Human breast cancer cells (left) are treated with a trial dose of the leukemia drug dasatinib (center) and then with a 10-fold stronger dose. (Image courtesy of Seth Corey)
Northwestern.edu, August 30, 2010, by Jessica krinke — Researchers at Northwestern University are pioneering ways to shoot out the tires from breast cancer’s getaway car in a high-speed chase of drugs and carcinogenic criminals.
That’s because breast cancer itself doesn’t kill until it metastasizes, or travels, to other sensitive organs, invades and then grows. But a new clue to stopping this destructive spree surprisingly came from pediatric research.
Dr. Seth Corey is a pediatric oncologist at Children’s Memorial Hospital and professor of cellular and molecular biology at Northwestern University’s Feinberg School of Medicine. They’ve found that dasatinib, a drug already used to eliminate leukemia in the bone marrow, may also prevent mobility in breast cancer, keeping it from invading vital organs.
But even though dasatinib is FDA-approved for the treatment of leukemia, the likelihood of your doctor prescribing it for breast cancer just yet is slim. The Northwestern research team hopes that dasatinib’s clinical trials will help determine what kinds of breast cancer respond to it best. By mapping the biological signatures of varying cancer types this way, fingerprints of these malignant flight-risks to assist in diagnosis and further targeted treatment may not be far off.
Seth Corey (image courtesy of Jessica Krinke/MEDILL)Medill Reports asked Corey about his team’s research, and what the future may hold for dasatinib and breast cancer.
Q) What is the basic aim of your research?
A) My primary interest is in leukemia, which is a cancer of the bone marrow – the site of [all] blood cell production. Cancer cell behavior is this: they proliferate, they do not differentiate, and they do not die. But for solid tumors, which is everything but leukemia, the cancer cells also have additional characteristics that make them malignant, and that is the ability for them to invade local tissues, spread to different sites and to metastasize as in the liver, the bone, the brain. Those are the more common sites for breast cancer metastasis.
Q) What makes breast cancer unique among cancers?
A) I’m a pediatric oncologist, and even though death due to cancer remains the most common cause of non-accidental death in children and adolescents, it’s uncommon. Maybe about 12,000 cases of new pediatric cancer are diagnosed each year in the United States. The total for adult cancers is about 1.5 million people each year.
Every cancer is different, and even within different [cancers] there are different types and different levels of aggressiveness. Breast cancer is a public health concern because around 180,000 women are diagnosed each year, so it’s one of the most common cancers to occur.
Q) Is leukemia a very common cancer in children?
A) Acute lymphoblastic leukemia (ALL) is the most common type of childhood cancer, although in adults it’s very rare. ALL occurs with about 3,500 cases per year, so it’s a little less than a third of all pediatric cancers.
ALL has been the focus in childhood cancer and, over the past 40 years or so, it has gone from a disease that was almost uniformly fatal to a disease that’s almost uniformly curable. We’ve gone from a roughly five-year survival rate in about 1960 or so of 8 percent to a five-year survival rate in 2010 of like 90-92 percent. It’s been an achievement of modern chemotherapy.
Q) So how did leukemia in children lead you to study breast cancer?
A) Christina Pichot gets a lot of the credit for helping to steer the lab and my thoughts in the direction of breast cancer. Chrissy was a graduate student then, she just got her PhD in March and she was interested in breast cancer. She began to look at Src kinase and how its levels and expression patterns correlated with different types of breast cancer. Src kinase is an enzyme, which is a protein that speeds up chemical reactions a million-fold. It remodels the cytoskeleton and the plasma membrane [of a cell].
[She] found that levels [of Src kinase] were highest in those breast cancer tissues that were the most aggressive and invasive. What she did was manipulate the expression of this protein by turning it off. And she found that cells didn’t invade as well, didn’t migrate as well and didn’t form finger-like projections, invadapodia, which help break down the barrier and facilitate the initial steps in cancer cell invasion. When cancer cells take up residence and continue to grow, forming metastasists, that’s what kills people.
Chrissy started to look at a drug, dasatinib, which is an FDA-approved drug for a form of leukemia called Chronic Myeloid Leukemia (CML). We found that [blocking] the Src kinases didn’t so much stop the cells from surviving, but it kind of got them to stop growing as quickly. But what it also did, and I think this is something that needs to be exploited, is that it did affect their ability to migrate, to invade and to form those finger-like projections of invadapodia.
