Acute Myocardial Infarction Pts Research Articles

P878Prevalence and prognosis of patients with myocardial infarction with nonobstructive coronary arteries: a nationwide registry based study

Abstract Background There are conflicting data about the proportion and prognosis of patients (pts) with acute myocardial infarction (AMI) with nonobstructive coronary arteries (MINOCA). Purpose To define the incidence and prognosis of MINOCA pts in different types of AMI. Methods The Hungarian Myocardial Infarction Registry (HUMIR) is a nationwide, mandatory database in which the clinical and demographic informations of patients with AMI are recorded. Between January 1, 2014 and June 30, 2018, a total of 45,223 AMI (ST-elevation myocardial infarction (STEMI) n=22,469) pts were registered. After excluding pts with previous AMI, PCI, CABG, and congestive heart failure, 2003 MINOCA pts were found (MINOCA group), while 43,220 AMI pts had obstructive coronary artery disease (MI-CAD group). Results The proportion of pts with MINOCA disease was 4.4% among the total pts with AMI. The prevalence was higher in the non ST-elevation myocardial infarction (NSTEMI) group (n=1546, 6.8%) than in the STEMI (n=457, 2.0%) group. The pts with MINOCA disease were slightly younger compared to the pts with MI-CAD (mean age 64.0±14.4 vs. 65.5±12.2 years respectively). The proportion of women was higher in the MINOCA group than in the MI-CAD group (55.7% vs. 36.5%). At discharge, pts with MINOCA disease were less likely to be prescribed certain drugs compared to the pts with MI-CAD. These include aspirin (85.4% vs. 95.6%), RAAS blockers (83.8% vs. 90.4%), statins (86.2% vs. 94.7%), β-blockers (86.8% vs. 89.8%) for the MINOCA and MI-CAD groups respetively. At the 1-year follow-up, the incidence of new AMI events was 1.6% in the MINOCA group compared with 5.0% in the MI-CAD group (HR=2.79). All-cause mortality was higher among the pts with MI-CAD compared to the pts with MINOCA disease. In the MINOCA group, among the pts with NSTEMI, men and women had similar outcomes at 30 days, but men had somewhat higher mortality at one and two years. In contrast, in the STEMI group, women had higher mortality compared to men at all time points during the study (Table 1). Mortality among MINOCA and MI-CAD pts Mortality MINOCA (n=2003) MI-CAD (n=43,220) MINOCA – STEMI MINOCA – NSTEMI Men (n=218) Women (n=239) Men (n=669) Womenr (n=877) 30-day 5.9% [4.9–7.0] 8.4% [8.1–8.7] 8.7% [4.9–12.4] 13.4% [9–17.6] 4.3% [2.8–5.9] 4.4% [3.1–5.8] 1-year 12.5% [11.0–14.0] 15.6% [15.3–16.0] 12.1% [7.6–16.4] 20.3% [15–25.2] 12.2% [9.6–14.7] 10.8% [8.7–12.8] 2-year 16.7% [14.9–18.5] 19.9% [19.5–20.3] 18.2% [12.4–23.6] 23.6% [17.8–29] 16.9% [13.8–20] 14.3% [11.7–16.7] 95% confidence interval in brackets. Conclusion The population-level incidence of MINOCA disease was 4.4% in AMI; the incidence was higher in the NSTEMI group compared to the STEMI group (6.8% vs. 2.0%). Despite the benign anatomy, the long-term prognosis is poor, especially in women after STEMI: 1 out of 4 pts died at the two-year follow up. Acknowledgement/Funding None

Air pollution and short-term clinical outcomes of patients with acute myocardial infarction.

