#cardiologist in salem
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Alfred Ashford in Resident Evil: Code Veronica X (2000)
#crimson's gifs: resident evil#Resident Evil#RE#Resident Evil: Code Veronica X#RE: Code Veronica X#RE: CVX#Alfred Ashford#Alfred (CVX)#Salem if youre reading this go see a fucking cardiologist you crazed ass Alfred Loving idiot (affectionately)
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Best Heart Specialist Hospital in Salem | AASAI Health Centre
Compassionate Hearts, Expert Care!
Welcome to Aasai Health Centre, the premier destination for cardiac care in Salem. With a steadfast commitment to excellence and a team of dedicated professionals, we are proud to be recognized as the Best Heart Specialist Hospital in Salem. At Aasai Health Centre, we understand the importance of providing compassionate care and cutting-edge treatments to our patients, making us the top choice for individuals seeking the Best Cardiologist in Salem.
Led by a team of renowned cardiologists and specialists, Aasai Health Centre is dedicated to delivering world-class cardiac care to patients of all ages. Our state-of-the-art facility boasts advanced technology and innovative treatments, ensuring that our patients receive the highest quality care available. What sets Aasai Health Centre apart as the Best Cardiac Hospital in Salem is our comprehensive approach to heart health. From preventive screenings and diagnostics to complex interventions and rehabilitation programs, we offer a full spectrum of services designed to meet the unique needs of each patient.
Guiding You Towards a Stronger Heart!
At Aasai Health Centre, we believe in empowering our patients to take control of their heart health through education and support. Our team of experts works closely with patients to develop personalized treatment plans tailored to their specific needs and goals, ensuring the best possible outcomes. In addition to our exceptional medical care, Aasai Health Centre is committed to providing a comfortable and welcoming environment for our patients and their families. From our friendly staff to our state-of-the-art facilities, we strive to create a healing space where patients can feel at ease throughout their journey to heart health.
Whether you are seeking preventive care, diagnostic services, or specialized treatment, you can trust Aasai Health Centre to provide the highest level of care and support. With our unwavering dedication to excellence and our commitment to patient-centered care, we are proud to be the Best Heart Specialist Hospital in Salem. In conclusion, Aasai Health Centre is dedicated to providing world-class cardiac care to the community of Salem. With a team of renowned cardiologists and specialists, state-of-the-art facilities, and a patient-centered approach to care, we are proud to be recognized as the Best Cardiac Hospital in Salem. If you are seeking the Best Cardiologist in Salem or require specialized cardiac care, we invite you to experience the difference at Aasai Health Centre.
AASAI Health Centre
392, 1st Cross Street, New Fairlands,
Salem, Tamilnadu
Pincode - 636016,
India.
Our Specialist Doctors
Dr. K.V. ASAITHAMBI, M.D.,
Consultant Physician and Diabetologist
Dr. A. RAJARAM PRASAD, M.D., D.M.,
Interventional Cardiologist
Our Timings
Monday : 08:00 AM - 05:00 PM
Tuesday : 08:00 AM - 05:00 PM
Wednesday : 08:00 AM - 05:00 PM
Thursday : 08:00 AM - 05:00 PM
Friday : 08:00 AM - 05:00 PM
Saturday : 08:00 AM - 01:00 PM
Sunday : Closed
Call us : +91 - 96007 33266
Phone : 0427 - 2442345
E-Mail - [email protected], [email protected]
#best cardiologist in salem#best heart specialist hospital in salem#salem heart specialist hospital#best cardiac hospital in salem#best cardio doctor in salem#heart specialist doctor in salem#best heart surgeon in salem
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Dr. Morris Salem - phaware® interview 483
Dr. Morris Salem is a pediatric congenital cardiologist and adult congenital heart disease specialist at Kaiser Permanente in Southern California. He takes care of patients of all ages, from fetuses to elderly individuals. Dr. Salem's primary focus is interventional cardiac catheterization, specifically the closure of holes in the heart. He also deals with pulmonary hypertension and collaborates with referring physicians throughout Southern California. Dr. Salem works within the Kaiser system, which provides care to all patients regardless of age, race, or financial abilities. My name is Dr. Morris Salem. I am a pediatric congenital cardiologist as well as an adult congenital heart disease specialist at Kaiser Permanente in Southern California. I take care of patients from San Diego to Bakersfield, all around Southern California. The age groups are really from fetuses all the way up to 80, 90 year-olds, so cradle to grave. Just to give you a little idea of what a typical day for me is, today is a Monday. I came in this morning. I went over to the OB facilities, where I saw several fetuses. These are babies inside their mothers who have been diagnosed with heart problems. That was my morning, counseling these families, helping them to understand what to expect, how we can shepherd this pregnancy along so that they have a healthy delivery. Once the baby comes out, then we can take over from there. That led to noontime, where I did a consultation on a 65-year-old with a hole in her heart that we're hoping to be able to close in a noninvasive, or, I should say, less invasive, fashion, where she would stay in the hospital overnight and go home the next day. Very briefly, I'll be talking to a family of a 4-year-old who was born with a heart problem that was inadvertently not picked up until very recently. We're going to try to help that child have a healthy and happy, normal, active life. So a typical day for me is very unpredictable. I never know what I'm going to be dealing with. I never know the age groups of the patients I'm going to be dealing with. I come in, it could be a baby, it could be a fetus, it could be an adult. It keeps me on my toes. What makes it exciting is that it's always different. It's always interesting. It's always unpredictable. I never know what I'm dealing with as compared to other types of doctors, where they might see one type of patient day in and day out. That is not what I do. My primary focus is interventional cardiac catheterization. We have a program here where we are very, very aggressive in transcatheter procedures and specifically with closure of holes inside the heart. We get referrals from all over Southern California. Part of our protocol is to do a diagnostic catheterization to really go inside and make sure that we're not missing anything, any diagnoses that have been potentially missed. As part of that, we measure pressures. We measure oxygen levels. We measure all sorts of different values and take pictures in all the different portions of the heart and the lungs to understand exactly what these numbers are. Is it okay for us to proceed with these interventional procedures, or are we going to do more harm by trying to intervene? One of the procedures that we're very involved in is, again, the closure of these septal defects, specifically atrial septal defects. In the olden days, this is prior to 2000, most of these procedures were being done surgically. The patients would get referred to surgery, the surgeon would operate not really knowing or understanding exactly what the pressures were inside the heart and the lungs. A lot of those patients did not do very well. Now, with these alternative techniques that we have using devices, we are very, very careful to know and understand precisely what the pressures are. That's specifically to try to avoid these potential complications that can occur if you actually do proceed with the closure. What we do is we measure everything, and if the numbers