Trends in treatment and outcomes for acute myocardial infarction: 1975-1995

PURPOSE: To review the trends in treatment and survival for patients with acute myocardial infarction over the last 20 years. MATERIAL AND METHODS: Studies were identified through MEDLINE searches and review of study bibliographies. Additional data were obtained from the Health Care Financing Administration including data from Medicare claims files (part A). Thirty-day mortality rates were calculated using Medicare data and case fatality rates from the National Hospital Discharge Survey. Published meta-analyses were used to determine treatment effects. Published studies were included if they reported the use of therapies for acute myocardial infarction at a population level. Trends in the demographic characteristics of the patients as well as infarct characteristics, medication use, and revascularization were recorded. RESULTS: The use of acute treatments that are known to improve survival among patients with myocardial infarction has increased markedly during the last 20 years, leading to an estimated 9.6% reduction (from 27.0% to 17.4%) in 30-day mortality. After adjusting for potential interactions between therapies, the increase in use of aspirin, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and reperfusion can explain 71% of the decrease in the 30-day age- and sex-adjusted mortality rate from 1975 to 1995. The greatest effect of a given therapy was that of aspirin, which accounted for 34% of the decrease in 30-day mortality, followed by thrombolysis (17%), primary angioplasty (10%), beta-blockers (7%), and ACE inhibitors (3%). If other treatments (such as heparin or nonprimary angioplasty), whose effects on mortality are less certain, are included, up to 90% of the decrease in 30-day mortality can be explained by changes in treatment. CONCLUSIONS: The primary reason for the decrease in early mortality from myocardial infarction during the last 20 years appears to be increased use of effective treatments.     

Geographic variation in health care utilization and outcomes in veterans with acute myocardial infarction

OBJECTIVES: To examine regional variation in health care utilization and outcomes during acute and chronic care of veterans following acute myocardial infarction (AMI), identifying potentially modifiable variables and processes of care that influence patient outcomes. METHODS: Using national VA databases, we identified all veterans hospitalized at any VA Medical Center (VAMC) for AMI between October 1990 and September 1997. Demographic, inpatient, outpatient, mortality, and readmission data were extracted for 4 regions: Northeast, South, Midwest and West. Multivariable Cox proportional hazards regression models, controlled for comorbidity, were used to assess predictors of time to death and readmission. RESULTS: We identified 67,889 patients with AMI. Patient demographic characteristics by region were similar. Patients in the Northeast had more comorbid conditions and longer lengths of stay during the index AMI hospitalization. Region of the country independently predicted time to death, with lower risk of death in the Northeast (hazard ratio [HR] = 0.875; 95% confidence interval [95% CI], 0.834 to 0.918; P < .0001) and West (HR = 0.856; 95%CI, 0.818 to 0.895; P = .0001) than in the South. Patients in the Northeast and West also had more cardiology or primary care follow-up within 60 days and at 1 year post-discharge than patients in the South and Midwest. Outpatient follow-up accounted for a significant portion of the variation in all-cause mortality. CONCLUSION: Substantial geographic variation exists in subsequent clinical care and outcomes among veterans hospitalized in VAMCs for AMIs. Outpatient follow-up was highly variable and associated with decreased mortality. Further studies are needed to explore the causes of regional variation in processes of care and to determine the most effective strategies for improving outcomes after AMI.     

New approaches to treatment of myocardial infarction

Survival of patients with acute transmural infarction is largely related to the size of the myocardial infarction. The goal of thrombolytic therapy in acute myocardial infarction is maximal salvage of myocardium by reestablishment of flow in the occluded infarct-related artery and the establishment and maintenance of a patent infarct-related artery. Results of randomized trials show a significant reduction in mortality in patients who have undergone thrombolysis. A patent infarct-related artery, even in the absence of a change in left ventricular function, is associated with reduced mortality. The Thrombolysis in Myocardial Infarction Trial and the European Cooperative Trial showed that recombinant tissue-type plasminogen activator is superior to streptokinase in reestablishing flow in a totally occluded artery. Experimental and clinical evidence suggests that thrombolysis and thrombosis occur simultaneously, and that lysis appears to increase both thrombin and platelet activity. Effective reduction of thrombosis accelerates thrombolysis. Rethrombosis after thrombolysis is due to anchored residual thrombus, which alters the hemorrheology of blood flow and produces a highly thrombogenic substrate that is largely due to residual fibrin-bound thrombin. Platelet deposition is directly related to severity of residual stenosis and shear rate. Thrombin appears to be the most potent of the 5 potential stimulators of platelet activation during arterial thrombosis. Proper anticoagulation can play an important role in reducing thrombosis. Experimental evidence strongly supports the use of heparin during and after thrombolysis. A recently reported study shows continued reduction of residual stenosis after 1 month of vigorous anticoagulation with intravenous heparin and subsequent oral anticoagulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

