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PubMed1993

[Infarction expansion and ventricular remodelling after acute myocardial infarction].

Infarct expansion (IE) and ventricular remodelling (VR) are interdependent pathophysiologic processes in the heart following acute myocardial infarction (AMI), and may contribute to dilatation of the left ventricle, heart failure, left ventricular aneurysm and/or rupture, and poor prognosis. IE and VR are demonstrated by echocardiography, and are usually seen with large, transmural, anterior AMI, hypertension and persisting occlusion of the infarct-related coronary artery. All myocardial tissue components are involved in IE and VR, and local generation of growth factors, vasoactive mediators, oxygen-derived free radicals, and activation of the renin-aldosterone-angiotensin system may have pathophysiological significance. These mechanisms can provide the opportunity for therapy, and evidence suggests that treatment with angiotensin converting enzyme-inhibitors can attenuate IE and VR.

Animals↗
PubMed1993

Right ventricular infarction vs. left ventricular infarction: review of pathophysiology, medical treatment, and nursing care.

Myocardial infarction is a significant health problem causing tremendous morbidity and mortality in the United States. Differences exist between right and left ventricular wall myocardial infarction which influence the treatment and nursing care rendered. Knowledge of the pathophysiology and management of right versus left ventricular infarction is important in providing proper patient care.

Humans↗
PubMed1977

Effects of perhexiline on survival time and infarct size in experimental myocardial infarction.

The effects of perhexiline on survival time and infarct size were studied in three animal models. Dogs pretreated orally with perhexiline, 200 mg/day/14 days, and monitored under anesthesia for 30 hours after ligation of the left anterior descending coronary artery (LAD) had infarct weights of 9.1+/-1.9 g as compared to 15.2+/-1.0 g in paired untreated controls (P less than .02). Twelve of 15 perhexiline-pretreated dogs survived the duration of these studies while only 5 of 15 control animals survived for the same period of time (P less than .05). Serum creatine phosphokinase activity was significantly lower in the treated dogs at 9, 12 and 15 hours after ligation (P less than .05). Conscious dogs, pretreated orally with perhexiline 200 mg/day/7 days or 400 mg/day/7 days and monitored without anesthesia or analgesia for 72 hours after coronary ligation had smaller infarcts (P200=26+/-5; P400=26+/-4; C=39+/-5 g; P less than .05) lower plasma peak creatine phosphokinase activity (P less than .05) and reduced heart rate (P400=198+/-8; C=226+/-8 beats/min; P less than .05) and reduced incidence of ventricular ectopic beats (P less than .05). In pentobarbital anesthetized open-chest dogs, perhexiline (3 mg/kg i.v.) reduced the sum of S-T segment elevation after left anterior descending coronary artery occlusion from 32+/-3 to 14+/-1 mV (P less than .001); this effect was associated with and/or preceded by a reduction in arterial pressure (101+/-4 to 78+/-5 mm Hg; P less than .001) and heart rate (151+/-8 to 138+/-7 beats/min P less than .025; Circumflex flow increased from 38+/-4 to 83+/-8 ml/min (P less than .01). In noninfarcted open-chest dogs, perhexiline administration (3 mg/kg i.v.) resulted in increases in coronary blood flow, narrowing of arterial-coronary sinus O2 difference and a 14% reduction in myocardial O2 consumption. The protective effects of perhexiline on the ischemic myocardium appear to result from reductions in heart rate and associated decrease in myocardial O2 demand as well as an antiarrhythmic effect.

Animals↗
PubMed1996

[Measurement of ejection fraction after acute myocardial infarction. A comparison of measurements by means of radionuclide technique one week and 8 weeks after the infarction].

Left ventricular ejection fraction was measured in 54 patients by means of radionuclide technique at one week after, and again at eight after acute myocardial infarction that had been treated with streptokinase. In 17 patients (31%) ejection fraction increased and in 15 patients (28%) it decreased > or = 5 ejection fraction units. In 22 patients (41%) ejection fraction remained unchanged. No obvious difference were found between the three groups as regards infarct localization, infarction size (enzyme activity), or level of first ejection fraction measurement. There was a statistically significant (p < 0.05) longer delay from start of chest pain until treatment was started among the patients with increased ejection fraction than among the patients with decreased ejection fraction.

