Tissue-factor antigen and activity in human coronary atherosclerotic plaques

BACKGROUND: Coronary atherosclerotic-plaque thrombosis is a key event in the pathogenesis of unstable angina and myocardial infarction. Although plaque rupture or fissuring frequently occurs in atherosclerosis, only a small proportion of ruptured plaques develop thromboses. METHODS: Tissue-factor antigen and activity were measured in atherectomy samples from 50 consecutive patients with coronary artery disease (stable angina n = 19, unstable angina n = 24, and myocardial infarction n = 7). FINDINGS: Median tissue-factor antigen and activity concentrations were significantly higher in plaques from patients with unstable angina and myocardial infarction than in those from patients with stable angina (antigen: 66.1 pg/mg [interquartile range 43.8-82.5] vs 32.4 pg/mg [9.8-43.4], p = 0.0001; activity: 0.22 mU/mg [0.17-0.41] vs 0.13 mU/mg [0.05-0.16], p = 0.0004). INTERPRETATION: Tissue-factor, an initiator of the coagulation cascade, may account for the different thrombotic responses to the rupture of human coronary atherosclerotic plaques.     

Precision and accuracy of bone landmarks in characterizing hand and wrist position

We have investigated the relationship between plasma endothelin (ET) concentrations and several clinical characteristics in 31 patients with acute myocardial infarction (MI). ET levels were also measured in 10 age-matched healthy subjects, 9 patients with unstable angina, and 20 patients with chronic heart disease. In patients with MI, although no significant relationship was observed between plasma ET concentrations and measured hemodynamic parameters, plasma levels were higher in patients with pulmonary congestion than in those without this complication (1.61 +/- 0.29 vs 1.21 +/- 0.33 fmol/ml; p < 0.01). No significant difference in plasma ET levels was found between cardiac and peripheral sampling sites (pulmonary artery; 1.07 +/- 0.28, right atrium; 1.02 +/- 0.28, peripheral artery; 1.12 +/- 0.23, peripheral vein; 1.14 +/- 0.38 fmol/ml: N.S.), or among patients with uncomplicated MI, unstable angina (1.00 +/- 0.32 fmol/ml), and healthy subjects (1.01 +/- 0.29 fmol/ml). Increased level were observed in patients with decompensated heart failure due to chronic heart disease, but were not found in patients without pulmonary congestion (1.62 +/- 0.60 vs 1.11 +/- fmol/ml; p < 0.01). These observations suggest that plasma ET concentrations are elevated in the presence of congestive heart failure or severe ventricular depression, but are not persistently increased by myocardial ischemia per se.     

Lipoprotein(a) as a risk predictor for cardiac mortality in patients with acute coronary syndromes

AIMS: Raised lipoprotein(a) concentrations are considered to be a risk factor for atherothrombotic diseases. We examined whether baseline concentrations were a risk factor for an adverse outcome in patients admitted with acute coronary syndromes. METHODS AND RESULTS: Five hundred and nineteen patients admitted with suspected acute coronary syndromes were studied and followed prospectively for a median of 3 years. The prognostic significance of a baseline lipoprotein(a) concentration of > or = 30 mg x dl(-1) or lower for subsequent cardiac death was assessed in patients with myocardial infarction (266) and unstable angina (197) and compared with other variables in regression models. In patients with myocardial infarction, a baseline lipoprotein(a) concentration of > or =30 mg x dl(-1) was associated with a 62% increase in subsequent cardiac death compared to the lower concentration group (29.8% vs 18.6%, Log rank P=0.04). In a multivariate regression model a baseline lipoprotein(a) concentration of > or = 30 mg x dl(-1) retained its significance as an independent predictor of cardiac death (P=0.037). In patients with unstable angina, baseline concentrations of > or = 7.9 mg x dl(-1) were found to be significant predictors of cardiac death in univariate (P=0.021) and multivariate (P=0.035) regression models. CONCLUSION: Baseline lipoprotein(a) concentrations in patients admitted with acute coronary syndromes are associated with an increased risk of cardiac death. For patients with myocardial infarction a concentration of > or = 30 mg x dl(-1) appears appropriate as a risk discriminator; for patients admitted with unstable angina, however, much lower concentrations of lipoprotein(a) appear to be prognostically important.     

