Staffing and equipping emergency medical services systems: Rapid identification and treatment of acute myocardial infarction

Each year, about 1,250,000 people in the United States experience an acute myocardial infarction (AMI). Emergency medical services (EMS) systems play a key part in the prehospital care and transportation of AMI patients. Rapid, state-of-the-art treatment by EMS personnel is essential for improving AMI survival and outcomes, as dramatized by the patient who is the victim of out-of-hospital cardiac arrest. In order to improve the prehospital care provided to AMI patients, this article by the Access to Care Subcommittee of the National Heart Attack Alert Program Coordinating Committee makes a number of recommendations regarding the staffing and equipping of EMS systems. The recommendations cover the “chain of survival” concept, universal and enhanced 9-1-1, emergency medical dispatching, ground ambulance specifications, automated external defibrillators, advanced life support coverage, medical direction, 12-lead electrocardiograms, and prehospital thrombolysis.     

Early identification of patients with acute myocardial infarction

In conclusion, early identification of AMI requires the utilization of three main criteria: (1) History and physical examination; (2) 12-lead electrocardiography, and (3) serum protein markers of myocardial cell death. The history may indicate admission for AMI exclusion or unstable angina, although these data remain largely subjective. The physical examination provides few clues in subtle presentations of myocardial cell death, and instead identifies patients with left ventricular dysfunction, often with failure. The 12-lead ECG is an insensitive early indicator of AMI, often identifying 50% or fewer of these patients. Currently, thrombolytic therapy or invasive catheterization techniques such as PTCA are based on 12-lead depictions of acute injury patterns. Finally, serum markers of AMI, particularly myoglobin, CPK-MM isoforms, and new monoclonal antibody assays for CPK-MB may allow early identification of patients with AMI with nondiagnostic ECGs.     

低分子量肝素治疗急性缺血性脑血管病研究

目的 研究低分子量肝素（LMWH）治疗急性缺血性脑血管病（AICVD）的疗效和安全性。方法 对64例AICVD患者皮下注射LMWH并与口服阿司匹林或盐酸噻氯匹啶的72例作对照研究,观察两组治疗前后神经功能缺损程度、出血时间（CT）、凝血酶原时间（PT）血小板计数（PLT）的变化,并比较两组出血性梗死、下肢深部静脉血栓发生率。结果 LMWH治疗组的疗效明显优于阿司匹林或盐酸噻氯匹啶对照组。CT、PT、PLT在两组间及治疗前后无明显变化。LMWH可有效地阻止缺血性卒中的进程,减少短暂性情绪脑缺血发作（TIA）向脑梗死转化,不增加出血性卒中的发生率。结论 LMWH对AICVD的疗效明显优于阿司匹林或盐酸噻氯匹啶,安全性高,特别适于治疗进展型卒中,中阻止TIA向脑梗死转化,减少下肢深部静脉血栓发生率。     

General pharmacologic treatment of acute myocardial infarction

The general pharmacotherapeutic issues surrounding AMI are complex and expanding, especially with regard to treatment aimed at the [table: see text] culprit, coronary atherosclerotic thrombus. Basic, well-established therapy includes the routine administration of oxygen, nitroglycerin, aspirin, and at times morphine, with selected cases invoking caution with respect to these agents (e.g., nitroglycerin and the risk of hypotension in right ventricular infarction; contraindication to nitrolycerin in patients on sildenafil). Cardioprotective agents, especially beta-adrenergic antagonists, should be considered early in light of their demonstrated benefit; others, such as ACE inhibitors, need not be administered in the ED. Heparin, both UFH and the newer LMWHs, have well-established roles in acute coronary syndromes. The GP IIb/IIIa inhibitors are the most recent addition to the pharmacologic armamentarium; their role is evolving rapidly as research on this frontier continues. Table 2 reviews recommended dosing of selected agents in acute coronary syndromes.     

