment to moment.

Because of this, there is no ejection of the blood in spurts. There is no ‘heartbeat’. The patient’s own heart is still beating but the continuous flow from the device masks their pulse, meaning it is often undetectable at the wrist or neck.

And the Hemopump lives on in spirit of newer devices. Abiomed’s newest heart prototype, Impella, uses similar technology boosted by leaps in modern engineering. It has a motor so small it sits inside the device at the end of the catheter, rather than outside of the body. The Impella is the smallest heart pump in use today – it’s not much bigger than a pencil – and as of March 2015 has been approved by the FDA for clinical use, supporting the heart for up to six hours in cardiac surgeries.

Meanwhile, at the Texas Heart Institute, the HeartMate II is being developed. Like the Hemopump, it doesn’t replace the heart but rather works like a pair of crutches for it. About the size and weight of a small avocado, the HeartMate II is suitable for a wider range of patients than the SynCardia and has, on paper, a significantly longer lifespan – up to ten years. Since its FDA approval in January 2010, close to 20,000 people – including former US Vice President Dick Cheney – have received a HeartMate II, 20 of whom have been living with the device for more than eight years. All with an almost undetectable pulse.

The Future of Heart Transplants

I try to imagine a world full of people with no pulse. How, in such a future, would we determine if a person were alive or dead? “That is very easy,” says William (Billy) Cohn, a surgeon at the Texas Heart Institute, bringing my existential philosophizing to a halt. “When we pinch our thumb and it goes from pink to white and immediately back to pink, this means blood is flowing through the body. You can also tell if someone is still alive if they are still breathing.”

He admits that once more of these devices are implanted into patients we will need a standard method of determining such a person’s vitals. Cohn imagines them wearing bracelets or even having tattoos to alert people to their pulseless state.

I wonder how people will take to hearts that literally don’t beat. Perhaps it will be the same as when patients were offered the first heart transplants: resistance, followed by acceptance due to overwhelming need.

“Any new procedure is going to have critics,” says surgeon Denton Cooley. “On the day that Christiaan Barnard did the first heart transplant, the critics were almost as strong, or stronger, than the proponents of [artificial] heart transplantation,” he says. “A lot of mystery goes with the heart, and its function. But most of the critics, I thought, were ignorant, uninformed or just superstitious.”

Cooley performed the first US heart transplant in May 1968. And at 94 years old he still treasures the memory of the day, in 1969, when he implanted the first artificial heart into Haskell Karp and the “satisfaction that came from seeing that heart supporting that man’s life.”

“I had always thought that the heart has only one function, and that is to pump blood,” he says. “It’s a very simple organ in that regard.”

thanks to: http://blogs.discovermagazine.com/

Causes of Secondary Hypertension ::

Secondary hypertension (secondary high blood pressure) is high blood pressure that's caused by another medical condition. Secondary hypertension differs from the usual type of high blood pressure (essential hypertension), which is often referred to simply as high blood pressure. Essential hypertension, also known as primary hypertension, has no clear cause and is thought to be linked to genetics, poor diet, lack of exercise and obesity.

Secondary hypertension can be caused by conditions that affect your kidneys, arteries, heart or endocrine system. Secondary hypertension can also occur during pregnancy.

Proper treatment of secondary hypertension can often control both the underlying condition and the high blood pressure, which reduces the risk of serious complications — including heart disease, kidney failure and stroke.

In about 5% of cases, the underlying causes of Hypertension is known such hypertension is called Secondary Hypertension. The commonest causes of Secondary Hypertension is renal disease. Causes of Secondary Hypertension are as follows ::

1. Alcohol
2. Obesity
3. Pregnancy (pre-eclampsia)
4. Renal disease (most common causes)
• Acute glomerulonephritis
• Chronic glomerulonephritis
• Polycystic kidney disease
• Renal tumour
• Renal artery stenosis
• Chronic pyelonephritis
5. Endocrine disease
• Phaeochromocytoma
• Cushing’s syndrome
• Primary hyperaldosteronism (Conn’s syndrome)
• Glucocorticoid-suppressible hyperaldosteronism
• Hyperparathyroidism
• Acromegaly
• Primary hypothyroidism
• Thyrotoxicosis
• Congenital adrenal hyperplasia due to 11-β-hydroxylase or 17α-hydroxylase deficiency
• Liddle’s syndrome
• 11-β-hydroxysteroid dehydrogenase deficiency
6. Cardiovascular causes
• Co-arctation of aorta
• Takayasu's disease

See More >>>>>>>>
http://healthmedicalinfohmi.blogspot.com/…/causes-of-second…

What happens in the brain when the heart stops?

"A research project funded by the Austrian Science Fund FWF is now set to provide scientific insights into one of these still unsolved mysteries: what goes on in the brain of people who are on the brink of death due to cardiac arrest and have memories of the time when their heart had stopped after resuscitation? Although a very rare occurrence, such experiences are reported from time to time. From a scientific point of view they are hard to explain, since electrical activity in the brain ceases seconds after the blood supply is interrupted – or does it? Scientists are still at a loss, but project head Roland Beisteiner is convinced that there are explanations for such events. "Although no comprehensive evidence of brain activity during cardiopulmonary resuscitation (CPR) has been found so far, this doesn't mean that it doesn't exist", observes the neurologist from the Medical University of Vienna and explains that an increasing amount of data, for instance from coma patients or the realm of anesthesia, points to the fact that the brain has great capacities for regeneration and information processing invisible to outside observers."

"World first" Australian surgeons have successfully performed a heart transplant with a heart that had stopped beating.

In a game-changing breakthrough, Australian surgeons have successfully performed a heart transplant with a heart that had stopped beating.

Image: Daily Telegraph

Doctors and scientists at St Vincent’s Hospital in Sydney, Australia recently transplanted two circulatory dead hearts, which were no longer beating, into two patients, both of whom are now recovering well.

Currently, donor hearts are taken from brain dead patients whose hearts are still beating, which limits the number of hearts available for transplant.

But the donor hearts used for these world-first transplants had been dead for at least 20 minutes, and were revived using a ground-breaking preservation fluid before being successfully transplanted into patients with heart failure.

Bob Graham, the executive director of the Victor Chang Cardiac Research Institute, who led the research team, told Elizabeth Jackson from the ABC that this will mean around 30 percent more people will be able to have heart transplants.

