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PubMed2005

Randomized evaluation of the effects of filter-based distal protection on myocardial perfusion and infarct size after primary percutaneous catheter intervention in myocardial infarction with and without ST-segment elevation.

BACKGROUND: In acute myocardial infarction, distal embolization of debris during primary percutaneous catheter intervention may curtail microvascular reperfusion of the infarct region. Our randomized trial investigated whether distal protection with a filter device can improve microvascular perfusion and reduce infarct size after primary percutaneous catheter intervention. METHODS AND RESULTS: We enrolled 200 patients who had angina within 48 hours after onset of pain plus at least 1 of 3 additional criteria: ST-segment elevation, elevated myocardial marker proteins, and angiographic evidence of thrombotic occlusion. Among the patients included (83% men; mean age, 62+/-12 years), 100 were randomly assigned to the filter-wire group and 100 to the control group. The primary end point was the maximal adenosine-induced Doppler flow velocity in the recanalized infarct artery; the secondary end point was infarct size estimated by the volume of delayed enhancement on nuclear MRI. ST-segment elevation myocardial infarction was present in 68.5% of the patients; the median time from onset of pain was 6.9 hours. In the filter-wire group, maximal adenosine-induced flow velocity was 34+/-17 compared with 36+/-20 cm/s in the control group (P=0.46). Infarct sizes, assessed in 82 patients in the filter-wire group and 78 patients in the control group, were 11.8+/-9.3% of the left ventricular mass in the filter-wire group and 10.4+/-9.4% in the control group (P=0.33). Thirty-day mortality was 2% in filter-wire group and 3% in the control group. CONCLUSIONS: The filter wire as an adjunct to primary percutaneous catheter intervention in myocardial infarction with and without ST-segment elevation did not improve reperfusion or reduce infarct size.

Aged↗
PubMed2006

Characterization of the peri-infarct zone by contrast-enhanced cardiac magnetic resonance imaging is a powerful predictor of post-myocardial infarction mortality.

BACKGROUND: Accurate risk stratification is crucial for effective treatment planning after myocardial infarction (MI). Previous studies suggest that the peri-infarct border zone may be an important arrhythmogenic substrate. In this pilot study, we tested the hypothesis that the extent of the peri-infarct zone quantified by contrast-enhanced cardiac magnetic resonance (CMR) is an independent predictor of post-MI mortality. METHODS AND RESULTS: We studied 144 patients with documented coronary artery disease and abnormal myocardial delayed enhancement (MDE) consistent with MI. A computer-assisted, semiautomatic algorithm quantified the total infarct size and divided it into the core and peri-infarct regions based on signal-intensity thresholds (>3 SDs and 2 to 3 SDs above remote normal myocardium, respectively). The peri-infarct zone was normalized as a percentage of the total infarct size (%MDE(periphery)). After a median follow-up of 2.4 years, 29 (20%) patients died. Patients with an above-median %MDE(periphery) were at higher risk for death compared with those with a below-median %MDE(periphery) (28% versus 13%, log-rank P<0.01). Multivariable analysis showed that left ventricular systolic volume index and %MDE(periphery) were the strongest predictors of all-cause mortality (adjusted hazard ratio [HR] for %MDE(periphery), 1.45 per 10% increase; P=0.002) and cardiovascular mortality (adjusted HR, 1.51 per 10% increase; P=0.009). Similarly, after adjusting for age and left ventricular ejection fraction, %MDE(periphery) maintained strong and independent associations with all-cause mortality (adjusted HR, 1.42; P=0.005) and cardiovascular mortality (adjusted HR, 1.49; P=0.01). CONCLUSIONS: In patients with a prior MI, the extent of the peri-infarct zone characterized by CMR provides incremental prognostic value beyond left ventricular systolic volume index or ejection fraction. Infarct characteristics by CMR may prove to be a unique and valuable noninvasive predictor of post-MI mortality.

Aged↗
PubMed1987

Steroid administration after myocardial infarction promotes early infarct expansion. A study in the rat.

