Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Infarction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed1991

Comparative effects of APSAC and rt-PA on infarct size and left ventricular function in acute myocardial infarction. A multicenter randomized study.

BACKGROUND: Recombinant tissue-type plasminogen activator (rt-PA or alteplase) and anisoylated plasminogen streptokinase activator complex (APSAC or anistreplase) have been demonstrated to limit infarct size significantly and to preserve left ventricular function when injected soon after acute myocardial infarction. However, as yet, the efficacy and safety of these two thrombolytic agents have not been directly compared in one trial; this was the aim of this study. METHODS AND RESULTS: One hundred eighty-three patients suffering from a first acute myocardial infarction were randomly allocated to either APSAC (30 units over 5 minutes) or single-chain rt-PA (100 mg over a 3-hour period) within 4 hours of the onset of symptoms. Global and regional left ventricular function were assessed from contrast angiography an average of 5.3 +/- 2.3 days after initial therapy. Radionuclide angiography and thallium-201 single-photon emission computerized tomography were performed before hospital discharge. Infarct size was assessed by single-photon emission computerized tomography and expressed in percentage of the total myocardial volume. Ninety patients received APSAC and 93 received rt-PA within a mean period of 172 +/- 52 minutes after the onset of symptoms. The two groups were similar in age, location of the acute myocardial infarction, Killip class, and time of randomization. The patency rate of the infarct-related artery was 72% in the APSAC group and 76% in the rt-PA group (NS). Initial and predischarge left ventricular ejection fraction as well as infarct size were similar in both therapeutic groups (0.50 +/- 0.14 versus 0.52 +/- 0.12 for initial and 0.48 +/- 0.10 versus 0.47 +/- 0.10 for predischarge ejection fraction, 11 +/- 7% versus 9 +/- 7% for infarct size, respectively, for APSAC- and rt-PA-treated patients). Bleeding complications requiring blood transfusion occurred in one APSAC patient and in two rt-PA patients. One patient in the rt-PA group died of a massive intracranial hemorrhage. At the end of the 3-week follow-up period, five APSAC patients (5.5%) and seven rt-PA patients (7.5%) had died. CONCLUSIONS: The early infusion of APSAC or rt-PA in acute myocardial infarction produced a similar patency rate, limitation of infarct size, and preservation of left ventricular systolic function with an equivalent rate of bleeding complications.

Anistreplase↗
PubMed1994

Long-term prognostic importance of patency of the infarct-related coronary artery after thrombolytic therapy for acute myocardial infarction.

BACKGROUND: After thrombolytic therapy, long-term patency of the infarct-related artery may reduce arrhythmias, limit ventricular dilatation, and provide collaterals to another infarct zone if further infarction occurs. However, independent long-term prognostic value of infarct artery patency has not been shown. METHODS AND RESULTS: We followed 312 patients with first myocardial infarction treated < 4 hours after pain onset with thrombolysis (streptokinase [n = 188] or recombinant tissue-type plasminogen activator [n = 124]). At 28 +/- 11 days, cardiac catheterization was performed. Flow of the infarct-related artery was assessed by the TIMI scoring system, and a scoring system relating coronary stenoses and flow to the amount of myocardium supplied was also used. Follow-up was for 39 +/- 13 months. Cardiac death occurred in 5.8% of patients, and there were two noncardiac deaths. Revascularization was performed in 11.5% of patients. On univariate and multivariate analysis, ventricular function (ejection fraction, P = .006 and .02, or end-systolic volume index, P = .01 and .06) was the most important prognostic factor. Patency of the infarct-related artery measured as TIMI 3 flow was marginally significant on univariate analysis (P = .08) but not on multivariate analysis (P = .2). Patency was an independent prognostic factor in univariate and multivariate analysis when measured as an occlusion score (amount of myocardium supplied by an occluded artery, P = .01 and < .05). When the ejection fraction was > or = 50%, only occluded arteries supplying > 25% of the left ventricle affected prognosis adversely. If the ejection fraction was < 50%, occluded arteries supplying < 25% of myocardium also adversely affected prognosis. Treadmill exercise duration 4 weeks after infarction was the only other prognostic factor identified. CONCLUSIONS: Ventricular function and infarct-related artery patency are independent prognostic factors after thrombolytic therapy for acute myocardial infarction.