The successful transplants were the result of a collaboration between the Victor Chang Cardiac Research Institute in Sydney and St Vincent’s Hospital.

Michelle Gribilar, 57, had the first transplant of this kind a few months ago, and is now recovering well. The second recipient, Jan Damen, underwent the surgery a fortnight ago and is now in recovery. Both suffered congenital heart failure.

The scientists developed a special preservation solution that works on a “heart in a box” to keep the dead heart healthy even without blood flow.

Graham explained the process to ABC:

“[Five minutes after the donor has died] we can take the heart out and we can put it on a console where we connect it up with blood going through the heart and providing oxygen.

"Gradually the heart ... starts beating again, and we can keep it warm and we can transport it on this console and we also give it a preservation solution that allows it to be more resistant to the damage of lack of oxygen.

"So those two things coming together almost like a perfect storm have allowed this sort of donation, this sort of transplantation of a heart that has stopped beating to occur. Before that it wasn't possible.”

Find out more in Graham’s interview over at ABC.

Source: ABC, Daily Telegraph

The evolution of pacemakers

Engineering Heartbeats: The Evolution of Artificial Pacemakers

Arrhythmia—a cardiac disease in which the heart beats irregularly or at an abnormal pace—is caused by faulty electrical signal generation within the heart at the SA node. Recognizing the electrical properties of the heart, engineers created a treatment device, the artificial pacemaker, by applying principles of electrical engineering. The device controls the rate and rhythm of the heartbeat by overriding faulty natural signals with generated electrical pulses. The first pacemaker was created in the 1920s, and subsequent innovations in batteries, transistors, and microprocessors allowed the pacemaker to be portable, wearable, and eventually implantable. Today, pacemakers can be programmed for different rates and automatic regulatory functions, but they are still limited in battery life and have risks of infection or failure. Engineers are applying the concepts of piezoelectricity and ultrasound to address these problems, and the results are promising for a new generation of smaller, safer pacemakers.

Introduction

We like to think we have complete control over our bodies – looking, touching, and moving wherever we want. However, there is one thing we cannot systematically control with our minds: our heartbeat. Even when the brain is resting at night, the heart never fails to keep beating at the same rate. This is because the heart serves the critical function of facilitating blood circulation, which in turn supplies oxygen to different organs in the body. A timely and constant delivery of oxygen is critical for proper body function: our cells rely on oxygen to perform basic tasks like cellular respiration, the process that harvests energy to fuel cellular activities. The interruption of the body’s oxygen supply for even a few minutes can have catastrophic effects, like the death of brain cells [1]. One of the most common medical conditions that can lead to interrupted blood supply is arrhythmia, when the heart beats at an abnormal rate due to heart signaling malfunctions. To treat this problem, engineers applied principles of electrical engineering and created the artificial pacemaker, a device placed in the chest or abdomen that generates electrical pulses to control the rate and rhythm of the heartbeat. Since the first artificial pacemaker of the 1920s, pacemakers have undergone significant improvements over the years through the combined efforts of electrical engineers and medical doctors. Moreover, different engineering disciplines have now been applied to the development of the pacemaker, and these new techniques offer exciting potential for pacemakers of the future.

How the Heart Works

To understand the clever engineering behind artificial pacemakers, we must first understand how the heart works. The heart is a hollow and highly muscular structure that pumps blood throughout the blood vessels by repeated rhythmic contractions. In the average human with a resting heart rate of 72 beats per minute, 5 liters of blood are pumped through the heart every minute – roughly the total volume of blood in the human body [1]. Unlike most human organs, the heart is not controlled by the nervous system. In fact, the electric signals that trigger heartbeats originate in the heart itself. The heart contains autorhythmic cardiac muscle cells that contract and relax on their own, even outside the body. These cells form the sinoatrial (SA) node located on the top right chamber of the heart (the right atrium) and the atrioventricular (AV) node located in the wall dividing the left atrium from the right. These two nodes are pictured in the heart in Fig. 1.

J. Heuser/Patrick J. Lynch; C. Carl Jaffe, MD

Figure 1: The SA node (marked by the number 1) and the AV node (marked by the number 2) create and conduct the heart's electrical signals.

The SA node (sometimes called the pacemaker) generates electrical impulses similar to nerve impulses at the start of every cardiac cycle, setting the rate and timing at which the rest of the heart contracts [1]. The impulses then spread rapidly through the top of the heart, causing uniform contraction in both atria. As the impulses reach the AV node (the “relay station”), they are slightly delayed and then conducted to the apex at the bottom of the heart. From here the impulses are spread throughout the ventricular walls, creating a strong contraction that pumps blood out of the heart into the rest of the body [11]. Depending on the different activities we perform, our body speeds up or slows down the heart’s tempo by regulating the SA node [1].

Abnormal Heartbeats: Arrhythmias

When the SA node doesn’t function correctly, the heart can beat too fast, too slow, or with an irregular rhythm. These problems are called arrhythmias and can be classified into three major subtypes: bradycardia (when the heart beats too slowly), tachycardia (when the heart beats too quickly), and fibrillation (when the atria or ventricles quiver instead of contract). When the heart doesn’t beat at the correct rate, blood and oxygen are not delivered effectively, and can result in fatigue, shortness of breath, or fainting. In severe cases, arrhythmias can cause severe organ damage, loss of consciousness, or even death [2]. Arrhythmias can arise from natural aging, heart muscle damage from a heart attack, medications, and several genetic conditions.

Over three million people with arrhythmia worldwide are treated with an implant device called the artificial pacemaker [3]. A pacemaker generates regular low energy pulses that overcome the faulty electrical signaling from the SA node, prompting the heart to beat at a normal rate. Even though the concept behind pacemakers is straightforward, the execution is not as easy.

The Evolution of Pacemakers

Although the correlation between electricity and the human heartbeat had been found as early as the 1800s, electro-stimulation devices for the heart did not appear until a century later [4]. The very first pacemaker was developed in the late 1920s almost simultaneously by both Australian anesthesiologist Mark Lidwell and American physiologist Albert Hyman. In 1928, Lidwell created an external device that delivered alternating current through a needle that was inserted directly into the patient’s ventricle. In 1932, Hyman created a similar device he named “artificial pacemaker,” a term still used today. The device was intended to restore a normal heartbeat to patients whose hearts had stopped. It consisted of a large, hand-wound current-generating motor and a bipolar needle that encompasses both negative and positive electrodes. The current generated was delivered through the bipolar needle into the right atrium (where the natural impulse originates) at rates of 30, 60, or 120 per minute. Despite his efforts, Hyman’s work faced many technical problems as well as opposition from the medical and social community. Hyman’s experiments were rejected by the Journal of the American Medical Association, no one agreed to manufacture the device, and some even regarded it as the work of the devil [4].