Aged↗
PubMed1996

[Long-term recovery of regional wall motion in patients with medically treated anterior myocardial infarction: quantitative assessment of the post-infarction left ventriculograms].

The effect of medical treatment without reperfusion therapy on the long-term recovery of regional wall motion was evaluated retrospectively in 28 patients with transmural acute anterior myocardial infarction who had coronary angiography and left ventriculography at 1-6 months after the onset of the episode and were followed for a mean of 65 months. In all patients, initial coronary angiography revealed significant stenosis in only the left anterior descending artery (LAD). All patients were treated medically without reperfusion therapy (such as thrombolytic therapy, angioplasty, or bypass grafting). The regional wall motion in the LAD territory was measured by the centerline method using the right anterior oblique projection. Long-term improvement in anterior wall motion is unlikely in patients with patent LAD or underdeveloped collaterals to the LAD (38%). However, subsequent anterior wall motion frequently improved among patients with severely stenotic or occluded LAD (63%) and well-developed collaterals (73%). Therefore, the anterior wall motion of some LAD-related infarctions improves spontaneously, the extent of coronary collaterals is an important determinant of long-term improvement, and the improvement in wall motion is completed within the early period of acute anterior infarction in patients with patent LAD.

Angiocardiography↗
PubMed1996

[Myocardial infarction--risks and procedures. Longitudinal observation of a population of 280,000 women and men--Project POL-MONICA Krakow. I V: Prognosis of non-invasive treatment in myocardial infarction within 28 days since its onset].

The objective of a paper was to assess in the observational study the early determinants of outcome in patients with acute myocardial infarction (MI)) in one province of Poland (Tarnobrzeg Voivodship). The studied group were 1858 hospitalized men and women registered in POL-MONICA Kraków study with clinical diagnosis of myocardial infarction or acute coronary heart disease, who fulfilled the criteria for definite or possible myocardial infarction according to The WHO MONICA Project. The main out-come measure was death before the end of 28th day after the onset. Patients with shock were at the highest risk to die-relative risk (RR) = 21.47, 95% confidence interval (CI) = 12.86-35.83. The other characteristics, which increased risk independently were: left ventricular failure (LVF) (RR = 2.51, 95% CI = 1.54-4.10) and age (RR = 1.03, 95% CI = 1.01-1.05) per one year. Male sex and diabetes were not related to the risk of death. After adjustment to age, sex, shock, LVF and diabetes, lower risk was found in patients treated with antiplatelet agents (RR = 0.41, 95% CI = 0.29-0.59), with beta-blockers (RR = 0.48, 95% CI = 0.31-0.75) and with nitrates (RR = 0.62, 95% CI = 0.39-0.98), which were used in 66.2%, 33.1% and 97% of events respectively. Higher risk was found in patients treated with diuretics.

Adrenergic beta-Antagonists↗
PubMed1997

Effects of RheothRx on mortality, morbidity, left ventricular function, and infarct size in patients with acute myocardial infarction. Collaborative Organization for RheothRx Evaluation (CORE).