Long-term (10-year) outcome in patients with unstable angina pectoris treated by coronary balloon angioplasty

OBJECTIVES: We sought to examine completed 10-year survival and event-free survival in patients with stable and unstable angina pectoris treated by coronary balloon angioplasty. BACKGROUND: Patients with unstable angina are at increased risk for recurrent acute coronary events. METHODS: The study included 208 consecutive patients (133 with stable and 75 with unstable angina pectoris) undergoing angioplasty from 1984 to 1986. The balloon crossed the lesion in 185 patients (121 with stable and 64 with unstable angina pectoris). Angioplasty was performed in patients with unstable angina pectoris 12+/-15 days (median 8) after symptom onset. Patients with unstable angina pectoris were classified retrospectively into Braunwald class I (n=3), class II (n=20), class III (n=28), class B (n=52) and class C (n=12). Follow-up data were obtained from hospital charts, telephone interview and official death certificates where applicable. The study had >80% power to detect a clinically significant 20% difference in survival and a 20% difference in event-free survival between the stable and unstable patient groups. RESULTS: Despite similar baseline characteristics, early (40-day) mortality was slightly higher in patients with unstable angina (4.7% [3 of 64 patients] vs. 0.8% [1 of 121 patients], p=NS). Long-term outcome was not different, because survival curves were parallel thereafter (10-year survival was 83% for those with stable and 77% for those with unstable angina, p=NS). Survival free of myocardial infarction or coronary artery bypass graft surgery at 10 years was 53% in patients with stable and 47% in patients with unstable angina (p=NS), and survival free of infarction, bypass surgery or repeat angioplasty was 32% for both groups at 10 years. In patients with Braunwald class III unstable angina, 10-year survival was 80%, as compared with 85% in other patients with unstable angina, due to the early hazard (p=NS). Survival and event-free survival were similar in patients who had had a recent myocardial infarction (Braunwald class C) and in patients with acute electrocardiographic changes. Repeat hospital admissions were not more frequent in patients with unstable angina (3.1+/-3.5 vs. 3.0+/-2.6, p=NS). CONCLUSIONS: Ten-year survival and event-free survival were similar in patients with stable and unstable angina pectoris treated by coronary balloon angioplasty, with no evidence of an increased rate of recurrent cardiovascular events in the unstable group.     

Initial experience with the use of abciximab in the salvage treatment of acute coronary thrombosis in the Hemodynamics Laboratory

The optimal treatment of acute thrombotic complications in the Catheterization Laboratory has not been defined yet, due to the limited efficacy shown by various pharmacological regimens, even when associated to coronary angioplasty (PTCA). The aim of our study was therefore to evaluate the effects of abciximab (ReoPro), a new potent inhibitor of the platelet glycoprotein IIb/IIIa, when administered as a "rescue" treatment for acute thrombotic coronary occlusion during diagnostic or interventional procedures. Sixteen patients (12 males, 4 females, mean age 59.3 +/- 9.2 years, range 43-77 years), with unstable angina and consecutively treated with abciximab due to clinical instability attributable to coronary thrombosis angiographically proven during PTCA (9 cases) or diagnostic angiography (7 cases), were identified. The individual angiographic films and medical records were then reviewed in order to evaluate the effects of treatment on coronary flow, thrombus size and occurrence of in-hospital adverse events: death, non-fatal acute myocardial infarction (AMI), need for urgent myocardial revascularization and hemorrhage. The administration of abciximab, in association with PTCA (associated in turn with stent implantation in 8 cases), induced a significant increase of coronary TIMI flow grade (0.3 +/- 0.6 vs 2.4 +/- 0.9; p < 0.05) and a significant decrease of thrombus "score" (size) 2.4 +/- 0.9 vs 1.3 +/- 0.6; p < 0.01). No deaths nor need for urgent myocardial revascularization were observed; in 31% of cases (5 patients) evolution towards AMI occurred, while however 94% of cases (15 patients) had a coronary occlusion before treatment. No major hemorrhagic complications were observed, while in 12% of cases (2 patients) a groin hematoma associated with moderate hemoglobin drop, developed. In conclusion, the administration of abciximab, associated with the common "rescue" interventional procedures, in patients with acute thrombotic coronary occlusion in the Catheterization Laboratory, appears to be effective in restoring adequate coronary flow and reducing the thrombus size (limiting therefore the evolution towards AMI), and safe, not having been associated with significant hemorrhagic complications.     