心肌梗死患者的康复治疗

心肌梗死患者的康复治疗包括循序渐进和按部就班的康复运动训练、对患者及家属的医学康复指导和对患者心脏功能及身体状况的定期评定 ,其目的是尽可能使患者恢复正常生活。实际上 ,心肌梗死的康复治疗始于发病当日 ,并且 ,由于冠心病是一个慢性和逐渐发展的过程 ,因此 ,这种康复治疗是终生的 ,大致可分为住院阶段、出院后阶段和维持阶段。1住院阶段以往认为 ,急性心肌梗死患者应强制卧床休息3— 6周 ,但这样处理常可引起长期卧床的不良后果 ,有时比心肌梗死疾病本身对患者的危害还要大。长期卧床的常见不良后果有 :1卧床 3周体力可下降2 0 %…     

Enhanced cardiac production of matrix metalloproteinase-2 and -9 and its attenuation associated with pravastatin treatment in patients with acute myocardial infarction

Previous experimental studies have demonstrated that MMPs (matrix metalloproteinases) contribute to LV (left ventricular) remodelling. We hypothesized that cardiac MMPs are activated in patients with AMI (acute myocardial infarction) and, if so, MMP production may be attenuated by statins (3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) through their cardiovascular protective actions. We studied 30 patients, ten control patients with stable angina pectoris and 20 patients with AMI, in whom LV catheterization at the chronic stage was performed 22+/-12 days (value is mean+/-S.D.) after the onset of AMI. Blood samples were collected from the CS (coronary sinus) and a peripheral artery. In patients with AMI, the levels of MMP-2 and MMP-9 were significantly (P<0.05) higher in the CS than the peripheral artery (MMP-2, 853+/-199 compared with 716+/-127 ng/ml; MMP-9, 165+/-129 compared with 98+/-82 ng/ml), whereas no significant differences were observed in the patients with angina pectoris. The CS-arterial concentration gradients of MMP-2 and MMP-9 correlated positively with BNP (brain natriuretic peptide) levels (MMP-2, R=0.68, P<0.01; MMP-9, R=0.59, P<0.05) and LV end-diastolic volume index (MMP-2, R=0.70, P<0.01; MMP-9, R=0.70, P<0.01). When patients with AMI treated with 10 mg of pravastatin or without (n=10 in each group) were compared, this statin therapy significantly (P<0.05) decreased the CS-arterial concentration gradients of MMP-2 (69+/-43 compared with 213+/-185 ng/ml) and MMP-9 (14+/-27 compared with 119+/-84 ng/ml). In conclusion, the enhanced production of cardiac MMP-2 and MMP-9 is associated with LV enlargement and elevated BNP levels in patients with AMI. A pleiotropic effect of statins appears to be associated with the modulation of cardiac MMP activation, which may be potentially beneficial in the attenuation of post-infarction LV remodelling.     

急性心肌梗死患者心肺复苏后溶栓治疗的研究

目的探讨急性心肌梗死(AMI)患者心肺复苏(CPR)后静脉溶栓的可行性及预后。方法AMI并发呼吸心跳骤停患者42例。治疗组25例，心肺复苏后即刻静脉给予尿激酶150～200万U，30min内静脉注射；对照组17例，在心肺复苏后予除静脉溶栓外的积极抢救治疗。观察其自主循环和呼吸恢复率，24h存活率及出院存活率，自主循环和呼吸恢复时间及出血发生率。结果治疗组的自主循环恢复率、自主呼吸恢复率，24h存活率和出院存活率明显高于对照组，自主循环恢复时间、自主呼吸恢复时间明显短于对照组。结论AMI患者心肺复苏后进行溶栓治疗，能明显提高患者的自主循环、自主呼吸恢复率、24h存活率、出院存活率，缩短自主循环、自主呼吸恢复时间，且不增加继发出血发生率。     

Reteplase: a new thrombolytic for the treatment of acute myocardial infarction

OBJECTIVE: To summarize the published data on reteplase, the most recent thrombolytic agent approved by the Food and Drug Administration for use in the management of acute myocardial infarction in adults. DATA SOURCES: Published data on reteplase identified by MEDLINE searches (January 1985-June 1997), as well as other pertinent literature. DATA SYNTHESIS: Reteplase is a new thrombolytic agent derived from human tissue plasminogen activator. Its mechanism of action is similar to that of alteplase, but it differs in pharmacokinetic and pharmacodynamic properties. Certain structural changes contribute to differences in pharmacokinetic properties such as a prolonged half-life (15 min), which allows it to be administered as two 10-MU bolus injections. Reteplase has been shown to have fibrin specificity similar to that of alteplase, but with a lower binding affinity for fibrin. This enables reteplase to bind to the thrombus repeatedly and increases its fibrinolytic potential. In clinical trials, reteplase demonstrated more rapid and complete coronary patency compared with alteplase, without a significant increase in clinical adverse events. However, the improvement in coronary artery patency with reteplase versus alteplase did not result in a reduction in mortality in the GUSTO III trial. CONCLUSIONS: Despite evidence that use of reteplase results in an improved coronary artery patency rate versus accelerated infusion alteplase, an improvement in mortality rate with reteplase was not shown. Reteplase may have an advantage over alteplase due to a more rapid and simpler dosing regimen, but the significance of this difference is yet to be determined.     