BACKGROUND: Previous studies suggested that RheothRx (poloxamer 188) reduces infarct size and improves left ventricular (LV) function in acute myocardial infarction (AMI). We therefore evaluated the effects of various doses of RheothRx in 2948 patients presenting with AMI. METHODS AND RESULTS: Patients were randomized to a control group (n = 963) or to receive RheothRx. Patients receiving RheothRx were allocated to receive a 1-hour bolus only (regimen A, n = 844), an additional 11-hour infusion at a low dose (target serum concentration of 0.5 mg/mL) (regimen Y, n = 490), or an additional 23-hour infusion at a low dose (regimen B, n = 483). Three higher doses (1-hour bolus+low-dose infusion for 47 hours, 1-hour bolus+high dose, target serum concentration of 1.0 mg/ml for 24 hours, or 1-hour bolus+high dose for 48 hours) were discontinued because of high rates of renal dysfunction (8.8%). Renal dysfunction was also observed at lower doses (regimen A, 3.1%; Y, 2.7%; and B, 4.1%) compared with the control patients (1.0%). There was no significant difference in the composite outcome of death, cardiogenic shock, or reinfarction at 35 days (all RheothRx, 13.6%; control, 12.7%). There was a higher incidence of sinus tachycardia (24.7% versus 21.6%, P = .02), atrial flutter (3.0% versus 1.3%, P = .019), atrial fibrillation (10.2% versus 7.3%, P = .082), pericarditis (6.6% versus 4.7%, P = .055), and clinical (21.9% versus 17.9%, P = .005) and radiological (15.3% versus 12.3%, P = .12) evidence of heart failure. This was associated with a lower LV ejection fraction (n = 1053) in treated patients (by = -0.02, P = .026), but there was little difference (P = .34) in infarct size (n = 1088). CONCLUSIONS: In this study of nearly 3000 patients, RheothRx had no effect on mortality, reinfarction, or cardiogenic shock and an adverse effect on renal function, LV ejection fraction, and various clinical manifestations of LV dysfunction or heart failure.

Acute Kidney Injury↗
PubMedDate not supplied

Factors influencing the time to thrombolysis in acute myocardial infarction. Time to Thrombolysis Substudy of the National Registry of Myocardial Infarction-1.

BACKGROUND: The Time to Thrombolysis Substudy of the National Registry for Myocardial Infarction provided the opportunity to identify factors that delay thrombolytic treatment of patients with ST-segment elevation acute myocardial infarction. PARTICIPANTS: Forty-two participating registry hospitals volunteered for the Time to Thrombolysis Substudy. METHODS: A case report form was developed to collect time points for emergency department arrival (door), recording of the electrocardiogram (ECG) (data), entry of the order to give a thrombolytic drug (decision), and initiation of the thrombolytic infusion (drug) as defined by the National Heart Attack Alert Program. The impact of mode of transportation to the hospital, sex, policy-driven cardiology consultation and/or contact of the primary care physician on door-to-drug time, and each component interval were determined in 1755 patients who were treated with recombinant tissue-type plasminogen activator (A1-teplase). The t test was used for comparison of means and the nonparametric sign test was used for medians. RESULTS: A minority of patients arrived at the hospital by ambulance, although more women (49.6%) arrived by ambulance than men (40.9%). However, women arrived at hospitals significantly later after onset of symptoms than men. It took half as long for patients arriving by ambulance to be seen by the physician than those who transported themselves to the hospital. It took longer for women to have the initial 12-lead ECG recorded than men. The decision to order a thrombolytic agent was delayed by 22 minutes and median door-to-drug time by 21 minutes in those patients who had a cardiac consultation over those in whom the drug was ordered and infusion was initiated by the emergency physician. Although the initial 12-lead ECG showed ST-segment elevation in 86% of patients who received the thrombolytic drugs, with no difference between men and women and no difference in the rate of cardiology consultation between men and women (77%), door-to-decision time and door-to-drug time were substantially longer for women having consultation than men. There was no significant difference in door-to-decision time between men and women when no consultation was performed, but it still took longer for a drug infusion to be initiated in women. Contacting the primary care physician delayed the decision to give a thrombolytic drug by 18 minutes and the administration of the drug by 20 minutes, but there were no differences between men and women. Preparation of the drug in the pharmacy resulted in significant delay compared with mixing it in the emergency department. CONCLUSIONS: Hospital practices and policies, including contacting the primary care physician prior to the initiation of a lytic drug, cardiology consultation, and preparation of the drug in the pharmacy rather than in the emergency department, significantly delay the goal of early treatment of patients with ST segment elevation acute myocardial infarction. Delays in hospital arrival for women are compounded by delays in the decision to treat them with a thrombolytic drug and initiation of the drug therapy in those women who receive consultation compared with men. Other delays in acquiring the first ECG and initiating the drug infusion in women are not explained.

Aged↗
PubMed1998

Prediction of right ventricular infarction from standard surface ECG in patients with inferior myocardial infarction.

