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PubMed2004

Relation between late patency of the infarct-related artery, left ventricular function, and clinical outcomes after primary percutaneous intervention for acute myocardial infarction (CADILLAC trial).

The importance of sustained patency of the infarct-related artery after primary percutaneous coronary intervention for acute myocardial infarction is controversial. We examined serial measures of left ventricular function and clinical outcomes in 280 patients with an initially occluded infarct artery in whom Thrombolysis In Myocardial Infarction trial grade 3 flow was achieved and routine follow-up angiography was performed 7 months after percutaneous coronary intervention. Reocclusion of the infarct artery was associated with decreased event-free survival, and the degree of restenosis was an independent predictor of the lack in improvement in left ventricular ejection fraction over time.

Aged↗
PubMed2005

Infarct-related coronary artery patency and medication use prior to ST-segment elevation myocardial infarction.

In patients who have ST-segment elevation myocardial infarction (STEMI), a patent infarct-related artery on the initial angiogram is associated with improved clinical outcomes, including decreased mortality. The present study assessed the influence of administering aspirin, beta blockers, statins, and angiotensin-converting enzyme inhibitors before STEMI on infarct-related artery patency. Our data demonstrate that patients who have STEMI and receive these medications on an outpatient basis before the event have a higher likelihood of having a patent infarct-related artery compared with patients who do not receive these medications. Further, our data demonstrate a graded association according to the number of such medications being administered: the likelihood of a patent infarct-related artery increased to >50% as the number of these medications increased.

Adrenergic beta-Antagonists↗
PubMed2006

A unicenter, randomized, double-blind, parallel-group, placebo-controlled study of Melatonin as an Adjunct in patients with acute myocaRdial Infarction undergoing primary Angioplasty The Melatonin Adjunct in the acute myocaRdial Infarction treated with Angioplasty (MARIA) trial: study design and rationale.

BACKGROUND: Experimental studies have documented the beneficial effects of the endogenously produced antioxidant, melatonin, in reducing tissue damage and limiting cardiac pathophysiology in models of experimental ischemia-reperfusion. Melatonin confers cardioprotection against ischemia-reperfusion injury most likely through its direct free radical scavenging activities and its indirect actions in stimulating antioxidant enzymes. These actions of melatonin permit it to reduce molecular damage and limit infarct size in experimental models of transient ischemia and subsequent reperfusion. STUDY DESIGN: The Melatonin Adjunct in the acute myocaRdial Infarction treated with Angioplasty (MARIA) trial is an unicenter, prospective, randomized, double-blind, placebo-controlled, phase 2 study of the intravenous administration of melatonin. The primary efficacy end point of this study is to determine whether melatonin treatment reduces infarct size determined by the cumulative release of alpha-hydroxybutyrate dehydrogenase (area under the curve: 0 to 72 h). Other secondary end points will be the clinical events occurring within the first 90 days: death, sustained ventricular arrhythmias, resuscitation from cardiac arrest, cardiogenic shock, heart failure, major bleedings, stroke, need for revascularization, recurrent ischemia, re-infarctions and rehospitalization. IMPLICATIONS: The MARIA trial tests a novel pharmacologic agent, melatonin, in patients with acute myocardial infarction and the hypothesis that it will confer cardioprotection against ischemia-reperfusion injury. If successful, the finding would support the use of melatonin in therapy of ischemic-reperfusion injury of the heart.

Adult↗
PubMed2004

Quantitative assessment of infarct size in vivo by myocardial contrast echocardiography in a murine acute myocardial infarction model.

