Palabras del cardiólogo Luis De la Fuente en el Journal of Invasive Cardiology

Publicado en el Journal of Invasive Cardiology, año 2002 Luis de la Fuente: As one of the oldest cardiologists here, I have enjoyed hearing so much of the history of Interventional Cardiology this morning. Most of the treatment modalities for cardiogenic shock have already been discussed today and I also absolutely agree that the patient in cardiogenic shock must be treated as soon as possible to open the occluded artery in the case of an acute myocardial infarction. I would like to comment on how we see cardiogenic shock from the South. First of all, allow me to review some history that may explain why we don't see as much cardiogenic shock in Argentina. With Favaloro, going back to 1969, we were convinced that myocardial revascularization was a very good procedure to improve blood flow to the ischemic heart, and the problem for us from then on would be the treatment of the acute coronary syndromes, especially the acute myocardial infarction and its complications. When we returned to Argentina from the U.S. in January 1970, we performed the first coronary angiography without any complications in 5 patients with acute myocardial infarction showing that this procedure was safe and feasible. In 1971, Favaloro wrote a book on myocardial revascularization and he said that one day acute myocardial infarction would be treated the same way that we were treating a “dead leg” — that is, given oxygenated blood to the infarcted area. However, at that time there was a good deal of pathological work in animals, primarily in dogs, showing that if oxygenated blood was given to an acute myocardial infarction area in the first hours, you would transform an anemic infarction into an hemorrhagic one and it would be very deleterious. We did not agree with this concept. On the contrary, we thought that monkey hearts would be more like our hearts. In 1972, we conducted studies in monkeys, ligating the left anterior descending artery and releasing the ligature after 6 hours and we could prove by left ventricular cineangiography that the left ventricular function improved dramatically after we released the ligature. Our studies showed that if we could revascularize the infarcted area in the first 6 hours, we could diminish the size of the infarct. From then on we started doing bypass surgery in acute myocardial infarction. Our work was presented at the American College of Cardiology meetings and was seen with enthusiasm by some doctors and with a lot of skepticism and criticism by others. We were invited to publish our experience, but our manuscripts were rejected by the reviewers, saying that the coronary and left ventriculogram pre and post were beautiful but that we were crazy. This is enough for the history. Years went by and physicians in Argentina gradually became educated on what to do when a patient with an acute myocardial infarction develops angina pectoris and/or continue to have ischemic changes either by EKG or Holter. It became evident that these patients could have an extension of the infarct or a new infarct in a different territory and they should be studied by angiography immediately. They also learned that in about 40% of the patients the first manifestation of coronary artery disease is an acute myocardial infarction or sudden death. If a patient has angina pectoris or others signs and/or symptoms of myocardial ischemia he has a real advantage because he can consult his cardiologist before any serious event. We stressed to the cardiologist that when a patient has an infarcted ventricular mass of near 40% he will go into cardiogenic shock and his prognosis will be very poor. We also told them that a patient with single vessel disease does not always have a relatively good prognosis. It is very important to know, not only the severity of the lesion and type of plaque, but also the location, the size of the artery and the absence or presence of adequate collateral circulation. A large left anterior descending artery can irrigate up to 33% of the left ventricular mass, very close to the 38-40% necessary to produce a cardiogenic shock. In our experience with acute myocardial infarction complicated by a severe mitral regurgitation produced by the rupture of the posterior papillary muscle, close to 25% of this patients had either a very large superdominant right coronary or circumflex arteries. These patients can also go in cardiogenic shock. In conclusion, I would say that the best treatment for cardiogenic shock is its prevention. Perhaps that is why, in Argentina, we currently don't see many patients in cardiogenic shock. However when we do see a patient with acute myocardial infarction in true cardiogenic shock we act more or less in the same way that Dr. Shawl has outlined. We also agree that there must be an cardiac interventionist on call 24 hours a day.