Abstract Background PCSK9i on top of high intensity statins have shown clinical benefit in patients after Acute Myocardial Infarction (AMI) who are not at LDL-c target. The ESC Task Force has defined guidance for the prescription of PCSK9i. Among patients discharged after AMI, the rate of those eligible for PCSCK9i is poorly documented. Methods We used data from the nationwide French FAST-MI 2015 registry. PSCK9-eligible patients were defined as those discharged with high intensity statins with expected-LDL>140 mg/dL, or >100mg/dL if they had additional high risk features such as diabetes with renal dysfunction or hypertension, multivessel coronary disease, associated peripheral artery disease or recurrent MI. The expected LDL-c was estimated from admission LDL-c and changes in lipid-lowering treatment. The rate of eligible patients was estimated from actual treatment and optimized treatment (i.e. addition of ezetimibe). Results Among 5291 pts included, 4715 (89%) were discharged with statins, at high intensity in 3655 (71%). Expected LDL was 71mg/dL (IQ 56, 95). Among patients discharged with high intensity statins, 3146 (59%) had an expected LDL-c<100/mg (figure, in green). PCSK9-eligible patients were those with LDL-c>140mg/dL (n=178, 3.3%, in red) and, among those with LDL-c 100–140mg/dL (n=331, 6.2%, in yellow), patients who had additional risk features (n=227 (4%)). As a result, the population eligible for PSCK9i according to the ESC guidance would represent 7.6% (405 pts) of the population admitted with AMI. Expanding the indication to patients with statins, but not at high intensity would add 159 (3%). Conversely, optimizing discharge treatment with ezetimibe would reduce the rate of eligible patients to 3% (181 pts, in brown). Conclusions In real life, according to the ESC Task Force, 7.6% of the whole population admitted for AMI would be eligible for PCK9i. This rate could be reduced to 3% with the addition of ezetimibe.

BACKGROUND:Experimental and clinical evidence suggests that cyclosporine may attenuate reperfusion injury and reduce myocardial infarct size. We aimed to test whether cyclosporine would improve clinical outcomes and prevent adverse left ventricular remodeling.METHODS:In a multicenter, double-blind, randomized trial, we assigned 970 patients with an acute anterior ST-segment elevation myocardial infarction (STEMI) who were undergoing percutaneous coronary intervention (PCI) within 12 hours after symptom onset and who had complete occlusion of the culprit coronary artery to receive a bolus injection of cyclosporine (administered intravenously at a dose of 2.5 mg per kilogram of body weight) or matching placebo before coronary recanalization. The primary outcome was a composite of death from any cause, worsening of heart failure during the initial hospitalization, rehospitalization for heart failure, or adverse left ventricular remodeling at 1 year. Adverse left ventricular remodeling was defined as an increase of 15% or more in the left ventricular end-diastolic volume.RESULTS:A total of 395 patients in the cyclosporine group and 396 in the placebo group received the assigned study drug and had data that could be evaluated for the primary outcome at 1 year. The rate of the primary outcome was 59.0% in the cyclosporine group and 58.1% in the control group (odds ratio, 1.04; 95% confidence interval [CI], 0.78 to 1.39; P=0.77). Cyclosporine did not reduce the incidence of the separate clinical components of the primary outcome or other events, including recurrent infarction, unstable angina, and stroke. No significant difference in the safety profile was observed between the two treatment groups.CONCLUSIONS:In patients with anterior STEMI who had been referred for primary PCI, intravenous cyclosporine did not result in better clinical outcomes than those with placebo and did not prevent adverse left ventricular remodeling at 1 year. (Funded by the French Ministry of Health and NeuroVive Pharmaceutical; CIRCUS ClinicalTrials.gov number, NCT01502774; EudraCT number, 2009-013713-99.).

