在急诊科设立胸痛中心对胸痛患者诊疗时间的影响

目的在急诊科设立胸痛中心并研究其对急性胸痛患者诊疗时间的影响。方法在急诊科设立急性胸痛中心,每周开诊3d,时间随机确定,其余时间由急诊科按常规流程对胸痛患者进行诊疗,由研究者对急性胸痛患者的病因和诊疗时间进行注册登记。结果2006年1月至2007年12月因急性非创伤性胸痛就诊北京军区总医院急诊科或胸痛中心的患者共696例,心源性胸痛244例（35％）,包括急性心肌梗死141例（20％）,不稳定型心绞痛81例（12％）,稳定型心绞痛17例（2．4％）,主动脉夹层2例（0．3％）,急性肺栓塞3例（0．4％）;非心源性胸痛452例（65％）,呼吸系统41例（6％）,消化系统70例（10％）,胸膜骨骼肌肉41例（6％）,神经精神或其他299例（42％）。经胸痛中心诊治的胸痛患者的诊疗时间与常规诊疗流程相比都有所缩短。急性心肌梗死（70．1±31．7）min vs（115±40．5）min（P〈0．01）;不稳定型心绞痛（228±54）min vs（264±78）min（P=0．02）;非心源性胸痛（108±66）min vs （126±96）min（P=0．03）。结论急性胸痛患者的病因中,心源性者占35％,以急性心肌梗死和不稳定型心绞痛为主;非心源性者占65％。胸痛中心模式能显著缩短急性胸痛患者的诊疗时间。     

Risk factors and prognosis after discharge for patients admitted because of suspected acute myocardial infarction with and without confirmed diagnosis

The prognosis regarding cardiac events--acute myocardial infarction (AMI) or cardiac death after discharge--was evaluated in 257 patients admitted because of suspected AMI due to chest pain, but in whom AMI was not confirmed (non-AMI patients). The findings and patient prognoses were compared with those of 275 patients with confirmed AMI. All patients were younger than 76 years and free of severe chronic diseases, and no cause of chest pain other than possible ischemic heart disease was found. The patients were followed for cardiac events for 11 to 24 months (median 14). The prognoses for the non-AMI patients were significantly better than those for the AMI patients (p = 0.05). The proportion without a cardiac event after 1 year was estimated at 91% and 86%, respectively. In the non-AMI patients, angina pectoris, previous AMI and electrocardiographic changes on admission (intraventricular block and permanent or transient ST-T changes) were significant predictors of cardiac events by univariate and multivariate analysis. In the AMI patients, female gender, heart failure, previous AMI and angina pectoris were significant predictors of cardiac events by univariate analysis. With use of multivariate analysis, female gender, heart failure and angina pectoris were independent predictors of cardiac events. Thus, non-AMI patients admitted with chest pain have a high risk of cardiac events after discharge. The risk is highest when there is evidence of coronary artery disease (electrocardiographic changes on admission and angina pectoris or previous AMI.     

Comparison of clinical presentation of acute myocardial infarction in patients older than 65 years of age to younger patients: the Multicenter Chest Pain Study experience

To assess whether the manifestations of acute ischemic heart disease in the elderly are less typical than in younger patients, the presenting clinical features and their associated relative risks for acute myocardial infarction (AMI) were compared in 2,625 patients greater than or equal to 65 years of age and 5,109 patients less than 65 years of age. These patients were evaluated for acute chest pain in the emergency departments of 7 hospitals. The same features were associated with increased relative risks for AMI in younger and elderly patients. The relative risks among older patients, however, were consistently closer to 1.0 for classic features, including male gender, pressure-like quality of pain, substernal location, typical pattern of pain radiation and electrocardiographic evidence of ischemia or AMI. Analyses for the endpoint "acute ischemic heart disease" (i.e., AMI or unstable angina) yielded similar findings. Elderly patients were more likely to be admitted to the hospital (56 vs 35%; p less than 0.0001) and to the coronary care unit (37 vs 23%; p less than 0.0001) in the absence of either AMI or unstable angina. These data support the hypothesis that diagnosis of acute chest pain is especially difficult in elderly patients.     