Whether steroids lead to thinner scars and larger aneurysms by delaying collagen deposition or worsening infarct expansion before significant collagen deposition begins is unknown. Rats underwent either transmural infarction by left coronary ligation or sham operation. Both infarct and sham rats were randomized to methylprednisolone 50 mg/kg i.p. X 4 or saline treatment within 24 h after operation. Sacrifice occurred before (3 d) or after (7 d) collagen deposition typically begins. Despite similar infarct size, infarct wall thickness was 1.35 +/- 0.08 mm in the saline and 0.99 +/- 0.12 mm in the methylprednisolone group (P less than 0.001) at 3 d. This decrease in wall thickness was explained by a decrease in the number of myocytes across the infarct wall (r = 0.99; P less than 0.001), suggesting that steroids promote myocyte slippage. Furthermore, methylprednisolone caused no further infarct thinning or cavity dilatation beyond 3 d. Thus, high-dose methylprednisolone given within 24 h after transmural infarction worsens infarct expansion before collagen is laid down by promoting the slippage of necrotic myocytes.

Animals↗
PubMed1993

Comparative effects of early and late reperfusion of the infarct-related coronary artery and collateral circulation which develops after infarction on left ventricular size and function.

This study assesses the effects of early and late reperfusion of the infarct-related coronary artery and collateral circulation developed after infarction on left ventricular morphology and function in 22 patients with a first acute anterior myocardial infarction and without long-standing preinfarction angina. The patients were categorized into 4 groups: group A-5 patients with successful reperfusion within 6 h after the onset of infarction: group B-6 patients with late patency of the infarct-related coronary artery; group C-6 patients without recanalization of the infarct-related coronary artery who had good collateral circulation (collateral index (CI) = 2 or 3); and group D-5 patients without recanalization who had either poor or no collateral circulation (CI = 0 or 1). The left ventricular size and function were evaluated by means of contrast left ventriculography during the chronic stage of infarction. The left ventricular global and regional functions were preserved better (p < 0.05) in group A than in the other three groups. Although there was no difference in regional wall motion of the infarct area among groups B, C and D, the ejection fraction was greater (p < 0.05) and the percentage perimetric circumference was smaller (p < 0.05) in groups B and C than in group D. Among the 4 groups, the left ventricular end-diastolic volume index tended to be greater in group D. Thus, these results suggest that blood supply to the infarct area is essential for the preservation of left ventricular size and function regardless of the timing and route.

Adult↗
PubMed1997

Effect of infarct-related artery patency and late potentials on late mortality after acute myocardial infarction.

OBJECTIVE: To assess the effect of patency of the infarct-related artery and the presence of late potentials on late cardiac mortality after myocardial infarction. MATERIAL AND METHODS: We studied the influence of the infarct-related artery patency and the presence of late potentials during signal-averaged electrocardiography on late mortality in 124 survivors of acute myocardial infarction. In addition, we assessed predictive factors of cardiac mortality by univariate and multivariate statistical analysis. RESULTS: A study group of 98 men and 26 women (mean age, 59 years) who were survivors of acute myocardial infarction underwent follow-up for a mean of 3.6 +/- 1.0 years. Immediate reperfusion therapy (thrombolysis or direct angioplasty) was accomplished in 71 patients (57%). During follow-up, 13 cardiac-associated deaths occurred. Infarct-related artery patency was strongly associated with improved survival, but the presence of late potentials did not correlate with increased mortality, even among patients with impaired left ventricular function. Univariate and multivariate analyses identified occluded infarct-related arteries, prior myocardial infarction, reduced left ventricular ejection fraction, and advanced age, but not late potentials, as predictors of increased late cardiac mortality. CONCLUSION: These data suggest that coronary angiography may, but signal-averaged electrocardiography may not, identify patients with increased late risk of cardiac-related death after myocardial infarction. The low mortality among patients who have undergone successful reperfusion therapy may reduce the ability of noninvasive tests to distinguish between high- and low-risk patients.

Analysis of Variance↗
PubMed1999

Long-term prognostic value of the stenosis of the infarct-related artery and the presence of viable myocardium in akinetic ventricular regions in infarcted patients.

