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At least 199 records · Page 11Linked to original sources
PubMed1991

Intravenous streptokinase in acute myocardial infarction (I.S.A.M.) trial: serial evaluation of left ventricular function up to 3 years after infarction estimated by radionuclide ventriculography. I.S.A.M. Study Group.

The Intravenous Streptokinase in Acute Myocardial Infarction (I.S.A.M.) trial was a prospective, placebo-controlled, double-blind multicenter trial of high-dose short-term intravenous streptokinase in acute myocardial infarction administered within 6 h after the onset of symptoms. Global and regional left ventricular ejection fractions were determined by radionuclide ventriculography in a subset of 120 patients 3 days, 4 weeks, 7 months, 18 months and 3 years after acute myocardial infarction. In patients with anterior myocardial infarction, left ventricular ejection fraction was higher in the streptokinase than in the placebo group 3 days after acute infarction (49 +/- 14% vs. 40 +/- 11%, p = 0.02). This difference of about 10% units in ejection fraction persisted during the 3 year follow-up period. Among streptokinase-treated patients, regional left ventricular ejection fraction was higher within the infarct zone as well as in remote myocardium throughout the follow-up period. Among patients with inferior infarction, no significant differences between the treatment and control groups were demonstrable with respect to global and regional left ventricular ejection fraction. Thus, intravenous administration of streptokinase within 6 h after the onset of symptoms of acute myocardial infarction preserves left ventricular function over a period of greater than or equal to 3 years in patients with acute anterior myocardial infarction. It improves regional myocardial function within the infarct zone as well as in remote areas. In patients with acute inferior myocardial infarction, benefit from intravenous streptokinase is of only minor degree.

Creatine Kinase↗
PubMed1991

Coronary patency, infarct size and left ventricular function after thrombolytic therapy for acute myocardial infarction: results from the tissue plasminogen activator: Toronto (TPAT) placebo-controlled trial. TPAT Study Group.

Infarct size, left ventricular function and infarct-related coronary artery patency were examined in 108 patients who took part in a previously reported placebo-controlled trial of recombinant tissue-type plasminogen activator (rt-PA) in acute myocardial infarction. Coronary angiography was performed 17 +/- 0.8 h after initiation of treatment in 47 patients (group A) or at 10 days in 61 patients (group B). Both groups underwent radionuclide ventriculography 3.8 +/- 0.8 h and again on day 9 after treatment and quantitative thallium scintigraphy on day 8. In group A, the infarct-related artery was patent in 53%; these patients had a smaller global (15.1 +/- 2.5% vs. 25.7 +/- 4.7%, p = 0.029) and regional (14.7 +/- 2.5% vs. 24.1 +/- 4.7%, p = 0.044) fixed thallium defect than did those with an occluded artery. Infarct regional ejection fraction improved by 10.1 +/- 2.1% between early and late studies when the infarct-related artery was patent and by 4.8 +/- 1.4% if it was occluded (p = 0.048); changes in global and noninfarct regional ejection fraction were similar irrespective of perfusion status. Infarct regional ejection fraction and fixed thallium defect were inversely related only when the infarct-related artery was occluded (r = -0.83, p less than 0.0001). In group B, 10 day patency of the infarct-related artery was 67%; there was no difference in patency by treatment assignment or in left ventricular function or infarct size between patients with and without infarct-related artery patency. There was no evidence of an effect of rt-PA therapy beyond that expressed through coronary patency alone in either group A or group B.

Coronary Vessels↗
PubMed2006

Relationship between infarct artery location, epicardial flow, and myocardial perfusion after primary percutaneous revascularization in acute myocardial infarction.

