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PubMed1995

Acute myocardial infarction--the angiographic picture: new insights into the pathogenesis of myocardial infarction.

The angiographic appearance of the coronary arteries were examined in 302 patients with stable angina pectoris and compared to 308 patients with acute myocardial infarction, who received high-dose intravenous thrombolytic therapy, in order to elucidate the underlying angiopathological picture in the two diseases. In each group coronary lesions were present in proximal segments of the arteries and were closely related to bifurcations. Lesions were more extensively distributed in the coronary tree in patients with stable angina and they had an average of 5.4 lesions per patient, compared to the acute myocardial infarction group who had only 2.4 lesions. Also, in the acute myocardial infarction patients, four-fifths of the culprit arteries were patent, 104 (34%) had a ruptured plaque, 22 (7%) had an ulcerated plaque and in 190 (62%) the lesions were eccentric. The study shows that patients with myocardial infarction who are suitable for thrombolysis have a unique coronary angiographic picture and the acute episode is caused by sudden rupture of a localized atheromatous plaque which initiates an obstructive thrombotic cascade.

Angina Pectoris↗
PubMed1989

Thrombolysis and Angioplasty in Myocardial Infarction (TAMI-1) trial: influence of infarct location on arterial patency, left ventricular function and mortality.

The influence of infarct location on arterial patency, left ventricular function and mortality after 150 mg of intravenous recombinant tissue-type plasminogen activator (rt-PA) and selective coronary angioplasty was studied in 386 patients with acute myocardial infarction. In 329 patients with acute and 1 week angiograms, the 90 min infarct-related artery patency rate after rt-PA in the left anterior descending, the left circumflex and the right coronary artery was 77, 68 and 68%, respectively. Angioplasty, performed in half the patients, resulted in a final acute patency rate of 93%, which was not related to arterial distribution. Repeat catheterization and revascularization were required in 12% of patients before day 7 and were independent of arterial distribution. The reocclusion rate for the right coronary artery (21%) was higher than that for the left anterior descending (12%) or left circumflex (5%) artery (p = 0.01). Acute and 1 week contrast ventriculograms suitable for analysis were available in 266 patients. Whereas serial left ventricular ejection fraction did not improve during the course of this study, serial regional wall motion (centerline chord method) improved in each arterial distribution. The in-hospital mortality rate of 6% was not related to arterial distribution, although death was twice as likely with proximal compared with distal lesions. Ten of 11 patients who died in the group with the left anterior descending artery as the infarct-related artery had a lesion proximal to the first septal perforator branch.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Clinical importance of thrombocytopenia occurring in the hospital phase after administration of thrombolytic therapy for acute myocardial infarction. The Thrombolysis and Angioplasty in Myocardial Infarction Study Group.

OBJECTIVES: The purpose of this study was to examine the incidence and clinical implications of thrombocytopenia that occurs in hospital after administration of thrombolytic therapy for acute myocardial infarction. BACKGROUND: The use of thrombolytic therapy in patients with acute myocardial infarction has improved mortaltiy rates, but hemorrhage remains a major complication. Because thrombocytopenia may be associated with hemorrhage after thrombolytic therapy, we examined the incidence and clinical implications of thrombocytopenia after administration of thrombolytic therapy for acute myocardial infarction. METHODS: The patient population comprised 1,001 patients enrolled in Phases 2, 3 and 5 of the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) trial and the urokinase trial. Patients received recombinant tissue-type plasminogen activator, urokinase or combination therapy in various dosing schemes. All patients received heparin, aspirin and a calcium-channel blocking agent. Thrombocytopenia occurring anytime after thrombolytic therapy was defined as a nadir platelet count either < 100,000/microliters or < 1/2 baseline. Blood loss was quantified by a bleeding index. Multiple logistic regression was used to evaluate the independent contribution of thrombocytopenia in a model predicting in-hospital mortality. RESULTS: Thrombocytopenia occurred in 16.4% of patients, with no difference among the thrombolytic regimens. Patients with thrombocytopenia had a lower median acute ejection fraction and a higher likelihood of three-vessel coronary artery disease than patients without thrombocytopenia. Patients with thrombocytopenia had more hemorrhage, a higher in-hospital mortality rate and a more complicated hospital course than patients without thrombocytopenia, even after consideration of other important variables, including age, acute ejection fraction, number of diseased vessels, bypass surgery and use of intraaortic balloon counterpulsation. CONCLUSIONS: Thrombocytopenia after thrombolytic therapy is a common event and is associated with excess hemorrhage and mortality. Platelet counts should be monitored daily after administration of thrombolytic therapy because the appearance of thrombocytopenia identifies a subset of patients at increased risk for hemorrhage and death.

