Very Long-Term Memory for Information Taught in School

The long-term relative benefits of thrombolysis and mechanical reperfusion therapy following acute myocardial infarction (AMI) have not been established. The purpose of this study was to compare left ventricular function, left ventricular remodeling and late outcome after AMI for different reperfusion therapies. Thirty consecutive patients suffering their first anterior wall myocardial infarction with coronary stenoses limited to the left anterior descending coronary artery were studied. They included 10 patients who underwent intracoronary thrombolysis (ICT), 10 who underwent PTCA and 10 who underwent noninterventional medical treatment. All patients underwent coronary angiography (CAG) during the acute phase of AMI and also during the follow-up period, and left ventriculography during the follow-up period and clinical follow-up was performed (mean clinical follow-up period: 53 +/- 31 months). No significant difference in global ejection fraction was noted among the groups, although the end-diastolic volume index (EDVI) in the PTCA group (79.4 +/- 17.5 ml/m2) was significantly smaller than in the noninterventional (106.1 +/- 25.1 ml/m2) and ICT (107.9 +/- 28.3 ml/m2) group (p < 0.05). The regional wall motion index (RWMI) for the anterior region in the PTCA group (-2.7 +/- 0.8) was greater (p < 0.05) than in the noninterventional (-3.4 +/- 0.6) and ICT (-3.3 +/- 0.6) groups. A significant linear correlation was found between EDVI and % diameter stenosis and also between RWMI and % diameter stenosis following reperfusion (p = 0.01). There was no difference in the incidence of cardiac death, nonfatal reinfarction, bypass surgery or congestive heart failure among the groups. Disturbed left ventricular regional wall motion and remodeling benefit most from angioplasty because of prompt restoration of adequate blood flow. However, there was no difference in late outcomes following AMI among the three groups.     

ESPRIT: a European study of the prevention of reocclusion after initial thrombolysis with duteplase in acute myocardial infarction

BACKGROUND: The goal of thrombolytic treatment in acute myocardial infarction is reperfusion of the infarct-related coronary artery. Duteplase is a double-chain recombinant tissue-type plasminogen activator. Its efficacy and safety were evaluated in patients with acute myocardial infarction treated within 4 h of onset of chest pain in this multicentre, open, non-controlled trial. METHODS AND RESULTS: A total of 273 patients were enrolled and treated with duteplase 0.6 MU.kg-1 over 4 h, with concomitant oral aspirin and intravenous heparin. Coronary arteriography was performed at 60 min, 90 min and approximately 24 h after the start of duteplase infusion to assess the perfusion grade (TIMI scoring) of the infarct-related coronary artery. Safety was assessed by monitoring patients closely for bleeding and for all other adverse experiences during the 72-h study period. Reinfarction during the study period was also recorded, and deaths at any time during the period in hospital were documented. TIMI grade 2 or 3 patency of the infarct-related coronary artery at 90 min was achieved in 70% of the patients and 7% of these "patent' infarct-related coronary arteries had reoccluded by 20 to 36 h. Clinical reinfarction during the 72-h study period was observed in 7%. Total in-hospital mortality was 8%. Serious or life-threatening bleeding occurred in 4% of the patients. There was one haemorrhagic stroke, and this was fatal. CONCLUSIONS: Weight-adjusted duteplase infusion, together with oral aspirin and intravenous heparin, in acute myocardial infarction resulted in patency of the infarct-related coronary artery and a safety profile comparable to those reported for the other form of tissue-type plasminogen activator, alteplase. However, there remains a problem with reocclusion and reinfarction after initially successful thrombolysis.     

Importance of infarct-related artery patency for recovery of left ventricular function and late survival after primary angioplasty for acute myocardial infarction

