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PubMed2006

Cardiac overexpression of monocyte chemoattractant protein-1 in transgenic mice prevents cardiac dysfunction and remodeling after myocardial infarction.

Myocardial infarction (MI) is accompanied by inflammatory responses that lead to the recruitment of leukocytes and subsequent myocardial damage, healing, and scar formation. Because monocyte chemoattractant protein-1 (MCP-1) (also known as CCL2) regulates monocytic inflammatory responses, we investigated the effect of cardiac MCP-1 overexpression on left ventricular (LV) dysfunction and remodeling in a murine MI model. Transgenic mice expressing the mouse JE-MCP-1 gene under the control of the alpha-cardiac myosin heavy chain promoter (MHC/MCP-1 mice) were used for this purpose. MHC/MCP-1 mice had reduced infarct area and scar formation and improved LV dysfunction after MI. These mice also showed induction of macrophage infiltration and neovascularization; however, few bone marrow-derived endothelial cells were detected in MHC/MCP-1 mice whose bone marrow was replaced with that of Tie2/LacZ transgenic mice. Flow cytometry analysis showed no increase in endothelial progenitor cells (CD34+/Flk-1+ cells) in MHC/MCP-1 mice. Marked myocardial interleukin (IL)-6 secretion, STAT3 activation, and LV hypertrophy were observed after MI in MHC/MCP-1 mice. Furthermore, cardiac myofibroblasts accumulated after MI in MHC/MCP-1 mice. In vitro experiments revealed that a combination of IL-6 with MCP-1 synergistically stimulated and sustained STAT3 activation in cardiomyocytes. MCP-1, IL-6, and hypoxia directly promoted the differentiation of cardiac fibroblasts into myofibroblasts. Our results suggest that cardiac overexpression of MCP-1 induced macrophage infiltration, neovascularization, myocardial IL-6 secretion, and accumulation of cardiac myofibroblasts, thereby resulting in the prevention of LV dysfunction and remodeling after MI. They also provide a new insight into the role of cardiac MCP-1 in the pathophysiology of MI.

Animals↗

PubMed1975

[Risk factors in postoperative myocardial infarction].

Myocardial infarction after major surgery occurred 25 times in 214 patients who had previously sustained infarcts. Analysis of data obtained before, during and after 335 operations in these patients revealed the following pathogenetic factors in the infarction: (1) The patient with the highest coronary risk had arterial hypertension of at least 160/95 mmHg and advanced arteriosclerosis combined with coronary arterial, peripheral arterial, cerebrovascular, and renovascular disease. (2) Myocardial necrosis occurred when oxygen supply was reduced, as evidenced from a fall in systolic blood pressure to 70 mmHg or less during operation or anaemia (RBC smaller than or equal to 3,5 times 10-6/mul) early after operation. (3) Risk of infarction was highest during the early postoperative stress period with elevated plasma catecholamine levels and thus an increased myocardial oxygen demand.

Aged↗

PubMed1997

Correlation of thallium uptake with left ventricular wall thickness by cine magnetic resonance imaging in patients with acute and healed myocardial infarcts.

Myocardial infarction (MI) is characterized by cellular necrosis which undergoes fibrotic transformation over time. Cine magnetic resonance imaging (MRI) offers high-resolution 3-dimensional images of the left ventricular myocardium, allowing sampling of the myocardial wall thickness over the entire left ventricle. Tomographic (single-photon emission computed tomography [SPECT]) thallium images also provide 3-dimensional information on the location and level of thallium uptake, which has been shown to correlate with myocardial viability. The purposes of this study were: (1) to examine the relation between both end-diastolic and end-systolic wall thickness and normalized thallium-201 uptake over the left ventricle in a group of patients with MI, (2) to examine the relation between regional wall thickening and normalized thallium uptake, and (3) to examine the relation between thallium uptake and wall thickness both early and late after infarction. Twenty-four patients with MI underwent stress, redistribution, and reinjection thallium SPECT imaging and cine MRI within several days. Seventeen patients underwent imaging late after infarction and 7 underwent imaging early after infarction. Normalized thallium activity was correlated with MRI wall thicknesses at both end-diastole and end-systole for 18 segments for each ventricle. In addition, end-diastolic and end-systolic wall thicknesses were grouped by their corresponding thallium activity levels into percentiles. End-systolic wall thickness correlated significantly with normalized thallium uptake in 14 of 18 segments, end-diastolic wall thickness in only 4 of 18 segments, and wall thickening in only 3 of 18 segments. Mean values for end-diastolic and end-systolic wall thicknesses corresponding to severely reduced (<50%) normalized thallium activity were 9.9 +/- 1.1 and 8.5 +/- 0.6, respectively. Using receiver-operating curve analysis, end-systolic wall performed as a better diagnostic parameter than end-diastolic wall for identifying severely reduced thallium activity levels. For all levels of thallium activity, end-diastolic wall thicknesses were all thinner late versus early after MI, whereas end-systolic wall thickness was thinner only in the segments corresponding to severely reduced thallium activity. Based on these results, end-systolic wall thickness is the best noninvasive anatomic parameter of myocardial scar.