Early detection of acute myocardial infarction by measurement of mass concentration of creatine kinase-MB

The diagnostic sensitivity and performance of immunoenzymometric measurements of creatine kinase (CK)-MB mass concentrations in the early diagnosis of acute myocardial infarction (AMI) were examined and compared with the sensitivities and performances of CK and CK-MB activity, in the context of simultaneous measurements of CK, CK-MB activity, and CK-MB mass concentrations in serially drawn blood samples obtained immediately from 36 patients with AMI and 126 patients with chest pain on admission to the emergency room of the department of internal medicine. In the 36 patients with AMI, who were all admitted no later than 4 hours after the onset of chest pain, pathologic increase occurred significantly earlier in CK-MB mass than in both CK and CK-MB activity, with a median difference of 1 hour each. In patients coming to the emergency room (51 with AMI, 51 with angina pectoris and 24 with chest pain not related to coronary artery disease), CK-MB mass was the best diagnostic measurement for AMI of all markers tested (significantly higher efficiency, Youden index and likelihood ratio than both CK and CK-MB activity). Before initiating thrombolytic therapy, the sensitivity of CK-MB mass is significantly higher than CK-MB activity during the 0- to 6-hour period and significantly higher than CK activity during the 2- to 4-hour period after the onset of chest pain. Consequently, it is often possible to diagnose an AMI on the basis of increased CK-MB mass concentrations even at a time when CK and CK-MB activities are still within the reference interval.     

Diagnostic implications for myocardial ischemia of the circadian variation of the onset of chest pain

To determine whether the occurrence of chest pain is randomly distributed during the day and to study whether the time of onset is useful in discriminating among causes of chest pain, patients older than 30 years who presented to 7 emergency departments with a chief complaint of chest pain unexplained by trauma or chest x-ray abnormalities were studied. A total of 7,759 patients presented during the study period; of these, 3,990 presented within 6 hours of the onset of pain and were included in the primary analysis. Chest pain caused by acute myocardial infarction, unstable angina pectoris and stable angina pectoris was more likely to begin during the period from 6 AM to noon than would be expected if the onset were uniformly distributed during the day (relative risks 1.15, 1.29 and 1.32, respectively), but chest pain that was caused by nonischemic cardiac causes and by noncardiac causes was also more likely to begin during the same time period (relative risks 1.28 and 1.17). Although chest pain from coronary arterial causes had a distinct circadian variation, the time of onset of pain was not a helpful criterion for determining the cause of chest pain.     

Diagnostic changes in serum creatine kinase MM isoenzyme sub-bands after the onset of acute myocardial infarction

The authors quantified the change of CK-MM isoforms in the first available serum sample from 16 patients each with acute myocardial infarction (AMI) and angina pectoris and 16 normal individuals as well. The average MM3/MM1 ratio in the normal group was 0.24 +/- 0.12, in angina group 0.21 +/- 0.13, and in AMI group 0.52 +/- 0.30 (P less than 0.001, as compare with the first two groups). The first blood sample of AMI was obtained in 3.0 +/- 1.9 hours after the onset of chest pain. Half of them (8/16) had a ratio of MM3/MM1 greater than 0.50 and the change occurred as early as 30 min after the attack. In contrast, the total CK and CK-MB in the three groups were within normal limits at the same time, they were 85.8 +/- 24.4 U/L for CK and 3.2 +/- 1.1% for CK-MB in patients with AMI, 66.7 +/- 18.0 U/L, 2.7 +/- 1.6% in angina pectoris and 71.4 +/- 24.5 U/L, 3.0 +/- 1.1% in normal subjects respectively. Accordingly, diagnostic change of CK-MM isoforms was the earliest among the enzymes after the onset of AMI.     