BACKGROUND: Patients with inferior myocardial infarction (MI) have a 45% chance of having concurrent right ventricular infarction (RVI); of these, 5-10% suffer hemodynamic collapse. Immediate correct diagnosis and appropriate management of such patients is vital. ST-segment elevation in the right precordial V4 lead (V4R) has a high diagnostic value in identifying RVI, but this determination requires additional time and cost. An attempt was made to use a collection of patients' standard surface electrocardiograms (ECG) to find any available data to detect RVI and to lead to a new way to diagnose RVI. METHODS: Fifty patients (males/females, 44/6; mean age, 64.3 +/- 6.9 years) with acute inferior myocardial infarction were enrolled in a first group to develop new diagnostic criteria for RVI. As a first step, the ST-segment change in every standard surface ECG lead was analyzed and compared with corresponding changes in V4R. RVI was diagnosed by typical clinical symptoms (chest pain for more than 30 minutes, ST elevation > 0.1 mV and enzyme changes) accompanying ST elevation of more than 0.1 mV in V4R (by Lopez-Sendon criteria) and echocardiographic findings. RVI was diagnosed in 24 (48%) patients using ECG. The new criteria were then tested in a secondary group of 48 patients (males/females, 43/5; mean age, 65.5 +/- 7.9 years) with inferior MI. RESULTS: Analysis of these patients found that ST depression in lead I and aVL was a specific characteristic of RVI (I + aVL > 0.2 mV). This criterion was applied to another group of patients with acute inferior MI to check the predictive value (sensitivity, 94.7%; specificity, 89.7%; positive predictive value, 85.7%; negative predictive value, 96.3%). CONCLUSIONS: In patients with evolving inferior MI, standard surface ECG analyzed for this criterion could aid clinical recognition of concomitant RVI.

Aged↗
PubMed1998

Associations of fibrinogen, factor VII and PAI-1 with baseline findings among 10,500 male participants in a prospective study of myocardial infarction--the PRIME Study. Prospective Epidemiological Study of Myocardial Infarction.

The contribution of coagulation factors and fibrinolytic variables to the development of ischaemic arterial disease is still not clearly established. The PRIME study is a prospective cohort study of myocardial infarction in men aged 50-59 years and recruited from three MONICA field centers in France (Lille, Strasbourg and Toulouse) and the center in Northern Ireland (Belfast). Baseline examination included measurement of plasma fibrinogen, factor VII, and PAI-1 activity in over 10,500 participants. We investigated the associations of these haemostatic variables with cardiovascular risk factors, prevalent atherosclerotic disease and geographical area. Fibrinogen level increased with age, smoking, waist-to-hip ratio, LDL-cholesterol, and it decreased with educational level, leisure physical activity, alcohol intake and HDL-cholesterol. Factor VII activity increased with body mass index, waist-to-hip ratio, triglycerides. HDL- and LDL-cholesterol. PAI-1 activity increased with body mass index, waist-to-hip ratio, triglycerides, alcohol intake, smoking, and decreased with leisure physical activity. PAI-1 level was higher in diabetic subjects than in subjects without diabetes. Cardiovascular risk factors explained 8%, 9%, and 26% of the total variance in fibrinogen, factor VII, and PAI-1, respectively. Compared with participants without prevalent cardiovascular disease, those with previous myocardial infarction (n = 280), angina pectoris (n = 230), or peripheral vascular disease (n = 19) had significantly higher levels of fibrinogen. but those with stroke (n = 67) had not. PAI-1 activity showed a similar pattern of association. The odds ratio for cardiovascular disease associated with a rise of a one standard deviation in fibrinogen and PAI-1 was 1.31 (95% confidence interval: 1.20 to 1.42, p <0.001) and 1.38 (95% confidence interval: 1.27 to 1.49, p<0.001), respectively. After adjustment for cardiovascular risk factors, these associations were attenuated but remained highly significant. There was no significant association between factor VII activity and prevalent cardiovascular disease. Fibrinogen level and, to a lesser extent, factor VII and PAI-1 activity were higher in Northern Ireland than France after adjustment for the main cardiovascular risk factors. These geographical variations are consistent with the 2 to 3-fold higher incidence of myocardial infarction in Northern Ireland than France. Our results provide further epidemiological evidence for a possible role of fibrinogen and PAI-1 in the pathogenesis of coronary heart disease.