Ambient air pollution is well-known to be a serious risk factor for cardiovascular diseases, stroke, and death. However, the association between air pollutants (AP) exposure and short-term clinical outcomes in acute myocardial infarction (AMI) patients (pts) has not been elucidated well. In the present study, 37880 AMI pts were enrolled from October 2005 to December 2013 in a nationwide large-scale, prospective, multicentre Korea AMI registry (KAMIR registry; http://www.kamir.or.kr). We obtained data on AP (e.g., NO2 , SO2 , CO, O3 and PM10 ) from the Korean National Institute of Environmental Research (NIER; http://www.nier.go.kr). Clinical endpoints included death, recurrent myocardial infarction (Re-MI), any revascularization and composite of all-cause death and Re-MI. Exposure to AP is defined as the average exposure to AP within 24hours before AMI admission. We observed that a 0.01 part per million (ppm) increase in NO2 concentration, 0.001ppm increase in SO2 concentration, and 0.1ppm increase in CO concentration each increased the risk of total death by 9.7% (95% CI, 6.2%-13.4%), 1.9% (95% CI, 0.3%-3.6%), and 2.1% (95% CI, 0.5%-3.9%), respectively. Exceptionally, O3 decreased the risk of total death by 0.6% (95% CI -0.2% to -1.0%) per 0.01ppm increase. PM10 was not related to any cardiovascular events. AP were each stratified into five quintiles according to ranges of AP levels. After adjusting analysis for risk variables, only high quintiles (Q4, Q5) of NO2 were positively associated with total death, cardiac death and MI, while SO2 , CO, O3 and PM10 were shown to be not related to any cardiovascular events at all levels. In AMI patients, each AP and its concentration has shown a different effect to short-term mortality and cardiovascular events.

Abstract 11414: Comparison of the Cardiovascular and Bleeding Risks in Patients With Acute Myocardial Infarction Newly Treated With Ticagrelor versus Clopidogrel in East Asia: A Nationwide Propensity-matched Cohort Study in Taiwan

Background: The Platelet Inhibition and Patient Outcomes (PLATO) trial showed that ticagrelor improved clinical outcomes in patients (pts) with acute coronary syndrome compared with clopidogrel. There were few real world data on the efficacy and safety of ticagrelor in East Asians in whom bleeding is a major concern with potent antithrombotic drugs. Methods: We conducted a nationwide population-based cohort study by using 2012 to 2014 Taiwan National Health Insurance Research Database. The 18-month clinical outcomes in pts with acute myocardial infarction (MI) treated with ticagrelor vs. clopidogrel were compared. Overall, we identified 27,339 acute MI pts (mean age 62.2 years, 71% male) who survived 30 days after the acute MI attack and took dual antiplatelet agents. Cohorts of ticagrelor and clopidogrel were 1:8 matched based on propensity score. The primary efficacy endpoints were all-cause death, recurrent MI or ischemic stroke. The safety endpoints consisted of major gastrointestinal (GI) bleeding and intracerebral hemorrhage (ICH). Results: In unmatched cohorts, ticagrelor-treated pts (n = 2,844) were younger with fewer comorbidities than clopidogrel-treated pts (n = 24,495). The 18-month primary efficacy endpoint rate was lower in ticagrelor group (10.1 vs. 18.3%, p < 0.001). In ticagrelor group, the risks of ICH (0.3%) and ICH + GI bleeding (2.9%) were similar to the data reported in the PLATO trial (ICH 0.3% and non-CABG related TIMI major bleeding 2.8%). After propensity matching, we obtained 2,389 ticagrelor users and 19,112 clopidogrel users in the cohort. After adjusting for clinical characteristics, the 18-month primary efficacy endpoint rate was 21% lower in ticagrelor than in clopidogrel group (10.5 vs. 16.0%, adjusted HR, 0.79; 95% CI, 0.68-0.93). The composite safety endpoint rate was not different between ticagrelor and clopidogrel group (3.2 vs. 4.1%, adjusted HR, 1.01; 95% CI, 0.74-1.37). Subgroup analyses show consistent benefits of ticagrelor in old pts (≥ 75 years) and in pts with diabetes, heart failure or previous MI. Conclusions: In the real world acute MI Taiwanese pts, ticagrelor offered better cardiovascular protection than clopidogrel without increasing the major bleeding risk.

