If I'm missing, or not taking messages sorry – I'm more angry about letting my friends down than YOU will ever be at being let down! Unfortunately that is sometimes a side effect of Cancer! Mea Culpa: may I blame being short fused & grumpy on it too! My first symptoms presented in Nov-1998 – Follow The Trail on >DIARY of CANCER< Immediately Below!
The Importance Of Speedy NHS Treatment Can NOT Be Over-estimated!
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Hi,
lets look at Heart Attacks in a little more detail, and just how important speedy attention is.One can but hope that someone in the Welsh Health Service reads this article – someone in a position to bypass and thus overcome the crass mismanagement of the Welsh EU Regional branch of the British NHS, under Labour control in the devolved misgovernance that goes with EU regional Assemblies!
I well remember the staggering incompetence of the NHS at The Royal Gwent when I suffered my heart attack – how I survived their utter mismanagement, tardy diagnosis and utter incompetenc is something of a miracle.It is not just emergency care through A&E or MAU I have experienced unconcionable delays in SAU also – not to mention presenting with classic symptoms of urinary tract cancer in November 1997 yet they took until July 2001 to make a diagnosis and even then it was only the intervention of Daniel Foggo, a perspnal friend and leading investigative journalist for then The Sunday Telegraph, quizzing the Gwent as to why the delay in operating for a radical open nephrectomy by September 2001. My Consultant informed me that I was very lucky as the cancer was on the verge of breaking out of the kidney to make survival extremely unlikely and that my life had been saved by Daniel’s intervention!
Then again a few years later whilst having bladder cancer dealt with via TURBC a sinister growth was noted and although I asked if the surgeon could immediately procede to remove it I was told it was ‘above his pay grade’ to make that decision, or words to that effect. I waited from the op on 31-Dec-2010 for a scan in Apr-2011 – by which time I had fully developed tumours in my abdomen and cancerous lymph glands which presented me with a life expectancy of 2 to 3 months!I was fortunate and whether by virtue of luck, harsh treatment, general constitution or attitude, or more likely a combination of the four I am still here today.
In the treatment of cancer speed of action plays an all important part – however the treatment of Heart Attacks is even more dramatically dependent on wasting no time and acting as rapidly as possible, as shown in the articles below.
How I survived a Heart Attack at 06:15hrs. 19-N0v-2012 I will never know, a Heart Attack that went totally untreated by the NHS in the hopelessly mismanaged Labour controlled devolver Welsh EU Assembly Region as I drove myself from my Doctor’s in Chepstow to find parking and find the MAU in the Royal Gwent in Newport, where I waited around for hours in pain and was even told to walk some distance to the radiology dempartment to wait yet further for a scan before finding my way back to MAU – actual drugs to try to curb the pain and deal with the heart attack were not administered until around 03:00hrs. 20-Nov-2012, the following morning!
A Sea Change in Treating Heart Attacks
The death rate from coronary heart disease has dropped 38 percent in a decade. One reason is that hospitals rich and poor have streamlined emergency treatment.
CAMDEN, N.J. — Yvette Samuels was listening to jazz late one night when she felt a stabbing pain down her left shoulder. She suspected a heart attack — she had heard about the symptoms from watching a Rosie O’Donnell standup routine on television — and managed to scratch on the door that connected her single room to her neighbor’s. He found her collapsed on the floor.
Paramedics arrived minutes later and slapped electrocardiogram leads on her chest, transmitting the telltale pattern of a heart attack to Our Lady of Lourdes Medical Center here.
As the ambulance raced through the streets, lights swirling, sirens screaming, Ms. Samuels, who took phone orders for a company that delivers milk, asked the paramedic, “Can this kill me?” He murmured yes, then told the driver, “Step on it!” She thought to herself, “This will be my last view of the world, the last time I will see the night sky.”
Instead, she survived, her heart undamaged, the beneficiary of the changing face of heart attack care. With no new medical discoveries, no new technologies, no payment incentives — and little public notice — hospitals in recent years have slashed the time it takes to clear a blockage in a patient’s arteries and get blood flowing again to the heart.
The changes have been driven by a detailed analysis of the holdups in treating patients and a nationwide campaign led by the American College of Cardiology, a professional society for specialists in heart disease, and the American Heart Association. Hospitals across the country have adopted common-sense steps that include having paramedics transmit electrocardiogram readings directly from ambulances to emergency rooms and summoning medical teams with a single call that sets off all beepers at once.
What Is A Heart Attack?
The heart has four chambers, which are separated by valves and surrounded by muscle.
The right side pumps blood back to the lungs for more oxygen.
The left side pumps oxygen-rich blood through the body.
Cardiac arteries supply oxygen-rich blood to the heart muscles.
If an artery becomes clogged or blocked, the downstream muscle is starved of blood.
“It may not be long before cardiovascular disease is no longer the leading cause of death” in the United States, said Dr. Michael Lauer, the director of the Division of Cardiovascular Sciences at the National Heart, Lung and Blood Institute.
The reinvention of protocols to hasten treatment is part of a broad rethinking of how to tackle coronary heart disease, which accounts for one of every seven deaths in the United States or 375,000 a year. Just this month, powerful drugs from the first new class of medicines to lower bad cholesterol levels in a generation nearedapproval by the Food and Drug Administration, raising hopes that they will further reduce the death rate from heart disease. At the same time, new, less invasive methods for replacing aged heart valves are raising hopes that ailing patients will be able to live longer. And researchers are immersed in resolving issues that remain unsettled: the utility of stents to treat the heart pain known as angina and the ideal level for blood pressure.