Increased release of the soluble form of the adhesion molecules L-selectin and ICAM-1 but not E-selectin during attacks of angina pectoris

Summary Myocardial ischemia leads to the activation of neutrophils as well as endothelial cells. The interaction between these cells is dependent on certain adhesion glycoproteins which are expressed on their surface. Adhesion of neutrophils to endothelium, mediated by adhesion molecules, has been shown to result in coronary capillary plugging and impairment of coronary blood flow. In certain conditions, upon cell activation, adhesion proteins may be released in soluble form into the circulating blood. The purpose of our study was to verify whether myocardial ischemia occurring during angina episodes results in the release of the soluble adhesion molecules, L-selectin, E-selectin, and intracellular adhesion molecule-1 (ICAM-1), into the circulation. Plasma samples were collected by venepuncture from 15 patients admitted to the emergency room with chest pain caused by attacks of angina pectoris and 15 patients with noncardiac chest pain. To confirm the diagnosis, all patients underwent an exercise stress test and, if not conclusive,^99mTc MIBI SPECT or coronary arteriography. Another set of plasma samples were taken from each patient in the absence of chest pain. In addition, blood for analysis was obtained from 15 sexand age-matched healthy subjects. Soluble adhesion molecules plasma levels were measured by standard enzyme-linked immunosorbent assay. In patients with angina pectoris, plasma levels of soluble L-selectin estimated during chest pain were significantly higher than in the control group and decreased in the absence of chest pain. Similarly, the mean concentration of soluble ICAM-1 at the time of angina onset was significantly elevated in the patients in comparison with the control group and remained higher, although not significantly, in the absence of chest pain. In patients with noncardiac chest pain, plasma levels of soluble L-selectin did not differ significantly from those observed in control subjects. In this group of patients, the plasma levels of soluble ICAM-1 estimated during pain onset and in the absence of this symptom were not significantly elevated. On the contrary, the mean values of soluble E-selectin in the patients with ischemic cardiac pain during chest pain and in the absence of this symptom, as well as those in the patients with noncardiac chest pain during or without symptoms, remained unchanged in comparison with the control group. During attacks of angina pectoris an increase in the plasma levels of the soluble adhesion molecules, ICAM-1 and L-selectin, was noted, possibly reflecting activation of neutrophils and endothelial cells during myocardial ischemia. However, Eselectin plasma levels remained unchanged in response to myocardial ischemia.Presented in part at the American College of Cardiology Session, Anaheim, CA, 1997, and published in abstract form in JACC 1997; 29/2 supplement A, 336A.The work was supported in part by grant from Komitet Badañ Naukowych.     

Diabetes mellitus prevents ischemic preconditioning in patients with a first acute anterior wall myocardial infarction

OBJECTIVES: This study was undertaken to assess whether prodromal angina could have beneficial effects in diabetic patients with acute myocardial infarction (AMI). BACKGROUND: Prodromal angina occurring shortly before the onset of AMI is associated with favorable outcomes by the mechanism of ischemic preconditioning. However, little is known about the impact of diabetes on ischemic preconditioning. METHODS: We studied 611 patients with a first anterior wall AMI who underwent emergency catheterization within 12 h after the onset of chest pain: 490 patients without diabetes and 121 patients with non-insulin treated diabetes. Prodromal angina was defined as angina episode(s) occurring within 24 h before the onset of AMI. Serial contrast left ventriculograms were obtained in 424 patients at the time of acute and predischarge catheterization. RESULTS: In non-diabetic patients, prodromal angina was associated with lower peak creatine kinase (CK) value (3,068 +/- 2,647 IU/l vs. 3,601 +/- 2,462 IU/l, p = 0.037), larger increase in left ventricular ejection fraction (LVEF) (10.1 +/- 13.0% vs. 5.8 +/- 13.4%, p = 0.004) and lower in-hospital mortality (3.4% vs. 9.3%, p = 0.015). On the contrary, in diabetic patients, there was no significant difference in peak CK value (3,382 +/- 2,520 IU/l vs. 3,233 +/- 2,412 IU/l, p = NS), the change in LVEF (6.7 +/- 13.8% vs. 7.1 +/- 12.4%, p = NS) and in-hospital mortality (8.8% vs. 11.0%, p = NS) between patients with and patients without prodromal angina. CONCLUSIONS: Prodromal angina limited infarct size, enhanced recovery of LV function and improved survival in non-diabetic patients with AMI. However, such beneficial effects of prodromal angina were not observed in diabetic patients, suggesting that diabetes might prevent ischemic preconditioning.     