Cardiac Catheterization↗
PubMed1994

Spontaneous delayed recovery of perfusion and contraction after the first 5 weeks after anterior infarction. Evidence for the presence of hibernating myocardium in the infarcted area.

BACKGROUND: In patients with ventricular dysfunction caused by stunning or hibernation, it is not clear when complete recovery of the salvaged myocardium occurs after acute myocardial infarction. The purpose of this study was to determine whether a delayed recovery of perfusion and contraction continues even after the subacute phase. METHODS AND RESULTS: We prospectively studied 71 consecutive male patients with first uncomplicated Q-wave anterior infarction. Resting regional blood flow distribution and contraction were assessed quantitatively 5 weeks and 7 months after the acute phase by serial sestamibi tomography and two-dimensional echocardiography. Coronary angiography also was performed in 52 patients. Overall, at 7 months there was an improvement in the perfusion defect severity (1019 +/- 811 versus 1365 +/- 821 at 5 weeks, P < .001) as well as in the extent of abnormal wall motion (28 +/- 19% versus 32 +/- 15%, P < .001) and left ventricular ejection fraction (53 +/- 14% versus 50 +/- 13%, P < .01). Among the 68 of 71 patients showing resting perfusion defects at 5 weeks, two groups were identified: 47 (group 1) who showed a significant (beyond the reproducibility limits) 7-month reduction of the resting perfusion defect, and 21 patients (group 2) in whom the perfusion defect remained unchanged. Ejection fraction and the extent of abnormal wall motion significantly (P < .01) improved in group 1 but not in group 2. Despite the presence of a comparable perfusion defect size between the two groups at 5 weeks after infarction, group 1 already showed a better regional and global ventricular function (P < .05). No significant differences were found between the two groups regarding age, medical therapy, the extent of underlying coronary disease, thrombolysis in the acute phase, Thrombolysis in Myocardial Infarction grade of the infarct-related vessel, and presence of collaterals on angiography. CONCLUSIONS: After anterior Q-wave infarction, the recovery of perfusion and wall motion may continue well after the subacute phase. Several patients exhibit relative hypoperfusion in viable tissue as late as 5 weeks after infarction, and a significant improvement of perfusion in the infarcted area commonly is observed between 5 weeks and 7 months. This delayed improvement of perfusion is associated with a delayed improvement of contractile function in the infarcted area after the first 5 weeks, which may continue for up to 7 months, suggesting the presence of hibernating myocardium in the infarcted area. Despite similar perfusion defect sizes, the level of regional function can be different at 5 weeks, and measurements taken around this time may not accurately estimate the eventual recovery of function.

Adult↗
PubMed1995

Infarct size after acute myocardial infarction measured by quantitative tomographic 99mTc sestamibi imaging predicts subsequent mortality.

