Angiographic morphology in unstable angina pectoris

Complex morphology occurs frequently in unstable angina; however, its relation to symptomatic presentation, timing of angiography and hospital outcome has not been investigated. Accordingly, coronary angiography was performed 5 +/- 2 days after qualifying rest pain in 101 consecutive patients presenting with acute coronary insufficiency (n = 67) or crescendo angina (n = 34). Significant coronary artery disease was defined as any greater than or equal to 50% stenosis, and complex morphology as any stenosis with irregularity, overhang or thrombus. Eight of the 67 patients presenting with acute coronary insufficiency later proved to have a myocardial infarction as the qualifying event (creatine kinase twice normal with elevation of MB fraction). There were no myocardial infarctions in the crescendo angina group. Complex morphology occurred in 61% of patients. Thrombus alone occurred in 27% of patients with unstable angina without myocardial infarction, with similar frequencies between the 2 clinical groups. In contrast, intraluminal thrombi were identified in 78% of patients with acute coronary insufficiency who later proved to have a myocardial infarction as the qualifying event. The need for urgent catheterization (less than 48 hours) prompted by recurrent symptoms was associated with the angiographic findings of intraluminal thrombus (46%) and complex morphology (83%). The presence of complex morphology and intracoronary thrombus was associated with a higher incidence of in-hospital cardiac events, i.e., revascularization, myocardial infarction and death, independent of the incidence of multivessel disease.     

Clinical characteristics determining the mode of presentation in patients with acute coronary syndromes

Objectives. The purpose of this study was to examine clinical characteristics of patients with acute coronary syndromes to identify factors that influence the mode of presentation.

Background. In acute coronary syndromes, presentation with myocardial infarction or unstable angina has major prognostic implications, yet clinical factors affecting the mode of presentation are not well defined.

Methods. A prospective cohort study was made of 1,111 patients with acute coronary syndromes. Baseline demographic, clinical and biochemical data were compared in groups with myocardial infarction (n = 633) and unstable angina (n = 478).

Results. The risk of myocardial infarction relative to unstable angina was increased by age >70 years (odds ratio [OR] 2.21; 95% confidence interval [CI] 1.33 to 3.66), male gender (OR 1.56; CI 1.13 to 2.16) and cigarette smoking (OR 1.49; CI 1.09 to 2.03). A rise in admission creatinine from the 10th to the 90th centile of the distribution also increased the odds of myocardial infarction (OR 1.30; CI 1.05 to 1.94). Conversely, the risk of myocardial infarction relative to unstable angina was reduced by previous treatment with aspirin (OR 0.37; CI 0.27 to 0.52), hypertension (OR 0.64; CI 0.47 to 0.86) and previous acute coronary syndromes (OR 0.36; CI 0.26 to 0.51) and revascularization procedures (OR 0.36; CI 0.21 to 0.62).

Conclusions. The clinical presentation of acute coronary syndromes may be influenced by various factors that have the potential to influence the coagulability of the blood, the collateralization of the coronary circulation and myocardial mass. Myocardial infarction is favored by cigarette smoking, advanced age and renal impairment, while unstable angina is favored by treatment with aspirin, hypertension, previous revascularization and previous coronary syndromes.     

The prognosis for patients with new-onset angina who have undergone cardiac catheterization