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.     

Unstable angina in coronary intensive care units without hemodynamics: is admissible a strategy limiting the indications for coronarography?

In coronary care units (CCU) without cardiac catheterization facilities, coronary angiography is rarely carried out when a successful medical treatment in the acute phase of unstable angina has been obtained. However, the unstable angina still has an uncertain prognosis when the remission of pain is obtained with drugs. This study presents a follow-up of 147 consecutive patients (aged 66.8 +/- 10.4 years) admitted to our CCU in 1991 and 1992 for unstable angina; 33 of them (22.4%) were in Braunwald class I. 2 (1.4%) in class II and 112 (76.2%) in class III. The patients were treated according to the usual therapy protocols and class III patients received i.v. heparin. In selected cases we used thrombolysis (10 patients) and intra-aortic balloon pump (5 patients). During hospitalization 1 patient died (0.7%), 5 patients (3.4%) suffered an acute myocardial infarction and 9 patients (6.1%) had angina. Stabilization of unstable angina was achieved in 132 patients (89.9%): in 113 (76.8%) during the first 48 hours, and in 19 (12.9%) later. Coronary angiography was carried out in non-stabilized patients and in 46 (34.8%) of the 132 with successful treatment (Group I). Eighty-six patients, without indication to coronary angiography were discharged in medical therapy (Group II). During the follow-up (mean of 15.0 +/- 9.0 months) Group I 10 patients (18.2%) had cardiac events (death, myocardial infarction, or recurrent angina) vs 26 of Group II (p < 0.05). In Group I coronary angiography together with clinical criteria of high risk allowed the identification of candidates to coronary revascularization (61.8% of Group I patients while). These data show that the initial success of treatment during the acute phase of unstable angina should not be considered as a favourable prognostic index. Coronary angiography appears to be indicated for clinical evaluation and therapeutical decision.     

C-reactive protein as a marker for acute coronary syndromes

BACKGROUND: For several years, acute coronary syndromes have been perceived as causing the most hospital admissions, and even hospital mortality. The syndrome of unstable angina frequently progresses to acute myocardial infarction but its pathogenesis is poorly understood, and prognosis determination is still problematic. We tested the hypothesis that measurement of the C-reactive protein in patients admitted for chest pain could be a marker for acute coronary syndromes. METHODS AND RESULTS: We studied 110 patients admitted with suspected ischaemic heart disease, but without elevated serum creatine-kinase levels at the time of hospital admission. Patients were subsequently divided into two groups based on their final diagnosis: group 1 comprised patients with unstable angina; group 2 patients with acute myocardial infarction. We measured the C-reactive protein at the time of hospital admission. The concentration of C-reactive protein was elevated in 59% of the patients with a final diagnosis of acute myocardial infarction, and in 5% of the patients with a final diagnosis of unstable angina, (P < 0.001). CONCLUSION: This study indicates that C-reactive protein levels measured at the time of admission in patients with suspected ischaemic heart disease could be a marker for acute coronary syndromes, and helpful in identifying patients at high risk for acute myocardial infarction. Measurement of C-reactive protein may have practical clinical significance in the management of patients hospitalized for suspected acute coronary syndromes.     