OBJECTIVES: The purpose of this study was to evaluate the importance of late infarct-related artery patency for recovery of left ventricular function and late survival after primary angio-plasty for acute myocardial infarction. BACKGROUND: Infarct-related artery patency is thought to improve late survival by its effect on preservation of left ventricular function. Patency may also enhance late survival by preventing left ventricular dilation and reducing arrhythmias, independent of myocardial salvage. However, most studies have not shown patency to be an independent predictor of survival when late left ventricular function is taken into account. METHODS: We followed up 576 hospital survivors of acute myocardial infarction treated with primary angioplasty for 5.3 years. Ejection fraction and infarct-related artery patency were determined at follow-up catheterization at 6 months. Predictors of late cardiac survival were determined using Cox regression models. RESULTS: Patients with patent arteries had more improvement and a better late ejection fraction than patients with occluded arteries (56.3% vs. 47.9%, p = 0.001). In patients with acute ejection fraction < 45%, late survival was better in those with patent versus occluded arteries (89% vs. 44%, p = 0.003), but patency was not a significant predictor after improvement in ejection fraction was taken into account. In patients with a large anterior infarction, patency was a significant independent predictor of late survival. CONCLUSIONS: Infarct-related artery patency is important for recovery of left ventricular function, and in patients with acute ejection fraction < 45%, patency is important for late survival. Our data are consistent with the hypothesis that the survival benefit is due primarily to the effect of patency on recovery of left ventricular function. In patients with a large anterior infarction, patency appears to provide an additional late survival benefit independent of myocardial salvage. These observations support the need for additional clinical trials of late reperfusion in patients with a large anterior infarction.     

The differing prognostic utility of exercise radionuclide ventriculography in coronary artery disease patients with and without prior myocardial infarction

Previous studies have documented the prognostic utility of left ventricular ejection fraction response to exercise primarily in populations without prior myocardial infarction. We undertook a study to assess the prognostic utility of exercise left ventricular ejection fraction and segmental wall motion response during exercise radionuclide ventriculography in coronary artery disease patients with and without prior myocardial infarction. METHODS: We examined the comparative prognostic utility of left ventricular ejection fraction and segmental wall motion response during upright bicycle exercise radionuclide ventriculography in 419 coronary artery disease patients with (n = 217) and without (n = 202) prior myocardial infarction using univariate and multivariate hierarchical regression analyses. RESULTS: During an average followup period of 61 months, 96 patients (23%) suffered cardiac events, including 55/217 (25%) of the patients with prior myocardial infarction and 41/200 (21%) of the patients without prior myocardial infarction (p = ns). Both cumulative Kaplan-Meier survival analyses and stepwise hierarchical Cox survival analyses demonstrated that peak left ventricular ejection fraction < 55% was a significant predictor of cardiac events in patients without prior myocardial infarction (p = 0.04), whereas an exercise wall motion worsening score > or = 2 was a significant predictor in patients with a prior myocardial infarction (p = 0.0001). CONCLUSIONS: The prognostic utility of exercise radionuclide ventriculography variables differ according to the presence or absence of prior myocardial infarction. Global function, assessed by peak left ventricular ejection fraction, adds the greatest prognostic information in patients without prior myocardial infarction, whereas regional function, assessed by exercise wall motion worsening, is the best predictor among patients with prior myocardial infarction.     

Early angiotensin converting enzyme inhibitor therapy after experimental myocardial infarction prevents left ventricular dilation by reducing infarct expansion: a possible mechanism of clinical benefits

OBJECTIVE: To examine the effects of early angiotensin-converting enzyme (ACE) inhibitor therapy after myocardial infarction on infarct expansion in an experimental rat model. BACKGROUND: ACE inhibitor therapy within 24 h of acute myocardial infarction (AMI) reduces mortality by unknown mechanism(s). METHODS: Rats underwent permanent coronary artery occlusion. A treated group received enalapril (1.9+/-0.2 mg/kg) daily in drinking water beginning 2 h after coronary artery occlusion, a time too late to reduce infarct size. Rats were sacrificed 2 days or 2 weeks after myocardial infarction. Hearts were arrested and fixed at a constant pressure, then sectioned and photographed for morphometric analysis. RESULTS: Infarcts in the control group expanded between 2 days and 2 weeks after myocardial infarction (expansion index 0.7+/-0.1 versus 2.5+/-0.4, P< 0.05). However, infarct expansion remained unchanged in the enalapril group between 2 days and 2 weeks after myocardial infarction (expansion index 0.8+/-0.1 versus 1.3+/-0.1, NS). Two weeks after myocardial infarction, the enalapril group had fewer expanded infarcts than the control group (expansion index 1.3+/-0.1 versus 2.5+/-0.4, P< 0.05). While left ventricular volume increased in the control group between 2 days and 2 weeks after myocardial infarction (0.17+/-0.01 ml versus 0.36+/-0.03 ml, P< 0.05), it remained constant in the enalapril group (0.22+/-0.02 ml versus 0.25+/-0.03 ml, NS). Two weeks after myocardial infarction, the left ventricles were larger in the control group than in the enalapril group (0.36+/-0.03 ml versus 0.25+/-0.03 ml, P< 0.05). CONCLUSIONS: Treatment with enalapril initiated 2 h after AMI prevented left ventricular dilation by limiting infarct expansion. This may explain the mechanism by which ACE inhibitor therapy started within 24 h of an AMI improves survival 5-6 weeks after infarction.     

