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PubMed1978

[Coronary atherosclerosis, coronary thrombosis and myocardial infarction in autopsy cases. 9th communication: relationship of coronary thrombosis and myocardial infarction (author's transl)].

The autopsy reports of the Pathological Institute Erfurt of the period from 1.1.1951 until 31.12.1969 were scored for cases of myocardial infarction and coronary thrombosis. Among 2,393 morphologically analysed myocardial infarctions 454 coronary thromboses (18.97 per cent) were found. Males were significantly more affected than females. Fresh infarcts showed significantly more thromboses than callous infarcts. We found fresh and occluding vessel thromboses more frequently in fresh infarctions. The analysis of age distribution yielded an increase of the rate of thrombosis in cases with myocardial infarction. On the other hand, the frequency of infarctions in cases with a coronary thrombosis was decreasing. It is suggested that the risk for infarctions is larger in younger people with coronary thrombosis than in older ones. No infarctions were detected in 165 cases of thrombosis. Preferably this group includes those cases in which the patients deceased within 6 to 8 hours and, therefore, the infarction was not morphologically detectable.

Adult↗
PubMedDate not supplied

Temporal changes in sequential quantitative thallium-201 imaging following myocardial infarction in dogs: comparison of four- and twenty-four-hour infarct images.

Thallium-201 ((201)T1) myocardial perfusion imaging allows definition of zones of myocardial infarction and ischemia. The temporal changes in sequential quantitative (201)T1 infarct imaging was studied 4 and 24 hours in dogs subjected to closed-chest anterior wall myocardial infarction. A temporal decrease in (201)T1 imaged infarct areas was noted in 10 of 13 animals. In no animal did the infarct area increase. The imaged infarct area decreased by an average of 30% from 12.9 ± 6.2 cm(2) at 4 hours to 9.1 ± 5.1 cm(2) at 24 hours (p < 0.001), and involved 34 ± 16% of the total (201)T1 left ventricular distribution at 4 hours and 22 ± 14% at 24 hours (p < 0.001). The magnitude of temporal change in imaged infarct area was not predicted by initial image defect or final histopathologic infarct size. Thus, the results of (201)T1 infarct imaging in the early period of infarction are clearly dependent upon the time at which the procedure is performed.

Animals↗
PubMed1994

Cerebral infarction within six hours of onset: prediction of completed infarction with technetium-99m-HMPAO SPECT.

UNLABELLED: Technetium-99m-HMPAO can be used to evaluate abnormal brain perfusion in the hyperacute stage of stroke. METHODS: We investigated cerebral blood flow using 99mTc-HMPAO SPECT in 31 patients within 6 hr after the onset of cerebral infarction and analyzed the relationship between abnormal perfusion and morphological changes on follow-up CT scans. Patients were classified into an infarct group and a noninfarct group, and the lesions on SPECT images were divided into infarct and peri-infarct regions. RESULTS: Among a total of 30 infarct regions, three lesions studied at 1.5, 2.5 and 5 hr after the ictus showed local hyperperfusion suggestive of early postischemic hyperemia, while the other 27 lesions demonstrated local hypoperfusion. All of the peri-infarct regions showed moderate hypoperfusion. The noninfarct group consisted of five patients, four of whom showed no perfusion abnormalities. The lesion-to-contralateral radioactivity ratios for the infarct and peri-infarct regions were respectively 0.48 +/- 0.14 and 0.75 +/- 0.10 in the patients with hypoperfusion, while the right-to-left ratio in the noninfarct group was 0.97 +/- 0.10. CONCLUSION: This SPECT study of cerebral blood flow demonstrates that local hyperperfusion occurs in some infarcts even within 6 hr of onset and that infarcted and morphological viable brain can be distinguished by a lesion-to-contralateral radioactivity ratio of 0.6 within this time range.

Adult↗
PubMed1997

Acute ischemic ventricular arrhythmias in pigs with healed myocardial infarction: comparative effects of ischemia at a distance and ischemia at the infarct zone.