Comparison of coronary angiographic findings in acute and chronic first presentation of ischemic heart disease

BACKGROUND: It is generally assumed that the clinical manifestations of ischemic heart disease occur randomly on the same underlying pathological process. Therefore, coronary angiographic findings should be similar whether the first presentation of ischemic heart disease is acute myocardial infarction or uncomplicated chronic stable angina. METHODS AND RESULTS: We studied 102 patients (men < or = 60 years old, women < or = 65 years old) presenting with either acute myocardial infarction as first manifestation of coronary artery disease with a concomitant coronary angiogram (55 patients; mean age, 50.2 years) or stable angina for at least 2 years with no history, ECG, or left ventriculographic evidence of any acute event and with an angiogram performed at least 2 years after initial symptoms (47 patients; mean age at symptom onset, 51.7 years). These angiograms were evaluated blindly for severity (number of vessels diseased, stenoses > or = 50%, occlusions), extent of disease (with an index derived by assigning a score of 0-3 per segment, depending on the proportion of lumen length irregularity and dividing the sum by the number of visualized segments), and pattern (discrete: three or fewer loci of disease never involving more than 50% of the length of any segment or diffuse: anything exceeding this). Patients with unheralded myocardial infarction had fewer vessels diseased, fewer stenoses and occlusion, and a lower extent index than those with uncomplicated stable angina (mean +/- SD of 1.3 +/- 0.8 versus 2.1 +/- 0.8, p < 0.001; 2.1 +/- 1.8 versus 3.9 +/- 1.8, p < 0.001; 0.6 +/- 0.6 versus 1.0 +/- 0.9, p < 0.02; and 0.6 +/- 0.5 versus 1.2 +/- 0.5, p < 0.001, respectively). A discrete pattern was present in 54.5% of patients with unheralded infarction and in only 8.5% of those with uncomplicated angina (p < 0.001). CONCLUSIONS: These very different angiographic findings suggest that unheralded acute myocardial infarction and uncomplicated chronic stable angina do not occur randomly on a common atherosclerotic background but rather that additional factors, such as a varying propensity to thrombosis, may predispose to one or the other of these two clinical syndromes.     

The protective effect of captopril on the ischemic myocardium in dogs through coronary sinus retroperfusion

The protective effect of coronary sinus retroperfusion of Captopril on the ischemic myocardium was observed in dogs with acute myocardial infarction (AMI). The results showed that the infarction size and the level of coronary sinus plasma endothelin (ET) and manodialdenyde (MDA) were smaller and lower when Captopril was administered by coronary sinus retroperfusion than that by systemic intravenous injection. These results suggest that (1) Captopril can be distributed adequately in the local ischemic myocardial zones when administered by coronary sinus retroperfusion in the presence of coronary artery occlusion, (2) Captopril can more effectively protect ischemic myocardium by inhibition of the ET release and against the oxygen free radicals in ischemic myocardial area when used by coronary sinus retroperfusion.     

Cataract extraction rates in Olmsted County, Minnesota, 1980 through 1994

Management of Q-wave acute myocardial infarction (AMI) has been shown to differ between the United States and Canada, with more catheterization and revascularization procedures performed in the United States, but with little or no apparent difference in clinical outcomes. No previous studies have evaluated management differences for the acute coronary syndromes of unstable angina pectoris and non-Q-wave AMI. We therefore compared treatments and outcomes between 14 United States and 4 Canadian tertiary care centers participating in an observational registry of all consecutive admissions for unstable angina or non-Q-wave AMI between 1990 and 1993. A random, stratified sample was selected for detailed assessment and follow-up. There were 1,733 patients enrolled in United States centers and 642 in Canadian ones. In United States centers patients were less likely to receive intravenous nitroglycerin, heparin, beta blockers, calcium antagonists, or > or = 2 anti-ischemic agents. Coronary arteriography during index hospitalization was equally frequent in both countries (63.4% vs 66.9%, p = 0.781), but at 6 weeks and 1 year coronary arteriography was slightly less frequent in the United States patients. Revascularization by coronary angioplasty or bypass surgery was equivalent at 6 weeks and 1 year; however, there were trends toward less angioplasty and more bypass surgery in the United States than in Canada. Patients at United States centers stayed in the hospital fewer days than patients at Canadian centers (mean 8.2 vs 12.1 days, p <0.001). Death or AMI by 6 weeks was not different (4.8% vs 4.4%, p = 0.633), nor was it different at 1 year (10.0% vs 10.2%, p = 0.836). The combined outcome of death, AMI, or recurrent ischemia was more common in United States than in Canadian patients at 6 weeks (18.4% vs 13.9%, p = 0.004). Our findings indicate that United States physicians and hospitals did not consistently utilize more resources and were not more aggressive than their Canadian counterparts when treating acute coronary syndromes during this period.     

