The History of Coronary Angioplasty
It’s hard to believe but true. When I finished medical school in 1980 we as physicians still did not know what caused myocardial infarctions. It was the classic chicken and the egg question. Autopsies showed some people had clots in their heart arteries and some did not. Some people believed that the clots caused the myocardial infarctions and some people believed that the myocardial infarctions caused the clots.
It took a groundbreaking study by Dr. Marcus DeWood of Seattle and published in the N Engl J Med 1980 Oct 16;303(16):897-902 to solve the problem. He catheterized 322 patients within 24 hours of their infarction. Although that doesn’t sound so groundbreaking now, when he did it this was unheard of. Many of these people were very sick and there was nothing that could be done for them. Angioplasty was developed but not in widespread use and thrombolytic therapy was not yet known. Many of the patients were taken to emergency surgery for reperfusion.
Let me digress for a minute. I will relate a story that Dr Andreas Gruentzig the man who invented coronary angioplasty related to me. I was in a cath lab at Emory University with Dr. John Douglas, who is one of the Grand Masters of angioplasty. We were doing an angioplasty in a cath room because someone who was having a cath closed his artery on the table. This was not an infrequent occurrence in the early days of cath. As this was the “wrong” room Dr. Gruentzig poked his head in to see what was going on. When he came into the room he saw what was going on and told us this story.
Although history states that the first coronary angioplasty was done in Zurich Switzerland in September of 1977, the first angioplasty in a human occurred prior to that. It was in just such a case that a patient closed his left anterior descending artery after a cath and his colleagues called upstairs for him to “bring down his balloons.” He did and he opened the artery successfully. This was the first reperfusion therapy by balloon in history. Dr Gruentzig then told his colleagues not to stop the heparin, a blood thinner that we used at the time. They of course did not listen and soon after the artery closed again and the patient went to emergency surgery. Laughing 6 years later, he warned us not to stop the heparin and walked out of the room. It is so vivid to me because it was the last time I saw him. He died in a private plane crash 2 days later at the age of 46.
DeWood found that in 110 of 126 patients in the first four hours of a heart attack had a complete occlusion of the heart artery and that this percentage decreased the longer past four hours someone went. This was the answer as to why the autopsies sometimes showed clot in the artery and sometimes did not. The autopsies were never correlated to the length of time after the symptoms of heart attack started.
Next…what we are still learning.
Tags: Angioplasty, Myocardial Infarction
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January 5th, 2010 at 7:31 pm
[...] A recent blog discussed the fact that clots cause myocardial syndromes. Stable clots induce STEMI and unstable or waxing and waning clots cause ACS or acute coronary syndrome. The differences between the unstable and stable clots are not fully understood but much of the difference is due to platelet activation and much of that activation is due to smoking.The question has now become why do the clots form? What does the inside of the artery look like and can these changes be predicted and prevented. I have blogged before that a large portion perhaps up to 40% of myocardial infarctions is not caused by severely diseased arteries. What I mean is the extent of blockage in these arteries is less than 50% of the lumen. It was believed that the arteries in the less severe disease states suffered from edge “cracking”. When the normal artery meets the abnormal plaque a fragile zone is created and under the right circumstances ruptures. This micro crack exposes the blood to abnormal components and the clotting cascade starts. [...]
June 1st, 2010 at 6:57 am
You post great articles. Bookmarked !