Influence of infarct-zone viability on left ventricular remodeling after acute myocardial infarction

BACKGROUND: The relation between residual myocardial viability after acute myocardial infarction (AMI) and ventricular remodeling has yet to be fully elucidated. We hypothesized that the presence of residual viability would favorably influence left ventricular remodeling after AMI and that serial changes in left ventricular dimensions might be related to the extent of myocardial viability in the infarct zone. METHODS AND RESULTS: Ninety-three patients with a first AMI successfully treated with primary coronary angioplasty underwent two-dimensional echocardiography within 24 hours of admission and low-dose dobutamine echocardiography at a mean of 3 days after AMI. Two-dimensional echocardiography and coronary angiography were obtained in all patients 1 and 6 months after coronary angioplasty. On the basis of dobutamine echocardiography responses, patients were divided in two subsets: those with (n=48; group I) and those without (n=45; group II) infarct-zone viability. There was no difference in minimal lesion diameter and infarct-related artery patency at 1 and 6 months between the two groups. Group II patients had significantly greater end-diastolic (76+/-18 versus 53+/-14 mL/m2; P<.0003) and end-systolic (42+/-17 versus 22+/-11 mL/m2; P<.0003) volumes at 6 months than did patients in group 1. The extent of infarct-zone viability was significantly inversely correlated with percent changes in end-diastolic volumes at 6 months (r=-.66; P<.000001) and was the most powerful independent predictor of late left ventricular dilation. CONCLUSIONS: After reperfused AMI, the degree of left ventricular dilation, when it occurs, is inversely related to the extent of residual myocardial viability in the infarct zone. Thus, the absence of residual infarct-zone viability discriminates patients who develop progressive left ventricular dilation after reperfused AMI from those who maintain normal left ventricular geometry.     

Very early thrombolysis in acute myocardial infarction--a light at the end of the tunnel

Myocardial damage in acute myocardial infarction is a time-dependent process. Thrombolytic therapy effectively opens the coronary artery, restores coronary blood flow and prevents ongoing necrosis. We examined the effect of very early thrombolytic therapy (including prehospital administration) in a consecutive group of 510 patients with myocardial infarction on the following factors: mortality, complications and the preservation of left ventricular function. The treatment was given to 89 at home (time delay to treatment 1.2 +/- 0.6 h) and 421 in hospital (2.0 +/- 1.0 h). Twelve patients died in hospital and major hemorrhage occurred in 10. The arterial patency rate in 416 patients who underwent coronary angiography 6 days later was 82%. Infarct size measured by left ventriculography was determined by the area at risk, the delay time until the initiation of thrombolytic therapy, the total duration of ischemic pain and the degree of restoration of arterial blood flow. We conclude that early thrombolytic therapy, particularly prehospital management, is feasible and safe and reduces infarct size and mortality. A further decrease in the delay to initiation of treatment and more effective thrombolytic therapy will further decrease mortality and myocardial damage.     

Effect of early enalapril therapy on left ventricular function and structure in acute myocardial infarction

Infarct expansion starts within hours to days after transmural myocardial injury. Previous echocardiographic and left ventriculographic studies demonstrated that angiotensin-converting enzyme (ACE) inhibitor therapy limits left ventricular dilatation, particularly in patients with anterior wall acute myocardial infarction (AMI) or impaired left ventricular function. Forty-three patients with an acute Q-wave AMI were randomized within 24 hours of symptom onset to intravenous enalaprilat (1 mg) or placebo. Patients were then given corresponding oral therapy and followed for 1 month. Predrug and 1-month gated blood pool scans were obtained in 32 patients to evaluate changes in cardiac volumes and ejection fraction. Twenty-three patients underwent magnetic resonance imaging at 1 month to evaluate left ventricular infarct expansion. Blood pressure decreased at 6 hours but returned to baseline in both groups after 1 month of therapy. The change in cardiac volumes from baseline to 1 month differed between the placebo (end-diastolic volume +16 +/- 5 ml, end-systolic volume +8 +/- 6 ml), and enalapril (end-diastolic volume -8 +/- 9 ml and end-systolic volume -14 +/- 7 ml) groups (p < 0.05 vs placebo). Global and infarct zone ejection fractions improved significantly at 1 month in the enalapril group (+6 +/- 3% and 19 +/- 5%, respectively) but did not change over 1 month in the placebo group. Infarct segment length and infarct expansion index by magnetic resonance imaging were significantly less in those treated with enalapril, suggesting less infarct expansion in this group. Thus, early administration of enalaprilat to patients presenting with a first Q-wave AMI prevents cardiac dilatation and infarct expansion.     