BACKGROUND: 99mTc sestamibi is a recently developed radioisotope that has been used to measure myocardium at risk and infarct size. The relation between these measurements and subsequent patient outcome has not yet been demonstrated. METHODS AND RESULTS: Two hundred seventy-four consecutive patients with acute myocardial infarction underwent tomographic 99mTc sestamibi imaging on arrival at the hospital (to measure myocardium at risk before reperfusion therapy) and at hospital discharge (to measure the amount of salvaged myocardium and final infarct size). Defect size on the sestamibi images was quantified using a threshold value of 60% of peak counts from the circumferential count profile curves generated for five representative slices of the left ventricle. Patients were followed after hospital discharge to evaluate the association between final infarct size and subsequent mortality. The median defect size measured was 27% of the left ventricle at presentation to the hospital (range, 0% to 77%) and was 12% of the left ventricle at hospital discharge (range, 0% to 68%). Almost one half of the patients had a final infarct size of < or = 10%. The median amount of myocardium salvaged was 9% (range, -31% to 75%). During a median duration of follow-up of 12 months, there were 10 deaths (7 cardiac and 3 noncardiac) and 1 resuscitated out-of-hospital cardiac arrest. There was a significant association between infarct size and overall mortality (chi 2 = 8.66, P = .003) and cardiac mortality (chi 2 = 11.89, P < .001). Two-year mortality was 7% for patients whose infarct size was > or = 12% versus 0% for patients whose infarct size was < 12%. There also was a significant association between myocardium at risk and cardiac mortality (chi 2 = 6.87, P = .009). There was no association between myocardium at risk and overall mortality or between amount of myocardium salvaged and either overall mortality or cardiac mortality. CONCLUSIONS: Larger infarct size measured by 99mTc sestamibi imaging after acute myocardial infarction is associated with increased mortality risk during short-term follow-up.

Aged↗
PubMed2003

Extracellular concentrations of non-transmitter amino acids in peri-infarct tissue of patients predict malignant middle cerebral artery infarction.

BACKGROUND AND PURPOSE: Space-occupying brain edema is a life-threatening complication in patients with large middle cerebral artery (MCA) infarction. To determine predictors of this detrimental process, we investigated alterations of extracellular non-transmitter amino acid concentrations in peri-infarct tissue. METHODS: Thirty-one patients with infarctions covering >50% of the MCA territory in early cranial CT scans were included in the study. Probes for microdialysis, intracranial pressure, and tissue oxygen pressure were placed into the noninfarcted ipsilateral frontal lobe. Positron emission tomography imaging was performed in 16 of these patients to measure cerebral blood flow in the tissue around the neuromonitoring probes. RESULTS: Fourteen of the 31 patients developed a malignant MCA infarction, and 17 did not. The patients in the malignant group had significantly lower extracellular concentrations of non-transmitter amino acids than those in the benign group in the first 12 hours of neuromonitoring. At this time, CBF values determined in regions of interest around the probes by positron emission tomography and tissue oxygen pressure showed that the monitored tissues were not yet infarcted, and no differences in transmitter amino acids concentrations were found between the 2 groups. Furthermore, extracellular concentrations of non-transmitter amino acids were negatively correlated with size of infarction. CONCLUSIONS: We assume that reduction of non-transmitter amino acid concentrations reflects an expansion of the extracellular space by vasogenic edema formation in peri-infarct tissue of patients with malignant MCA infarction. Our findings facilitate early prediction of malignant edema formation and may help to increase knowledge of the pathophysiology of the peri-infarct zone of large MCA infarction.

Amino Acids↗
PubMed1999

Measurement of initial N-acetyl aspartate concentration by magnetic resonance spectroscopy and initial infarct volume by MRI predicts outcome in patients with middle cerebral artery territory infarction.

BACKGROUND AND PURPOSE: (1)H MR spectroscopy can be used to study biochemical changes occurring in the brain in stroke. We used it to examine the relationship between metabolite concentration (N-acetyl aspartate [NAA], lactate, cholines and creatines), size of infarct, clinical deficit, and 3-month clinical outcome in patients with middle cerebral artery (MCA) territory infarction. METHODS: Thirty-one patients with acute MCA territory infarction were recruited within 72 hours of the onset of symptoms. Single-voxel short echo time stimulated echo acquistion mode spectroscopy was used to obtain metabolite data from the infarct core. Metabolite concentrations were determined with use of variable projection time domain-fitting analysis. Infarct size was determined with T2-weighted images. Patient outcome groups at 3 months were "independent," "dependent," or "dead." RESULTS: All patients (100%; 95% CI 75% to 100%) who had an infarct >70 mL did poorly. Eighteen of 20 patients (90%; 95% CI 68% to 99%) with a core NAA concentration <7 mmol/L did poorly at 3 months, whereas 7 of 11 patients (64%; 95% CI 31% to 89%) with an initial NAA concentration >7 mmol/L did well. Combining these results showed that all patients who had an initial infarct volume >70 mL did poorly, irrespective of the NAA concentration. Of those patients with infarcts <70 mL, those who had a core NAA concentration >7 mmol/L did well (88%; 95% CI 47% to 100%), whereas those with a lower NAA concentration did poorly (80%; 95% CI 44% to 97%). There was no association between other metabolite concentrations and outcome. CONCLUSIONS: Infarct volume and NAA concentration can together predict clinical outcome in MCA infarction in humans.