Aged↗
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↗
PubMed2005

Preprocedural Thrombolysis in Myocardial Infarction (TIMI) flow significantly affects the extent of ST-segment resolution and myocardial blush in patients with acute anterior myocardial infarction treated by primary angioplasty.

BACKGROUND: Although the benefits of primary angioplasty for ST-segment elevation myocardial infarction (STEMI) have been demonstrated, the prognostic role of early recanalization in these patients has yet to be investigated. The aim of the study was to evaluate the impact of preprocedural Thrombolysis in Myocardial Infarction (TIMI) flow on the extent of myocardial reperfusion in patients with anterior STEMI treated with primary angioplasty. METHODS: Our population consisted of 754 consecutive patients with anterior STEMI treated by primary angioplasty from April 1997 to October 2001. All angiographic, clinical, and follow-up data were prospectively collected. RESULTS: Preprocedural TIMI flow was related to postprocedural TIMI 3 flow (P < .0001), ST-segment resolution (P = .009), myocardial blush grade (P < .0001), enzymatic infarct size (P < .0001), and predischarge ejection fraction (P < .0001), even in the analysis restricted to patients with postprocedural TIMI 3 flow. These data explain the observed significant impact of preprocedural TIMI flow on 1-year mortality. CONCLUSIONS: This study shows that in patients with anterior STEMI, poor preprocedural TIMI flow is associated with impaired perfusion, larger infarct size, and 1-year mortality. This study suggests that all efforts should be made to obtain optimal restoration of antegrade flow as early as possible before angioplasty. Further studies are needed to investigate the impact of early adjunctive pharmacological therapy on preprocedural TIMI flow and mortality in these high-risk patients.

Angioplasty↗
PubMed2005

A randomized trial comparing clopidogrel versus ticlopidine therapy in patients undergoing infarct artery stenting for acute myocardial infarction with abciximab as adjunctive therapy.

AIM: To evaluate the impact of a clopidogrel therapy on the effectiveness of myocardial reperfusion in patients with ST-segment elevation acute myocardial infarction (AMI) undergoing routine infarct-related artery (IRA) stent implantation and receiving routine abciximab therapy. BACKGROUND: Inflammatory processes after mechanical restoration of flow in AMI play a central role in decreasing the effectiveness of reperfusion at microcirculatory level. Several studies suggest that clopidogrel may exert a protective effect against adverse cardiovascular events by virtue of its anti-inflammatory properties. METHODS: A total of 133 patients with a first ST-elevation AMI were randomized to clopidogrel (600-mg loading dose before IRA stenting followed by 75 mg daily, n = 66) or ticlopidine (500 mg before IRA stenting followed by 250 mg twice daily, n = 67). The primary end point was scintigraphic infarct size at 1 month. The secondary end points were ST-segment elevation resolution within 3 hours of procedure and 1-month clinical outcome, as a composite of death, reinfarction, target vessel revascularization, and stroke within 1 month of the index procedure. RESULTS: The 1-month technetium 99m sestamibi scintigraphy revealed similar infarct size (16.2% +/- 14.6% vs 15.0% +/- 14.1%, P = .703) and severity (0.48 +/- 0.18 vs 0.49 +/- 0.15, P = .592) in the clopidogrel group as compared with the ticlopidine group. Three-hour ST-segment resolution rate was similar in the 2 study groups (86% vs 89%, P = .642). At 1 month, there was no difference in major cardiovascular adverse event rate (3% vs 3%, P = .988). Discontinuation of thienopiridine therapy within the first month occurred in no patient randomized to clopidogrel and in 3 (4.5%) patients randomized to ticlopidine (P = .082). CONCLUSION: Clopidogrel has no impact on the effectiveness of myocardial reperfusion in patients with AMI treated routinely with stenting and abciximab. However, clopidogrel, administered as a 600-mg loading dose followed by 75 mg daily, is safe and at least as effective as the standard ticlopidine therapy in this subgroup of patients.

