Blog Archives

December 16th, 2009

FDA Advisers Recommend Expanding Crestor to Patients Without High Cholesterol

An FDA advisory panel voted 12 to 4 on Tuesday to expand the use of rosuvastatin (Crestor) to patients with normal cholesterol levels and no history of cardiac disease, according to the Associated Press.

The panel’s recommendation was based on last year’s JUPITER trial, in which rosuvastatin cut cardiovascular risk in patients with normal LDL cholesterol but high C-reactive protein levels.

The manufacturer said it “would focus on marketing the drug to patients with health issues that put them at increased risk of heart problems, such as a smoking habit or family history of hypertension,” the AP reports.

The FDA is expected to make its decision in early 2010.

December 9th, 2009

Bleeding With PCI: We’re Making The Problem Worse

In a recent editorial regarding the management of ACS patients, we emphasized the importance of early risk stratification to identify patients who would most benefit (or not benefit) from intensive antithrombotic therapy or an invasive cardiac procedure. 

However, a recently published study reported that 22% of dialysis patients  undergoing PCI received an antithrombotic agent (enoxaparin or eptifibatide) that was contraindicated in individuals with renal disease.  Not surprisingly, the use of these agents was associated with an increased risk of major bleeding and death. 

As inverventionalists, do we know how to assess (and minimize) bleeding risks in our PCI patients? 

December 7th, 2009

Dabigatran vs Warfarin: War or Peace?

CardioExchange Editors: Given the results of both your RE-COVER study and the recently published RE-LY study, should anybody still be using warfarin?

Goldhaber: Warfarin is not going to fade away into oblivion.  Anyone currently stable on warfarin has little reason to abandon this time-tested drug.  If once monthly INRs are usually in the therapeutic range, and if there have been no bleeding or clotting complications, why “rock the boat”?  By the way, warfarin’s fighting back.  It’s been around since 1954, so we know all of its potential complications.  And it’s inexpensive.  With a large ongoing NHLBI trial to test rapid turnaround genetic testing to prescribe a more precise starting dose of warfarin, and with (mostly) insurance-reimbursed point-of-care fingerstick self-testing of INR, effective prescription of warfarin is more widespread now than ever before.  Keep in mind that nurse and pharmacist-run Anticoagulation Clinics have also enhanced the safety and efficacy of warfarin prescription. Finally, dabigatran has not been tested in important thrombotic conditions such as for prophylaxis against venous thromboembolism during hospitalization for medical illness or for prevention of thrombosis with mechanical prosthetic heart valves.  At the moment, dabigatran is not FDA approved for any condition in the United States.  And nowhere has it yet received regulatory approval for stroke prevention in atrial fibrillation or for treatment (along with a required initial course of low molecular weight heparin or fondaparinux) for acute venous thromboembolism.

CardioExchange Editors: If it were to receive FDA approval, what situations would you consider to be prohibitive for dabigatran?

Goldhaber:
Very few.  Inability to comply with a twice daily medication.  Renal failure.  Gastric discomfort not alleviated by taking dabigatran with food.  Keep in mind that a small minority of patients (3%) suffers excruciating gastric discomfort.  They can’t tolerate dabigatran and should use warfarin.  Contraindications also include any active bleeding condition or bleeding predisposition that would ordinarily prohibit use of warfarin.

CardioExchange Editors:
Given that very few patients in RE-COVER had even mild renal dysfunction, how cautious do you think we should be in situations where the creatinine clearance is above 30 but below 50 ml/minute, knowing that dabigatran is 80% renally excreted?

Goldhaber:
We need to be cautious using dabigatran in patients with chronic kidney disease, especially the creatinine clearance might drift down below 30 ml/minute.  Major bleeding is an ominous prognostic sign for patients with either arterial or venous thrombotic illness.  Patients with renal failure (creatinine clearance <30 ml/minute) should use warfarin, which is metabolized by the liver, not the kidney.

CardioExchange Editors:
Although the difference was not statistically significant, people with a prior VTE appeared to do better on warfarin versus dabigatran in RE-COVER.  Why might this be the case?

Goldhaber:
It has been long observed by “blood clot docs” that patients who are established on warfarin and clinically stable have much better control of the INR and far fewer problems than “warfarin naïve” patients.  So, I’d expect that these patients already taking warfarin are, in a sense, pre-selected to do well.  All the kinks of anticoagulation have been pretty much been worked out for them.

Comments are closed on this post, but please join the conversation at our Dabigatran Resource Round-Up.

December 4th, 2009

The Final CMS Rule Is Flawed

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The Centers for Medicare and Medicaid Services (CMS) Final Rule on the cardiology fee schedule (download the entire 450-page document here) is an ill-conceived policy change that will drastically affect the practice of cardiology in the United States. Relying on limited, unrepresentative data from the Physician Practice Information survey (PPIS) done by the AMA, the CMS determined that the cost of delivering care in a cardiology practice (the practice expense) went down by 40% in the last three years. Those of you involved in managing practices know that costs haven’t dropped at all — in fact, they have typically risen by several percentage points each year. A 40% drop is totally out of touch with reality.