An evaluation of the use made of cosmetic and functional prostheses by unilateral upper limb amputees

PURPOSE: To review the available data on the treatment of chronic stable angina and formulate a rational approach to the use of pharmacologic therapy, percutaneous transluminal coronary angioplasty (PTCA), and coronary artery bypass graft surgery (CABG). DATA SOURCES: A MEDLINE search of English-language literature published between 1976 and 1996 and the bibliographies of relevant articles. STUDY SELECTION: Primary research articles, meta-analyses, and meeting abstracts related to the management of chronic stable angina with an emphasis on comparisons of medical therapy, PTCA, and CABG. DATA EXTRACTION: Three trials comparing medical therapy with PTCA, seven trials comparing medical therapy with CABG, and nine trials comparing PTCA with CABG. DATA SYNTHESIS: Low-risk patients with single-vessel coronary artery disease and normal left ventricular function had greater alleviation of symptoms with PTCA than with medical treatment; mortality rates and rates of myocardial infarction were unchanged. In high-risk patients (risk was defined by severity of ischemia, number of diseased vessels, and presence of left ventricular dysfunction), improvement of survival was greater with CABG than with medical therapy. In moderate-risk patients with multivessel coronary artery disease (most had two-vessel disease and normal left ventricular function), PTCA and CABG produced equivalent mortality rates and rates of myocardial infarction. CONCLUSIONS: In low-risk patients, a strategy of initial medical therapy is reasonable. In moderate-risk patients, PTCA and CABG produce similar mortality rates and rates of myocardial infarction but PTCA-treated patients require more revascularization procedures. In high-risk patients, CABG is usually preferred.     

PROTECT (Prospective Reinfarction Outcomes in the Thrombolytic Era Cardizem CD Trial): a randomized, double-blind clinical trial of diltiazem versus atenolol in secondary prophylaxis post non-Q wave myocardial infarction

OBJECTIVE: To describe the rationale and design of the Prospective Reinfarction Outcomes in the Thrombolytic Era Cardizem CD Trial (PROTECT). DESIGN: A multicentre, randomized, double-blind, parallel-group comparison of once daily beta-therapy versus heart rate lowering calcium channel blocker therapy, in the reduction of one-year nonfatal reinfarction and cardiovascular death (combined primary end-point) initiated 24 to 96 h post non-Q wave myocardial infarction. SETTING: One hundred and twenty hospitals across Canada. PATIENTS: Over 7500 women and men aged 21 years or older with enzyme-confirmed non-Q wave infarction and without significant left ventricular systolic dysfunction will be recruited over two years. INTERVENTIONS: Once daily beta-blocker therapy (oral atenolol, 50 to 200 mg) versus once daily calcium channel blocker therapy (oral diltiazem 120 to 360 mg) with follow-up for up to three years. CONCLUSIONS: The PROTECT will be the largest all-Canadian cardiovascular trial to date and will compare two commonly prescribed agents for secondary prophylaxis following non-Q wave infarction. The scientific question addressed by the PROTECT is of major public health importance and the results of the study will directly affect current clinical practice.     

Randomized trial of direct coronary angioplasty versus intravenous streptokinase in acute myocardial infarction