Alcohol Drinking↗
PubMed1995

Randomized, Placebo-Controlled Study of Lamifiban with Thrombolytic Therapy for the Treatment of Acute Myocardial Infarction: Rationale and Design for the Platelet Aggregation Receptor Antagonist Dose Investigation and Reperfusion Gain in Myocardial Infarction (PARADIGM) Study.

The benefits of thrombolytic therapy in the treatment of acute myocardial infarction are incontrovertible. Large-scale studies combining angiographic and clinical end-points have demonstrated a perfusion-mortality relationship, with the highest survival rate among patients with early restoration of TIMI grade 3 coronary arterial flow. Despite advances in thrombolytic strategies, a substantial number of patients fail to rapidly achieve and maintain adequate coronary perfusion with thrombolysis. Conjunctive therapy with aspirin has proven useful in thrombolytic regimens, likely countering the heightened platelet activity central to acute coronary syndromes. The antiplatelet effect of aspirin is relatively weak compared with that of glycoprotein IIb/IIIa platelet receptor antagonists, which block the final common pathway of platelet aggregation. Lamifiban is a nonpeptide glycoprotein IIb/IIIa receptor antagonist. In early experimental studies, Lamifiban in combination with thrombolytic therapy has been shown to effectively restore coronary arterial patency, and phase I and phase II data have shown its use to be safe. To determine the optimal dose with regard to safety and efficacy of Lamifiban to be used with thrombolytic therapy in a large-scale trial, a phase II study is underway. The Platelet Aggregation Receptor Antagonist Dose Investigation and Reperfusion Gain in Myocardial Infarction (PARADIGM) study is a randomized, placebo-controlled study of Lamifiban in 400 patients receiving thrombolysis as treatment for acute myocardial infarction. By studying 90-minute angiography, platelet aggregation, continuous electrocardiography, and clinical outcome in PARADIGM, important insights will be obtained to determine the optimal dose of Lamifiban for phase III study. We provide the background and rationale for the study of Lamifiban in PARADIGM and other ongoing studies in acute coronary syndromes.

Journal Article↗
PubMed2004

IL-6 levels in acute and post myocardial infarction: their relation to CRP levels, infarction size, left ventricular systolic function, and heart failure.

BACKGROUND: Inflammatory mechanisms in heart disease are of great interest. The proinflammatory cytokine interleukin (IL) 6 has been linked to increased morbidity in unstable angina pectoris and depressed myocardial function in heart failure (HF). METHODS: We studied the relation of IL-6 levels to C-reactive protein (CRP), infarction size, left ventricular function, and HF in acute myocardial infarction (MI) and after hospital discharge in 31 consecutive patients (19 males, mean age 69+/-13 years). Blood sampling for IL-6 was performed on admittance, four times on day 1, twice on day 2, and once daily on days 3-5, and 6 and 12 weeks later. Clinical signs of HF were evaluated daily during hospitalization and after 6 and 12 weeks. Echocardiography was performed on day 3 and at 6 weeks. RESULTS: IL-6 showed a curved time course with elevated levels already on admittance (mean+/-S.D. 19.3+/-26.9 ng/l), thereafter increasing to a peak on days 1 and 2 (maximum 68.5+/-152.9 ng/l), and then declining rapidly to lower, although not normalized, levels during hospitalization and at 6 and 12 weeks. CRP showed a similar time pattern, but with a later peak and a seemingly less rapid decline in levels. Mean levels of IL-6 and CRP on days 1-5 correlated highly (r=0.794, p<0.0001). IL-6 and infarction size did not correlate. HF during hospitalization and at 6 weeks was not related to IL-6; however, patients with HF at 12 weeks had higher IL-6 levels, both at 6 and 12 weeks. Patients on ACE inhibitors or diuretics at discharge had higher IL-6 levels at 6 weeks. IL-6 during hospitalization was not related to LVF; yet, patients with depressed LVF in the hospital and at 6 weeks had higher IL-6 levels at 6 and 12 weeks. CONCLUSIONS: IL-6 in acute MI shows a curved time course and is highly correlated to CRP. It peaks on days 1 and 2 and remains elevated even after 12 weeks. Increased IL-6 levels after hospital discharge are associated with HF and depressed LVF. Whether anti-inflammatory agents will influence left ventricular dysfunction and outcome postacute MI has yet to be determined.