BACKGROUND: The myocardium bordering a healed infarction undergoes electrophysiological and autonomic neural derangements that may interact with a new ischemic episode to promote arrhythmias. Therefore, peri-infarction ischemia may be more arrhythmogenic than ischemia at a distance from the infarct zone, but this is not known. METHODS AND RESULTS: Forty-two anesthetized open-chest pigs with a 1-month-old myocardial infarction induced by permanent ligature of the distal left anterior descending coronary artery (LAD) underwent a coronary reocclusion at either the proximal LAD (group 1, peri-infarction ischemia, n=21) or at the circumflex coronary artery (group 2, ischemia at a distance, n=21). Ventricular arrhythmias were analyzed during 60 minutes of coronary reocclusion and during programmed electrical stimulation. Infarct size was measured, and underperfusion at the occluded area was estimated by recording 99mTc-tetrofosmin activity. Weights of acute ischemic (23+/-9 versus 21+/-9 g) and healed infarction (10+/-6 versus 10+/-3 g), baseline LV pressure and peak of LV dP/dt, and radiotracer activity at the occluded area (3+/-2% versus 5+/-2% of normal tissue) were comparable between the two groups. Compared with group 2, group 1 showed more ventricular premature beats (median, 136 versus 59; P=.008), a higher incidence of spontaneous sustained ventricular tachycardia (57% versus 19%, P=.02) and ventricular fibrillation (76% versus 47%, P=.05), and greater electrical inducibility of sustained ventricular tachycardia (65% versus 28%, P=.03) but comparable induction of ventricular fibrillation. CONCLUSIONS: Ischemia superimposed at the border of a 1-month-old myocardial infarction is more arrhythmogenic than ischemia at a distance from the infarct zone in swine. Data suggest the presence of electrophysiological instability at the peri-infarction zone.

Animals↗
PubMed1997

Effects of patency of infarct-related coronary artery on acute outcome in acute myocardial infarction patients undergoing urokinase therapy. Collaborative Research Group on Thrombolysis.

OBJECTIVE: To study the effects of patency of infarct-related coronary artery on acute outcome in cases of acute myocardial infarction undergoing urokinase therapy. METHODS: One thousand one hundred and thirty-eight cases of acute myocardial infarction admitted in 37 collaborative hospitals were given urokinase intravenously with a standard program. Patency of infarct-related coronary artery assessed by uniform criteria occurred in 757 patients (66.5%) and non-patency in 381 patients (33.5%). Four-week mortality and frequency of various severe complications were compared between patency patients and non-patency patients. RESULTS: The 4-week mortality in patients with patency was 3.4% versus 21.8% in those without patency (P < 0.001). Frequencies of various severe complications, such as heart failure, shock, ventricular fibrillation, bundle branch blocks and mechanical complications (P < 0.01), and complete atrioventricular block (P < 0.05) were much higher in patients without than in those with patency. In large sized infarcts such as high lateral plus anterior wall infarction the difference in 4 week mortality was even more obvious between patients with and without patency (2.6% vs 32.7%, P < 0.001). Using Cox proportional hazards regression model analysis, patency of infarct-related coronary artery was defined as the most important independent predictor of 4-week mortality. The risk ratio for occluded versus patent infarct-related coronary artery was 6.69. CONCLUSION: On univariate and multivariate analyses, patency of the infarct-related coronary artery was the most important prognostic factor for acute outcome in acute myocardial infarction.

Adult↗
PubMed2005

Posterior cerebral artery infarction from middle cerebral artery infarction.

BACKGROUND: While it is known that posterior cerebral artery (PCA) infarction may simulate middle cerebral artery (MCA) infarction, the frequency and localization of this occurrence are unknown. OBJECTIVE: To determine the frequency of PCA infarction mimicking MCA infarction and the territory of the PCA most commonly involved in this simulation. DESIGN: We studied 202 patients with isolated infarction in the PCA admitted to our stroke center to determine the frequency of PCA infarction simulating MCA infarction, the involved PCA territory, and the patterns of clinical presentation. RESULTS: We found 36 patients (17.8%) with PCA ischemic stroke who had clinical features suggesting MCA stroke. The PCA territory most commonly involved was the superficial PCA territory (66.7%), followed by the proximal PCA territory (16.7%) and both the proximal and the superficial PCA territories (16.7%). The principal stroke mechanism was cardioembolic (54.1%) in the superficial PCA territory, lacunar (46.2%) in the proximal PCA territory, and undetermined (40.2%) in both the proximal and the superficial territories. Among the 36 patients, the most common clinical associations were aphasia (13 patients), visuospatial neglect (13 patients), and severe hemiparesis (7 patients). CONCLUSIONS: Posterior cerebral artery infarction simulating MCA infarction is more common than previously thought. Early recognition of the different stroke subtypes in these 2 arteries may allow specific management.

Aged↗
PubMed2004

[Study of postmyocardial infarction scar-formation mechanisms: advantage of an experimental myocardial infarction model in mice].