Q) How can readers imagine this for themselves?
A) You can think of it like a car. A car needs to move and the way it moves is turning on the engine and running on the four tires. So the idea is to knock out all the tires so our cancer car won’t move. If you can shoot out the tires of the car with a drug like dasatinib, then you’re going to slow down the cancer cell and extend peoples’ lives.
Q) Is dasatinib something someone who currently has breast cancer can ask her doctor about?
A) One goal is to make the disease go away, but an alternative goal is to have stable disease in check. If you can’t cure somebody of a cancer, you can make it a chronic disease. I think most people could live with that. The question is how to incorporate dasatinib into a multi-drug regimen as a second-line or third-line therapy for women with refractory, or relapsed, breast cancer.
New view: May Griffith holds up a biosynthetic replacement cornea.
Credit: Ottawa Hospital Research Institute
The results of a two-year study are as good as those achieved with donor corneas.
MIT Technology Review, August 30, 2010, by Nora Schultz
Patients with impaired vision because of a damaged cornea could soon regain their sight without need of a human donor transplant. Instead, such patients could be aided by an artificial but biosynthetic implant. One such implant has now been tested in patients over two years, and the results are as good as, or even better than, those achieved with donor corneas.
The transparent tissue that covers the surface of the eyes, the cornea, can be damaged by injury, infection, or inflammation, causing the eye to lose much of its ability to refract light and focus images on the retina. Such damage has caused loss of vision in millions of people around the world. The best treatment for cornea damage remains a transplant, but donor corneas are in chronically short supply.
Plastic replacements have been available for decades, but their implantation is still plagued by side effects such as infection and glaucoma. “They remain a last resort option for patients where all other options have failed, including donor transplants,” says Joachim Storsberg at the Fraunhofer Institute for Applied Polymer Research in Potsdam, Germany. Storsberg is developing plastic implants but was not involved with the current work.
Several other research groups are working on artificial corneas made from materials that encourage cell growth and are less likely to be rejected. But this is the first time the long-term effectiveness of such an implant has been tested in humans.
May Griffith of Linköping University in Sweden and Ottawa Hospital Research Institute, along with colleagues, developed the implant for patients with damage to only the top layers of the cornea. A partner company, Fibrogen, engineered yeast cells to manufacture the human protein collagen. The team then chemically cross-linked this collagen and let it harden in a mold in the shape of corneas, which they then implanted in place of the damaged cornea layers of 10 patients.
Although the implants do not contain any live cells, they mimic the flexible scaffold material that makes up the bulk of the stroma, the thickest layer of the cornea, which is essentially a natural hydrogel consisting mostly of collagen.
“Although donor corneas remain the gold standard, Griffith’s approach looks like it’s a close second, and very promising, at least if you don’t have persistent infections that destroy the regenerating tissue,” says Storsberg.
Griffith’s team reports this week in the journal Science Translational Medicine that two years after implantation, cells had repopulated the implants, and the outermost epithelial cell layer, which protects the eye from infection, had grown back over the implant in all patients. Vision in all ten patients improved to levels comparable to that of patients who have received donor corneas–but only when those ten patients also wore contact lens. “This is because stitches on the implants introduced bumps that impaired vision and need to be smoothed by contact lenses,” says Griffith. But using different suturing methods or replacing the stitches by gluing the implants to the eye with tissue adhesives could solve this problem, she argues, adding that the team has had encouraging results testing such alternatives in preliminary follow-up work.
The team also observed regenerating nerves in all the corneas, and in nine out of 10 patients, the nerves grew all the way to the center of the implant, a result Griffith is particularly excited about. “The nerves are really important for the long-term health of the rest of the cornea–but regeneration does not happen reliably even in donor corneas,” she says. Her long-term expectation is that the implant will slowly degrade and be completely replaced by the natural scaffold regenerated by the cells that have repopulated the cornea.
Christopher Ta, an associate professor at Stanford University who’s working on another kind of hydrogel substitute for donor corneas, is also optimistic about Griffith’s work, which he says “has the potential to revolutionize the field of cornea transplantation. It is possible to see widespread use of this type of engineered cornea in the next five years.”
