Although mortality rates from coronary heart disease in the western countries have declined in the last few decades, morbidity caused by this disease is increasing and a substantial number of patients still suffer acute coronary syndrome (ACS) and sudden cardiac death. Acute coronary syndrome occurs as a result of myocardial ischaemia and its manifestations include acute myocardial infarction and unstable angina. Culprit plaque morphology in these patients varies from thrombosis with or without coronary occlusion to sudden narrowing of the lumen from intraplaque haemorrhage. The coronary artery plaque morphologies primarily responsible for thrombosis are plaque rupture, and plaque erosion, with plaque rupture being the most common cause of acute myocardial infarction, especially in men. Autopsy data demonstrate that women <50 years of age more frequently have erosion, whereas in older women, the frequency of rupture increases with each decade. Ruptured plaques are associated with positive (expansive) remodelling and characterized by a large necrotic core and a thin fibrous cap that is disrupted and infiltrated by foamy macrophages. Plaque erosion lesions are often negatively remodelled with the plaque itself being rich in smooth muscle cells and proteoglycans with minimal to absence of inflammation. Plaque haemorrhage may expand the plaque rapidly, leading to the development of unstable angina. Plaque haemorrhage may occur from plaque rupture (fissure) or from neovascularization (angiogenesis). Atherosclerosis is now recognized as an inflammatory disease with macrophages and T-lymphocytes playing a dominant role. Recently at least two subtypes of macrophages have been identified. M1 is a pro-inflammatory macrophage while M2 seems to play a role in dampening inflammation and promoting tissue repair. A third type of macrophage, termed by us as haemoglobin associated macrophage or M(Hb) which is observed at site of haemorrhage also can be demonstrated in human atherosclerosis. In order to further our understanding of the specific biological events which trigger plaque instability and as well as to monitor the effects of novel anti-atherosclerotic therapies newer imaging modalities in vivo are needed.

Update on acute coronary syndromes: the pathologists' view

The primary cause of cardiac morbidity and mortality in developed countries is ischemic (coronary) heart disease. The incidence of this disease is virtually all due to atherosclerosis, and ischemic heart disease is also the most prevalent disease in the industrialized world, causing over 40% of all deaths in the United States and Western Europe. In Japan, the incidence of ischemic heart disease due to coronary atherosclerosis is gradually increasing as well. Compared with the classical nomenclature of atherosclerosis; that is, fatty streak, fibrous plaque and complicated lesions, the term Stary's classification has been universally accepted because it reflects the more recently acquired knowledge about the morphological and biochemical details of the processes in coronary atherosclerosis, which have been obtained by new strategies such as angioscopy, intravascular ultrasound and molecular biological methods. The term Stary's classification has been applied for the coronary atherosclerosis of patients with acute coronary syndrome at the National Cardiovascular Center, for the analysis of predisposing atherosclerosis of these patients. The recent findings regarding acute coronary syndrome resulting from a rupture of coronary atherosclerotic plaques indicate that this syndrome is probably the most important mechanism underlying the sudden onset. It has been found that the risk of plaque rupture may depend more on plaque composition than on plaque size. Plaques rich in soft extracellular lipids and macrophages are possibly more vulnerable to plaque rupture. Two of the goals of the present review are to clarify how plaque disruption occurs and to elucidate the relationship between plaque disruption and coronary risk factors in elderly Japanese patients with acute coronary syndrome. Coronary stents have been shown to be efficacious in the treatment of acute and threatened closure complicating percutaneous transluminal coronary angioplasty (PTCA) and have produced encouraging initial results in the prevention of restenosis. In the autopsy study of restenosis after PTCA, it was observed that dense caps of collagen fibers in the adventitia in the vicinity of the disrupted internal elastic laminae were present in all of the remodeling lesions. It is suggested that remodeling, which resulted in adventitial scarring, is one of the major causative factors of restenosis after PTCA. The long-term success of stenting, however, remains limited by the occurrence of late in-stent restenosis, with an incidence of 20-42% depending on the stent design and the patient population studied. Another aim of the present review is to describe the pathological mechanism of restenosis after PTCA and/or stent replacement and, consequently, the vascular remodeling that occurs around adventitial tissue after PTCA and intimal hyperplasia that is chronically irritated by a foreign body granulomatous reaction after stenting. Finally, the results of the investigation of the effect of a tissue factor pathway inhibitor on the prevention of interventional restenosis is described.

Coronary atherosclerosis and interventions: pathological sequences and restenosis.