OBJECTIVES: The objective of this study was to obtain preliminary data on the relative clinical utility of direct coronary angioplasty compared with that of intravenous thrombolytic therapy for patients with acute myocardial infarction. BACKGROUND: The relative merits of intravenous thrombolytic therapy and direct coronary angioplasty as treatment for acute myocardial infarction are incompletely understood, and randomized trials of these treatments have been extremely limited. METHODS: One hundred patients with ST segment elevation presenting to a single high volume interventional center within 6 h of the onset of chest pain were randomized to receive either streptokinase (1.2 million U intravenously over 1 h) or immediate catheterization and direct coronary angioplasty. Patients were excluded for age > or = 75 years, prior bypass surgery, Q wave infarction in the region of ischemia or excessive risk of bleeding. All patients were then treated with aspirin (325 mg orally/day) and heparin (1,000 U intravenously/h) for 48 h until catheterization was performed to determine the primary study end point, namely, infarct-related artery patency at 48 h. Secondary end points were in-hospital death, left ventricular ejection fraction at 48 h and time to treatment. RESULTS: There was no difference in the baseline characteristics of the two treatment groups. Overall patient age was 56 +/- 10 years, 83% of patients were male, 11% had prior infarction, 40% had anterior infarction and 97% were in Killip class I or II. Although time to treatment was delayed in the angioplasty group (238 +/- 112 vs. 179 +/- 98 min, p = 0.005), there was no difference in 48-h infarct-related artery patency or left ventricular ejection fraction (patency 74% vs. 80%; ejection fraction 59 +/- 13% vs. 57 +/- 13%; angioplasty vs. streptokinase, p = NS for both). There were no major bleeding events, and the mortality rate with angioplasty (6%) and streptokinase (2%) did not differ (p = NS). CONCLUSIONS: These results suggest that intravenous thrombolytic therapy might be preferred over coronary angioplasty for most patients because of the often shorter time to treatment.     

Aspirin versus coumadin in the prevention of reocclusion and recurrent ischemia after successful thrombolysis: a prospective placebo-controlled angiographic study. Results of the APRICOT Study

BACKGROUND: Successful coronary thrombolysis involves a risk for reocclusion that cannot be prevented by invasive strategies. Therefore, we studied the effects of three antithrombotic regimens on the angiographic and clinical courses after successful thrombolysis. METHODS AND RESULTS: Patients treated with intravenous thrombolytic therapy followed by intravenous heparin were eligible when a patent infarct-related artery was demonstrated at angiography < 48 hours. Three hundred patients were randomized to either 325 mg aspirin daily or placebo with discontinuation of heparin or to Coumadin with continuation of heparin until oral anticoagulation was established (international normalized ratio, 2.8-4.0). After 3 months, in which conservative treatment was intended, vessel patency and ventricular function were reassessed in 248 patients. Reocclusion rates were not significantly different: 25% (23 of 93) with aspirin, 30% (24 of 81) with Coumadin, and 32% (24 of 74) with placebo. Reinfarction was seen in 3% of patients on aspirin, in 8% on Coumadin, and in 11% on placebo (aspirin versus placebo, p < 0.025; other comparison, p = NS). Revascularization rate was 6% with aspirin, 13% with Coumadin, and 16% with placebo (aspirin versus placebo, p < 0.05; other comparisons, p = NS). Mortality was 2% and did not differ between groups. An event-free clinical course was seen in 93% with aspirin, in 82% with Coumadin, and in 76% with placebo (aspirin versus placebo, p < 0.001; aspirin versus Coumadin, p < 0.05). An event-free course without reocclusion was observed in 73% with aspirin, in 63% with Coumadin, and in 59% with placebo (p = NS). An increase of left ventricular ejection fraction was only found in the aspirin group (4.6%, p < 0.001). CONCLUSIONS: At 3 months after successful thrombolysis, reocclusion occurred in about 30% of patients, regardless of the use of antithrombotics. Compared with placebo, aspirin significantly reduces reinfarction rate and revascularization rate, improves event-free survival, and better preserves left ventricular function. The efficacy of Coumadin on these end points appears less than that of aspirin. The still-high reocclusion rate emphasizes the need for better antithrombotic therapy in these patients.     

Treatment with ramipril improves systolic function even in patients with mild systolic dysfunction and symptoms of heart failure after acute myocardial infarction