Desktop Cancer Check
By TR Editors
Photo Credit: Christopher Harting
MIT Technology Review, September/October 2010
A device that analyzes blood levels of prostate-specific antigen (PSA) is one of the first doctor’s-office uses of microfluidics–technology that can manipulate fluids on a chip at microscopic scales. When a cartridge bearing a blood sample is inserted into the tabletop device, an accurate reading can be completed in 15 minutes, helping monitor the health of patients with prostate cancer. The procedure used now involves sending a sample to a lab for analysis, which often takes a day or two. The device received European approval in June.
A Methicillin-resistant Staphylococcus Aureus (MRSA) bacteria strain is seen in a petri dish at a microbiological laboratory in Berlin, in this March 2008 file photo. Some British patients who underwent plastic surgery in South Asia now carry a new gene that has the potential to turn bacteria into the latest antibiotic resistant superbug, such as MRSA, according to an article published Wednesday in the journal Lancet Infectious Diseases. Credit: (Fabrizio Bensch/Reuters)
FORBES.com, August 30, 2010 — Austria’s health ministry is reporting two cases of a new gene that allows bacteria to become a superbug.
The ministry says experts at the medical university in the southern city of Graz detected the gene, known as NDM-1, in two people, both of whom are believed to have been infected in hospitals abroad.
A statement Friday said a person from Pakistan was released in good health from Graz’s university clinic last year after successful treatment. It said another person from Kosovo is still under medical supervision there.
Researchers say the gene – which appears to be circulating widely in India – alters bacteria, making them resistant to nearly all known antibiotics.
Superbugs: ‘Slow Motion Doom and Gloom,’ Experts Says
The overuse of antibiotics has contributed to the increase in antibiotic resistant bugs. Over time, bacteria grow stronger than the treatments they may be regularly exposed to. And, according to many experts, there’s no end in sight.
“It’s slow motion doom and gloom,” say the experts. “We are feeling the limited availability of active antibiotics, and we’re put in situations where we don’t have active therapies to treat cases.”
Although researchers are not able to reverse the superbug genes, it is possible to slow the spread of superbugs, according to Dr. William Schaffner, chairman of preventive medicine at Vanderbilt University Medical Center.
“Antibiotics are used when they don’t have to be used, and are continued for too long,” said Schaffner.
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The podcast team is taking a brief summer break, but we’re back with a full show next week
ANNUAL UPDATE FROM TARGET HEALTH INC. – Highlights of the Year
We would like to thank the loyalty and feedback of our over 3,200 readers, some of whom have been receiving ON TARGET since 1995.
Several times a year we are asked what Target Health does and what are our accomplishments. The following summarizes what has happened over the last 12 months.
In 2010, Target Health celebrated its 17th year as a New York City-based, full-service e*CRO with full-time staff dedicated to all aspects of Drug and Device Regulatory Affairs, Clinical Research, Biostatistics, Data Management, Internet-based clinical trials (Target e*CRF®), Medical Writing, and Strategic Planning. We also provide fully validated software for clinical trials.