We investigated the prognostic significance of new-onset angina in patients in whom coronary anatomic characteristics were known. New onset angina was defined as angina of less than 3 months duration. Consecutive patients (n = 1727) with significant coronary artery disease (diagnosed at cardiac catheterization) and who had not had a prior myocardial infarction or congestive heart failure were studied. In patients with new-onset angina (n = 329) there was a higher incidence of single-vessel disease (43% vs 27%) and a lower incidence of triple-vessel (23% vs 35%) and left main artery (5% vs 10%) disease compared with patients with chronic angina (n = 1398). Patients were classified by the presence or absence of preinfarction angina (severe and prolonged angina at rest requiring hospitalization to rule out myocardial infarction). In patients treated without surgery and who did not have preinfarction angina, survival at 1 year was 97% for patients with new-onset angina and 98% for those with chronic angina (p = .27). Among patients not treated surgically who did not have preinfarction angina, at 1 year 16% with new-onset angina and 7% with chronic angina had suffered a cardiac event (nonfatal myocardial infarction or death, p = .006). In patients treated surgically who did not have preinfarction angina, survival at 1 year was 96% both for those with new-onset angina and those with chronic angina (p = .99). The risk of an event in patients treated surgically at 1 year was not statistically different in patients with new-onset angina and those with chronic angina (12% vs 11%, p = .27). Survival and event-free rates were lower in patients with preinfarction angina than in patients who did not have it.(ABSTRACT TRUNCATED AT 250 WORDS)     

Unstable angina--clinical course and medical management including antiplatelet treatment

One hundred patients with unstable angina who were treated medically were classified into 2 groups of non-crescendo and crescendo angina and reviewed regarding their clinical course for 24 months on the average. Thirty-four patients with non-crescendo angina had an occurrence of recurrent angina in 7 patients (21%), myocardial infarction in 2 (6%) and death in none, while 66 patients with crescendo angina had a significantly higher occurrence of recurrent angina in 29 (44%) and myocardial infarction in 14 (21%), p less than 0.05 in both angina and infarction. There were 4 (6%) deaths in patients with crescendo angina in spite of similar clinical backgrounds. Modern medical treatments of unstable angina include nitrates, beta blockers, calcium antagonists as well as antiplatelet and thrombolytic therapy. We conclude that our patients under active medical treatment have more favorable prognosis than once thought and that classification of unstable angina into non-crescendo and crescendo angina according to the early clinical course appears to be useful both for a selection of treatments and for an assessment of prognosis.     

Treatment of unstable angina pectoris.

Unstable angina pectoris may be manifested as new-onset angina, a change in the anginal pattern, pain at rest with associated electrocardiographic (ECG) changes, or postinfarction angina. Of these, pain at rest with ischemic ECG changes is known to be associated with the poorest prognosis. The pathogenesis of unstable angina pectoris involves a combination of a fixed atherosclerotic obstruction and a dynamic component related to coronary vasoconstriction, thrombus formation, or both. Long-acting nitrates, inhibitors of platelet aggregation, beta blockers, and calcium antagonists are among the agents that have been shown to be effective in the medical management of unstable angina. A study now in progress is evaluating the routine use of thrombolytic therapy for this indication. Although alleviation of symptoms and prevention of death and myocardial infarction are important therapeutic goals, the overall efficacy of a particular medical therapy can best be assessed by objective evaluation of its ability to control ischemia, using such techniques as exercise scintigraphy and ambulatory ECG monitoring. Cardiac catheterization and revascularization are indicated for patients with unstable angina who continue to experience symptoms or who show evidence of silent ischemia despite medical therapy. A study is under way to determine the advisability of routine revascularization of such patients. Revascularization will provide symptomatic relief in most patients with unstable angina and may prolong survival and improve left ventricular function in certain subsets.     

Comparison of Complete and Incomplete Revascularization by Coronary Angioplasty for Unstable Angina