Adult↗
PubMed1988

Reduced early diastolic extension in the infarcted portion in patients with old myocardial infarction.

To study relaxation characteristics of the infarcted myocardium, cyclic changes in the global left ventricular (LV) volume were measured in 20 patients with old myocardial infarction (OMI) and 17 normals (Normal) and those in the regional segment length were measured in 9 patients with anterior old myocardial infarction (anterior OMI) and 11 normals. The LV volume was calculated by using biplane LV cineangiograms. The regional segment length was calculated by measuring the spatial length between the 2 points of the ramifying branches on the left coronary arteries by using biplane coronary cineangiograms. The LV filling volume before atrial contraction (VR) was significantly less in the OMI compared with that in the normals (Normal 38 +/- 6 (mean +/- SD) ml/m2 vs 30 +/- 7 ml/m2: p less than 0.01), while filling volume by atrial contraction (Va) did not significantly differ (Normal 15 +/- 4 ml/m2 vs OMI 17 +/- 5 ml/m2). The lengthening of the segmental wall during diastole before atrial contraction (%LR) in the infarcted portion was 5.0 +/- 2.9% which was also significantly less than that in the non-infarcted portion (9.6 +/- 4.2%). The extent of lengthening by atrial contraction (%La) did not differ between the 2 portions (non-infarcted portion 3.8 +/- 1.1% vs infarcted portion 3.5 +/- 1.2%). Reduction of %LR was speculated to be caused by the incomplete relaxation in the myocardium adjacent to the infarcted portion and stiff myocardium in the infarcted portion. This study suggests that the infarcted myocardium may lead to a reduction of diastolic expansion before atrial contraction.

Angina Pectoris↗
PubMed1993

Noninvasive evaluation of total occlusion of infarct-related coronary artery after a first myocardial infarction.

Previous studies have demonstrated that the long-term prognosis after acute myocardial infarction in patients whose infarct-related artery remains occluded is worse than that in those with anterograde flow. To determine how to identify patients with occluded infarct-related arteries noninvasively, 143 consecutive patients after a first myocardial infarction underwent exercise testing and dipyridamole thallium scintigraphy. The incidence of total occlusion was higher in inferior/posterior infarction than in anterior infarction (29/53 vs 28/90; p = 0.005). In patients with inferior/posterior infarction, discriminant analysis revealed a sensitivity of 79%, a specificity of 88% and an accuracy of 83% (p = 0.0005) in identifying those with an occluded infarct-related artery. In patients with anterior infarction, the analysis showed a sensitivity of 68%, a specificity of 85% and an accuracy of 79% (p < 0.0001) in identifying those with an occluded artery. These results indicate that noninvasive study may be useful in the evaluation of total occlusion of the infarct-related coronary artery.

Adult↗
PubMed1976

Superimposition of transmural infarction following acute subendocardial infarction; how frequent?

Thirty-five consecutive patients with acute subendocardial infarction admitted to the coronary care unit during a 15-month period were identified and analyzed for location of infarction, and for the in-hospital course in terms of recurrent chest pain, the occurrence of a second infarction, and the clinical status at the end of hospitalization. Thirteen patients developed a transmural infarction sometime between 3 and 21 days (average, ten days) after the initial subendocardial infarction. The transmural infarction was defined by a separate episode of severe and prolonged chest pain, late development of QRS alteration, and an appropriate elevation of the creatine phosphokinase concentration. Our experience with acute subendocardial infarction, hertofore regarded as a relatively benign event, indicates that the immediate prognosis of the patient who sustains his first episode of subendocardial infarction is not at all benign, and, indeed, subendocardial infarction frequently heralds transmural infarction within the acute phase of the disease.

