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Guia de practica clinica de la ESC para el manejo del infarto agudo de miocardio en pacientes con elevacion del segmento ST : Grupo de Trabajo para el manejo del infarto agudo de miocardio con elevacion del segmento ST de la Sociedad Europea de Cardiologia (ESC)

During the evolution of coronary atherosclerosis, growth factors, cytokines, and other molecules are involved in cell recruitment, migration, and proliferation. Endothelin is an endothelial-derived vasoconstrictor peptide that possesses mitogenic properties. In this review, current evidence is provided that suggests that endothelin fulfills proposed criteria to be considered an atherogenic peptide because of its mitogenic and proliferative properties, as well as its inter-actions with known atherogenic factors. In addition, a proposed role of endothelin in the evolution of atherosclerosis is outlined.

Objectives. This study sought to evaluate treatment of early intracoronary stent thrombosis. Background. Although refinements in intracoronary stent implantation technique and pharmacologic treatment have reduced the frequency of early stent thrombosis, stent thrombosis remains a feared complication of this procedure. Optimal treatment for stent thrombosis is still undefined. Methods. Twenty-nine patients (44 stents) with early (≤30 days) coronary stent thrombosis over a 5-year period at our institution were identified. Treatment and outcome of stent thrombosis were analyzed. Results. Mean (±SD) time from implantation to stent thrombosis was 6.1 ± 5 days. Twenty-three patients were treated with catheter-based therapies (angioplasty alone in 14, angioplasty and intracoronary urokinase in 7, intracoronary urokinase alone in 2). Flow was restored without residual thrombus in 11 (48%) of the catheter-treated patients (6 of 14 with angioplasty alone, 4 of 7 with angioplasty and urokinase, 1 with urokinase alone). Of the 23 patients, 2 died despite restoration of anterograde flow, and 9 were referred for emergent or urgent bypass surgery because of residual thrombus and refractory angina despite restoration of blood flow. Of the remaining six patients, five were treated medically and one with coronary bypass surgery; three died. Acute myocardial infarction evolved in 26 patients (90%), including 20 (87%) of the 23 catheter-treated patients. Conclusions. Stent thrombosis is associated with severe adverse outcomes. Although catheter-based therapies are effective in restoring patency in a majority of patients, patients are referred frequently for coronary bypass surgery because of residual thrombus and refractory angina. These findings suggest that alternative or adjunctive therapies for stent thrombosis are needed.

The objective of the study was to identify patients with anterior wall acute myocardial infarction (AMI) at high risk of postinfarction left ventricular dysfunction (LVD). This study population included all patients admitted with a diagnosis of anterior wall AMI (ST segment elevation of1 mm in 2 or more precordial leads) without history or ECG evidence of antecedent AMI,who underwent assessment of left ventricular ejection fraction (LVEF) during emergency hospitalization. ST segment deviation from baseline was measured manually 0.08 s after the J point in all leads. Patients (n = 81) were classified into two groups based on the configuration of the QRS complex and ST segment: ST1 mm with preserved (pattern A; n = 60) or distorted terminal QRS (emergence of the J point at a level above the lower half of the R wave or disappearance of the S wave in leads with an Rs configuration; pattern B; n = 21). LVD (LVEF40%) was significantly more prevalent in patients with pattern B than pattern A (48 vs. 12%; p = 0.002). There was no correlation between the number of leads with ST segment elevation and LVD (p = 0.47). The sum of ST segment elevation in involved leads correlated weakly, yet significantly with LVEF (R = -0.22; p0.05). In conclusion, patients with anterior wall AMI and pattern B in the initial ECG are at high risk of post-AMILVD.

Summary: The purpose of the study was to determine whether the initial electrocardiographic pattern is predictive of in-hospital mortality in inferior wall acute myocardial infarction. It is commonly perceived that patients with acute myocardial infarction presenting with greater ST elevation have a worse prognosis. The initial electrocardiogram of patients (n = 213) with inferior wall myocardial infarction was categorized based on the pattern of ST-segment elevation in inferior leads: (A) ST

This study assesses the electrocardiographic (ECG) morphologic differences between early (24 h) and late (24 h) episodes of ST segment reelevation after acute myocardial infarction. We studied the records of 101 consecutive patients with acute myocardial infarction whose admission ECG demonstrated ST segment elevation with positive T waves, without pathological Q waves in the relevant leads, and without signs of bundle branch block or left ventricular hypertrophy. Thirty-five patients had 44 episodes of early ST segment reelevation, while 22 patients experienced 26 late episodes of ST segment reelevation. Seven patients experienced both early and late episodes. Early episodes of ST segment reelevation was seen more often after thrombolytic therapy: 43% (32 of 74 patients) versus 11% (3 of 27 patients) (P0.006). No differences were found in the incidence of late episodes between those who underwent (23%) or did not undergo (19%) thrombolytic therapy. Two patterns of ST segment elevation were distinguished. Pattern A with positive T waves, ST segment elevation (or = 0.1 mV), but without distortion of the terminal portion of the QRS complex. Pattern B characterized by positive T waves, ST segment elevation (or = 0.1 mV) with distortion of the terminal portion of the QRS complex. Each ECG was categorized according to these two patterns. The admission ECG pattern was A in 75 patients, and B in 26. No significant differences were found between patients with early, late, or no episodes of ST segment reelevation in the appearance of pattern A or B on admission.(ABSTRACT TRUNCATED AT 250 WORDS)