BACKGROUND: Clinical signs of heart failure such as pulmonary rales and dyspnea, ventricular dysfunction, and ventricular arrhythmia are independent predictors of a poor prognosis after acute myocardial infarction (AMI). HYPOTHESIS: The study aimed to assess the effect of ramipril treatment on mildly depressed left ventricular (LV) systolic function, assessed by atrioventricular (AV) plane displacement in patients with congestive heart failure after AMI. METHODS: The study was a substudy in the Acute Infarction Ramipril Efficacy Study, a double-blind, randomized, place-bo-controlled trial of ramipril versus placebo in patients with symptoms of heart failure after AMI. In all, 56 patients were included in the main study, 4 refused to participate in the substudy, and 4 were excluded for logistical reasons. Echocardiography was performed at entry and after 6 months. Patients who underwent coronary artery bypass grafting during the follow-up period were excluded. RESULTS: At baseline, the patients had modest LV dysfunction, and mean AV plane displacement of 9.7 mm. During follow-up, AV plane displacement increased in ramipril-treated patients from 9.5 to 10.9 mm (p < 0.01). No statistically significant changes were seen in the placebo group. CONCLUSIONS: Ramipril improves LV systolic function in patients with clinical signs of heart failure and only modest systolic dysfunction after AMI. Measurement of AV plane displacement is a simple and reproducible method for detection of small changes in systolic function and may be used instead of ejection fraction in patients with poor image quality.     

Successive ischemic events to a first acute myocardial infarct treated with fibrinolysis. An analysis of GISSI-2 patients considered reperfused by a clinical criterion. Participants in the GISSI-2 study. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico

BACKGROUND: The fast normalisation of the ST, after thrombolysis, is early sign related to coronary artery reperfusion and to prognosis of acute myocardial infarction (AMI). The aim of this analysis is the evaluation, in the large patients cohort of the GISSI-2 trial, of the relationship between the ST segment evolution after fibrinolytic therapy of AMI and recurrent ischaemic events [angina-reinfarction-ischaemia to exercise testing (ET)] at 30 and 180 days from randomisation. METHODS: Patients with first confirmed IMA and ECG before randomisation and 4 hours later, are chosen from GISSI-2 trial. A decrease > or = 50% of the sigma ST elevation is adopted as cutoff for predicting coronary artery patency. Recanalisation is deemed to have occurred in group A patients versus not reperfused group B patients. The studied events are: angina, reinfarction, mortality, at 30 and 180 days from randomisation; ischemia to ET SL of 4-6 week. The results are presented in terms of Mantel-Haenszel odds ratios (OR) and 95% confidence intervals. RESULTS: Group A patients n. 5307 experienced versus group B patients n. 2718 a higher incidence of--in-hospital angina: 10.3% vs 7.9% OR 1.30 (1.11-1.52)-180 days reinfarction: 2.9% Vs 1.7% OR 1.66 (1.19-2.30)-Ischaemia to ET 25.4% vs 21.4% OR 1.24 (1.08-1.43), and a lower in-hospital mortality: 3.8% vs 8.5% OR 0.39 (0.32-0.48). CONCLUSIONS: Patients having indirect signs of early reperfusion post thrombolysis for IMA experience a higher in-hospital and 180 days recurrent ischaemia and a lower mortality; this fact can allow early identification of the patients who can receive a benefit from different therapeutical strategies.     

The effect of L-DOPA on the motor activity of mouse fetuses

Most patients with acute myocardial infarction do not receive or are ineligible for thrombolytic therapy, and thus their prognosis is worse than that of the populations studied in the major, randomized, lytic therapy trials. We need to devise a cost-effective strategy with which to appropriately stratify these patients. Simple, easily ascertained clinical variables that are evident soon after hospital admission can identify higher-risk patients, who are likely to be older and less able to adequately complete an exercise test. In some patients, nuclear imaging tests are appropriate; low-dose dobutamine echocardiography and ambulatory ECG monitoring may also have a role. Greater use of routine cardiac catheterization (with assessment of ventricular function) might be the most appropriate way to stratify patients because it may overcome some of the limitations of noninvasive testing, will clearly define high-risk patients, and may facilitate early discharge from the hospital. Left ventricular function and the patency of the infarct-related artery will be determined, and patients with left main coronary disease, significant three-vessel coronary artery disease, and two-vessel coronary disease (especially with proximal left anterior descending coronary artery involvement) will be identified. An aggressive strategy of revascularization to improve survival in appropriate patients may be employed. Greater use of routine coronary arteriography after acute myocardial infarction would inevitably lower the threshold for inappropriate, potentially risky, and expensive further interventions. We need to focus our attention on the most appropriate strategies for the management of patients whose prognosis is worse than the prognosis of those who receive lytic therapy after acute myocardial infarction.     