look favorable, we then proceed with the catheterization. If the numbers are not favorable, then what we try to do is do additional studies in the cath lab while the patient is still there to measure the response to various different medications so that we can offer the patient additional treatments so that someday we can come back and potentially close the hole in a much safer way. Pulmonary hypertension is a big part of what we have to deal with, especially with patients who are born with these septal defects, whether they're between the upper chambers of the heart or the lower chambers of the heart. It's something that we see a lot of, and understanding the hemodynamics is very, very important before you can manage them with any kind of procedure. When I first started my job, I used to travel to different hospitals, but I became so much busier that that just proved to be impossible driving around Los Angeles. It was really a waste of time, all those hours is going from hospital to hospital in a car. What we've developed is really a network model where a lot of doctors actually know me and they have my cell phone contact information. From San Diego all the way to Bakersfield, I get a lot of phone calls from these referring physicians who run things by me. if the patient sounds like there's something that needs to be done or intervened on or that we need to evaluate further, they're referred all the way up to Los Angeles where I can see them and deal with them, whether it's through some kind of a diagnostic procedure or a CT scan, MRI, or whatever the procedure may be. But that's how the referrals come up to us. One of the advantages of the Kaiser system -- we're a massive, massive system close to 5 million members. And one of the advantages here is that we don't have to think about whether a patient is actually covered for a particular procedure or a particular problem. Once the patient is within our system, they get taken care of regardless of age, race, financial abilities. We take care of everybody once they're within our system. Oftentimes, that's without any out-of-pocket expenses. Once they're in the Kaiser system, and the Kaiser system has different ways we get members, we have a lot of unions, we have individual companies that sign up for coverage. We have individual patients who find us through the internet, but we also have about a 20% rate of Medi-Cal patients. These are patients who typically do not have the resources to get private insurance, but they're assigned to Kaiser. Regardless of who they are, how they get Kaiser, and how they're assigned to one of the various different hospitals within Southern California, once they're within our system, we get them, we take care of them, whatever they need. When I see a pregnant mother with her husband who have come in and they've had a recent diagnosis of a baby or fetus with a severe type of heart problem, it always comes as a shock to these families. As one would expect, both parents always internalize this, and they feel that it's their fault. That they did something wrong. That they didn't do something properly, they didn't eat the right kinds of foods, or they didn't exercise enough. Or maybe they walked by somebody who was smoking marijuana or something, anything. They reach for straws. It is incredibly difficult to try to impress upon these families that this really has nothing to do with that. It is not their fault. These types of rare problems occur through nobody's fault, and regardless of how well you take care of yourself, what you do, that's not to say that you shouldn't do all of those things, but when it does happen, it's not your fault. We are here to help these parents and these families through this process and make sure that their children get the best care possible and the latest technology that is available to make sure that they live a long and healthy, happy life. Honestly, whether you're 6 or 16 or 60, it makes no difference. You deserve the same exact quality of care, which is the absolute best that we can give you. My name is Dr. Morris Salem, and I'm aware that my patients are rare.
Learn more about pulmonary hypertension trials at www.phaware.global/clinicaltrials. Follow us on social @phaware Engage for a cure: www.phaware.global/donate #phaware Share your story: [email protected]
Listen and View more on the official phaware™ podcast site
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Shanmuga Hospital offers the best when it comes to executing complex heart treatments with a high success rate, as it houses some of the best heart surgeons in Salem.
The medical professionals working at Shanmuga hospital possess several years of expertise in the field. As one of the top multispecialty hospitals in Salem, Shanmuga hospital provides exceptional healthcare services in a number of specialties including diabetology, urology, neurology, pediatrics, hematology, orthopaedics, obstetrics & gynecology, gastroenterology and so on.
#heart hospital in salem#heart hospital#cardiologist in salem#shanmuga hospital#cardiology#heart treatment
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❝The world is a painting and i hold the brush.❞
MEET…
Julian Porter
Age: 34
Birthday: May 8
Gender/Pronouns: Cis Male, He/Him
Hometown: Cambridge, England
Length of time in Salem: 9 months
Occupation: Pediatrician
Faceclaim: Rege-Jean Page
HIS STORY
Julian Porter is a man used to being the best. It's in his blood, in his bones, in his very DNA: there is no mountain he can't climb. And who can blame him, when the best is all he's ever known? Born in Cambridge, England, Julian was raised by a renowned cardiologist and professor of medicine for a mother and a groundbreaking trauma surgeon for a father. Both of his elder siblings followed in their footsteps, racing to the forefront of their own medical disciplines; there was no other path forward for him, and he wouldn't have had it any other way.
While first his parents and then his siblings were relatively absent, Julian never minded. Growing up, he was always busy himself, busy enough never to notice when the halls of his house were quiet, when the front door would open and close in the dawn hours of morning. "Lonely" never even crossed Julian's mind; after all, he understood from a young age the sacrifices that came with being a doctor, the way one's life wasn't always their own. It mattered little to him, his days and evenings filled with studying--he would settle for nothing less than top of his class--or football practices or time with friends. Something of a social butterfly, Julian was sure to always be seen, always be present, but he held himself back from ever truly growing close with most of his peers.
And then he was eighteen with his life before him, and out of nowhere, Julian found himself truly, hopelessly, bored. An unexpected offer granted him exactly the new challenge he needed: he was offered a scholarship to play football--soccer, from then on out, though he always scoffed at the word--at a university in the States. While wary, his parents acquiesced quickly; after all, there was little doubt that Julian would become a doctor no matter where he went to school first.
This, too, came easy to him; he breezed through his classes, the sleepless nights putting in the work never phasing him. His sport gave him a much-needed outlet, kept him in shape, and gave him a glowing social life. But then, in his junior year, it seemed Julian had finally flown too close to the sun. In the final game of the season, he had to be taken off the field in a stretcher. A serious injury, but one he would recover fully from before the next season started. It didn't matter, not to Julian; he stepped down from the team. He'd been good, better than good, and he refused to be remembered as anything else, refused to return to the team at anything less than his full capabilities.