In the early 1950s, the first portable pacemaker was created by Canadian electrical engineer John Hopps [12]. The new pacemaker was a bulky external unit powered through household outlets, and it was considered “portable” since it could be wheeled around among different outlets. Instead of driving a conductive needle straight into the heart, Hopps’s device took the transvenous approach: electricity was delivered through a flexible bipolar catheter inserted through a vein into the right atrium of the heart. As a result, patients’ heart rates were successfully controlled without painful chest contractions. Nonetheless, the devices were not very desirable since they had low mobility and often contributed to other health complications. Because the pacemaker was external, infection often occurred in the chest along the lead [4].

In the late 1950s to early 1960s, several breakthroughs were achieved, eliminating the major problems with external pacemakers and shaping them into what they are today. Inspired by the rhythmic output of electronic metronomes, electrical engineer Earl E. Bakken and his brother-in-law (founders of the leading medical electronics company Medtronic Inc.) created the first battery-operated, wearable pacemaker [12]. The electronic metronomes used a circuit element called a transistor, which is a small semiconductor that switches signals on and off [5]. Bakken’s device combined the rather simple transistor-based circuits from the metronome with a miniature mercury battery that was able to supply power for around 1000 hours. This innovation significantly improved the size and mobility of pacemakers, allowing them to be worn on the neck or strapped onto the body of a patient [4].

Shortly after Bakken’s wearable pacemaker was developed, Swedish surgeon and engineer Ake Senning and physician Rune Elmqvist produced the first implantable pacemaker [4]. They made use of one of the first silicon transistors at the time, which significantly lowered the energy needed to power the pacemaker. In addition, they replaced the mercury battery with a nickel-cadmium battery that is rechargeable through an antenna [4]. This allowed the pacemaker to become the size of a Kiwi shoe polish can, small enough to be implanted in a patient’s chest [12]. (A Kiwi can, in fact, served as the mold for the first prototype of Senning’s and Elmqvist’s design.) Since then, the technology of implantable pacemakers for long-term therapy has developed rapidly with advancements in electronic technology, giving rise to the pacemakers available to patients today [4].

Modern Pacemakers

How They Work

Today’s artificial pacemakers have improved significantly from the early models. Modern pacemakers weigh less than an ounce, and they are only slightly larger than the size of a wristwatch face. In addition, they not only have the ability to pace heartbeats through electric currents, but they can also monitor the heart’s natural electrical activity [6].

National Heart Lung and Blood Institute (NIH)/National Heart Lung and Blood Institute (NIH)

Figure 2: The pacing system includes one or two leads, which are inserted through a heart-bound vein, and the pacemaker itself, which is implanted in the chest.

A pacing system has two major components, pictured in Fig. 2: the pacemaker and the pacing lead(s). The pacemaker unit consists of a small lithium battery (the generator), a microprocessor with memory and electrical circuits, a metal case, and a plastic connector block to which the lead is attached [7]. The pacing lead is a strong and highly flexible plastic-insulated wire designed to withstand the constant bending and twisting resulting from body and heart movements [6]. The pacing lead contains electrodes that act as both electricity conductors and sensors. The lead collects information about the electrical activity from the heart and sends it to the microprocessor in the pacemaker. The microprocessor, which is essentially a computer, records the heart’s electric activity and rhythm. If an abnormal natural electric pulse is detected, the computer directs the generator to create a small current that travels through the leads into the heart. In some cases, the pacemakers are also responsive to the particular rate of the heart’s beat: by sensing changes in blood temperature and breathing, the pacemaker can speed up or slow down the heart’s rate according to the activities that the patient is performing [7]. In addition, the pacemakers can be adjusted through a radio frequency remote control device called a “programmer.” By placing the programmer over the pacemaker, doctors can access recordings of the heart’s activity, reprogram the signaling rate, and check the status of the battery [6].

Where They Go

The surgical procedure to implant a pacemaker is rather simple, usually taking around one to two hours. The placement of pacemakers is usually considered a minor surgery, as only a minor incision and local anesthesia are needed [13]. Through the incision, one or more pacing leads connected to the pacemaker are inserted into a vein close to the collarbone and moved into the desired position in the heart with the help of an X-ray [7]. The pacemaker is then inserted into a pocket under the skin just below the collarbone where the incision is made.

The positioning of the leads depends on the type of pacing the patient needs. Pacemakers are capable of two types of pacing: single-chamber pacing and dual-chamber pacing. In single-chamber pacing, only one lead is placed inside the heart, either in the right atrium or the right ventricle. A lead placed in the right atrium is used to correct faulty signaling from the SA node, where natural impulses are generated. If placed in the right ventricle, the lead is used to correct faulty signal transmission at the AV node, which is responsible for propagating signals throughout the rest of the heart. (This problem with the AV node is a condition called heart block.) When both the SA node and the AV node are defective, dual-chamber pacing is needed. Dual-chamber pacing has two leads, one attached to the right atrium and one in the right ventricle. In the case of dual-chamber pacing, the microprocessor determines which of the two leads—if not both leads—will deliver an impulse depending on the readings delivered from the sensors [6].

The Future of Pacemakers

Although pacemakers have significantly improved over the years, they still cannot offer long-term solutions to conditions like arrhythmia. One of the major downsides of modern pacemakers is that they have a battery life of five to seven years. This lifespan is much better than the early devices, but it is still not ideal for patients who require long-term treatment. When the batteries run out, they have to be replaced surgically, which is not only expensive but also increases the risk of infection. Another downside is the difficulty associated with placing the leads. Placing leads can be extremely difficult in certain patients, such as those with cardiovascular diseases. If the leads fail, major surgeries with a high risk of infection may be required to remove them [9]. Nonetheless, several ongoing studies show great potential for solving these problems.

