How does a physician treat a heart attack where the blood flow to the heart muscle is suddenly cut off by a blocked artery? In the most severe cases, the ST segments on the ECG are elevated, signalling that a major part of the heart muscle is at risk. It’s called a STEMI (ST-Elevated Myocardial Infarction). And, if you subscribe to the concept that the heart and circulation are like the plumbing in your house, like Dr. Charles Dotter did (he invented the concept of angioplasty and, in his offbeat humorous way, he used the graphic to the left as his logo), then you would assume there are two major ways to treat the problem: use Drano to dissolve the blockage or use a mechanical roto-rooter to clear it out.
In a way, that’s the big question I discussed in my previous post which was a critique of Dr. Nortin Hadler’s article, “The End of the Era of Coronary Angioplasty.” Briefly, Dr. Hadler opines that angioplasty is seldom necessary in STEMI cases because lytic agents, a.k.a. “clot-busters,” can effectively dissolve the blood clot that is causing the blockage; in other words, use Drano. But, while clot-busters certainly have their place, especially in situations where the patient is very far from a PCI-capable hospital, the gold standard for the treatment of STEMI remains angioplasty, or primary percutaneous coronary intervention, or pPCI, or the “roto-rooter.”
Several readers sent in questions and comments to my previous post, looking for data supporting my assertion that pPCI is superior, assuming a patient can be revascularized within an hour or two. In order to keep that article to a manageable length, I had decided not to get into quoting the studies that have been done over the past decade-plus that have shown a clear benefit for pPCI, and I probably should have! Most clinicians in the field know these well.
One of the most important studies was published in Circulation in 2003: the DANAMI-2 study which is even mentioned by Dr. Hadler in his article. Interestingly, however, Hadler doesn’t footnote it, perhaps because, if you read the study, you’d have seen that in a cohort of 1,572 patients, the primary endpoint of reinfarction, stroke or death at 30 days was reached in 8.5% of the patients in the angioplasty group, as compared with 14.2% in the fibrinolysis group, a very significant difference. This difference held at the 8-year followup analysis: roto-rooter was better than Drano!
Dr. Hadler dismisses the DANAMI-2 study, saying that it was biased against lytic therapy because the more stable the patient the more likely they were to be transferred expeditiously. The only problem with his point is that the most critical patients specifically were excluded from DANAMI-2 for that very reason. Moreover, the DANAMI-2 trial was stopped prematurely on ethical grounds because the interim results showed such a clear benefit for angioplasty — in other words, it was judged unethical to continue randomizing patients to lytic therapy when pPCI had shown such a pronounced benefit. So Dr. Hadler’s call for a randomized controlled trial seems uninformed by the known data. And there have been other trials, almost all of which have mirrored these results.
Additionally, the DANAMI-2 trial enrolled patients during the early era of pPCI, from 1997-2001. Transport, procedural and pharmacologic pPCI therapies have advanced significantly since then; most likely the mortality benefit of pPCI is underestimated by DANAMI-2.
A final point is that, as with all medical issues, it’s not either-or. It’s not pPCI vs. fibrinolytic therapy. The two are both strategies and in specific locales, patient populations, length of time since symptom onset, etc., etc., etc. both should be considered or combined. The state of Minnesota, for example, has a very advanced helicopter transfer protocol for STEMI patients. And whether or not they use “clot-busters’ totally depends on how far away the patient is from the PCI-capable hospital.
So…can’t we all just get along?