Graduation came and went, and Julian began med school at Harvard. With each aced test and each professor's praise, his already-strong ego only grew--and the worst part was, it was justified. Julian was damned good at what he did, and refused to settle for less than perfection. Sure, some of his classmates gave him a run for his money, but there was never a doubt that he was one of the best among the best. Residency nearby only sealed this, and when his residency ended, he stayed on, rising through the hospital's ranks until his name was known throughout the community.
At the top of his game, with nowhere further to climb, Julian did something that shocked his coworkers, his family: he quit, quit for some smaller town, nonprestigious practice in Salem. His friend, his rival, his coworker had just inherited it, and invited him to join her. Without a second thought, he left to start this new challenge. Nine months into his time in Salem, Julian is still settling into this new setting, but it's nothing more than something new for him to excel at.
PERSONALITY
+ confident, competent, determined
- arrogant, abrasive, selfish
Julian is played by KRIS.
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While I’m in an oversharing mood
I mentioned in my last post about a local doctor that was essentially run out of town and arrested by the Texas Rangers for pushing pills... but there’s actually a whole story here about how the asshat was unethical to extremes and instituted a new family policy of never going alone to see any sort of doctor for any reason.
Enter one Doctor John Dang, owner of a local gym (Dang Gym) and medical practice, and generally well respected in the community at large and was seen as the go-to person for general medical needs and fitness needs (since he ran the only gym in town outside of the ones for schoolkids use in school hours and functions).
Seems nice enough on the surface right? Good man with a respectable, albeit funny, name in the community and essentially a staple of the town.
Well, what no-one really knew, talked about, or understood (take your pick), was that he was a medically licensed pervert and prescription drug dealer. We’re talking two counts of sexual assault of a minor/child, one count of assault, two charges of sexual assault, and no less than one count of insurance fraud (which is surprisingly NOT tied in to his pill pushing/dealing).
He would see an opportunity with patients needing just bare minimum painkillers, and prescribe the more expensive, and often time more addictive, substance, usually opiods, to create a demand and hook his patients to keep them coming back for more.
After they became dependent on him (emotionally, medically, or otherwise), that is when he would take advantage of his victims, as cited in the current 6 indictments against Dang. The insurance fraud, while unrelated at the moment to his pill pushing and sexual misdeeds, involved reporting allegedly stolen items from his home of no less than $115,000 USD in value.
Salem, the point of this story???
The point is hush, I’m getting there.
For about a year and a half before his clinic mysteriously shuttered its doors, he was the Primary Care Physician for my S.O. and... the atmosphere when he entered the room was always odd enough to make me want to usher them out and try to find a replacement. Regardless, I stayed with them through every visit, even as he prescribed them Beta-blockers for a heart-condition that was manageable without medication (we cut caffeine out of their diet and no heart issues since!) and never once thought to send us to see a cardiologist. That recommendation came to us from the E.R. one night after a particularly bad episode, back before it got filled up with dumbasses and became a joke.
When the cardiologist commented on how odd it was to be prescribed Beta-blockers instead of consulting a cardiologist, we both agreed it was time to drop Dang like a bad penny...
And that’s when, roughly a year and a half later, the rumors started to fly that he was on the run, practically chased out of town for the reasons stated earlier as the local paper broke the story of his victims coming forward. He was found a few towns over and essentially dragged back in to town to face the courts.
Lucky for him, the D.A. and nearly every lawyer in town knows him and his family on some level and cannot handle his case in any way, shape or form.
Unfortunately, the same cannot be said of the lawyers that replaced the one he was initially assigned or paid for, as they come from the DFW area and have no ties to the town, including the D.A. that is now in charge of the case.
No updates have happened on his trial in nearly a year, but the last I had heard was that his bond was set just shy of $1million USD on just those 6 indictments alone. The charges involving his pill pushing and opiod peddling have not been settled one way or another to my knowledge.
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tag game!!
tagged by: @daechwitatamic, @sugarwithtea, @lvoekook, @mercurygguk
name: nixie
sign: leo
height: 152 cm (im short, i know)
time: 10.45pm
birthday: 25 july
favorite band/artist: bts (duh), txt, harry styles, taylor swift, anthony ramos,
last movie: havent watched one in ages. i think it was a rewatch of "yes boss"
last show: i know the show but i dont know the show name
when i created this blog: march 2021
what i post: chaos, reblogs, my edits (new!) and rambles
last thing i googled: transcription and translation
other blogs: @bts-crack (bts incorrect quotes and other chaos)
do i get asks: yes, sometimes! please send me more <3
following: 772 (yea i have to clear stuff out)
followers: 139 🥺🥺🥺🥺
average hours of sleep: 4.5-5h
instruments: none but i want to be able to play my guitar thats collecting dust beside my bed. once upon a time, i knew how to play the piano...
what i’m wearing: over-sized sleep shirt, short shorts and my blanket over my shouders
dream job: cardiologist (its not gonna happen lol)
dream trip: south korea, japan, australia, paris, greece and so many other places i cant remember
nationality: india
favorite songs: (lately)
bad decisions - bts, Benny blanco and snoop dogg
PS5 - Salem Ilese, TXT and Alan Walker
this is why we cant have nice things - taylor swift
tagging: @yoongukie-ff, @gimmethatagustd, @pjiminbloomx, @mochakat, @meirkive, @haliiimede (no pressure)
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so i decided to do a little switcheroo and bring my girl cassidy to houghton. she’s A Lot so i apologize in advance her shit. without further ado, let me introduce you all to my babe.
first of all, here is her stat page
most of her info you can find in her bulletpoints on the main, but here’s a tl;dr
cassie was born in salem. her mother her had when she was only sixteen years old and unlike most of her peers at houghton, she didn’t grow up wealthy.
she has a really bad relationship with her father, who had an on-and-off relationship with her mother until the latter finally moved on and married a rich cardiologist.
cassidy always pretended that her step father was her real father at school, because she wanted to fit in with the rest of houghton’s elite. her plan worked, and she joined the windsors in her sophomore year and quickly became one of the most popular girls at school. in her junior year, she also became the captain of cheerleading squad.
when dante was chosen as their new leader, the two of them had a power struggle. cassidy and dante always had a rivalry, and he wanted to get rid of her before she could sabotage him. so, he ended up stabbing her in the back and spilled her secret of how she grew up poor. in a fit of rage, she ended up punching him and kicking him in the groin rip.
so cassidy got suspended from school, got demoted on the cheer squad and was unanimously voted out of the windsors.
right now she’s kind of a social pariah. most of her friends cast her out, which hurt her tremendously, but in hindsight she also happy about not having to deal with their fake shit anymore. after getting demoted, she dropped out of the cheer squad.
cassidy HATES the windsors. like she loaths them and everyone close to them. my girl is bitter and vicious af so... you’ve been warned.
personality wise, she’s kind of a judgemental bitch, but after her fall from the top, she softened up a little bit, at least towards other people who reside on the bottom of the social hierarchy.
connections that i would like for her are her ex friends/enemies, new friends, exes, romantic flings, frenemies, all that good stuff. you all know i suck at plotting but i try.