Abciximab↗
PubMed2006

What is the frequency and functional and clinical significance of complex lesions in non-infarct-related arteries after fibrinolysis for acute ST-elevation myocardial infarction?

BACKGROUND: Observational data suggest that the diffuse inflammatory nature of coronary disease may be expressed by the presence of unstable coronary lesions in multiple vessels in patients with acute myocardial infarction. The aim of our study was to investigate the existence of complex lesions in nonculprit vessels in patients with ST-elevation myocardial infarction and to assess their clinical and functional significance. METHODS: We evaluated 974 non-infarct-related arteries (nIRAs) in 439 patients presenting within 6 hours of acute ST-elevation myocardial infarction. Coronary angiograms and electrocardiograms (ECGs) were obtained 60 minutes after fibrinolysis and systematically analyzed in core angiographic and ECG laboratories. Complex lesions in nIRA were identified according to prior criteria, that is, stenosis > 50% with one of the following: overhanging edges, markedly irregular borders, ulceration, or thrombus. RESULTS: Complex lesions were identified in 85 (8.7%) of 974 nIRAs. Seventy-three (16.7%) of 439 patients had at least 1 complex lesion in a nIRA, with 10 of the 73 patients having > 1 nIRA affected. There were no differences in baseline total ST deviation on the qualifying ECG between patients with or without nIRA complex lesions. TIMI 3 flow in nIRAs occurred less frequently in vessels with complex lesions (50.8% vs 81.5%, P < .001), a difference maintained when nIRAs with stenosis between 50% and 99% were analyzed (P < .006). Patients with nIRA complex lesions had a higher inhospital incidence of congestive heart failure (16.4% vs 6.3%, P = .007) and a trend toward more recurrent ischemia (13.7% vs 7.4%, P = .102). CONCLUSION: These findings provide new evidence supportive of the concept that active coronary lesions occur simultaneously in > 1 vessel, while also attesting to their functional and clinical significance.

Adolescent↗
PubMed2006

Antecedent left ventricular mass and infarct size in ST-elevation myocardial infarction.

BACKGROUND: Increased left ventricular mass index (LVMI) is associated with a greater incidence of acute myocardial infarction (AMI), but there are no data regarding its impact on infarct size. OBJECTIVES: The objective of this study was to determine whether LVMI impacts on infarct size. METHODS: We analyzed consecutive patients with a first ST-elevation AMI and successful reperfusion of the culprit artery who underwent an echocardiographic assessment of LVMI and regional wall motion score index (RWMSI) <72 hours post AMI. RESULTS: Of the 165 patients (76.4% men) with a mean age of 61.0 +/- 13.9 years, 53.9% had anterior wall involvement and 59.3% had increased LVMI. There were no significant differences in baseline characteristics between patients with and without increased LVMI, except for a greater prevalence of hypertension among patients with increased LVMI (44.0% vs 22.4%, P < .001). The distributions of anterior wall AMI location and culprit artery involvement were similar between the groups. Patients with increased LVMI were more likely to present with single-vessel coronary artery disease (P = .04) and heart failure upon presentation (P = .03). There was no significant difference between patients with and without increased LVMI in peak creatine kinase (2106.8 +/- 1642.7 vs 2551.2 +/- 2357.4 U/L, P = .16) or RWMSI (1.62 +/- 0.44 vs 1.61 +/- 0.38, P = .91). In addition, no correlation was observed between LVMI as a continuous variable and RWMSI (r = 0.11, P = .18) or peak creatine kinase values (r = 0.02, P = .81). CONCLUSIONS: Among patients with a first ST-elevation AMI and successful reperfusion, antecedent increased LVMI was fairly common and did not impact on infarct size.

Aged↗
PubMed2005

Usefulness of the presence of peripheral vascular disease in predicting mortality in acute myocardial infarction patients treated with primary angioplasty (from the Primary Angioplasty in Myocardial Infarction Database).