Adult↗

PubMed1999

Effects of aspirin and trapidil on cardiovascular events after acute myocardial infarction. Japanese Antiplatelets Myocardial Infarction Study (JAMIS) Investigators.

Aspirin therapy confers conclusive net benefits in the acute phase of evolving myocardial infarction, but no clear evidence of benefit from the long-term use of aspirin after acute myocardial infarction (AMI) has been shown in any single study. This multicenter study, the Japanese Antiplatelets Myocardial Infarction Study, was performed to find out whether aspirin or trapidil would improve clinical outcome compared with no antiplatelets in postinfarction patients. The study was a multicenter, open-label, randomized controlled trial of aspirin 81 mg/day, trapidil 300 mg/day, and no antiplatelets in patients with AMI admitted within 1 month from the onset of symptoms. Seven hundred twenty-three patients were enrolled at 70 hospitals in 18 prefectures of Japan; 250 were randomly assigned to treatment with 81 mg aspirin (aspirin group), 243 to that with trapidil (trapidil group), and 230 were not given antiplatelet agents. The mean follow-up period was 475 days. This study demonstrated that long-term use of aspirin at the dose of 81 mg/day reduced the incidence of recurrent AMI compared with the group receiving no antiplatelets after AMI (p = 0.0045) and that trapidil also reduced the occurrence of reinfarction compared with the group receiving no antiplatelets, but the difference was not significant (p = 0.0810). The incidence of cardiovascular events including cardiovascular death, reinfarction, uncontrolled unstable angina requiring admission to hospital, and nonfatal ischemic stroke was reduced in the group receiving 300 mg trapidil daily compared with the group receiving no antiplatelets (p = 0.0039). The use of aspirin 81 mg/day provided almost no benefit over no antiplatelets therapy in the incidence of cardiovascular events. In conclusion, low-dose aspirin (81 mg) effectively prevented recurrent AMI in postinfarction patients after thrombolysis or coronary angioplasty when used over a long term. Furthermore, the long-term use of trapidil resulted in a significant reduction in the incidence of cardiovascular events.

Aged↗

PubMed1985

Metoprolol in acute myocardial infarction. Development of myocardial infarction. The MIAMI Trial Research Group.

The effect of metoprolol on the development of an acute myocardial infarction (AMI) during days 0 to 3 and on late first and recurrent infarctions during days 4 to 15 has been investigated. Signs on electrocardiogram (ECG) were well balanced between the treatment groups at entry; 70% of patients had signs of suspected AMI and 19% of patients had normal ECGs. The remaining patients had abnormal ECGs but actual infarction could not be localized. The localization of suspected AMI was equivalently distributed in the 2 groups before randomization. Metoprolol altered the distribution of patients diagnosed during days 0 to 3 as having definite, possible or no AMI (p less than 0.02). In the placebo group, there were more patients with definite AMI (72.5% vs 70.5%) and less with possible AMI (5.6% vs 7.4) than in the metoprolol group. A larger proportion of patients developed a Q-wave infarction during days 0 to 3 in the placebo group (53.9%) compared with the metoprolol group (50.9%, p = 0.024). No difference in the effect of metoprolol regarding localization of the early AMI was observed. Late first myocardial infarction development (days 4 to 15) was observed in 20 patients (0.7%) in each group. Recurrent myocardial infarction tended to develop more frequently during days 4 to 15 in the placebo group compared with the metoprolol group (3.9% vs 3.0%, p = 0.08).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗

PubMed1990

[Ealuation of thrombolytic treatment of acute myocardial infarct using myocardial scintigraphy with Tc-99-MIBI. Immediate results and follow-up after one year].