Troponin T in patients with low grade or atypical angina. Identification of a high risk group for short- and long-term cardiovascular events

AIMS: Cardiac troponin T is an established marker of cardiovascular risk in patients with severe angina pectoris. Data are scarce on patients admitted to a coronary care unit with low grade or atypical angina pectoris to rule out myocardial infarction. METHODS AND RESULTS: We investigated 106 patients (57.4 SD 11.6 years) with low grade (Braunwald class I) or atypical symptoms out of 702 patients admitted to the coronary care unit with suspected acute myocardial infarction. Serum concentrations of troponin T were measured at admission and 4 h later. In hospital cardiovascular events including acute myocardial infarction, life threatening cardiac arrhythmias, congestive heart failure, and death were recorded. Patients were additionally observed after 3 and 6 months post-discharge regarding acute myocardial infarction, unstable angina, rehospitalization for cardiac causes and death. The patients were divided into a troponin T positive (> or =0.2 microg x 1(-1) at admission or 4 h later; n=11) and a troponin T negative group. The mean value of troponin T 4 h after admission in the positive group was 0.58 microg x 1(-1). Of the troponin T positive patients, 0.82 (0.95 CI: 0.48-0.98) had a cardiovascular event during their stay in hospital vs 0.41 (0.95 CI: 0.31-0.52) of troponin T negative patients (P<0.05). In the troponin T positive group 0.64 (0.95 CI: 0.31-0.89) developed myocardial infarction in hospital vs 0.07 (0.95 CI: 0.03-0.15) in the troponin T negative group (P<0.001). Troponin T predicts outcome after 3 and 6 months significantly (P<0.05). CONCLUSION: Troponin T identifies patients with low grade or atypical angina at risk of severe short- and long-term cardiovascular events. Therefore, troponin T adds substantial information in patients with ruled out acute myocardial infarction. Troponin T positive patients have to be observed carefully regardless of their symptom intensity and may have to receive early cardiac catheterization; troponin T negative patients could be released safely from the coronary care unit early.     

Treatment of ostial lesions of the left anterior descending coronary artery with Palmaz-Schatz coronary stent

We evaluated acute and long-term clinical and angiographic results of elective Palmaz-Schatz coronary stent implantation for left anterior descending coronary artery (LAD) ostial stenosis in 23 consecutive patients. Eight patients had stable angina, 14 had unstable angina, and 1 had recent myocardial infarction. Sixteen patients had single-vessel, 5 had double-vessel, and 2 had triple-vessel disease. Clinical success without major complications (death, acute myocardial infarction, emergency coronary artery bypass grafting) was obtained in all cases and technical success in 20 cases (86.9%). After stenting, minimal lumen diameter increased from 1.05 +/- 0.45 mm to 2.89 +/- 0.52 mm (p < 0.001), and percent diameter stenosis decreased from 65.49% +/- 13.36% to 2.94% +/- 19.93% (p < 0.001). One case of subacute thrombosis and no major bleeding occurred. Twenty patients were followed-up for 6 months, during which no acute cardiac event (death, acute myocardial infarction) was observed. Eighteen patients were eligible for follow-up coronary angiography; restenosis (> or = 50% diameter stenosis) was observed in 4 (22.2%). Minimal lumen diameter was 1.77 +/- 0.55 mm, percent diameter stenosis was 39.66% +/- 17.62%, late loss was 1.01 +/- 0.69 mm, net gain was 0.79 +/- 0.55 mm, and loss index (late loss/acute gain) was 0.53 +/- 0.37. This study suggests that elective Palmaz-Schatz stent implantation may be a safe and successful treatment of LAD ostial lesions and provides a large increase in lumen diameter.     