Highlights of the year included:
- Three regulatory approvals using Target e*CRF (NDA 1; PMA 1; Canadian 1)
- Pfizer’s license of Protalix’s taliglucerase alfa. Target Health assisted Protalix from pre-IND to NDA in 5.5 years, including a full eCTD NDA submission
- eCTD IND/NDA programs
- Full management of a 90 center study in ulcerative colitis
- Dr. Park on the FDA biomarker task force for Gaucher disease
- Target Health member of the CTTI Steering Committee
- Release of:
- Target e*CRF® v1.10 (EDC made simple)
- Target Document® v 1.6 (Document management)
- Target e*CTMS™ v 1.3 (Clinical trial management system)
- Target e*Pharmacovigilance™ v 1.0 (Safety monitoring)
- Target Encoder® v 1.2 (MedDRA and WHO Drug coder)
- Target e*CTR™ v 1.0 (Electronic Clinical Trial Record)
In 2010, Target Health was directly involved with three regulatory approvals (2 US, 1 Canada). There are now 19 unique products that used Target e*CRF® for their pivotal trials
- NDA/MAA – ellaOne® (HRA Pharma) EDC ; Monitoring; DM; Statistics; Writing
- CANADIAN DEVICE – AUGMENT™ Bone Graft (Biomimetic Therapeutics) – EDC
- NDA – ULESFIA – (Summers Laboratories, Inc./Sciele) – EDC; Monitoring; DM; Statistics; Writing; Toxicology; NDA (eCTD)
- NDA/MAA – DEGARELIX – (Ferring Pharmaceuticals) -EDC
- BLA – ARCALYST (Regeneron Pharmaceuticals) – EDC
- NDA/MAA – MENOPUR (Ferring Pharmaceuticals) – EDC ; DM; Statistics
- NDA/MAA – BRAVELLE (Ferring Pharmaceuticals) – EDC; DM; Statistics
- PMA – GEM 21S (Biomimetic Therapeutics) – EDC ; Monitoring; DM; Statistics; Writing
- PMA – REPEL CV (Synthemed, Inc. Approved) – EDC ; Monitoring; DM; Statistics; Writing; PMA (eCopy)
- PMA – Nine (9) Diagnostic Approvals (Abbott Laboratories) – EDC
- 510(k) – One (1) Diagnostic Approval (Abbott Laboratories) – EDC
- NDA Cystic Fibrosis – Submitted 2008 – Monitoring; DM; Statistics; Writing; NDA preparation
- NDA Gaucher Disease – Submitted 2009 – Monitoring; DM; Statistics; Writing; NDA preparation
Target Health now represents over 30 companies at FDA from all over the world including England, France, Germany, Israel, Korea, Switzerland and the US.
1. 2010: NDA ellaONE (HRA Pharma)
HRA Pharma was granted marketing authorization by the European Commission for ellaOne® (ulipristal acetate), the next generation emergency contraceptive. For this program, Target Health provided monitoring, data management, biostatistics and medical writing services. Target e*CRF® was used for the Phase 3 studies.
2. PMA (Abbott Diagnostics)
Abbott Diagnostics received approval of the first assay to detect both antigen and antibodies to Human Immunodeficiency Virus (HIV). This assay is approved for use as an aid in the diagnosis of HIV-1/HIV-2 infection in adults including pregnant women. It is also the first assay for use as an aid in the diagnosis of HIV-1/HIV-2 infection in children as young as two years old. Target e*CRF® was used for the pivotal trial.
3. MDL AUGMENT™ Bone Graft (Biomimetic Therapeutics)
Biomimetic Therapeutics received Health Canada approval of Augment Bone Graft for use as an alternative to autograft in foot and ankle fusion surgery. For this program, Target e*CRF® was used for the pivotal trial.
4. INDs / CTAs
d. Fatty liver
e. Gaucher disease (Canada)
f. Growth Impairment
5. Orphan Drug
a. Scleroderma (US and EU)
6. FDA Meetings
a. Cushing’s syndrome
b. Emergency contraception
c. Gaucher disease
d. Hereditary angioedema
e. Hormone replacement therapy
f. Ulcerative colitis
g. Women’s Health
7. Electronic Submissions
Target Health has expertise in preparation and publishing of electronic submissions and is an FDA approved vendor for electronic submissions through the Electronic Submissions Gateway (ESG).
CLINICAL TRIAL SOFTWARE PACKAGES
Clinical Trial Software Packages
Target e*CRF®: Target e*CRF has now been used in over 250 clinical trials since 1999. Largest trial to date is over 7,000 patients.
Target Document®: Target Document is a USER-FRIENDLY, INEXPENSIVE; HIGHLY SOPHISTICATED, Web-based, document management system that allows authorized users to view, download, and manage any document for their organization. – No More paper – Target Document features include: 1) 21 CFR Part 11 compliance; 2) routing for electronic signatures; 3) email alerts; 5) communication tools.
Target Encoder®: Target Encoder is a user-friendly, inexpensive; highly sophisticated, Web-based, coding system that allows authorized users to automatically code MedDRA and WHO Drug and other types of dictionaries. Target Encoder is fully integrated with Target e*CRF.