The aim of the study was to investigate Single Photon Emission Computed Tomography (SPECT) with technetium-99m esakis-2-methoxy isobutyl isonitrile (Tc-99m-MIBI) as a means of evaluating the results of intravenous thrombolytic treatment in patients with acute myocardial infarction. In addition, the evolution of myocardial perfusion pattern was studied. The study group included 15 patients (12 males and 3 females, mean age 57 +/- 8 years) with acute myocardial infarction admitted to the coronary care unit within 4 hours of the onset of symptoms. All patients were injected with 740 MBq of Tc-99m-MIBI before starting the thrombolytic therapy (rt-PA 100 mg i.v. in 3 hours); SPECT was performed 3 to 6 hours later. The tomographic study was repeated 5 days later. Ten patients were re-examined using Tc-99m-MIBI SPECT one year after the acute event. Taking into account the clinical, electrocardiographic and enzymatic data and the findings of two-dimensional echocardiography performed both on the fifth day and after one month, patients were divided into two groups: group A (8 patients) with probably effective reperfusion, group B (7 patients) probably unaffected by therapy. The infarct related vessel was patent in all group A patients and in 2 of the 7 patients of group B. The percent decrease in the perfusion defect size between the first and second scintigraphic studies showed a significant difference between the two groups: group A 61.2 +/- 6.8, group B 4.7 +/- 2.4% (p less than 0.002). A significant difference was also found when the results of the admission scintigraphy were compared with those of the control 1 year after: group A 80.8 +/- 8.7%, group B 20.8 +/- 13.8% (p less than 0.02). The percent decrease in the perfusion defect size between the 5-day and 1-year images was also significantly different in the two groups: group A 52.9 +/- 20.9%; group B 17.8 +/- 12% (p less than 0.02). The late perfusion improvement involved mainly the sub-epicardial layers. In conclusion, Single Photon Emission Computed Tomography with Tc-99m-MIBI clearly identified patients with effective reperfusion after thrombolytic treatment and distinguished them from subjects unaffected by therapy. Both, successfully and unsuccessfully treated patients showed a late perfusion improvement which was more evident in the successfully treated patients.

Female↗

PubMed2002

Effects of atorvastatin on stroke in patients with unstable angina or non-Q-wave myocardial infarction: a Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) substudy.

BACKGROUND: This report describes the effect of intensive cholesterol lowering with atorvastatin on the incidence of nonfatal stroke, a secondary end point, in a randomized, placebo-controlled trial of patients with unstable angina or non-Q-wave myocardial infarction. The primary end point, a composite of death, nonfatal myocardial infarction, resuscitated cardiac arrest, or recurrent symptomatic myocardial ischemia with objective evidence requiring emergency rehospitalization, was reduced from 17.4% in the placebo group to 14.8% in the atorvastatin group over the 16 weeks of the trial (P=0.048). METHODS AND RESULTS: Strokes were adjudicated by a blinded end-point committee using standard clinical and imaging criteria. The outcomes of nonfatal stroke and fatal plus nonfatal stroke were analyzed by time to first occurrence during the 16-week trial. Of 38 events (in 36 patients) adjudicated as fatal or nonfatal strokes, 3 were classified as hemorrhagic, one as embolic, and 29 as thrombotic or embolic; 5 could not be categorized. Nonfatal stroke occurred in 9 patients in the atorvastatin group and 22 in the placebo group (relative risk, 0.40; 95% confidence intervals, 0.19 to 0.88; P=0.02). Fatal or nonfatal stroke occurred in 12 atorvastatin patients and 24 placebo patients (relative risk, 0.49; 95% confidence intervals, 0.24 to 0.98; P=0.04). All 3 hemorrhagic strokes occurred in the placebo group. CONCLUSION: Intensive cholesterol lowering with atorvastatin over 16 weeks in patients with acute coronary syndromes reduced the overall stroke rate by half and did not cause hemorrhagic stroke. These findings need to be confirmed in future trials.