BACKGROUND: The association between infarct artery location, reperfusion success, and clinical outcomes after primary percutaneous coronary intervention (PCI) has not been characterized. We examined the infarct artery-specific impact of epicardial and myocardial flow and reperfusion after primary PCI for acute myocardial infarction. METHODS: Among 2082 patients undergoing primary PCI in the CADILLAC trial, myocardial blush grade, TIMI flow grade, ST-segment resolution, and clinical outcomes were analyzed according to the infarct artery. RESULTS: Baseline clinical characteristics did not significantly differ between patients experiencing infarction in the left anterior descending (LAD, 37%) versus left circumflex (18%) and right coronary artery (46%) distributions. Baseline left ventricular function was reduced, and collateral flow was less commonly present in patients with infarction involving the LAD. Achievement of final TIMI-3 flow, grade 3 myocardial blush, and ST-segment resolution >70% was also significantly less common in anterior infarction. Patients with anterior versus nonanterior infarction had significantly higher mortality at 30 days (3.4% vs 1.3%, P = .0006) and 1 year (6.5% vs 2.9%, P < .0001) and had increased 1-year rates of reinfarction (3.6% vs 1.7%, P = .009) and ischemic target vessel revascularization (16.1% vs 11.7%, P = .006). By multivariate analysis, LAD infarction was a powerful independent predictor of 1-year mortality (odds ratio 2.45, P = .009). CONCLUSIONS: Acute myocardial infarction involving the LAD distribution is associated with reduced left ventricular function, less frequent collateral flow, impaired myocardial perfusion and decreased reperfusion success, findings associated with reduced survival, and increased major adverse cardiac events compared with other vascular territories. These data provide mechanistic insights to the adverse prognosis of patients with anterior infarction.

Aged↗
PubMed2004

The sequential changes in myocardial thickness and thickening which occur during acute transmural infarction, infarct reperfusion and the resultant expression of reperfusion injury.

AIM: Successful primary PTCA (with TIMI 3 reflow) in patients with acute transmural infarction has been observed to result in an immediate abnormal increase in wall thickness associated with persisting abnormal post-systolic thickening. To understand the sequential changes in regional deformation during: (i) the development of acute transmural infarction, (ii) upon TIMI grade 3 infarct reperfusion and (iii) during the subsequent expression of reperfusion injury the following correlative experimental study was performed in a pure animal model in which there was no distal dispersion of thrombotic material causing either no reflow or secondary microvascular obstruction. METHODS: In 10 closed-chest pigs, a 90 min PTCA circumflex occlusion was used to induce a transmural infarction. This was followed by 60 min of TIMI 3 infarct reperfusion. M-mode ultrasound data from the "at risk" posterior wall infarct segment and from a control remote non-ischemic septal segment were acquired at standardized time intervals. Changes in regional deformation (end-diastolic (EDWT), end-systolic (ESWT) and post-systolic (PSWT) wall thickness, end-systolic strain (epsilonES) and post-systolic strain (epsilonps)) were measured. RESULTS: In this pure animal model of acute transmural infarction/infarct reperfusion (with no pre-existing intra-luminal thrombus), the induced changes in wall thickness and thickening were complex. During prolonged occlusion, after an initial acute fall in ESWT, there was no further change in systolic deformation to indicate the progression of ischaemia to infarction. Both transmurally infarcted and reperfused-infarcted myocardium retained post-systolic thickening indicating that this parameter, taken in isolation, is not a consistent marker of segmental viability and, in this regard, should be interpreted only in combination with other indices of segmental function. The most striking abnormality induced by reperfusion was an immediate increase in EDWT which then increased logarithmically over a 60 min period as reperfusion injury was further expressed. PS did not change significantly during reperfusion. Histology confirmed the wall thickness changes on reperfusion to be due to massive extra-cellular oedema. CONCLUSIONS: The identification of an acute increase in regional wall thickness in a reperfused infarct zone by cardiac ultrasound following primary PTCA might be used in patients to both identify successful infarct reperfusion and to monitor the presence, extent and resolution of the oedema associated with reperfusion injury.

Animals↗
PubMed2005

Effects of primary angioplasty for acute myocardial infarction on early and late infarct size and left ventricular wall characteristics.