A recent study by the Department of Aerospace Engineering at the University of Michigan in Ann Arbor offers a promising solution to battery life limitations. Instead of running on lithium batteries, the proposed device uses piezoelectricity—e​lectricity generated from motion, which in this case is the heartbeat. The idea was taken from a light unmanned aircraft that is powered by the vibrations of its own wings. Based on a wide variety of simulated heartbeats, researchers found that the energy harvested from heartbeats were ten times more than the energy required for modern pacemakers. The potential for power-harvesting devices is extremely exciting, since it promises a power source that is a smaller (half the size of the batteries currently in use) and allows pacemakers to be self-powering [8].

Research efforts have also been devoted to exploring possible replacements for pacing leads. Cambridge Consultants, a company based in England, has engineered a pacing system that eliminates the need for leads altogether. The device uses a miniscule electrode—only the size of a grain of rice—that receives electric signals wirelessly though ultrasounds. The size of the electrodes allows them to be implanted directly onto the heart with a catheter (a thin flexible tube). The pacemaker is implanted in the chest, and then it sends ultrasonic pulses that create vibrations in the electrode, which turns into a current to stimulate the heart. Though the device is still in research phase, it shows great potential after the successful completion of several clinical trials [10].

With the today’s rapid rate of technological evolution, there is no doubt that pacemakers will keep getting smaller and more resilient in the near future.

References

• • [1] Jane B. Reece, Lisa A. Urry, Michael L. Cain, et al, Campbell Biology, Boston, MA: A Pearson Education Company, 2011, pp. 902-904.
  • [2] U. D. o. H. &. H. Services, "NIH," NIH, 28 Feb 2012. [Online]. Available: http://www.nhlbi.nih​.gov/health/health-t​opics/topics/pace/. [Accessed 28 March 2013].
  • [3] M. C. Staff, "Mayo Clinic," Mayo Clinic, 15 Oct 2010. [Online]. Available: http://www.mayoclini​c.com/health/pacemak​er/MY00276. [Accessed 28 March 2013].
  • [4] O. Aquilina, "A brief history of cardiac pacing," Images in Paediatric Cardiology, vol. 8, no. 2, pp. 17-81, 2006.
  • [5] "The Transistor," Nobelprize.org, [Online]. Available: http://www.nobelpriz​e.org/educational/ph​ysics/transistor/?em​_x=22. [Accessed 29 March 2013].
  • [6] Medtronic, Inc, "For your pacemaker - Patient Manual," October 2008. [Online]. Available: http://manuals.medtr​onic.com/wcm/groups/​mdtcom_sg/@emanuals/​@era/@crdm/documents​/documents/contrib_1​17089.pdf. [Accessed 29 March 2013].
  • [7] Heart Rhythm Society, "Pacemaker," Heart Rhythm Society, 2013. [Online]. Available: http://www.hrsonline​.org/Patient-Resourc​es/Treatment/Pacemak​er#axzz2OzM2efcw. [Accessed 28 March 2013].
  • [8] B. B. Deena Beasley, "Scientists say heartbeat, not battery, could power pacemakers," Reuters, 4 Nov 2012.
  • [9] C. Bates, "The amazing pacemaker powered by your own heartbeat instead of batteries - and is smaller than a one penny piece," Daily Mail, 5 Nov 2012.
  • [10] T. E. Online, "Total control of the heart," The Economist, 15 Nov 2011.
  • [11] NIH Heart, Lung and Blood Institute, "Your Heart's Electrical System NHLBI, NIH." N.p., n.d. Web. 22 Apr. 2013. .
  • [12] Biotele, "History of Pacemakers." n.d. Web. 2 May 2013.
  • [13] WebMD, "Pacemaker placement." n.d. Web. 3 May 2013.

Thankshttp://illumin.usc.edu/271/engineering-heartbeats-the-evolution-of-artificial-pacemakers/

Train your heart to protect your mind

Exercising to improve our cardiovascular strength may protect us from cognitive impairment as we age, according to a new study by researchers at the University of Montreal. "Our body's arteries stiffen with age, and the vessel hardening is believed to begin in the aorta, the main vessel coming out of the heart, before reaching the brain. Indeed, the hardening may contribute to cognitive changes that occur during a similar time frame," explained Claudine Gauthier, first author of the study. "We found that older adults whose aortas were in a better condition and who had greater aerobic fitness performed better on a cognitive test. We therefore think that the preservation of vessel elasticity may be one of the mechanisms that enables exercise to slow cognitive aging."
The researchers worked with 31 young people between the ages of 18 and 30 and 54 older participants aged between 55 and 75. This enabled the team to compare the older participants within their peer group and against the younger group who obviously have not begun the aging processes in question. None of the participants had physical or mental health issues that might influence the study outcome. Their fitness was tested by exhausting the participants on a workout machine and determining their maximum oxygen intake over a 30 second period. Their cognitive abilities were assessed with the Stroop task. The Stroop task is a scientifically validated test that involves asking someone to identify the ink colour of a colour word that is printed in a different colour (e.g. the word red could be printed in blue ink and the correct answer would be blue). A person who is able to correctly name the colour of the word without being distracted by the reflex to read it has greater cognitive agility.
The participants undertook three MRI scans: one to evaluate the blood flow to the brain, one to measure their brain activity as they performed the Stroop task, and one to actually look at the physical state of their aorta. The researchers were interested in the brain's blood flow, as poorer cardiovascular health is associated with a faster pulse wave,at each heartbeat which in turn could cause damage to the brain's smaller blood vessels. "This is first study to use MRI to examine participants in this way," Gauthier said. "It enabled us to find even subtle effects in this healthy population, which suggests that other researchers could adapt our test to study vascular-cognitive associations within less healthy and clinical populations."
The results demonstrated age-related declines in executive function, aortic elasticity and cardiorespiratory fitness, a link between vascular health and brain function, and a positive association between aerobic fitness and brain function. "The link between fitness and brain function may be mediated through preserved cerebrovascular reactivity in periventricular watershed areas that are also associated with cardiorespiratory fitness," Gauthier said. "Although the impact of fitness on cerebral vasculature may however involve other, more complex mechanisms, overall these results support the hypothesis that lifestyle helps maintain the elasticity of arteries, thereby preventing downstream cerebrovascular damage and resulting in preserved cognitive abilities in later life."
The findings were published in Neurobiology of Aging on August 20, 2014.
SEE MORE at - http://medicalxpress.com/news/2014-08-heart-mind.html
Photo - Credit: Rice University
Train your #heart to protect your #mind

ECG ::

Complete cardiac transplant

Ever wondered what heart transplant surgery really looks like? Watch this. But be warned, this is graphic content and not for the... faint of heart. 
Almost half a century ago, the world’s first heart transplant was performed in South Africa in 1967. The following year, Australia’s first heart transplant was performed by Dr Harry Windsorat St Vincent’s Hospital in Sydney. 