Lack of Speed Kills
In a heart attack, a blocked artery prevents blood from reaching an area of heart muscle. At first, cells are merely stunned, but as minutes tick by, they start to die. The way to save the heart is to open the blocked artery by pushing in a catheter, inflating a tiny balloon that shoves the blockage aside, and holding the artery open by inserting a stent, a tiny wire cage.
But leading cardiologists had despaired of reaching a national goal set by the American College of Cardiology and the American Heart Association of getting this done for at least half of heart attack patients within 90 minutes of arrival at a hospital. Often it took more than two hours for blood to flow to a patient’s heart again.
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Procedures at Lourdes allow cardiologists like Dr. Thierry Momplaisir, right, and nurse Krista Damirgian to start working on a patient faster.Credit Mark Makela for The New York Times
Now, nearly all hospitals treat at least half their patients in 61 minutes or less, according to the most recent data from the American College of Cardiology. At Yale-New Haven Hospital, where half the patients used to have to wait at least 150 minutes before their arteries were opened, the median time is now 57 minutes. At the Mayo Clinic and at major academic centers like NewYork-Presbyterian Hospital, it is 50 minutes — a statistic that, amazingly, Lourdes matches.
Some cardiologists still express sadness at the price many patients paid when care was much slower. Dr. Mahesh Bikkina, the director of the cardiac catheterization laboratory at St. Joseph Regional Medical Center in Paterson, N.J., tells his trainees about the old days: heart muscles that tore, with blood leaking out of holes, and valves that ruptured, leading to sudden death if not repaired immediately with open-heart surgery.
“I tell them you will read about these things in textbooks,” Dr. Bikkina said. “You will almost never see them.”
Dr. Brahmajee Nallamothu, a University of Michigan cardiologist, said he remembered patients who became cardiac cripples after long delays in receiving treatment, their hearts so damaged that the slightest exertion exhausted them.
“What I feel about this, what is really meaningful to me, is when we finally stopped saying, ‘You know, this stuff happens,’ and started taking control and saying, ‘This is not acceptable,’ ” Dr. Nallamothu said.
The improvements in treatment have spilled over into the care of stroke victims. Neurologists watched with envy as cardiologists slashed their times. For strokes, too, the time it takes to be treated with the clot-dissolving drug tPA is of the essence. “Time is brain,” neurologists say. They began to copy the cardiologists.
“Seeing that someone else could do it was remarkably motivating and a little bit competitive,” said Dr. Lee H. Schwamm, the chief of stroke services at Massachusetts General Hospital. “If they can do it, why can’t we?”
The payoff from the changes has been breathtaking, experts say.
“Heart disease mortality is dropping like a stone. This is a reason why,” said Dr. Eric Peterson, a cardiology researcher at Duke. “And stroke has fallen to fifth as a major killer. This is a reason why.”
Treating a Heart Attack
Doctors must first reopen the blocked artery and restore the flow of blood to the heart muscles.
Doctors insert a hollow catheter through the groin or an arm, threading it up a major artery and into the heart.
A deflated balloon is passed through the catheter to the site of the blockage.
The balloon is surrounded by a metal mesh stent. Inflating the balloon opens the artery and locks the stent in place.
Hospitals have been working to reduce the time needed to insert stents in patients having heart attacks.
A City at Risk
No city seemed more in need of improved heart care than Camden, where 42 percent of the population lives in poverty and heart disease risk factors abound, according to various studies. Obesity is rampant, as are high cholesterol levels, high blood pressure and smoking. A quarter of the population ages 50 to 59 who were hospitalized for any reason had diabetes. The vast majority of residents are Hispanic or African-American, groups with a relatively high prevalence of heart disease.
Most Camden residents having a heart attack are rushed to Lourdes, a medium-size Roman Catholic hospital founded in 1950 by the Franciscan Sisters of Allegany to serve the poor. It looks like a bisque-colored wedding cake perched high on a hill, with a statue of the Virgin Mary on top, hands folded in prayer. Its beige corridors are hushed, with no crackling intercom announcements to disturb the quiet. The staff members say they have a mission to serve their patients with reverence. Some have roots that go deep. One nurse, Brian Shannon, was born at Lourdes, as were his children. His mother worked there as a nurse for 35 years.
The Lourdes cardiology department has long felt pretty cocky about how it was doing. Heart care is the hospital’s specialty, and without its revenue, said Dr. Reginald Blaber, who runs the medical center’s cardiovascular disease program, Lourdes would have to close its doors.
Articles in this series will explore new approaches to treating heart disease.
Part 1A Sea Change in Treating Heart Attacks
Part 2Building a Better Valve
In 2007, the first year of a national campaign to speed treatment, half the patients at Lourdes waited at least 93 minutes before their arteries were opened. By 2011, Lourdes had a median treatment time of 71 minutes.
But at a staff meeting that year, Dr. Blaber challenged members of his team to do better. He pointed out that 16 percent of patients had to wait more than 90 minutes. “What if that one time when it took more than 90 minutes it was your mom?” he asked them.
Staff members set up what they called the D2B task force, standing for door to balloon time — the crucial period from when the patient enters the hospital until the cardiologist can thread a balloon into the blocked artery, inflate it, push the blockage aside and let blood flow again. They broke down the process, looking for opportunities to shave off a minute or two.