Patients with acute myocardial infarction (AMI) often have multiple co-morbidities that influence outcome. We sought to evaluate the impact of peripheral vascular disease (PVD) on the outcome of patients with AMI treated with primary angioplasty. We evaluated 3,716 patients with AMI who underwent emergency catheterization with planned primary angioplasty in the Primary Angioplasty in Myocardial Infarction trials. Patients with a history of PVD (claudication, stroke, or transient ischemic attack) were compared with patients without PVD. Of the 3,716 patients, 394 (10.6%) had PVD and were older, more often women, and more frequently had a history of diabetes mellitus, hypertension, smoking, congestive heart failure, angina, myocardial infarction, and coronary revascularization. They presented more often with a heart rate >100 beats/min, Killip class >1, lower ejection fraction, and multivessel disease. No difference was found in stent use, final percentage of stenosis, or Thrombolysis In Myocardial Infarction 3 flow. Patients with PVD had a twofold increased in-hospital mortality (5.3% vs 2.6%, p = 0.0021). The difference remained significant at 1 month, 6 months, and 1 year (12.6% vs 6%, p < 0.0001). In multivariate logistic regression analysis, a history of PVD was an independent predictor of in-hospital mortality and death at 1 year (odds ratio 1.64, 95% confidence interval 1.04 to 2.57, p = 0.032). In conclusion, patients with AMI with PVD have increased co-morbidities and higher mortality despite treatment with primary angioplasty. The presence of PVD is an independent predictor of in-hospital mortality and death at 1 year.

Aged↗
PubMed2006

Time course of microvascular resistance of the infarct and noninfarct coronary artery following an anterior wall acute myocardial infarction.

Previous studies have suggested that coronary flow velocity reserve (CFVR) in the early phase of acute myocardial infarction (AMI) is abnormal in infarcted and remote regions. This study determined the coronary microvascular resistance of infarct-related arteries (IRAs) and non-IRAs during AMI and at follow-up in patients who were treated with primary percutaneous intervention. In 73 patients with a first anterior wall AMI, baseline and minimal microvascular resistance in IRAs and non-IRAs immediately after reperfusion and at 1-week and 6-month follow-up were calculated as the ratio of mean transvascular pressure gradient to mean baseline and to adenosine-induced hyperemic blood flow velocity, respectively. CFVR in IRAs increased from 1.6 +/- 0.4 after reperfusion to 1.9 +/- 0.5 at 1 week and to 3.0 +/- 0.8 at 6 months (p <0.0001) and in non-IRAs from 2.4 +/- 0.5 to 2.7 +/- 0.6 at 1 week to 3.3 +/- 0.6 at 6 months (p <0.0001). Minimal microvascular resistance in IRAs and non-IRAs (3.2 +/- 1.7 and 2.2 +/- 0.6 mm Hg/second/cm, respectively) decreased significantly at follow-up (2.0 +/- 0.6 and 1.7 +/- 0.6 mm Hg/second/cm at 1 week and 1.8 +/- 0.6 and 1.8 +/- 0.7 mm Hg/second/cm at 6 months, respectively). After correction for rate-pressure product, baseline microvascular resistance after reperfusion and at 6 months did not significantly differ between IRAs and non-IRAs. In conclusion, minimal microvascular resistance is higher in infarcted and noninfarcted regions during AMI than at follow-up. The low CFVR in remote regions during AMI is probably due more to disturbed autoregulation than to increased myocardial workload.

Adult↗
PubMed2006

Uridine-5'-triphosphate (UTP) reduces infarct size and improves rat heart function after myocardial infarct.

We have previously found that uridine 5'-triphosphate (UTP) significantly reduced cardiomyocyte death induced by hypoxia via activating P2Y(2) receptors. To explore the effect of UTP following myocardial infarction (MI) in vivo we studied four groups: sham with or without LAD ligation, injected with UTP (0.44microg/kg i.v.) 30min before MI, and UTP injection (4.4microg/kg i.v.) 24h prior to MI. Left ventricular end diastolic area (LVEDA), end systolic area (LVESA) fractional shortening (FS), and changes in posterior wall (PW) thickness were performed by echocardiography before and 24h after MI. In addition, we measured different biochemical markers of damage and infarct size using Evans blue and TTC staining. The increase in LVEDA and LVESA of the treated animals was significantly smaller when compared to the MI rats (p<0.01). Concomitantly, FS was higher in groups pretreated with UTP 30min or 24h (56+/-14.3 and 36.7+/-8.2%, p<0.01, respectively). Ratio of infarct size to area at risk was smaller in the UTP pretreated hearts than MI rats (22.9+/-6.6, 23.1+/-9.1%, versus 45.4+/-7.6%, respectively, p<0.001). Troponin T and ATP measurements, demonstrated reduced myocardial damage. Using Rhod-2-AM loaded cardiomyocytes, we found that UTP reduced mitochondrial calcium levels following hypoxia. In conclusion, early or late UTP preconditioning is effective, demonstrating reduced infarct size and superior myocardial function. The resulting cardioprotection following UTP treatment post ischemia demonstrates a reduction in mitochondrial calcium overload, which can explain the beneficial effect of UTP.