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Biomed Grid | Association Between Timp-3/Angiotensin II, Profile and Cardiac Remodeling in Patients with Essential Hypertension and Heart Failure with Mid- Range Ejection Fraction
Abstract
Background and Aims: Arterial hypertension (AH) is a leading cause for heart failure with mid-range ejection fraction (HfmrEF). The aim of our study was to:
1. Measure levels of tissue inhibitor of matrix metalloprotease-3 (TIMP-3) and Angiotensin II (AII) in sera of patients with AH and HFmrEF.
2. In sera of controls.
Material and Methods: 56 patients with AH and HfmrEF were examined, mean age 65.62±9.69; and 22 age and sex matched healthy subjects, mean age 56.4±5.53. 41 of patients were with hypertension mediated organ damage and 15 were without. Patients were divided in two subgroupssubjects with left ventricular hypertrophy (n=32); (HFmrEF+LVH) and subjects without left ventricular hypertrophy (n=24); (HFmrEF-LVH). ELISA was used for measuring AII and TIMP-3.
Results: Patients with HFmrEF-LVH showed higher levels of TIMP-3: 7.747 (1.21916.725) than HFmrEF+LVH 4.693 (2.06210.463); (KW=0.48; p=0.48) and healthy controls 6.460 (1.00712.520); (p>0.05), but not significantly. TIMP3 showed correlation with grade of AH (r=0.85; p=0.02) and stage of AH (r=-0.52; p=0.05); and PLVW (r=-0.40; p=0.03). Patients with HFmrEF+LVH showed statistically significantly higher levels of AII: 8.533 (1.47713.009) than HFmrEF-LVH 1.333 (0.4776.932) and healthy controls 1.539 (0.2745.218); (KW=3.48; p=0.04). AII correlated with TIMP-3 (r=-0.50; p=0.0001), hypertensive cerebrovascular damage (r=0.57; p=0.0009), DBP (r=0.30; p=0.05), stage with AH (r=0.47; p=0.001); CK-MB (r=0.42; p=0.002) and UA (r=0.35; p=0.02).
Conclusion: Our data suggest an association between changes in levels of TIMP-3/Angiotensin II profile and cardiac remodeling. Determination of serum TIMP-3/Angiotensin II profile may be a useful method for monitoring of development and progression of LVH.
Abbreviations: BMI- Body Mass Index; DBP- Diastolic Blood Pressure; HDL- High Density; Lipoprotein Cholesterol; HFmrEF+LVH- Mid-Range Ejection Fraction and Left Ventricular Hypertrophy; HFmrEF-LVH- Mid-Range Ejection Fraction Without Left Ventricular Hypertrophy; LDL- Low Density Lipoprotein Cholesterol; SBP- Systolic Blood Pressure
Introduction
Traditionally cardiac extracellular matrix (ECM) is thought to be a relatively inactive structure, which takes the role as scaffolding for cardiac myocytes and vessels. Recent studies show evidence that cardiac ECM is metabolically active and dynamic structure. Changes in cardiac ECM turnover are suspected of contributing to the genesis and progression of heart failure [1]. Degradation of ECM’s structural proteins occurs through the action of matrix metalloproteinases (MMPs), which are regulated by tissue inhibitor of metalloproteinases (TIMPs). TIMP-3 is the only TIMP that is ECM-bound and could exert tissue-specific effects [2,3]. However, the exact role of TIMP3 in hypertension remains to be understood. The detection of subclinical left ventricular hypertrophy (LVH) is made difficult by several factors. “Firstly, the clinical disease processes do not cause signs and symptoms; consequently, LV remodeling may remain an unrecognized and insidious process for a prolonged period of time. Secondly, LVH is not easily detectable using standard clinical means such as a patient’s history, physical exam or electrocardiography (ECG). Specialized testing tools are usually needed for that subspecialty expertise to perform and interpret” [4].
There is growing evidence that supports the notion that angiotensin II (AII) may directly cause cardiovascular and renal diseases, independent of its hypertensive effect. Thus, recent in vivo work, coupled with in vitro findings, has provided new insights into the molecular and cellular mechanisms of AII-mediated cardiovascular and renal diseases [5]. Angiotensin II exerts direct effects on vascular remodeling and function [6]. TIMP-3 could be implicated in the progression of vascular diseases, independently from its ability to inhibit MMPs. In this regard, in vitro and in vivo adenoviral overexpression of TIMP-3, but not TIMP-1 or -2, has shown to promote apoptosis in vascular smooth muscle cells. In vivo experiments have shown that this effect was not achieved when synthetic MMP inhibitor was used [7,8]. Arterial hypertension (AH) is a leading cause for large number of heart failure (HF) cases. Heart failure with mid-range ejection fraction (HFmrEF) is a syndrome, defined by: (1)-Left ventricular ejection fraction (LVEF%)-40-49%; (2)-Symptoms and/or signs of heart failure; (3a)-Elevated levels of natriuretic peptides; (3b)-At least one additional criterion: relevant structural heart disease (left ventricular hypertrophy/left atrial enlargement) or diastolic dysfunction- 2016 European Society of Cardiology (ESC) Guidelines for the diagnosis and treatment of acute and chronic heart failure [9].