They decided to have paramedics do an electrocardiogram, which can show the characteristic electrical pattern of the heart that signals a heart attack, as soon as they reached the patient and transmit it directly to the emergency room. That meant the staff could spring into action the moment the ambulance pulled in. The hospital designated a beige phone on a counter in the E.R. for calls from paramedics.
They eliminated a big time sink — the requirement that a cardiologist look at the electrocardiogram and decide if an interventional cardiologist, who would open the blocked artery, should see it, too. Why not just give the emergency room doctor authority to call in the specialist?
It made a huge difference, Dr. Blaber said. Before, the E.R. doctor would fax an electrocardiogram to him. “The fax machine would go eh, eh, eh,” he said. And then he’d look at it: “ ‘Oh, God, I can’t read it. Send it again.’ Five minutes go by, seven minutes go by, 10 minutes go by. ‘Yeah, it’s a Stemi,’ ” he would say, using the acronym for a heart attack. “‘Let’s call the interventionalist.’ ”
In another change, the hospital operator began summoning members of the heart attack team with a single phone call that sounded their beepers simultaneously. And each member of the staff on call was required to be within 30 minutes of the hospital. Karl Madrid, a nurse, now spends on-call nights at his parents’ house in Voorhees, N.J. Dr. Ibrahim Moussa, a cardiologist, sleeps in his scrubs at a Crowne Plaza hotel four miles from the hospital when he is on call.
Photo
A physical therapist, Laura Funk, assisting Yvette Samuels, who was preparing for a short walk in the hallway at Lourdes as she recovered from a heart attack.Credit Jessica Kourkounis for The New York Times
The relatively languid step-by-step preparation of patients in the emergency room was transformed. Now when a patient arrives, staff members swarm the stretcher and within five minutes undress the patient, place defibrillator pads on the chest, insert two intravenous lines, shave the patient’s groin where the catheter will be inserted and snaked up to the heart, supply oxygen through a cannula in the nose, and provide medications like morphine, a blood thinner, and a drug to control heart rhythms.
One room has been designated for heart attack patients and is kept stocked with the necessary supplies, to avoid last minute scrambles for wires or catheters.
And a requirement that long consent forms be filled out before the team could get to work was jettisoned. The hospital’s lawyers advised that in an emergency, the team could get by with the patient’s name, date of birth and Social Security number.
“Everybody was anxious,” said Dr. Audrey Sernyak, a cardiologist who led the D2B team. “Everybody was giving up a lot of control. And everybody worried it might not go smoothly.”
But treatment times plunged.
Learning From the Swift
The heart story began nearly a decade ago when Dr. Krumholz, the Yale cardiologist, had an idea.
Medicare had created a national database showing how long it took hospitals across the country to get heart patients’ arteries opened. It was a bell curve year after year, and the times were not getting any better. But there were a few hospitals at the tail end of the curve that year after year were treating people in an hour or so.
Dr. Krumholz and his colleagues visited the 11 best performing hospitals. They were not famous institutions or major medical centers, said Elizabeth Bradley, a professor of public health at Yale and a leader in the project. Some were community hospitals; others were far from major population centers. The investigators recorded every detail of how the hospitals got things done and ended up with a short list of what the stellar performers had in common — procedures Lourdes later adopted.
They included paramedics’ transmitting electrocardiogram readings to emergency rooms, E.R. doctors’ deciding whether a person was likely having a heart attack, and hospital operators’ summoning treatment teams with a single call. These hospitals also continually measured performance.
Dr. Krumholz said he was particularly struck by the role of emergency room doctors. Interventional cardiologists were giving up the power to decide if they and the entire staff required to open an artery needed to dash in, often in the middle of the night.
“It is very rare for a group to give up power and get nothing in return,” he said. “You are saying, ‘You can call me at 3 in the morning and I am not going to question you.’ ”
At Yale, and most other places, Dr. Krumholz said, the procedures had been very different, with a long telephone chain of doctors and other staff members called one by one as precious minutes ticked by.
“A patient would come in, and the emergency room doctor would see him,” Dr. Krumholz recalled. “He would say, ‘O.K. I think we should call the primary care doctor.’ The primary care doctor would say: ‘I think we should call a cardiologist. I wonder which cardiologist to call.’ Sometimes, the first cardiologist was not available, so another had to be called. The cardiologist would call an interventional cardiologist, the specialist who could open the artery. The hospital page operator would try to find phone numbers for nurses and technicians and start calling each one in turn. Finally, when the staff had arrived, the patient would be wheeled into the cardiac catheterization lab to have his artery opened.
The problem was even worse if a patient went first to a community hospital that could not open an artery with a stent, said Dr. Nallamothu, of the University of Michigan. His group joked that a community hospital nearby was “30 minutes by car and three hours by ambulance” because it took so long for the community hospital emergency room to call the university’s emergency room and for the long chain of telephone calls to be completed.
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A 15-ton statue of the Virgin Mary atop Our Lady of Lourdes Medical Center. The hospital is in Camden, N.J., one of the poorest cities in the United States.Credit Mark Makela for The New York Times
The Yale researchers then surveyed a random sample of 365 hospitals and discovered that those that used one or more of six specific strategies to cut down on the time it took to get patients to the treatment room and open their arteries did better than those that had not, and that as more strategies were used, patients were being treated increasingly faster.
“We were shocked,” Dr. Bradley said. The results were so much better than she had hoped.
Dr. Krumholz and his colleagues persuaded The New England Journal of Medicine to publish their already accepted paper in the same week at the end of November 2006 that the American College of Cardiology announced a national campaign to get hospitals to change their ways. Twelve hundred committed to doing so.
