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The guidelines of the European Society of Cardiology, published in 2003, consider primary angioplasty as the preferred treatment strategy in acute coronary syndromes with ST-segment elevation, if the procedure can be performed within 90 min after first medical contact. We report the experience of three Alsacian centers running a common prospective registry with 2504 consecutive patients enroled between January 1999 and December 2004. The average age of the patients was 62 years with a proportion of 24% women. The time delay "pain to admission" was > or =3 hours in 55.9% of the cases. The treatment delay "door to catheterisation needle" was 59 min and the mean delay "door-to-reperfusion" was 79 min. The study population was representative of the real world including subsets of patients with a particulary high risk profile: age > or =70 years in 33%, a Killip grade > or =3 in 11.5%, rescucitated sudden death in 6.6% and cardiogenic shock in 10.9% of the patients respectively. The immediate procedural success rate (Timi 3 flow) in the treated coronary artery was 96.5%. The overall inhospital mortality-rate was 9.3%. The combinations of rescucitated sudden death--cardiogenic shock or age > or =75 years--cardiogenic shock were associated with a poor clinical outcome and mortality rates of 69% and 72.6% respectively, where as in the absence of abovementioned clinical high risk settings, the mortality rate was as low as 1.4%. The overall bleeding complication rate was 1.4%. The policy of systematic primary angioplasty in acute coronary syndromes with ST-Segment elevation appears to be coherent. The procedural complications and the in-hospital mortality rates were low, except in the presence of above mentioned clinical high risk settings.

Rupture of the pulmonary artery or of one of its branches during a Swan-Ganz catheterisation is a rare complication which remains lethal in about 50% of cases. The risk factors and mechanisms of this complication have been previously described. There are two means of treatment: intensive care and specific medical or surgical treatment. In this case, the rupture of the pulmonary artery occurred during Swan-Ganz catheterisation and was treated by coil embolisation. This simple and rapid technique seems to be very promising.

Complete thrombosis of the left main coronary artery is a rare angiographic finding and usually gives rise to cardiogenic shock during unstable angina or myocardial infarction. The prognosis of this condition is very dependent on the collateral coronary circulation and the myocardial protection seems to depend on the rapidity of revascularisation. Two therapeutic approaches may be envisaged; emergency coronary bypass grafting or percutaneous angioplasty, the natural history being particularly disastrous. The authors report the case of a 42-year-old patient with complete occlusion of the left main stem responsible for unstable angina and acute pulmonary oedema. The outcome with angioplasty in the acute phase associated with surgical revascularisation four days later, was good.

Intracoronary thrombolysis showed the chronological order of clinical electric and biological changes following the reestablishment of coronary flow. These changes make up the reperfusion syndrome; ST segment changes are part of this syndrome. They occur in practically all cases at the moment of reperfusion. The ST elevation may regress more or less rapidly or, on the contrary, increase transiently to a greater or lesser degree. When associated with other criteria of reperfusion-enzyme changes, arrhythmias, ST changes contribute to the indirect diagnosis of reestablishment of coronary flow. Rapid decrease in ST segment elevation is usually associated with a good myocardial outcome. The prognostic significance of transient increases in ST elevation--so called "reperfusion ischaemia"--is not fully understood, in particular its relationship to myocardial reperfusion injury. The myocardial prognosis after reperfusion may be the "biological" sum of cellular lesions due to ischaemia and reperfusion.

Myocardial infarction is an anatomical and therefore functional amputation of some of the myocardial tissues. Moments after acute coronary occlusion, a cascade of metabolic, mechanical and electrical ischaemia related events is observed. Contraction stops and regional left ventricular akinesis (then dyskinesis) occurs in the zone at risk of irreversible myocardial damage. This is partially compensated by hyperkinetic motion of non-ischaemic myocardium. The degree of alteration of the global ejection fraction is the resultant of these akinetic and hyperkinetic wall motions. It is lower in cases of anterior myocardial infarction, of occlusion of the proximal segment of the left anterior descending artery and of multivessel disease. Its eventual outcome depends on coronary blood flow. If the artery responsible is recanalized early, the global ejection fraction stabilises or improves. When this does not happen, the global ejection fraction decreases. The end-diastolic volume, an indicator of left ventricular remodeling, increases in relation to the size of the infarct and to the persistence of coronary artery occlusion. The delay before the appearance of the first irreversible lesions, the rate of their propagation within the myocardial wall and the presence of reperfusion lesions are poorly understood factors in the clinical setting and influence the efficacy of methods of myocardial protection.

Acute myocardial infarction is the result of sudden coronary occlusion in the absence of a collateral circulation. There main factors are required for this to occur: an acute parietal lesion on a stenosis of variable, sometimes minor, importance; local coronary vasoconstriction and a platelet and fibrin thrombus. Parietal fissuration is the commonest "trigger" of coronary spasm and the thrombotic cascade. All factors of coronary occlusion are potentially reversible--vasodilation--platelet anti-aggregation--physiological fibrinolysis--remodeling and cicatrisation of the plaque, thereby explaining cases of spontaneous regression of occlusion (10% at 1 hour; 20% at 6 hours; 30% at 24 hours; 50 to 70% at 1 year). The pathogenesis of myocardial infarction with angiographically normal coronary arteries may be reviewed and attributed to acute parietal fissuration at a non-significant or angiographically undetectable plaque resulting in occlusive thrombosis. In this case, the role of other pathogenic factors is also discussed (diabetes, oral contraception, haemostatic abnormalities, platelet disorders...).

