This study sought to assess the rate of acute Thrombolysis In Myocardial Infarction (TIMI) trial grade 3 patency that can be achieved with the combination of prehospital thrombolysis and standby rescue angioplasty in acute myocardial infarction. No large angiographic study has been performed after prehospital thrombolysis to determine the 90-minute TIMI 3 patency rate in the infarct-related artery. Hospital outcome and artery patency were compared to 170 matched patients treated with primary angioplasty. Prehospital thrombolysis was applied 151 ± 61 minutes after the onset of pain in 170 patients (56 ± 12 years, 86% men), using recombinant tissue-type plasminogen activator, streptokinase, or eminase. Emergency 90-minute angiography was performed in every case. All patients in whom thrombolysis failed underwent rescue angioplasty. After thrombolysis alone, TIMI grade 3 flow in the infarct-related artery was observed in 108 patients (64%), TIMI grade 2 in 12 (7%), and TIMI grade 0 or 1 in 50 (29%). Rescue angioplasty was successful in 47 of 50 attempts. Overall, TIMI 3 patency was achieved in 91%, and additionally TIMI 2 flow in 7% of patients, an average of 113 ± 39 minutes after thrombolysis and 55 ± 19 minutes after admission. Therefore, <2 hours after thrombolysis, only 2% of patients had persistent occlusion (TIMI 0 or 1) of the infarct-related artery. In-hospital mortality was 4% overall (7 of 170), and 3% in the 155 patients in whom TIMI 3 was obtained during the acute phase. Severe hemorrhagic complications occurred in 14 patients (8%) with 2 fatal cerebral hemorrhages (7% of patients required transfusions). The matched comparison with primary PTCA showed no significant difference in hospital outcome. Combined prehospital thrombolysis, 90-minute angiography, and rescue angioplasty yield a high rate of acute TIMI 3 patency rate early after thrombolysis and hospital admission. A randomized, prospective comparison between these 2 reperfusion strategies may be now warranted.

This study assessed the prognostic value of cardiac troponin I (cTnI) and C-reactive protein (CRP) in unstable angina, and specifically in patients with angiographically proven coronary artery disease. These biochemical parameters, which are related to myocardial injury or to systemic inflammation, may help in short-term risk stratification of unstable angina. We prospectively studied 195 patients with unstable angina, 100 of whom had angiographically proven coronary artery disease (with normal creatine kinase [CK] and CK-MB mass). Serum concentrations of cTnI (N <0.4 ng/ml) and CRP (N <3 mg/L) were measured at admission, 12, and 24 hours later. The rate of in-hospital major adverse cardiac events (death, myocardial infarction, or emergency revascularization) was higher in patients with increased cTnI within the first 24 hours, regardless of the results of coronary angiography (23% vs 7%; p <0.001). Conversely, events occurred at similar rates in patients with or without increased CRP. In patients with angiographic evidence of coronary artery disease, multivariate analysis showed that increased cTnI within 24 hours of admission (35 patients) was an independent predictor of major adverse cardiac events (odds ratio 6.7, range 1.7 to 27.3), but not cTnI levels at admission and CRP at 0, 12, and 24 hours. Thus, both in unselected patients with unstable angina and in patients with angiographically proven coronary artery disease, increased cTnI within 24 hours of admission, but not CRP, is a predictor of in-hospital clinical outcome. We also found a temporal link between cTnI increase and late elevation of CRP, suggesting that systemic inflammation may partially be a consequence of myocardial injury.

The principal objective of treatment of the acute phase of myocardial infarction is the obtention of TIMI 3 complete patency. Usually, only a minority of patients receives thrombolytic therapy and complete reperfusion in unusual. Between June 1988 and April 1996, 700 consecutive patients were admitted to Bichat hospital within 6 hours of the onset of transmural myocardial infarction (81% men; age 59 +/- 13 years). The objective of treatment was to obtain maximal coronary patency in the acute phase, either by thrombolysis (with systematic angiography at 90 minutes and salvage angioplasty in case of failure), or primary angioplasty or conventional treatment (usually in cases of spontaneous reperfusion). The emergency angiography and angioplasty procedures were performed by a medical team on 24 hour duty. During the acute phase, 316 patients received intravenous thrombolysis (angiography at 90' in 302 patients with salvage angioplasty in 79 patients), 304 underwent primary angioplasty (TIMI 3 artery in 85% of cases) and 80 underwent conventional treatment (including 52 cases of angiographically documented spontaneous reperfusion). Therefore, a 81% (566/700) rate of patent TIMI 3 arteries was obtained. The hospital mortality was 8.9%, lower in TIMI 3 arterial patency (6%) than TIMI 2 (20%) or TIMI 0-1 (23%), p < 0.001. The mortality was 4% in patients treated by thrombolysis. Therefore, a reperfusion strategy associating thrombolysis and/or angioplasty provides a high TIMI 3 patency rate in the acute phase of myocardial infarction with a low mortality (6%) in consecutive, unselected patients.