According to the Heart Foundation, the procedure usually takes between three and six hours, and will be one of two types of transplant operations. An orthotopic heart transplant is the most common type (as seen above), and this involves removing the diseased heart from the body through an incision made in the middle of the chest. A donor heart is then placed inside.

Under rare circumstances, selected patients can undergo heterotopic heart transplants, which allow the donor heart to piggy-back onto the existing heart. Double hearts are a good solution for patients with heart problems that cause them to have extremely high blood pressure in the pulmonary artery, which is the blood vessel that transport the blood from the heart to the lungs. The pressure that builds up because of this can cause the heart muscle to be weakened - a condition known as cardiomyopathy. If a patient is approved for a heterotopic heart transplant, the donor heart acts as an extra pump to help out the patient's weakened heart.

Source: Heart Foundation

இதயத்திற்கு இதமான செய்தி...... இதயத்தில் அடைப்பு உள்ளதா?

இதோ உடனே செல்லுங்கள் .திருவனந்தபுரம் காட்டாகடை அருகில் உள்ள பன்னியோடு சுகுமாரன் வைத்தியர் அவர்கள் இலவசமாக வைத்தியம் செய்கிறார்.நாடித்துடிப்பை பார்த்தே உங்கள் நோயை கண்டுபிடிக்கிறார்..வெள்ளிக்கிழமை தவிர்த்து மற்ற எல்லாநாட்க்களிலும் வைத்தியம் .இதயத்தில் அடைப்பு உள்ளவர்களுக்கு மூன்று மாத மருந்துக்கு 2700 ரூபாய் ஆறு நாட்கள் மருந்து உட்கொண்டாலே ரத்த குழாய் அடைப்பு மாறுகிறது .பணம் கொடுக்க வசதியில்லாதவருக்கு இலவசம் .தேவையுள்ளவர் இந்த வாய்ப்பை நழுவவிடாதீர் .


மிகமிக முக்கியமான தகவல் என்பதால் இதனை அதிகமான அளவில் பகிர்ந்து உங்களுடைய நண்பர்களுக்கு இத்தகைய தகவல் சென்றுசேர உதவுங்கள் இதனால் யாரவது ஒருவர் பயன்பெற்றாலும் நம் அனைவருக்கும் மகிழ்ச்சியே.....


தகவல் கே.எம்.ஷாவிடம் இருந்து.

How stress causes heart attacks?

New research suggests films of bacteria are keeping heart attack-causing plaque out of the blood stream, but stress hormones are setting them free.

Image: Bernard B. Lanter/Binghamton University

Scientists have long thought that stress triggers heart attacks, but they’ve never been able to work out how. Now new research has identified the bacteria that may be involved.

It's long been suspected that bacteria attaches to and infects plaque - a substance that builds up in arteries when cholesterol combines with fat and calcium, and can harden over time to cause heart attack or stroke. Researchers from Binghamton University in New York set out to study which bacteria were involved, and whether the process was being affected by stress.

Using fluorescent tags, they discovered more than 10 species of bacteria clustered tightly around plaque, including Pseudomonas aeruginosa - a bacteria known for growing in clumps called biofilms (red in the microscope image above, the artery is green).

According to lead researcher David Davies, these biofilms can affect the risk of cardiovascular disease by binding tightly to plaque and stopping them from entering the bloodstream. And he suspected that stress hormones were breaking them down.

His team tested this theory by growing P. aeruginosa biofilms in artificial arteries in the lab. As Sara Reardon reports for Nature, they then flooded the system with stress hormone noradrenaline to see what happened.

What they found was that noradrenaline triggers the body’s cells to release iron, which in turn breaks down the bonds that hold P. aeruginosa biolfilms together.

And as collateral damage, the plaque is also set free, their research suggests. The results are published in mBio.

More work needs to be done to determine whether this same mechanism is happening in humans and animals, but if it pans out, it “introduces a completely unexpected potential culprit” for heart attacks, Davies told Nature.

One criticism so far is that the amount of noradrenaline released in the experiment is much higher than would be present in the human body, but it’s possible that lower levels could have a similar affect - we’ll just have to wait and see.

In the meantime, let’s all try to stress less…

Source: Nature

Acute Myocardial Infarction Management

Management of a patient with acute myocardial infarction (AMI) is a medical emergency. Local guidelines for the management of myocardial infarction should be followed where they exist.

Pre-hospital management :-

- Arrange an emergency ambulance if an AMI is suspected. Take an electrocardiogram (ECG) as soon as possible, but do not delay transfer to hospital, as an ECG is only of value in pre-hospital management if pre-hospital thrombolysis is being considered.
- Advise any patient known to have ischaemic heart disease to call for an emergency ambulance if the chest pain is unresponsive to glyceryl trinitrate (GTN) and has been present for longer than 15 minutes or on the basis of general clinical state - eg, severe dyspnoea or pain.
- Cardiopulmonary resuscitation and defibrillation in the event of a cardiac arrest.
- Oxygen: do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:
a. People with oxygen saturation less than 94% who are not at risk of hypercapnic respiratory failure, aiming for saturation of 94-98%.
b. People with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target saturation of 88-92% until blood gas analysis is available.
- Pain relief with GTN sublingual/spray and/or an intravenous opioid 2.5-5 mg diamorphine or 5-10 mg morphine intravenously with an anti-emetic.[2] Avoid intramuscular injections, as absorption is unreliable and the injection site may bleed if the patient later receives thrombolytic therapy.
- Aspirin 300 mg orally (dispersible or chewed).
- Insert a Venflon® for intravenous access and take blood tests for FBC, renal function and electrolytes, glucose, lipids, clotting screen, C-reactive protein (CRP) and cardiac enzymes (troponin I or T).
- Pre-hospital thrombolysis is indicated if the time from the initial call to arrival at hospital is likely to be over 30 minutes. The National Institute for Health and Clinical Excellence (NICE) recommends using intravenous bolus (reteplase or tenecteplase) rather than an infusion for pre-hospital thrombolysis.