Target e*CTMS™: Target e*CTMS is a user-friendly, inexpensive; highly sophisticated, Web-based, clinical trial management system. A new clinical trial starts with identification of the sponsor and project name. Investigators, IRBs and users are maintained within the CTMS and can be easily assigned to a project. All staff within a clinical site can be identified with their title and contact information, as well as shipping addresses which could be different from the head office. As the site commits to participate in the clinical trial, a site number can be assigned. Once IRB approval is obtained, and all regulatory documents have been identified as received, an alert can be sent out via email to allow for drug shipment. Target e*CTMS provides many additional features such as: 1) Decision Logs, 2) Meeting Logs with uploading of the meeting minutes, 3) Questions and Answers, 4) Status of Regulatory Submissions and Deliverables, and 5) Monitor Site Visit Tracking with document upload.
Target Batch Edit Checks: With Target e*CRF®, batch edit checks are now integrated with the electronic query system within the study. Target e*CRF® runs the edits and displays the results of those edits through a discrepancy review screen integrated with the query system.
Target e*Pharmacovigilance™: Target e*CRF integrates EDC with a pharmacovigilance module by 1) allowing the principle investigators to enter a narrative, 2) allowing the medical monitor to enter a narrative and then have the EDC system generate an approved version of Form 3500A or CIOMS for regulatory submission with the ability to control the original and followup submissions.
Target eClinical Trial Record (Target e*CTR™): Target e*CTR allows the clinical study sites to perform direct data entry into any EDC system, and at the same time generates a read-only electronic document, which can be designated as the primary source data (eSource). These data, maintained in a secure, read-only trusted 3rd party environment, are available to the clinical study sites, monitors and regulatory agencies in a human readable format.
EDC vendor for 2 NIH grants in Juvenile Rheumatoid Arthritis at the Cleveland Clinic and University of Washington. Collaboration with the Biotechnology Center at SUNY Stony Brook, Rutgers and UMDNJ (the Medical School of New Jersey) and NYU School of Medicine.
Dr. Mitchel is a Course Director for Center for Biotechnology, Fundamentals of the Bioscience Industry, SUNY Stony Brook School of Medicine.
|3rd degree burns||Dermatology||Menopausal symptoms|
|Adhesion prevention||Emergency contraception||Nocturia|
|Atopic dermatitis||Erectile dysfunction||Osteoporosis|
|Bladder cancer||Gaucher’s disease||Ovarian cancer|
|Bone fractures||Growth Impairment||Pancreatic cancer|
|Brain Imaging||Hereditary angioedema||Pre-eclampsia diagnostic|
|Cardiac implant device||Head lice||Prostate cancer|
|Colorectal cancer||HIV diagnostic||Transdermal drug delivery|
|Cushing’s disease||Infertility||Ulcerative colitis|
|Cystic fibrosis||Juvenile rheumatoid arthritis||Wound Healing|
1. Mitchel J, Park G, Lynch S. Phase 1 Clinical Trials and Exploratory Phase 2 Clinical Trials. Book Chapter in Principles in Clinical Oral Health Research, Edited by: William Giannobile (University of Michigan Clinical Center), Brian Burt and Robert Genco (State University of New York at Buffalo) Chapter 11: 2009.
2. Dye, BA and Mitchel J. Data Management in Oral Health Research. Book Chapter in Principles in Clinical Oral Health Research, Edited by: William Giannobile (University of Michigan Clinical Center), Brian Burt and Robert Genco (State University of New York at Buffalo) Chapter 6: 2009.
3. Mitchel, J, Kim, YJ, Choi, JH, et al. The Final eFrontier. Applied Clinical Trials, Online, 1 May 2010
4. Morrison, B, Cochran, C, Giangrandec, J, et al. A CTTI Survey of Current Monitoring Practices. Society For Clinical Trials, May 2010
Target Health (www.targethealth.com) is a full service eCRO with full-time staff dedicated to all aspects of drug and device development. Areas of expertise include Regulatory Affairs, comprising, but not limited to, IND (eCTD), IDE, NDA (eCTD), BLA (eCTD), PMA (eCopy) and 510(k) submissions, execution of Clinical Trials, Project Management, Biostatistics and Data Management, EDC utilizing Target e*CRF®, and Medical Writing.
Target Health has developed a full suite of eClinical Trial software including:
1) Target e*CRF® (EDC plus randomization and batch edit checks)
2) Target e*CTMS™
3) Target Document®
4) Target Encoder®
5) Target Newsletter®
6) Target e*CTR™ (electronic medical record for clinical trials).
Target Health’s Pharmaceutical Advisory Dream Team assists companies in strategic planning from Discovery to Market Launch. Let us help you on your next project.