Doctors and hospitals began competing to see who could have the best times. The initiative tapped into professional pride and a thirst to be the best. And, of course, hospitals wanted patients.
Within a few years, times were dropping all over the nation.
But then a debate arose.
A paper by Dr. Peterson, the Duke cardiologist, and his colleagues, published in The New England Journal of Medicine in 2013, said that even though times had plummeted, the death rates for heart attack patients whose arteries were opened with balloons and stents had not budged. Could it be that faster just seemed better but that it actually made no difference to patient outcomes?
“That was demoralizing,” Dr. Krumholz said. But he did an analysis that found that the universe of heart attack patients being treated with stents and balloons had changed markedly. It used to be just the younger and healthier people who were more likely to have their arteries opened. Now, as the procedure became more popular and so many more people were treated this way, the group included more older and sicker people.
Dr. Peterson concluded that analyses like his and Dr. Krumholz’s had challenges. The problem, he said, is that it is hard to accurately compare treatments given at different points. Nonetheless, the consensus — which he shares with Dr. Krumholz and other leading cardiologists — is that the shorter times and improved medical care contributed to the declining death rates and better outcomes for heart attack patients.
A Never-Ending Mission
At Lourdes, the push to be faster — and to fix the problems that slow things down — continues.
The weekend that Ms. Samuels was rushed to Lourdes, two other heart attack patients were brought in. First was Kevin Whisler, 43, a postal worker by day and forklift operator by night. He had been having what he thought was heartburn for two days, gulping Tums, Rolaids and Pepcid. Finally, on Saturday night, March 28, he went to an urgent care center, where a practitioner did an electrocardiogram and called an ambulance.
“You’ve got to be kidding me,” Mr. Whisler said. “I go in for heartburn and now you tell me I’m having a heart attack?”
Mr. Whisler’s doctor had prescribed a statin for his high cholesterol level and a medication for his diabetes. But Mr. Whisler said he thought he was too young to be taking pills every day and was trying to control his risk factors with diet.
In Less Than an Hour, a Heart Is Pumping Again
Doctors at Our Lady of Lourdes Medical Center in Camden, N.J., were able to clear Yvette Samuels’s blocked artery 55 minutes after she arrived at the emergency room.
Around 1:30 a.m. on March 29Ms. Samuels has a heart attack. She receives an electrocardiogram in the ambulance.
Clock startsat 1:54 a.m.The ambulance delivers Ms. Samuels to the emergency room.
6 minutesStaff members prepare her for surgery. The emergency room doctor orders another EKG before paging the heart attack team.
9 minutesA single phone call pages the heart attack team. An operating room is prepared.
33 minutesThe heart attack team begins to arrive. A cardiologist obtains consent from Ms. Samuels and prepares to move her.
41 minutesMs. Samuels is moved to the operating room, where doctors begin surgery on her heart.
55 minutesat 2:49 a.m.A balloon and stent inserted into Ms. Samuels’s wrist and maneuvered to her heart clear her blocked artery.
He was stunned by the speed with which things happened at Lourdes. Lying in his hospital bed the next day, he said he felt great and was going home in another day, inspired now to take his medications.
But at a staff meeting the next Monday morning, no one was happy with Mr. Whisler’s time — 72 minutes. The reason though, had nothing to do with the hospital; it was an issue with the urgent care center. The peeved cardiologist who treated him, Dr. Thierry Momplaisir, complained that the center did not notify the hospital that it had a heart attack patient or transmit his electrocardiogram. The emergency department was not prepared for his arrival, and it took 12 minutes before Mr. Whisler had another electrocardiogram. When the doctor saw the characteristic pattern, she asked the hospital operator to page the heart attack team.
Dr. Momplaisir was paged just as he was about to take a shower and go to a gala for the hospital. He pulled on his scrubs and jumped into his black Mercedes-Benz, speeding from his home in Villanova, Pa., in 20 minutes. But look at all the time that was wasted, he told the group.
It took a speedy 55 minutes from the time Ms. Samuels arrived at the hospital until her artery was opened, but the time could have been even better, Dr. Momplaisir said. She had her heart attack around 1:30 a.m. on Sunday, March 29. The paramedics transmitted her electrocardiogram to the emergency room. The beige phone in the E.R. dedicated to heart attacks rang, and a doctor picked it up. “We have a Stemi, female, age 49, 10 minutes out,” a paramedic said.
The only doctor in the E.R. that night was dealing with three life-threatening emergencies: a stroke patient and two people in respiratory distress who needed breathing tubes. The doctor, who declined to be identified for this article, explained her decisions to her colleagues Dr. Alfred Sacchetti and Dr. Blaber. She knew what to do when that phone rang — decide if she agreed the patient was having a heart attack. If she did, she would instruct the hospital operator to call in the heart attack team. But, Dr. Sacchetti said, the decision this time was not so clear cut. It was, he said, a judgment call.
Ms. Samuels was only 49 and her symptoms, as described, seemed ambiguous. So the doctor decided to get the emergency room ready so that as soon as Ms. Samuels arrived, she could be evaluated and have another electrocardiogram. If she was having a heart attack, the cardiac team would be paged. That, Dr. Sacchetti said, was a reasonable course.
But the cardiologist on call, Dr. Momplaisir, was annoyed. He rushed in from home, as he had for Mr. Whisler a few hours earlier, but 10 minutes had been wasted waiting for the ambulance to arrive at the emergency room before he was paged.