Journal Article↗
PubMed2004

Post-infarct left ventricular free wall rupture-not always a lethal complication of acute myocardial infarction.

Post-myocardial infarction cardiac rupture is an important complication and cause of death in the period following myocardial infarction. It is rarely diagnosed before death. However, early diagnosis is crucial as successful treatment is possible with surgery. A successful outcome is sometimes compromised by difficult anatomy or an extensive infarct. Presentation, diagnosis and treatment of cardiac rupture is reviewed in this article, and is illustrated by five cases of cardiac rupture.

Journal Article↗
PubMed1998

A Randomized, Blinded Study of Two Doses of Novastan(R) (Brand of Argatroban) Versus Heparin as Adjunctive Therapy to Recombinant Tissue Plasminogen Activator (Accelerated Administration) in Acute Myocardial Infarction: Rationale and Design of the Myocardial Infarction using Novastan(R) and T-PA (MINT) Study.

Thrombolytic therapy has become a standard treatment for selected patients with acute myocardial infarction (MI). Various thrombolytic agents have been shown to decrease mortality. However, current thrombolytic agents still suffer significant shortcomings, such as a low optimal reperfusion rate delayed reperfusion. and incomplete myocardial perfusion. Furthermore, cyclic flow variations and reocclu.sions remain a significant cause of late morbidity and mortality. In thrombolysis with tissue plasminogen activator (t-PA), heparin seems to play an important role. However, it has several features that suggest that it may not be the optimal adjunct to thrombolytics, including weak and indirect action on thrombin, little access to clot-bound thrombin, inhibition by acute-phase plasma proteins, and its direct stimulation of platelet aggregation. Argatroban (NOVASTAN(R)), a small-molecule, synthetic, direct thrombin inhibitor, has several potential advantages over heparin, and prior studies suggest superior thrombin inhibition with favorable pharmacokinetic and pharmacodynamic properties warranting further investigation The Myocardial Infarction using NOVASTAN (R) and t-PA (MINT) study is a phase II, single-blind, angiographic trial directly comparing heparin versus two doses of argatroban in 120 patients with ST-elevation MI who present within 6 hours of symptom onset. The primary objective of the MINT trial is to assess the TIMI grade 3 flow and TIMI Frame Count at 90 minutes after the initiation of t-PA. This trial will also evaluate the safety of the combination of t-PA, argatroban, and aspirin. The incidence of clinical or silent ischemia, will be monitored. All patients will be followed up to 30 days for the composite endpoint of death, nonfatal recurrent myocardial infarction, coronary artery bypass surgery, PTCA, recurrent ischemia, and shock/new-onset heart failure.

Journal Article↗
PubMed2006

Hemicraniectomy after middle cerebral artery infarction with life-threatening Edema trial (HAMLET). Protocol for a randomised controlled trial of decompressive surgery in space-occupying hemispheric infarction.

BACKGROUND: Patients with a hemispheric infarct and massive space-occupying brain oedema have a poor prognosis. Despite maximal conservative treatment, the case fatality rate may be as high as 80%, and most survivors are left severely disabled. Non-randomised studies suggest that decompressive surgery reduces mortality substantially and improves functional outcome of survivors. This study is designed to compare the efficacy of decompressive surgery to improve functional outcome with that of conservative treatment in patients with space-occupying supratentorial infarction METHODS: The study design is that of a multi-centre, randomised clinical trial, which will include 112 patients aged between 18 and 60 years with a large hemispheric infarct with space-occupying oedema that leads to a decrease in consciousness. Patients will be randomised to receive either decompressive surgery in combination with medical treatment or best medical treatment alone. Randomisation will be stratified for the intended mode of conservative treatment (intensive care or stroke unit care). The primary outcome measure will be functional outcome, as determined by the score on the modified Rankin Scale, at one year.