Acute Disease↗

PubMed2006

Selective spatiotemporal induction of matrix metalloproteinase-2 and matrix metalloproteinase-9 transcription after myocardial infarction.

Myocardial remodeling after myocardial infarction (MI) is associated with increased levels of the matrix metalloproteinases (MMPs). Levels of two MMP species, MMP-2 and MMP-9, are increased after MI, and transgenic deletion of these MMPs attenuates post-MI left ventricular (LV) remodeling. This study characterized the spatiotemporal patterns of gene promoter induction for MMP-2 and MMP-9 after MI. MI was induced in transgenic mice in which the MMP-2 or MMP-9 promoter sequence was fused to the beta-galactosidase reporter, and reporter level was assayed up to 28 days after MI. Myocardial localization with respect to cellular sources of MMP-2 and MMP-9 promoter induction was examined. After MI, LV diameter increased by 70% (P < 0.05), consistent with LV remodeling. beta-Galactosidase staining in MMP-2 reporter mice was increased by 1 day after MI and increased further to 64 +/- 6% of LV epicardial area by 7 days after MI (P < 0.05). MMP-2 promoter activation occurred in fibroblasts and myofibroblasts in the MI region. In MMP-9 reporter mice, promoter induction was detected after 3 days and peaked at 7 days after MI (53 +/- 6%, P < 0.05) and was colocalized with inflammatory cells at the peri-infarct region. Although MMP-2 promoter activation was similarly distributed in the MI and border regions, activation of the MMP-9 promoter was highest at the border between the MI and remote regions. These unique findings visually demonstrated that activation of the MMP-2 and MMP-9 gene promoters occurs in a distinct spatial relation with reference to the MI region and changes in a characteristic time-dependent manner after MI.

Animals↗

PubMed2002

Exercise training following myocardial infarction improves myocardial perfusion assessed by thallium-201 scintigraphy.

AIM: We assessed the effects of a 6-week exercise programme on the thallium-201 myocardial perfusion characteristics of patients following myocardial infarction. METHODS: Twenty-five patients presenting with a first acute myocardial infarction were randomised into two groups: (i) those undergoing a supervised exercise training programme over 6 weeks (n=15) and (ii) a control group who did not attend the exercise programme (n=10). All underwent three sequential stress thallium myocardial perfusion scans at 10 days, 6 weeks and 3 months after infarction. The stress conditions were identical on each occasion. The images were analysed using a polar plot with a computer assisted algorithm comparing stress and redistribution data. Values for extent, severity and percentage redistribution of the thallium images were generated. RESULTS: A total of 29 perfusion defects were identified, 18 in the exercise group and 11 in the control group. Over 3 months in the exercise group the mean extent of the stress image defect fell from 109+/-64 to 95+/-51 pixels (P<0.05) while in the control group there was an increase from 133+/-57 to 144+/-57 pixels (P=ns). Stress defect severity fell in the exercise group from 581+/-417 to 494+/-346 S.D. (P<0.05) but increased in the control group from 765+/-494 to 877+/-543 S.D. (P=ns). On redistribution imaging in the exercise group a significant decrease was observed in both extent (94+/-56 to 76+/-43 pixels (P<0.05)) and severity (541+/-387 to 438+/-291 S.D. (P<0.05)) of the defects. However in the control group no significant change was observed for extent (125+/-54 to 125+/-52 pixels) or severity (745+/-485 to 820+/-503 S.D.) of the redistribution defects (P=ns). Reversibility of the defects increased slightly in both the exercise group (from 14.6+/-17 to 17.5+/-20%) and the control group (5.2+/-5 to 9.6+10%) (P=ns). CONCLUSION: Following myocardial infarction a 6-week exercise programme improves myocardial perfusion characteristics. An exercise programme should be integrated into cardiac rehabilitation protocols for patients after infarction.