急性心肌梗死诊断和治疗新概念

1　急性心肌梗死诊断新概念1.1　心肌梗死概念及定义心肌梗死可以从临床症状、心电图、生物化学和病理学等几个方面来定义。心肌梗死的定义也具有社会和心理学意义 ,即健康主要问题的标记 ,也是疾病流行的统计和临床试验的结果。以往 ,WHO定义以下二点或三点同时存在可以诊断心肌梗死 :(1)典型临床症状 (如胸部不适 ) ;(2 )酶学升高 ;(3)典型心电图出现 ,包括出现病理性 Q波的出现。然而 ,目前临床实践、健康监护系统、以及流行病学研究和临床试验 ,均需要准确的心梗定义。而且随着敏感和特异的血清生物学标志物和现代影像技术的出现 ,更…     

Study of postmyocardial infarction scar-formation mechanisms: advantage of an experimental myocardial infarction model in mice

Myocardial infarction involves scar-formation mechanisms in which inflammation, proliferation, cell differentiation, apoptosis and angiogenesis all play a role. Better knowledge of the scar-formation process would be helpful in developing new therapies. The authors have generated a mouse model for infarction because its possible application in transgenic mice would allow the role of target genes in postinfarction scar-formation mechanisms to be studied. An infarction is caused by ligating the descending branch of the left coronary artery. At various times after ligation, the mice are sacrificed to determine the size of the infarction, left ventricular function and the overall myocardial scar-formation process. Early mortality was 10%. Between the fourth and sixth day postsurgery, 25% of mice died of a ruptured, infarcted left ventricle. The size of the infarctions diminished with time, while the surface of the left ventricle increased. In hemodynamics, 15 and 30 days after infarction, left ventricle telediastolic pressure was higher, telesystolic pressure was lower and contractility in indexes had collapsed. After an inflammatory phase in which polynuclear neutrophils colonized the scar, granulation tissue set in with a proliferation of myofibroblasts and growth of new blood vessels. These cells disappeared from the scar gradually, leaving behind a matrix rich in collagen and devoid of any contractile properties. The authors have characterized a murine model of myocardial infarction, with applications in transgenic mice and in view of establishing new agents in postmyocardial infarction repair.     

Demographic description and outcomes of a metropolitan network for myocardial infarction treatment

Objective:The objective of the study was to describe the myocardial infarction treatment network and compare in-hospital mortality in patients undergoing either primary angioplasty or pharmacoinvasive strategy in Mexico City and a broad metropolitan area.Methods:Cohort study including patients with ST-elevation myocardial infarction. We recorded demographic and clinical data, laboratory tests and in-hospital mortality in patients that underwent primary angioplasty and pharmacoinvasive strategy. Kaplan-Meier analysis was used to assess mortality and Cox-regression assessed mortality risk factors.Results:Three hundred forty patients from a network of 60 hospitals and 9 states were analyzed. Of the total population, 166 were treated with pharmacoinvasive strategy and 174 with primary angioplasty. Door to thrombolytic time was 54 min and door to wire crossing time was 72.5 min; no differences in total ischemia time were demonstrated. No differences for in-hospital mortality (6.3% vs. 5.4%, p = 0.49) were found when comparing pharmacoinvasive and primary angioplasty groups. The main predictors for in-hospital mortality were: glucose > 180 mg/dl (HR 3.73), total ischemia time > 420 min (HR 3.18), heart rate > 90 bpm (HR 5.46), Killip and Kimball > II (HR 11.03), and left ventricle ejection fraction < 40% (HR 3.21).Conclusions:This myocardial infarction network covers a large area and constitutes one of the biggest in the world. There were no differences regarding in-hospital mortality between pharmacoinvasive strategy and primary angioplasty. Pharmacoinvasive strategy is an effective and safe option for prompt reperfusion in Mexico.Key words: Myocardial infarction, Thrombolytic therapy, Angioplasty, Mortality     