MethodsClinical draft
All patients were residing in the vicinity of the Pleven University Hospital. Subjects’ sera were taken from October 2016 to May 2017. All the procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional or regional) and with the Helsinki Declaration of 1975, as revised in 2000. Approval of local Ethics Committee was obtained and informed consent from adult research participants was obtained too. The study group consisted of 56 patients with AH and HFmrEF, mean age 65.62±9.69. Forty-one of patients were with hypertension mediated organ damage (HMOD) and 15 were without. Patients were divided in two subgroups- subjects with mid-range ejection fraction and left ventricular hypertrophy (n=32), mean age 62.5±12.58 years (HFmrEF+LVH); subjects with mid-range ejection fraction without left ventricular hypertrophy (n=24), mean age 60.4±8.4 years (HFmrEF-LVH) (Table 1). These values were compared to serum TIMP-3/Angiotensin II profile in 22 age and sex matched controls with no family history of diabetes, atherosclerosis or hypertension, mean age 56.4±5.53 years.
Table 1: Clinical data of patients with heart failure with mid-range ejection fraction and left ventricular hypertrophy and without left ventricular hypertrophy and healthy controls.
Note 1: Data are presented as mean±SD
Hypertension-Mediated Organ Damage Assessment: All patients were examined for HMOD via anamnesis (for established cardiovascular or premature CVD, renal, cerebrovascular or ophthalmological damage) and physical examination and pulse pressure assessment (in older people) >_60mmHg.
Instrumental tests
a. Arterial blood pressure was measured using a standard anearoid sphygmomanometer, to the nearest 2 mmHg, in the dominant arm after at least 10-min rest in supine position.
b. ECG was performed for LVH assessment (Sokolow–Lyon index >35 mm, or R in aVL >_11 mm; Cornell voltage duration product >2440mm.ms, or Cornell voltage >28mm in men or >20mm in women).
c. Echocardiography was performed with General Electric (Vivid S5) with 4-MHz transducer. All measurements were obtained according to ESC 2015 criteria for Cardiac Chamber Quantification by Echocardiography [10]. Echocardiographic LVH [LV mass index: men >50 g/m2.7; women >47 g/m2.7 (height in m2.7); indexation for BSA may be used in normalweight patients; LV mass/BSA g/m2 >115 (men) and >95 (women)].
Laboratory tests
1. Serum uric acid, glucose were determined. Total cholesterol, triglyceride concentrations, HDL were measured by enzyme assay (Boehringer Mannheim, Mannheim, Germany). LDL was calculated via Friedewald formula.
2. Serum creatinine levels were measured and moderate CKD with eGFR >30–59 mL/min/1.73 m2 (BSA) or severe CKD eGFR <30 mL/min/1.73 m2 were assessed
If any HMOD was found, then patient was further consulted with a referring specialist (cardiologist, nephrologist, neurologist, ophthalmologist).
Elisa
Enzyme-linked immunosorbent assay (ELISA) was used for measuring AII and TIMP-3 levels. TIMP-3 levels were measured in serum samples using enzyme-linked immunosorbent assay (R&D Systems, Minneapolis, MN, DY973) according to the manufacturer’s instructions. Angiotensin II levels were measured in serum samples using enzyme-linked immunosorbent assay ALPCO Diagnostics (Salem, MA, USA, 74-ANGHU-E01) according to the manufacturer’s instructions.
Statistical analyses
The research data was processed with the computer programs EXCEL (Microsoft Corporation, Redmond, WA) and STATGRAPHICS plus (Manugistics, Rockville, MD) for WINDOWS. All results were described in tables, graphs, numerical values (mean ± SD, share indicators and correlations). For assessment and conclusions in the case of normal distribution the Student t-test, Fisher’s F-test (ANOVA) and post-hoc tests (LSD, Tukey HSD, Scheffe, Bonferroni, Newman-Keuls, and Duncan) were used, and for distribution, different from the normal – the K-W (Kruskal-Wallis)-test. The level of significance was determined as p < 0.05. In cases with different from normal distribution, median was used (M), together with first and third quartile Q1 and Q3; (twenty-fifth and seventy-fifth percentile P25 and 75P).
Results
Serum TIMP-3 levels in patients were lower than controls 5.051 (2.06210.463) vs. 6.460 (1.00712.520) (p>0.05), but not significantly. Patients with HFmrEF-LVH showed higher levels of TIMP-3: 7.747 (1.21916.725) in comparison with HFmrEF+LVH- 4.693 (2.06210.463); (KW=0.48; p=0.48) and healthy controls 6.460 (1.00712.520) (p>0.05), but not significantly. TIMP3 showed correlation with grade of AH (r=0.85; p=0.02) and stage with AH (r=-0.52; p=0.05); and PLVW (r=-0.40; p=0.03). AII levels in patients were statistically significantly higher than controls- 8.952 (1.86915.782) vs. 1.539 (0.274 5.218); (KW=2.77; p=0.05). Patients with HFmrEF+LVH showed statistically significantly higher levels of AII- 8.533 (1.47713.009) than HFmrEF-LVH 1.333 (0.4776.932) and healthy controls 1.539 (0.274 5.218); (KW=3.48; p=0.04). AII showed correlation with TIMP-3 (r=- 0.50; p=0.0001), hypertensive cerebrovascular damage (r=0.57; p=0.0009), DBP (r=0.30; p=0.05), stage with AH (r=0.47; p=0.001); CK-MB (r=0.42; p=0.002) and UA (r=0.35; p=0.02).
Discussion
The conceptual role for AII, as a local mediator of fibrosis, is suggested by studies in which circulating AII is chronically increased from either endogenous or exogenous sources [11]. Mounting evidence points towards an authentic signalling capacity for TIMPs distinct from their MMP-inhibitory activity. It also seems to play an important role in the regulation of apoptosis, cell survival, growth, migration, differentiation, angiogenesis, inflammation and overall ECM remodelling. Due to these mechanisms TIMPs could play a vital role in the process of cardiac remodelling [12,13]. A suggestion about a link between TIMPs and the renin–angiotensin-system is firstly given by Kang [14]. They identified human angiotensin- II-type-2-receptor as a novel TIMP-3 interacting partner, linking TIMP-3 with the renin–angiotensin system. Although, the pathophysiological roles and signaling mechanisms of angiotensin-IItype- 2-receptor are still largely unknown, but they were shown to be increased during hypertrophy and ischemic heart disease. Our results show decreased TIMP-3 levels and increased AII in all patients. Interestingly, the TIMP-3/AII profile is different according to presence of LVH. This can be described by the next findings: TIMP-3 levels in patients with HFmrEF-LVH are statistically significantly higher than those in HFmrEF+LVH. On the contrary- AII levels in HFmrEF-LVH are statistically significantly lower than these in HFmrEF+LVH.
