早期靜脈注射貝它阻斷劑可能對急性心肌梗塞有害


  March 15, 2005(奧蘭多)-根據發表於美國心臟學會(ACC)2005年會中發表的The Clopidogrel and Metoprolol Infarction Trial Second Chinese Cardiac Study(COMMIT/CCS-2)試驗結果發現,以靜脈注射metoprolol接著口服metoprolol,並不如預期中的是「無疑的獲勝者」,而且可能事實上對許多病患來說是項風險。
  
  英國牛津大學臨床試驗中心主任之一的Rory Collins醫師表示,IV貝它阻斷劑接著口服貝它阻斷劑確實可以降低早期再梗塞的風險,但是也會增加心因性休克的風險,這個風險抹消了任何其他的好處;Collins醫師於臨床試驗座談中發表COMMIT/CCS-2試驗結果,並且在ACC記者會中討論這些發現。
  
  在這項試驗中,metoprolol可以降低每1000位接受治療病患中5位的院內再梗塞絕對風險(P=.001),以及每1000位接受治療病患中,6位發生心室顫動的風險(P<.001);但是這項治療卻會增加1000位病患中,11位發生心因性休克的風險(P<.00001)。
  
  高風險病患,特別是心臟衰竭或是低血壓病患,是心因性休克的高危險群,而接受血栓溶解療法的低風險病患會因為這個療法而受益;因此,Collins醫師表示,這項療法應該用來針對那些低風險病患。
  
  Collins醫師向Medscape表示,在急性心肌梗塞時使用貝它阻斷劑已經被質疑許多年,但是少數試驗數據持續這個爭論;相反的,COMMIT試驗隨機分派了22,927位病患接受Mmetoprolol,而22,922位病患接受安慰劑;他表示,有這樣大規模的試驗數據,我們現在具有關於這個作用的證據。
  
  麻州波士頓哈佛醫學院助理教授Christopher Cannon醫師表示,COMMIT/CCS-2試驗結果對處理急性心肌梗塞有很大的貢獻。
  
  但是Cannon醫師附帶表示,以metoprolol來說,我認為我們已經學到如何適當使用這類「應該已經是證據充足的」藥物,而且我認為新的試驗數據可以幫助我們降低這些病患的風險,而且使適合的病患因此獲益;Cannon醫師是Collins醫師發表COMMIT/CCS-2試驗結果臨床試驗座談中的共同主席,同時也是這項研究的討論專家。
  
  然而,Cannon醫師表示,這項試驗結果是出乎意料的,早期的試驗結果顯示,靜脈注射貝它阻斷劑的療程是有益的。

Early IV Beta Blockade May Be<

By Peggy Peck
Medscape Medical News

March 15, 2005 (Orlando) — The Clopidogrel and Metoprolol Infarction Trial Second Chinese Cardiac Study (COMMIT/CCS-2) found that beta blockade with intravenous (IV) metoprolol followed by oral metoprolol is not the "sure winner" that many expected, and may in fact be risky in a significant number of patients, according to results reported here at the American College of Cardiology (ACC) 2005 Annual Scientific Session.

Rory Collins, MD, codirector of the clinical trials unit at Oxford University in the U.K., said that while IV beta blockade followed by oral metoprolol does reduce the risk of early reinfarction, it also increases the risk of cardiogenic shock, "which wipes out any benefit." Dr. Collins presented the COMMIT/CCS-2 findings at a late-breaking clinical trials session and discussed them during an ACC press conference.

In the study, metoprolol reduced the absolute risk of in-hospital reinfarction by five cases per 1,000 treated (P = .001) and ventricular fibrillation was reduced by six cases per 1,000 treated (P < .001). "But it increased the risk of cardiogenic shock by 11 cases per 1,000 (P < .00001)," Dr. Collins said.

Higher-risk patients, typically those with heart failure or hypotension, were most at risk for cardiogenic shock, while low-risk patients who had undergone thrombolytic therapy benefited from the treatment. "Therefore, the treatment should be targeted to those patients presenting with a lower-risk profile," Dr. Collins said.

The use of beta blockade during acute MI has been hotly debated for several years, but there have been few data to sustain the argument, Dr. Collins told Medscape. By contrast, COMMIT randomized 22,927 patients to metoprolol and 22, 922 to placebo. "With numbers this large, we now have very clear evidence about the effects," he said.

Christopher Cannon, MD, an associate professor at Harvard Medical School in Boston, Massachusetts, noted that the COMMIT/CCS-2 findings make a "significant contribution to the management of acute myocardial infarction."

But Dr. Cannon added that in terms of metoprolol, "I think we've learned the appropriate use of this previously 'ought-to-be-established' class, and I think the new data will help avoid any excess risk in these patients and allow appropriate benefit in patients who can derive it." He cochaired the late-breaking clinical trials session at which Dr. Collins presented the COMMIT/CCS results, and he served as discussant for the paper.

Dr. Cannon, however, characterized the results as unexpected, noting that earlier studies suggested an advantage for the IV beta blockade regimen.

ACC 2005 Annual Scientific Session. Late-breaking clinical trials. Presented March 9, 2005.

Reviewed by Gary D. Vogin, MD

    
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