Early definition of treatment outcomes after reperfusion therapy for myocardial infarction

AIMS: Early definition of treatment outcomes, including coronary patency and infarct size, after reperfusion therapy for myocardial infarction (MI) is desirable to identify patients requiring further intervention. METHODS AND RESULTS: Patients receiving reperfusion therapy for a first MI had continuous 12-lead ST segment monitoring to document reperfusion and ischaemia time. Infarct size was measured by 12-lead QRS score and radionuclide scintigraphy ((201)Tl single-photon emission computed tomography, SPECT) at 1 week, and left ventricular function by echocardiography at 1 week and 1 month. Resolution of ST elevation accurately detected TIMI 2 or 3 reperfusion (predictive accuracy 93%) in 55 patients undergoing immediate angioplasty, but ST recovery was delayed (17+/-14min) after angiographic reperfusion. A multivariate model, including risk region and ischaemia time, accurately predicted MI size (R(2)=0.80, P<0.00001) in these patients. The same model, prospectively applied on Day 1 to 154 patients receiving thrombolytic therapy, accurately predicted MI size, measured by QRS score (R(2)=0.88, P<0.0000001) and (201)Tl SPECT (R(2)=0.75, P<0.000001) at 1 week for individual patients. Regional myocardial wall motion at 1 month was directly correlated with MI size predicted by the model on Day 1 (r=0.73, P<0.0001). CONCLUSIONS: Use of ST segment monitoring during reperfusion therapy facilitates early prediction of treatment outcomes, including coronary reperfusion, infarct size and ventricular function.     

Right ventricular myocardial infarction: presentation and acute outcomes

Acute inferior wall myocardial infarction can be complicated by right ventricular myocardial infarction (RVMI), and the excess mortality cannot be fully explained by mechanical reasons. The authors try to systematically assess the incidence, clinical presentation and early outcomes of right ventricular infarction in a tertiary-care setup. Their study was a prospective observational series of consecutive patients with RVMI. All patients with acute inferior myocardial infarction (n=135) were enlisted. RVMI was diagnosed by > or = 1 mm ST elevation in lead V(4R) in a right-sided electrocardiogram. Right ventricular (RV) infarction occurred in 37% (n=50) of patients with acute inferior infarctions. Patients with isolated inferior infarction served as controls (n=85). Echocardiography was performed within 24 hours of admission. From both groups, 66% qualified for thrombolysis. The incidence of hypotension-bradycardia and heart blocks requiring pacing support was much higher in right ventricular infarction (n=21) than in inferior infarction (n=13). Clinically manifest RV dysfunction (raised jugular venous pulse [JVP], hypotension, tricuspid regurgitation) and right ventricular dilation detected by echocardiography were seen in only 13 patients. The in-hospital mortality rate was significantly higher (n=8, 16%) in right ventricular infarction group than in inferior infarction group (n=3, 3.5%). Right ventricular infarction was seen in a third of inferior myocardial infarctions (IMIs), but hemodynamically evident right ventricular dysfunction occurred in only a tenth of acute IMIs. Nevertheless, the acute in-hospital mortality rate of patients with right ventricular infarction was much higher than in those with inferior infarction owing to arrhythmic and mechanical complications.     