When a "culprit lesion" can be identified in a patient with unstable angina, it may be possible to achieve clinical improvement with incomplete revascularization. We analyzed actuarial survival free of an event (severe angina, myocardial infarction, coronary artery bypass graft, or death) at 6, 12, 18, and 24 months in 83 patients with multi-vessel disease and unstable angina who had undergone successful percutaneous transluminal coronary angioplasty (PTCA); revascularization was complete in 31 patients and incomplete in 52. Event-free survival in 85 patients with single-vessel disease and unstable angina who had undergone successful PTCA also was analyzed. Event-free survival at 24 months was worse in the multivessel disease patients than in the single-vessel disease patients (62% vs 85%; P = 0.001). Multivessel disease patients with complete revascularization had the same event-free survival as those with incomplete revascularization (63% vs 61%; P NS). Diagnostic angiograms revealed thrombus or an irregular ulcerated lesion in 42 of the multivessel disease patients. The event-free survival of these 42 patients was not different from that of the multivessel disease patients as a whole (64% vs 60%; P NS). We conclude that in patients with multivessel disease and unstable angina the event-free survival after PTCA is poorer than in patients with single-vessel disease and unstable angina. In the former patients, event-free survival does not necessarily depend on the completeness of revascularization. The outcome of patients who have intra-coronary thrombus or an irregular ulcerated lesion resembles the outcome of patients who lack these findings. (J Interven Cardiol: 1988:1:1)     

Nitrates for unstable angina

Summary The termunstable angina encompasses heterogeneous clinical syndromes. Fissuring of an atherosclerotic coronary artery plaque with superimposed platelet deposition, with or without additional thrombus formation, is invariably responsible for a prolonged episode of angina at rest, increasing frequency of angina at rest, or with minimal exertion of less than 4 weeks in duration and early postinfarction angina. Plaque progression, rather than plaque fissuring, is the most likely mechanism for progressive reduction in walking distance due to angina in patients who previously have stable angina. Coronary artery spasm is responsible for Prinzmetal's variant angina, but its exact role in other forms of unstable angina is unknown. The mainstay of treatment of unstable angina (prolonged episode of angina at rest and recent onset angina at rest, or with minimal exertion with a crescendo pattern) is aspirin, heparin, or both. Both aspirin and intravenous (IV) heparin or their combination reduce early mortality and the incidence of acute myocardial infarction in patients hospitalized with unstable angina. However, these agents do not promptly relieve chest pain. There are no placebo-controlled studies evaluating the usefulness of nitrates in unstable angina. In open-label studies, continuous therapy with IV nitroglycerin (NTG) for 24 hours or longer has been shown to relieve chest pain in patients with rest angina refractory to therapy with other antianginal agents, including long-acting nitrates. Recurrence of chest pain in patients receiving IV NTG is a common problem and probably represents development of pharmacologic tolerance, but this can be overriden by dose escalation; protracted tolerance during short-term use of IV NTG is usually not a problem. In the acute phase of unstable angina, IV NTG is the preparation of choice as the dose can be rapidly titrated up or down. There is no role of intermittent nitrate therapy in the acute phase of unstable angina. Once the patient is stable for 12–24 hours, IV NTG should be tapered gradually and intermittent therapy with a long-acting nitrate, as outlined for the treatment of stable angina, instituted. Aspirin reduces mortality and morbidity during long-term therapy and should be continued indefinitely. Routine use of morphine and other potent analgesics is not recommended. Patients who do not respond to IV NTG or in whom IV NTG is contraindicated should be treated with a beta-blocker devoid of intrinsic sympathomimetic activity, provided there are no contraindications to beta-blocker therapy. The role of calcium channel blockers in patients nonresponsive to IV NTG is less well defined. In patients already receiving beta-blockers and nitrates, the addition of nifedipine may be beneficial. However, monotherapy with nifedipine or other first-generation dihydropyridines is not recommended. Although there are no large trials of diltiazem or verapamil in unstable angina, these agents are often used in patients who are not candidates for beta-blocker therapy. Patients who are refractory to intensive medical therapy are candidates for coronary angiography and revascularization procedures, provided the coronary anatomy is suitable for such procedures.     