Aged↗

PubMed1998

Randomized, controlled trial of RheothRx (poloxamer 188) in patients with suspected acute myocardial infarction. RheothRx in Myocardial Infarction Study Group.

BACKGROUND: Patients with acute myocardial infarction (AMI) who are not eligible for thrombolytic therapy or primary coronary angioplasty are distinguished by advanced age, complicated medical histories, relatively frequent use of prior revascularization procedures, and worse outcomes than their counterparts who are eligible for reperfusion therapy. METHODS AND RESULTS: The purpose of this randomized, controlled trial was to determine whether RheothRx, a hemorheologic agent, reduced myocardial infarct size and improved left ventricular function in patients who had suspected AMI at the time of hospital admission and were not eligible for reperfusion therapy. Patients were randomly assigned to RheothRx (n = 97) or placebo (n = 99). Patients in the two groups were similar with respect to age, sex, medical history, and clinical presentation. Enzyme evidence of AMI was present in 69% of the treatment group and 70% of the placebo group. Infarct size measured before hospital discharge was similar in the two groups (14.1% +/- 18.5% vs 11.7% +/- 14.1%, p = 0.60), although left ventricular ejection fraction was lower in the treatment group (47 +/- 14 vs 52 +/- 11, p = 0.026). Hospital mortality rate was 11.3% and 7.1% in patients receiving RheothRx and patients receiving placebo, respectively (p = 0.30). There was a higher occurrence of acute renal dysfunction in the RheothRx group (12% vs 2%, p = 0.005). Because of changes in drug dosage necessitated by the occurrence of acute renal dysfunction, the trial was stopped. CONCLUSIONS: In this study of patients who had suspected AMI and were not eligible for thrombolytic therapy, RheothRx did not decrease infarct size or favorably alter outcome. The need for effective treatment for this large patient population remains largely unmet.

Acute Kidney Injury↗

PubMed1996

Length of hospital stay after acute myocardial infarction in the Myocardial Infarction Triage and Intervention (MITI) Project registry.

OBJECTIVES: This study sought to identify current trends in length of stay in patients with an acute myocardial infarction and to evaluate which demographic, clinical, procedural and hospital-related factors explain the variation and reduction in length of stay observed during the study period. BACKGROUND: Hospital length of stay is an important contribution to cost of care. Previous studies of length of stay after acute myocardial infarction have been performed largely on administrative data bases and do not reflect current practice patterns. METHODS: We used univariate and multivariate models to evaluate which demographic, clinical and administrative factors influenced length of stay in 11,932 patients with acute myocardial infarction admitted to 19 Seattle-area hospitals between 1988 and 1994. RESULTS: Length of hospital stay decreased from (mean +/- SD) 8.5 +/- 8.2 to 6.0 +/- 5.8 days during the study period. Demographic and clinical characteristics known at the time of admission explained only 6% of variation in length of stay, whereas hospital complications, procedure use and type of admitting hospital explained an additional 27% of variation. The use of primary angioplasty and early diagnostic coronary angiography predicted a shorter length of stay; however, none of the measured variables explained the 29% reduction in length of stay that occurred between 1988 and 1994. CONCLUSIONS: Although hospital complications, procedure use and hospital characteristics are important predictors of length of hospital stay, none of these factors explains the 29% reduction in length of stay observed in postmyocardial infarction patients between 1988 and 1994. It is likely that unmeasured economic and administrative factors play important roles in influencing hospital length of stay.

Aged↗

PubMed1995

Value of rescue percutaneous transluminal coronary angioplasty following unsuccessful thrombolytic therapy in patients with acute myocardial infarction. Thrombolysis in Myocardial Infarction Investigators.