TWO-YEAR CLINICAL OUTCOMES OF ACUTE MYOCARDIAL INFARCTION PATIENTS WITH MYOCARDIAL BRIDGE AND/OR CORONARY ARTERY SPASM WITHOUT OBSTRUCTIVE LESIONS

Coronary artery spasm (CAS) has been identified as an alternative cause for acute myocardial infarction (AMI) patients (pts). However there is few data on the prognosis in these pts. Therefore we aimed to compare the prognosis between AMI pts due to myocardial bridge (MB) and/or CAS without

Low magnesium is not a significant predictor of hard events in acute myocardial infarction

BackgroundAlthough magnesium (Mg) has recognized cardioprotective properties and hypomagnesemia is common in patients with acute myocardial infarction (AMI), data regarding the role of Mg as prognostic factor for adverse events are scarce, as well as there are conflicting results on the use of Mg as adjuvant therapy in AMI. AimTo evaluate the role of Mg as predictor for hard events (HE, all cause death, and nonfatal myocardial infarction) in AMI patients. Design and patientsWe studied 406 AMI patients (306 males, age: 67±12years, mean±SD). Patient data were collected from the Institute electronic databank which saves demographic, clinical, instrumental, therapeutical and follow-up data of all patients admitted to our Coronary Unit. ResultsDuring a mean follow-up period of 21±18months, the combined endpoint accounted for 63 HE, 44 (11%) deaths (35 cardiac deaths), 19 (5%) nonfatal MI.The multiple regression model identified glycemia as the only independent determinant of Mg in AMI pts. (T value=−2.8, standard coefficient=−0.15, p<0.01). The Kaplan–Meier survival estimates failed to show a significantly worst outcome in patients presenting low Mg (<0.783mmol/L, 25th percentile). Aging (>67years—50th percentile), and ejection fraction (<40%) remained as prognostic factors for HE in the adjusted Cox multivariate proportional hazard model (HR=2.8, 95% CI=1.6–5, p<0.001; HR=3.2, 95% CI=1.9–5.3 p<0.001, respectively). ConclusionThe present findings do not support a significant role of low Mg as predictor for HE in AMI.

CRT-200.36 Long-term Clinical Outcomes in Patients With Acute Myocardial Infarction With Co-morbidity: 3-year Follow-up Results After Propensity Score Matched Analysis

Patients (pts) with acute myocardial infarction (AMI) are associated with a higher mortality rate and usually have higher incidence of co-morbid condition. However, long-term clinical outcomes of AMI pts with comorbidity are unclear. Among 12,431 pts enrolled in a nationwide in Korea AMI Registry (

Abstract 11133: The Incidence and Predicting Factors of Heart Failure After First Acute Myocardial Infarction: A Population[[Unable to Display Character: &amp;#8208;]]Based Study in Taiwan

Background: Early coronary revascularization and medical therapy advancement improve the survival of patients (pts) with acute myocardial infarction (AMI). However, survivors of AMI are at heightened risk of developing heart failure (HF) and there is a paucity of information regarding this issue in Asian countries. This study described the temporal trends in the incidence of HF after the first AMI and the predicting factors of HF development in Taiwan. Methods: We conducted a nationwide population-based cohort study by using 1999 to 2009 National Health Insurance Research Database. Pts aged≧18 years, with no history of HF, who hospitalized with a first AMI between January 2002 and December 2008 were identified and followed up for one year. The primary outcome was HF. We evaluated the incidence of HF during the index hospitalization, 30 days, 6 months, and one year after the discharge. The predicting factors of HF were identified by Cox proportional hazard model. Results: Overall, 42,011 first AMI pts (mean age 64.4 ± 13.8 years; male 75.0%) from 2002 to 2008 were identified. The HF incidence during the index hospitalization was 14.8%. After exclusion of HF during the hospitalization, the overall HF prevalence at 30 days, 6 months, and 1 year was 9.6%, 14.2%, and 16.8%, respectively. The HF prevalence at 1 year declined from 17.9% to 14.9% (p&lt;0.05) from 2002 to 2008. The independent predicting factors of HF after the first AMI were elder age (≧65 years) (adjusted HR 1.81, 95% CI 1.51-2.18), diabetes mellitus (adjusted HR 1.30, 95% CI 1.21-1.41), chronic kidney disease (adjusted HR 1.41, 95% CI 1.20-1.65), use of loop diuretics within 30 days after the discharge (adjusted HR 2.21, 95% CI 2.00-2.43), and recurrent AMI (adjusted HR 2.43, 2.16-2.74). Conclusions: Survivors of AMI without prior HF remain at risk of developing HF in Taiwan and most episodes occur within 6 months after AMI. Five important clinical factors of HF were identified that may help us for risk stratification.