Aged↗
PubMed1995

Vectorcardiography in experimental myocardial infarction. Serial changes and correlation between QRS loop change and the infarction size.

The objectives of this study were to examine the serial vectorcardiographic changes following acute myocardial infarct and to assess the relationship between QRS loop changes and infarct size. Fifty adult male Long-Evans rats of 250-350 gm body weight were used to study experimental acute myocardial infarction induced by coronary artery ligation. Vectorcardiograms (VCG) of the Frank lead system were recorded before, and 1 day and 7 days after operation. Animals were sacrificed on the 7th day for histological quantitation of infarct area ratios. We found that (1) before operation, rats have ST elevation, probably due to early repolarization. (2) After coronary artery ligation, ECG showed characteristic dome-shaped ST elevation at 1 hr after ligation which returned to normal during the first day. Abnormal Q waves appeared thereafter. (3) After ligation, maximum QRS vector, ST vector and maximum T vector were reduced in magnitude the first day and recovered by the 7th day. The vectors tended to shift their direction to the right and to the posterior. QRS-T angle, however, widened as time went on. About half of the rats revealed changes in the inscription direction of the QRS loop and abnormal QRS morphology also appeared in about half of the ligated rats. (4) Those in whom abnormal QRS loop morphology and/or biting appeared had significantly larger infarct area ratios (p < 0.01). (5) Change in QRS loop inscription direction seemed not to be related to the infarct size. (6) In the LS plane, the difference in max QRS vector magnitude between the 1st and 7th days significantly correlated with the infarct area ratio (r = 0.533, p < 0.05). In the H plane, the change in the max QRS vector magnitude at the 7th day correlated with the infarct area ratio (r = -0.531, p < 0.05). In the F plane, changes in the direction of the max QRS vector were significantly correlated to the infarct area ratio both on the first (r = 0.431, p < 0.05) and 7th days (r = 0.531, p < 0.05). It is concluded that the VCG, like the ECG, had evolutional changes in AMI and that the QRS loop seen on vectorcardiography has only a slight correlation with the histological myocardial infarct size.

Animals↗
PubMed2002

Relationship between infarction location and size to QT dispersion in patients with chronic myocardial infarction.

The relationship between the location and size of an infarction and QT dispersion was investigated in 84 Japanese patients with chronic myocardial infarction (54 with anteroseptal infarction and 30 with inferior infarction). The control group consisted of 23 subjects without ischemic heart disease (13 normal subjects and 10 hypertensive patients). Corrected QT dispersion (maximum corrected QT interval minus minimum corrected QT interval: QTc dispersion), was significantly larger in the anterior infarction group than in the control group (69.9+/-21.5 msec vs 53.0+/-17.6 msec), while the inferior infarction group showed no significant difference from control subjects. QTc dispersion was significantly greater in the patients with large anterior infarcts than in those with small anterior infarcts (80.5+/-20.5 msec vs 61.9+/-18.8 msec). In patients with chronic myocardial infarction, QT dispersion is influenced by the infarct location and size. Accordingly, interpretation of QT dispersion data should take these factors into consideration.

Electrocardiography↗
PubMed1978

[Restricted myocardial infarction. Coronary angiographic and ventriculographic findings. Comparison with acute coronary insufficiency and transmural infarction].

