Archive for the ‘Pharmacotherapy of Cardiovascular Disease’ Category

Subarachnoid hemorrhage care at Mayo Clinic in Rochester, Minn., ranks No. 1 for neurology and neurosurgery in the U.S. News & World Report Best Hospitals rankings

Reporter: Aviva Lev-Ari, PhD, RN


A Mayo Clinic study found that 63.3 percent of people treated for aneurysmal subarachnoid hemorrhages at Mayo Clinic in Rochester, Minnesota, from 2001 to 2013 had no or few lasting symptoms.

Mayo Clinic in Phoenix/Scottsdale, Ariz., and Mayo Clinic in Jacksonville, Fla., are ranked among the Best Hospitals for neurology and neurosurgery by U.S. News & World Report.




The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes (see the image below). It occurs in various clinical contexts, the most common being head trauma. However, the familiar use of the term SAH refers to nontraumatic (or spontaneous) hemorrhage, which usually occurs in the setting of a ruptured cerebral aneurysm or arteriovenous malformation (AVM).

The classic presentation can include the following:

  • Sudden onset of severe headache (the classic feature)
  • Accompanying nausea or vomiting
  • Symptoms of meningeal irritation
  • Photophobia and visual changes
  • Focal neurologic deficits
  • Sudden loss of consciousness at the ictus
  • Seizures during the acute phase

Physical examination findings may be normal or may include the following:

  • Mild to moderate BP elevation
  • Temperature elevation
  • Tachycardia
  • Papilledema
  • Retinal hemorrhage
  • Global or focal neurologic abnormalities

Complications of SAH include the following:

  • Hydrocephalus
  • Rebleeding
  • Vasospasm
  • Seizures
  • Cardiac dysfunction


Diagnosis of SAH usually depends on a high index of clinical suspicion combined with radiologic confirmation via urgent noncontrast CT, followed by lumbar puncture or CT angiography of the brain. After the diagnosis is established, further imaging should be performed to characterize the source of the hemorrhage.

Laboratory studies should include the following:

  • Serum chemistry panel
  • Complete blood count
  • Prothrombin time (PT)/activated partial thromboplastin time (aPTT)
  • Blood typing/screening
  • Cardiac enzymes
  • Arterial blood gas (ABG) determination

Imaging studies that may be helpful include the following:

  • CT (noncontrast, contrast, or infusion)
  • Digital subtraction cerebral angiography
  • Multidetector CT angiography
  • MRI (if no lesion is found on angiography)
  • Magnetic resonance angiography (MRA; investigational for SAH)

Other diagnostic studies that may be warranted are as follows:

  • Baseline chest radiograph
  • ECG on admission
  • Lumbar puncture and CSF analysis

See Workup for more detail.


Current treatment recommendations include the following:

  • Antihypertensive agents (eg, IV beta blockers) when mean arterial pressure exceeds 130 mm Hg
  • Avoidance of nitrates (which elevate ICP) when feasible
  • Hydralazine and calcium channel blockers
  • Angiotensin-converting enzyme (ACE) inhibitors (not first-line agents in acute SAH)
  • In patients with signs of increased ICP or herniation, intubation and hyperventilation

Other interventions for increased ICP are as follows:

  • Osmotic agents (eg, mannitol)
  • Loop diuretics (eg, furosemide)
  • IV steroids (controversial but recommended by some)

Surgical treatment to prevent rebleeding includes the following options:

  • Clipping the ruptured aneurysm
  • Endovascular treatment [1(ie, coiling)

The choice between coiling and clipping usually depends on the location of the lesion, the neck of the aneurysm, and the availability and experience of hospital staff.



Pharmaco-Therapy for SAH

  • Nimodipine is a drug used for SAH

Nimodipine is a second generation calcium channel blocker used in the treatment of cerebral vasospasm after subarachnoid hemorrhage.  Nimodipine is not widely used and has not been implicated in causing clinically apparent acute liver injury.