AIMSTo determine the effect of sex on reperfusion therapy and early mortality after acute myocardial infarction.METHODSWe analysed the characteristics, the reperfusion interventions, and in-hospital mortality in 400 consecutive patients (320 men and 80 women) admitted during the first 6 h of acute myocardial infarction and treated by primary angioplasty, or intravenous thrombolysis with rescue angioplasty.RESULTSThe differences between men and women were age (57 vs 67 years, P = 0.001), systemic hypertension (33 vs 50%, P = 0.02), cigarette smoking (79 vs 30%, P = 0.0001) and contraindications to thrombolysis (28.5 vs 42.5%, P = 0.02). Successful reperfusion of the infarct-related artery was achieved in 84% of patients of both sexes. In-hospital mortality was 7.2% in men and 18.7% in women (P = 0.001). Multivariate analysis was performed by linear logistic regression in order to compare several embedded models, using repeated maximum likelihood ratio tests. The best model involved the variables of cardiogenic shock and age. Addition of the variable 'sex' did not improve the predictive power of this model (P > 0.5).CONCLUSIONDuring acute myocardial infarction, similar successful early reperfusion rates can be achieved in men and women, despite the lower eligibility of women for thrombolytic therapy. Although in-hospital mortality was higher in women than men, the best predictive model of mortality was the combination of age and cardiogenic shock. Therefore, sex does not appear to be an independent predictor of mortality.

Objectives. This study sought to assess the maximal rate of acute Thrombolysis in Myocardial Infarction (TIMI) grade 3 patency that can be achieved in unselected patients.Background. Early and complete (TIMI grade 3 flow) reperfusion is an important therapeutic goal during acute myocardial infarction. However, thrombolysis, although widely used, is often contraindicated or ineffective. The selective use of primary and rescue percutaneous transluminal coronary angioplasty (PTCA) may increase the number of patients receiving reperfusion therapy.Methods. A cohort of 500 consecutive unselected patients with acute myocardial infarction were prospectively treated using a patency-oriented scheme: Thrombolysis-eligible patients received thrombolysis (n = 257) and underwent 90-min angiography to detect persistent occlusion for treatment with rescue PTCA. Emergency PTCA (n = 193) was attempted in patients with contraindications to thrombolysis, cardiogenic shock or uncertain diagnosis and in a subset of patients admitted under ''ideal conditions.'' A small group of patients (n = 38) underwent acute angiography without PTCA. Conventional medical therapy was used in 12 patients with contraindications to both thrombolysis and PTCA.Results. Ninety-eight percent of patients received reperfusion therapy (thrombolysis, PTCA or acute angiography), and angiographically proven early TIMI grade 3 patency was achieved in 78%. Among patients with TIMI grade 3 patency, thrombolysis alone was, the strategy used in 37%, emergency PTCA in 40% and rescue PTCA after failed thrombolysis in 15%; spontaneous patency occurred in 8%.Conclusions. Reperfusion therapy fan be provided to nearly every patient (98%) with acute myocardial infarction. Rescue and direct TCA provided effective early reperfusion to patients id whom thrombolysis failed or was excluded. (C) 1997 by the American College of Cardiology.

AIMS:Prospectively to compare success rate and complications in percutaneous transluminal coronary angioplasty using two doses of heparin.METHODS AND RESULTS:Four hundred patients undergoing coronary angioplasty were randomly assigned to receive 15,000 IU (group A) or 100 IU.kg-1 (group B) of heparin. The angioplasty success rate was 95% of both groups. Stents were placed in 28.5% and 26.5% of patients in groups A and B, respectively (P = 0.73). The primary endopoint (freedom from death, myocardial infarction, unplanned revascularization or bailout stenting) occurred in 91% vs 95% of patients in groups A and B, respectively (odds ratio: 1.88, 95% CI: 0.80-4.50, P = 0.12). Haemoglobin loss was 0.36 +/- 1 and 0.27 +/- 0.9 g.dl-1 in groups A and B, respectively (P = 0.37). The time to sheath removal (735 +/- 265 vs 558 +/- 246 min) and the time to transfer to a stepdown unit (12.7 +/- 4.5 vs 9.8 +/- 4.2 h) were longer in groups A (P = 0.0001 for both comparisons).CONCLUSION:A weight-adjusted low dose of intravenous heparin is at least as safe as a fixed high dose for coronary angioplasty. It allows earlier sheath removal and discharge to a stepdown unit.

The role of systematic emergency percutaneous transluminal coronary angioplasty (PTCA) in patients with spontaneous reperfusion during myocardial infarction is debated. We retrospectively examined the inhospital outcome of 47 consecutive patients with myocardial infarction < 6 hours and angiographically proven spontaneous patency of the infarct artery managed without initial PTCA. There was one death (2.1%) and no incidence of reinfarction. Predischarge angiography showed regression of the culprit coronary lesion to < 50% stenosis in 23% of the patients, therefore obviating the need for PTCA. However, 17% of the patients had acute recurrent ischemia, requiring emergency intervention in 10.6%. Comparison with matched patients in whom Thrombolysis in Myocardial infarction grade 3 patency was achieved by thrombolysis or by primary PTCA showed that patients with spontaneous patency tended to have smaller infarctions, as judged from a lower peak creatine kinase level (1132 +/- 1002, 2051 +/- 1536, and 2715 +/- 2146 i.u., respectively; p = 0.001) and a higher left ventricular ejection fraction (56.4%, 47.9%, and 48.7% respectively; p = 0.02). In conclusion, these patients have an excellent inhospital outcome, with evidence of less myocardial damage than in patients in whom reperfusion therapy was required to achieve TIMI 3 patency. Initial conservative treatment appears safe.