Management initiated in hospital :-

- If not already done, insert a Venflon® for intravenous access and take blood tests for cardiac enzymes (troponin I or T), FBC, renal function and electrolytes, glucose, lipids, CRP, and clotting screen.
- Continue close clinical monitoring, oxygen therapy and pain relief.
- ECG monitoring: features that increase the likelihood of infarction are: new ST-segment elevation; new Q waves; any ST-segment elevation; new conduction defect. Other features of ischaemia are ST-segment depression and T-wave inversion.

Reperfusion

Patency of the occluded artery can be restored by percutaneous coronary intervention (PCI) or by giving a thrombolytic drug. PCI is the preferred method. Compared with fibrinolysis, PCI results in less reocclusion, improved left ventricular function and improved overall outcome (including reduced risk of stroke).

Primary percutaneous coronary intervention (PCI)

= PCI (or percutaneous transluminal coronary angioplasty - PTCA) is regarded as superior to fibrinolysis in the management of AMI and is becoming increasingly available for initial patient care.
= Primary angioplasty provides an early assessment of the extent of the underlying disease.
= Any delay in primary PCI after a patient arrives at hospital is associated with higher mortality in hospital. Time to treatment should therefore be as short as possible. Door (or diagnosis) to treatment time should be less than 90 minutes, or less than 60 minutes if the hospital is PCI ready and symptoms started within 120 minutes.
= There is general agreement that PCI should be considered if there is an ST elevation acute coronary syndrome, if symptoms started up to 12 hours previously.
= Patients should receive a glycoprotein IIb/IIIa inhibitor to reduce the risk of immediate vascular occlusion, and should also receive either unfractionated heparin, a low molecular weight heparin (eg, enoxaparin), or bivalirudin.
= Prasugrel in combination with aspirin is an option for the prevention of atherothrombotic events in patients with acute coronary syndromes and undergoing PCI if immediate primary PCI is necessary, stent thrombosis occurs during treatment with clopidogrel, or the patient has diabetes mellitus.
= Balloon angioplasty following myocardial infarction reduces death, nonfatal myocardial infarction and stroke compared with thrombolytic reperfusion. However, up to 50% of patients experience restenosis and 3% to 5% recurrent myocardial infarction.
= There is no evidence to suggest that primary stenting reduces mortality when compared with balloon angioplasty but stenting seems to be associated with a reduced risk of re-infarction and target vessel revascularisation.

Fibrinolytic drugs

For patients who cannot be offered PCI within 90 minutes of diagnosis, a thrombolytic drug should be administered along with either unfractionated heparin (for maximum two days), a low molecular weight heparin (eg, enoxaparin) or fondaparinux. Thrombolytic drugs break down the thrombus so that the blood flow to the heart muscle can be restored to prevent further damage and assist healing.

Antithrombotic therapy without reperfusion therapy

- In patients presenting within 12 hours after the onset of symptoms but reperfusion therapy is not given, or in patients presenting after 12 hours, aspirin, clopidogrel and an antithrombin agent (heparin, enoxaparin or fondaparinux) should be given as soon as possible.
- For patients who do not receive reperfusion therapy, angiography before hospital discharge is recommended (as for patients after successful fibrinolysis) if no contra-indications are present.

Coronary bypass surgery

Other initial management :
1. Antiplatelet agent
2. Beta-blockers
3. Angiotensin-converting enzyme (ACE) inhibitors
4. Cholesterol-lowering agents
5. Patients who have a left ventricular ejection fraction of 0.4 or less and either diabetes or clinical signs of heart failure should receive the aldosterone antagonist eplerenone (started within 3-14 days of the myocardial infarction and ideally after ACE inhibitor therapy) unless contra-indicated by renal impairment or hyperkalaemia (left ventricular function should be assessed in all patients with AMI during the initial hospital admission).
6. Cardiac assessment and revascularisation

CAUSES OF HYPERTENSION ::

இதய மாற்று சிகிச்சைக்குக் காத்திருப்பவர்களுக்கு செயற்கை இதயம் ரெடி:

உறுப்பு மாற்று அறுவை சிகிச்சைகளும் செயற்கை உறுப்புகளைப் பொருத்தும் முறைகளும் நாளுக்கு நாள் அதிகரித்து வருகின்றன. இவற்றின் உச்சகட்ட வளர்ச்சியாக, இதயம் செயலிழந்து, இதய மாற்று சிகிச்சைக்குக் காத்திருப்பவர்களுக்கு மாற்று இதயம் கிடைக்கும் வரை உயிரைப் 'பிடித்து' வைக்க செயற்கை இதயத்தைப் பொருத்தும் அறுவை சிகிச்சையும் தற்போது பிரசித்தமாகி வருகிறது. சமீபத்தில் பிரான்சில் 'கார்மட்' எனும் உயிரி மருந்தியல் துறை நிறுவனம் புதிய செயற்கை இதயத்தை வடிவமைத்து சாதனை புரிந்துள்ளது.

மாரடைப்பு வந்தவரின் இதயத்தில் எல்லா தமனி ரத்தக் குழாய்களும் அடைபட்டு ஆஞ்சியோ பிளாஸ்டி, பைபாஸ் சிகிச்சை எதுவும் பலனளிக்காமல் போனால், அவருக்குச் செயற்கை இதயத்தைப் பொருத்தலாம். இதயத்தின் கீழறைகள் இரண்டும் மிகவும் பாதிக்கப்பட்டு, மகா தமனிக்குள்ளும், நுரையீரல் தமனிக்குள்ளும் ரத்தத்தைச் செலுத்த முடியாத அளவுக்கு இதயம் செயலிழந்து போனாலும் இதைப் பொருத்தலாம். இதய இடைச் சுவர்களில் துளை விழுந்து அல்லது இதயத்தில் உள்ள எல்லா வால்வுகளும் பழுதடைந்து, இதயம் பலூன்போல் விரிந்துவிட்டால் செயற்கை இதயம் பயன்படும்.