BACKGROUND: Recent studies have reported that adequate perfusion of the infarct-related artery improves survival in patients with myocardial infarction, independently of left ventricular pump function. However, it is not known whether or not this reduction in mortality is independent of myocardial viability within the infarct zone. The aim of this study was to evaluate the prognostic value of the patency of the infarct artery and the presence of myocardial viability in akinetic regions in patients with myocardial infarction. METHODS: Low-dose dobutamine echocardiography was performed in 154 patients with recent or previous myocardial infarction and known coronary anatomy. In each patient three vascular regions were defined. Each akinetic region was considered viable if function improved during dobutamine echocardiography, and irrorated by a not stenotic akinetic area-related artery if the supplying vessel had a stenosis < 75% or had been successfully revascularized within 1 month of dobutamine echocardiography. RESULTS: At follow-up of 34 +/- 14 months, 19 patients died of cardiac death. At univariate Cox analysis end-diastolic and end-systolic volumes, ejection fraction, previous myocardial infarction, regional wall motion score index, and stenosis of the akinetic area-related artery were related to mortality. At multivariate analysis, stenosis of the akinetic area-related artery remained a significant predictor of mortality (p = 0.04), with higher mortality (13/66 vs 6/88, p = 0.02) in patients with a stenotic akinetic area-related artery, without differences in ejection fraction (35 +/- 9 vs 34 +/- 10%). Mortality was lower in patients with myocardial viability if they had a not stenotic akinetic area-related artery (1/43 vs 4/21, p = 0.02), while no difference was found among non-viable patients, with or without stenosis of the akinetic area-related artery (5/45 vs 9/45). CONCLUSIONS: The present study confirms the prognostic role of the patency of the infarct-related artery. However, it suggests that the lower mortality in patients with a patent artery supplying akinetic infarcted regions is related to the presence of myocardial viability in these regions.

Aged↗
PubMed2003

Delayed secondary phase of peri-infarct depolarizations after focal cerebral ischemia: relation to infarct growth and neuroprotection.

In focal cerebral ischemia, peri-infarct depolarizations (PIDs) cause an expansion of core-infarcted tissue into adjacent penumbral regions of reversible injury and have been shown to occur through 6 hr after injury. However, infarct maturation proceeds through 24 hr. Therefore, we studied PID occurrence through 72 hr after both transient and permanent middle cerebral artery occlusion (MCAo) via continuous DC recordings in nonanesthetized rats. PIDs occurred an average 13 times before reperfusion at 2 hr and then ceased for an average approximately 8 hr. After this quiescent period, PID activity re-emerged in a secondary phase, which reached peak incidence at 13 hr and consisted of a mean 52 PIDs over 2-24 hr. This phase corresponded to the period of infarct maturation; rates of infarct growth through 24 hr coincided with changes in PID frequency and peaked at 13 hr. In permanent MCAo, PIDs also occurred in a biphasic pattern with a mean of 78 events over 2-24 hr. Parameters of secondary phase PID incidence correlated with infarct volumes in transient and permanent ischemia models. The role of secondary phase PIDs in infarct development was further investigated in transient MCAo by treating rats with a high-affinity NMDA receptor antagonist at 8 hr after injury, which reduced post-treatment PID incidence by 57% and provided 37% neuroprotection. Topographic mapping with multielectrode recordings revealed multiple sources of PID initiation and patterns of propagation. These results suggest that PIDs contribute to the recruitment of penumbral tissue into the infarct core even after the restoration of blood flow and throughout the period of infarct maturation.

Animals↗
PubMed1991

[Effect of diabetes mellitus and blood glucose on the size of cerebral infarction and causes of death. Neuropathological study of 77 cases of infarction in the sylvian artery area].

The influence of diabetes mellitus and hyperglycemia on cerebral infarction has been studied on 77 patients who died of infarcts in the territory of the middle cerebral artery. The size of the infarcts was assessed by transferring the surface of the infarcted area onto 8 schematic drawings corresponding to 8 brain slices and measuring this surface by means of a planimeter. An infarction volume index (IVI) was calculated by measuring the ratio of the infarcted area to the theoretical area of the middle cerebral artery territory on the 8 slices. The causes of death were assessed by full post-mortem examination. There was no statistically significant difference in size of infarcts and causes of death between diabetics and non-diabetics. However, the stroke-to-death interval was shorter (p = 0.05) in non-diabetic patients. It appears from this study that diabetes mellitus has no deleterious effect on cerebral infarction. Equally, there were non statistically significant differences in size of infarcts, stroke-to-death interval and causes of death between patients with and without hyperglycemia.