BACKGROUND:Nitric oxide (NO) donors, in addition to their vasodilator effect, decrease platelet aggregation and inhibit vascular smooth muscle cell proliferation. These actions could have beneficial effects on restenosis after coronary balloon angioplasty.METHODS AND RESULTS:In a prospective multicenter, randomized trial, 700 stable coronary patients scheduled for angioplasty received direct NO donors (infusion of linsidomine followed by oral molsidomine) or oral diltiazem. Treatment was started before angioplasty and continued until 12 to 24 hours before follow-up angiography at 6 months. The primary study end point was minimal lumen diameter, assessed by quantitative coronary angiography, 6 months after balloon angioplasty. Clinical variables were well matched in both groups. However, despite intracoronary administration of isosorbide dinitrate, the reference diameter in the NO donor group was significantly greater than in the diltiazem group on the preangioplasty, postangioplasty, and follow-up angiograms. Pretreatment with an NO donor was associated with a modest improvement in the immediate angiographic result compared with pretreatment with diltiazem (minimum luminal diameter, 1.94 versus 1.81 mm; P = .001); this improvement was maintained at the 6-month angiographic follow-up (minimal lumen diameter, 1.54 versus 1.38 mm; P = .007). The extent of late luminal narrowing did not differ significantly between groups (loss index in the NO donor and diltiazam groups, 0.35 +/- 0.78 and 0.46 +/- 0.74, respectively; P = .103). Restenosis, defined as a binary variable (> or = 50% stenosis), occurred less often in the NO donor group (38.0% versus 46.5%; P = .026). Combined major clinical events (death, nonfatal myocardial infarction, and coronary revascularization) were similar in the two groups (32.2% versus 32.4%).CONCLUSIONS:Treatment with linsidomine and molsidomine was associated with a modest improvement in the long-term angiographic result after angioplasty but had no effect on clinical outcome. The improved angiographic result related predominantly to a better immediate procedural result, because late luminal loss did not differ significantly between groups.

Among 498 patients hospitalised for myocardial infarction during a three year period, 194 (39%) were aged over 70 (mean age: 78.6 +/- 6), including 99 women and 95 men. Comparison of this group of patients with those aged under 70 showed a significantly higher hospital mortality (17.5% v. 6.5%) (p < 0.01) and a higher acute complication rate (60.8% v. 23.7% (p < 0.01), in particular after the age of 75. Twenty-eight patients were treated by thrombolysis (14.4% v. 50.6%) (p < 0.05), with a 79.2% patency rate in follow-up angiography at 48 h, and only one non-fatal hemorrhagic complication. Eighty-six patients were investigated by coronary arteriography (44.9% v. 87.2% (p < 0.05) without any complication. Mean ejection fraction was 57.3 +/- 13.5%. Fifty patients were treated by angioplasty (24.6% v. 57%) (p < 0.01) including 15 during the acute phase, with primary success in 40 of them (80%). Ten patients underwent coronary bypass following their infarction (5.1% v. 6.25%) (NS) with two per- or postoperative deaths (20%). Follow-up study revealed high secondary mortality with an overall survival rate at one year of 59.6% v. 81% in patients aged under 70 (p < 0.01). In total, infarction in the elderly is characterised by high mortality and morbidity as compared with infarctions in patients aged under 70, and requires active management during the acute phase, assessed according to the physiological status and age of the patient.

Many enzyme systems such as glutathione peroxidase (GPx) or superoxide dismutase (SOD) neutralise the oxygen derived free radicals produced during myocardial reperfusion by thrombolysis. Erythrocytic SOD, plasma and erythrocytic GPx and their cofactor selenium, substances reacting with thiobarbituric acid (TBARS) were analysed by repeated sampling between T0 and 48 hours in 24 patients treated by thrombolysis for acute myocardial infarction. Angiographic control was undertaken systematically between 60 and 180 minutes after initiating thrombolytic therapy : 18 patients had a patent vessel and 6 patients had an occluded vessel recanalised in 5 cases by angioplasty. Biological analysis was performed in the 23 patients successfully revascularised by thrombolysis, eventually completed by angioplasty. The plasma GPx decreased non-significantly between T0 and 2 hours from 246.8 +/- 53.3 to 233 +/- 39 U/ml with a significant increase between 2 and 48 hours from 233 +/- 39.2 to 294 +/- 76 U/ml, whereas the erythrocytic GPx rose significantly and constantly between T0 and 48 hours from 34.8 +/- 7.1 to 37.6 +/- 7.5 U/gHb with significant consumption of selenium between TO and 4 hours from 81.2 +/- 14 to 68.5 +/- 12.6 mu g/l. The erythrocytic SOD increased significantly between T0 and 48 hours from 318.9 +/- 40.8 to 337 +/- 59 U/gHb. Finally, the analysis of plasma TBARS showed a non-significant rise between T0 and 30 minutes from 1.59 +/- 0.30 to 1.71 +/- 1.43 mm/l with a return to the basic line values after about 2 hours. These results show a significant increase in the activity of enzymes protecting against the liberation of oxygen free radicals, such as erythrocyte or plasma GPx and erythrocyte SOD between T0 and 48 hours with consumption of selenium, cofactor of GPx, and an increase in circulating lipid peroxydes in acute myocardial infarction heated by thrombolysis. They also illustrate the oxidative stress which occurs in this situation.