Rescue percutaneous transluminal coronary angioplasty (PTCA) has been advocated as a mechanical method to achieve reperfusion in instances where the myocardial infarct artery remains occluded after thrombolytic therapy. Most prior reports of rescue PTCA have been observational and analyses of value have been inconclusive. To evaluate the benefit of rescue PTCA, we studied 133 patients enrolled in the Thrombolysis in Myocardial Infarction Phase I Open Label and Phase II trials who had an occluded infarct-related artery after thrombolytic therapy. According to protocol, 100 consecutive patients had no rescue PTCA performed (no rescue group), and 33 consecutive patients underwent protocol-directed rescue PTCA (rescue group). The 2 cohorts were compared for clinical and angiographic outcome. Baseline characteristics of the 2 groups were similar. Rescue PTCA was attempted in each rescue group patient and was successful in 82%. At 21 days the mortality rate was 12% in the rescue group and 7% in the no rescue group (p = NS). Failed rescue PTCA was associated with a mortality of 33%. Reinfarction occurred in 6% of patients in the rescue group, and in 5% of those in the no rescue group (p = NS). At 21 days, mean left ventricular ejection fraction was 51 +/- 13% in the rescue group and 48 +/- 12% in the no rescue group (p = NS). We conclude that the routine use of rescue PTCA does not appear to offer significant benefit beyond that of contemporary medical therapy after thrombolytic failure.

Angioplasty, Balloon, Coronary↗

PubMed2003

Angiographic assessment of reperfusion in acute myocardial infarction by myocardial blush grade.

BACKGROUND: Angiographic successful reperfusion in acute myocardial infarction has been defined as TIMI 3 flow. However, TIMI 3 flow does not always result in effective myocardial reperfusion. Myocardial blush grade (MBG) is an angiographic measure of myocardial perfusion. We hypothesized that optimal angiographic reperfusion is defined by TIMI 3 flow and MBG 2 or 3. METHODS AND RESULTS: In 924 consecutive patients with TIMI 3 flow after angioplasty for acute myocardial infarction, we prospectively studied the value of MBG. End points were death, MACE, enzymatic infarct size, and residual left ventricular ejection fraction. Follow-up was 16+/-11 months. Of the 924 patients, 101 (11%) patients had MBG 0 or 1. Mortality was significantly higher in patients with MBG 0 or 1 compared with patients with MBG 2 or 3 (relative risk, 4.7; 95% CI, 2.3 to 9.5; P<0.001). The combined incidence of MACE was higher in patients with MBG 0 or 1 compared with patients with MBG 2 or 3 (relative risk, 1.8; 95% CI, 1.1 to 2.8; P=0.009). Enzymatic infarct size was larger (1437+/-2388 versus 809+/-1672, P=0.001) and left ventricular ejection fraction was lower (37.7+/-10.6 versus 43.8+/-11.1, P<0.001) in patients with MBG 0 or 1 compared with patients with MBG 2 or 3. CONCLUSIONS: MBG is a strong angiographic predictor of mortality in patients with TIMI 3 flow after primary angioplasty. Enzymatic infarct size is larger and residual left ventricular ejection fraction is lower in patients with MBG 0 or 1 compared with MBG 2 or 3. Angiographic definition of successful reperfusion should include both TIMI 3 flow as well as MBG 2 or 3.

Angioplasty↗

PubMed1999

Imaging of Myocardial Perfusion with SonoVuetrade mark in Patients with a Prior Myocardial Infarction.

Myocardial contrast echocardiography (MCE) is an evolving noninvasive imaging technique that can be used to assess regional myocardial perfusion. MCE relies upon the detection of nonlinear ultrasound signal from gas-filled microbubbles during their microvascular transit, resulting in tissue opacification. Provided that the relation between myocardial microbubble concentration and video intensity (VI) is within the linear range, VI measured from any myocardial region reflects the relative tissue concentration of microbubbles, which is influenced by three factors: (1) microbubble concentration in blood; (2) the myocardial blood volume fraction; and (3) microbubble destruction that occurs within the ultrasound beam. In this article, we discuss how these three factors may influence myocardial perfusion information provided by MCE and highlight the importance of image processing. In order to illustrate these concepts, we examine data obtained during perfusion imaging in patients with prior myocardial infarction using intermittent harmonic imaging at various ultrasound pulsing intervals (PIs) during bolus and continuous venous infusions of a second-generation microbubble agent (SonoVue(trade mark)). Our results suggest that evaluation of resting perfusion is most accurate when both myocardial blood volume and blood velocity are assessed. This information is provided only with continuous infusions of microbubbles during imaging protocols that vary the ultrasound PI.