WebMD.com, August 26, 2010 — More than 1 million Americans have heart attacks each year. A heart attack, or myocardial infarction (MI), is permanent damage to the heart muscle. “Myo” means muscle, “cardial” refers to the heart, and “infarction” means death of tissue due to lack of blood supply.
What Happens During a Heart Attack?
The heart muscle requires a constant supply of oxygen-rich blood to nourish it. The coronary arteries provide the heart with this critical blood supply. If you have coronary artery disease, those arteries become narrow and blood cannot flow as well as they should. Fatty matter, calcium, proteins, and inflammatory cells build up within the arteries to form plaques of different sizes. The plaque deposits are hard on the outside and soft and mushy on the inside.
When the plaque is hard, the outer shell cracks (plaque rupture), platelets (disc-shaped particles in the blood that aid clotting) come to the area, and blood clots form around the plaque. If a blood clot totally blocks the artery, the heart muscle becomes “starved” for oxygen. Within a short time, death of heart muscle cells occurs, causing permanent damage. This is a heart attack.
While it is unusual, a heart attack can also be caused by a spasm of a coronary artery. During a coronary spasm, the coronary arteries restrict or spasm on and off, reducing blood supply to the heart muscle (ischemia). It may occur at rest and can even occur in people without significant coronary artery disease.
Each coronary artery supplies blood to a region of heart muscle. The amount of damage to the heart muscle depends on the size of the area supplied by the blocked artery and the time between injury and treatment.
Healing of the heart muscle begins soon after a heart attack and takes about eight weeks. Just like a skin wound, the heart’s wound heals and a scar will form in the damaged area. But, the new scar tissue does not contract. So, the heart’s pumping ability is lessened after a heart attack. The amount of lost pumping ability depends on the size and location of the scar.
Heart Attack Symptoms
Symptoms of a heart attack include:
- Discomfort, pressure, heaviness, or pain in the chest, arm, or below the breastbone
- Discomfort radiating to the back, jaw, throat, or arm
- Fullness, indigestion, or choking feeling (may feel like heartburn)
- Sweating, nausea, vomiting, or dizziness
- Extreme weakness, anxiety, or shortness of breath
- Rapid or irregular heartbeats
During a heart attack, symptoms last 30 minutes or longer and are not relieved by rest or nitroglycerin under the tongue.
Some people have a heart attack without having any symptoms (a “silent” myocardial infarction). A silent MI can occur in any person, though it is more common among diabetics.
What Do I Do if I Have a Heart Attack?
After a heart attack, quick treatment to open the blocked artery is essential to lessen the amount of damage. At the first signs of a heart attack, call for emergency treatment (usually 911). The best time to treat a heart attack is within one to two hours of the first onset of symptoms. Waiting longer increases the damage to your heart and reduces your chance of survival.
Keep in mind that chest discomfort can be described many ways. It can occur in the chest or in the arms, back, or jaw. If you have symptoms, take notice. These are your heart disease warning signs. Seek medical care immediately.
How Is a Heart Attack Diagnosed?
To diagnose a heart attack, an emergency care team and ask you about your symptoms and begin to evaluate you. The diagnosis of the heart attack is based on your symptoms and test results. The goal of treatment is to treat you quickly and limit heart muscle damage.
Tests to Diagnose a Heart Attack
- ECG . The ECG (also known as EKG or electrocardiogram) can tell how much damage has occurred to your heart muscle and where it has occurred. In addition, your heart rate and rhythm can be monitored.
- Blood tests. Blood may be drawn to measure levels of cardiac enzymes that indicate heart muscle damage. These enzymes are normally found inside the cells of your heart and are needed for their function. When your heart muscle cells are injured, their contents — including the enzymes — are released into your bloodstream. By measuring the levels of these enzymes, the doctor can determine the size of the heart attack and approximately when the heart attack started. Troponin levels will also be measured. Troponins are proteins found inside of heart cells that are released when they are damaged by ischemia. Troponins can detect very small heart attacks.
- Echocardiography. Echocardiography is an imaging test that can be used during and after a heart attack to learn how the heart is pumping and what areas are not pumping normally. The “echo” can also tell if any structures of the heart (valves, septum, etc.) have been injured during the heart attack.