Aged↗
PubMed1990

Exercise-induced ST-segment elevation in leads over infarcted area and residual myocardial ischemia in patients with previous myocardial infarction.

The purpose of this study was to evaluate the clinical significance of exercise-induced ST elevation in patients who had previous myocardial infarction. Electrocardiographic leads were placed over the infarcted area in 65 patients who had previous myocardial infarction (PMI; isolated left anterior descending coronary artery disease). All patients also had stress thallium scan. Exercise-induced ST changes in leads placed over patients' infarcted areas were compared with the extent of both their myocardial ischemia [thallium ischemic score (TIS)] and the area of their infarcted tissue [defect score (DS)]. The latter was derived from a circumferential profile analysis. In patients who had PMI less than three months after the onset of myocardial infarction (n = 36), the left ventricular ejection fraction (LVEF) and the extent of abnormal left ventricular wall motion did not significantly differ from those in patients with exercise-induced ST elevation (greater than 2 mm, n = 26; less than 2 mm, n = 10). In patients who had PMI more than three months after the onset of myocardial infarction (n = 29), patients with high exercise-induced ST elevation (greater than 2 mm, n = 15) showed left ventricular dyskinesis more frequently than those with low ST elevations (less than 2 mm, n = 14). In addition, the former showed higher DS and lower TIS than the latter. In patients who had PMI less than three months after onset (n = 26), 73% of those with ST elevations with prominent upright T waves (n = 15) also had transient thallium defects in their infarcted areas. They also had higher LVEF and TIS than those with low ST elevations (less than 2 mm, n = 11). These results indicated that exercise-induced ST elevations in leads placed over the infarcted areas are to be interpreted differently depending on the degree of recovery of injured myocardial tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Circulation↗
PubMed1989

[Clinical features of patients with spontaneous recanalization of the infarct-related artery during evolving acute myocardial infarction].

The clinical features of 124 patients with incompletely obstructed infarct-related arteries during the early stages of myocardial infarction (Group 1) were compared with those of 212 patients having completely occluded coronary arteries (Group 2). Coronary angiography was performed within 12 hours after onset of symptoms in all cases. Patients treated with emergency coronary angioplasty were excluded from the study. Thrombolytic therapy, performed in both groups whenever intracoronary thrombi were detected, was successful in 61% of Group 2. Results were as follows: 1. In Group 1, three-vessel disease was observed more frequently than one-vessel disease (49 vs 27%, p less than 0.005). 2. The peak level of CPK was higher in Group 2 (p less than 0.001), and left ventricular ejection fraction was higher in Group 1 (66 +/- 16 vs 56 +/- 14%, p less than 0.01). 3. Either significant ST elevation or the Q wave was more commonly absent in Group 1 (31 vs 12%, p less than 0.01; 49 vs 12%, p less than 0.001). 4. Improvement of ejection fraction was observed in Group 1, but not in Group 2 even if the infarct-related artery was recanalized within six hours. 5. Extension of an infarct area was more common in Group 1 compared to Group 2 which was successfully treated with thrombolytic therapy (12 vs 3.9%, p less than 0.05). 6. The most important cause of death was extension of an infarct area in Group 1 and pump failure in Group 2, though hospital mortality rates were similar in both groups. It was concluded that patients with myocardial infarction having incompletely obstructed infarct-related coronary arteries have better left ventricular function and higher rates of non-Q myocardial infarction compared with those who had completely obstructed coronary arteries. However, extensions of infarcted areas commonly occur in these patients.

Aged↗
PubMed1986

[Infarct size in patients with acute myocardial infarction estimated by emission computed tomography with technetium-99m pyrophosphate: relation to creatine phosphokinase release].

