Eosinophilic coronary periarteritis (vasospastic angina and sudden death), a new type of coronary arteritis: report of seven autopsy cases and a review of the literature.

A previously reported autopsy case of eosinophilic coronary periarteritis (ECPA, or isolated eosinophilic coronary periarteritis, IECPA), and an additional six autopsy cases of ECPA are reported. In addition, another four autopsy cases of ECPA reported in the literature are discussed. Fifteen cases of ECPA with spontaneous coronary dissection (hematoma), which appeared in the literature from 1987 to 2011, are also reviewed. The characteristic clinico-pathological findings of ECPA are: (a) variant angina (Prinzmetal's vasospastic angina) appeared mainly from evening to early in the morning; (b) allergy or allergic history could be identified in only three of a total of 11 cases; (c) sudden unexpected death (sudden cardiac death) usually occurred early in the morning; (d) eosinophilic inflammation limited to the adventitia and periadventitial soft issue appeared in the epicardial large coronary arteries, chiefly in the left coronary anterior descending artery; (e) fibrinoid necrosis or granuloma could not be found in or around the inflammatory area; (f) no type of vasculitis could be found in any other tissues or organs (i.e., localized and non-systemic periarteritis); (g) ECPA was frequently accompanied by spontaneous coronary arterial dissection (SCAD) in the affected wall; and (h) ECPA without SCAD appeared mainly in men (male/female ratio was 8:3), while EPCA with SCAD appeared in almost all female cases (male/female ratio was 1:14). Although the etiology and pathogenesis are still unknown, we believe that ECPA (with or without SCAD) might be a distinct new type of coronary arteritis.

Did the widespread use of long-acting calcium antagonists decrease the occurrence of variant angina?

BACKGROUND: We have not often encountered variant angina (VA) since the use of long-acting calcium antagonists (L-CAs) became widespread. OBJECTIVES: This study examined the frequency of VA retrospectively. METHODS: and results: We diagnosed angiographically confirmed coronary spastic angina (CSA) in 349 consecutive patients using selective spasm provocation tests from January 1991 to December 2002. During this period, 3,148 diagnostic cardiac catheterizations and 1,515 selective spasm provocation tests were performed. Seventy-four of these 349 patients (21.2%) had VA. Coronary spasms were defined as transient luminal narrowings of > 99%, and VA was defined as an ST elevation during spontaneous attacks or noninvasive stress tests. We classified the 12 years of the study into four periods of 3 years each. No tendency to decrease for the ratio of the number of patients with CSA and the number of selective spasm provocation tests was observed among the four time periods (18%, 24%, 32%, and 23%, respectively). However, the number of patients with VA (28, 33, 9, and 4) and the VA/CSA ratio (32%, 28%, 14%, and 5%, respectively) in the four group significantly decreased. The frequency of administration of calcium antagonists (CAs) before hospital admission (49% vs 33%, respectively; p < 0.05) was significantly higher in the last time period (from 2000 to 2002) than in the first period (from 1991 to 1993). L-CAs were administered in > 90% of CSA patients who had been medicated with CAs before hospital admission in the last period (from 2000 to 2002), while L-CAs were administered in only 20% in the former period (from 1991 to 1993). The administration of statins and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers before hospital admission gradually increased according to the period passed, but not significantly. CONCLUSION: The frequency of VA has decreased in Japan, possibly due to the widespread use of therapy with L-CAs.

William Heberden and Myron Prinzmetal: angina pectoris.

The most significant accounts of angina pectoris appeared in the medical literature separated by nearly two centuries. They were Heberden's initial description of classic angina and Prinzmetal's report of the variant form. Angina pectoris represents a transient myocardial oxygen deficiency. It is usually related to atherosclerotic coronary artery disease, but there are a number of less common etiologies, most notably aortic stenosis. Stable and unstable forms exist, with stable angina being further subclassified as being of one of four patterns: classic, variant, atypical, and angina equivalent.

[Diagnostic criteria and classification of unstable stenocardia and lesions in the coronary bed]. / Diagnosticheskie kriterii, klassifikatsiia nestabil'noi stenokardii i porazhenie pri nei koronarnogo rusla.

A total of 128 patients with unstable angina pectoris (UAP) have been examined. Personal data of clinical examinations and the literature data enabled the authors to elaborate diagnostic criteria of UAP. Classification of UAP with consideration of its history, the clinical course of the disease and changes in the coronary arteries found with coronarography is offered. Almost half of patients with UAP begin to feel it while in perfect health. In 1/3 of cases only therapeutic treatment made the symptoms regress. It is established that UAP occurs mainly due to the changes in the system of left coronary artery. Very often stenosis of the main branch of this artery is observed.

Clinical spectrum of "unstable angina".

In order to determine the natural evolution of different clinical types of "unstable angina", 167 patients were included in a prospective study. After angiography, 11 (6.5%) were excluded because they had no significant coronary lesions. The remaining 156 were sorted into different groups according to their clinical characteristics and were followed up for a period of 24 months at least. After that follow-up period, mortality and incidence of acute myocardial infarction (AMI) were as follows: angina of recent onset (Class III--IV NYHA): 8.5% (3/35) and 34.2% (12/35). Progressive angina: 7.4% (2/27) and 7.4% (2/27). Intermediate syndrome: 41.6% (10/24) and 37.5% (9/24). Prinzmetal's angina: 10% (1/10) and 10% (1/10). Post acute myocardial infarction angina: 35% (7/20) and 10% (2/20). Acute persistent ischemia: 2.5% (1/40) and 20% (8/40). Comparison of these figures pointed out significant differences (p less than 0.001 for mortality and p less than 0.03 for AMI incidence respectively). We conclude that it is clinically possible to identify different groups within the so-called unstable angina. Such a division not only allows for the creation of more homogeneous groups, but it contributes to a more rational therapeutic approach and also permits identification of high risk prodromes of greater complications, such as myocardial infarction or sudden death.