BACKGROUND: In vivo measurement of the infarct size in a small animal model is still challenging. The purpose of this study was to evaluate the feasibility of quantitative assessment of infarct size by myocardial contrast echocardiography (MCE) in the acute myocardial infarction (AMI) model of the rat. METHODS: In 32 Sprague-Dawley rats with AMI, we measured total myocardial area (TMA) and infarct area (IA) of the rats by MCE study (MCE method). They were compared with those of postmortem heart measured by planimetry after histochemical staining with triphenyl tetrazolium chloride solution (TTC method). Simple TTC staining was done in 13 rats (Group 1). To reduce the postmortem change, continuous aortic and left ventricular (LV) pressure was loaded during TTC staining in 19 rats (Group 2). RESULTS: The TMA, IA, and IA/TMA ratio measured by the MCE method were 38.4+/-3.4 mm2, 18.3+/-0.8 mm2, and 0.37+/-0.02 in Group 1, and 43.7+/-1.8 mm2, 15.8+/-1.1 mm2, and 0.37+/-0.02 Group 2, respectively. Those measured by the TTC method were 66.1+/-2.2 mm2, 29.3+/-1.1 mm2, and 0.44+/-0.01 in Group 1, and 65.9+/-2.5 mm2, 26.5+/-1.7 mm2, and 0.40+/-0.02 in Group 2, and 65.9+/-2.5 mm2, 26.5+/-1.7 mm2, and 0.44+/-0.02 in Group 2, respectively. Compared with the TTC method, the MCE method underestimated the TMA and IA in both groups (p<0.001). There was no difference in TMA and IA between the two groups in both methods. IA/TMA ratio showed significant correlation between the two methods in both groups (r=0.85, p<0.001). CONCLUSION: The IA/TMA ratio measured by the MCE method may be useful for in vivo estimation of the myocardial infarct size in the AMI model of the rat.

Animals↗
PubMed2007

Role of pre-infarction angina and inflammatory status in the extent of microvascular obstruction detected by MRI in myocardial infarction patients treated by PCI.

BACKGROUND/OBJECTIVES: The extent of microvascular obstruction (MVO) during myocardial infarction referred to as the "no-reflow phenomenon", may determine myocardial damage. Our study aimed to investigate the incidence and the influencing factors of MVO in patients with ST-elevation myocardial infarction (STEMI) treated by primary percutaneous intervention (PCI). PATIENTS, METHODS: Using contrast-enhanced MRI, microvascular obstruction was defined as early hypoenhancement. Contrast defects were scored from 0 (no hypoenhancement) to 3 (strong hypoenhancement). 50 patients (56+/-11 years) with STEMI underwent PCI. Contrast-enhanced MRI (6+/-2 days after STEMI) and biochemical parameters were evaluated. RESULTS: Microvascular obstruction (score 1 to 3) was observed in 90% of the patients and major microvascular obstruction (score 2-3) in 54%. In univariate analysis, leukocytes and CRP levels were associated with MVO, whereas pre-infarction angina and prior medication by aspirin or calcium channel antagonist appeared protective. Microvascular obstruction intensity positively correlated with baseline inflammation status assessed by C-reactive protein and leukocytes (rho=0.43 and rho=0.44; p=0.003), the peak of CK (rho=0.56; p=0.01) or Troponin I (rho=0.59; p=0.01) and negatively correlated with LVEF (rho=-0.44; p=0.002). Multivariate analysis identified the absence of pre-infarction angina as the only independent predictor for microvascular obstruction (odds ratio, 8.35, 95% confidence interval 1.27-54.71; p=0.027). CONCLUSION: MRI-detected microvascular obstruction has a high incidence in patients with STEMI treated by primary PCI and determines post-MI LVEF even in patients with post PCI TIMI 3 flow score. Pre-infarction angina appears to be an independent determinant of the extent of MVO detected by MRI.

Adult↗
PubMed2005

Quantitative measurement of infarct size by contrast-enhanced magnetic resonance imaging early after acute myocardial infarction: comparison with single-photon emission tomography using Tc99m-sestamibi.