Nimodipine is a second generation calcium channel blocker used in the treatment of cerebral vasospasm after subarachnoid hemorrhage.  Nimodipine is not widely used and has not been implicated in causing clinically apparent acute liver injury.



Nimodipine (nye moe’ di preen) belongs to the dihydropyridine class of calcium channel blockers (similar to amlopidine and felodipine) and is used to treat cerebral vasospasm after subarachnoid hemorrhage.  Like other calcium channel blockers, nimodipine acts by inhibition of the influx of calcium ions into smooth muscle cells during depolarization which results in vasodilation.  Nimodipine has high lipid solubility and was developed specifically to treat cerebral vasospasm.  Clinical trials have suggested that nimodipine reduces infarct size and complications after subarachnoid hemorrhage.  Nimodipine was approved for use in the United States in 1988 but is not widely used, largely because of its restricted indications.  Nimodipine is available in generic forms and under the commercial name Nimotop as capsules of 30 mg.  The recommend dose in adults is 60 mg every 4 hours for 21 days starting as soon as possible or within 96 hours of the diagnosis of subarachnoid hemorrhage.  Like most calcium channel blockers, nimodipine is generally well tolerated and side effects are largely due to its vasodilating activities and can include headache, dizziness, flushing, fatigue, nausea, diarrhea, peripheral edema, palpitations and rash.


Hepatotoxicity, Outcome and Management

Nimodipine has been associated with only rare reports of serum enzyme elevations during therapy.  These elevations are usually mild, transient and not associated with symptoms or need for dose modification.  Nimodipine is not widely used and has not been linked to instances of clinically apparent liver injury.  Thus, hepatotoxicity from nimodipine must be rare, if it occurs at all.


Likelihood score: E  (Unlikely cause of clinically apparent liver injury).


The reason why some calcium channel blockers cause liver injury (verapamil, diltiazem, amlodipine) while others (such as nimodipine) do not is not known. Because liver injury from calcium channel blockers is rare, those that are uncommonly used may just not have had enough exposures to manifest idiosyncratic cases of liver injury. Nimodipine is metabolized in the liver largely via CYP 3A4 and is susceptible to drug-drug interactions with agents that induce or inhibit CYP 3A4.


Drug Class:  Cardiovascular AgentsCalcium Channel Blockers


Other Drugs in the Subclass, Calcium Channel Blockers:  AmlodipineDiltiazemFelodipineIsradipineNicardipineNifedipineNisoldipineVerapamil




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Acute Coronary Syndrome (ACS): Strategies in Anticoagulant Selection: Diagnostics Approaches – Genetic Testing Aids vs. Biomarkers (Troponin types and BNP)

Curator: Aviva Lev-Ari, PhD, RN


UPDATED on 3/17/2018

An NT-proBNP <300 pg/ml strongly excludes the presence of acute HF.

J Am Coll Cardiol. 2018 Mar 20;71(11):1191-1200. doi: 10.1016/j.jacc.2018.01.021.

N-Terminal Pro-B-Type Natriuretic Peptide in the Emergency Department: The ICON-RELOADED Study


A breakthrough in emergence of

  • Genetic Testing Aids as a Personalized approach, genomics-based approach to selecting antiplatelet therapy, for reduction in ischemic and bleeding events, and
  • Biochemical Biomarker approaches for dosing anti-thrombotic drugs are presented here.

“This study fills in a part of the puzzle of genomic testing,” said Craig Beavers, PharmD, of the University of Kentucky in Lexington. “It shows we can use genomic information in clinical decision making. It was interesting that there appeared to be a change in prescribing based on genomics.”


At 12 months, 25.9% of patients receiving standard care had experienced the trial’s primary composite endpoint — cardiovascular death, non-fatal MI or stroke, and Bleeding Academic Research Consortium (BARC) 3-5 major bleeding — compared with 15.8% of patients receiving an anticoagulant drug on the basis of genetic testing (P<0.001), reported Diego Ardissino, MD, of Azienda Ospedaliero-Universitaria di Parma in Italy, and colleagues.