Journal Article↗

PubMed1975

Distributions of several agents useful in imaging myocardial infarcts.

Myocardial cell death due to infarction is accompanied by an influx of calcium ion. The calcium ion seems to localize in crystalline structures that form within mitochondria and resemble hydroxyapatite. Based on this phenomenon 99mTc-stannous pyrophosphate has been successfully used to image myocardial infarcts within 24 hr of infarction and 1 hr following tracer administration both in dogs and patient volunteers. In this report, canine distribution studies of 99m-Tc-pyrophosphate are compared with similar studies with 99mTc-stannous polyphosphate, 99mTc-stannous 1, hydroxy-ethylidene-1, 1-disodium phosphonate diphosphonate), and 18F as sodium fluoride. Pyrophosphate polyphosphate, and diphosphonate are each potentially useful in myocardial infarct imaging but bone uptake of 18F occurs sufficiently early to prevent the use of this radionuclide in infarct scintigraphy.

Animals↗

PubMed1998

Comparison of double bolus urokinase versus front-loaded alteplase regimen for acute myocardial infarction. Thrombolysis in Myocardial Infarction in Korea (TIMIKO) study group.

This study was performed to compare the double bolus urokinase regimen with the front-loaded alteplase regimen for acute myocardial infarction. Double bolus urokinase is an easy, safe, and effective thrombolytic regimen with comparable results to standard front-loaded alteplase in acute myocardial infarction.

Adolescent↗

PubMed1986

Pathogenesis of impending myocardial infarction and acute myocardial infarction: clinical and angiographic evaluation of coronary thrombosis as a precipitating factor.

In order to investigate the role of coronary thrombosis as a precipitating factor of acute myocardial infarction (AMI), we examined coronary angiographic findings in 89 patients with AMI taken within 24 hours of the onset and in 42 patients with prolonged angina attack of impending myocardial infarction (impending MI) taken within 50 hours of the last angina attack. Furthermore, in the patients with impending MI, the effects of intracoronary and intravenous thrombolytic therapy and anticoagulant therapy used to prevent impending MI from developing into AMI, were also studied. (1) In 72 of 89 patients (81%) with AMI, coronary thrombi were detected angiographically. The thrombi were detected most frequently (88%) in angiographs taken within 3 hours of onset. (2) In 23 of 42 patients with impending MI, coronary thrombi were detected angiographically. In 6 patients with coronary thrombi who underwent intracoronary thrombolysis during angina attack, occlusive coronary thrombi in ischemia-related vessels were the observed, and recanalization by thrombolysis with intracoronary urokinase infusion relieved chest pain and improved ECG changes. (3) The incidence of AMI in 42 patients with impending MI who were treated with intracoronary and intravenous thrombolytic therapy and anticoagulant therapy was significantly less than in the conventional therapy group (80 patients) (11.9% vs. 27.5%; p less than 0.05). In 4 of 5 patients with developing AMI, coronary thrombi were detected angiographically in the acute phase of impending MI. These results indicate that coronary thrombosis plays an important role not only in the precipitation of impending MI but also in the development of impending MI to AMI.

Angina Pectoris↗

PubMed2005

A rare cause of myocardial infarction: acute inferoposterior myocardial infarction after successful intravenous thrombolytic treatment of mechanical mitral prosthetic valve thrombosis.

Prosthetic valve thrombosis is a rare and dreaded complication of patients with mechanical valves, particularly those in the mitral position. A 45-year-old female with status post prosthetic mitral valve replacement was admitted to the hospital with acute pulmonary edema. Echocardiography showed mitral valve thrombosis which was treated with tissue plasminogen activator (t-PA). During t-PA infusion she developed acute inferoposterior myocardial infarction. Coronary angiography showed normal coronary arteries. Presented case had acute inferoposterior myocardial infarction secondary to coronary emboli after the successful thrombolytic treatment of prosthetic mitral valve thrombosis.

Echocardiography↗