The findings at coronary arteriography and ventricular angiography in 52 patients with a restricted myocardial infarct were compared with those of 106 patients with acute coronary insufficiency and 100 with transmural infarcts. Certain features place restricted myocardial infarction in an intermediate category when compared with the two other syndromes. The percentage of coronary occlusions was significantly higher in transmural infarction (23.5%) and in restricted infarction (16.6%) than in acute coronary insufficiency 6.8%). Study of the vessel beyond a tight stenosis (greater than or equal to 75% was particularly effective in clearly separating the three groups. As a result, 63% of patients with coronary insufficiency, 40% of these with restricted infarcts, and only 23% of patients with a transmural infarct could be referred for surgery. Ventricular angiography showed a close relationship between restricted infarction and acute coronary insufficiency because ventricular function appeared normal or subnormal (localised hypokinesia) in 69% and 81% of cases respectively, compared with 4% of cases of transmural infarction. Restricted myocardial infarction appears to resemble coronary insufficiency, but shows elevation of enzymes and often more marked disease of distal vessels.

Acute Disease↗
PubMedDate not supplied

Accelerated infusion of streptokinase in acute myocardial infarction results in better TIMI flow grade in infarct-related artery.

Bolus followed by rapid infusion of tissue plasminogen activator results in higher grade of TIMI flow in infarct-related artery as compared to slow infusion. In the present study, an accelerated regimen of streptokinase given over 15 minutes was compared with conventional infusion over one hour in 47 patients presenting within 12 hours of acute myocardial infarction. Forty-seven patients (44 males, 3 females; mean age 54.0 +/- 1.1 years) were randomly allocated to receive 1.5 million units of streptokinase either over 15 minutes (group 1, n = 24) or over one hour (group 2, n = 23) at a mean interval of 5.4 +/- 3.6 hours after onset of symptoms. All the patients received aspirin and intravenous heparin (1000 U/hr) for 96 hours after thrombolysis. Coronary angiography was performed in 43 patients (22 in group 1, 21 in group 2) prior to discharge from the hospital (mean 7 +/- 2.1 days after acute myocardial infarction) and patency of the infarct-related artery and grade of TIMI flow were determined. Infarct-related artery was patent (TIMI 2/3 flow) in 19 (86.4%) patients in group 1 as compared to 12 (57.1%) in group 2 (p < 0.05). TIMI grade 3 flow in the infarct-related artery was present in 13 (59.1%) in group 1 as compared to 7 (33.3%) in group 2 (p = 0.1). There was no significant difference between group 1 and 2 in time of presentation (mean 5.3 +/- 3.9 hrs vs 5.5 +/- 3.2 hrs), time to needle in hospital (25.6 +/- 11.2 min vs 26.3 +/- 6.2 min), site of infarct (anterior myocardial infarction 12 in group 1 vs 11 in group 2), relief of pain at 90 min (13 vs 12), more than 50 percent reduction of ST elevation at 90 minutes (17 vs 12) and left ventricular ejection fraction (48.8 +/- 9.1% vs 49.8 +/- 16.0%), respectively. Streptokinase was well tolerated in both the groups, although hypotension was more common with the accelerated regimen (5 in group 1 vs 3 in group 2; p = NS). Thus, 'accelerated' streptokinase given over 15 minutes in patients presenting within 12 hours of acute myocardial infarction is well tolerated and results in higher grades of TIMI flow in the infarct-related artery as compared to the "conventional" one-hour infusion regimen.

Adult↗
PubMed2005

Gated SPECT evaluation of outcome after abciximab-supported primary infarct artery stenting for acute myocardial infarction: the scintigraphic data of the abciximab and carbostent evaluation (ACE) randomized trial.