Alcohol and acute myocardial infarction

A number of studies from different countries and several large-scale meta-analyses have reported reduced coronary heart disease rates among those regularly consuming mild to moderate amounts of alcohol compared with those abstaining from alcohol. In contrast, various studies have also reported that heavy alcohol consumption promotes the progression of atherosclerosis and that binge drinking might trigger embolic stroke and acute myocardial infarction. We discuss the association between alcohol consumption and acute myocardial infarction on the basis of evidence from literature published recently. Alcohol consumption has both favourable and unfavourable effects on metabolism, lipid profile, blood coagulation and fibrinolysis, blood pressure and vascular tone depending on the amount of alcohol consumed and the way that it is drunk (i.e. drinking habits). We conclude that it is extremely important to warn people of the risks associated with binge drinking and to encourage them to remain within the recommended safe limits for alcohol consumption.     

Arrhythmias and acute myocardial infarction

The most common arrhythmias associated with inferior-wall and anterior-wall myocardial infarction are bradycardia and supraventricular and ventricular tachycardia. Optimal treatment approaches are based on the pathophysiology of the infarct and the presence of contributing medical factors (eg, congestive heart failure, metabolic disorders). Temporary or permanent pacemaker therapy is helpful in some patients. Sudden death due to arrhythmia after myocardial infarction may be predicted and avoided in certain situations.     

Reducing time to treatment in acute myocardial infarction.

The earliest possible initiation of reperfusion therapy is necessary to prevent extended necrosis, preserve ventricular function, and reduce morbidity and mortality from acute myocardial infarction. Therefore, improving the time to thrombolysis is a critical goal of patient management. Four complementary strategies have been employed in an attempt to shorten the time to thrombolytic therapy: (1) public education to shorten the delay in summoning help, (2) prehospital thrombolysis by trained emergency-response personnel, (3) implementation of emergency department thrombolysis protocols, (4) and the use of rapid diagnostic techniques to confirm acute myocardial infarction. Currently available fibrinolytic agents do not lend themselves to emergency use. Therefore, new thrombolytic agents have been bioengineered with characteristics that make them better suited for use in this setting. Two of these agents, TNK-t-PA and nPA, have extended half-life profiles that permit single-bolus dosing--an important consideration when fibrinolytic therapy is initiated outside the coronary care unit. The most effective system will integrate these complementary strategies to deliver continuous patient care from the time of the call for help, through emergency response, transportation, hospital admission, assessment, and initiation of thrombolytic therapy.     

Pheochromocytoma and acute myocardial infarction

When a pheochromocytoma is manifested as an acute myocardial illness, diagnosis may be difficult to make. If the tumor is suspected early enough, a workup can be done while the complications of the myocardial illness are being controlled (as in our case). The tumor can then be expeditiously removed before any further problems develop. The case presented here underscores the importance of maintaining a high index of suspicion for a pheochromocytoma in any patient who has an unexpected myocardial event.     

Rapid monocyte kinetics in acute myocardial infarction are sustained by extramedullary monocytopoiesis

Monocytes (Mo) and macrophages (MΦ) are emerging therapeutic targets in malignant, cardiovascular, and autoimmune disorders. Targeting of Mo/MΦ and their effector functions without compromising innate immunity's critical defense mechanisms first requires addressing gaps in knowledge about the life cycle of these cells. Here we studied the source, tissue kinetics, and clearance of Mo/MΦ in murine myocardial infarction, a model of acute inflammation after ischemic injury. We found that a) Mo tissue residence time was surprisingly short (20 h); b) Mo recruitment rates were consistently high even days after initiation of inflammation; c) the sustained need of newly made Mo was fostered by extramedullary monocytopoiesis in the spleen; d) splenic monocytopoiesis was regulated by IL-1β; and e) the balance of cell recruitment and local death shifted during resolution of inflammation. Depending on the experimental approach, we measured a 24 h Mo/MΦ exit rate from infarct tissue between 5 and 13% of the tissue cell population. Exited cells were most numerous in the blood, liver, and spleen. Abrogation of extramedullary monocytopoiesis proved deleterious for infarct healing and accelerated the evolution of heart failure. We also detected rapid Mo kinetics in mice with stroke. These findings expand our knowledge of Mo/MΦ flux in acute inflammation and provide the groundwork for novel anti-inflammatory strategies for treating heart failure.