PHARMCLO is the first trial to combine clinical characteristics with genetic information to inform the choice of P2Y12 receptor antagonist in patients with ACS, Ardissino said in a presentation at the American College of Cardiology annual meeting. The study was simultaneously published in the Journal of the American College of Cardiology.

“Selecting treatment on the basis of genetic data in addition to considerations concerning the patients’ clinical characteristics may lead to a more personalized, and therefore more efficient, antiplatelet therapy, thus reducing both ischemic and bleeding risk,” he said. “PHARMCLO is the first step of a new approach that will see a shift in emphasis away from trying to discover ever-more potent anti-thrombotic drugs, and toward ensuring that the right therapy is given to each individual patient.”

However, PHARMCLO was halted after about a fourth of the intended population was recruited. The Ethics Committee of Modena (Italy) required the trial to be prematurely stopped because of a lack of in vitro diagnosis certification for the testing instruments. The original patients were still followed, Ardissino stated.

The authors enrolled 888 patients, and randomly assigned them to be tested for

  • three genes associated with resistance to clopidogrel (Plavix), and then were assigned a
  • treatment based on clinical data informed by the testing results.
  • Tested genes were ABCB1, 2C19*2 and 2C19*17 with the STQ3 system.
  • Another group was assigned to treatment without reference to genetic testing.
  • Standard of care treatment was with Clopidogrel, Ticagrelor (Brilinta), or Prasugrel (Effient).
  1. Clopidogrel was more frequently used in the standard arm (50.7% versus 43.3%), while
  2. Ticagrelor in the pharmacogenomic arm (42.6% versus 32.7%, P<0.05) and
  3. Prasugrel were used equally in both.

The primary endpoint hazard ratio was 0.58 versus the standard arm (95% CI 0.43-0.78, P<0.001).

Previous studies have shown Prasugrel and Ticagrelor to be superior to Clopidogrel at preventing ischemic events. However, prasugrel and ticagrelor, which are more potent, are also known to increase the risk of bleeding. The findings suggest that having more information about a specific patient’s likely response to clopidogrel can help doctors weigh this trade-off, Ardissino said.


The STANDARD OF CARE in Diagnosis of Acute Coronary Syndrome (ACS) using BioMarkers in serum blood relays of values of Troponin types and BNP for dosing anti-thrombotic drugs.

The team at LPBI Group published the following articles on this topic:

A search into our Journal Archive for “Acute Coronary Syndrome” yielded 210 articles

  1. High Sensitivity Troponin (hs cTn) Assays 

  • Previously undiscerned value of hs-troponin

Curators: Larry H. Bernstein, MD, FCAP and Aviva Lev-Ari, PhD, RN

  • Recent Insights into the High Sensitivity Troponins for Acute Coronary Syndromes

Curator: Larry H Bernstein, MD, FCAP

  • Dealing with the Use of the High Sensitivity Troponin (hs cTn) Assays: Preparing the United States for High-Sensitivity Cardiac Troponin Assays

Author and Curator: Larry H Bernstein, MD, FCAP and Author and Curator: Aviva Lev-Ari, PhD, RD

  • Preparing the United States for High-Sensitivity Cardiac Troponin Assays

Curator: Larry H Bernstein, MD, FCAP


2. BNP and proBNP

Brain natriuretic peptide (BNP), also known as B-type natriuretic peptide, is a hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume, decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis. The net effect of these peptides is a decrease in blood pressure due to the decrease in systemic vascular resistance and, thus, afterload. Additionally, the actions of both BNP and ANP result in a decrease in cardiac output due to an overall decrease in central venous pressure and preload as a result of the reduction in blood volume that follows natriuresis and diuresis.