This study examines whether patients with inferior wall acute myocardial infarction (AMI) and maximal ST-segment depression in left precordial leads are at higher risk for in-hospital mortality. The charts of patients (n = 213) with inferior wall AMI and an initial electrocardiogram that displayed peaked, tall T waves or ST-segment elevation with upright T waves in inferior leads were reviewed, after excluding patients with inverted T waves in inferior leads (n = 75). ST-segment deviation from baseline was measured for all leads. Patients were classified into 3 types: I = no precordial ST-segment depression; II = sum of ST-segment depression in leads V1 to V3 equal to or more than the sum of ST-segment depression in leads V4 to V6; and III = maximal precordial ST-segment depression in leads V4 to V6. Thirty-six patients (17%) died in the hospital. In-hospital mortality rates for patients with types I and II were 12% and 10%, respectively, compared with 41% for those with type III (p < 0.0001). Mortality rates in surviving patients were similar for all types up to 1 year after infarction. Multivariate logistic regression models for in-hospital mortality by ST-segment depression type adjusted for age, previous AMI, diabetes mellitus, and thrombolytic therapy revealed that type III pattern was a strong predictive factor for in-hospital mortality (odds ratio = 4.9, p = 0.0008, 95% confidence interval 1.93 to 12.26). Thus, patients with inferior wall AMI and maximal precordial ST-segment depression in leads V4 to V6 are at high risk for in-hospital mortality.

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Subacute closure is a well recognized complication of stent implantation [l-6]. The time course of the phenomenon (occurrence within the first month and usually within the first 10 days following stent implantation), morbidity and mortality associated with it (50-90% incidence of myocardial infarction mortality approximately 20%, and the need for urgent coronary bypass graft surgery approximately 30%), and factors associated with the development of the event (residual dissection, inlet or outlet obstruction, incomplete stent apposition and residual thrombus) have been relatively well described. Fortunately with the widespread use of high pressure balloon inflation, post-deployment inflation, and the shift in adjunctive medications from Coumadin to aspirin and ticlopidine, the incidence appears to have declined substantially and is less than approximately 2-3% [7]. As stent usage continues to increase, and as stents are placed in less favorable vessels, the incidence, however, may again increase. There are a variety of approaches to the patient with subacute closure of a stent. The etiology is usually thrombotic and includes both red blood cells, fibrin and platelets [8]. Potential approaches can be seen in Table 1. Although thrombolytic therapy is a

Background: Devices designed to facilitate or replace conventional percutaneous transluminal coronary angioplasty have been introduced in recent years. Objectives: To characterize the changes in percutaneous coronary interventional practice over 16 years and to assess the relative use of these new devices. Methods: We performed a retrospective analysis of all patients who underwent percutaneous coronary revascularization at Mayo Clinic, Rochester, Minn, during a 16-year period (1980-1995) and characterized the changes in procedural and clinical factors. Results: The number of coronary interventional procedures performed increased from 38 in 1980 to 1284 in 1995. Atherectomy and laser angioplasty were incorporated in 1988; their use peaked in 1994 (17% of procedures) but decreased to 9.9% by 1995. In contrast, the use of intracoronary stents has increased steadily since 1990. By 1995, intracoronary stents were placed in 48.2% of procedures. The success rate improved from 55.3% in 1980 to 91.4% in 1995, although patients were older (51 ±10 [means±SD] years in 1980 vs 63±12 years in 1995), had more extensive coronary artery disease (0% with multivessel disease in 1980 vs 47.4% in 1995), had more complex lesions, and often underwent intervention in the peri-infarction setting (2.6% of procedures in 1980 vs 17% in 1995). The rate of referral to emergency coronary bypass surgery after percutaneous procedures declined from 5.2% in 1980 to 0.4% in 1995. Conclusions: Current coronary interventional practice is expanding and improving. In contrast to intracoronary stents that have greatly affected current practice, other new devices are used infrequently. Conventional angioplasty, with or without intracoronary stents, remains the dominant treatment strategy. Arch Intern Med. 1997;157:677-682

To the Editor.— In their article in the April 1991 issue of theArchives, Angeli et al 1 compared the efficacy of sublingual captopril and nifedipine in immediate treatment of hypertensive emergencies. The authors imply that the sublingual route is the optimal means of orally administering nifedipine in hypertensive emergencies. However, a few studies have shown that nifedipine is poorly absorbed through the oral mucosa, 2 and, thus, the efficacy of sublingual nifedipine may be attributed to its ultimate gastric absorption. The bite-and-swallow method is the most efficacious route of administering nifedipine orally. The authors also state that there is general medical consensus that prompt control of blood pressure is required in hypertensive emergencies. The fact is that while sublingual nifedipine produces a rapid fall in blood pressure within 5 to 10 minutes, 3 it can also cause symptomatic hypotension in the acute treatment of severe hypertension. 4 Cerebral infarction