Three hundred and twenty eight patients (238 men, 90 women) with an average age of 63.5 +/- 18 years admitted consecutively for acute myocardial infarction over a 24 month period (March 1989-March 1991) were followed up at one year by out-patient appointment, questionnaire or telephonic enquiry. The average delay before hospital admission was 6.7 +/- 44 hours (1 h-48 h). The infarct was transmural in 82% of cases, anterior in 45.3%, inferior in 46.3% and lateral in 8.4% of cases. Forty eight per cent had one or several complications during the hospital period with a 10.4% hospital mortality rate. Thirty eight per cent of patients underwent primary thrombolysis and 9% had primary angioplasty. Seventy four per cent of patients had coronary angiography; 41% underwent deferred angioplasty and 6% surgical revascularisation. The global 1 year survival rate was 81.4%. At follow-up, 52.6% of patients were asymptomatic, 31% had signs of cardiac failure and 18% had residual angina. Sixty five per cent were treated with 2 or 3 drugs; 6% underwent secondary angioplasty and 2.8% secondary coronary bypass surgery. Of the 34% of active subjects, 61.4% declared having returned to full-time professional activity. Therefore, in 1992, a continuous reduction of infarct-related mortality and morbidity was observed.

The isoforms of creatinine kinase (CK) and myoglobin were analysed by serial samplings in 45 patients admitted consecutively for myocardial infarction treated by thrombolysis according to the usual indications. Angiographic controls were carried out systematically in the first 24 hours, including 20 cases at the end of thrombolysis. The patients were divided into two groups according to the patency of the infarct related artery: Group I (n = 35) with a patent vessel and Group II (n = 10) with an occluded vessel; 4 patients in Group II were successfully revascularised by angioplasty. The total CK had a higher peak value in Group II (2,393 +/- 1,991 UI/l at 547 +/- 247 min versus 2,888 +/- 2,189 IU/l at 584 +/- 395 min) but the difference was not statistically significant. The analysis of CK isoforms showed the MM3/MM1 ratio to be higher at the 2nd hour in Group I (3.74 +/- 2.37 versus 3.09 +/- 1.43) with a faster increase, without attaining statistical significance. A fourth CK MM fraction was observed at the 2nd hour in 71% of patients in Group I compared with only 20% of patients in Group II. Analysis of myoglobin showed a significantly earlier peak value in Group I (1,218 +/- 1,117 micrograms/l at 133 +/- 62 min versus 1,309 +/- 1,549 micrograms/l at 210 +/- 84 min). The sensitivity and specificity of these different markers were respectively 40%, 86%, 77%, and 60%, 70% and 67% for the CK (peak before 8 hours), the MM3/MM1 ratio (increase of over 35% in the first hour) and myoglobin (peak before 2 hours).(ABSTRACT TRUNCATED AT 250 WORDS)

Three hundred and twenty eight patients (238 men, 90 women) with an average age of 63.5 +/- 18 years admitted consecutively for acute myocardial infarction over a 24 month period (March 1989-March 1991) were followed up at one year by out-patient appointment, questionnaire or telephonic enquiry.The average delay before hospital admission was 6.7 +/- 44 hours (1 h-48 h).The infarct was transmural in 82 % of cases, anterior in 45.3 inferior in 46.3 % and lateral in 8.4 % of cases. Forty eight per cent had one or several complications during the hospital period with a 10.4 % hospital mortality rate.Thirty eight per cent of patients underwent primary thrombolysis and 9 % had primary angioplasty.Seventy four per cent of patients had coronary angiography; 41 % underwent deferred angioplasty and 6 % surgical revascularisation.The global 1 year survival rate was 81.4 %.At follow-up, 52.6 % of patients were asymptomatic, 31 % had signs of cardiac failure and 18 % had residual angina. Sixty five per cent were treated with 2 or 3 drugs; 6 % underwent secondary angioplasty and 2.8 % secondary coronary bypass surgery.Of the 34 % of active subjects, 61.4 % declared having returned to full-time professional activity.Therefore, in 1992, a continuous reduction of infarct-related mortality and morbidity was observed.