These results can be summarized with the next two ratios:
i. Profile of patients with HFmrEF-LVH- increased TIMP-3/ decreased AII
ii. Profile of patients with HFmrEF+LVH- decreased TIMP-3/ increased AII
Our results are consistent with authors [15] who found that recovery of TIMP-3 content in the failing myocardium is associated with reversing cardiac remodeling, highlighting the influence of this critical matrix constituent in maintaining normal cardiac structure and function. We report the existence of an association between changes in levels of TIMP-3/Angiotensin II profile and cardiac remodeling. Determination of serum TIMP-3/Angiotensin II profile may be a useful method for monitoring of development and progression of LVH in patients with essential hypertension and heart failure with mid-range ejection fraction. This is a pilot study. Although these findings should be confirmed in a larger study, our data suggest that changes in the TIMP-3/AII balance may play an important role in the structural, functional, and clinical manifestations of cardiac remodeling. However further examination and prospective studies are needed to clarify the MMP-independent biological functions of TIMP-3 and fully understand its effects and exact relevance on contributing to the cardiac remodeling.
Conflict of Interest
Authors declare no conflict of interest
Read More About this Article: https://biomedgrid.com/fulltext/volume4/association-between-timp-3angiotensin-ii-profile.000753.php
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#Biomedgrid#American Journal of Biomedical Science & Research#Family medicine#Regenarative medicine#Journals on vaccination#journals on neuro imaging#biomedical journal articles
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DNA
I, like many people I know on this same health and wellness journey, have always struggled with weight. I heard the terms ‘big-boned’ and ‘slow metabolism’ thrown around a lot inside and around my family when I was growing up. Starting around puberty I started having to fight like hell to keep from being bigger. At my lowest point I resorted to horrible habits that lead down the dark path of disordered eating that so many can relate to. That journey alone could, and probably one day when I am ready, will be its own blog post. From the time I was old enough to realize that some people can dispense nearly anything, in any quantity into their body and still maintain a slim physique and others of us have to painstakingly watch every calorie we consume, I began to resent my genetic coding.
Surely that was the problem, right? If some people could eat the same things that I did and didn’t need to work out as hard as I did, or even at all to stay smaller than me, surely my metabolism must be the issue. I realized there was no way to remedy this, it was just the way I was made. I had never really noticed during my childhood that both of my parents and also the overwhelming majority of my family was overweight. Until my mother’s battle with fibromyalgia and multiple sclerosis began, a little extra weight had never stopped them from doing anything. My mom used to zoom around our little three bedroom in Winston-Salem keeping a damn near immaculate house (it would have been immaculate if not for me and my brother). My father taught my brother and I how to play basketball, baseball, volleyball, tennis, even badminton from a young age and even served as coach on a few of our teams over the years.
But here I was, standing in front of this seemingly insurmountable issue: my body was not built equal to others. I want to be clear, it is not that being overweight (eventually even being labeled as ‘morbidly obese’) was my only issue. I began having headaches and migraines when I was just ten years old. When I was eighteen I was diagnosed with acute recurring pancreatitis. My freshman year of high school I realized that my adapting body was now allergic and intolerant to a number of things that I had never had issue with prior. I was in high school when I was told I (already) was showing signs of arthritis in my ankles and knees. These issues are all treatable and I have found ways to cope with every single one of them; they pale in comparison to what millions of people face daily, but I want you to know what I was feeling internally when my initial efforts to lose weight were failing.
At this point, I was probably 25 or 26. I wasn’t happy with my body shape after I had graduated from college. Like many students, I ate poorly in school and didn’t make exercise the priority that I should have. I overloaded my schedule to ensure I could graduate a full year early and in the process took on an unrealistic amount of stress. I had then, after graduating, thrown myself head first into the work force. Working shortly as a bank teller on my feet all day until I started what is now my career at a lab company. My weight had shot up well above 225 by this point and after injuring myself, I had to sideline myself from the little exercise I had been doing – running with my dog. It certainly seems dramatic now, but at the time I felt thoroughly defeated. Like my body just would not cooperate. I let myself sink deeper and deeper into a depression. My psychiatrist prescribed me medication after medication, each one packing on more pounds. I once took an antipsychotic drug that packed over sixty pounds on me in a little over a month’s time. I knew something needed to change but I couldn’t muster the will to do anything.
Fast forward to February 2019. I was sitting around one evening looking at some pictures my husband and I had printed from our trip to Bermuda the previous year. He had long since settled in and started playing games on his Xbox for the night but I couldn’t stop studying them. I was so big, the biggest I had ever been. That summer I had been prompted to join Weight Watchers. My starting weight at the beginning of this journey was just over 287 lbs. It startles me even now as I look at the computer screen and see that number staring back. I was a shell of the athlete I had once been. Weight Watchers had not done much, if anything for me. I was flirting with disordered eating again as a result of the plan and had settled back into using exercise as punishment for overeating or not eating the right things before I had decided to quit for my sanity. But February 28, 2019 as I sat there looking at those photos, something inside me clicked into place. I decided that I needed to start exercising again. In a healthy way. In a structured way. On a schedule that I could incorporate into my schedule and stick to. Above all, I needed to be able to hold myself accountable. Or I would fail. I had done it over and over again, failure always the endgame.
So that Thursday evening, I got up and searched for an overnight bag small enough to serve as a gym bag. I packed all the essentials I would need to get ready in various sized plastic baggies and tucked them all into my makeshift gym bag along with a towel, work outfit and accessories, earbuds, straight iron, and hair dryer. I set my alarms. I sat out a water bottle for the morning. I laid out the closest thing I had to workout clothes, some black yoga pants, a tshirt, and a sports bra. Sat them on top of my socks and shoes. Something amazing happened the next morning that shocked even me: I got up and actually went to the gym. I don’t even remember how long I did each thing or what all I did, only that I went and gave it my all. And then I kept going and kept going.