The outcome was excellent, though — Ms. Samuels’s artery was opened fast enough to save her heart muscle. There was no permanent damage, Dr. Momplaisir said.
Ms. Samuels is overwhelmingly grateful that she got to the hospital in time.
“I am the face of life,” she said.
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This phone in the Lourdes emergency room is used only to alert the heart attack team that a patient is on the way.Credit Mark Makela for The New York Times
That same night, the beige phone rang again. Another heart attack. This time it was a 63-year-old woman, Carmen Pierce, who lives with her daughter in a trailer nearby. “I was sweating from my head on down,” she said. “And I felt a pinching, in my shoulder, in my back. ”
She has diabetes and thought the problem must be low blood sugar. Her daughter gave her orange juice, but Ms. Pierce passed out holding the glass. Her daughter called 911.
This time, the emergency room doctor immediately told the hospital operator to page the staff and the backup cardiologist on call; Dr. Momplaisir was busy with Ms. Samuels. The cardiologist, Dr. Moussa, was sound asleep in his scrubs in his eighth-floor room at the Crowne Plaza. He arrived at the hospital just as Ms. Pierce was being wheeled in on a gurney. She and her daughter were crying in fear as staff members converged on her.
“Listen, we will get you through this,” Dr. Moussa said.
Ms. Pierce started to crash by the time they got her to the operating room. Three of her arteries were obstructed and one was totally blocked, causing her heart attack. That one was calcified, making it difficult to push the artery open.
It took 52 minutes to stabilize her and open her calcified artery.
“I don’t know what they did, but the pain was gone,” Ms. Pierce said afterward from her hospital bed.
She was lucky, Dr. Moussa said. “If she had stayed home, her heart would have stopped.”
Nights like that, he added, “are what we live for.”
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!
.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings. . Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar. . You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
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YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!
.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
.
Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
.
You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
.
YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .
I found this interesting but make of it what you will.
I tend to question the cause of my heart attack as I gave up smoking in 2001 having smoked cigars since the late 1960s. I NEVER add salt to food, we only use the bare minimum of salt in cooking, if atall.
I also do not eat junk foods – in fact there seems no reason for me to have had a heart attack – I wonder to what extent the removal of a cancerous kidney 12 years ago played a part, also did Sodium play any part in the blocking off of my right corunary artery from end to end?
Simple steps may identify patients that hold onto excess sodium
IMAGE:Evan A. Mulloy, a second-year medical student at the Medical College of Georgia at Georgia Regents University and Dr. Gregory A. Harshfield, a hypertension researcher who directs the Georgia…
Augusta, Ga. – Getting a second urine sample and blood pressure measure as patients head out of the doctor’s office appears an efficient way to identify those whose health may be in jeopardy because their bodies hold onto too much sodium, researchers report.
“We want to prove that you can easily and efficiently identify these patients,” said Evan A. Mulloy, a second-year medical student at the Medical College of Georgia at Georgia Regents University. “We want this to become a part of our routine standard of care.”
Using the simple method, researchers looked at 19, 10-19 year-olds seeing a pediatric nephrologist. They found eight were sodium retainers and seven of these were already hypertensive. “Eight kids were holding onto sodium and the amounts ranged anywhere from a few milligrams to hundreds of milligrams over the course of a doctor’s visit,” Mulloy said.
The findings are featured as a poster presentation at the American Heart Association‘s High Blood Pressure Research 2013 Scientific Sessions Sept. 11-14 in New Orleans.
About 1 in 3 blacks and 1 in 5 whites retain too much sodium following stress, driving fluid retention and blood pressure levels up, said Dr. Gregory A. Harshfield, a hypertension researcher who directs the Georgia Prevention Center at GRU’s Institute of Public and Preventive Health.
Years ago, Harshfield identified this impaired ability in some blacks and wanted to take the next logical step: finding an easy, inexpensive way to identify these individuals. His studies, funded by the National Institutes of Health, have already shown sodium retainers respond well to angiotensin receptor blockers. These drugs, which reduce blood vessel constriction, are widely used to treat hypertension but, ironically, they often are considered ineffective in blacks, Harshfield said. Studies at MCG and elsewhere have shown angiotensin promotes sodium retention directly and it increases aldosterone, another hormone that enhances sodium retention.
For the new study, Mulloy recruited patients as they came into the pediatric nephology clinic at Children’s Hospital of Georgia where patients have their blood pressure taken and provide a urine sample as part of their routine visit. Those who agreed to participate had both steps repeated at the conclusion of their visit for comparison sake.
The idea was that the stress of going to the doctor would be sufficient to cull out the sodium retainers. Increased sodium retention is one way the body responds to stress but normally, as soon as the stress passes, the extra sodium gets excreted in the urine.
To be effective, they knew the method for identifying retainers had to fit easily into a regular doctor’s visit. Knowing patients are sodium retainers will go a long way in helping physicians identify optimal therapies, including prevention strategies, Mulloy said. They are now using the method in adults seeing a general internist.
“Salt sensitivity is a great concept but it’s never been implemented into the clinical arena. We think this is a measure of salt sensitivity,” Harshfield said. Nearly 31 percent of American adults are hypertensive and more than half do not have their high pressure under control, according to the Centers for Disease Control and Prevention.
In a related poster presentation at the AHA meeting, the MCG team also presents early evidence that potassium supplementation could help maintain a healthier sodium level following stress.
