1/4. Complete rupture of the posterior papillary muscle caused by late reperfusion for acute myocardial infarction.We describe a patient with acute mitral regurgitation due to complete rupture of the papillary muscle immediately after successful late reperfusion for inferior myocardial infarction. An 81-year-old woman was admitted complaining of mild chest discomfort. Although the electrocardiograms, biochemical test results, and her clinical history showed that several days had passed since the onset of acute myocardial infarction, a late coronary stenting was performed. Immediately after successful stenting, she suddenly developed acute pulmonary edema, leading to cardiogenic shock. In addition to high pulmonary capillary wedge pressure (mean 35 mmHg), color Doppler imaging revealed massive mitral regurgitation caused by complete rupture of the posterior papillary muscle. Emergent mitral valve replacement with a prosthetic valve was performed, saving the patient. Hence, late reperfusion should be considered carefully when treating a patient with a high risk, such as an elderly patient or a patient with single-vessel disease or initial transmural myocardial infarction.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
2/4. Clinicopathological study of myocardial infarction with normal or nearly normal extracardiac coronary arteries. Quantitative analysis of contraction band necrosis, coagulation necrosis, hemorrhage, and infarct size.In order to clarify the pathogenesis of acute myocardial infarction (MI) in hearts with normal coronary arteries, infarct size, and the extent of contraction band necrosis (CBN), coagulation necrosis, and hemorrhage were quantitatively examined using an image analyzer in 5 autopsy cases of MI with normal or nearly normal extracardiac coronary arteries. One patient died 40 h after acute MI. A second patient with acute MI due to severe spasm of segment 6, confirmed by cineangiography, died three days later. The third patient had already suffered a subarachnoid hemorrhage, and died 10 h after the onset of acute MI. The fourth patient had aortic stenosis and regurgitation. She developed acute MI due to total occlusion of segment 6, confirmed by cineangiography 4 h after the onset, and died 61 days later. autopsy revealed old anteroseptal MI with normal coronary arteries and valvular thrombi. The fifth patient had a malignancy, and died one day after the onset of acute MI. autopsy revealed multiple occlusive thrombi in the small intramural coronary arteries of the left ventricular wall supplied by segment 14, without any stenosis in the feeding vessel. Most infarcts were localized in the territory supplied by 1 or 2 of the 3 epicardial coronary arteries, and coincided with the clinically diagnosed infarct site. The infarct size ranged from 3%-26% of the left ventricular wall, and infarcts were generally localized to the inner third of the wall (67 /- 20%). Histological examination of the four patients with acute MI revealed diffuse CBN (86 /- 14% of the infarcted area) and/or hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
3/4. Acute myocardial infarction shortly after negative exercise test and reperfusion by intracoronary thrombolysis.A 67-year-old man developed an acute myocardial infarction shortly after normal exercise testing. His clinical history and findings from emergency coronary arteriography suggested that coronary artery spasm followed by intraluminal thrombosis might have been responsible for the myocardial infarction. Although intracoronary thrombolysis two hours after the onset of chest pain provided continued patency of an occluded vessel, serial myocardial perfusion scintigraphies documented myocardial injury, which was probably induced by reperfusion, rather than myocardial salvage.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
4/4. Rapid reversal of no-reflow using Abciximab after coronary device intervention.The no-reflow phenomenon is a reduction in epicardial coronary artery blood flow without mechanical vessel obstruction. Early descriptions of this syndrome involved reperfusion after myocardial infarction. More recently, the no-reflow phenomenon has been recognized after brief ischemic times associated with coronary interventions. It is clearly a negative prognostic indicator. The proposed mechanism is multi-factorial and may involve small vessel vasospasm and potentially platelet-mediated loss of capillary autoregulation. Because of the potential role of platelets in the genesis of the no-reflow state, we administered Abciximab to two patients with no-reflow phenomenon following catheter interventions. In both of these settings, rapid distal runoff was reestablished within minutes after treatment with the platelet glycoprotein 2B/3A inhibitor.- - - - - - - - - - ranking = 2keywords = vessel (Clic here for more details about this article) |