Adenosine Triphosphate↗
PubMed2004

Preinfarction angina does not alter infarct size and in hospital outcome after acute myocardial infarction with ST elevation.

BACKGROUND: Preinfarction angina has been reported to limit infarct size, in a manner analogous to experimental preconditioning. However, other studies have reported inconsistent results. We aimed to investigate prospectively the role of preinfarction angina on infarct size and in hospital outcome. METHODS: Ninety-nine patients were divided into three groups according to the timing of angina: the group "< 48 h" reported angina within the last 48 h, the group "> 48 h" earlier than 48 h and the group "acute" no angina before infarction. Myocardial injury was estimated by creatine kinase, creatine kinase-MB, troponin I and C-reactive protein. In hospital events included death, recurrent ischemia, congestive heart failure and atrioventricular block. RESULTS: Clinical characteristics, thrombolysis administration and the magnitude of enzymes released were not statistically different among the three groups: peak creatine kinase was 2139+/-1714 U/l for the >48 h group, vs. 2344+/-1634 U/l for the acute group, vs. 2209+/-1384 U/l for the <48 h group (p=0.88). Peak creatine kinase-MB was 124+/-104 U/l for the >48 h group, vs. 168+/-182 U/l for the acute group, vs. 154+/-108 U/l for the <48 h group (p=0.62). Peak troponin I, peak C-reactive protein and in hospital outcome also did not differ statistically in the three groups; p=0.5, p=0.45. CONCLUSIONS: Infarct size estimated by cardiac enzymes and by the marker of C-reactive protein, as well as in hospital clinical prognosis are not different in patients with and without preinfarction angina. It seems, therefore, that preinfarction angina confers ischemic conditions inadequate to mimic preconditioning.

Angina, Unstable↗
PubMed2004

Significance of exercise-induced ST segment elevation in Q leads in patients with a recent myocardial infarction and an open infarct-related artery Analysis with angiography, intracoronary myocardial contrast echocardiography and cardiac magnetic resonance.

AIMS: The significance of exercise-induced ST segment elevation in Q leads in patients with a recent myocardial infarction and without significant residual stenosis in the infarct-related artery has not been defined. We aimed to elucidate the role of myocardial perfusion and viability in this scenario. METHODS AND RESULTS: Sixty-six patients with a first myocardial infarction, single-vessel disease and an open artery were studied. Myocardial perfusion was assessed with angiographic blush, intracoronary myocardial contrast echocardiography and magnetic resonance. Myocardial viability was quantified by means of magnetic resonance (transmural extent of necrosis). Exercise-induced ST elevation in Q leads was observed only in 13 cases (20%); 53 patients (80%) did not show this finding. The group with ST elevation had fewer cases with normal perfusion: Blush 3 (15% vs. 74%, p=0.001), myocardial contrast echocardiography score >0.75 (8% vs. 81%, p=0.001) and magnetic resonance score >0.75 (31% vs. 68%, p=0.03). Similarly, myocardial viability (necrosis <50%) was less frequent in patients with ST elevation (8% vs. 72%, p=0.001). CONCLUSION: In patients with a first myocardial infarction and without residual ischemia, exercise-induced ST segment elevation in Q leads is an uncommon finding and it is related to a more damaged coronary microcirculation and to less viable myocardium.

Angioplasty, Balloon, Coronary↗
PubMed2005

Excess weight at time of presentation of myocardial infarction is associated with lower initial mortality risks but higher long-term risks including recurrent re-infarction and cardiac death.