While analyzing another cohort of young healthy blacks, Harshfield and Office Associate Deborah L. Stewart noted that sodium retainers in the group still dumped potassium. Normally, potassium and sodium are dumped at the same time, Stewart said. They are writing a grant now to explore whether potassium supplementation is an inexpensive and safe method to improve sodium excretion.
Stewart, who has worked with Harshfield for a year, helping write grants, abstracts and analyze data, is completing her undergraduate degree in biology with plans to move into a role as research assistant. Mulloy has worked with Harshfield for three consecutive summers, beginning when he was an undergraduate at William & Mary.
###
Toni Baker
Communications Director
Medical College of Georgia
Georgia Regents University
706-721-4421 Office
706-825-6473 Cell tbaker@gru.edu
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!
.
If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
.
Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
.
You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
.
YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .
this article from National Geographic in 2007 makes an interesting read:
Healing the Heart
Mending Broken Hearts
Cheeseburgers, smoking, stress, the rise of the couch potato: These are the usual suspects on the list of risk factors for heart disease, a malady reaching global epidemic proportions. Now discoveries about genetic triggers may help us spot trouble before it starts.
By Jennifer Kahn
Photograph by Robert Clark
Gloria Stevens is lying on her back, sedated but alert, staring at an image of her own beating heart. Metaphorically, Gloria’s heart is the very core of her emotional self—not to be worn on the sleeve, much less displayed on an overhead monitor. More literally, it is a blood-filled pump about the size of a clenched fist whose rhythmic contractions have kept Gloria alive for 62 years, and with a little tinkering will keep her going for an indeterminate number more.
At this moment, her doctor is threading a thin catheter up through her femoral artery from an incision in her groin, on into the aorta, and from there into one of the arteries encircling Gloria’s heart. At the tip of the catheter is a small balloon. The doctor gently navigates the tip to a spot where plaque has narrowed the artery’s channel by 90 percent. With a quick, practiced movement he inflates the balloon to push back the artery wall, deflates the balloon, then inserts an expandable stent—it looks like a tiny tube of chicken wire—that will keep the passage open. As Gloria watches on the monitor, the crimp in her artery disappears, and a wide laminar flow gushes through the vessel, like a river in flood.
The procedure is over. It has lasted only half an hour. In all likelihood, Gloria will be able to go home the next day. So will a few thousand other patients in the United States undergoing such routine angioplasty—more than a million of them a year. Pipe fixed, patient cured, right?
Wrong.
Because of her treatment, Gloria’s quality of life will likely improve. She’ll breathe easier and maybe live longer. But she is hardly cured. Her coronary atherosclerosis—a hardening and narrowing of the arteries that supply the heart with oxygen-rich blood—still leaves her vulnerable to future blockages and coronary heart disease.
Although hearts suffer many maladies—valves leak, membranes become inflamed—coronary heart disease, which can lead to heart attack and ultimately to heart failure, is the number one killer of both men and women in the United States, where 500,000 die annually. Worldwide, it kills 7.2 million people every year. Exacerbated by the export of Western lifestyle—motorized transport, abundant meat and cheese, workdays conducted from the comfort of a well-padded chair—incidence of the disease is soaring.
To help stem this lethal tide, cardiologists can prescribe such cholesterol-lowering drugs as statins to help keep arteries clear. They can advise patients to change their habits, or they can operate to fix an immediate problem. Angioplasty is one procedure, and surgery to bypass the diseased arteries is another—each year more than 400,000 bypasses are performed in the U.S. Transplants can replace severely damaged hearts, and artificial ones can keep people alive while they wait for a donor heart. But in the face of an impending global epidemic, none of these stopgap measures addresses the essential question: Who gets heart attacks and why?
The human heart beats 100,000 times a day, propelling six quarts of blood through 60,000 miles (97,000 kilometers) of vessels—20 times the distance across the U.S. from coast to coast. The blood flows briskly, surging out of a ten-ounce (0.3 kilograms) heart so forcefully that large arteries, when severed, can send a jet of blood several feet into the air. Normally the relentless current helps keep blood vessels clean. But where an artery bends, tiny eddies form, as in a bend in a river. This is where bits of sticky, waxy cholesterol and fat can seep into the artery wall and oxidize, like butter going rancid. Other matter piles up too. Eventually, the whole mass calcifies into a kind of arterial stucco, or plaque.
Until recently, cardiologists approached heart disease as a plumbing problem. Just as mineral deposits restrict the flow of water through a pipe, an accretion of plaque impedes the flow of blood through an arterial channel. The more crud in the system, the greater likelihood that a dammed artery will trigger a heart attack. Doctors now dismiss this “clogged-pipes model” as an idea whose time has passed. It’s just not that simple.
Most heart attacks are caused by plaque embedded within the artery wall that ruptures, cracking the wall and triggering the formation of a blood clot. The clot blocks the flow of blood to the heart muscle, which can die from lack of oxygen and nutrients. Suddenly, the pump stops pumping.
Contrary to the clogged pipes model, heart attacks generally occur in arteries that have minimal or moderate blockage, and their occurrence depends more on thekindof plaque than on the quantity. Scientists have been struggling to figure out what type is most responsible. Paradoxically, findings suggest that immature, softer plaques rich in cholesterol are more unstable and likely to rupture than the hard, calcified, dense plaques that extensively narrow the artery channel. But understanding the root cause of the disease will require much more research. For one thing, human hearts, unlike plumbing fixtures, are not stamped from a mold. Like the rest of our body parts, they are products of our genes.