Among 498 patients hospitalised for myocardial infarction during a three year period, 194 (39%) were aged over 70 (mean age: 78.6+/-6), including 99 women and 95 men. Comparison of this group of patients with those aged under 70 showed a significantly higher hospital mortality (17.5% v. 6.5%) (p<0.01) and a higher acute complication rate (60.8% v. 23.7% (p<0.01), in particular after the age of 75. Twenty-eight patients were treated by thrombolysis (14.4% v. 50.6%) (p<0.05), with a 79.2% patency rate in follow-up angiography at 48 h, and only one non-fatal hemorrhagic complication. Eighty-six patients were investigated by coronary arteriography (44.9% v. 87.2% (p<0.05) without any complication. Mean ejection fraction was 57.3 +/- 13.5%. Fifty patients were treated by angioplasty (24.6% v. 57%) (p<0.01) including 15 during the acute phase, with primary success in 40 of them (80%). Ten patients underwent coronary bypass following their infarction (5.1% v. 6.25%) (NS) with two per- or postoperative deaths (20%). Follow-up study revealed high secondary mortality with an overall survival rate at one year of 59.6% v. 81% in patients aged under 70 (p<0.01). In total, infarction in the elderly is characterised by high mortality and morbidity as compared with infarctions in patients aged under 70, and requires active management during the acute phase, assessed according to the physiological status and age of the patient.

The authors report a case of myocardial infarction in a 27 year old patient by simultaneous thrombosis of the left anterior descending and right coronary arteries in an angiographically normal coronary circulation. The young age of the patient, the absence of the usual risk factors and a normal angiographic network after arterial recanalisation by angioplasty led to the search for a risk factor of thrombosis. This showed a qualitative deficiency of protein S and the absence of any other abnormality of coagulation or fibrinolysis. This case raises the question of a causal relationship between a hereditary protein S deficiency and thrombotic arterial occlusion.

This study reports two cases of acute severe Coxsackie virus B4 myocarditis in which the immediate clinical signs suggested the acute phase of myocardial infarction, apparently antero-lateral in the first case in a context of cardiogenic shock and infero-lateral in the second case, in the context of acute pulmonary edema. Both cases were characterized by the severity of the initial signs. Numerous other cases of acute Coxsackie virus B myocarditis, simulating myocardial infarction, have been reported in the literature and these contexts deserve to be recognized earlier as they call for specific treatment. The immediate outcome was favorable in both cases but required massive cardiological intensive care in the first patient. Long term follow-up was excellent.

This study reports two cases of acute severe Coxsackie virus B4 myocarditis in which the immediate clinical signs suggested the acute phase of myocardial infarction, apparently antero-lateral in the first case in a context of cardiogenic shock and infero-lateral in the second case, in the context of acute pulmonary edema. Both cases were characterized by the severity of the initial signs. Numerous other cases of acute Coxsackie virus B myocarditis, simulating myocardial infarction, have been reported in the literature and these contexts deserve to be recognized earlier as they call for specific treatment. The immediate outcome was favorable in both cases but required massive cardiological intensive care in the first patient. Long term follow-up was excellent.

During a 20 year period, 285 patients were hospitalised for infectious endocarditis (IE) in the Department of Cardiology of the Ernest-Conseil Hospital in Tunis and 86 of them, i.e. 30%, developed a vascular complication (VC). Among these 86 patients, there were a total of 108 lesions, including 52 neurological complications, 14 peripheral acute ischemic syndromes, 16 peripheral arterial aneurysms, 9 aortic aneurysms, 7 pulmonary embolisms, 6 splenic infarctions and 4 coronary lesions. The mortality in this patient group proved to be slightly greater than in the series as a whole, in particular concerning patients with multiple lesions and those with an artificial valve. No prognostic difference was seen between patients with a VC of aneurysmal type and of ischemic type, but the presentation and severity of lesions was very variable. The vascular complication was a presenting feature of IE in almost 40% of cases. The organism found most often was the streptococcus, above all in ischemic type IE as well as in the total patient group. Similarly, the preferential site was aortic, above all for aneurysmal type IE. Ultrasonography revealed a higher incidence of vegetations in this series of patients, above all in ischemic type VC, but anatomical studies have shown this to be an investigation of moderate sensitivity and poor specificity, poorly correlated from a prognostic standpoint with the risk of embolism. The conclusion of the study is above all the need to prevent such complications: embolic complications by early antibiotic treatment and valve replacement and aneurysmal complications by methodical routine angiographic evaluation and appropriate treatment.