As you might imagine, these alleged drops in practice expense have affected the formula by which RVU reimbursement is calculated. This leads to very significant cuts in scheduled payments to cardiology practices, especially those with large imaging practices (particularly the 36% cut in nuclear imaging). In our own practice, the projected impact in 2010 will be a 12% reduction in Medicare revenue as well as reduced reimbursement by all payers with contracts tied to the resource-based relative value scale (RBRVS). (The ACC offers a Practice Impact Calculator to help you determine how these cuts will affect your practice.) These reductions will continue over the next four years, and that does not include the additional 21.2% cut in physician payments mandated under the sustainable growth rate (SGR) formula.

Our practice will need to make significant program and service cuts to preserve our viability. Many practices in the country will be similarly hurt. If imaging shifts to the hospitals, costs will rise significantly, because in 2010, planned Medicare reimbursement to hospitals for these studies is nearly triple the rates set for physician practices.

The ACC has provided excellent leadership on this issue, advocating in Washington for all cardiologists. Their efforts have stimulated a strong grass roots movement and may have been responsible for spreading the impact of these cuts over the next four years. Still, the ACC is unsatisfied with this result and is fighting hard for further reversals of this misguided CMS policy. Without question, this change will affect access and service for our patients needing quality cardiac care. I hope that you’ll agree with me and with the ACC about this rule. Whatever your thoughts, I strongly encourage you to do two things: write your representative in congress and share your thoughts below with the CardioExchange community.

December 3rd, 2009

Sensitive Troponin Assay: Who Needs It? Not Me!

Sensitive assays for troponin (see here and here) improve early diagnosis of acute myocardial infarction and risk stratification.  However, according to a recent NEJM study, sensitive assays detect low circulating levels of cardiac troponin in the great majority (98%) of patients who have stable coronary artery disease and preserved LV systolic function.
 
In many emergency departments, serum troponin levels are part of the routine “screening labs.” Not uncommonly, elevated levels are found in patients without ACS, which leads to unnecessary admissions, cardiac evaluations, and procedures. Indiscriminant use of sensitive assays for troponin will only exacerbate this problem.
 
Do I really need (or want) access to a more sensitive assay for troponin?  I’m not convinced. It may be more harmful than helpful to the patient and physician.

December 2nd, 2009

Cardiology in the Big Tent
Helping our fellows make the most of a national meeting

I remember the first national meetings I attended as a fellow. They were sensory overload experiences: Huge crowds, stargazing at the cardiology luminaries, preparing and overpreparing for my own talks (attended by few beyond my closest friends), staying up too late at the lobby bars.

Now, seeing this experience through the eyes of our own fellows, I’ve found that unless we provide some guidance, they don’t get as much out of the meeting as they should. We send each fellow to one national meeting a year (more, if they are presenting). Here is a version of the email we send them before the meeting:

Prepare in advance. The meeting is enormous, and if you wait to decide what to do, you will spend your day running back and forth across the conference center without learning much

Focus on full or half sessions rather than individual talks
You will usually learn more from the didactic lectures/symposia than the research talks, unless the talks are in an area of particular interest to you.
Identify one or two clinical areas in which you feel you need more depth of knowledge, or that we have not focused on sufficiently, and learn about these areas in depth

2.    Remember that this is a business trip, not a vacation

Have a great time . . . but remember that you represent the program at all times
Be an ambassador for the program
Attend as much of the meeting as possible each day

3.     You do not need to attend your own faculty’s programs

This is your opportunity to get exposure to experts outside our institution

4.     You should plan to attend your co-fellows’ presentations and poster sessions

Friendly faces make a huge difference to colleagues who are presenting

I’d be interested to know your program’s policies regarding the national meetings. How important are these meetings to the overall fellowship experience? Did you learn anything new? Was the networking valuable? Is it worth the expense to send the fellows to the big meetings, or would the money be better spent on other educational opportunities?

December 1st, 2009

New Guidelines on Perioperative Use of Beta-Blockers: POISE for a DECREASE?

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By now, there’s a good chance you’ve heard that the American College of Cardiology and the American Heart Association updated their guidelines on the perioperative use of beta-blockers in patients who undergo noncardiac surgery. Perhaps you’ve been thinking about the implications for practice. I certainly have, but then again I chaired the group that wrote the update, and I’d like to share my own reflections, which don’t necessarily represent the official stance of the ACC or the AHA.