Comparison of clinical features of non-Q wave and Q wave myocardial infarction

The clinical spectrum and outcome of 119 patients with acute non-Q wave myocardial infarction (NQMI) were studied, in comparison with those of 354 patients with acute Q wave myocardial infarction (QMI). The patients with NQMI had a significantly higher incidence of preinfarction angina (73% vs 63%), previous myocardial infarction (43% vs 22%), multivessel disease (73% vs 51%), postinfarction angina (55% vs 21%), and recurrent myocardial infarction during follow-up for an average of 25 months (17% vs 8%). NQMI patients also had a lower rate of complication of pump failure and smaller infarct size estimated by peak creating phosphokinase (CPK) levels (1361 +/- 1243 vs 2711 +/- 1684 IU/L) than those with QMI. There was no difference in in-hospital mortality between the two groups (17% vs 17%). However, death due to cardiac rupture was exclusively noted in the QMI group. The present study suggests that NQMI is more unstable than QMI in the clinical course.     

Unstable angina: from physiopathology to therapeutics]

Unstable angina is a term which encompasses several clinical syndromes (crescendo angina, angina de novo, resting angina, postinfarction angina), intermediary between stable angina and myocardial infarction. The results of coronary angioscopy have allowed differentiation of accelerated effort angina which seems related to ulceration of an atheromatous plaque from resting angina, more commonly associated with intraluminal thrombosis. The diagnosis of unstable angina is clinical and justifies immediate hospital admission to a coronary care unit because of the risk of myocardial infarction and/or sudden death. Medical management comprises triple anti-ischemic therapy (nitrate derivatives, betablockers, calcium antagonists), anticoagulants and platelet antiagregants. Randomised therapeutic trials versus placebo have shown that this treatment decreases the incidence of refractory angina and myocardial infarction. Several studies are under way to assess the role of thrombolytic therapy in unstable angina. When unstable angina is refractory to maximal medical therapy, emergency coronary angiography should be performed. However the outcome is usually favourable and coronary angiography can be performed several days after the acute event. The coronary lesion responsible for unstable angina is often "complex", an eccentric, irregular, severe stenosis or appearances of thrombosis. Whenever possible, depending on the coronary lesion, myocardial revascularisation by coronary angioplasty or aorto-coronary bypass should be proposed. Surgical treatment has been shown to be more effective (symptomatic relief, improved survival) than medical therapy in patients with triple vessel disease. However, the results of studies comparing medical or surgical treatment with coronary angioplasty are not yet available.     

Unstable Angina: Good Long-Term Outcome After a Complicated Early Course

Objectives. This study was performed to investigate the long-term outcome of patients with unstable angina within subgroups of the Braunwald classification.

Background. Long-term follow-up studies of patients with unstable angina are rare and date from more than two decades ago. This study was performed to establish the prognosis of different subgroups of patients with unstable angina (Braunwald criteria) during a 7-year follow-up period.

Methods. We registered a well defined group of 417 consecutive patients, admitted to the hospital for suspected unstable angina. The definite diagnosis was unstable angina in 282 patients (68%) and evolving myocardial infarction in 26; in 109 patients (26%), the symptoms were attributed to other or nonspecific causes. Patients with definite unstable angina were subclassified according to the Braunwald classification. Survival, survival without infarction and survival without infarction or intervention were determined for each class.

Results. After a median follow-up period of 94 months, the mortality rate in the first year was 6% and 2% to 3% in the following years. The frequency of revascularization was 47% in the first year, and that for myocardial infarction was 11% in the first year and 1% to 3% thereafter. The Braunwald classification appeared to be appropriate for risk stratification in the first year. However, at 7 years the event rates in all classes were similar. In particular, the Braunwald classification had no long-term impact on mortality or infarction rates. However, patients with acute angina at rest or postinfarction angina and patients with extensive anginal treatment had high intervention rates.

Conclusions. To our knowledge, this study is the first to demonstrate that despite a complicated course during the first year, current management results in good long-term outcome in patients with unstable angina.     