OBJECTIVES: The aim of this research was to evaluate kinetics and extent of myocardial contrast enhancement (CE) in comparison with single-photon emission computed tomography (SPECT) early after acute myocardial infarction (AMI). BACKGROUND: Quantification of infarct size serves as a surrogate end point in evaluating new therapies of AMI. Contrast-enhanced magnetic resonance imaging (CeMRI) of the myocardium is a promising new method for identification of irreversible tissue injury. METHODS: A total of 33 patients were examined by CeMRI and SPECT 7 +/- 2 days after AMI and successful coronary intervention. After gadolinium-diethylenetraimine pentaacetic acid injection (0.2 mmol/kg), continuous short-axis slices of the left ventricle (LV) were acquired every 7 min up to 42 min using different inversion times (TI). Myocardial CE at each imaging time point was quantified and compared with corresponding SPECT perfusion defect. RESULTS: All patients showed myocardial CE in the infarct region. A constant TI for CeMRI resulted in a decrease of signal intensity and extent of CE on late acquisitions. With TI adjustment, infarct image intensity peaked at 21 min with a contrast of 478% of remote myocardium and remained at this level up to 42 min after contrast injection (437%); CE extent was stable over time and agreed well with SPECT within an average difference of 3% of the LV myocardium, yielding the best correlation at 28 min (r = 0.86). CONCLUSIONS: In patients after AMI and successful reperfusion, CE is stable over time and matches well with SPECT perfusion defect; CeMRI under standardized conditions can accurately assess myocardial infarct size in vivo and may be attractive for serving as a surrogate end point early after AMI.

Adult↗
PubMed2005

High serum erythropoietin level is associated with smaller infarct size in patients with acute myocardial infarction who undergo successful primary percutaneous coronary intervention.

OBJECTIVES: We investigated whether a higher serum erythropoietin (EPO) level in patients with acute myocardial infarction (MI) subjected to successful primary percutaneous coronary intervention (PCI) can predict a smaller infarct size determined by creatine kinase (CK) release. BACKGROUND: Erythropoietin has been shown to protect cardiomyocytes from ischemia-reperfusion injury in rodents. METHODS: We prospectively studied 101 patients with first MI who received successful primary PCI within 12 h from the onset of MI. Blood samples were collected to examine the serum EPO level after the primary PCI and within 24 h from the onset of MI. RESULTS: The peak CK level and cumulative CK release were significantly lower in the above-median EPO group than in the below-median EPO group. Thrombolysis In Myocardial Infarction (TIMI) grades and collateral grades before PCI, infarct-related coronary arteries, time to the successful reperfusion from the onset of MI, and serum creatinine levels were similar in the two EPO groups. A stepwise multiple regression analysis revealed that the absolute serum EPO level (mU/ml) as well as TIMI grades after PCI and preinfarction angina was an independent predictor for the cumulative CK release. CONCLUSIONS: These data suggest that a high endogenous EPO level can predict a smaller infarct size in patients with acute MI subjected to successful primary PCI. This might be attributed to the potentially protective effect of endogenous EPO against ischemia-reperfusion injury in humans.

Aged↗
PubMed1997

Conservative management of patients with acute myocardial infarction and spontaneous acute patency of the infarct-related artery.

The role of systematic emergency percutaneous transluminal coronary angioplasty (PTCA) in patients with spontaneous reperfusion during myocardial infarction is debated. We retrospectively examined the inhospital outcome of 47 consecutive patients with myocardial infarction < 6 hours and angiographically proven spontaneous patency of the infarct artery managed without initial PTCA. There was one death (2.1%) and no incidence of reinfarction. Predischarge angiography showed regression of the culprit coronary lesion to < 50% stenosis in 23% of the patients, therefore obviating the need for PTCA. However, 17% of the patients had acute recurrent ischemia, requiring emergency intervention in 10.6%. Comparison with matched patients in whom Thrombolysis in Myocardial infarction grade 3 patency was achieved by thrombolysis or by primary PTCA showed that patients with spontaneous patency tended to have smaller infarctions, as judged from a lower peak creatine kinase level (1132 +/- 1002, 2051 +/- 1536, and 2715 +/- 2146 i.u., respectively; p = 0.001) and a higher left ventricular ejection fraction (56.4%, 47.9%, and 48.7% respectively; p = 0.02). In conclusion, these patients have an excellent inhospital outcome, with evidence of less myocardial damage than in patients in whom reperfusion therapy was required to achieve TIMI 3 patency. Initial conservative treatment appears safe.