To evaluate the usefulness of single photon emission computed tomography (SPECT) with technetium-99m-pyrophosphate (99mTc-PYP) for estimating infarct size, we compared SPECT data with maximum creatine phosphokinase values. Background threshold was established in a series of phantom experiments. When a 40% cut-off was applied, the SPECT data most closely approximated actual phantom volumes. Therefore, the 40% cut-off level was used in the present study. In 10 patients with acute myocardial infarction, planar 99mTc-PYP myocardial scintigraphy and SPECT using a rotating gamma camera were performed two days after the initial myocardial infarction episode. The maximum creatine phosphokinase value (CPKmax) was also measured repeatedly following the episode. When the infarct size measured by SPECT using transaxial images and calculated by the pixel counts, it correlated very closely with CPKmax (r = 0.94). Most studies so far have reported that the CPKmax level reflects infarct size. We conclude that the infarct size as measured by 99mTc-PYP SPECT closely approximates the actual infarct size, and that this method is useful to determine the severity of infarcts clinically. Among the 10 patients in this series, three of five with infarcts greater than 60 ml died of pump failure. Therefore, we may be able to predict prognosis after accumulating more such cases and improving the methodology.

Aged↗
PubMed1984

Verapamil in two reperfusion models of myocardial infarction. Temporary protection of severely ischemic myocardium without limitation of ultimate infarct size.

The ability of verapamil to protect severely ischemic myocardium was assessed in dogs using 40 minutes of temporary coronary occlusion. Reperfusion was established for 4 days after which infarcts were sized histologically. Untreated dogs developed subendocardial infarcts (the more moderately ischemic subepicardial region being salvaged by reperfusion). Pretreatment with verapamil reduced the size of these subendocardial infarcts from 34 +/- 8 to 8 +/- 3% of the ischemic circumflex vascular bed at risk (identified by postmortem perfusion of the previously occluded and unoccluded arteries with different dyes). Thus, verapamil prevented cell death in the severely ischemic subendocardial region for the 40-minute test period. In a second study to establish whether verapamil could delay cell death for a longer period of time in the less severely ischemic subepicardial region, a 3-hour period of coronary occlusion was used. This period of occlusion caused infarcts averaging 60 +/- 6% of the ischemic area at risk in untreated dogs. Dogs treated with verapamil 15 minutes postocclusion and throughout the remaining 165 minutes of the 3-hour test period had no limitation of infarct size (53 +/- 3% of the area at risk). In this 3-hour study, the effect of variation in collateral blood flow on infarct size was evaluated by plotting infarct size versus subepicardial collateral flow. Verapamil neither improved collateral flow nor altered the relationship between infarct size and baseline collateral flow. Thus, pretreatment with verapamil prevented necrosis of severely ischemic myocytes, when reperfusion was established at 40 minutes, but failed to prevent necrosis of moderately ischemic myocardium and thus failed to limit infarct size when the period of coronary occlusion was prolonged to 3 hours and treatment was started 15 minutes after the onset of ischemia.

Animals↗
PubMed1993

Effects of late reperfusion on infarct expansion and infarct healing in conscious rats.

We examined the effects of late reperfusion on infarct expansion and infarct healing process in conscious rats. Coronary occlusion and reperfusion were carried out in conscious rats 1 week after appropriate surgical preparations. The rats were randomized into the following four groups: sham operated, permanent occlusion, early reperfusion (i.e., reperfusion performed 1 hour after occlusion), and late reperfusion (i.e., reperfusion performed 6 hours after occlusion). Histological examination was performed 7 days after coronary occlusion. In the early reperfusion group, infarct size and expansion were reduced when compared to the permanent occlusion group. In rats subjected to late reperfusion, infarct size and expansion were not different from those in the permanent occlusion group. The extent of unresorbed necrotic myocardium in areas of infarcted scar was reduced in both early and late reperfusion groups. Infiltration by neutrophilic cells into areas of necrotic myocardium 16 hours after myocardial infarction was increased in both reperfusion groups. Infiltration by macrophages 3 days after infarction was also increased in both reperfusion groups. Late reperfusion, therefore, does not affect infarct expansion, but does contribute to the acceleration of the infarct healing process.