Angiographic aspects of unstable angina

One-hundred and ninety-four patients with unstable angina pectoris (91 "in crescendo" angina and 103 new onset angina) underwent coronary angiography. The angiographic data from both groups were compared in order to discover whether angiographic aspects were related to the various clinical symptoms of coronary artery disease. Patients with recent onset angina had a significant increase (p less than 0.0001) of mono-vessel disease, whereas multi-vessel disease was prevalent in patients with "in crescendo" angina pectoris. Higher prevalence of coronary collaterals was observed in patients with "in crescendo" angina (p less than 0.005). No significant difference was observed in ejection fraction of the two groups. A further analysis was performed in 100 patients with unstable angina pectoris but without prior myocardial infarction (42 "in crescendo" angina and 58 recent onset angina). Also in these patients were found the same results; with the exception of ejection fraction which was more slight in patients with "in crescendo" angina (p less than 0.01). These data confirm that patients with unstable angina are an heterogeneous group in which comparison is unreliable and that the severity of clinical symptoms is not related to the degree of angiographic coronary lesions.     

Correlation between clinical course and quantitative analysis of the ischemia related artery in patients with unstable angina pectoris, refractory to medical treatment

Patients with unstable angina, refractory to intensive medical therapy, are at high risk for developing thrombotic complications, such as recurrent ischemia, myocardial infarction and coronary occlusion during coronary angioplasty. As both platelet aggregation and/or thrombus formation play an important role in this ongoing ischemic process, a monoclonal platelet GPIIb/IIIa receptor antibody (c7E3) or thrombolytic therapy (alteplase) might be able to modify the clinical course and underlying coronary lesion morphology. To evaluate whether alteplase or c7E3 could influence the incidence of complications, we randomized 36 and 60 patients, respectively to alteplase or placebo, or c7E3 or placebo. All patients exhibited dynamic ECG changes and recurrent pain attacks, despite maximal tolerated medical therapy. Patients were randomized in both studies after initial angiography had demonstrated a culprit lesion amenable for angioplasty. After study drug infusion quantitative angiography was repeated and angioplasty performed. Recurrent ischemia during study drug infusion occured in 5, 6, 9 and 16 patients from the alteplase, placebo, c7E3 and placebo group, respectively. Major events defined as death, myocardial infarction or urgent intervention occurred in 7, 3, 1 and 7 patients, respectively. Two patients died: one in the alteplase group and one in the placebo group from the c7E3 study. The first patient due to retroperitoneal hemorrhage, the second as a result of recurrent infarction. Qualitative angiography showed resolution of clots in the c7E3 group only, while the same group of patients showed in 20% an improvement in TIMI flow grade, without deterioration in any patient from this group. Quantitative angiography showed a significant improvement in percentage diameter stenosis in the c7E3 group, which was not observed in all three other groups, although differences between groups were not significant. Alteplase infusion in patients with refractory unstable angina did not change the clinical course, nor the coronary morphology, c7E3 on the other hand, both improved the clinical course and the coronary lesion morphology and rheology in the same category of patients.     

Coronary angioplasty in unstable angina. Immediate and short-term results

We report the results of percutaneous transluminal coronary angioplasty (PTCA) in 67 consecutive patients with unstable angina. Twenty patients had new onset (less than 2 months) angina, 33 patients had crescendo angina and 14 had early postinfarction angina. Fifty-one patients had one-vessel disease, 12 patients had two-vessel disease and two patients had three-vessel disease; two patients had a stenosis of a venous graft. In cases with multivessel disease, we performed only the dilatation of the ischaemia-related vessel identified by morphologic features of coronary lesion and electrocardiographic changes during chest pain. The procedure was successful in 54 cases (80.6%). Seven patients (10.4%) had major complications. Emergency coronary artery bypass graft surgery was performed in 6 cases (8.9%) because of occlusion of the left anterior descending artery; despite emergency operation one patient died and two patients sustained a myocardial infarction. One patient had occlusion of the right coronary artery and inferior myocardial infarction. In all patients in whom angioplasty was successful unstable angina disappeared. At 6 months follow-up there were no infarctions or deaths but 14 of 42 patients (33%) had recurrent angina. Restenosis occurred in 16 of 33 patients (48%) who had repeat coronary angiography. Four patients with recurrence of unstable angina had repeat angioplasty; it was successful in 3 cases. One patient died of refractory cardiac arrest. The mortality rate of 71 procedures performed in 67 patients was 2.8% (2/71) and the overall myocardial infarction rate was 4.2% (3/71).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular risk and therapeutic benefit of coronary interventions for patients with unstable angina according to the troponin T status.