Hyponatremia predicts the acute (type 1) cardio-renal syndrome

Background: The acute (type 1) cardio-renal syndrome (CRS) refers to an acute worsening of heart function leading to acute kidney injury (AKI), and frequently complicates acute decompensated heart failure (ADHF) and acute myocardial infarction (AMI). The aim of this study was to investigate whether hyponatremia, a surrogate of profound neurohormonal activation, could identify patients (pts) at risk for AKI. Methods: We studied the association between hyponatremia and AKI (defined as an increase of >0.3 mg/dl in creatinine above baseline) in 2 separate cohorts: 1) pts with ADHF (n=525) and 2) pts with AMI (n=1184 STEMI pts). Hyponatremia was defined as sodium <136 mmol/L. The association between hyponatremia and AKI was determined using logistic regression, adjusting for age, gender, baseline renal function, diabetes, hypertension, hemoglobin, BNP levels in the ADHF cohort, Killip class in the AMI cohort, and ejection fraction. Results: Hyponatremia was present on admission in 156 pts (19.7%) with ADHF and in 244 pts in AMI (21%). In ADHF, AKI occurred in 82 (22%) pts without hyponatremia and 54 (35%) with hyponatremia (P=0.0003). In AMI, AKI occurred in 135 (17%) pts without and 109 (27%) pts with hyponatremia (P<0.001). In a multivariable logistic regression model, the adjusted odds ratio for AKI was 1.90 among ADHF pts with hyponatremia (95% CI 1.25-2.88; P=0.003), and 2.06 among AMI pts with hyponatremia (95% CI 1.48-2.87; P<0.0001). When sodium was used as a continuous variable, the risk for AKI was inversely related to sodium levels (Figure). ![Figure][1] Probability of AKI Conclusion: Hyponatremia predicts the development of AKI in two clinical scenarios that frequently lead to the type I CRS. These data suggest that neurohormonal activation contribute to the development of acute CRS. [1]: pending:yes

Toll Like Receptor 4 in Acute Myocardial Infarction

Previous studies on Toll-like receptor 4 (TLR 4), which are identified as central innate immune receptors, were done for local (at plaque rupture site) and systemic expression of TLR 4 from mononuclear concentrate (MNC) in acute myocardial infarction (AMI) pts. TLR inhibition is considered as a emerging new therapeutic modality for LV remodeling. We want to study difference of expression of TLR 4 on MNC and plasma in AMI pts. Even though, for TLR 4 protein detection in plasma requires higher concentration on the lymphocytes and to be secreted into plasma, but still, if plasma detected TLR 4 has same prognostification importance as from TLR 4 of MNC then, TLR 4 detection from plasma may be used at bed side.

248 Presence of endothelial colony-forming cells is associated with reduction of microvascular obstruction limiting infarct size and left ventricular remodelling: MRI study in acute myocardial infarction

Endothelial colony-forming cells (ECFCs) have proliferative and vasculogenic capacities and can be detected in patients (pts) with myocardial infarction (MI). High ECFC levels reportedly lead to positive left ventricular (LV) remodelling after acute MI, but the mechanism of this improvement has never been assessed. We evaluated the relationship between ECFC levels and microvascular obstruction (MVO), and the impact of this relation on infarct size and LV remodelling at 6 months as assessed by magnetic resonance imaging (MRI). 109 pts<75 years old, admitted with a first MI within 12 hours of onset of symptoms were enrolled. Peripheral blood samples were drawn to assess number of ECFC colonies (culture cells). Measurements of infarct size by MRI were performed at day 5 and 6 months. ECFC colonies were detected in 51/109 pts (47.2%) at admission (ECFC pos pts). At 5 days, MVO was more frequently observed (63% vs 33%; p = 0.003) and of greater magnitude (7 ± 6% vs 3 ± 5%, p = 0.0004) in ECFC neg patients versus ECFC pos pts respectively. At 6 months, there was a significantly greater reduction in infarct size in ECFC pos pts (−33.7 ± 33.2% vs −15.1 ± 24.6%, ECFC pos vs ECFC neg respectively; p = 0.003). This reduction in infarct size was associated with a significant improvement in LV ejection fraction and a significant reduction in LV end diastolic and systolic volumes in ECFC pos pts. A significant positive correlation was observed among ECFC pos pts between MVO at day 5 and infarct size at 6 months (r 2 =0.58, p<0.0001), while the number of ECFC colonies was significantly correlated with the relative change in infarct size at 6 months MRI (r 2 =0.33, p<0.0001). The presence of ECFC colonies is associated with a reduced degree of microvascular obstruction early after myocardial infarction, leading to reduced infarct size and positive LV remodelling at 6 months and can be considered as a marker of microvascular integrity in acute MI pts.