Clinical and angiographic features of patients with an occluded versus a patent infarct vessel after intravenous streptokinase for acute myocardial infarction

Despite early treatment with thrombolytic agents for acute myocardial infarction, a significant portion of patients fail to achieve a patent infarct artery. To study the various factors related to achieving patency in the infarct vessel, 201 patients who received streptokinase within six hours of symptoms were studied. All patients underwent cardiac catheterization during the same hospitalization at 5.40 +/- 3.26 days after admission. Forty-five (22.4%) patients were found to have an occluded infarct artery (group 1) and 156 (77.6%) had a patent infarct vessel (group 2). There was no difference in the time from onset of symptoms to receiving streptokinase between the two groups. The two groups were similar to each other with regard to age, gender, history of myocardial infarction or angina, and major risk factors for coronary disease. Coagulation parameters before and after streptokinase therapy, reflecting the lytic state, were similar in both groups. The left ventricular end diastolic pressure was significantly higher and the left ventricular ejection fraction was significantly lower in group 1 than in group 2. These observations suggest that despite early initiation of thrombolytic therapy in patients with acute myocardial infarction, a significant portion of patients fail to achieve a patent infarct artery. This failure cannot be explained by the observed clinical parameters or the lytic state after streptokinase.     

Interleukin-8 expression in bronchoalveolar lavage cells in the evaluation of alveolitis in idiopathic pulmonary fibrosis

OBJECTIVES: We evaluated the relationship between alterations in coronary flow velocity during the acute phase of acute myocardial infarction (AMI) and the recovery of left ventricular wall motion in patients who underwent successful primary angioplasty. BACKGROUND: The status of the coronary microcirculation is the major determinant of the prognosis of patients who have had successful reperfusion after AMI. Animal studies have shown that dynamic changes in regional flow are associated with the extent of infarction. Evaluation of alterations in coronary flow velocity in infarcted arteries may provide information about microcirculatory damage. METHODS: Flow velocity of the distal anterior descending artery was continuously monitored with the use of a Doppler guide wire immediately after recanalization for 18 +/- 4 h in 19 patients who underwent successful primary angioplasty after anterior AMI. Subjects were divided into two groups on the basis of the time course of alterations in average peak velocity (APV). Group D consisted of patients who had progressive decreases in APV through the next day (n = 9), and Group I comprised patients with an increase in APV after a transient decline (n = 10). Ejection fraction (EF) and regional wall motion (RWM) were assessed by left ventriculography performed on admission and at discharge. RESULTS: The APV at the end of monitoring was greater in group I than in group D. In group I, EF and RWM were significantly improved at discharge. The change in EF was greater in group I than in group D (17 +/- 9% vs. 4 +/- 9%, p = 0.007), as was the change in RWM (0.96 +/- 0.23 vs. 0.13 +/- 0.36 SD/chord, p < 0.0001). CONCLUSIONS: The alteration in flow velocity in recanalized infarcted arteries is related to left ventricular recovery. A progressive decrease in velocity after angioplasty implies no reflow, which is associated with a poor recovery of left ventricular function. Reperfusion injury may account in part for this phenomenon.     

Independent impact of thrombolytic therapy and vessel patency on left ventricular dilation after myocardial infarction. Serial echocardiographic follow-up