AIMS: Elevation of troponin T in patients with unstable angina is predictive of adverse outcomes. Since no advanced therapeutic concept for such high-risk patients has been established, we investigated cardiac risk prior to, during, and after coronary revascularization in patients with unstable angina stratified according to the troponin T status. METHODS AND RESULTS: Out of 351 patients with unstable angina, troponin was elevated for 36% of the patients as determined by qualitative bedside tests. The patients were followed during hospitalization and 30 days after discharge for incidence of death and myocardial infarction. In troponin-positive patients, clinical symptoms were more refractory to medical treatment than in troponin-negative patients (78% vs 44%;P=0.002). Although these patients were catheterized earlier (1.6 vs 3.4 days;P=0.005) and more frequently (95% vs 69%;P<0.001), troponin-positive patients suffered a higher incidence of cardiac events prior to scheduled revascularization (death, myocardial infarction; 6.4% vs 0.4%;P<0.001). The angiogram for troponin-positive patients confirmed a more severe coronary artery disease requiring revascularization (69% vs 50%;P=0.001). Also the following coronary intervention was more complicated (death, myocardial infarction; 15.3% vs 4.8%;P=0.02). During the 30-day follow-up period, cardiac risk remained elevated for troponin-positive patients. CONCLUSIONS: Troponin T rapid testing reliably identified high-risk patients with unstable angina. A higher event rate was observed prior to and particularly in association with the coronary intervention. Coronary revascularization did not abrogate the increased risk of troponin-positive patients during the 30-day follow-up.     

Comparison of clinical and angiographic features and longterm follow-up events between patients with variant angina and patients with ST elevation myocardial infarction

We investigated to what extent patients with variant angina and significant coronary stenosis (>or=70%) present a clinical and angiographic profile similar to patients with ST elevation myocardial infarction. Thus, the clinical and angiographic features as well as follow-up events of 200 patients were prospectively analyzed and were compared with those of 422 patients with a first ST elevation myocardial infarction survivors of the early phase (3 days) and those of 70 patients with variant angina and non significant stenosis. Age and incidence of smoking, systemic hypertension, diabetes and maximum ST elevation were similar in the 2 groups. Furthermore, among patients with significant coronary stenosis, stenosis severity and the proportion of eccentric lesions were also comparable. Incidence of recent-within 30 days prior to admission-angina at rest was higher in variant angina patients with significant stenosis (67% vs. 27%, p<0.001) than in those with myocardial infarction but long standing angina at rest (>30 days) was low and comparable in these 2 groups (15% vs. 11%, ns). Also, in a 5-year follow-up most patients from these 2 groups were free from angina at rest (86% vs. 84%) which in variant angina patients was largely attributable to a high revascularization rate (72%). Moreover, the rate of myocardial infarction/cardiac death (20% vs. 19%) was also similar. Patients with variant angina and non-significant stenosis, however, had longer antecedent angina, more frequent follow-up angina and a lower incidence of cardiac events than the other 2 groups. Thus, these findings suggest that patients with variant angina and significant coronary stenosis generally behave as an acute coronary syndrome-likely associated with an acutely complicated plaque-rather than as recurrent vasospastic angina, and should be managed accordingly.     