UNLABELLED: The effects of reperfusion on early and late infarct size and left ventricular wall characteristics were studied by performing cine-magnetic resonance imaging, first-pass perfusion, and delayed enhancement imaging in 22 patients at five days and five months after successful primary angioplasty for first acute myocardial infarction. Infarct size, end-diastolic wall thickness, and segmental wall thickening were quantified, and the extent of microvascular obstruction (MO) was evaluated qualitatively. Infarct size decreased by 31%. Segments without MO had early increased wall thickness and late partially normalized wall thickening. Segments with MO showed late wall thinning and no functional recovery at five months. OBJECTIVES: We aimed to study the effects of early successful primary angioplasty for ST-segment elevation acute myocardial infarction (AMI) on early and late infarct size and left ventricular (LV) wall characteristics. BACKGROUND: Early reperfusion treatment for AMI preserves LV function, but the effects on early and late infarct size, end-diastolic wall thickness (EDWT), and segmental wall thickening (SWT) are not well known. METHODS: In 22 patients with successful primary angioplasty for first AMI, cine-magnetic resonance imaging (MRI), first-pass perfusion, and delayed-enhancement imaging was performed at five days and five months. The extent of microvascular obstruction (MO) was evaluated on perfusion images. Infarct shrinkage was defined as the difference between the volume of delayed-enhancement at five days and five months. The EDWT and SWT were quantified on cine-MRI. RESULTS: Infarct shrinkage occurred to the same extent in small and large infarctions [r = 0.92; p < 0.001], with a mean decrease of 31% (35 +/- 21 g to 24 +/- 17 g). Dysfunctional segments without MO had an increased EDWT at five days compared with remote myocardium (9.2 +/- 1.7 mm vs. 8.4 +/- 1.7 mm; p < 0.001). At five months, EDWT in these segments became comparable to the thickness of remote myocardium (7.8 +/- 1.6 mm vs. 7.6 +/- 1.4 mm; p = 0.60), and SWT improved (21 +/- 15% to 40 +/- 24%; p < 0.001) but remained impaired (40 +/- 24% vs. 71 +/- 29%; p < 0.001). Segments with MO demonstrated wall thinning at five months (6.4 +/- 1.3 mm vs. 7.6 +/- 1.4 mm; p = 0.006) and no significant recovery in SWT (12 +/- 14% to 17 +/- 20%; p = 0.15). CONCLUSIONS: Infarct size decreased by 31%. Segments without MO had early increased wall thickness and late partial functional recovery. Segments with MO showed late wall thinning and no functional recovery at five months.

Angioplasty, Balloon, Coronary↗
PubMed2002

Utility and limitation of treadmill exercise echocardiography for detecting significant coronary stenosis in infarct-related arteries in patients with healed myocardial infarction.

This clinical study examines the diagnostic accuracy of exercise echocardiography for detecting significant coronary stenoses in infarct-related arteries in patients with healed myocardial infarction. Quantitative coronary angiography and exercise echocardiography using treadmill testing were performed within 2 weeks of each other in 123 patients with a prior myocardial infarction. Coronary lumen diameter stenosis > or =50% by quantitative coronary angiography and the lack of a hyperdynamic response on exercise echocardiography was considered significant. For detection of infarct-related coronary lesions, treadmill exercise echocardiography was highly sensitive (91%) but less specific (59%) than for detection of non-infarct-related artery lesions. The 2 groups of patients with large and small infarct sites had similar sensitivity for detection of residual stenosis of the infarct-related artery (88% vs 96%, p = NS); however, the specificity of the small infarct sites for this purpose was significantly higher than that of the large infarct sites (86% vs 33%, p < 0.01). When remote ischemia was detected on exercise echocardiography, the specificity of exercise echocardiography was significantly lower (33% vs 70%, p < 0.05) than when remote ischemia was not present. Thus, although there is high sensitivity, the specificity of treadmill exercise echocardiography for detecting infarct-related artery lesions is limited. However, high specificity is maintained when the infarct size is small and/or remote ischemia is not present.

Chi-Square Distribution↗
PubMed2001

Fibrinogen and C-reactive protein on admission as markers of final infarct size after primary angioplasty for acute myocardial infarction.