Clinical Outcomes in Patients with Acute Left Circumflex/Obtuse Marginal Occlusion Presenting with Myocardial Infarction

Acute occlusion of left circumflex (LCx) or obtuse marginal (OM) arteries can present as ST elevation myocardial infarction (STEMI) or non-ST elevation myocardial infarction (NSTEMI). NSTEMI patients (pts) with occlusions have worse outcomes than those without occlusions, but no studies specifically examine outcomes in acute myocardial infarction (AMI) pts with LCx/OM occlusion. This study aims to define the incidence of NSTEMI in pts presenting with LCx/OM occlusion and analyzes clinical characteristics and outcomes in those presenting with NSTEMI compared to STEMI. A review of our catheterization and STEMI database was performed to identify AMI pts presenting with LCx or OM occlusion from 1/1/2007 to 7/31/2009 at the Medical College of Virginia. Patients were divided into STEMI and NSTEMI groups, and a chart review was performed. Primary end-points were in-hospital mortality (HM), cardiogenic shock (CS), and in-hospital CHF. Secondary end-points included peak CK-MB and time to catheterization, as well as combined end-points of 1-month mortality, and recurrent AMI and CHF. Fifty-six pts met inclusion criteria, 54% of whom presented with NSTEMI. STEMI pts were significantly more likely to meet the primary end-points, as well as the combined secondary end-points. They had shorter times to catheterization but larger infarct sizes. Patients with left or mixed coronary dominance were more likely to have STEMI. AMI pts with LCx/OM occlusion present with NSTEMI as often as STEMI. Those with NSTEMI have better outcomes, which may be related to right coronary dominance. Patients with acute LCx or OM occlusion present with NSTEMI as often as STEMI, but those with STEMI have worse outcomes. The difference in presentation may be related to coronary dominance.

AS-155: Midterm Angiographic and Clinical Outcomes of Sirolimus- versus Paclitaxel-versus Zotarolimus-Eluting Stents in Patients with Acute Myocardial Infarction

The safety and efficacy of different types of drug-eluting stents (DES) in patients (pts) with acute myocardial infarction (AMI) has not been clarified. We compared 6-month angiographic and clinical outcomes of AMI pts who received 3 common DES types.

P149: D-ribose improves cardiac indices in patients undergoing “off” pump coronary arterial revascularization

Patients (pts) with coronary artery disease (CAD) may undergo revascularization using an “off” pump cardiopulmonary bypass (OPCAB) technique. OPCAB has gained acceptance with proper pt selection, including pts presenting with acute myocardial infarction (MI). Increased morbidity and mortality rates may occur, especially with acute MI pts, in which lower tissue levels of adenosine triphosphate (ATP) may play a key role. Ribose (R), a natural occurring pentose sugar, has demonstrated not only accelerated myocardial ATP return of depressed energy levels, but also functional benefits in pts with cardiovascular disease.

Concurrent G-CSF and GM-CSF administration for the induction of bone marrow-derived cell mobilization in patients with acute myocardial infarction: a pilot study evaluating feasibility, safety and efficacy.

To verify feasibility and safety of bone marrow stem cells (BMC) mobilization in patients (pts) with acute myocardial infarction (AMI) and to monitor the clinical effects of BMC mobilization in terms of myocardial perfusion and function. Eight male pts (median age: 50.5 years) treated with a primary PTCA were enrolled. The mobilization regimen consisted of G-CSF 5 microg/kg/12 h from day 0 to day +2 and GM-CSF 2.5 microg/kg/24 h. All pts underwent coronary angiography, intracoronary doppler flow study, echocardiography, and nuclear thallium scan before treatment and at 6 months. All pts showed increased values of WBC and circulating CD34+ following cytokine administration. No patient died. All patients completed a 6-months follow-up: target lesion revascularization rate was 12,5%, target vessel revascularization rate was 37.5%, angiographic mean ejection fraction increased from 49.8+/-11.9 to 55.4+/-8.7 (p=NS), mean coronary flow reserve from 1.63+/-0.42 to 2.5+/-0.4 (p=0.001), mean Thallium uptake raised from 55.56+/-16.42% to 67.56+/-13.66% (p=0.01), and normally perfused segments from 16% to 52% (p=0.01). Cytokine-induced BMC mobilization is feasible in AMI pts. Improvements of myocardial perfusion can be expected after PTCA associated with G-CSF and GM-CSF induced mobilization. Further studies are required to define the role of BMC-mobilization and the most effective cytokine combination.