Differences in inflammatory activity at the onset of acute myocardial infarction according to the clinical presentation of preinfarction angina

It is unknown whether the pathogenetic mechanisms underlying acute myocardial infarction (AMI) differ according to the clinical presentation of preinfarction angina, so the present study measured plasma levels of C-reactive protein (CRP) in 280 patients with AMI in whom serum creatine kinase levels were normal on admission and increased subsequently. Patients were classified into 3 groups according to the type of preinfarction angina: no angina (n=95), stable angina (n=48), and unstable angina (n= 137). Patients with unstable angina were subdivided according to the Braunwald classification: class IB (n=39), class IIB (n=22), and class RIB (n=76). There were no differences among the 5 groups in baseline characteristics. CRP on admission was significantly higher and the level of physical activity at symptom onset was significantly lower in the Braunwald class RIB group than in the other groups, but no differences were observed among the other groups. Patients with preinfarction Braunwald class IIB unstable angina had higher CRP levels on admission and symptom onset at a lower level of physical activity. In such patients, the pathogenetic mechanisms may differ from those in other subsets of patients with AMI and active inflammation may play a more important role in AMI onset.     

急性冠状动脉综合征患者血运重建的预后

目的 入选2003年7月1日至2005年9月30日在我院接受血运重建治疗的6005例患者,1年后对患者进了解接受血运重建治疗的急性冠状动脉综合征患者的近期和长期预后.方法 行电话或门诊随访.比较ST段抬高心肌梗死(STEMI)、非ST段抬高急性心肌梗死(NSTEMI)和不稳定性心绞痛患者的临床和预后[不良心脑血管事件(MACCE)包括伞因死亡、非致死性心肌梗死、非致死性卒中和再次血运重建]情况.结果 共4865例患者,其中STEMI患者955例,NSTEMI患者263例,不稳定性心绞痛患者3647例,3组患者的院内和18个月生存率(分别为96%、98%和98%)差异无统计学意义,不稳定性心绞痛患者18个月MACCE发生率较低(STEMI,NSTEMI和不稳定性心绞痛3组无事件生存率分别为86%、86%和89%).结论 接受血运重建的STEMI、NSTEMI和不稳定性心绞痛患者临床情况有所差异,但是近期和长期病死率相似,不稳定性心绞痛患者的长期MACCE发生率低.

Abstract：

Objective To evaluate short-term and long-term prognosis of revascularization in patients with acute coronary syndrome. Methods A total of 6005 patients who received coronary revascularization in our institution between July 2003 and September 2005 were enrolled. The patients were followed up in clinic or by telephone after discharge between September 2006 and November 2006. The clinical and prognosis data of all-cause mortality, neo-myocardial infarction, nonfatal stroke, and rerevascularization of ST-segment elevation myocardial infarction ( STEMI ) , non ST-segment elevation myocardial infarction ( NSTEMI) and major adverse cardiovascular and cerebrovascular events ( MACCE) were analyzed. Results Among 4865 acute coronary syndrome patients, 955 cases were STEMI; 263 cases were NSTEMI; and 3647 cases were unstable angina ( UA) pectoris. There were no significant difference for in-hospital mortality and late mortality ( 18 month survival 96% , 98% and 98% ) between patients with STEMI, NSTEMI and UA. Patients with UA had lower MACCE rate (18 month non-MACCE survival of STEMI, NSTEMI and UA group were 86% , 86% , and 89% respectively). Conclusions Despite different clinical characteristics, patients with STEMI, NSTEMI and UA undergoing revascularization had similar short-term and long-term mortality. Patients with UA had lower MACCE rate.     

112例不稳定型心绞痛患者介入治疗的临床评价

目的 探讨不稳定型心绞痛患者介入治疗的安全性及临床效果。方法 不稳定型心绞痛112例．反复发作时即行冠状动脉造影,明确病变后对“罪犯”血管行经皮冠状动脉介入治疗,术后残余狭窄小于10％,前向血流按心肌梗死溶栓治疗临床实验（thrombolysisinmyocardialinfarction,TIMI）血流分级3级为手术成功;随访6月,分析即时及远期效果。结果 手术成功率100％,所有病例均随访6月,其中,17例（15％）患者在经皮冠状动脉介入术后3-6个月再发心绞痛,发作时心电图或平板负荷试验提示心肌缺血,此17例均再次冠状动脉造影提示“罪犯”血管支架内再狭窄,再次行经皮冠状动脉介入术。其余病例术后6个月内未再发心绞痛。随访期间无1例再发心肌梗死或死亡。结论 早期介入治疗不稳定型心绞痛患者是有效的治疗方法,手术成功率及安全性高,近期和远期临床效果满意。     