BACKGROUND: In acute myocardial infarction (AMI) treated conservatively or with thrombolysis, marked increases of C-reactive protein (CRP) and fibrinogen have been observed. No data are however available concerning a possible relation between CRP and fibrinogen levels on admission and markers of infarct size after obtaining thrombolysis in myocardial infarction (TIMI) flow III by primary angioplasty. METHODS: We studied 34 patients with a first AMI (29 men, mean age 54+/-11 years) who were treated with primary angioplasty (TIMI flow III in all patients, no concomitant treatment with glycoprotein IIb-IIIa antagonists) within 6 h of onset of pain. CRP and fibrinogen levels on admission were determined and related to the following markers of infarct size: peak creatine kinase MB (CKMB) levels, radionuclide left ventricular ejection fraction (LVEF) at discharge and thallium-201 single-photon emission computed tomography (SPECT) infarct size at 1 month. RESULTS: Median CRP levels were 0.4 mg/dl (range 0.09-3 mg/dl), median fibrinogen levels 412 mg/dl (range 198-679 mg/dl), mean CKMB was 178+/-151 U/l, mean LVEF 52+/-8% and mean thallium-201 infarct size 7+/-6%. Although CRP levels were related to fibrinogen levels on admission (r=0.56, P=0.002), only fibrinogen levels were related to markers of infarct size (r=0.58, P=0.001 for CKMB, r=-0.44, P=0.01 for LVEF and r=0.64, P=0.001 for thallium-201 infarct size). No relation was found between CRP or fibrinogen levels on admission and the extent of coronary artery disease or the myocardial area at risk. In multiple regression analysis, the relation between fibrinogen and markers of infarct size was independent of CRP levels and the duration of pain on admission. CONCLUSIONS: These findings indicate a relation between fibrinogen levels on admission and myocardial infarct size in patients treated with primary angioplasty for AMI. This relation seems to be independent of CRP levels and the duration of pain on admission. If confirmed in larger patient populations, fibrinogen levels on admission could have an important value for risk stratification and more aggressive reduction of infarct size in patients who are treated with primary angioplasty.

Acute Disease↗
PubMed1991

Late potentials on signal-averaged electrocardiograms and patency of the infarct-related artery in survivors of acute myocardial infarction.

This study evaluated the relation between patency of the infarct-related artery and the presence of late potentials on the signal-averaged electrocardiogram (ECG) in 124 consecutive patients (98 men, 26 women; mean age 59 years) with acute myocardial infarction receiving thrombolytic therapy, acute percutaneous transluminal coronary angioplasty or standard care. All patients were studied by coronary angiography, measurement of ejection fraction and signal-averaged ECG. The infarct-related artery was closed in 51 patients and open in 73. Among patients with no prior myocardial infarction undergoing early attempted reperfusion therapy, a patent artery was associated with a decreased incidence of late potentials (20% versus 71%; no significant difference in ejection fraction). In the 48 patients receiving thrombolytic agents within 4 h of symptom onset, the incidence of late potentials was 24% and 83% among patients with an open or closed artery, respectively (p less than 0.04). The most powerful predictors of late potentials were the presence of a closed infarct-related artery, followed by prior infarction and patient age. Among patients receiving thrombolytic agents within 4 h of symptom onset, the only variable that was predictive of the presence of late potentials was a closed infarct-related artery. These data imply that reperfusion of an infarct-related artery has a beneficial effect on the electrophysiologic substrate for serious ventricular arrhythmias that is independent of change in left ventricular ejection fraction as an index of infarct size. These findings might explain, in part, the low late mortality rate in survivors of myocardial infarction with documented reperfusion of the infarct-related artery.

Angioplasty, Balloon, Coronary↗
PubMed1999

Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction: results of a multicenter, randomized, placebo-controlled trial: the Acute Myocardial Infarction STudy of ADenosine (AMISTAD) trial.

OBJECTIVES: The Acute Myocardial Infarction STudy of ADenosine (AMISTAD) trial was designed to test the hypothesis that adenosine as an adjunct to thrombolysis would reduce myocardial infarct size. BACKGROUND: Reperfusion therapy for acute myocardial infarction (MI) has been shown to reduce mortality, but reperfusion itself also may have deleterious effects. METHODS: The AMISTAD trial was a prospective, open-label trial of thrombolysis with randomization to adenosine or placebo in 236 patients within 6 h of infarction onset. The primary end point was infarct size as determined by Tc-99 m sestamibi single-photon emission computed tomography (SPECT) imaging 6+/-1 days after enrollment based on multivariable regression modeling to adjust for covariates. Secondary end points were myocardial salvage index and a composite of in-hospital clinical outcomes (death, reinfarction, shock, congestive heart failure or stroke). RESULTS: In all, 236 patients were enrolled. Final infarct size was assessed in 197 (83%) patients. There was a 33% relative reduction in infarct size (p = 0.03) with adenosine. There was a 67% relative reduction in infarct size in patients with anterior infarction (15% in the adenosine group vs. 45.5% in the placebo group) but no reduction in patients with infarcts located elsewhere (11.5% for both groups). Patients randomized to adenosine tended to reach the composite clinical end point more often than those assigned to placebo (22% vs. 16%; odds ratio, 1.43; 95% confidence interval, 0.71 to 2.89). CONCLUSIONS: Many agents thought to attenuate reperfusion injury have been unsuccessful in clinical investigation. In this study, adenosine resulted in a significant reduction in infarct size. These data support the need for a large clinical outcome trial.