Maisel A, Krishnaswamy P, Nowak R, McCord J, Hollander J, Duc P, Omland T, Storrow A, Abraham W, Wu A, Clopton P, Steg P, Westheim A, Knudsen C, Perez A, Kazanegra R, Herrmann H, McCullough P (2002). “Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure“. N Engl J Med347 (3): 161–7. 


The team at LPBI Group published the following articles on this topic:

  • Effect of Coronary Atherosclerosis and Myocardial Ischemia on Plasma Levels of High-Sensitivity Troponin T and NT-proBNP in Patients With Stable Angina

  • More on the Performance of High Sensitivity Troponin T and with Amino Terminal Pro BNP in Diabetes

Writer and Curator: Larry H. Bernstein, MD, FCAP

  • Erythropoietin (EPO) and Intravenous Iron (Fe) as Therapeutics for Anemia in Severe and Resistant CHF: The Elevated N-terminal proBNP Biomarker

Co-Author of the FIRST Article: Larry H. Bernstein, MD, FCAP. Reviewer and Curator of the SECOND and of the THIRD Articles: Larry H. Bernstein, MD, FCAP and Article Architecture Curator: Aviva Lev-Ari, PhD, RN

  • Highlights of LIVE Day 1: World Medical Innovation Forum – CARDIOVASCULAR • MAY 1-3, 2017  BOSTON, MA • UNITED STATES

Aviva Lev-Ari, PhD, RN


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 Cholesterol Lowering Novel PCSK9 drugs: Praluent [Sanofi and Regeneron] vs Repatha [Amgen] – which drug cuts CV risks enough to make it cost-effective?

Reporter: Aviva Lev-Ari, PhD, RN


Did Amgen’s Repatha cut CV risks enough to make it cost-effective? Analysts say no

Sanofi, Regeneron’s Praluent pulls off PCSK9 coup with 29% cut to death risks in most vulnerable patients
SEE our curations on PCSK9 drugs:

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ODYSSEY Outcomes trial evaluating the effects of a PCSK9 inhibitor, alirocumab, on major cardiovascular events in patients with an acute coronary syndrome to be presented at the American College of Cardiology meeting on March 10.

Reporter: Aviva Lev-Ari, PhD, RN


For PCSK9 inhibitors, the effect on major adverse cardiovascular events has always fallen short of expectations based on cholesterol lowering.

But cardiovascular risk reduction is complicated. There is more to the puzzle than cholesterol. Some drugs lower both cholesterol and prevent cardiovascular events, but some people think that the two effects are actually not that closely related.

Milton Packer MD

In a previous trial (FOURIER), another PCSK9 inhibitor had only a modest benefit on its primary endpoint, and it did not reduce cardiovascular death, although the magnitude of cholesterol lowering was striking.

In another trial (SPIRE), a third PCSK9 inhibitor, the clinical trial was terminated prematurely by Pfizer because of reduction of the effect of the drug (a humanized but not fully humanized antibody) due to development of neutralizing antibodies in some of the patients. Actually, in patients treated for more than a year who did not develop neutralizing antibodies, a beneficial effect was seen.

The ODYSSEY Outcomes trial is evaluating the effects of a PCSK9 inhibitor,alirocumab, on major cardiovascular events in patients with an acute coronary syndrome within the prior year. The drug lowers serum cholesterol dramatically, and some are hopeful that that effect will translate into an important reduction in the risk of major adverse cardiovascular events. If you believe that cholesterol reduction inevitably leads to the prevention of cardiovascular death, myocardial infarction and stroke, then you would have high expectations for the ODYSSEY trial.

ODYSSEY. The trial uses a somewhat more aggressive treatment strategy and has a longer follow-up period than its predecessors. So maybe the benefit will be large. Maybe the drug will even reduce cardiovascular death or all-cause mortality.

In order to enrich the population for cardiovascular events, the trial enrolled patients with an acute coronary syndrome within the prior year. These patients are at high risk of having a recurrence. The problem is that risk is not necessarily related to changes in cholesterol, especially the events occurring early in the trial. And in this type of trial, the analysis tends to give extra weight to early events.