Animals↗
PubMed1995

Risk stratification for malignant arrhythmic events in patients with an acute myocardial infarction: role of an open infarct-related artery and the signal-averaged ECG.

BACKGROUND: There is increasing evidence that an open infarct-related artery results in increased electrical stability of the heart and that this effect is at least in part responsible for the favorable outcome of these patients. In the thrombolytic era the optimal strategy for risk stratification remains controversial. This study examined the predictors of serious arrhythmic events during the first year after myocardial infarction. METHODS: A total of 222 patients with acute myocardial infarction, 41.4% of whom were treated with thrombolysis, were studied. At hospital discharge, signal-averaged electrocardiography was performed on 196 subjects and Holter monitoring on 200. One hundred and ninety-seven patients underwent coronary angiography. Left ventricular ejection fraction was determined in 201 subjects. RESULTS: An open infarct-related artery was documented in 106 patients. The incidence of late potentials was 34% (66 patients). Twenty-four patients (10.8%) had an arrhythmic event during follow-up (sudden death in seven, sustained ventricular tachyarrhythmias in 15, unexplained syncope in two). Signal-averaged electrocardiography had a sensitivity of 94% and a specificity of 72% for prediction of arrhythmic events. An occluded infarct-related artery was 78% sensitive and 58% specific, a left ventricular ejection fraction below 40% had a sensitivity of 71% and specificity of 80%, and Holter monitoring was only 38% sensitive and 92% specific. A combination of late potentials plus an occluded infarct-related artery was 68% sensitive and 84% specific. Positive predictive value was low for all variables examined, but could be improved by the combination of several risk factors. The highest positive predictive value was provided by the combination of an abnormal signal-averaged ECG and complex ventricular arrhythmias on ambulatory ECG. On multivariate analysis, in rank order, presence of late potentials, ejection fraction below 40%, high-grade ventricular ectopic activity and an occluded infarct-related artery were predictive of arrhythmic events. CONCLUSION: Among patients surviving an acute myocardial infarction, the occurrence of malignant arrhythmic events can be reliably predicted by the combination of an abnormal signal-averaged ECG, left ventricular dysfunction, complex ventricular arrhythmias on Holter monitoring and an occluded infarct-related artery at the time of hospital discharge.

Action Potentials↗
PubMed1996

Transplantation of fetal myocardial tissue into the infarcted myocardium of rat. A potential method for repair of infarcted myocardium?

BACKGROUND: Unlike skeletal myocytes, mammalian adult cardiomyocytes cannot regenerate after injury. A possible strategy to increase viability and augment ventricular function after myocardial injury is fetal myocardial tissue transplantation. The engrafted fetal cells are a potential source of growth factors and can be used for cardiomyocyte-based gene therapy. The purpose of our study was to test the feasibility and efficiency of fetal cardiomyocyte transplantation into a model of myocardial infarction. METHODS AND RESULTS: We subjected rats after myocardial infarction to three protocols of therapy. In the first protocol, tissue fragments of cultured human fetal ventricles were injected into the scar 7 to 24 days after infarction. The rats were treated with intraperitoneal injections of 12.5 mg.kg-1.d-1 cyclosporine. In the second protocol, fragments of cultured fetal rat ventricles were injected into the scar 9 to 17 days after infarction. A third group of animals with myocardial infarction was treated with injection of saline into the scar (control). After 7 to 65 days post-transplantation, hearts were harvested and processed for electron microscopy and alpha-actin immunohistochemistry. Toluidine blue staining and electron microscopy revealed the presence of engrafted human and rat cardiomyocytes in the infarcted myocardium up to 14 and 65 days after transplantation, respectively. The morphology was similar to that of cultured fetal cardiomyocytes. The engrafted fetal tissues were also stained positive for alpha-actin, which is unusual for the adult rat myocardium. Examination of control hearts detected infarcted tissue only, and alpha-actin staining was limited to vessel walls. CONCLUSIONS: Fetal cardiomyocyte tissue can be implanted and survive in the infarcted myocardium. This experimental approach may provide a therapeutic strategy for cardiomyocyte-based gene therapy for introduction of therapeutic proteins into myocardial infarction.

Actins↗