Adenosine↗
PubMed1999

Decreased no-reflow in patients with anterior myocardial infarction and pre-infarction angina.

AIMS: Pre-infarction angina is associated with better outcome after myocardial infarction. The aim of this study was to assess whether pre-infarction angina is associated with decreased no-reflow after coronary recanalization. METHODS AND RESULTS: Twenty-three patients underwent intracoronary myocardial contrast echocardiography during the acute phase of anterior myocardial infarction after successful recanalization, and before hospital discharge. Myocardial perfusion was graded semi-quantitatively in the area at risk (dyssynergic segments). Global left ventricular function was assessed by radionuclide angiography on days 8 and 42 and regional wall motion was assessed by 2D echocardiography on days 0 and 42. Fourteen patients had pre-infarction angina (angina less than 7 days before myocardial infarction) and nine did not. Baseline characteristics were similar in the two groups. The myocardial contrast echocardiography perfusion score in the area at risk after recanalization was higher in the patients with pre-infarction angina than in those without (0.72 +/- 0.19 vs 0.53 +/- 0.22, P=0.04), and the incidence of no-reflow (myocardial contrast echocardiography perfusion score < or =0.5) was lower (14% vs 56%, P=0.04). This difference persisted 8 +/- 2 days after myocardial infarction (0. 87 +/- 0.11 vs 0.69 +/- 0.26, P=0.04), and was associated with greater mid-term (day 42) improvement in left ventricular function in patients with pre-infarction angina than in those without, as assessed by changes in radionuclide left ventricular ejection fraction (+5.8 +/- 8.1% vs -3.3 +/- 4.6%, respectively;P=0.01) and by changes in regional wall motion score on 2D echocardiography (-0. 61 +/- 0.39 vs -0.24 +/- 0.17, respectively;P=0.04). CONCLUSION: Pre-infarction angina is associated with preservation of the microvasculature, reflected by reduced no-reflow. This may be a mechanism underlying greater recovery of left ventricular function in patients with pre-infarction angina.

Adult↗
PubMed1993

Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators.

BACKGROUND: Despite anecdotal evidence suggesting that heavy physical exertion can trigger the onset of acute myocardial infarction, there have been no controlled studies of the risk of myocardial infarction during and after heavy exertion, the length of time between heavy exertion and the onset of symptoms (induction time), and whether the risk can be modified by regular physical exertion. To address these questions, we collected data from patients with confirmed myocardial infarction on their activities one hour before the onset of myocardial infarction and during control periods. METHODS: Interviews with 1228 patients conducted an average of four days after myocardial infarction provided data on their usual annual frequency of physical activity and the time, type, and intensity of physical exertion in the 26 hours before the onset of myocardial infarction. We compared the observed frequency of heavy exertion (6 or more metabolic equivalents) with the expected values using two types of self-matched analyses based on a new case-crossover study design. The low frequency of heavy exertion during the control periods was validated by data from a population-based control group of 218 subjects. RESULTS: Of the patients, 4.4 percent reported heavy exertion within one hour before the onset of myocardial infarction. The estimated relative risk of myocardial infarction in the hour after heavy physical exertion, as compared with less strenuous physical exertion or none, was 5.9 (95 percent confidence interval, 4.6 to 7.7), Among people who usually exercised less than one, one to two, three to four, or five or more times per week, the respective relative risks were 107 (95 percent confidence interval, 67 to 171), 19.4 (9.9 to 38.1), 8.6 (3.6 to 20.5), and 2.4 (1.5 to 3.7). Thus, increasing levels of habitual physical activity were associated with progressively lower relative risks. The induction time from heavy exertion to the onset of myocardial infarction was less than one hour, and symptoms usually began during the activity. CONCLUSIONS: Heavy physical exertion can trigger the onset of acute myocardial infarction, particularly in people who are habitually sedentary. Improved understanding of the mechanisms by which heavy physical exertion triggers the onset of myocardial infarction and the manner in which regular exertion protects against it would facilitate the design of new preventive approaches.