Thirty out of 287 patients (10.4 %) admitted to hospital for infective encodarditis between December 1970 and January 1990 had neurological complications.Twenty-three patients had native valve infectious endocarditis and 7 had prosthetic valve endocarditis. The clinical features were charactarised by the frequency of aortic valve involvement (23 out of 30) and other complications, especially cardiac failure (16 cases) and peripheral vascular manifestations (7 cases).The commonest organism was the staphylococcus (53 % of identified organisms) but the number of negative blood cultures was high (50 % of cases).The neurological complication was often the presenting symptome of the endocarditis (19 cases) but it occurred after bacteriological cure in 4 cases. The complications observed were cerebral ischemia (16 cases), cerebral haemorrhage (11 cases), coma (2 cases), and one peripheral neuropathy causing a Claude Bernard Horner syndrome. These complications presented with hemiplegia in 17 cases, a meningeal syndrome in 8 cases, a convulsion in 1 case, a Von Wallenberg syndrome in 1 case, and a Claude Bernard Horner syndrome in 1 case. Twelve patients had a transient or permanent neurological coma.Cerebral CT scan showed ischemic lesions in 7 cases and haemorrhagic lesions in 10 cases. Carotid angiography demonstrated mycotic aneurysms in 6 patients.Twelve patients died: the cause of death was neurological coma (7 cases), low cardiac output (4 cases) and haemorrhagic shock (1 case). Four patients underwent neurosurgery: 3 for clipping a mycotic aneurysm and 1 for drainage of an intracerebral haematoma.Poor prognostic factors were: coma, cardiac failure, cardiac valve prosthesis and, above all, the extent and multiplicity of the neurological lesions.The authors propose the following measures to improve the prognosis:early surgery in cases of large and/or mobile vegetations especially when the infecting organism is a staphylococcus and when a systemic embolism has occurred;routine CT scanning and/or digitised cerebral angiography in all patients with infective encodarditis to detect surgically accessible mycotic aneurysms.

Thirty out of 287 patients (10.4%) admitted to hospital for infective endocarditis between December 1970 and January 1990 had neurological complications. Twenty-three patients had native valve infectious endocarditis and 7 had prosthetic valve endocarditis. The clinical features were characterized by the frequency of aortic valve involvement (23 out of 30) and other complications, especially cardiac failure (16 cases) and peripheral vascular manifestations (7 cases). The commonest organism was the staphylococcus (53% of identified organisms) but the number of negative blood cultures was high (50% of cases). The neurological complication was often the presenting symptom of the endocarditis (19 cases) but it occurred after bacteriological cure in 4 cases. The complications observed were cerebral ischemia (16 cases), cerebral haemorrhage (11 cases), coma (2 cases), and one peripheral neuropathy causing a Claude Bernard Horner syndrome. These complications presented with hemiplegia in 17 cases, a meningeal syndrome in 8 cases, a convulsion in 1 case, a Von Wallenberg syndrome in 1 case, and a Claude Bernard Horner syndrome in 1 case. Twelve patients had a transient or permanent neurological coma. Cerebral CT scan showed ischemic lesions in 7 cases and haemorrhagic lesions in 10 cases. Carotid angiography demonstrated mycotic aneurysms in 6 patients. Twelve patients died: the cause of death was neurological coma (7 cases), low cardiac output (4 cases) and haemorrhagic shock (1 case). Four patients underwent neurosurgery: 3 for clipping a mycotic aneurysm and 1 for drainage of an intracerebral haematoma. Poor prognostic factors were: coma, cardiac failure, cardiac valve prosthesis and, above all, the extent and multiplicity of the neurological lesions. The authors propose the following measures to improve the prognosis: early surgery in cases of large and/or mobile vegetations especially when the infecting organism is a staphylococcus and when a systemic embolism has occurred; routine CT scanning and/or digitised cerebral angiography in all patients with infective endocarditis to detect surgically accessible mycotic aneurysms.