That first morning at the gym I posted to my story on Instagram about my workout. It was my way of keeping myself accountable. I knew I had to put myself out there and risk everyone knowing if I failed to keep myself determined and accountable. Those accountability posts evolved over time and now include pics of my Fitbit showing my workout stats, a sweaty selfie (always now!), and the screens from machines I’ve used showing distance, or various pieces of equipment I’ve used during a workout. Over time I eventually decided to repurpose an old Instagram account specifically for my fitness journey to help inspire others who are trying to find the motivation to do amazing things in their own lives, or need an accountability buddy.
Everything was going pretty well until one night last summer my mom called me and told me they were taking dad to the emergency room for chest pain. They were sure it was just horrible indigestion but Byron and I felt differently. Our worst fears were confirmed when he required a second dose of nitroglycerin. They transferred him after some testing to a bigger area hospital and he was admitted. They scheduled a scan to determine damage, blockages, etc. Then everything was moved up. I left work and Byron did too. They determined that my dad had a total of five blockages and would require a quadruple bypass. In between meetings with the medical staff, trying to keep my dad’s spirits up, and calming my mother’s nerves I looked up as much about the procedures, long term effects, required hospitalization, etc until I couldn’t read anymore. The day came for his surgery with what felt like turbo speed. A kind staff volunteer led me back to the prep room where my dad was being prepped for surgery and meeting his various team members. I told my dad how much I loved him, what he meant to us and kissed him before stepping out into the hallway, rounding the corner and collapsing. I cried harder in those five minutes than I have ever cried in my entire life. And my husband can tell you, I am a crier. I hoped my dad would make it through the surgery, but we had no certainty. And if he did make it, I was almost certain things would never be the same.
I did all the things you are supposed to do when a relative discovers they have heart disease: told my PCP, got blood work done, had a visit with a cardiologist, underwent the ECG and stress tests to determine I am not at risk right now. I was so frustrated when I made the first of those appointments, thinking selfishly to myself how my genetics were just the gift that keeps on giving. I know it seems callous but that was my honest thought coming through all of this. If we weren’t at risk, none of this would have happened.
I’ll fast forward again here, my dad recovered fine and entered the cardiac rehab program via the hospital. The Cardiac Rehab program was an immense blessing to our family. Many of the family’s questions regarding the new normal and expectations during recovery were answered. It taught my parents healthier alternatives for meals and what my dad should be eating to keep his risks for a repeat event as low as possible. Additionally, the rehab program helped him build his strength back up by slowing introducing a cardio routine. Even though by this point I had been working on regularly for the better part of the year, I still learned quite a few things from my dad’s rehab instruction. He is still not 100% but he is well on his way, with new habits in hand to boot.
During my dad’s cardiac rehab program, I gave him one of my old Fitbit watches that I was no longer using. We synced up and started challenging one another to weekly step challenges. On days that I barely felt like getting up and going to work, let alone working out, I found my dad’s journey especially inspirational in helping me get out of bed and exercise anyway. If he could have his chest opened up, his ribs broken and sewn back together and his heart literally stopped for a short while and he could recover and show my ass up on a challenge, I needed to up my game. I needed to dig deeper. And I have always been up for a good challenge.
One morning I was at Planet Fitness on the treadmill, when a song by Kendrick Lamar came on my playlist. I had heard it what seems like 1,000 times before and it had always been a ‘get your blood flowing’ kind of song, like most of his stuff is for me. But this particular morning, it really struck a chord with me. “DNA” talks about how one is built, whether you have ambition, whether you hustle hard. I knew in that moment, taking in every single second of this rap song with new eyes, that your DNA isn’t about your metabolism, or your hair color, or your susceptibility to allergies or headaches. Your DNA is about what is instilled in you. Whether you have grit. Whether you get back up every time you get knocked down or you stay down and make excuses. My dad, my hero, my first role model, has shown me not just in our coaching years but in his fire to get back up and show life what he’s got is what DNA is all about. That fire that burns deeply within me is in large part due to him. I am so thankful that he is still here and for this kick-ass DNA that he has given me.
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#best cardiologist in salem#best cardio doctor in salem#heart specialist doctor in salem#best heart surgeon in salem
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Episode 483 - Dr. Morris Salem
Dr. Morris Salem is a pediatric congenital cardiologist and adult congenital heart disease specialist at Kaiser Permanente in Southern California. He takes care of patients of all ages, from fetuses to elderly individuals. Dr. Salem's primary focus is interventional cardiac catheterization, specifically the closure of holes in the heart. He also deals with pulmonary hypertension and collaborates with referring physicians throughout Southern California. Dr. Salem works within the Kaiser system, which provides care to all patients regardless of age, race, or financial abilities.
Learn more about pulmonary hypertension trials at www.phaware.global/clinicaltrials. Follow us on social @phaware Engage for a cure: www.phaware.global/donate #phaware Share your story: [email protected]
Listen and View more on the official phaware™ podcast site
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This is My Cardiologist, the synth pop band I was in ten years ago, with my very talented friends Salem and Selena on vocals, auxiliary synth and guitar. I wrote the lyrics and programmed the sequencers. We only played two shows before people started moving away, but I’m really proud of this album.
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Waited a month for a cardiologist appointment, got there, sat in the exam room for five min. and then the doctor comes in and says "I don't know why you're here." Turns out (I already knew this), the cardio doc doesn't treat POTS! So they tried to refer me to a neurologist, only for the neurologist to say 'hey, we don't treat this either!!' Best part is they don't even know who to send me to. They're waiting for my mom to find a POTS specialist near us to refer me to. If anyone knows any dysautonomia docs around Charlotte or Winston Salem area in NC, please let me know!
#dysautonomia#pots#potsie#chronic illness#spoonie#i love how the ppl who r supposed to b taking care of me have no idea what theyre doing!!!!!!!!!!!!!#no one cares
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AHA News: Common Prostate Cancer Treatment May Increase Risk of Fatal Heart Condition
MONDAY, Aug. 5, 2019 (American Heart Association News) — Many men with prostate cancer rely on common testosterone-blocking drugs as a part of their treatment. But those so-called antiandrogens also might put them at risk for a deadly heart condition, according to new research.
In a study published Monday in the American Heart Association journal Circulation, researchers looked at how several testosterone-blocking drugs affect the heart’s QT interval – the time it takes the heart cells to recharge in between beats.
The longer a QT interval, typically measured by an electrocardiogram, the more at risk a person is to develop serious heart rhythm problems and a condition called torsade de pointes, which can result in sudden death. Women naturally have a longer QT interval than men, and they are at higher risk for this form of arrhythmia.