BACKGROUND: It has been shown that successful reperfusion of the infarct-related artery by thrombolysis can prevent left ventricular dilation after acute myocardial infarction; these beneficial effects were detected from several days to several months after infarction. To date, however, no study has shown that these effects can be demonstrated within hours after the onset of infarction. Furthermore, data are scarce on the independent impact of thrombolytic therapy and late vessel patency on ventricular volume and function. The aim of this study was to assess separate effects of thrombolysis and patency of the infarct-related artery on left ventricular size and function by serial two-dimensional echocardiographic examinations. METHODS AND RESULTS: We evaluated 131 consecutive patients with first acute myocardial infarction by two-dimensional echocardiography in the following sequence: days 1, 2, 3, 7, and after 3 and 6 weeks. Intravenous streptokinase was administered in 81 patients, and 50 patients were treated without thrombolysis. Left ventricular end-diastolic volume, end-systolic volume, and ejection fraction were determined from apical two- and four-chamber views using the Simpson biplane formula and normalized to body surface area. Coronary angiography was performed in 107 patients after a mean of 26.0 +/- 20.2 (mean +/- SD) days after infarction. Patency of the infarct-related artery was assessed using TIMI criteria, with 54 considered patent (TIMI 3) and 53 with TIMI grade < 3. On day 1, end-systolic volume was significantly higher in patients not receiving thrombolysis (37.7 +/- 15.3 versus 33.0 +/- 10.6 mL/m2, P = .045). End-systolic volume (ESVi) was significantly higher in patients treated without thrombolysis throughout the study, whereas significant differences in end-diastolic volume (EDVi) were detected from day 3 (P = .041) onward and in ejection fraction (EF) from day 2 (P = .025) onward, all differences becoming progressively more significant with time (6-week values: EDVi, 78.8 +/- 25.4 versus 65.9 +/- 15.7 mL/m2, P = .001; ESVi, 45.4 +/- 22.6 versus 33.9 +/- 15.1 mL/m2, P = .002; EF, 45.1 +/- 11.6% versus 50.2 +/- 10.1%, P = .018). Patients with an occluded infarct-related artery (TIMI < 3) demonstrated highly significant differences at 6 weeks compared with patients with patent vessels (EDVi, 76.8 +/- 24.7 versus 65.2 +/- 15.6 mL/m2, P = .006; ESVi, 44.6 +/- 23.3 versus 31.9 +/- 12.2 mL/m2, P = .001; EF, 45.0 +/- 11.6% versus 52.1 +/- 9.0%, P < .001), but these differences developed more slowly than that seen among the thrombolytic subgroups. Indeed, multivariate analysis demonstrated that thrombolysis was the major determinant of initial volumes (P = .08, .02, and .08 for EDVi, ESVi, and EF, respectively), while vessel patency was the overwhelming determinant of subsequent changes (P = .0033, .0002, and .0024 for EDVi, ESVi, and EF, respectively). Additionally, ventricular volumes were significantly higher and ejection fractions lower in patients with anterior versus inferior infarction, but even adjusting for these differences as well as those associated with age, sex, and initial ventricular volume, the additive and independent impact of thrombolysis and infarct vessel patency persisted. CONCLUSIONS: These data indicate that the beneficial effect of thrombolysis on left ventricular size and function can be demonstrated in the earliest phases of acute myocardial infarction and that subsequent changes are mediated primarily through patency of the infarct-related artery. Thrombolytic therapy and late vessel patency thus have an additive and complementary impact in reducing ventricular dilation after myocardial infarction.     

Myocardial contrast echocardiography versus dobutamine echocardiography for predicting functional recovery after acute myocardial infarction treated with primary coronary angioplasty

OBJECTIVES: We sought to compare myocardial contrast echocardiography with low dose dobutamine echocardiography for predicting 1-month recovery of ventricular function in acute myocardial infarction treated with primary coronary angioplasty. BACKGROUND: The relation between myocardial perfusion and contractile reserve in patients with acute myocardial infarction, in whom anterograde flow is fully restored without significant residual stenosis, is still unclear. METHODS: Thirty patients with acute myocardial infarction treated successfully with primary coronary angioplasty underwent intracoronary contrast echocardiography before and after angioplasty and dobutamine echocardiography 3 days after the index infarction. One month later, two-dimensional echocardiography and coronary angiography were repeated in all patients and contrast echocardiography in 18 patients. RESULTS: After coronary recanalization, 26 patients showed myocardial reperfusion within the risk area, although 4 did not. At 1-month follow-up, all patients had a patient infarct-related artery without significant restenosis. Both left ventricular ejection fraction and wall motion score index within the risk area significantly improved in the patients with reperfusion ([mean +/- SD] 38 +/- 8% vs. 48 +/- 12%, p < 0.005; and 2.35 +/- 0.5 vs. 2 +/- 0.6, p < 0.001, respectively), but not in those with no reflow. Of the 72 nonperfused segments before angioplasty, 27 showed functional improvement at follow-up. Myocardial contrast echocardiography had a sensitivity and a negative predictive value similar to dobutamine echocardiography in predicting late functional recovery (96% vs. 89% and 89% vs. 93%, respectively), but a lower specificity (18% vs. 91%, p < 0.001), positive predictive value (41% vs. 86%, p < 0.001) and overall accuracy (47% vs. 90%, p < 0.001). CONCLUSIONS: Microvascular integrity is a prerequisite for myocardial viability after acute myocardial infarction. However, contrast enhancement shortly after recanalization does not necessarily imply a late functional improvement. Thus, contractile reserve elicited by low dose dobutamine is a more accurate predictor of regional functional recovery after reperfused acute myocardial infarction than microvascular integrity.