The challenge in this update was to reconcile sometimes conflicting new data, most notably from the POISE and DECREASE-IV trials, to produce a clinically relevant document for guiding clinicians in this area. First, here are a few of the key points from the update:

  • Continue beta-blockers in noncardiac surgery patients who are already receiving them appropriately (class I recommendation). Discontinuation of beta-blockade is not recommended.
  • It’s reasonable to consider beta-blockers in high-risk patients (e.g., those with known coronary disease or multiple risk factors for cardiac complications) who are undergoing intermediate- or high-risk surgeries (class IIa recommendation). In general, the fewer risk factors the patient has, the less strong the case for using perioperative beta-blockade.
  • When starting beta-blockers in advance of an elective procedure, (1) allow sufficient time for titration to heart rate and blood pressure, as tolerated preoperatively and throughout the perioperative period; and (2) maintain vigilance for hypovolemia, infection, or other potential causes of tachycardia that may require adjustment, or even discontinuation, of beta-blocker therapy.
  • Routine perioperative use of beta-blockers is not recommended, particularly not fixed, higher-dose regimens started on the day of surgery.

The new guidelines support much of what I was already doing in the clinic for elective, noncardiac surgery patients who were at risk for cardiac complications: weighing the pros and cons of beta-blocker therapy, initiating it “low and slow,” and adjusting up from there. However, the POISE study further clarified that beta-blockers can be associated with risk in this clinical setting, particularly in fixed, higher-dose regimens started on the day of surgery. The onus is on us as clinicians to select patients for therapy — and monitor them — thoughtfully.

By the way, the European Society of Cardiology also recently issued its guidelines on perioperative care for patients undergoing noncardiac surgery.. The recommendations, which are worth your time to review, differ in some respects from ours (e.g., the ESC has three class I indications for beta-clockers, whereas we have only one). However, I believe that the core message to clinicians is similar: Choose patients judiciously, start therapy well in advance of elective procedures, adjust as tolerated, and monitor patients carefully.

So, let me ask, how are you using beta-blockers perioperatively in the wake of the new data? What “clinical pearls” can you share from your experiences? And what are you telling your patients about what’s changed and what hasn’t? I’m curious to hear, and undoubtedly so are your colleagues.

November 30th, 2009

Even Very Low Levels of Cardiac Troponin T Linked to Heart Failure, Cardiovascular Death

Even very low levels of cardiac troponin T are associated with increased risk for heart failure and cardiovascular death among patients with stable heart disease, according to an industry-funded study in the New England Journal of Medicine.

Using a highly sensitive assay, researchers tested for troponin T in nearly 3700 adults with stable coronary artery disease and preserved left ventricular function, and then followed them for roughly 5 years. (The assay is not commercially available.)

The test detected very low troponin T levels in nearly all subjects — levels that would have gone undetected using conventional assays, the researchers write. Even at these low concentrations, increasing troponin T was associated with elevated risk for cardiovascular death or heart failure (but not MI).

November 29th, 2009

Return to POBA?

We almost never do plain old balloon angioplasty in our place anymore. To many, that technique seems so last century. We have moved on to better procedures that have made restenosis a relatively rare occurrence.

We have even changed the name of the procedure. If an intern on rounds utters the word “angioplasty,” we quickly correct him or her, using the opportunity to teach the meaning of “percutaneous coronary intervention.”  Angioplasty, we say, derives from Greek words meaning “molding of the vessel” — whereas PCI involves more than molding, often the implantation of a stent.

The problem with stenting is that we have exchanged a higher risk of restenosis, an annoying but generally non-life-threatening event, for a lower risk of stent thrombosis, an often abrupt, often catastrophic closure of the vessel that can result in AMI and death. The stent thrombosis risk can be mitigated with dual antiplatelet therapy — aspirin and a thienopyridine — but only if the patient can purchase the pills and take them.

During the last two weeks, experiences with several of my patients who received stents for the treatment of AMI had me reflecting on our progress. As their hospitalizations came to a close, it became clear that they could not afford clopidogrel and had few options. The price of the antiplatelet drugs, in addition to the other medications their care required, represented a heavy burden for these individuals. Pharmaceutical company assistance programs require at least a month and a lot of paperwork. And cost is not the only problem; some of my patients have developed contraindications to dual antiplatelet therapy during hospitalization, putting them in an especially difficult position.

I know that one of my patients, despite all pleading and efforts to make the pills affordable, will almost certainly not buy and take them. He is an undocumented resident who has lived in our area for 14 years. He occasionally finds work as a painter and has a loving family and many friends. He has a warm smile, even though he has just survived a devastating MI with many complications — including a retroperitoneal bleed requiring multiple transfusions — which only makes our discharge instructions more difficult to give.

Would he have been better off with a POBA and the risk of restenosis? If so, could we have known that in advance?

I worry that for some patients, we have set up a dangerous situation in our attempts to do good and provide the most advanced care.

November 24th, 2009

Expand or Restrict Primary PCI?

At last week’s AHA meeting, a late breaking clinical trial reported that STEMI patients in Massachusetts who underwent primary PCI at hospitals without cardiac surgery on site had similar rates of death, MI, and target vessel revascularization at 1 year as those who underwent primary PCI at hospitals with cardiac surgery on site.  In contrast, the recently released AHA/ACC updated STEMI guidelines make the development of regional systems of STEMI care “a matter of utmost importance.”
 
Should primary PCI be limited to regional centers, or should it continue to be performed at hospitals without cardiac surgery on site to maximize access to it?