Several epidemiological studies have shown that the prevalence of ischemic heart disease is higher in occupational drivers than in people with other occupations. Although occupation categories can be surrogate measures for coronary risk factors, the relationships between taxi driving and severity of coronary heart disease (CHD) has not been investigated. Even more important, the contribution of risk factors to the severity of CHD in taxi drivers remains unclear. Our study tested the hypothesis that taxi driving could be associated with the severity of CHD. We also examined the relation between this occupation and risk factors and social lifestyle. We analyzed the coronary angiograms of 57 consecutive male taxi driver patients and compared them with those of 215 age-adjusted male non-taxi-driver patients. The number of diseased vessels and risk factors were compared between two groups. The prevalence of myocardial infarction and multi-vessel disease was higher in the taxi-driver patients than in the non-taxi-driver patients. The taxi-driver patients had higher prevalence of body mass index (BMI), diabetes, and smoking, higher levels of low-density lipoprotein cholesterol (LDL-C), and lower levels of apolipoprotein AI (ApoAI). Multiple logistic regression analysis showed that multi-vessel disease was associated with BMI and diabetes mellitus in taxi-driver patients. The taxi-driver patients were characterized by more extensive coronary atherosclerosis associated with higher prevalence of diabetes mellitus and obesity. These characteristics may be explained by in part their working environment.

Characteristics of Coronary Heart Disease in Japanese Taxi Drivers as Determined by Coronary Angiographic Analyses

OBJECTIVE—To analyse the prodrome of acute myocardial infarction in relation to the plaque morphology underlying the infarct.
DESIGN—A retrospective investigation of the relation between rupture and erosion of coronary atheromatous plaques and the clinical characteristics of acute myocardial infarction. The coronary arteries of 100 patients who died from acute myocardial infarction were cut transversely at 3 mm intervals. Segments with a stenosis were examined microscopically at 5 µm intervals. The clinical features of the infarction were obtained from the medical records.
RESULTS—A deep intimal rupture was encountered in 81 plaques, whereas 19 had superficial erosions only. There were no differences in the location of infarction, the incidence of hypertension, diabetes mellitus, or hyperlipidaemia, diameter stenosis of the infarcted related artery, Killip class, Forrester's haemodynamic subset, or peak creatine kinase between plaque rupture and plaque erosion groups. The presence of plaque rupture was associated with significantly greater incidences of leucocytosis, current smoking, and sudden or unstable onset of acute coronary syndrome. In patients with unstable preinfarction angina, new onset rest angina rather than worsening angina tended to develop more often in the plaque rupture group than in the plaque erosion group (p = 0.08).
CONCLUSIONS—Plaque rupture causes the sudden onset of acute myocardial infarction or unstable preinfarction angina, which may be aggravated by smoking and inflammation.


Keywords: acute coronary syndrome; plaque rupture; white blood cell; preinfarction angina

https://heart.bmj.com/content/heartjnl/83/1/64.full.pdf

Is preinfarction angina related to the presence or absence of coronary plaque rupture

A brief review of epidemiological studies on ischemic heart disease in Japan.

Histopathological study of acute myocardial infarction and pathoetiology of coronary thrombosis: A comparative study in four districts in Japan.

To clarify the patho-etiologic factors of Japanese myocardial infarction, a comparative pathological study of myocardial infarction in the Osaka, Akita, Wakayama, and Hokkaido districts, and an extensive histopathological study of 94 autopsy cases with acute myocardial infarct (AMI) in less than 4 weeks at Osaka were carried out. Although AMI in Akita was highly complicated by hypertension, AMI in Osaka was associated with a history of diabetes mellitus and hypercholesterolemia, especially in the young generation (under 59 years of age); hypercholesterolemia was related to the occurrence of AMI. Moreover, in spite of increases in transmural myocardial infarct (TMI) in Osaka, Hokkaido and Wakayama, Akita showed an equal ratio of TMI and subendcardial myocardial infarct. In AMI in Osaka, significant stenosis (more than 75% stenosis) of the coronary artery was of the same grade between the proximal and distal portions in the epicardial coronary artery. AMI in Akita, however, showed more severe stenosis in the proximal than the distal portion. A high incidence (88.3%) of thrombosis formation corresponding to the site of infarction was observed in AMI in Osaka. Moreover, ruptured atheromatous plaques were identified as being responsible for 62.6% of the coronary thrombosis cases, and a high incidence (70.0%) of foamy cell infiltration was disclosed. Thus, it can be concluded that ruptured atheromatous plaque is a major factor in the progression of coronary atherosclerosis and/or thrombosis, which might be due to the process of plaque softening.

Histopathological study of acute myocardial infarction and pathoetiology of coronary thrombosis: a comparative study in four districts in Japan

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Histopathological study of acute myocardial infarction and pathoetiology of coronary thrombosis: A comparative study in four districts in Japan.

Histopathological study of acute myocardial infarction and pathoetiology of coronary thrombosis: a comparative study in four districts in Japan