Aged↗
PubMed1998

The clinical implications of no reflow demonstrated with intravenous perfluorocarbon containing microbubbles following restoration of Thrombolysis In Myocardial Infarction (TIMI) 3 flow in patients with acute myocardial infarction.

Intravenous injections or infusions of perfluorocarbon-exposed sonicated dextrose albumin microbubbles were given 2.4 +/- 1.6 days following acute myocardial infarction to 45 consecutive patients. Patients were divided into 3 groups: patients with Thrombolysis In Myocardial Infarction (TIMI) grade 3 angiographic flow but persistent myocardial contrast defects by echocardiography (no reflow), patients with TIMI 3 flow and myocardial contrast enhancement (reflow), and patients with TIMI grade 0 to 2 flow in the infarct vessel. Thirty-five patients had TIMI 3 flow at the time of contrast study. Of these, 25 had evidence of reflow with intravenous contrast, whereas 10 (29%) still had contrast defects. At follow-up, end-systolic volume index decreased significantly in patients who exhibited reflow (21 +/- 8 ml/m2 at baseline to 18 +/- 8 ml/m2 at follow-up; p = 0.04), whereas those with no reflow had a significant increase (26 +/- 9 ml/m2 at baseline to 32 +/- 9 ml/m2 at follow-up; p = 0.006). A persistent contrast defect in the infarct zone demonstrated with intravenous ultrasound contrast following restoration of TIMI grade 3 flow in the infarct vessel identified patients likely to have deterioration in both regional and global systolic function.

Aged↗
PubMed1995

Design of a placebo-controlled clinical trial of long-acting diltiazem and aspirin versus aspirin alone in patients receiving thrombolysis with a first acute myocardial infarction. Incomplete Infarction Trial of European Research Collaborators Evaluating Prognosis Post-Thrombolysis (diltiazem) (INTERCEPT) Research Group.

Several pharmacologic forms of adjunctive therapy, designed to enhance the efficacy of thrombolysis following acute myocardial infarction (AMI), are being explored. However, few studies have assessed the use of standard secondary prevention therapies (beta-blockers, angiotensin-converting enzyme inhibitors, magnesium, calcium antagonists, etc.) for antecedent thrombolysis. Although calcium antagonists have not been shown to alter post-AMI mortality, diltiazem has been shown to reduce recurrent nonfatal infarction and myocardial ischemia following non-Q-wave AMI. Because both non-Q-wave AMI and AMI treated with thrombolytic therapy result in early reperfusion and clinical manifestations of "incomplete infarction" (i.e., aborted transmural infarction), we hypothesize that prophylactic administration of diltiazem to AMI patients who receive thrombolysis before other therapies might decrease ischemic complications. We have initiated a multicenter, randomized, placebo-controlled, double-blind, parallel-group comparison of long-acting diltiazem 300 mg/day and aspirin 160 mg/day versus aspirin 160 mg/day alone in up to 920 patients with an uncomplicated first AMI (no heart failure or left ventricular dysfunction) within 36 to 96 hours of receiving thrombolysis. Active enrollment is under way at 46 centers in the United Kingdom, Belgium, The Netherlands, and Denmark. This trial (known as the Incomplete INfarction Trial of European Research Collaborators Evaluating Prognosis Post-Thrombolysis [diltiazem], or INTERCEPT) represents the first long-term, large-scale, prospective study of a calcium antagonist administered post-thrombolysis as adjunctive therapy to AMI patients in which the primary trial objective is to assess the effect of blinded therapy on the 6-month cumulative occurrence of a combined clinical end point (cardiac death, recurrent nonfatal AMI, and medically refractory ischemia).

Adolescent↗
PubMed1999

Expression of Gi-2 alpha and Gs alpha in myofibroblasts localized to the infarct scar in heart failure due to myocardial infarction.