Don Steffensen was putting duck-hunting decoys out on a small lake one fall afternoon in southwestern Iowa when his heart attack hit. The infarction was massive and unexpected. It’s likely that Steffensen survived only because a buddy was carrying nitroglycerin tablets and quickly slipped one under his friend’s tongue. Nitroglycerin is used to make dynamite; in the body, a heavily diluted form releases nitric oxide, which signals the smooth muscle cells in veins and arteries to relax, dilating the vessels.
The Steffensen clan is enormous: more than 200 relatives spread over three generations, many of the youngest are now dispersed from Iowa to New York and beyond. Although heart trouble is common in the family, it had never struck anyone as unusual. “I attributed it to diet,” shrugs Tina, a slim 38-year-old and the family’s only vegetarian.
It was a reasonable conclusion. The Steffensens were raised on the kind of farm food that the state is famous for—ham balls, meatloaf, pie, macaroni and cheese—and still popular even as careers have moved indoors. Driving north through cornfields to meet some of the family in Buffalo Center, I dined at a restaurant offering deep-fried sandwiches. A single ham and cheese hoagie—dunked in hot fat and served sizzling—seemed capable of stopping a heart all on its own.
But could the high incidence of heart trouble among the Steffensens be related to something else besides high-fat diets? Eleven years after Don’s attack, his wife, Barbara, happened to overhear a doctor describing a study about the genetics of heart attacks.
Curious, Don and 20 of his relatives each sent a vial of blood to the Cleveland Clinic, where the research was being conducted. Eric Topol, a cardiologist and genetics researcher at the clinic, spent a year studying their DNA. Each person’s genome comes with millions of individual variations, but Topol was looking for something distinctive—and shared only by the members of the clan with heart trouble. The mutation he and his team finally spotted, in a gene calledMEF2A, produced a faulty protein. “We knew we had something,” Topol says. “But the question was: How does this sick protein, present at birth, lead to heart attacks 50 years later in life?”
Topol himself is as lean as a greyhound and weathered in a cowboyish way. He talks slowly and eats minimally: salads for dinner and high-fiber cereal for breakfast. He doesn’t eat lunch at all. Like almost every cardiologist I’ve talked to, he takes statins preventively, and his cholesterol count is a low 135. His children, 22 and 25, also eat uncommonly well for their ages. “People have looked at the cadavers of men in their 20s who died in car accidents or as casualties of war, and nearly all had arterial cholesterol deposits,” Topol said as we walked to his lab. “This disease starts much earlier than people realize.”
Using endothelial cells (which line the inside of the artery wall) grown in culture, Topol set about figuring out what theMEF2Amutation does. He and his coworkers created some cells carrying the Steffensen variant, and others with the normal form of the protein. Both cell proteins were tagged fluorescent green so their locations could be visualized on a computer screen. The resulting images revealed a striking difference.
In a normal cell, all theMEF2Aprotein was inside the nucleus; on the screen, the cell resembled a fried egg with a fluorescent green yolk. But in the cells carrying the mutated version, the nucleus did not glow; instead the cell membrane was edged by a thin, luminous green line: a layer ofMEF2Aprotein, trapped where it cannot serve its usual purpose. Topol believes that this defect affects the integrity of the coronary artery walls, rendering them more vulnerable to cracking when the plaque embedded in them ruptures. And each crack brings an increased chance of a heart attack.
Since this discovery, the Steffensens have become famous, appearing on shows like60 Minutes II. Their mutant gene turns up in a Robin Cook novel titledMarker, about a health insurance company in New York that secretly screens patients for theMEF2Amutation and then kills them to preempt future medical-care payouts. Lively reading, but the Steffensen gene is an unlikely target for an insurance company, in part because it is an uncommon genetic defect.
Topol’s study did find that although dysfunctionalMEF2Ais very rare, the chance of heart disease in those carrying it may approach 100 percent. Most other genetic variations identified thus far increase the risk by much less. As it turns out, Topol himself carries a bum gene:apoE4, which affects inflammation in the arteries. UnlikeMEF2A, it is common; every fourth person has it.
“Heart disease is not a one- or two-gene problem,” says Steven Ellis, a Cleveland Clinic cardiologist who oversees a 10,000-person genetic study known as GeneBank that collects DNA samples from patients who enter hospitals with atherosclerosis. Ellis, like most cardiac researchers, suspects that dozens of genes end up contributing to a predisposition: Some affect arterial integrity, others inflammation (which both causes and exacerbates arterial cracks), and still others the processing of lipids (the fats and cholesterol that turn into plaques). Of the several dozen genes, each may contribute just one percent to a person’s total risk—an amount that may be compounded, or offset, by outside factors like diet. As one doctor told me, any person’s heart attack risk is “50 percent genetic and 50 percent cheeseburger.”
The point of tracking down all these small mutations, Ellis explains, is to create a comprehensive blood test—one that could calculate a person’s genetic susceptibility by adding up the number of risky (and, eventually, beneficial) variables. Combined with other important factors, such as smoking, weight, blood pressure, and cholesterol levels, doctors could decide which patients need aggressive treatment, such as high-dose statins, and which ones are likely to benefit from exercise or other lifestyle changes. Some genes already can predict whose cholesterol level will respond strongly to dietary changes and whose won’t. Assessing risk is crucial, Ellis says, because heart disease is often invisible. In fact, 50 percent of men and 64 percent of women who die of heart disease die suddenly, without experiencing any previous symptoms.
Although standard tests can detect atherosclerosis, they aren’t foolproof. They may reveal plaques, but give no indication whether or not they are life-threatening. Tests like angiography, for example, where doctors inject a dye into the bloodstream and track it with x-rays, can show how much blood is flowing through an artery, but not discern the plaques embedded inside the artery wall—often the culprit in a heart attack.