Carotid atherosclerotic plaque instability in patients with acute myocardial infarction

The instability of atherosclerotic plaque is partly determined by local factors, but systemic factors such as infection, inflammation, autoimmunity or genes might also be important. We aimed to analyze whether patients with acute myocardial infarction (AMI) might have a higher proportion of unstable plaques in the carotid arteries compared with patients who had had no acute coronary events. Methods Sixty-nine consecutive patients with AMI (Group 1) and 95 patients without acute coronary events (Group 2) had carotid artery duplex ultrasounds. Carotid atherosclerosis was quantified by number of plaques in the two carotid arteries, intimal media thickening and degree of maximal stenosis. According to their morphology, plaques were divided into stable (fibrocalcific) and unstable (soft and/or not homogeneous). Results The two groups did not differ as regards age (66 ± 8 vs. 68 ± 19; p = 0.3), female sex (13% vs. 21%; p = 0.3), mean number of carotid plaques (2.8 ± 1 vs. 2.5 ± 2; p = 0.2), degree of stenosis (59 ± 2% vs. 36 ± 1%; p = 0.2) or intimal media thickening (1.04 ± 0.2 vs. 1.06 ± 0.2; p = 0.8). However, Group 1 pts more frequently had unstable carotid plaques compared with Group 2 (43% vs. 15%; p = 0.004), and had a greater number of unstable carotid plaques (0.51 ± 0.6 vs. 0.16 ± 0.4: p < 0.0001) and a higher ratio of unstable to stable plaque (19% vs. 8%; p = 0.005). In the overall population, logistic regression analysis showed that after adjustment for degree of maximal stenosis, the presence of coronary artery event (AMI pts) predicted the presence of unstable carotid plaque (OR: 4.3 95% CI: 2.0–9.2; p = 0.0002). Conclusion Patients with unstable coronary artery disease expressed clinically as AMI, frequently had unstable atherosclerotic plaques in other arterial sites such as carotid arteries. This finding supports the hypothesis that plaque instability might reflect a systemic process.

Morphopathology of myocardial infarction in hypertension. a postmortem study

Although a large series of studies identified hypertension as a major coronary risk factor for all the types of myocardial ischemic disease, only a few reports related the morphology of acute myocardial infarction (AMI) to hypertension. Remodeling from cardiac hypertrophy due to hypertension would often seem to lack in AMI hearts. The purpose of this study was to assess retrospectively the relationship between pre-existing hypertension and morphopathology of AMI. We re-examined 168 (56.7%) autopsy cases out of 296 affected by AMI. 108 (64%) were males and 60 (36%) females with a mean age of 64.3 ± 18 years. 27/168 AMI pts (16%) had hypertension (systolic blood pressure from 180 mmHg to 220 mmHg, and diastolic blood pressure from 90 mmHg to 115 mmHg). Anatomically, infarction was anterior 86 times (51%)-13 cases (15%) with hypertension-, inferior 49 times (29%)-9 cases (18%) with hypertension-, and anterior+inferior 33 times (20%)-5 cases (15%) with hypertension-. 10 hypertensive hearts (37%) showed postinfarction cardiac rupture (PCR) with cardiac hypertrophy (mean heart weight: 627 ± 188 gm, wall thickness 25 ± 3 mm versus respectively 400 ± 75 gm, and 14 ± 2 mm for non-hypertensive hearts and hypertensive hearts without PCR, P < 0.01). No change in pathologic patterns of AMI was seen. Multiple irregular narrowings less than 90% affected coronary tree of hypertensive hearts compared with hearts without hypertension (P < 0.01). No difference in occlusive thrombi. In conclusion, hypertension influenced morphopathology of AMI by a greater number of stenoses in the coronary tree and a major incidence of PCR accompanied by cardiac hypertrophy.