OBJECTIVE: Patients surviving large transmural myocardial infarction (MI) are at risk for congestive heart failure with attendant alteration of ventricular geometry and scar remodeling. Altered Gi-2 alpha and Gs alpha protein expression may be involved in cardiac remodeling associated with heart failure, however their expression in scar tissue remains unclear. METHODS: MI was produced in Sprague-Dawley rats by ligation of the left coronary artery. Gi-2 alpha and Gs alpha protein concentration, localization and mRNA abundance were noted in surviving left ventricle remote to the infarct, in border and in scar tissues from 8 week post-MI hearts with moderate heart failure. RESULTS: We observed a 4.5- and 5.0-fold increase in immunoreactive Gi-2 alpha protein concentration occurs in the border and scar regions vs. control values, respectively, in 8-week post-MI rat hearts. Similarly, immunoreactive Gs alpha protein concentration was increased 3.4- and 8.2-fold, respectively, in these tissues vs. controls. Double-fluorescence labeling and phenotyping studies revealed that both Gi-2 alpha and Gs alpha proteins were localized to myofibroblasts in the infarct scar and to viable myocytes bordering the scar. Northern analysis revealed that the Gi-2 alpha/GAPDH ratio was increased in both viable and scar regions (1.24- and 1.85-fold respectively) from experimental hearts when compared to sham-operated control values when compared to noninfarcted left ventricle, the value of this ratio in scar tissue was elevated approximately 1.5 fold. The Gs alpha/GAPDH ratio was significantly increased (1.28-fold) only in the scar region vs. control. CONCLUSION: Our results indicate a marked increase in the expression of Gi-2 alpha and Gs alpha from myofibroblasts of the infarct scar as well as remnant myocytes bordering the scar in 8-week post-MI rat hearts. We suggest that these changes may be associated with ongoing remodeling in the infarct scar in chronic post-MI phase of this experimental model.

Analysis of Variance↗
PubMed2000

Diltiazem in acute myocardial infarction treated with thrombolytic agents: a randomised placebo-controlled trial. Incomplete Infarction Trial of European Research Collaborators Evaluating Prognosis post-Thrombolysis (INTERCEPT)

BACKGROUND: Diltiazem reduces non-fatal reinfarction and refractory ischaemia after non-Q-wave myocardial infarction, an acute coronary syndrome similar to the incomplete infarction that occurs after successful reperfusion. We postulated that this agent would reduce cardiac events in patients after acute myocardial infarction treated initially with thrombolytic agents-a clinical application previously unexplored with heart-rate-lowering calcium antagonists. METHODS: A prospective, randomised, double-blind, sequential trial was done in 874 patients with acute myocardial infarction, but without congestive heart failure, who first received thrombolytic agents. Patients received either 300 mg oral diltiazem once daily, or placebo, initiated within 36-96 h of infarct onset, and given for up to 6 months. The trial primary endpoint was the cumulative first event rate of cardiac death, non-fatal reinfarction, or refractory ischaemia. Additional prespecified endpoints included several composites of non-fatal cardiac events (non-fatal reinfarction combined with refractory ischaemia, all recurrent ischaemia, or the need for myocardial revascularisation). The diagnosis of ischaemia, whether refractory or recurrent, and the need for myocardial revascularisation, was always based on objective electrocardiographical evidence of ischaemia, either at rest or on exertion. RESULTS: For the trial primary endpoint, 131 events occurred in the 444 placebo patients and 97 events in the 430 diltiazem patients (hazard ratio 0.79; 95% CI, 0.61-1.02; p=0.07). For non-fatal cardiac events, diltiazem treatment was associated with a relative decrease (0.76; 0.58-1.00) in the combined event rate of non-fatal reinfarction and refractory ischaemia. There was a similar decrease in the composite non-fatal endpoints of non-fatal reinfarction combined with all recurrent ischaemia (0.80; 0.64-1.00) and non-fatal reinfarction combined with the need for myocardial revascularisation (0.67; 0.46-0.96). The need for myocardial revascularisation alone was significantly reduced by 42% (0.61; 0.39-0.96). No major safety issues were encountered. CONCLUSIONS: Diltiazem did not reduce the cumulative occurrence of cardiac death, non-fatal reinfarction, or refractory ischaemia during a 6-month follow-up, but did reduce all composite endpoints of non-fatal cardiac events, especially the need for myocardial revascularisation.