Adult↗
PubMed2000

Prodromal unstable angina in acute myocardial infarction: prognostic value of short- and long-term outcome and predictor of infarct size.

BACKGROUND: An estimated 50% of patients with myocardial infarction have prodromal unstable angina. There is controversy over whether prodromal unstable angina identifies a group of patients at lower risk of short- and long-term death and the clinical importance of recording this event. METHODS: Of 207 patients enrolled at a single Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) site, 196 survived the 24 hours after presentation, achieved peak creatine kinase MB concentrations, and were classified as having either abrupt symptom onset or prodromal unstable angina in the 2 weeks before myocardial infarction. Creatine kinase MB peak was used to categorize infarct size as aborted myocardial infarction, minor myocardial damage, or extensive myocardial injury. Follow-up was performed at 24 hours, 30 days, 1 year, and 5 years. Multiple variables, including prodromal unstable angina, time to treatment, age, sex, previous infarction and infarct location, were analyzed for predicting infarct size. Also, these variables plus peak creatine kinase MB level and a combined variable of prodromal unstable angina and peak creatine kinase MB level were examined for predicting survival. RESULTS: Mortality rate was 2.5% within 24 hours, 9.0% at 30 days, 13.5% at 1 year, and 27.1% at 5 years. Patients categorized as either aborted infarction or minor myocardial damage were significantly more likely to have prodromal unstable symptoms (81.3% vs 51.2%, P <.001) and better survival at each follow-up period. Prodromal presentation was the most significant predictor of infarct size category (P =.001). Five-year survival was predicted by age (P <.0001), peak creatine kinase MB level (P =.007), infarct location (P =.009), the combined variables (P =.029), and prodromal unstable angina (P =.017). Prodromal unstable angina had the highest odds ratio for 5-year survival at 3.83 (95% confidence interval 1.27-11.47). CONCLUSIONS: Prodromal unstable angina is a strong predictor of infarct size and survival. Recognizing prodromal unstable angina is important for clinically assessing prognosis.

Adult↗
PubMed1993

Delayed recovery of myocardial perfusion after successful coronary angioplasty of infarct-related artery in patients with prior myocardial infarction.

We studied the status of myocardial perfusion before and after coronary angioplasty (PTCA) of infarct-related artery using stress thallium scan in patients with prior myocardial infarction. Twenty-six patients who had anterior myocardial infarction caused by single-vessel disease at the left anterior descending coronary artery were involved. Patients were classified into the following four groups according to the stress-redistribution thallium scintigraphic findings before PTCA: complete redistribution (two cases), incomplete redistribution (12 cases), partial redistribution (seven cases) and no redistribution (five cases). In the group with complete redistribution, the extent of residual ischaemia in the infarct area decreased significantly after PTCA but infarct size only slightly. In the groups with incomplete and partial redistribution, the extent of residual ischaemia and infarct size decreased significantly after PTCA. In contrast, the group with no redistribution showed a slight decrease in the extent of residual ischaemia and a gradual decrease in infarct size beginning 3 months after PTCA. Clinical findings including electrocardiogram indicated that the patients with incomplete redistribution had more viable myocardium and the patients with no redistribution had more scarring. The groups with incomplete and partial redistribution showed characteristics intermediate between complete and no redistribution. The change of infarct area after PTCA was different between the four groups, but both residual ischaemia and infarct size decreased in all groups. Thus, PTCA of the infarct-related coronary artery is useful even in the patients with prior myocardial infarction, even in patients with no redistribution shown by stress thallium scan.

Adult↗
PubMed2006

Laser microdissection and capture of pure cardiomyocytes and fibroblasts from infarcted heart regions: perceived hyperoxia induces p21 in peri-infarct myocytes.