Feasibility of Low-Molecular-Weight-Heparin (Fraxiparine) for Primary Stenting in Acute Myocardial Infarction

Background and objectives:The optimal anti-thrombotic strategy for primary stenting in acute myocardial infarction (AMI) is still controversial. We evaluated prospectively the efficacy and safety of low-molecularweight-heparin (LMWH) for primary stenting in AMI. Materials and Method:From 1/1997 to 7/1998, 54 AMI pts underwent primary stenting with 96% of procedural success rate (52/54). Of these, five pts were excluded from the study for warfarinization or use of GPIIb/IIIa inhibitor despite of successful stenting (TIMI 3 flow and less than 30% of residual stenosis). In 47 pts included in the study, 5,000-10,000 U of unfractionated heparin was administered (IV/bolus) bofore primary stenting. After sheath removal, LMWH (Fraxiparine, 7500 U/S.C.BID) maintained for 10.6±5.7 days. Aspirin and ticlopidine (500mg/day for ≥4 weeks) were given before stenting. Pts were followed to determine early (0-30 days) and late (31-180 days) major adverse cardiac events (MACE). Subsequent revascularization involving other coronary arteries did not constitute an end point. Results:In 47 Pts (M:F=32:15, age=57.7±11.3 yrs, range:37-88), 50 stents (Nir:38, micro:7, Jo:5, LAD:LCX:RCA=24:9:14) were implanted. Their immediate poststenting MLD and diameter-stenosis (%) were 2.9±0.4 mm, 4.3±8.7%, respectively. No patient showed subacute stent thrombosis or major bleeding requiring blood transfusion or surgery. During 0-30 days, the primary combined end point occurred in 2 (4.2%):one repeated angioplasty for in-stent restenosis;one hospital death for pump failure (1 of 2 Killip IV pts at admission). 44 patients were followed for 180 days and additional three TVR (3/44 (6.8%), one CABG, one repeatedangioplasty and one recurrrent myocardial infarction) occurred between 30-180 days due to recurrent ischemia. Conclusion:Anti-thrombotic therapy with LMWH (Fraxiparine) is safe and feasible for primary stenting in AMI. But to illuminate the impact on 논문접수일:1999년 3월 7일 심사완료일:1999년 6월 2일 교신저자:오동주, 152-703 서울 구로구 구로동 고려대학교 의과대학 순환기내과학교실 전화:(02) 818-6633·전송:(02) 866-1643 E-mail:hhansin@unitel.co.kr

127. Levels of functional versus intact fibrinogen in 140 patients with acute myocardial infarction treated with Reteplase

Reteplase, the novel K2P-deletion mutant of t-PA, was administered in a dose-finding multicenter study (GRECO) to 140 patients (pts) with acute myocardial infarction (AMI). 40 pts (group A) received an 18 mg (10 Megaunits (MU)) i.V. single bolus of Reteplase and 100 subsequent pts (Group B) were treated with a 27 mg (15 MU) i.v. single bolus. Fibrinogen (fbg) was measured using two different methods before (pre) and 2, 4, 8 and 24 h after Reteplase: the first fbg method was a clotting rate assay according to the Clauss method (functional fbg), the second an enzyme immunoassay (EAI) for immunologically intact fbg. In 10 out of the group B pts (group C; 27 mg) changes of fbg levels were measured in very close intervals until 18 days (dl8) after thrombolysis. Results: The levels of functional (Clauss) and intact (EIA) fbg differed significantly at each time point: A (Clauss/EIA; median values; [g/1]): Pre: 2.8/3.5; 2 h: 1.7/2.7 (60%/77% of the pre-bolus value of each method); 4 h: 1.7/2.7 (62%/76%); 8 h: 1.5/2.6 (54%/74%); 24 h: 2.2/3.0 (79%/86%) (p<0.001 between Clauss and EIA at any time of sampling). B: Pre: 2.6/3.2; 2 h: 1.0/2.1 (37%/66%); 4 h: 0.9/2.2 (36%/69%); 8 h: 1.0/2.2 (37%/69%); 24 h: 1.6/2.4 (63%/75%) (p<0.0005). C: Pre: 2.7/3.1; 30 min.: 1.6/2.5; 60 min.: 1.3/2.4; 2 h: 1.2/2.3; 4 h: 1.2/2.2 (44%/69%); 8 h: 1.3/2.2; 24 h: 1.8/2.5; 48 h: 2.8/2.7; 72 h: 4.1/3.6; d6: 4.7/3.8 (173%/123%); d9: 4.5/3.9 (167%/126%); d!2: 4.1/3.5; d!5: 3.9/3.2; d!8: 4.0/3.4 (p<0.05; exception: 48 h: not significant). Conclusions: The levels of functional (Clauss) fbg showed lower nadirs and higher rebound levels (C) compared to the intact (EAI) fbg levels. Lower nadirs measured by the Clauss method might reflect the disturbance of this method by fibrin(ogen) degradation products. Higher rebound levels of functional fbg (Clauss) might indicate newly synthesized fast clotting HMW (high molecular weight) fbg and therefore a risk factor for reocclusions in AMI pts treated with thrombolytic agents. In contrast to our previous studies in rt-PAtreated AMI pts, the pretreatment ratio of functional (Clauss) to intact (EAI) fbg here was <0.9 in groups A, B and C compared to 1.6 in the rt-PA study. © Pearson Professional Ltd 1996.