OBJECTIVES: To evaluate the influence of elevated body mass index (BMI) on short- and long-term survival following acute myocardial infarction (AMI). BACKGROUND: Recent studies suggest an obesity survival paradox in individuals undergoing percutaneous coronary intervention with better 30-day and 1-year outcomes in obese relative to normal weight patients. We tested a similar obesity paradox hypothesis following acute myocardial infarction. METHODS: Short- and long-term all-cause mortality, and risk of recurrent AMI were evaluated according to BMI status in 894 consecutive survivors of AMI <80 years of age admitted to the Mayo Clinic Coronary Care Unit between January 1, 1988 and April 16, 2001. Normal weight, overweight and obesity were defined as BMI <25, 25-29.9, and >30 kg/m(2), respectively. RESULTS: Overall mortality following hospital discharge was significantly lower in overweight and obese patients and was mostly attributable to lower 6-month mortality (adjusted HR = 0.47, P = 0.01 for BMI >25 kg/m(2)) relative to normal weight patients, while long-term mortality among 6-month survivors was similar in all 3 groups. The risk of recurrent AMI was higher in patients with BMI >25 kg/m(2) (adjusted HR = 2.30, P = 0.01). Overweight and obese patients were significantly more likely to die from cardiac rather than non-cardiac causes (P < 0.01). CONCLUSIONS: Following AMI, overweight and obese individuals although paradoxically protected from short-term death have a long-term mortality risk that is similar to normal weight individuals. Younger age at the time of initial infarction and fewer non-cardiovascular comorbidities presumably explain the short-lived obesity survival paradox following myocardial infarction.

Aged↗
PubMed2003

A randomized trial comparing primary infarct artery stenting with or without abciximab in acute myocardial infarction.

OBJECTIVES: We sought to evaluate the efficacy of abciximab as adjunctive therapy to routine infarct-related artery (IRA) stenting. BACKGROUND: The impact of abciximab on the efficacy of myocardial reperfusion and the outcome of patients with acute myocardial infarction (AMI) undergoing IRA stenting have not yet been defined. METHODS: In a randomized trial, we assigned 400 patients with AMI to undergo IRA stenting alone or stenting plus abciximab. The primary end point was a composite of death, reinfarction, target vessel revascularization (TVR), and stroke at one month. RESULTS: The incidence of the primary end point was lower in the abciximab group than in the stent only group (4.5% and 10.5%, respectively; p = 0.023), and randomization to abciximab was independently related to the risk of the primary end point (odds ratio 0.41, 95% confidence interval 0.17 to 0.97; p = 0.041). Early ST-segment resolution was more frequent in the abciximab group (85% vs. 68%, p < 0.001). Infarct size, as assessed by one-month technetium-99m sestamibi scintigraphy, revealed smaller infarcts in the abciximab group. At six months, the cumulative difference in mortality between the groups increased (4.5% vs. 8%), and the incidence of the composite of six-month death and reinfarction was lower in the abciximab group than in the stent only group (5.5% and 13.5%, respectively; p = 0.006). Six-month repeat TVR and restenosis rates were similar in the two groups. CONCLUSIONS: Abciximab plus IRA stenting should be considered the routine reperfusion strategy in patients with AMI undergoing primary percutaneous mechanical revascularization, especially in high-risk patients.

Abciximab↗
PubMed2006

Thrombus aspiration before primary angioplasty improves myocardial reperfusion in acute myocardial infarction: the DEAR-MI (Dethrombosis to Enhance Acute Reperfusion in Myocardial Infarction) study.

OBJECTIVES: This study sought to test the hypothesis that thrombus removal, with a new manual thrombus-aspirating device, before primary percutaneous coronary intervention (PPCI) may improve myocardial reperfusion compared with standard PPCI in patients with ST-segment elevation acute myocardial infarction (STEMI). BACKGROUND: In STEMI patients, PPCI may cause thrombus dislodgment and impaired microcirculatory reperfusion. Controversial results have been reported with different systems of distal protection or thrombus removal. METHODS: One-hundred forty-eight consecutive STEMI patients, admitted within 12 h of symptom onset and scheduled for PPCI, were randomly assigned to PPCI (group 1) or manual thrombus aspiration before standard PPCI (group 2). Patients with cardiogenic shock, previous infarction, or thrombolytic therapy were excluded. Primary end points were complete (>70%) ST-segment resolution (STR) and myocardial blush grade (MBG) 3. RESULTS: Baseline clinical and angiographic characteristics were similar in the 2 groups. Comparing groups 1 and 2: complete STR 50% versus 68% (p < 0.05); MBG-3 44% versus 88% (p < 0.0001); coronary Thrombolysis In Myocardial Infarction (TIMI) flow grade 3 78% versus 89% (p = NS); corrected TIMI frame count 21.5 +/- 12 versus 17.3 +/- 6 (p < 0.01); no reflow 15% versus 3% (p < 0.05); angiographic embolization 19% versus 5% (p < 0.05); direct stenting 24% versus 70% (p < 0.0001); and peak creatine kinase-mass band fraction 910 +/- 128 mug/l versus 790 +/- 132 mug/l (p < 0001). In-hospital clinical events were similar in the 2 groups. After adjusting for confounding factors, multivariate analysis showed thrombus aspiration to be an independent predictor of complete STR and MBG-3. CONCLUSIONS: Manual thrombus aspiration before PPCI leads to better myocardial reperfusion and is associated with lower creatine kinase mass band fraction release, lower risk of distal embolization, and no reflow compared with standard PPCI. (Thrombus Aspiration Before Standard Primary Angioplasty Improves Myocardial Reperfusion in Acute Myocardial Infarction; http://clinicaltrials.gov/ct/show/NCT00257153).