骨髓干细胞动员治疗急性心肌梗死研究进展

急性心肌梗死(AMI)的各种治疗手段均不能从根本上修复坏死心肌组织,彻底恢复心脏的正常收缩功能。因此,即使AMI的死亡率有所下降,但AMI后心衰的发病率仍居高不下。心脏移植又存在供体不足及免疫排斥等问题而难以在临床推广。随着干细胞生物学的飞速发展,采用生物学技术将多种来源的干细胞进行动员或自体心肌内移植,以增加有功能的心肌细胞数量,修复损伤心肌组织,降低心衰发生率已成为近年来心血管疾病研究领域的热点之一。其中尤以骨髓干细胞动员以其无创伤、无免疫排斥反应,不需要干细胞提取、培养、扩增等工作而备受亲睐。现结合文献…     

Regional myocardial and organ blood flow after myocardial infarction: application of the microsphere principle in man

A physiologic means of measuring the distribution of cardiac output and regional myocardial blood flow has been developed that uses human albumin microspheres labeled with carbon-11 (11C) and external detection with positron emission tomography. Ten patients with previous myocardial infarction were studied to investigate the level of blood flow in normal and infarcted segments of the heart. After diagnostic catheterization, 4 to 6 mCi of 11C on 2 to 3 million sterile microspheres (15 to 20 micron) were mixed and injected into the apex of the left ventricle during timed withdrawal of arterial blood to obtain reference flow values. Regional activity in brain, heart, lungs, liver, spleen, and kidneys was measured tomographically. Blood flow was calculated based on the relationship between total activity in a reference flow and tissue activity in tomograms of each organ (ml/min/100 g). No adverse effects were noted after injection of the microspheres. Successive myocardial tomograms showed no loss of activity. There were no significant differences in flow values in matched regions of paired organs. Mean cerebral flow was 52.4 +/- 10.0 ml/min/100 g in the frontal lobes, 54.4 +/- 8.8 in the temporal lobes, 67.6 +/- 8.2 in the occipital lobes, and 53.0 +/- 9.4 in the basal ganglia. Flow was 16.0 +/- 8.4 ml/min/100 g (range 0 to 40.0) in the center of infarcted myocardium and 82.0 +/- 32.0 in the remote segments. This method meets most of the demands for use of microspheres to measure tissue blood flow. The wide range of flow values in infarcted myocardium may be a function of infarct size, spatial resolution, or pathologic evidence of islands of viable tissue. Patients with angina had high flow values in the infarcted segment, whereas those with heart failure had significantly lower values. Surviving myocardium in the region of the infarct may need to be considered if patients complain of angina, particularly when treatment is aimed at preserving ventricular function.     

Regional myocardial shape alterations in patients with anterior myocardial infarction

Objective: To assess the impact of regional left ventricular curvature in patients with an acute anterior myocardial infarction on ventricular volume.Methods: Left ventricular curvature was calculated at 100 points from apical four chamber echocardiograms of 68 patients with an acute anterior wall infarction. Curvature at any point of the contour was defined as the reciprocal of the radius of the circle that intersects that point tangentially and was independent of volume and geometric assumptions. Curvature, volume and shape of the patient group was compared with these measurements in 20 normal volunteers.Results: Diastolic curvature differed at the borderzone of the infarct and the apical area. In the basal septal area (point 9–18) mean curvature was lower in the patient group (0.1±2.7 versus 2.1±0.7; p<0.0001) as compared to the normal individuals. In the mid-septal area (point 22 to 27), mean curvature was more concave (– 0.1±2.6) in the patient group corresponding to in the normal population (– 0.4±1.3) p<0.005. In the apex point 52 and 53 diverged with a curvature of 9.9±1.9 in patients versus 9.4±2.9 p<0.005 in normal individuals. Systolic curvature diverged at the basal septum (point 1–4) with a mean curvature of 1.4±1.1 in patients compared to 3.5±2.5 in normal individuals p<0.01. Curvature differed also in the mid-septal region (point 9–29) with a curvature of – 1.7±1.2 in patients versus 0.4±0.9 (p<0.01) in normal individuals and in the apical septum (point 48–52) with a curvature of 16.6±5.2 in patients and 13.9±2.6 (p<0.0001) in healthy individuals. Separation of patients with the greatest curvature alteration to those with minor curvature change revealed, that baseline curvature analysis can discriminate patients at risk for left ventricular remodelling.Conclusion: Regional curvature analysis correctly identifies the geometric changes induced by myocardial infarction. Apical systolic curvature can distinguish those patients that are at risk for left ventricular remodelling from those who are not at risk.