இப்படிப் பலருக்கும் பயன் தருகின்ற செயற்கை இதயத்தைக் கண்டுபிடிக்கும் முயற்சி 50 ஆண்டுகளுக்கு முன்பே தொடங்கிவிட்டது. அமெரிக்காவிலுள்ள ஹூஸ்டன் மருத்துவமனை ஆராய்ச்சியாளர்கள்தான் இதில் முன்னோடிகள். இந்த மையத்தைச் சேர்ந்த டாக்டர் ராபர்ட் ஜார்விக் என்பவர் 1982ல் வடிவமைத்த 'ஜார்விக் & 7' (Jarvik 7) எனும் செயற்கை இதயம், மருத்துவ உலகில் மிகவும் பிரபலம்.

இது பாலியுரேத்தேன் எனும் பிளாஸ்டிக்கால் உருவாக்கப்பட்டது. ஒரு நெல்லிக்காய் அளவு பேட்டரியில் இயங்குகின்ற 'ஜார்விக் &7' கருவியை நோயாளி யின் பழுதடைந்த இதயத்தோடு பொருத்தி விடுகிறார்கள். இதில் 2 பலூன்கள் இதயத்தை ஒட்டி யிருக்கும். ஒரு சிறிய குழாய் மூலம் பலூனுக்குள் காற்று செல்கிறது. அக்காற்று தருகின்ற அழுத்தத்தில் பலூன்கள் விரிந்து சுருங்கும்போது இதயமும் இயங்குகிறது. பேட்டரி சார்ஜ் குறைந்துபோன காரை 4 பேர் பின்பக்கத்திலிருந்து தள்ளிவிட்டு நகரச் செய்வதைப் போலத்தான் இதுவும்.

இதைப் பயன்படுத்துவதில் பல சிரமங்கள் இருந்தன. இதன் பேட்டரி இணைந்த கருவி ஒரு பெரிய கேமரா அளவிற்கு இருக்கும். இதை இடுப்பில் எந்நேரமும் சுமந்து கொண்டிருப்பது நோயாளிகளுக்குச் சிரமத்தைத் தந்தது. இது காற்றைச் செலுத்தும்போது ரத்தம் உறைந்து போனது. இது தருகின்ற காற்றழுத்தம் நுரையீரல்களின் செயல்பாட்டைத் தடுத்தது. இதன் செயற்கை வேதிப்பொருள்களை உடல் ஏற்றுக்கொள்ளாமல் நிராகரித்தது. எல்லாவற்றுக்கும் மேலாக, இது அதிகபட்சமாக 6 மாதங்களே செயல்பட்டது. ஆகையால், இதைவிட சிறந்த கருவியைக் கண்டுபிடிக்க ஆராய்ச்சியாளர்கள் முடுக்கிவிடப்பட்டனர்.

இதன் பலனாக போனிக்ஸ்&7 (Phoenix 7), அபியோகோர் (AbioCor), சின்கார்டியா (SynCardia) என்று பல செயற்கை இதயங்கள் செயலுக்கு வந்தன. இவை டைட்டானியம் மற்றும் பிளாஸ்டிக்கால் செய்யப்பட்டவை. இதயத்தின் வெளிப்பக்கத்திலிருந்து 'ஜார்விக்&7' இயங்கியது என்றால், இவை நோயாளியின் இதயத்துக்குள்ளேயே பொருத்தப்பட்டு செயல்பட்டன. பழுதடைந்து போன இதயத்தின் இரண்டு கீழறைகளையும் 4 வால்வுகளையும் அகற்றி விட்டு, அந்த இடத்தில் இக்கருவி ஒன்றை இணைத்து விட்டனர். இவற்றில் 2010ல் சிட்னி& செய்ன்ட் வின்சென்ட் மருத்துவமனையில், 50 வயது முதியவர் ஆஞ்சலோ தைகோனோ என்பவருக்குப் பொருத்தப்பட்ட சின்கார்டியா செயற்கை இதயம் மட்டும் 4 வருடங்களுக்குச் செயல்பட்டது. இதுவும் காற்றழுத்தம் மூலம் இதயத்தை இயங்கவைத்த காரணத்தால்... இதிலும் ரத்த உறைவு மற்றும் நுரையீரல்களில் காற்றழுத்தப் பிரச்னைகள் ஏற்பட்டன.

இன்னும் மேம்படுத்தப்பட்ட கருவிகளைக் கண்டுபிடிக்கும் முயற்சியில் இப்போது 'கார்மட்' எனும் செயற்கை இதயம் மூலம் பலன் கிடைத்துள்ளது. இதை உருவாக்கிய டாக்டர் அலென் கார்ப்பென்டியர் கூறுகையில், “எங்கள் நிறுவன ஆராய்ச்சியாளர்கள்தான் இக்கருவியைக் கண்டுபிடித்தார்கள் என்றாலும், டென்மார்க்கைச் சேர்ந்த ஐரோப்பிய ஏரோநாடிக் டிஃபன்ஸ் மற்றும் ஸ்பேஸ் நிறுவனம் இதை மேம்படுத்திக் கொடுத்தது. பாரீஸில் உள்ள ஜார்ஜஸ் போம்பிடௌ மருத்துவ மனையில் இதயம் செயலிழந்த 75 வயது முதியவருக்கு இது பொருத்தப்பட்டது. டாக்டர் கிறிஸ்டியன் லேட்டர்மெளலி இந்த அறுவைச் சிகிச்சையை மேற்கொண்டார்.

இது லித்தியம் பேட்டரி மூலம் இயங்குகிறது. பேட்டரியை இடுப்பில் அணிந்துகொள்ள வேண்டும். இது, சில உயிரிப்பொருள்களுடன் பசுவின் திசுக்களும் கொண்டு தயாரிக்கப்பட்டுள்ளதால், இயற்கை இதயத்துக்கு நிகராக இது கருதப்படுகிறது. ஆகவே, இதை உடல் எளிதாக ஏற்றுக்கொண்டது. இயற்கை இதயத்திலிருந்து செயற்கை இதயத்துக்கு ரத்தம் வருகின்ற இடம் பிளாஸ்டிக் இழைகளால் தயாரிக்கப்படாமல், பசுவின் திசுக்களால் தயாரிக்கப்பட்டதாலும், காற்றுக்குப் பதிலாக ஹைட்ராலிக் திரவத்தின் அழுத்தம் கொண்டு இது இயக்கப்படுவதாலும் ரத்தம் உறைந்து கட்டியாவது தடுக்கப்பட்டுள்ளது. இதில் சென்சார் மற்றும் கணினி தொழில்நுட்பமும் இணைந்துள்ளதால், காய்ச்சல், அயர்ச்சி, மகிழ்ச்சி போன்ற நோயாளியின் உடல், மன மாறுதல்களுக்கு ஏற்ப தன் இயக்க சக்தியை மாற்றிக் கொள்ளும் திறனும் இதற்கு உண்டு. இதன் எடை 900 கிராம். இது 5 ஆண்டுகளுக்கு நீடித்து உழைக்கும்” என்கிறார்.