To the Editor.— In the April 1990 issue of theArchives, Lipsy et al 1 reviewed the various histamine 2 receptor antagonists. I would like to comment on the section describing the drug interactions of histamine 2 antagonists and cardiovascular drugs. The authors state that the clearance of propranolol is decreased by both cimetidine and ranitidine, thus causing increased levels of propranolol in the blood. However, whereas cimetidine increases propranolol concentrations in the blood and potentiates β-blocking effects through inhibition of hepatic microsomal enzymes and reduction of hepatic blood flow, 2 ranitidine has no effect on propranolol metabolism or clearance. 2 The authors failed to address the interaction between histamine 2 receptor antagonists and the calcium-channel blockers that are becoming increasingly popular. Increased blood levels of diltiazem are detected when this drug is administered concurrently with ranitidine and, more so, with cimetidine. 3 Cimetidine causes increased levels of nifedipine, which might

The effect exerted by different hyperglycemic states on the pain threshold and on the analgesic potential of morphine was studied in male Sabra rats with the hot plate device. Hyperglycemia induced by an intraperitoneal injection of 0.014 mol/kg glucose or an acute or chronic diabetic state induced by streptozocin injection did not significantly alter the pain threshold. However, states of acute and chronic diabetes markedly blunted the analgesic effect of morphine (5 mg/kg). Sabra rats maintained on a cocktail of glucose-saccharin, thought to activate the release of endogenous opioids, demonstrated an increased pain threshold and rapidly developed resistance to the analgesic effect of morphine. Previous studies have shown that glucose in high concentration may interfere with the interaction of morphine on the opiate receptor. The influence of the diabetic state on β-endorphin synthesis and concentration in the central nervous system is another factor that might change pain perception in diabetes. We propose that in diabetes, generally, the pain threshold is adequately maintained, despite the antagonistic effect of glucose, partly due to a compensatory increased secretion of endogenous opioid peptides. We hypothesize that in patients with chronic painful diabetic neuropathy, these normal analgesic response mechanisms may be overwhelmed either by an excess of nociceptive impulses from diseased peripheral nerves or conceivably by a failure of endogenous opioid secretory response to the hyperglycemia.

Reports have shown increased systemic levels of endothelins during coronary artery bypass grafting in human beings. It was not known whether increased endothelin levels during coronary artery bypass grafting reflect a general systemic response to the surgical procedure or increased myocardial production of endothelins in response to ischemia and reperfusion. We therefore measured endothelin levels in the right atrium and proximal aorta of 15 patients undergoing coronary artery bypass grafting for anginal syndrome immediately before aortic crossclamping and again after cessation of cardiopulmonary bypass. In five patients, we also measured coronary sinus levels of endothelins during cardiopulmonary bypass circulation. We found that endothelin levels were elevated throughout the surgical procedure. Right atrial endothelin levels were significantly elevated after cessation of cardiopulmonary bypass circulation with respect to values immediately before aortic crossclamping (11.1 ± 3.1 vs 14.2 ± 3.7 pg/ml, p = 0.008), whereas endothelin levels in the proximal aorta did not rise significantly (10.5 ± 2.3 vs 11.6 ± 2.4 pg/ml, p > 0.5). Coronary sinus endothelin levels tended to decline temporarily during cardiopulmonary bypass circulation (11.1 ± 2.1 pg/ml before aortic crossclamping, 7.9 ± 1.9 1 minute after release of aortic crossclamp, and 9.9 ± 2.1 pg/ml after release of partial aortic crossclamping, p = 0.06). We conclude that the rise in right atrial endothelin levels during coronary artery bypass grafting reflects systemic production and secretion of endothelins, probably by vasculature or organs distal to the proximal aorta, and is not the result of increased myocardial production and secretion of endothelins. (J T horac Cardiovasc Surg 1996;112:531-6)

Objectives. This study was performed to examine the effect of intracoronary exogenous basic fibroblast growth factor (bFGF) on angiogenesis in infarcted myocardial regions.Background. Exogenous bFGF is a potent promoter of angiogenesis. Little information is available on its effect on myocardial angiogenesis.Methods. Myocardial infarction was induced in 10 pigs by intracoronary injection of microscopic beads. Four pigs served as a control group; in six pigs slow-release bFGF was delivered by the beads. Cardiac performance was evaluated by repeated echocardiographic measurement and angiogenesis was evaluated by immunohistochemical studies 14 days later.Results. As compared with control pigs, pigs treated with bFGF had higher microvessel counts (mean ± SEM) in both viable tissue (141 ± 27 per field vs. 39 ± 4, p = 0.01) and nonviable tissue (329 ± 26 per field vs. 95 ± 7, p < 0.001) within the infarct area. No significant differences in total regional left ventricular wall motion were noted between the two groups throughout the 14-day study period.Conclusions. In the swine, direct intracoronary application of bFGF to infarcted myocardium enhances myocardial neovascularization within 2 weeks.