Value and limitations of technetium-99m stannous pyrophosphate in the detection of acute myocardial infarction.

Technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial imaging was performed in 436 consecutive patients for the evaluation of chest pain and suspected acute myocardial infarction (AMI). Scintigrams were assessed independently by three observers with a 90% interobserver agreement. In 134 patients with documented AMI (97 TRANSMURAL, 37 NONTRANSMURAL), THE SENSITIVITY OF 99MTc-PYP imaging was significantly lower in patients with nontransmural AMI (41%) than in patients with transmural AMI (78%), 99mTc-PYP imaging correctly localized the site of transmural infarction in 53 patients (70%). A diffuse 99mTc-PYP uptake was found in nine (10%) of 91 patients with positive scintigrams: six of these had a transmural AMI and three nontransmural AMI. In 226 patients without AMI, the specificity of infarct imaging was 95%. A false-positive scintigram was found in 0%, 8%, 9%, and 2% of patients with unstable angina, progressive angina, stable angina, and noncardiac chest pain, respectively. A diffuse uptake was found in six (54%) of 11 patients with false-positive scintigrams. No patient with the clinical diagnosis of noncardiac chest pain showed discrete uptake. In 76 patients with uncertain diagnosis for AMI, 99Tc-PYP imaging was considered of value in 11 patients with ventricular conduction defects (two patients with WPW syndrome, nine patients with LBBB). These data suggest that: 1. 99mTc-PYP imaging is moderately sensitive in detecting and localizing transmural AMI and is insensitive in detecting nontransmural AMI; 2. A discrete 99mTc-PYP uptake is highly specific for AMI; 3. a diffuse uptake is neither sensitive to, nor specific for AMI. Myocardial imaging with 99m-Tc-PYP is of clinical value when the standard electrocardiographic and enzymatic techniques are inadequate for an accurate diagnosis of AMI.     

Chest pain of cardiac and noncardiac origin

Chest pain is one of the most common symptoms driving patients to a physician's office or the hospital's emergency department. In approximately half of the cases, chest pain is of cardiac origin, either ischemic cardiac or nonischemic cardiac disease. The other half is due to noncardiac causes, primarily esophageal disorder. Pain from either origin may occur in the same patient. In addition, psychological and psychiatric factors play a significant role in the perception and severity of the chest pain, irrespective of its cause. Chest pain of ischemic cardiac disease is called angina pectoris. Stable angina may be the prelude of ischemic cardiac disease; and for this reason, it is essential to ensure a correct diagnosis. In most cases, further testing, such as exercise testing and angiography, should be considered. The more severe form of chest pain, unstable angina, also requires a firm diagnosis because it indicates severe coronary disease and is the earliest manifestation of acute myocardial infarction. Once a diagnosis of stable or unstable angina is established, and if a decision is made not to use invasive therapy, such as coronary bypass, percutaneous transluminal coronary angioplasty, or stent insertion, effective medical treatment of associated cardiac risk factors is a must. Acute myocardial infarction occurring after a diagnosis of angina greatly increases the risk of subsequent death. Chest pain in women warrants added attention because women underestimate their likelihood to have coronary heart disease. A factor that complicates the clinical assessment of patients with chest pain (both cardiac and noncardiac in origin) is the relatively common presence of psychological and psychiatric conditions such as depression or panic disorder. These factors have been found to cause or worsen chest pain; but unfortunately, they may not be easily detected. Noncardiac chest pain represents the remaining half of all cases of chest pain. Although there are a number of causes, gastroesophageal disorders are by far the most prevalent, especially gastroesophageal reflux disease. Fortunately, this disease can be diagnosed and treated effectively by proton-pump inhibitors. The other types of non-gastroesophageal reflux disease–related noncardiac chest pain are more difficult to diagnose and treat. In conclusion, the cause of chest pain must be accurately diagnosed; and treatment must be pursued according to the cause, especially if the cause is of cardiac origin.     