- Cardiac catheterization. Cardiac catheterization, also called cardiac cath, may be used during the first hours of a heart attack if medications are not relieving the ischemia or symptoms. The cardiac cath can be used to directly visualize the blocked artery and help your doctor determine which procedure is needed to treat the blockage.
What Is the Treatment for a Heart Attack?
Once heart attack is diagnosed, treatment begins immediately — possibly in the ambulance or emergency room. Drugs and surgical procedures are used to treat a heart attack.
What Drugs Are Used to Treat a Heart Attack?
What Is the Treatment for a Heart Attack? continued…
The goals of drug therapy are to break up or prevent blood clots, prevent platelets from gathering and sticking to the plaque, stabilize the plaque, and prevent further ischemia.
These medications must be given as soon as possible (within one to two hours from the start of your heart attack) to decrease the amount of heart damage. The longer the delay in starting these drugs, the more damage can occur and the less benefit they can provide.
Drugs used during a heart attack may include:
- Aspirin to prevent blood clotting that may worsen the heart attack.
- Other antiplatelets, such as Plavix, to prevent blood clotting.
- Thrombolytic therapy (“clot busters”) to dissolve any blood clots in the heart’s arteries.
- Any combination of the above
Other drugs, given during or after a heart attack, lessen your heart’s work, improve the functioning of the heart, widen or dilate your blood vessels, decrease your pain, and guard against any life-threatening heart rhythms.
Are There Other Treatment Options for a Heart Attack?
During or shortly after a heart attack, you may go to the cardiac cath lab for direct evaluation of the status of your heart, arteries, and the amount of heart damage. In some cases, procedures (such as angioplasty or stents) are used to open up your narrowed or blocked arteries.
If necessary, bypass surgery may be performed in following days to restore the heart muscle’s supply of blood.
Treatments (medications, open heart surgery, and interventional procedures, like angioplasty) do not cure coronary artery disease. Having had a heart attack or treatment does not mean you will never have another heart attack; it can happen again. But, there are several steps you can take to prevent further attacks.
How Are Future Heart Attacks Prevented?
The goal after your heart attack is to keep your heart healthy and reduce your risks of having another heart attack. Your best bet to ward off future attacks are to take your medications, change your lifestyle, and see you doctor for regular heart checkups.
Why Do I Need to Take Drugs After a Heart Attack?
Drugs are prescribed after a heart attack to:
- Prevent future blood clots.
- Lessen the work of your heart and improve your heart’s performance and recovery.
- Prevent plaques by lowering cholesterol.
Other drugs may be prescribed if needed. These include medications to treat irregular heartbeats, lower blood pressure, control angina, and treat heart failure.
It is important to know the names of your medications, what they are used for, and how often and at what times you need to take them. Your doctor or nurse should review your medications with you. Keep a list of your medications and bring them to each of your doctor visits. If you have questions about, ask your doctor or pharmacist.
What Lifestyle Changes Are Needed After a Heart Attack?
There is no cure for coronary artery disease. In order to prevent the progression of heart disease and another heart attack, you must follow your doctor’s advice and make necessary lifestyle changes. You can stop smoking, lower your blood cholesterol, control your diabetes and high blood pressure, follow an exercise plan, maintain an ideal body weight, and control stress.
When Will I See My Doctor Again After I Leave the Hospital?
Make a doctor’s appointment for four to six weeks after you leave the hospital following a heart attack. Your doctor will want to check the progress of your recovery. Your doctor may ask you to undergo diagnostic tests (such as an exercise stress test at regular intervals. These tests can help your doctor diagnose the presence or progression of blockages in your coronary arteries and plan treatment.
Call your doctor sooner if you have symptoms such as chest pain that becomes more frequent, increases in intensity, lasts longer, or spreads to other areas; shortness of breath, especially at rest; dizziness, or irregular heartbeats.
WebMD Medical Reference
Reviewed by Robert J Bryg, MD
Study: New Coating for Hospital Walls, Surgical Equipment, Other Surfaces Kills MRSA
Reviewed by Laura J. Martin, MD
WebMD.com, August. 17, 2010, by Bill Hendrick — Biotech scientists at Rensselaer Polytechnic Institute have developed a coating for use in health care settings that they say kills the deadly MRSA germ.