“Testosterone is in part responsible for the protective effect in men,” said lead study author Dr. Joe-Elie Salem, an associate professor of cardiology and pharmacology at Sorbonne University in Paris. “We wanted to see if blocking testosterone with antiandrogens could lead to acute QT prolongation and sudden death.”
Salem and his colleagues used VigiBase, a global health database of reports of suspected adverse effects of medicines filed since 1968. They searched for cases of men with long QT, torsade de pointes or a sudden death associated with testosterone-blocking therapy.
Seven of the 10 drugs they reviewed were disproportionally associated with either long QT, torsade de pointes or sudden death. The drug enzalutamide, which is used to treat metastatic prostate cancer, was linked with more deaths than any other antiandrogen.
The impact and interaction of drugs on the heart’s rhythms “is an important issue that probably doesn’t get as much attention as it deserves in terms of drug safety,” said Dr. Richard J. Kovacs, Q.E. and Sally Russell Professor of Cardiology at the Indiana University School of Medicine. “When we actively search for cases of drug-induced torsade, such as this research team did, we find that the incidence of the problem is often orders of magnitude greater than what’s discovered by just passive surveillance.”
Salem said more research should explore the interaction between antiandrogens and other drugs and conditions that also can also prolong QT. For example, electrolyte disorders caused by low potassium can impact the heart’s rhythm.
“When you’re giving antiandrogen drugs, you should probably monitor for torsade de pointes and be very careful about controlling the other risk factors for QT prolongation,” Salem said.
Kovacs, who was not involved in the new study, recommended that before prescribing medication to patients who take antiandrogen drugs, doctors check CredibleMeds.org. The organization tracks medications that have a known or potential risk of QT prolongation.
The list includes dozens of drugs, including commonly prescribed antibiotics such as ciprofloxacin and antidepressants such as citalopram, known by its brand name, Celexa.
“If you have a patient who is taking an antiandrogen,” Kovacs said, “and you have a choice of prescribing an antibiotic that increases torsade de pointes risk and one that doesn’t, wouldn’t you choose the one that doesn’t?”
Kovacs suggested that oncologists and cardiologist work together to manage QT prolongation and the risk of torsade de pointes in high-risk prostate cancer patients.
“There are off-target effects, and they can be life-threatening,” he said. “How do you mitigate the risk? I think that’s the most important follow-up question.”
Copyright 2019 All right reserved
The post AHA News: Common Prostate Cancer Treatment May Increase Risk of Fatal Heart Condition appeared first on Be Healthy News.
AHA News: Common Prostate Cancer Treatment May Increase Risk of Fatal Heart Condition posted first on https://www.behealthynews.com
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Treatment Benefits of Remedē System Sustained Through 36 Months in Patients with Central Sleep Apnea
Treatment Benefits of Remedē System Sustained Through 36 Months in Patients with Central Sleep Apnea Find more on: The Elly Mackay Blog
Newly published results from 24- and 36-month data from the remedē System Pivotal Trial demonstrate long-term safety and sustained improvement in sleep metrics from phrenic nerve stimulation in adult patients with moderate to severe central sleep apnea (CSA). The study is published in Sleep and funded by Respicardia Inc, the remedē System.
“It is imperative that we understand the long-term results of phrenic nerve stimulation since CSA and its underlying disorders are chronic and progressive,” says Henrik Fox, MD, senior cardiologist at Ruhr-Universität Bochum, Bad Oeynhausen, Germany, in a release. “The durability of the clinical results seen in this trial further validates the remedē System as an effective, reliable, long-term treatment option for indicated patients.”
Patients from the remedē System Pivotal Trial were assessed at 24 months (full overnight, in-lab, attended polysomnogram) and 36 months (home sleep study of cardiorespiratory polygraphy) to evaluate sleep metrics and safety. All sleep studies were scored by a central sleep core laboratory.
The results at 24-months include:
99% reduction in the median of the central apnea index (CAI) from baseline
93% of patients had a reduction in the apnea-hypopnea index (AHI) from baseline
59% reduction in the median arousal index from baseline
Improved rapid eye movement (REM) sleep and the percentage and minutes of sleep with oxygen saturation less than 90%, which is an independent predictor of all-cause mortality in chronic heart failure
90% of patients were free from serious adverse events associated with the implant procedure, the remedē System, or delivered therapy through 24 months. No additional related serious adverse events were reported between 24 and 36 months.
The control arm showed similar results once therapy was activated after a pre-specified 6-month randomization period. The improvement in sleep metrics for both groups was sustained and consistent at 36 months.
The latest results build upon prior published data in The Lancet and the American Journal of Cardiology, which demonstrated that the remedē System significantly reduces the severity of CSA and improves sleep, quality of life and patient satisfaction, and the benefits are sustained.
Respicardia Initiates New Clinical Study
Respicardia also announced the initiation and first patient enrollments into a major new clinical study: the remedē System Therapy Study (rēST Study), a multi-center, prospective, open-label, single-arm study to collect safety and effectiveness data in approximately 500 remedē System patients in the United States and Europe for up to 5 years. To assess effectiveness, the study will evaluate changes in sleep metrics, daytime sleepiness, quality of life and, for patients with heart failure, core-lab determined cardiac remodeling biomarkers as well as functional capacity. The first global enrollments occurred July 9, 2019 at Novant Health Forsyth Medical Center in Winston-Salem, NC, and were implanted by Michael N. Drucker, MD, who says, “We are very excited to be leading the way and enrolling the first two patients into the rēST Study. Phrenic nerve stimulation has enormous potential to treat central sleep apnea patients who currently have few therapeutic options. The rēST Study will give us further insight into the impact of the therapy and long-term outcomes.”
“We are dedicated to offering physicians and their patients a clinically proven CSA treatment option with long-term safety and benefits,” says Peter Sommerness, president and CEO of Respicardia. “The 3-year data from the IDE Pivotal Trial combined with the initiation of the rēST Study further strengthens our clinical foundation and supports our commitment to improving patient outcomes.”
from Sleep Review http://www.sleepreviewmag.com/2019/07/treatment-remede-36months/
from Elly Mackay - Feed https://www.ellymackay.com/2019/07/12/treatment-benefits-of-remede-system-sustained-through-36-months-in-patients-with-central-sleep-apnea/
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