Calcium Channel Blockers↗
PubMed2002

Effects of losartan and captopril on mortality and morbidity in high-risk patients after acute myocardial infarction: the OPTIMAAL randomised trial. Optimal Trial in Myocardial Infarction with Angiotensin II Antagonist Losartan.

BACKGROUND: ACE inhibitors attenuate the detrimental effects of angiotensin II, and improve survival and reduce morbidity in patients with acute myocardial infarction and evidence of heart failure or left-ventricular dysfunction. Selective antagonism of the angiotensin type 1 receptor represents an alternative approach to inhibition of the renin-angiotensin system. We did a multicentre, randomised trial to test the hypothesis that the angiotensin II antagonist losartan would be superior or non-inferior to the ACE inhibitor captopril in decreasing all-cause mortality in high-risk patients after acute myocardial infarction. METHODS: 5477 patients 50 years of age or older (mean age 67.4 years [SD 9.8]), with confirmed acute myocardial infarction and heart failure during the acute phase or a new Q-wave anterior infarction or reinfarction, were recruited from 329 centres in seven European countries. Patients were randomly assigned and titrated to a target dose of losartan (50 mg once daily) or captopril (50 mg three times daily) as tolerated. The primary endpoint was all-cause mortality. Analysis was by intention to treat. FINDINGS: There were 946 deaths during a mean follow-up of 2.7 (0.9) years: 499 (18%) in the losartan group and 447 (16%) in the captopril group (relative risk 1.13 [95% CI 0.99-1.28], p=0.07). The results for the secondary and tertiary endpoints were as follows: sudden cardiac death or resuscitated cardiac arrest 239 (9%) versus 203 (7%), 1.19 (0.98-1.43), p=0.07, and fatal or non-fatal reinfarction 384 (14%) versus 379 (14%), 1.03 (0.89-1.18), p=0.72. The all-cause hospital admission rates were 1806 (66%) versus 1774 (65%), 1.03 (0.97-1.10), p=0.37. Losartan was significantly better tolerated than captopril, with fewer patients discontinuing study medication (458 [17%] vs 624 [23%], 0.70 [0.62-0.79], p<0.0001). INTERPRETATION: Since we saw a non-significant difference in total mortality in favour of captopril, ACE inhibitors should remain first-choice treatment in patients after complicated acute myocardial infarction. Losartan cannot be generally recommended in this population. However, it was better tolerated than captopril, and was associated with significantly fewer discontinuations. Although the role of losartan in patients intolerant of ACE inhibition is not clearly defined, it can be considered in such patients.

Aged↗
PubMed1997

Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. European Myocardial Infarct Amiodarone Trial Investigators.

BACKGROUND: Ventricular arrhythmias are a major cause of death after myocardial infarction, especially in patients with poor left-ventricular function. Previous attempts to identify and suppress arrhythmias with various antiarrhythmic drugs failed to reduce or actually increase mortality. Amiodarone is a powerful antiarrhythmic drug with several potentially beneficial actions, and has shown benefit in several small-scale studies. We postulated that this drug might reduce mortality in patients at high risk of death after myocardial infarction because of impaired ventricular function, irrespective of whether they had ventricular arrhythmias. METHODS: The European Myocardial Infarct Amiodarone Trial (EMIAT) was a randomised double-blind placebo-controlled trial to assess whether amiodarone reduced all-cause mortality (primary endpoint) and cardiac mortality and arrhythmic death (secondary endpoints) in survivors of myocardial infarction with a left-ventricular ejection fraction (LVEF) of 40% or less. Intention-to-treat and on-treatment analyses were done. FINDINGS: EMIAT enrolled 1486 patients (743 in the amiodarone group, 743 in the placebo group). Median follow-up was 21 months. All-cause mortality (103 deaths in the amiodarone group, 102 in the placebo group) and cardiac mortality did not differ between the two groups. However, in the amiodarone group, there was a 35% risk reduction (95% CI 0-58, p = 0.05) in arrhythmic deaths. INTERPRETATION: Our findings do not support the systematic prophylactic use of amiodarone in all patients with depressed left-ventricular function after myocardial infarction. However, the lack of proarrhythmia and the reduction in arrhythmic death support the use of amiodarone in patients for whom antiarrhythmic therapy is indicated.