The authors report two cases of pulmonary valve endocarditis which required emergency surgical treatment. A 74 year old patient with trivalvular endocarditis (pulmonary, aortic, mitral), due to Sptreptococcus D bovis, developed cardiogenic shock with acute pulmonary oedema and underwent double aortic and pulmonary valve replacement with Carpentier-Edwards prostheses and simple resection of a mitral valve vegetation. Another 36 year old drug addict developed isolated pulmonary valve endocarditis due to Staphylococcus aureus infection complicated by pulmonary regurgitation with right ventricular failure and by septic pulmonary embolism with persistent sepsis: he underwent pulmonary valve replacement with a Bravo 300 bioprosthesis. The postoperative course was uncomplicated in both cases, with interruption of the infection and normalisation of the haemodynamic status. The insidious and severe nature of pulmonary valve endocarditis is demonstrated by these two cases, confirming previous reports which have underlined the poor prognosis of this condition. Surgery has been shown to be effective and well tolerated and should be integrated early in the therapeutic strategy, the results being all the better when an aggressive attitude is taken.

The authors report two cases of pulmonary valve endocarditis which required emergency surgical treatment. A 74 year old patient with trivalvular endocarditis (pulmonary, aortic, mitral), due to Sptreptococcus D bovis, developed cardiogenic shock with acute pulmonary oedema and underwent double aortic and pulmonary valve replacement with Carpentier-Edwards prostheses and simple resection of a mitral valve vegetation. Another 36 year old drug addict developed isolated pulmonary valve endocarditis due to Staphylococcus aureus infection complicated by pulmonary regurgitation with right ventricular failure and by septic pulmonary embolism with persistent sepsis: he underwent pulmonary valve replacement with a Brave 300 bioprosthesis. The postoperative course was uncomplicated in both cases, with interruption of the infection and normalisation of the hemodynamic status. The insidious and severe nature of pulmonary valve endocarditis is demonstrated by these two cases, confirming previous reports which have underlined the poor prognosis of this condition. Surgery has been shown to be effective and well tolerated and should be integrated early in the therapeutic strategy, the results being all the better when an aggressive attitude is taken.

The pathogenic mechanism of unstable angina, a clinical expression of coronary heart disease, is similar to that of myocardial infarction. The main event is the instability of the atheromatous plaque adhering to the coronary intima leading to thrombosis and occlusion. Clinical manifestations can be severe since fatal or non-fatal myocardial infarction occurs in 3.9% and 5.4% of the case respectively. Adapted medical treatment can stabilize the situation in most patients, justifying early preventive treatment. Moreover, it has been estimated that a premonitory phase of angina had gone unnoticed or undiagnosed in one-half of all myocardial infarcts. In nearly all patients with unstable angina, coronarography is of major importance for rapidly defining an adapted therapeutic strategy. Myocardial revascularization (especially by angioplasty) is often needed to limit the risk of major cardiac events occurring within a short or moderate delay. Unfortunately, these procedures carry a supplementary risk of thrombosis. Thus the emphasis placed on measures capable of improving the anti-thrombotic risk in unstable angina by using new antiplatelet agents, or for certain patients at high risk of a major cardiac event, antithrombosis agents. Finally, the search for compounds capable of stabilizing the previously formed atheromatous plaque (and thus avoiding rupture) is a prime objective for an overall management strategy for patients with coronary heart disease.

The pathogenic mechanism of unstable angina, a clinical expression of coronary heart disease, is similar to that of myocardial infarction. The main event is the instability of the atheromatous plaque adhering to the coronary intima leading to thrombosis and occlusion. Clinical manifestations can be severe since fatal or non-fatal myocardial infarction occurs in 3.9% and 5.4% of the cases respectively. Adapted medical treatment can stabilize the situation in most patients, justifying early preventive treatment. Moreover, it has been estimated that a premonitory phase of angina had gone unnoticed or undiagnosed in one-half of all myocardial infarcts. In nearly an patients with unstable angina, coronarography is of major importance for rapidly defining an adapted therapeutic strategy. Myocardial revascularization (especially by angioplasty) is often needed to limit the risk of major cardiac events occurring within a short or moderate delay. Unfortunately, these procedures carry a supplementary risk of thrombosis. Thus the emphasis placed on measures capable of improving the anti-thrombotic risk in unstable angina by using new antiplatelet agents, or for certain patients at high risk of a major cardiac event, antithrombosis agents. Finally, the search for compounds capable of stabilizing the previously formed atheromatous plaque (and thus avoiding rupture) is a prime objective for an overall management strategy for patients with coronary heart disease.