MRSA, or methicillin-resistant Staphyloccus aureus, is a virulent bacterium that causes antibiotic-resistant infections, killing about 90,000 patients a year. Because it has been hard to battle, it is sometimes called a “superbug.”
But Rensselaer scientists say their coating, for use on surgical equipment, hospital walls, and other surfaces in health care settings, seems to be very effective in eradicating MRSA.
The study is published in ACS Nano, a journal of the American Chemical Society.
In tests, 100% of MRSA bacteria were killed within 20 minutes of contact with a surface painted with latex paint laced with the coating, the researchers say. The coating is made with lysostaphin, a naturally occurring enzyme, combined with carbon nanotubes.
“We’re building on nature,” Jonathan S. Dordick, PhD, director of Rensselaer’s Center for Biotechnology and Interdisciplinary Studies, says in a news release. “Here we have a system where the surface contains an enzyme that is safe to handle, doesn’t appear to lead to resistance, doesn’t leach into the environment, and doesn’t clog up with cell debris.”
When the superbugs came in contact with a painted surface, “they’re killed,” he says.
How It Works
Lysostaphin works by attaching itself to the bacterial cell wall, slicing it open, but is not toxic to human cells, Dordick says.
Researcher Ravi S. Kane, PhD, says the enzyme is attached to the carbon nanotube with a short, flexible polymer link, improving its ability to reach the MRSA bacteria.
“The more the lysostaphin is able to move around, the more it is able to function,” Dordick says.
Kane and Dordick worked With Dennis W. Metzger, PhD, and Ravi Pangule, a graduate student in chemical engineering, at Albany Medical College, where Metzger maintains strains of MRSA.
“At the end of the day, we have a very selective agent that can be used in a wide range of environments — paints, coating, medical instruments, doorknobs, surgical masks — and it’s active and it’s stable,” Kane says. “It’s ready to use when you’re ready to use it.”
They say their approach will likely prove superior to previous attempts at creating antimicrobial agents, some of which release biocides, which can lose effectiveness over time due to leaching into the environment and may have harmful side effects, the researchers say.
“We spent quite a bit of time demonstrating that the enzyme did not come out of the paint during antibacterial experiments,” he says. “Indeed, it was surprising that the enzyme worked as well as it did while remaining embedded near the surface of the paint.”
It’s unlikely, Kane says, that MRSA superbugs will develop resistance to a naturally occurring enzyme, which has “evolved over hundreds of millions of years to be very difficult for Staphyloccus aureus to resist.”
They also say their new coating can be washed repeatedly without losing effectiveness and that it has a dry storage shelf life of up to six months.
MRSA can infect the bloodstream, the lungs, and the urinary tract, and people can carry it without being sickened. Killing it on surfaces is important because MRSA is spread by contact and can be carried by people who touch infected objects.
Graphic Credit: Bryan Christie Design
MIT Technology Review, August 25, 2010 — Mere months after Kyoto University researchers announced in 2007 that they had discovered how to turn skin cells into induced pluripotent stem cells (iPS cells), Jacob Hanna used these new types of cells to cure mice of sickle-cell anemia, in which a genetic defect causes bone marrow to make defective red blood cells. Hanna, a fellow at the Whitehead Institute, took skin cells from a diseased mouse and reprogrammed them create iPS cells, which behave like embryonic stem cells, readily turning into any cell type in the body. He then corrected the sickle-cell genetic defect and prodded the iPS cells to develop into the type of marrow stem cell that manufactures a mouse’s blood cells. These healthy cells were transplanted back into the mouse, whose immune system accepted them as the animal’s own tissue. The treated mouse began producing healthy red blood cells on its own.
Hanna’s work was a turning point for iPS research, says George Daley, director of the Stem Cell Transplantation Program at Boston’s Children’s Hospital and a professor at Harvard Medical School: “It was a beautiful demonstration of a mouse model of a human disease, and really demonstrated the potential of iPS cells.”
Before iPS cells can be used to treat diseases such as sickle-cell anemia in humans, a lot of work has to be done to make sure they won’t cause adverse side effects and to improve the efficiency of deriving them from skin cells. Hanna is now developing simulations to understand what happens when cells are reprogrammed, and he’s searching for new types of human stem cells that could be easier to turn into adult cells.–Nidhi Subbaraman