Myocardial infarction caused by ischemia-reperfusion in the coronary vasculature is a focal event characterized by an infarct-core, bordering peri-infarct zone and remote noninfarct zone. Recently, we have reported the first technique, based on laser microdissection pressure catapulting (LMPC), enabling the dissection of infarction-induced biological responses in multicellular regions of the heart. Molecular mechanisms in play at the peri-infarct zone are central to myocardial healing. At the infarct site, myocytes are more sensitive to insult than robust fibroblasts. Understanding of cell-specific responses in the said zones is therefore critical. In this work, we describe the first technique to collect the myocardial tissue with a single-cell resolution. The infarcted myocardium was identified by using a truncated hematoxylin-eosin stain. Cell elements from the infarct, peri-infarct, and noninfarct zones were collected in a chaotropic RNA lysis solution with micron-level surgical precision. Isolated RNA was analyzed for quality by employing microfluidics technology and reverse transcribed to generate cDNA. Purity of the collected specimen was established by real-time PCR analyses of cell-specific genes. Previously, we have reported that the oxygen-sensitive induction of p21/Cip1/Waf1/Sdi1 in cardiac fibroblasts in the peri-infarct zone plays a vital role in myocardial remodeling. Using the novel LMPC technique developed herein, we confirmed that finding and report for the first time that the induction of p21 in the peri-infarct zone is not limited to fibroblasts but is also evident in myocytes. This work presents the first account of an analytical technique that applies the LMPC technology to study myocardial remodeling with a cell-type specific resolution.

Actins↗
PubMed1994

Rat and rabbit heart infarction: effects of anesthesia, perfusate, risk zone, and method of infarct sizing.

Rabbits and rats are becoming popular models for in vitro as well as in situ studies of myocardial infarction. In the present analysis we evaluated the results of several of our completed investigations and tested whether blood-free perfusate, anesthesia, or risk zone size affects infarction in these species. In addition, the influence of the method used for determining infarct size (histology or histochemistry) was examined in rabbits. All hearts experienced 30 min of regional ischemia followed by either 2-3 h of reperfusion in animals in which infarct size was assessed by staining with triphenyltetrazolium chloride or 72 h in those in which histological methods were used to measure infarct size. Eighteen rabbit and seven rat hearts perfused with Krebs buffer, seventeen open-chest rabbits, eight rats anesthetized with pentobarbital, and ten conscious rabbits were studied. Risk zone size measured with fluorescent particles was plotted against infarct size. Infarct size was linearly correlated with risk zone size and did not differ among models for each species. In rat hearts the regression line passed through the origin so that zero infarction occurred with zero risk zone size. However, in the rabbit heart there was no apparent infarction for risk zone sizes < 0.3 cm3. Although the relationship between risk zone and infarction was found to be remarkably independent of the model chosen, the nonzero intercept for the rabbit heart can be an important, previously unrecognized source of experimental variability when infarct size is expressed as a percentage of the risk zone.

Anesthesia↗
PubMedDate not supplied

White matter medullary infarcts: acute subcortical infarction in the centrum ovale.

Acute infarction confined to the territory of the white matter medullary arteries is a poorly characterised acute stroke subtype. 22 patients with infarction confined to this vascular territory on CT and/or MRI were identified from a series of 1,800 consecutive admissions to our stroke unit (1.2%) between August 1993 and March 1997. 19 patients had small infarcts (< 1.5 cm maximum diameter) and 3 large infarcts (> 1.5 cm). Small infarcts were associated with a history of smoking (69%), hypertension (58%), and hyperlipidaemia (37%), and less frequently with atrial fibrillation (21%). Significant (>50%) ipsilateral carotid stenosis (16%) was a less frequent finding in this group. Patients most commonly presented with weakness and/or sensory disturbance affecting mainly the upper limbs, but dysarthria, dysphasia, and ataxia were also seen. Large infarcts were infrequent in our series, but did not differ significantly from small infarcts with respect to clinical presentation or risk factor profiles (p > 0.05 for all comparisons). The majority of symptomatic patients with white matter medullary infarcts are associated with small (< 1.5 cm diameter) lesions and a risk factor profile consistent with small vessel disease. More data are required to elucidate the mechanism of larger (> 1.5 cm) infarcts. Because of the potential overlap between white matter medullary infarcts and internal watershed infarcts, suggested criteria for each are presented.