Extracardiac contributions to chest pain perception in patients 6 months after acute myocardial infarction

OBJECTIVES: The amount of perceived anginal pain in patients after infarction deserves the attention of the physician. This study sought to identify the modulating influence of extracardiac factors on persistent angina pectoris after myocardial infarction. METHODS AND RESULTS: A total of 552 male survivors of acute myocardial infarction (age 29 to 65 years, median 54 years) were followed for a period of 6 months; the affective state was assessed immediately after the acute event. The prognostic importance of postinfarction depression on chest pain perception was evaluated 6 months after the cardiac event in 376 patients. After the 6-month follow-up period, 199 (53%) of the patients with myocardial infarction had angina pectoris. Somatic risk factors and electrocardiographic data at initial testing did not contribute to the risk of having chest pain. However, patients with high levels of depression at initial testing had an almost 3-fold risk of having angina pectoris 6 months after the index event. Older age, lower social class status, and preinfarction angina were also significantly related to angina pectoris at the end of the study. Patients who were pain free before the index infarction reported significantly more symptoms of chest pain at the study end point (P 相似文献   

Effects of verapamil in preventing early postinfarction angina and reinfarction

Because verapamil is effective in the treatment of "preinfarction" angina, a single-blind, placebo-controlled trial was performed in 17 patients admitted to the coronary care unit with transmural acute myocardial infarction (AMI) to assess the effects of verapamil on angina and reinfarction after AMI. The study was terminated because results obtained in the initial 17 patients indicated that verapamil is not as effective in treating angina after AMI as it is in angina before AMI and does not prevent reinfarction. Continuous electrocardiographic monitoring during the first 3 days after AMI showed the presence of transient episodes of ST-segment elevation in 4 patients taking verapamil and 4 patients taking placebo. The total number and duration of transient ischemic episodes was similar in the 2 groups (46 vs 41 and 23 +/- 22 vs 17 +/- 15 minutes, respectively). The percentage of transient ischemic episodes accompanied by chest pain was similar in both groups (10%). The ischemic episodes were never preceded by important increases of heart rate. Four patients taking verapamil and 4 taking placebo had reinfarction within the first 10 days after the incident AMI. These findings suggest that the prevailing mechanisms of myocardial ischemia in the immediate post-AMI period could be different from those operating in angina before AMI.     

The importance of creatine kinase determination in identifying acute myocardial infarction among patients complaining of chest pain in an emergency room

The contribution of serum creatine kinase (CK) levels to the diagnosis of acute myocardial infarction (AMI) in an emergency room was studied in 252 patients presenting with chest pain. Thirty percent were ultimately diagnosed as having AMI. The electrocardiogram (ECG) identified 66% of patients with AMI who were evaluated within 4 h of onset of symptoms; while CK serum levels were elevated in only 9%. Among patients evaluated more than 4 h after the onset of symptoms, the ECG was helpful in diagnosing AMI in only 36.6%, while serum CK levels were high in 63.4%. CK testing added significantly to the diagnosis of AMI in patients already studied by ECG. We suggest that determination of serum CK levels in the emergency room is of value in the evaluation of patients complaining of chest pain 4 or more hours after the onset of symptoms.     

Chest pain in the emergency room. Importance of a systematic approach

OBJECTIVE: To evaluate the efficiency of a systematic diagnostic approach in patients with chest pain in the emergency room in relation to the diagnosis of acute coronary syndrome (ACS) and the rate of hospitalization in high-cost units. METHODS: One thousand and three consecutive patients with chest pain were screened according to a pre-established process of diagnostic investigation based on the pre-test probability of ACS determinate by chest pain type and ECG changes. RESULTS: Of the 1003 patients, 224 were immediately discharged home because of no suspicion of ACS (route 5) and 119 were immediately transferred to the coronary care united because of ST elevation or left bundle-branch block (LBBB) (route 1) (74% of these had a final diagnosis of acute myocardial infarction [AMI]). Of the 660 patients that remained in the emergency room under observation, 77 (12%) had AMI without ST segment elevation and 202 (31%) had unstable angina (UA). In route 2 (high probability of ACS) 17% of patients had AMI and 43% had UA, whereas in route 3 (low probability) 2% had AMI and 7 % had UA. The admission ECG has been confirmed as a poor sensitivity test for the diagnosis of AMI ( 49%), with a positive predictive value considered only satisfactory (79%). CONCLUSION: A systematic diagnostic strategy, as used in this study, is essential in managing patients with chest pain in the emergency room in order to obtain high diagnostic accuracy, lower cost, and optimization of the use of coronary care unit beds.     