Aged↗
PubMed1997

Role of infarction artery status in left ventricular remodeling after acute myocardial infarction.

The aim of this study was to evaluate the relation between the infarction artery status and left ventricular volumes, independently of regional ventricular dysfunction, at 4-6 weeks after a first myocardial infarction. The study group consisted of 100 patients, of whom 80 received thrombolytic treatment. Coronary and contrast left ventricular angiograms were performed at 36+/-5 days postinfarction. Left ventricular end-diastolic and end-systolic volumes were measured. The centerline chord motion method was used to calculate the extent of wall motion abnormality (percentage of chords with hypokinetic motion) and its severity (maximum units of S.D. below the normal wall motion reference). Minimum lumen diameter, patency and collateral flow in the infarction artery were also analyzed. Eight patients (group I) showed occlusion with poor collateral flow in the infarction artery, 22 patients (group II) occlusion with good collateral flow, 38 patients (group III) severe residual stenosis (minimum lumen diameter < or = 1 mm), and 32 patients (group IV) non-severe residual stenosis (minimum lumen diameter > 1 mm). Patients from group I presented greater wall motion abnormality in terms of both extent (P=0.005) and severity (P=0.007), and greater end-diastolic (P=0.07) and end-systolic (P=0.0008) volumes; there were no differences among groups II, III and IV. By stepwise multivariate regression analysis, the extent of wall motion abnormality was the main determinant of end-diastolic (P=0.0001) and end-systolic (P=0.0001) volumes; occlusion with poor collateral flow was also a significant independent factor for end-systolic volume (P=0.03). Total occlusion (including both with and without collaterals) and the minimum lumen diameter did not correlate with end-diastolic and end-systolic volumes. We concluded that (A) the extent of regional dysfunction is the primary determinant of left ventricular volumes at 4-6 weeks postinfarction. (B) The status of the infarction artery is a weak predictor of end-diastolic volume, which is the best descriptor of ventricular remodeling, although occlusion with poor collateral flow is associated to larger end-systolic volume.

Cardiac Volume↗
PubMed1999

[The characteristics, management and prognosis of the acute myocardial infarct patient in the Valencian Community in 1995: the results of the PRIMVAC Registry (The Registry Project of Acute Myocardial Infarct in Valencia, Alicante and Castellón). As representatives of the PRIMVAC investigators].

BACKGROUND AND OBJECTIVES: Regional registers of patients with acute myocardial infarction are scarce in Spain. The PRIMVAC register (Proyecto de Registro de Infarto agudo de Miocardio de Valencia, Alicante y Castellón) was initiated to obtain updated information on the management of these patients in the Valencia Autonomous Community. Data of the first twelve months of the register are presented. METHODS: The 17 participating hospitals cover 2,833,938 inhabitants. Demographic, clinical, procedural and outcome data as well as predictive variables of mortality were analysed in the patients with acute myocardial infarction during their stay in the coronary care units from 1 December 1994 to 30 November 1995. RESULTS: During 12 months, 2,377 patients were included. Mean age was 65.3 years (SD 11.9) and 23.2% were female. Left ventricular failure was present in 39.8%. Thrombolytic therapy was applied in 42.1% with a median time delay of 195 min from chest pain onset. This time was longer in the women (250 min) and in the elderly (210 min). The in-coronary-care-unit-mortality rate was 13.9%. Age, female gender, diabetes, previous myocardial infarction, Q wave and right ventricular infarction independently predicted increased early mortality. CONCLUSION: Present data show the feasibility of an acute myocardial infarction register in the Valencia Autonomous Community. Although an acceptable level of thrombolysis has been reached, the mortality rate is still high. The long delay in initiating thrombolysis, particularly in female and elderly patients is remarkable.