Trials like ODYSSEY are often designed to stop early if the results are unbelievably impressive. The ODYSSEY trial wasn’t stopped early.

the patients entering the ODYSSEY trial are starting out with a serum LDL <100 mg/dL or even <90 mg/dL. Is cholesterol really playing an important role at that level, especially when compared with noncholesterol factors?


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  1. Lungs can supply blood stem cells and also produce platelets: Lungs, known primarily for breathing, play a previously unrecognized role in blood production, with more than half of the platelets in a mouse’s circulation produced there. Furthermore, a previously unknown pool of blood stem cells has been identified that is capable of restoring blood production when bone marrow stem cells are depleted.


  1. A new drug for multiple sclerosis: A new multiple sclerosis (MS) drug, which grew out of the work of UCSF (University of California, San Francisco) neurologist was approved by the FDA. Ocrelizumab, the first drug to reflect current scientific understanding of MS, was approved to treat both relapsing-remitting MS and primary progressive MS.


  1. Marijuana legalized – research needed on therapeutic possibilities and negative effects: Recreational marijuana will be legal in California starting in January, and that has brought a renewed urgency to seek out more information on the drug’s health effects, both positive and negative. UCSF scientists recognize marijuana’s contradictory status: the drug has proven therapeutic uses, but it can also lead to tremendous public health problems.


  1. Source of autism discovered: In a finding that could help unlock the fundamental mysteries about how events early in brain development lead to autism, researchers traced how distinct sets of genetic defects in a single neuronal protein can lead to either epilepsy in infancy or to autism spectrum disorders in predictable ways.


  1. Protein found in diet responsible for inflammation in brain: Ketogenic diets, characterized by extreme low-carbohydrate, high-fat regimens are known to benefit people with epilepsy and other neurological illnesses by lowering inflammation in the brain. UCSF researchers discovered the previously undiscovered mechanism by which a low-carbohydrate diet reduces inflammation in the brain. Importantly, the team identified a pivotal protein that links the diet to inflammatory genes, which, if blocked, could mirror the anti-inflammatory effects of ketogenic diets.


  1. Learning and memory failure due to brain injury is now restorable by drug: In a finding that holds promise for treating people with traumatic brain injury, an experimental drug, ISRIB (integrated stress response inhibitor), completely reversed severe learning and memory impairments caused by traumatic brain injury in mice. The groundbreaking finding revealed that the drug fully restored the ability to learn and remember in the brain-injured mice even when the animals were initially treated as long as a month after injury.


  1. Regulatory T cells induce stem cells for promoting hair growth: In a finding that could impact baldness, researchers found that regulatory T cells, a type of immune cell generally associated with controlling inflammation, directly trigger stem cells in the skin to promote healthy hair growth. An experiment with mice revealed that without these immune cells as partners, stem cells cannot regenerate hair follicles, leading to baldness.


  1. More intake of good fat is also bad: Liberal consumption of good fat (monounsaturated fat) – found in olive oil and avocados – may lead to fatty liver disease, a risk factor for metabolic disorders like type 2 diabetes and hypertension. Eating the fat in combination with high starch content was found to cause the most severe fatty liver disease in mice.


  1. Chemical toxicity in almost every daily use products: Unregulated chemicals are increasingly prevalent in products people use every day, and that rise matches a concurrent rise in health conditions like cancers and childhood diseases, Thus, researcher in UCSF is working to understand the environment’s role – including exposure to chemicals – in health conditions.


  1. Cytomegalovirus found as common factor for diabetes and heart disease in young women: Cytomegalovirus is associated with risk factors for type 2 diabetes and heart disease in women younger than 50. Women of normal weight who were infected with the typically asymptomatic cytomegalovirus, or CMV, were more likely to have metabolic syndrome. Surprisingly, the reverse was found in those with extreme obesity.