UNLABELLED: We used gated SPECT to evaluate the impact of abciximab on the efficacy of myocardial reperfusion in patients with acute myocardial infarction undergoing infarct-related artery stenting. METHODS: The Abciximab and Carbostent Evaluation (ACE) trial randomized 400 infarct patients to stenting alone or stenting plus abciximab. One-month (99m)Tc-sestamibi gated SPECT was planned in a subgroup of consecutive patients to evaluate infarct size, infarct severity, left ventricular volumes, and ejection fraction. RESULTS: The final study population included 182 patients (99 randomized to abciximab and 83 to stenting alone). Gated SPECT revealed smaller infarcts in the abciximab group than in the stenting-alone group (14.3% +/- 11.7% vs. 18.1% +/- 13%, P < 0.02), and lower infarct severity (minimum-to-maximum count ratio = 0.47 +/- 0.17 vs. 0.41 +/- 0.15, P < 0.02), resulting in a smaller left ventricular end-diastolic volume index (57.8 +/- 20.0 vs. 64.6 +/- 20.8 mL/m(2), P = 0.03) and left ventricular end-systolic volume index (31.7 +/- 17.4 vs. 37.5 +/- 18.6 mL/m(2), P = 0.05) in the abciximab group. One-month left ventricular ejection fraction was significantly higher in patients randomized to abciximab (47.4% +/- 11.3% vs. 43.9% +/- 11.7%, P = 0.05). CONCLUSION: The use of abciximab therapy as an adjunct to infarct-related artery stenting leads to a reduction in infarct size and severity, resulting in smaller 1-mo left ventricular volumes and better left ventricular function. Gated SPECT appears to be an ideal tool for outcome assessment in infarct patients undergoing different treatment strategies.

Abciximab↗
PubMed1989

[Clinical methods for evaluating infarct size and its anatomic correlations. A study conducted with 193 cases. II. Evaluation of infarct size by determining maximal creatine phosphokinase in serum. Enzimatico-anatomic correlations].

AIMS: To compare the infarct size calculated by the peak serum CK method with the anatomic infarct size in a population dying of acute myocardial infarction. CONCEPT AND PLACE OF THE STUDY: To use the method of peak serum CK in the assessment of infarct size, calculated by a method developed by the authors, in a population dying of acute myocardial infarction in a coronary care unit. METHODS: 193 patients who successively died with acute myocardial infarction entered the study. After establishing the exclusion criteria the anatomical infarct size was measured using the method developed by the authors of myocardial slices after fixation of the heart and by the peak CK method. The two methods were correlated using linear regression curves. RESULTS AND CONCLUSIONS: A global correlation between the two methods was found although wide scattered values were found. After dividing the population in several subgroups, the analysis showed that survival below 48 hours, death in left ventricular failure, inferior infarcts and reinfarction influenced negatively this correlation. The anatomical method showed its value for this kind of evaluation having always in mind its known limitations. The enzyme method looked less discriminating as peak CK, obtained by 12 h sampling will seldom reflect the peaks of CK liberation curve. As the study was applied to a population of patients dying of acute myocardial infarction its results cannot be applied without caution to a population of survivors. We anticipate that in such a population peak CK will have a better correlation with real CK peaks even with 12 hours sampling and therefore reflecting more accurately infarct size.

Autopsy↗
PubMed1989

[Heart insufficiency in acute myocardial infarct. Long-term prognostic implications. Study of 213 cases of myocardial infarct].

OBJECTIVE: To evaluate intra-hospital and first year prognosis of the acute myocardial infarction. DESIGN: Univariate analysis of hospital and late mortalities in 21 characteristics on the evolution of the acute phase of myocardial infarction of patients sequentially admitted in a coronary care unit. SETTING: Coronary care unit and out patient clinic of a school hospital. PATIENTS: A group of 213 patients with acute myocardial infarction admitted sequentially in a coronary care unit was studied. MATERIAL AND METHODS: Making use of a computerized information system the following characteristics f the patients were prospectively studied: age, sex, previous history of myocardial infarction, angor, diabetes, hypertension and tabacism, presence of left ventricular dysfunction electrocardiographic localization of the infarction, presence of angor in the acute phase of the infarction, epistenocardic pericarditis, hypertensive reaction, hypotension, sinus tachycardia, sinus bradycardia, supraventricular disrhythmias, ventricular disrhythmias, A-V block, complete right bundle branch block, complete left bundle block and peak of CPK values. Univariate analysis was made between each one of these characteristics and hospitalar and one year mortalities. RESULTS: Statistically significant differences were obtained in the hospitalar mortality in the following characteristics: age (p less than 0.001), sex (p less than 0.03), previous history of diabetes (p less than 0.05) and tabagism (p less than 0.005), left ventricular disfunction (p less than 0.0005), hypotension (p less than 0.005), sinus tachycardia (p less than 0.0005), sinus bradycardia (p less than 0.024), A. V. block (p less than 0.004), and peak of CPK (p less than 0.05). Statistically significant differences were found in one year mortality in the following characteristics: age (p less than 0.001), left ventricular disfunction (p less than 0.02), sinus tachycardia (p = 0.0116) and peak of CPK (p less than 0.05). CONCLUSION: Influence in the hospitalar mortality was demonstrated by the following characteristics of the patients with myocardial infarction: age, sex, previous history of diabetes and tabagism, left ventricular disfunction, infarct size expressed by the peak values of CPK, sinus tachycardia, sinus bradycardia, hypotensive reaction in the acute phase of the myocardial infarction and A-V block. Mortality in the late phase infarction was influenced by age, left ventricular dysfunction, sinus tachycardia and peak values of CPK.