790-3 ECG Changes During the First 48 Hours of Myocardial Infarction are Similar in Pts with TIMI 2 and TIMI 3 and Differ from Pts with TIMI 0/1

It has been suggested that the ECG development (ST segment, QRS score) of acute myocardial infarction (MI) pts with TIMI 2 flow is closer to TIMI 0/1 than to TIMI 3. To study this, 358 acute MI pts treated with thrombolytic therapy were investigated. Sum of ST deviation (&Sigma;ST) and QRS score of the 12 lead ECG were calculated at 3 time points during the first 48 hours: ECG 1: on admission (mean 90 min alter onset of MI), ECG 2: mean 9 hours alter MI, and ECG 3: mean 36 hours after MI. ECG's were related to the TIMI flow determined from the last view of angiography 60 and 90 min after start of thrombolytic therapy. ECG TIMI TIMI 2 3 0/1 2/3 N 46 248 64 294 &Sigma;ST 1 16.1 ns 15.5 15.4 ns 15.6 (mm) 2 6.5 ns 5.3 10.2 *** 5.5 3 5.1 ns 4.7 6.1 * 4.8 ORS- 1 2.9 ns 2.9 2.6 ns 2.9 score 2 3.9 ns 4.5 4.5 ns 4.4 3 5.1 ns 5.2 6.3 ** 5.2 * p &lt; 0.05 ** p &lt; 0.01 *** p &lt; 0.0001 TIMI 2 patients have significantly less ECG changes at 9 hours and later than patients with TIMI 0/1 flow. Electrocardiographically, patients with TIMI2 flow behave like pts with TIMI 3 flow.

1023-111 Effects of Propranolol in Patients with Their First Acute Myocardial Infarction and Persistent Electrocardiographic ST Segment Depression in the Beta Blocker Heart Attack Trial

The available data suggest that patients (pts) recovering from an acute my ocardial infarction (AMI) who have persistent electrocardiographic (ECG) ST segment depression (STD) are at high risk for future cardiac events when compared with AMI pts without STD. There are little data on the long term effects of medical therapy on acute MI pts with STD. The objectives of this retrospective analysis were to examine in the Beta Blocker Heart Attack Trial (BHAT) the effects of propranolol in this high risk group. Of the 2877 first MI BHAT pts, 656 pts had persistent ECG STD from the time of admission until randomization (9.7 ± 3.1 days after index MI). Of these, 317 pts were randomized to the propranolol and 339 pts to placebo. There were no significant baseline differences (p &lt; 0.05) between the two groups. The median follow up was 24.6 months. Follow-up Events Propranolol Placebo p-value (n = 317) (n = 339) (Cox regression) Overall mortality 7.6% 13.6% 00078 Sudden death 4.7% 9.7% 00094 Definite or probable MI 3.8% 7.7% 0.037 MI andlor mortality 9.2% 17.4% 0.0011 Cox regression analysis, adjusting for baseline variables showed the relative risk of mortality and the relative risk of sudden death were 2.13 (1.22, 3.70) and 2.56 (1.27, 5.26) respectively in the placebo, compared to the propranolol group. It appears that propranolol therapy is effective in reducing cardiac events in pts recovering from an AMI with ECG STD.