Myocardial reperfusion is associated with a number of clinical, electrocardiographic (arrhythmias, conduction defects, ST segment changes), haemodynamic and biological events. The commonest arrhythmias are ventricular extra-systoles, rapid ventricular tachycardias, and accelerated idio-ventricular rhythms. Reperfusion bradycardias are less common. When the arrhythmia is related to ischaemia it usually regresses when perfusion is restored. Reperfusion of the inferior wall of the left ventricle is often associated with sinus bradycardia and hypotension. The ST segment changes may evolve in two different ways: progressive regression or accentuation of ST elevation. When the responsible artery is recanalized, there is an immediate rise in plasma enzyme and myoglobin concentrations. The peak CPK concentration is usually observed after the 12th hours. The diagnostic value of the reperfusion syndrome lies in the interpretation of rapid ventricular tachycardias, accelerated idio-ventricular rhythms, ST segment changes and immediate rise in plasma CPK levels. The clinical risks of the reperfusion syndrome are low, practically never rhythmic and only exceptionally haemodynamic.

The authors report their preliminary results with the Rotacs system in the reopening of chronic coronary artery occlusion by low-speed rotational angioplasty. This system improves the percentage of coronary recanalisation in cases where it is impossible to pass the guide wire alone. It seems to be an effective, low-cost complementary tool for the treatment of this type of lesion.

Coronary recanalisation rate is one of the parameters utilized to evaluate the effectiveness of a thrombolytic agent. This parameter can only be measured when the occlusion and reopening of the coronary artery involved are demonstrated by angiography. Moreover, this type of study enables the kinetics of drug activity to be accurately determined. When injected intravenously in doses of 30 units less than four hours after the onset of chest pain and when studied by this method, Eminase produces recanalisation in more than 60 per 100 of the cases. The time elapsed between injection and action is 45 minutes on average. The risk of early reocclusion is low (about 5%). The recanalisation rate obtained with Eminase is similar to that obtained with intracoronary streptokinase.

In a multicentre randomized open study conducted on two parallel groups the effectiveness of APSAC was compared with that of streptokinase (SK) in 116 cases of myocardial infarction treated during the first 2.75 hours. APSAC (30 IU) was administered by intravenous bolus injection over 2 to 5 minutes, and SK (1.5 million IU) by intravenous infusion over 60 minutes. The patency of the coronary artery responsible for myocardial infarction was evaluated by coronary arteriography performed 1.74 h on average after the beginning of treatment; it was 70 p. 100 in the APSAC group and 51 p. 100 in the SK group (p less than 0.05). The fall in plasma fibrinogen was similar in both groups (mean minimum level; 0.2 g/l). Haemorrhages occurred in 9/58 patients treated with APSAC (15.5 p. 100) and in 13/58 patients treated with SK (22.4 p. 100); these haemorrhages took place during the first 24 hours in 4 patients of the APSAC group and in 10 patients of the SK group. Five patients died: 2 in the APSAC group and 3 in the SK group. In a subgroup of 38 patients who underwent 3 control coronary arteriographies (at 90 min, 24 hours and 3 weeks), the patency rates were 63 p. 100, 82 p. 100 and 93 p. 100 respectively with APSAC and 44 p. 100, 86 p. 100 and 92 p. 100 respectively with SK (NS). No coronary reocclusion occurred in the APSAC group, as against 3 (1 early, 2 delayed) in the SK group. It is concluded that APSAC seems to be more effective than intravenous streptokinase; it is easier to administer (bolus injection) and does not carry a higher risk of haemorrhage.

Coronary recanalisation during the acute phase of myocardial infarction, especially by in situ infusion of thrombolytic agents, is accompanied in most cases by rapid regression of chest pain and a reduction in the degree of ST elevation. However, a multicentre retrospective study of 104 attempts at recanalisation, including 78 successful procedures, showed in 10 cases (12.8 p. 100), an apparently paradoxical accentuation of the chest pain with or without increased ST elevation, at the time of angiographically demonstrable recanalisation. This phenomenon may be interpreted as being the result of aggravation of the ischaemia of the border zone, the objective of therapy. Several pathogenic hypotheses, all with experimental proof, may be suggested to explain these observations (haemorrhagic infarction, non reperfusion, ischaemic contraction due to massive intracellular flow of calcium, etc.). It is usually associated with arrhythmias and may be considered to be a reliable sign of recanalisation. It may also explain certain cases of persistence of chest pain and ECG changes despite the demonstration of a permeable epicardial artery on initial coronary angiography.

The case of a 44 year old patient with inaugural postero-diaphragmatic myocardial infarction is reported. Coronary angiography performed at the 3 rd hour showed total occlusion of the right coronary artery at the level of its second segment. A streptokinase perfusion through a Judkins' catheter positioned in the ostium of the right coronary artery using Rentrop's technique, resulted in recanalisation of the vessel at the 45 th minute. Control coronary angiography on the 10 th day showed an angiographically normal right coronary circulation. The clinical course was complicated by a recurrence on the 12 th day with a new occlusion at the same level. This observation confirms: - the reality of acute coronary thrombosis as a mechanism of myocardial infarction in the absence of significant underlying atherosclerotic stenosis. - the value of early fibrinolytic therapy in situ for limitation of the infarcted myocardial tissues.