Successive ischemic events to a first acute myocardial infarct treated with fibrinolysis. An analysis of GISSI-2 patients considered reperfused by a clinical criterion. Participants in the GISSI-2 study. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico

BACKGROUND: The fast normalisation of the ST, after thrombolysis, is early sign related to coronary artery reperfusion and to prognosis of acute myocardial infarction (AMI). The aim of this analysis is the evaluation, in the large patients cohort of the GISSI-2 trial, of the relationship between the ST segment evolution after fibrinolytic therapy of AMI and recurrent ischaemic events [angina-reinfarction-ischaemia to exercise testing (ET)] at 30 and 180 days from randomisation. METHODS: Patients with first confirmed IMA and ECG before randomisation and 4 hours later, are chosen from GISSI-2 trial. A decrease > or = 50% of the sigma ST elevation is adopted as cutoff for predicting coronary artery patency. Recanalisation is deemed to have occurred in group A patients versus not reperfused group B patients. The studied events are: angina, reinfarction, mortality, at 30 and 180 days from randomisation; ischemia to ET SL of 4-6 week. The results are presented in terms of Mantel-Haenszel odds ratios (OR) and 95% confidence intervals. RESULTS: Group A patients n. 5307 experienced versus group B patients n. 2718 a higher incidence of--in-hospital angina: 10.3% vs 7.9% OR 1.30 (1.11-1.52)-180 days reinfarction: 2.9% Vs 1.7% OR 1.66 (1.19-2.30)-Ischaemia to ET 25.4% vs 21.4% OR 1.24 (1.08-1.43), and a lower in-hospital mortality: 3.8% vs 8.5% OR 0.39 (0.32-0.48). CONCLUSIONS: Patients having indirect signs of early reperfusion post thrombolysis for IMA experience a higher in-hospital and 180 days recurrent ischaemia and a lower mortality; this fact can allow early identification of the patients who can receive a benefit from different therapeutical strategies.     

Pathogenesis of acute coronary syndromes

Coronary artery diseases may categorized into asymptomatic disease, angina pectoris, myocardial infarction, chronic heart failure, and sudden coronary death. Unstable angina, acute myocardial infarction, and sudden cardiac death are known as the acute coronary syndromes. Coronary atheroma is unstable in the patients with acute coronary syndromes. Stable plaques will be unstable when dynamic alterations occur. The alterations are plaque rupture, plaque hemorrhage, coronary thrombosis and vasospasm. They act each other. We analysed the histopathology of coronary arteries who died of acute myocardial infarction in 85 cases. It showed that the risk factors of plaque rupture are clusters of form cells, eccentric plaque with soft lipid rich core, and thinning of fibrous cap in atheroma. Most of these cases ruptured at edge of the atheroma.     

Decreased baroreflex sensitivity in patients with stable coronary artery disease is correlated with the severity of coronary narrowing

Although studies have shown that arterial baroreflex sensitivity (BRS) is decreased in patients with acute myocardial infarction, BRS changes in patients with stable coronary artery disease (CAD) have not been studied extensively. We assessed BRS by the phenylephrine method in 55 normotensive and nondiabetic patients with chronic effort angina, old myocardial infarction, or both. The control group consisted of 24 age-matched patients without coronary lesions. To identify factors that determine BRS in stable CAD, we performed multivariate analysis using age, sex, left ventricular ejection fraction, pulmonary artery wedge pressure, resting systolic blood pressure, resting heart rate, the number of stenotic coronary arteries, history of myocardial infarction, and the presence or absence of angina pectoris as variables. BRS was significantly lower in patients with CAD than in control subjects (5.9 +/- 2.9 vs 6.9 +/- 2.4 ms/mm Hg, p < 0.05). In patients with CAD, BRS was inversely correlated with age, the resting heart rate, and the number of stenotic coronary vessels (p < 0.001, p < 0.005, and p < 0.005, respectively), but was independent of other clinical parameters, including the history of myocardial infarction. In control subjects, BRS was significantly correlated only with age. These results indicate that BRS is decreased in patients with stable CAD, and this decrease is correlated with the extent and severity of coronary narrowing.     