Soluble PECAM-1, but not P-selectin, nor osteonectin identify acute myocardial infarction in patients presenting with chest pain.

We sought to determine plasma levels of platelet/endothelial cell adhesion molecule-1 (PECAM-1), P-selectin, and platelet-derived osteonectin, and prospectively compare these data with the discharge diagnosis in patients presenting with chest pain in a community hospital Emergency Department. Soluble antigens were measured by ELISA in 44 subjects including patients with acute myocardial infarction (AMI) (n = 13), chest pain of noncardiac origin (n = 17), and compared to those of age- and sex-matched healthy controls (n = 14). Elevated soluble PECAM-1 (64.5 +/- 18.3 ng/ml, p = 0.019), but not P-selectin (149.5 +/- 49.8 ng/ml, p = NS), nor osteonectin (549. 5 +/- 159.1 ng/ml, p = NS), occurred in the AMI group as compared to patients with noncardiac chest pain (46.2 +/- 7.5 ng/ml, 118.2 +/- 40.1 ng/ml, and 619.4 +/- 74.4 ng/ml, respectively). Increased plasma PECAM-1 may serve as a useful marker in the early detection of patients with AMI. Larger studies will be necessary to confirm the utility of soluble PECAM-1 in identifying AMI among patients presenting with chest pain.     

Beat-to-beat electrocardiographic morphology variation in healed myocardial infarction

Using high-fidelity electrocardiographic (ECG) amplifiers, we measured subtle beat-to-beat ECG morphologic variations at different phases of the ECG complex. The electrocardiograms were recorded from 49 men with a documented Q-wave myocardial infarction and from 30 age-matched normal men. Forty consecutive beats were averaged to achieve an average ECG signal from which variance could be calculated. The relative variance, defined as the ratio between the integrated variance of the examined window and the integrated variance of the ECG signal that was close to full cycle length, was calculated at QRS onset and at offset in 2 frequency bands (4 to 40 and 60 to 120 Hz). Patients with healed infarction had a relative variance of 2.1 +/- 0.5 (mean +/- standard deviation [SD]) at QRS offset (a window of 40 ms), which was significantly lower than that of the healthy volunteers: 2.5 +/- 0.33 (mean +/- SD; p less than 0.02) at the low-frequency band. At the high-frequency band, patients with healed infarction had a significantly higher relative variance than the control subjects at QRS onset: 1.95 +/- 0.58 vs 1.55 +/- 0.35 (mean +/- SD; p less than 0.005). A model based on the numerous minor conduction abnormalities that exist in the chronically ischemic myocardium is presented to explain the changes in variance at the onset and offset of the QRS. The variance changes described can eventually serve as quantitative indexes of myocardial injury and electrical stability in patients with ischemic heart disease.     

Clinical implication of persistent ischemic chest pain on admission in patients with late reperfused acute myocardial infarction