Adult↗
PubMed1989

Clinical first myocardial infarction: coronary artery disease and old infarcts in 53 consecutive fatal cases from a coronary care unit.

The frequency and size of previous unrecognized myocardial infarction in patients with first clinical diagnosed acute myocardial infarction are unknown. In this study, 53 consecutive patients with clinical first acute myocardial infarction which proved fatal were studied postmortem. All showed acute infarction (inclusion criterium). Acute coronary thrombosis was found in 51 (96%). One-, two-, and three-vessel disease diagnosed by postmortem coronary angiography (diameter stenosis greater than or equal to 75%) was present in 17 (32%), 22 (42%), and 14 (26%), respectively. One or more old infarcts were found in 24 of the cases (45%) despite no history of previous myocardial infarction. Old infarcts were found in 86% of the hearts with three-vessel disease and in 55% of the hearts with two-vessel disease, but none were found in the hearts with one-vessel disease. The median weight of the old infarcts was 4 grams (range: 0.5 to 25 grams) corresponding to 5% (0.5 to 14%) of the ventricular myocardium. Thus, two- or three-vessel coronary artery disease and old infarcts are often present in patients dying from their clinical first acute myocardial infarction.

Adult↗
PubMed1986

[Definition and significance of the area at risk in myocardial infarct and the ischemic border zone in acute myocardial infarct].

Early localisation of infarction, estimation of infarct size and visualisation of metabolic and structural changes is of great importance for the management of acute myocardial infarction. This paper is based on an experimental model using a combination of in-vivo and in-vitro methods that allow the evaluation of the area at risk of infarction, the border zone and its changes over time. The purpose of the study was to characterize the topography and the time course of the border zone. The border zone forms an approximately 2 mm wide margin at the lateral edges of the infarct, with increasing width of the border zone along the subepicardium. Increasing duration of ischemia is associated with a dynamic sequence of events, not only within the area at risk of infarction but also in the peri-ischemic border zone, leading to an expansion of the subepicardial margin due to improved collateral blood flow over time. The area at risk of infarction is characterized by early distinct metabolic changes that were visualized as soon as 90 to 120 seconds following coronary artery occlusion. After 6 hours of occlusion almost the entire area at risk shows signs of irreversible injury due to severe hypoperfusion. The border zone, in contrast, is characterized by only moderate metabolic changes due to greater collateral perfusion (45 to 80% of the regional blood flow in the non-ischemic vascular bed). Several interventions were chosen and evaluated for their effects on the dynamic course of events within the area at risk of infarction and in the border zone. Interventions that have strong myocardial protective effects such as the combination of alpha- and beta-blockade, the application of specific O2-carriers (Perfluorocarbons) and pressure controlled retrograde perfusion via the coronary sinus ("PICSO"), not only reduce infarct size by 20 to 40% of the myocardium at risk of infarction, but also induce substantial topographic, functional and metabolic changes within the border zone.

Animals↗