Different clinical and prognostic aspects of angina pectoris in unstable phase

The purpose of this study was to focus on the clinical and angiographic characteristics of 113 patients with crescendo angina (Group I) as compared to 187 patients with angina of new onset (Group II), selected from a series of 474 consecutive subjects, admitted to our clinic between January 1976 and July 1983 because of recurrent episodes of spontaneous angina, who underwent cardiac catheterization and coronary angiography within one month of hospitalization. Group I patients showed a greater incidence of prior transmural myocardial infarction (p less than 0.01), arterial hypertension (p less than 0.01), multivessel disease (p less than 0.01) and a lower value of left ventricular ejection fraction (p less than 0.01) than Group II patients. In the latter group of patients anginal episodes were more frequently associated with S-T segment elevation than with S-T segment depression (p less than 0.001), while the opposite was found in patients with crescendo angina. Survival curves up to five years showed that medically treated patients with crescendo angina had a worse long-term prognosis than patients with unstable angina of new onset (p less than 0.01). On the contrary no difference was found between the surgically treated patients of the two groups. Our data suggest that the more diffuse involvement of the coronary tree associated with a more depressed left ventricular function may result in an unfavorable long-term prognosis in patients with crescendo angina as compared to those with unstable angina of new onset. Such a difference between the two groups was abolished by surgical treatment.     

Comparison of angioscopy,intravascular ultrasound imaging and quantitative coronary angiography in predicting clinical outcome after coronary intervention in high risk patients

Objectives. The purpose of this study was to identify qualitative or quantitative variables present on angioscopy, intravascular ultrasound imaging or quantitative coronary arteriography that were associated with adverse clinical outcome after coronary intervention in high risk patients.Background. Patients with acute coronary syndromes and complex lesion morphology on angiography are at increased risk for acute complications after coronary angioplasty. Newer devices that primarily remove atheroma have not improved outcome over that of balloon angioplasty. Intravascular imaging can accurately identify intraluminal and intramural histopathologic features not adequately visualized during coronary arteriography and may provide mechanistic insight into the pathogenesis of abrupt closure and restenosis.Methods. Sixty high risk patients with unstable coronary syndromes and complex lesions on angiography underwent angioscopy (n = 40) and intravascular ultrasound imaging (n = 46) during interventional procedures. In 26 patients, both angioscopy and intravascular ultrasound were performed in the same lesion. All patients underwent off-line quantitative coronary arteriography. Coronary interventions included balloon (n = 21) and excimer laser (n = 4) angioplasty, directional (n = 19) and rotational (n = 6) atherectomy and stent implantation (n = 11). Patients were followed up for 1 year for objective evidence of recurrent ischemia.Results. Patients whose clinical presentation included rest angina or acute myocardial infarction or who received thrombolytic therapy within 24 h of procedure were significantly more likely to experience recurrent ischemia after intervention. Plaque rupture or thrombus on preprocedure angioscopy or angioscopic thrombus after intervention were also significantly associated with adverse outcome. Qualitative or quantitative variables on angiography, intravascular ultrasound of off-line quantitative arteriography were not associated with recurrent ischemia on univariate analysis. Multivariate predictors of recurrent ischemia were plaque rupture on preprocedure angioscopy (p < 0.05, odds ratio [OR] 10.15) and angioscopic thrombus after intervention (p < 0.05, OR 7.26).Conclusions. Angioscopic plaque rupture and thrombus were independently associated with adverse outcome in patients with complex lesions after interventional procedures. These features were not identified by either angiography or intravascular ultrasound.