Effect of puerarin on plasma endothelin, renin activity and angiotensin II in patients with acute myocardial infarction

OBJECTIVE: To study the changes of endothelin (ET), renin activity (RA) and angiotensin II (AT-II) before and after puerarin treatment in patients with acute myocardial infarction (AMI). METHODS: Forty-three patients with AMI were divided into two groups, and were given puerarin and glucose-insulin-kalium (GIK) treatment respectively. Plasma ET, RA and AT-II were measured by radioimmunoassay (RIA) before and after treatment in different phases. RESULTS: It showed that plasma ET and RA, AT-II levels in AMI were higher than those in control group (P < 0.01). ET level was conversely correlated with RA and AT-II (P < 0.01). After treatment with puerarin, plasma levels of ET, RA and AT-II were recovered to normal in 3 days, but these data recovered to nearly normal until 7-14 days in group with GIK treatment. CONCLUSION: Puerarin might play an important role in regulating the imbalance of ET, RA and AT-II of patients with AMI.     

Myocardial contrast echocardiography versus dobutamine echocardiography for predicting functional recovery after acute myocardial infarction treated with primary coronary angioplasty

OBJECTIVES: We sought to compare myocardial contrast echocardiography with low dose dobutamine echocardiography for predicting 1-month recovery of ventricular function in acute myocardial infarction treated with primary coronary angioplasty. BACKGROUND: The relation between myocardial perfusion and contractile reserve in patients with acute myocardial infarction, in whom anterograde flow is fully restored without significant residual stenosis, is still unclear. METHODS: Thirty patients with acute myocardial infarction treated successfully with primary coronary angioplasty underwent intracoronary contrast echocardiography before and after angioplasty and dobutamine echocardiography 3 days after the index infarction. One month later, two-dimensional echocardiography and coronary angiography were repeated in all patients and contrast echocardiography in 18 patients. RESULTS: After coronary recanalization, 26 patients showed myocardial reperfusion within the risk area, although 4 did not. At 1-month follow-up, all patients had a patient infarct-related artery without significant restenosis. Both left ventricular ejection fraction and wall motion score index within the risk area significantly improved in the patients with reperfusion ([mean +/- SD] 38 +/- 8% vs. 48 +/- 12%, p < 0.005; and 2.35 +/- 0.5 vs. 2 +/- 0.6, p < 0.001, respectively), but not in those with no reflow. Of the 72 nonperfused segments before angioplasty, 27 showed functional improvement at follow-up. Myocardial contrast echocardiography had a sensitivity and a negative predictive value similar to dobutamine echocardiography in predicting late functional recovery (96% vs. 89% and 89% vs. 93%, respectively), but a lower specificity (18% vs. 91%, p < 0.001), positive predictive value (41% vs. 86%, p < 0.001) and overall accuracy (47% vs. 90%, p < 0.001). CONCLUSIONS: Microvascular integrity is a prerequisite for myocardial viability after acute myocardial infarction. However, contrast enhancement shortly after recanalization does not necessarily imply a late functional improvement. Thus, contractile reserve elicited by low dose dobutamine is a more accurate predictor of regional functional recovery after reperfused acute myocardial infarction than microvascular integrity.     