Journal Article↗
PubMed2004

Allograftic bone marrow-derived mesenchymal stem cells transplanted into heart infarcted model of rabbit to renovate infarcted heart.

OBJECTIVE: To investigate the directed transplantation of allograftic bone marrow-derived mesenchymal stem cells (MSCs) in myocardial infarcted (MI) model rabbits. MATERIALS AND METHODS: Rabbits were divided into 3 groups, heart infarcted model with MSCs transplanted treatment (MSCs group, n = 12), heart infarcted model with PBS injection (control group, n = 20), sham operation with PBS injection (sham group, n = 17). MSCs labelled by BrdUrd were injected into the MI area of the MSCs group. The same volume of PBS was injected into the MI area of the control group and sham group. The mortality, LVIDd, LVIDs and LVEF of the two groups were compared 4 weeks later. Tropomyosin inhibitory component (Tn I) and BrdUrd immunohistochemistry identified the engrafted cells 4 weeks after transplantation. RESULT: The mortality of the MSCs group was 16.7% (2/12), and remarkably lower than the control group's mortality [35% (7/20) (P < 0.05)]. Among the animals that survived for 4 weeks, the LVIDd and LVIDs of the MSCs group after operation were 1.17+/-0.21 cm and 0.74+/-0.13 cm, and remarkably lower than those of the model group, which were 1.64+/-0.14 cm and 1.19+/-0.12 cm (P < 0.05); the LVEF of the MSCs group after operation was 63+/-6%, and remarkably higher than that of the model group, which was 53+/-6% (P < 0.05). Among the 10 cases of animals that survived for 4 weeks in the MSCs group, in 8 cases (80%), the transplanted cells survived in the non MI, MI region and its periphery, and even farther away; part of them differentiated into cardiomyocytes; in 7 cases (70%), the transplanted cells participated in the formation of blood vessel tissue in the MI region. CONCLUSION: Transplanted allograftic MSCs can survive and differentiate into cardiomyocytes, form the blood vessels in the MI region. MSCs transplantation could improve the heart function after MI.

Animals↗
PubMed1996

Stenting of the Infarct-Related Artery During Complicated Angioplasty in Acute Myocardial Infarction.

The aim of this study was to assess safety and efficacy of coronary stenting as a strategy for improving PTCA suboptimal angiographic result. From March 1993 to December 1995, 104 patients underwent PTCA during acute myocardial infarction. Unplanned coronary stenting was required in 66 pts (63.5%). Procedural success was obtained in 64 pts (97%). Two patients had an unsuccessful stenting procedure: one patient for a suboptimal stent deployment and another for LAD reocclusion requiring emergency CABG (1.5%). Palmaz-Schatz stents were used in 60 pts (91%) and AVE micro-stent in 6 pts (9%). During the hospital course, subacute reocclusion of the vessel occurred in 3 pts (4.6%); one patient underwent a successful rePTCA while the other two underwent CABG. Two patients had vascular groin complications requiring surgical repair of the femoral artery. During hospitalization, one patient underwent elective CABG for early residual myocardial ischemia. At seventy-two hours from PTCA, one patient (1.5%) died as a result of intestinal infarct. Six months survival rate was 98.3% for 59 pts discharged alive from our department. Ten pts were symptomatic during the follow-up: One patient underwent PTCA on another vessel and the other underwent CABG for a multivessel disease. CABG was used in one patient who presented residual silent ischemia in multivessel coronary artery disease. At six months, the first group of patients (18 pts) underwent planned coronary angiography: Vessel patency was present in 17 patients. One patient had an asymptomatic reocclusion of the treated vessel. This study shows a good angiographic result obtained with intracoronary stenting during primary or rescue PTCA of the infarct-related artery. It does not appear to increase major in-hospital adverse events and may reduce the need for surgical revascularization, reducing in-hospital mortality rate and favorably affecting LVEF.

Journal Article↗