Researchers have been working to solve this problem with scanners that provide pictures of the arterial wall itself, but it’s a tricky task. Normal cardiac artery walls are about a millimeter thick. Coronary arteries move with every beat of the heart, 70 times a minute. It’s tough to get a clear image of something so small in constant motion.
Difficult, but not impossible. As I walk through the basement of the Cleveland Clinic, I pass a room containing a large, blue, plastic doughnut as tall as I am, with a woman’s legs sticking out of the middle. The doughnut is a computed tomography (CT) scanner, a kind of three-dimensional x-ray machine that’s also used for imaging tumors. The scanner, aided by medications that reduce a patient’s heart rate and an injectable dye that highlights the arteries, can produce startlingly clear pictures.
Scrolling through images on his computer monitor, Mario Garcia, the clinic’s director of cardiac imaging, retrieves one that looks like a black-and-white landscape photographed from a plane, with a single, large river running through it. As Garcia zooms in on the river, a series of white lumps appears on the bank—hard plaques bright with calcium. But there is also a tiny black smudge. “That’s the type we believe causes a heart attack,” he says with satisfaction, pointing to the smudge of soft plaque. “It’s a rare opportunity to see that.”
As compelling as the CT scan is, it’s still an imperfect tool for predicting heart disease. It’s expensive, for one, and the dose of radiation from the x-rays makes it ill suited for use in healthy-patient annual exams. And although it sees arterial plaques, even soft plaques inside arterial walls, it can’t reveal whether those plaques are likely to crack and cause a heart attack.
Until there are tests, genetic or otherwise, that give a clearer measure of risk, everyone would be advised to exercise, watch their diet, and take statins for elevated cholesterol—the same advice doctors gave when the clogged-pipes model of heart disease reigned unchallenged.
At the Cleveland Clinic, cardiologist Stephen Nissen has conducted several studies on statins such as Lipitor, which reduce the amount of LDL (“bad” low-density lipoprotein) cholesterol made by the liver. Nissen is an advocate of lowering cholesterol by any means necessary. Does he take a statin? “You bet!” he says. “I have no intention of dying of the disease I treat.” His LDL level is a paltry 51. Of eight cardiologists I spoke with, all but one were taking the medication. (Some studies now seem to show that lowering even normal cholesterol levels has a protective effect.) HDL (“good” high-density lipoprotein) cholesterol is another story. Nissen calls it the “arterial-wall garbage barge” because of its ability to remove cholesterol from clogged arteries. Not all HDL can do this; some is dysfunctional. But tests have shown that raising the HDL level in genetically engineered lab mice can shrink their arterial plaques.
A drug that could raise functional HDL levels in humans would likely become the next multibillion-dollar blockbuster, and a few are in various stages of testing. However, the trial of a Pfizer drug called torcetrapib ended in failure. Torcetrapib had been shown, in combination with Lipitor, to raise HDL levels 44 to 66 percent with a once-a-day pill. But the increase was not necessarily in functional HDL, and the drug was also associated with elevated blood pressure. In December, when data showed a 60 percent higher death rate in patients taking torcetrapib with Lipitor than in those taking Lipitor alone, Pfizer abruptly ended the trial.
It’s not clear whether the problem lay with one drug or an entire class of drugs. Until further research is completed, the several different statins on the market will remain the most prescribed class of drugs in the world, with 11.6 million prescriptions filled monthly in the U.S. alone. Pfizer’s Lipitor may be the best-selling drug ever made, with 12 billion dollars in annual worldwide sales.
But statins, like any drug, carry the risk of side effects: Muscle aches are a well-known effect, and periodic blood tests to check liver function are recommended. The fact is, many of us just like to eat cheeseburgers, watch television, and get around in cars. And it’s hard, says Leslie Cho, director of the Cleveland Clinic’s Women’s Cardiovascular Center, for a person to worry about a disease that hits ten years down the road—particularly since heart patients, unlike cancer patients, can’t easily observe the progress of their disease. “You’ve done damage over years, and it will take years to undo that damage,” she says. “That’s a very hard thing to sell to Americans. We do what we can, but then people go home.”
The good news is that genetic research continues to thrive. Should we want to, we will soon be able to know the state of our hearts—and our genes—in ever growing detail. That knowledge, and what we do with it, could make the difference between dying at 65 and living until 80. The choice, increasingly, will be ours.
To Spread The Facts World Wide To Give Others HOPE
I Have Been Fighting Cancer since 1997 & I’M STILL HERE!
I Have Cancer, Cancer Does NOT Have Me
I just want to say sorry for copping out at times and leaving Lee and friends to cope!
Any help and support YOU can give her will be hugely welcome.
I do make a lousy patient!
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If YOU want to follow my fight against Cancer from when it started and I first presented with symptoms in 1998 see The TAB at the Header of this Blog. called >DIARY of Cancer ….< just click and it will give you a long list of the main events in chronological order, many linked to specific blog postings.
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Thoughts, articles and comments will be in chronological order in the main blog and can be tracked in the >ARCHIVE< in the Left Sidebar.
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You may find the TABS >MEDICAL LINKS< and also >CANCER LINKS< of help, also many of the links in articles and >HOT LINKS< in the Sidebar.
.
YOU are welcome to call me, minded that I am NOT medically trained, if you believe I can help in ANY way. .
Life's Roller Coaster 