'கார்மட்' இதயம், அறிவியல் கண்டுபிடிப்பில் ஓர் அரிய வரம்!

via தினகரன்

quick exercise best for heart

A University of Queensland study has found high-intensity short-duration exercise provides better results than the recommended 30 minutes of daily exercise.
Researchers are looking at the benefits of high intensity interval training as the most effective way of reducing the risk of heart disease in people with metabolic syndrome.
Metabolic syndrome, suffered by 30 per cent of the Australian population, involves a combination of being overweight or obese and having either high blood pressure, high cholesterol or diabetes.
Professor Jeff Coombes at UQ’s School of Human Movement Studies said the trial was in early stages; but results had been promising.
“Out of the 25 participants who have taken part in the high intensity exercise program, seven no longer have metabolic syndrome,” Professor Coombes said.
“Participants observed improved weight loss and a reversal in high levels of cholesterol, blood sugar and blood pressure, as well as improved fitness levels.
“By simultaneously reducing these risk factors you significantly decrease the risk of heart disease, type 2 diabetes and stroke.
“Exercise is a proven way to manage many health problems, but these results show that short bursts of high intensity exercise could get the same, if not better, results in half the time.”
The study, conducted by PhD student Joyce Ramos, involved participants training three times a week for 16 weeks, with one group exercising at high intensity for on four-minute period and a second group exercising at high intensity for four four-minute periods.
Results were compared with a control group exercising moderately for half an hour.
"We are working to confirm these exciting results through a multi-centre international trial with 750 individuals," Prof Coombes said.
High-intensity interval training involves alternating short periods of intense exercise with less intense exercise in the same session.

Editor's Note: Original news release can be found here.

Microparticles cut heart damage

This is the first therapy that reduces heart attack damage and scarring by targeting the key driver of that damage.

Image: Sebastian Kaulitzki/Shutterstock

A University of Sydney discovery has the potential to transform the treatment of a heart attack, after a new approach boosted heart function and reduced heart scarring in preclinical studies.
The research breakthrough, published in Science Translational Medicine, involves injecting tiny "microparticles" into the bloodstream within 24 hours of a heart attack to reduce tissue damage made by inflammatory cells.
The discovery was made at the University of Sydney and is the result of an international collaboration with researchers at Northwestern University in the USA, and Bonn and Münster in Germany.
After a heart attack (myocardial infarction), much of the damage to heart muscle is caused by inflammatory cells that rush to the scene of the oxygen-starved tissue. But researchers found this damage was slashed in half when they used the microparticles to keep the highly damaging cells away.
"This is the first therapy that specifically targets a key driver of the damage that occurs after a heart attack," said Dr Daniel Getts, one of the original discoverers from the University of Sydney, now based at Northwestern University in the USA.
"There is no other therapy on the horizon that can do this. It has the potential to transform the way heart attacks and cardiovascular disease is treated," he said.
Nicholas King, Professor of Immunopathology at the University of Sydney and co-discoverer, said the power of the treatment was that the microparticles triggered a natural pathway that destroyed the inflammatory cells.
"We're very excited," Professor King said.
"This discovery means that we can prevent major tissue damage simply because the inflammatory cells pick up microparticles in the blood stream and are then diverted down a natural cell disposal pathway into the spleen."
The discovery also has huge potential beyond the cardiovascular system.
The research shows the microparticles reduce inflammatory damage and enhance tissue repair in disease models as diverse as multiple sclerosis, inflammatory bowel disease, peritonitis, viral inflammation of the brain and kidney transplant.
"The potential for this approach is quite extraordinary," Professor King said.
"It's amazing that such a simple approach can limit major tissue damage in such a wide range of diseases."
The next step is safety tests on the microparticles, which are tiny balls of absorbable material, 200 times smaller than the thickness of a human hair. They are made of a biodegradable compound, poly lactic-co-glycolic acid, used in absorbable surgical sutures and already approved for use in humans.
Clinical trials on heart attack patients should follow within two years at the University of Sydney.
The research was co-authored by Professor King from the University of Sydney, and Dr Getts and Professor Miller from Northwestern University.

Editor's Note: Original news release can be found here.

Scientists Develop World’s Smallest Blood Monitoring Implant That Tells Your Smartphone When You’re About To Have A Heart Attack

The world’s smallest medical implant has recently been revealed by a group of scientists at Ecole Polytechnique Fédérale de Lausanne (EPFL) in Switzerland. The device measures 14 millimeters only but can provide accurate data used to analyze levels of sugar in the blood, lactate and ATP. It is also capable of feeding data about the activity of the body as well as information about diseases like diabetes.

While implants aren’t really something new in today’s world, this new medical device can transmit data to smartphones via Bluetooth. Basically, data will be sent wirelessly to the owner’s smartphone, which will tell that he or she is about to get a heart attack, which is known to be a silent killer.

In case you’re wondering how this works – The implant will be induced into the part of the body that has few activities so its functions wouldn’t be disturbed. It is coated with an enzyme that reacts with blood-borne elements so that detectable signals can be sent to devices like smartphones. The implant has proven to be effective in preventing heart attack not because it directly interacts with the body’s activity but because it provides consistent information on levels of data it is programmed to read.

A heart attack, according to medical practitioners and experts, do not happen in a second. It is a progression and a process that can be prevented if only the subject knows what’s happening inside of him or her.

Hours leading to a heart attack, muscles starve for oxygen and when they couldn’t get enough, they break and fragments are carried out by blood in the circulation. These are among the things this medical implant could detect. If data are immediately fed to the smartphone, the user would know he or she needs to do some preventive measures or contact a physician immediately.

The implant can be recharged using a 100-milliwatt battery pack outside the body via inductive wireless charging and uses the skin to send off electrons.

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