Variations between countries in invasive cardiac procedures and outcomes in patients with suspected unstable angina or myocardial infarction without initial ST elevation. OASIS (Organisation to Assess Strategies for Ischaemic Syndromes) Registry Investigators

BACKGROUND: There are wide variations between countries in the use of invasive cardiac catheterisation and revascularisation procedures for patients with acute ischaemic syndromes. We studied the relation between rates of such procedures and rates of cardiovascular death, myocardial infarction, stroke, refractory angina, and major bleeding in a prospective, registry-based study in six countries with widely varying intervention rates. METHODS: 7987 consecutive patients presenting with unstable angina or suspected myocardial infarction without ST-segment elevation were recruited prospectively from 95 hospitals in six countries and followed up for 6 months. FINDINGS: The rates of all procedures were highest in patients in Brazil and the USA, intermediate in Canada and Australia, and lowest in Hungary and Poland. There were no significant differences in rates of cardiovascular death or myocardial infarction among these countries (4.7% overall [range 3.7-5.6] at 7 days; 11% overall [9-12] at 6 months). For the countries with the highest rates of invasive procedures (59%) versus the rest (21%) there was no difference in rate of cardiovascular death or myocardial infarction (adjusted odds ratio 0.88 at 7 days and 1.0 at 6 months). Rates of stroke were higher in Brazil and the USA than in the countries with lower intervention rates (adjusted odds ratio at 7 days 3.0, p=0.012; at 6 months 1.8, p=0.004) but rates of refractory angina at 7 days (0.7, p<0.001) and readmission for unstable angina at 6 months were lower (0.70, 0.63; both p<0.001). Comparison of results for hospitals without cardiac-catheterisation facilities and for those with such facilities gave adjusted odds ratios for cardiovascular death, myocardial infarction, or stroke at 6 months of 0.83 (10.6% vs 12.5%, p=0.05) and for refractory angina of 1.25 (19.3% vs 16.1%, p=0.09). INTERPRETATION: Higher rates of invasive and revascularisation procedures were associated with lower rates of refractory angina or readmission for unstable angina, no apparent reduction in cardiovascular death or myocardial infarction, but with higher rates of stroke. Randomised trials should assess the relative impact of conservative and more aggressive approaches to invasive cardiac procedures and revascularisations in patients with unstable angina.     

Impaired platelet production of nitric oxide predicts presence of acute coronary syndromes

BACKGROUND: Thrombus formation within a coronary vessel is the acute precipitating event in most acute coronary syndromes. Recently, constitutive nitric oxide synthase (cNOS) has been identified in human platelets, and platelet-derived nitric oxide has been shown to inhibit platelet recruitment after aggregation. However, its role in regulating platelet responses under normal or pathologic conditions has not yet been elucidated. METHODS and RESULTS: We examined nitric oxide (NO) production by platelets isolated from 87 patients undergoing coronary angiography, 37 with stable angina and 50 with unstable angina or a myocardial infarction within 2 weeks. After stimulation with 5 micromol/L ADP, platelet aggregation and NO production were simultaneously measured with an NO-selective microelectrode adapted for use in a standard platelet aggregometer. Mean (+/-SEM) platelet-derived NO production was 1.78+/-0.36 pmol/10(8) and 0.26+/-0.05 pmol/10(8) platelets in coronary patients with stable angina and acute coronary syndromes, respectively (P=0. 0001). By logistic regression analysis, heparin treatment (odds ratio 6.6, CI 1.9 to 22.8, P=0.003), lower platelet-NO production (odds ratio 4.0, CI 1.3 to 11.5, P=0.01), and extent of atherosclerosis (odds ratio 1.5, CI 1.1 to 2.0, P=0.02) were independent predictors of an acute coronary syndrome. In the subset of patients with angiographic evidence of atherosclerosis (n=83), logistic regression demonstrated that platelet NO production (odds ratio 3.9, CI 1.3 to 11.1, P=0.01) and heparin treatment (odds ratio 6.4, CI 1.9 to 22.0, P=0.004) were independent predictors of an acute coronary syndrome, whereas extent of atherosclerosis was not. CONCLUSIONS: In summary, aggregating platelets from patients with acute coronary syndromes produce less NO. Since platelet aggregation and thrombus formation are implicated in unstable angina and myocardial infarction, impaired platelet-derived NO production may contribute to the development of acute coronary syndromes.