Angioplasty, Balloon, Coronary↗
PubMed2005

The clinico-radiologic properties of deep small basal ganglia infarction: lacune or small striatocapsular infarction?

OBJECTIVE: Deep small basal ganglia infarction (DSBI) cannot be clearly classified as either lacune or striatocapsular infarction by their sizes only. We tried to elucidate clinical and other properties of DSBI to understand better in pathophysiology of ischemic lesion of basal ganglia. METHODS: We analyzed 36 patients with acute ischemic lesion of basal ganglia with the size varying from 1.5 to 3 cm in maximal diameters. We assessed clinical features, laboratory data, risk factors of stroke, and radiologic findings such as MRI and MR angiography. RESULTS: Patients with DSBI could be largely divided into two distinctive groups, small infarction with cortical sign (SICS) and lacunar syndrome (LS) according to their presence of cortical manifestations. Total of 11 patients were in SICS group and they showed cortical manifestations such as eyeball deviation, visual field defect, aphasia and neglect. They also showed severer non-cortical neurologic deficit compared with LS group. Whereas LS group showed various MRA patterns, 7 patients of SICS group (63.6%) showed proximal MCA stenosis in MRA. CONCLUSIONS: We found that many patients with DSBI could have the features of either lacune or striatocapsular infarction. Although they have similar morphologic characteristics but they are presumed to have different pathophysiologic mechanism.

Adult↗
PubMed2005

Cell transplantation preserves cardiac function after infarction by infarct stabilization: augmentation by stem cell factor.

OBJECTIVE: We hypothesized that implantation of adult mesenchymal stem cells after acute myocardial infarction mobilizes bone marrow precursor cells by activating the stem cell factor pathway, and that overdriving this pathway would enhance the beneficial effects of cell transplantation. METHODS: After coronary ligation, medium, mesenchymal stem cells, or stem cell factor-overproducing mesenchymal stem cells were injected into the anterior left ventricle. Cells from beta-galactosidase transgenic mice enabled tracking of injected cells. The global and local impact of the cells was evaluated by measuring cytokine levels, endothelial progenitor cells, and myocardial angiogenesis, and by addressing cardiomyogenesis with confocal microscopy. The impact on cardiac function was evaluated by pressure-volume loops. Ventricular morphometrics were measured after in situ perfusion-fixation of the hearts at physiologic pressures. RESULTS: Implantation of mesenchymal stem cells increased myocardial stem cell factor levels 2.0-fold, endothelial progenitor cell mobilization 2.7-fold, and myocardial angiogenesis 2.3-fold (P < .05), but did not induce mitogenesis in host cardiomyocytes or give rise to beta-galactosidase-expressing cardiomyocytes. Cell-transplanted groups had improved indices of cardiac function, including preload recruitable stroke work and end-systolic elastance (P < .001). Cell transplantation resulted in 2.0-fold smaller ventricular volumes (P = .001) and 2.0-fold reduced infarct scar area (P = .056), but had no effect on the volume of spared myocardium. Stem cell factor overproduction imparted greater functional benefit without inducing detectable histologic cardiomyocyte regeneration. CONCLUSION: Mesenchymal stem cell implantation after myocardial infarction facilitates functional cardiac regeneration without myocyte regeneration through augmentation of endogenous infarct repair, which is enhanced by stem cell factor.

Animals↗