Acute Disease↗
PubMed2001

The expression of the CD18 leucocyte integrin in a rabbit model of acute myocardial infarction: a pilot study of temporal changes and relationship to infarct size.

CD18 integrins mediate leucocyte adhesion to vascular endothelium. This represents the initial step in inflammatory cell infiltration following myocardial necrosis. The current study assessed whether the expression of these rapidly activated and readily measured adhesion receptors on circulating neutrophils would reflect the extent of cardiac damage in a rabbit model of acute myocardial infarction. Myocardial ischaemia/infarction was induced in anaesthetised adult male New Zealand white rabbits (n = 8) by ligation of the circumflex or marginal coronary artery. To control for the effects of anaesthesia and surgery, 4 rabbits underwent identical procedures without the induction of infarction. Absolute infarct size (in mg) and infarct size as a percentage of total left ventricular mass (relative infarct size) were calculated by differential staining and weighing of necrotic myocardium. Flow cytometry was used to determine cell surface expression of CD18 at six time points (baseline, 20 and 45 min of ischaemia and 20, 60 and 180 min of reperfusion). Absolute neutrophil CD18 expression and changes in expression over baseline were correlated with absolute and relative infarct size. Mean neutrophil CD18 expression increased significantly (from 2.42 +/- 0.20 to 3.07 +/- 0.29; p = 0.04) within 20 min of ischaemia. CD18 expression at 3 h did not predict absolute or relative infarct size (r = 0.40 and 0.37, respectively). The percentage change in cell surface CD18 expression (above baseline levels) was, however, correlated with both measures of infarct size (r = 0.76, p = 0.03, and r = 0.92, p = 0.001, respectively). In conclusion, in this rabbit model of myocardial infarction, neutrophil CD18 expression rises within 20 min of the induction of ischaemia but absolute values after 3 h of reperfusion are poor indicators of infarct size. Although percentage change in neutrophil CD18 levels over baseline correlates with infarct size there is considerable variation between individuals, limiting any clinical application.

Animals↗
PubMed1986

Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion.

Dilatation of infarcted segments (infarct expansion) may occur during recovery from myocardial infarction, but the fate of noninfarcted segments is uncertain. Accordingly, left ventricular geometric changes were assessed by left ventricular angiography and M mode echocardiography on admission and 2 weeks later in 30 patients with their first acute transmural myocardial infarction. All patients demonstrated chest pain, ST segment elevation with subsequent development of Q waves (15 anterior, 15 inferior), and elevation of cardiac enzymes. Sequential left ventricular angiographic and hemodynamic findings were available in these patients by virtue of their participation in a study of thrombolysis in acute myocardial infarction. By that study design, all patients treated successfully with thrombolytic therapy and demonstrating improvement of flow in an occluded coronary artery underwent repeat cardiac catheterization. At 2 weeks there was a significant decrease in left ventricular and pulmonary capillary wedge pressures (p less than .01), whereas both left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volume indexes increased (p less than .01). The increase in LVEDV correlated directly with the percentage of the ventriculographic silhouette that was akinetic or dyskinetic at the initial catheterization (r = .71, p less than .001). To assess regional changes in both infarcted and noninfarcted segments, serial endocardial perimeter lengths of both the akinetic-dyskinetic segments (infarction zone) and of the remainder of the cardiac silhouette (noninfarction zone) were measured in all patients who demonstrated at least a 20% increase in their LVEDV at 2 weeks after myocardial infarction. Notably, there was a mean increase of 13% in the endocardial perimeter length of infarcted segments and a 19% increase in the endocardial perimeter length of noninfarcted segments. Serial M mode echocardiographic studies showed no significant change in the wall thickness of noninfarcted myocardial segments. Hemodynamic changes that occurred in this subgroup of patients included significant decreases in left ventricular end-diastolic and pulmonary capillary wedge pressures (p less than .05) and significant increases in angiographic cardiac index (p less than .01) and LVESV index (p less than .01). We conclude that in patients who manifest cardiac dilatation in the early convalescent period after myocardial infarction, there is remodeling of the entire left ventricle including infarct expansion of akinetic-dyskinetic segments and volume-overload hypertrophy of noninfarcted segments.(ABSTRACT TRUNCATED AT 400 WORDS)

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