OBJECT: Although previous studies reported that late reperfusion might prevent left ventricular dilation after acute myocardial infarction (AMI), implication of persistent ischemic chest pain on admission remains to be investigated. This study was undertaken to assess the implication of persistent ischemic chest pain on in-hospital outcome and left ventricular function after late reperfused AMI. METHODS AND PATIENTS: We studied 63 patients with a first anterior AMI who underwent percutaneous coronary intervention 6 to 24 hours (11.2+/-4.5 hours) after the onset. Of 63 patients, 48 (76%) had persistent ischemic chest pain on admission. RESULTS: Incidence of in-hospital death, reinfarction or congestive heart failure was similar between the 2 groups. Pretreatment left ventricular ejection fraction and end-diastolic volume were similar between the 2 groups. Predischarge angiography was performed at 17+/-5 days after the onset. Late reperfusion prevented the dilation of left ventricular end-diastolic volume in patients with chest pain (78+/-12 to 75+/-17 ml/m2, p=0.15), but did not in those without (75+/-20 to 93+/-28 ml/m2, p=0.03). A multivariate analysis revealed that absence of persistent ischemic chest pain was an independent predictor of predischarge left ventricular end-diastolic volume >100 ml/m2 (odds ratio 0.10, p=0.04). CONCLUSIONS: Our data demonstrated that absence of persistent ischemic chest pain appears to be a simple and reliable marker which predicts left ventricular dilation after late reperfused AMI.     

One-year prognosis in patients hospitalized with a history of unstable angina pectoris

The prognosis during 1 year of follow-up in 715 patients admitted to one single hospital due to suspected acute myocardial infarction (AMI) with a history of unstable angina pectoris immediately preceding hospitalization is described. AMI developed in 192 patients (27%) during the first three days and in 255 patients (38%) during the first year. The mortality during hospitalization was 7% (50 patients) and during 1 year 19% (130 patients). Of the nonsurvivors, 54% died of AMI, 28% of congestive heart failure, and 20% of cardiogenic shock. Based on simple clinical parameters on admission to the emergency room, risk indicators for death during the following year could be identified as follows, in the order of significance: high age (p < 0.001), ST-segment depression on admission (p < 0.001), and a history of diabetes mellitus (p < 0.05). At admission to the emergency room, risk indicators for development of AMI during the following year were as follows: initial degree of suspicion of AMI (p < 0.001), electrocardiographic signs of acute ischemia on admission (p < 0.001), ST-segment elevation on admission (p < 0.01), age (p < 0.05), and lack of a previous history of chronic stable angina pectoris (p < 0.05). We conclude that, among patients admitted to hospital due to suspected AMI with a history of unstable angina pectoris immediately preceding hospitalization, 38% developed a confirmed infarction and 19% died during the following year.     

Temporal relation between left ventricular dysfunction and chest pain in coronary artery disease during activities of daily living

Forty-three ambulatory patients with angina of increasing frequency underwent continuous monitoring of left ventricular (LV) function for an average of 2.9 +/- 1.9 hours to determine the incidence and temporal sequence of LV dysfunction, ST-segment depression and chest pain. Indicators of ischemia were: a decrease in ejection fraction greater than 5% lasting greater than 1 minute; horizontal or downsloping ST-segment depression of greater than or equal to 1 mm; or onset of the patient's typical chest pain complex, or a combination of these. During the monitoring interval, subjects performed daily activities such as sitting, walking, climbing stairs and eating. In 11 patients, 22 episodes of chest pain or ST-segment depression, or both, were observed. Eighteen episodes were accompanied by a decrease in ejection fraction (9 patients); chest pain accompanied the decrease in ejection fraction during 13 episodes, whereas ST-segment changes occurred during 7. In 12 of 13 episodes the decrease in ejection fraction began earlier than the onset of chest pain, whereas in 1 patient ejection fraction decrease and chest pain onset started at the same time. The average interval from a decrease in ejection fraction to the onset of chest pain was 56 +/- 41 seconds (range 0 to 120). ST changes occurred after the onset of a decrease in ejection fraction in 6 of 7 episodes. The average interval from the onset of ejection fraction decrease and the onset of ST change was 99 +/- 91 seconds. These data suggest that LV dysfunction manifested by a decrease in ejection fraction is an earlier indicator of myocardial ischemia than is angina pectoris or electrocardiographic evidence of ischemia.     

Prognosis and risk indicators of death during a period of 10 years for women admitted to the emergency department with a suspected acute coronary syndrome

AIM: To describe the 10-year prognosis and risk indicators of death in women admitted to the emergency department with acute chest pain or other symptoms raising a suspicion of acute myocardial infarction (AMI). Particular interest was paid to women of 相似文献