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What Level of Blood Pressure (BP) should be Treated? Comments on the New Guidelines

Reporter: Aviva Lev-Ari, PhD, RN


UPDATED on 2/27/2018

ACC, AHA Fire Back at Charge of BP Guideline Conflicts

Open Payments system ‘replete with erroneous data’

by Crystal Phend,Senior Associate Editor, MedPage Today

February 14, 2018


“We remain completely convinced of the high value of the Hypertension Guideline for the long-term heart and brain health of the American public and have found nothing that would dispute the motives or actions of our distinguished volunteer authors. We have, however, noted areas where our processes could be improved and have modified them.”

Based on the Open Payments database, Romano had initially alleged that Kim Williams Sr., MD, of Rush University and past president of the ACC, who was on the guideline writing committee, “received $19,594 in 2015 and $20,000 in 2016 in grant funding from Boston Scientific. Boston Scientific sells a device called the Vessix renal denervation system to treat hypertension. He disclosed no relationship with Boston Scientific.”


ACC: 130/50 vs 140/90

Last year, the American Heart Association, the American College of Cardiology and many other cardiology organizations announced that the threshold for identifying hypertension had been officially lowered. The threshold for diagnosing and treating hypertension was now 130/80.

The document relies in part on the findings of the SPRINT trial, but no one really understands the blood pressures in that study. Strangely, the document applies its recommendations to people who were not even represented in the SPRINT trial. For example, it applies its recommendations to those with heart failure, even though there is no scientific basis for doing so.

Nevertheless, suddenly, 46% of Americans had hypertension. On the previous morning, 32% had the disease. Within 24 hours, millions of people were given a new label.

Furthermore, millions of people who thought they had well-controlled blood pressure (because it was below 140/90) now learned that they needed to do more to bring their blood pressures down.

In December, the American Academy of Family Physicians (AAFP) said they were not endorsing the new hypertension guideline.

American College of Physicians which proposed a target systolic blood pressure of 150 for people who were 60 years or older. Earlier this week, the ACP doubled down, issuing a statement criticizing the lower threshold.

The Fake Hypertension War – Medical politics and mud fights

by Milton Packer MD

Packer recently consulted for Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Cardiorentis, Daiichi Sankyo, Gilead, Novo Nordisk, Relypsa, Sanofi, Takeda, and ZS Pharma. He chairs the EMPEROR Executive Committee for trials of empagliflozin for the treatment of heart failure. He was previously the co-PI of the PARADIGM-HF trial and serves on the Steering Committee of the PARAGON-HF trial, but has no financial relationship with Novartis.

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FDA approval on 12/1/2017 of Amgen’s evolocumb (Repatha) a PCSK9 inhibitor for the prevention of heart attacks, strokes, and coronary revascularizations in patients with established cardiovascular disease

Reporter: Aviva Lev-Ari, PhD, RN


Evolocumab was first FDA approved in 2015 for patients with

  • familial hypercholesterolemia and
  • others who fail to achieve LDL cholesterol lowering through diet and maximally-tolerated statin therapy.

In the Repatha cardiovascular outcomes study (FOURIER), Repatha reduced the risk of

  • heart attack by 27 percent, the risk of
  • stroke by 21 percent and the risk of
  • coronary revascularization by 22 percent.2


U.S. Repatha Indication

Repatha is a PCSK9 (proprotein convertase subtilisin kexin type 9) inhibitor antibody indicated:

  • to reduce the risk of myocardial infarction, stroke, and coronary revascularization in adults with established cardiovascular disease.
  • as an adjunct to diet, alone or in combination with other lipid-lowering therapies (e.g., statins, ezetimibe), for treatment of adults with primary hyperlipidemia (including heterozygous familial hypercholesterolemia [HeFH]) to reduce low-density lipoprotein cholesterol (LDL-C).
  • as an adjunct to diet and other LDL‑lowering therapies (e.g., statins, ezetimibe, LDL apheresis) in patients with homozygous familial hypercholesterolemia (HoFH) who require additional lowering of LDL‑C.