Chi-Square Distribution↗
PubMed1998

Sequential changes in the localization of the type IV collagen alpha chain in the infarct zone: immunohistochemical study of experimental myocardial infarction in the rat.

Collagen, as a component of the extracellular matrix, have a role in the healing process after myocardial infarction (MI). For type IV collagen, a major structural protein present in the basal membrane of myocytes, six alpha chains [alpha 1 (IV)-alpha 6(IV)] have been identified. We examined the sequential changes in the appearance and localization of the alpha 1 (IV)-alpha 5(IV) after experimental MI in rats. Hearts were excised from 1 day to 8 weeks after permanent left coronary artery ligation. Immunohistochemical staining with monoclonal antibodies was performed. On day 3, staining for both alpha 1(IV) and alpha 2(IV) first appeared, forming a wavy pattern in the infarct peripheral zone, and the staining was not restricted to the cell membrane. The staining intensity and distribution for both alpha 1(IV) and alpha 2(IV) in the peripheral zone then gradually increased, reaching a maximum around day 7. The distribution progressed from the peripheral to the central zone of the infarct for 1-2 days, reaching the center point after 2 weeks. The staining distribution gradually decreased after reaching the maximum, but the staining had not completely disappeared at 8 weeks. In contrast, no positive staining for alpha 3(IV), alpha 4(IV) or alpha 5(IV) was observed at any time during the 8-week observation period. Thus, the present results demonstrated that in rats, type IV collagen consisting of alpha 1 and alpha 2 chains appears in the infarct zone at a relatively early phase after MI, indicating that type IV collagen composed of alpha 1 and alpha 2 chains contributes to infarct healing.

Animals↗
PubMed2001

Early assessment of regional myocardial blood flow and metabolism in thrombolysis in myocardial infarction flow grade 3 reperfused myocardial infarction using carbon-11-acetate.

OBJECTIVES: The aim of this study was to investigate the prognostic value of carbon-11-acetate (acetate) positron emission tomography (PET) after successful reperfusion of myocardial infarction (MI). BACKGROUND: Acetate PET allows the measurement of both myocardial flow and oxidative metabolism. The prognostic value of acetate measurements performed early (within 24 h) after Thrombolysis In Myocardial Infarction (TIMI) flow grade 3 reperfused MI is unknown. METHODS: In 18 patients with TIMI flow grade 3 reperfusion of their first MI, a dynamic acetate study was performed within 24 h of the acute event. At five days, nitrogen-13-NH3 (NH3) and fluorine-18-labeled fluorodeoxyglucose (FDG) PET studies were performed. Infarct-related areas were classified as "PET viable" or "PET nonviable," as assessed with NH3 and FDG, according to previously established criteria. At five days and three months, radionuclide angiography was performed for evaluation of left ventricular (LV) function. RESULTS: In infarct-related regions, myocardial blood flow, FDG uptake and oxygen consumption were decreased, compared with remote regions. However, oxygen consumption values, as measured with acetate in both PET-viable and PET-nonviable areas, as assessed with NH3 and FDG, were not significantly different (p = NS). A significant linear correlation was observed between global LV ejection fraction at three months and oxidative metabolism in the infarct-related area (r = 0.8, p < 0.0001). Multivariate analysis revealed that oxidative metabolism measurements in reperfused myocardium was the only significant predictor for recovery of LV function at three months (p < 0.05). CONCLUSIONS: Measurement of oxidative metabolism early after TIMI flow grade 3 reperfusion of MI offers important prognostic value concerning LV function at follow-up.

Acetates↗