Considerable Time From the Onset of Plaque Rupture and/or Thrombi Until the Onset of Acute Myocardial Infarction in Humans: Coronary Angiographic Findings Within 1 Week Before the Onset of Infarction

BackgroundIt has been thought that the thrombi and bleeding in plaques that occur after plaque rupture or endothelial damage from vessels with mild stenosis suddenly occlude the lumen and cause acute myocardial infarction (AMI). However, our hypothesis is that thrombi and bleeding may not suddenly occlude the lumen. Methods and ResultsThe study group consisted of 20 patients who had coronary angiograms performed within 1 week (3±3 days) before AMI and 20 control patients who had coronary angiograms performed 6 to 18 months (282±49 days) before AMI. The features of infarct-related coronary segments (IRCS) at 3 days before AMI were the presence of a significant stenosis of >50% (95% in incidence and 71±12% diameter stenosis) and Ambrose’s type II eccentric lesions (plus multiple irregularities), an indicator of plaque rupture and/or thrombi (60% [70%]), and the features at 1 year before AMI were mild stenosis of <50% (95% incidence and 30±18% diameter stenosis) with rare Ambrose’s type II eccentric lesions (plus multiple irregularities) (10% [10%]). The same relation was observed in each of the 4 subgroups with Q-wave infarction, non–Q-wave infarction, preceding effort angina within 1 month before AMI, and no preceding effort angina. ConclusionsThe appearance of marked progression and Ambrose’s type II eccentric lesion on coronary angiograms 3 days before AMI suggests the presence of a considerable time from the onset of plaque rupture and/or thrombi until the onset of AMI. These features may be predictors of AMI. The concept provides new insight into the mechanism and prevention of human AMIs.

[1]  T Suzuki,et al.  Process of progression of coronary artery lesions from mild or moderate stenosis to moderate or severe stenosis: A study based on four serial coronary arteriograms per year. , 1999, Circulation.

[2]  R. Califf,et al.  Relationship between delay in performing direct coronary angioplasty and early clinical outcome in patients with acute myocardial infarction: results from the global use of strategies to open occluded arteries in Acute Coronary Syndromes (GUSTO-IIb) trial. , 1999, Circulation.

[3]  R. Katori,et al.  Short-Acting Nifedipine and Diltiazem Do Not Reduce the Incidence of Cardiac Events in Patients With Healed Myocardial Infarction , 1997 .

[4]  T. Sakamoto,et al.  Serial changes of plasma plasminogen activator inhibitor activity in acute myocardial infarction: difference between thrombolytic therapy and direct coronary angioplasty. , 1995, American heart journal.

[5]  R. Califf,et al.  Noninvasive assessment of speed and stability of infarct-related artery reperfusion: results of the GUSTO ST segment monitoring study. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries. , 1995, Journal of the American College of Cardiology.

[6]  L. Shaw,et al.  Early and 1-year clinical outcome of patients' evolving non-Q-wave versus Q-wave myocardial infarction after thrombolysis. Results from The TIMI II Study. , 1995, Circulation.

[7]  S. Hosoda,et al.  Factors governing re-infarction in patients with myocardial infarction in Japan. , 1995, Japanese circulation journal.

[8]  S. Hosoda,et al.  Follow-up of 2,733 Japanese patients with myocardial infarction. , 1995, Japanese circulation journal.

[9]  K. Kanmatsuse,et al.  Thrombolytic therapy for acute myocardial infarction-effects, problems and strategies. , 1994, Japanese circulation journal.

[10]  H. Kennedy,et al.  Morphological and quantitative angiographic analyses of progression of coronary stenoses. A comparison of Q-wave and non-Q-wave myocardial infarction. , 1994, Circulation.

[11]  J. O’Keefe,et al.  Primary coronary angioplasty for acute myocardial infarction (the Primary Angioplasty Registry). , 1994, The American journal of cardiology.

[12]  M. Gotsman,et al.  Angiographic findings in the coronary arteries after thrombolysis in acute myocardial infarction. , 1992, The American journal of cardiology.

[13]  M. Fujita,et al.  Significance of preinfarction angina for preservation of left ventricular function in acute myocardial infarction. , 1992, American heart journal.

[14]  B Meier,et al.  Relation of the site of acute myocardial infarction to the most severe coronary arterial stenosis at prior angiography. , 1992, The American journal of cardiology.

[15]  F. Van de Werf,et al.  Angiographic assessment of the infarct-related residual coronary stenosis after spontaneous or therapeutic thrombolysis. , 1990, Journal of the American College of Cardiology.

[16]  K. Lee,et al.  Relationship between antecedent angina pectoris and short-term prognosis after thrombolytic therapy for acute myocardial infarction. Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group. , 1990, American heart journal.

[17]  W. Santamore,et al.  Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease? , 1988, Circulation.

[18]  V. Fuster,et al.  Angiographic progression of coronary artery disease and the development of myocardial infarction. , 1988, Journal of the American College of Cardiology.

[19]  R. W. Brower,et al.  Effect of continued rt-PA administration on the residual stenosis after initially successful recanalization in acute myocardial infarction--a quantitative coronary angiography study of a randomized trial. , 1987, European heart journal.

[20]  V. Fuster,et al.  Angiographic evolution of coronary artery morphology in unstable angina. , 1986, Journal of the American College of Cardiology.

[21]  M J Davies,et al.  Plaque fissuring--the cause of acute myocardial infarction, sudden ischaemic death, and crescendo angina. , 1985, British heart journal.

[22]  Louis E. Teichholz,et al.  Angiographie morphology and the pathogenesis of unstable angina pectoris , 1985 .

[23]  E. Falk Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis. Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi. , 1983, British heart journal.

[24]  A. Hutter,et al.  The incidence and pattern of angina prior to acute myocardial infarction: a study of 577 cases. , 1979, American heart journal.

[25]  M. Stowers,et al.  Warning symptoms before major myocardial infarction. , 1970, British heart journal.

[26]  T. Killip,et al.  Prodromata in Acute Myocardial Infarction , 1969 .

[27]  K. Simon,et al.  Early and 1-year clinical outcome of patients evolving non-Q-wave versus Q-wave myocardial infarction after thrombolysis: results from the TIMI II study. , 1995, Circulation.

[28]  放射線影響研究所 Technical report series , 1989 .

[29]  S L Winters,et al.  Angiographic morphology and the pathogenesis of unstable angina pectoris. , 1985, Journal of the American College of Cardiology.

[30]  H. S. Mueller,et al.  The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. , 1985, The New England journal of medicine.

[31]  HYPERTENSION and coronary heart disease: classification and criteria for epidemiological studies. , 1959, World Health Organization technical report series.

[32]  H. J. Smith,et al.  The prodromal symptoms of myocardial infarction. , 1954, Journal. Iowa State Medical Society.