The safety and effectiveness of Repatha have not been established in pediatric patients with HoFH who are younger than 13 years old.

The safety and effectiveness of Repatha have not been established in pediatric patients with primary hyperlipidemia or HeFH.

Eligible patients with high cholesterol (LDL-C ≥70 mg/dL or non-high-density lipoprotein cholesterol [non-HDL-C] ≥100 mg/dL) and established cardiovascular disease at more than 1,300 study locations around the world were randomized to receive Repatha subcutaneous 140 mg every two weeks or 420 mg monthly plus high- or moderate-intensity effective statin dose; or placebo subcutaneous every two weeks or monthly plus high- to moderate-intensity statin dose. Statin therapy was defined in the protocol as at least atorvastatin 20 mg or equivalent daily with a recommendation for at least atorvastatin 40 mg or equivalent daily where approved. The study was event driven and continued until at least 1,630 patients experienced a key secondary endpoint.

About Repatha® (evolocumab)
Repatha® (evolocumab) is a human monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9). Repatha binds to PCSK9 and inhibits circulating PCSK9 from binding to the low-density lipoprotein (LDL) receptor (LDLR), preventing PCSK9-mediated LDLR degradation and permitting LDLR to recycle back to the liver cell surface. By inhibiting the binding of PCSK9 to LDLR, Repatha increases the number of LDLRs available to clear LDL from the blood, thereby lowering LDL-C levels.1

About Amgen in the Cardiovascular Therapeutic Area
Building on more than three decades of experience in developing biotechnology medicines for patients with serious illnesses, Amgen is dedicated to addressing important scientific questions to advance care and improve the lives of patients with cardiovascular disease, the leading cause of morbidity and mortality worldwide.8 Amgen’s research into cardiovascular disease, and potential treatment options, is part of a growing competency at Amgen that utilizes human genetics to identify and validate certain drug targets. Through its own research and development efforts, as well as partnerships, Amgen is building a robust cardiovascular portfolio consisting of several approved and investigational molecules in an effort to address a number of today’s important unmet patient needs, such as high cholesterol and heart failure.

Homozygous Familial Hypercholesterolemia (HoFH): In 49 patients with homozygous familial hypercholesterolemia studied in a 12-week, double-blind, randomized, placebo-controlled trial, 33 patients received 420 mg of Repatha subcutaneously once monthly. The adverse reactions that occurred in at least 2 (6.1 percent) Repatha-treated patients and more frequently than in placebo-treated patients, included upper respiratory tract infection (9.1 percent versus 6.3 percent), influenza (9.1 percent versus 0 percent), gastroenteritis (6.1 percent versus 0 percent), and nasopharyngitis (6.1 percent versus 0 percent).

Immunogenicity: Repatha is a human monoclonal antibody. As with all therapeutic proteins, there is a potential for immunogenicity with Repatha.

Please contact Amgen Medinfo at 800-77-AMGEN (800-772-6436) or 844-REPATHA (844-737-2842) regarding Repatha® availability or find more information, including full Prescribing Information, at and


  1. Repatha® U.S. Prescribing Information. Amgen.
  2. Sabatine MS, Giugliano RP, Keech AC, et al, for the FOURIER Steering Committee and Investigators. N Engl J Med. Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease. 2017;376:1713-22.
  3. Cannon CP, et al. N Engl J Med. 2004;350:1495-1504.
  4. LaRosa JC, et al. N Engl J Med. 2005;352:1425-1435.
  5. Pederson TR, et al. JAMA. 2005;294:2437-2445.
  6. Search Collaborative Group Lancet 2010;376:1658–69.
  7. Cannon CP, et al. N Engl J Med. 2015;372:2387-2397.
  8. World Health Organization. Cardiovascular diseases (CVDs) fact sheet. Accessed October 30, 2017.



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