Myocardial infarction involves scar-formation mechanisms in which inflammation, proliferation, cell differentiation, apoptosis and angiogenesis all play a role. Better knowledge of the scar-formation process would be helpful in developing new therapies. The authors have generated a mouse model for infarction because its possible application in transgenic mice would allow the role of target genes in postinfarction scar-formation mechanisms to be studied. An infarction is caused by ligating the descending branch of the left coronary artery. At various times after ligation, the mice are sacrificed to determine the size of the infarction, left ventricular function and the overall myocardial scar-formation process. Early mortality was 10%. Between the fourth and sixth day postsurgery, 25% of mice died of a ruptured, infarcted left ventricle. The size of the infarctions diminished with time, while the surface of the left ventricle increased. In hemodynamics, 15 and 30 days after infarction, left ventricle telediastolic pressure was higher, telesystolic pressure was lower and contractility in indexes had collapsed. After an inflammatory phase in which polynuclear neutrophils colonized the scar, granulation tissue set in with a proliferation of myofibroblasts and growth of new blood vessels. These cells disappeared from the scar gradually, leaving behind a matrix rich in collagen and devoid of any contractile properties. The authors have characterized a murine model of myocardial infarction, with applications in transgenic mice and in view of establishing new agents in postmyocardial infarction repair.

Animals↗
PubMed1998

Observations of the treatment of women in the United States with myocardial infarction: a report from the National Registry of Myocardial Infarction-I.

BACKGROUND: To determine whether there are sex differences in the demographics, treatment, and outcome of patients with acute myocardial infarction in the United States, data from the National Registry of Myocardial Infarction-I from September 1990 to September 1994 were examined. METHODS: The National Registry of Myocardial Infarction-I is a national observational database consisting of 1234 US hospitals in which each hospital submits data from each patient with acute myocardial infarction to a central data collection center. For these analyses, the following variables were examined in 354 435 patients with acute myocardial infarction: demographics; use of medical therapy including thrombolytic agents; use of procedures including cardiac catheterization, percutaneous transluminal coronary angioplasty, and coronary artery bypass surgery; length of hospital stay; adverse events (stroke, major bleeding, or recurrent myocardial infarction); and causes of death. RESULTS: In comparison with men, women experiencing acute myocardial infarction in the United States are older, with 55.7% older than 70 years. Women have a higher mortality rate than men even when controlled for age and die less often from arrhythmia but more often from cardiac rupture whether or not thrombolytic therapy is used. Treatment with aspirin, heparin, or beta-blockers is less frequent in women. When thrombolytic therapy is used, women are treated an average of almost 14 minutes later than men and experience a greater incidence of major bleeding. Cardiac catheterization, percutaneous transluminal coronary angioplasty, and coronary artery bypass surgery are used less often in women. CONCLUSIONS: Observations from the National Registry of Myocardial Infarction-I document important sex differences in demographics, treatment, and outcome of patients with acute myocardial infarction in the United States.

Age Distribution↗
PubMed2000

One-year clinical outcomes and relative costs of primary infarct artery stenting versus angioplasty following systemic thrombolysis for acute myocardial infarction.

We investigated the clinical effectiveness and relative cost of two different infarct artery revascularization strategies in patients following systemic thrombolysis for acute myocardial infarction. The clinical efficacy and relative cost of stenting and angioplasty have not been investigated in patients requiring infarct artery revascularization after systemic thrombolysis for myocardial infarction. We prospectively enrolled 220 consecutive patients who received thrombolytic therapy for acute myocardial infarction and were subsequently treated with either angioplasty or primary stenting of the infarct artery. In-hospital and 1-year clinical outcomes, including death, myocardial infarction, and repeat revascularization, and total hospital costs over the 1-year study period were assessed. Compared to angioplasty, primary stenting resulted in lower in-hospital mortality (4% vs. 0%; P = 0.01) and reduced rates of repeat percutaneous or surgical revascularization (7% vs. 0%; P = 0.0009). At 1-year follow-up, stenting was associated with a lower death rate (6.25% vs. 0%; P = 0.002) and reduced repeat infarct artery revascularization (11% vs. 27%; P = 0. 001). Initial hospitalization costs were higher in the stent group ($11,818 +/- $3,377 vs. $9,723 +/- $8,661; P = 0.014) due primarily to catheterization laboratory-related expenditures ($7,346 +/- $2, 395 vs. $3,567 +/- $1,212; P = 0.0001). However, the cumulative 1-year medical cost difference between the two groups was not significant ($13,938 +/- $5,939 vs. $12,914 +/- $9,308; P = 0.33). Following thrombolytic therapy, primary infarct artery stenting reduced in-hospital and 1-year mortality and revascularization rates compared to angioplasty. Stenting was associated with higher initial hospital costs, which were off-set by lower revascularization rates, resulting in comparable total hospitalization costs after 1 year. These findings have important clinical and economic implications in an increasingly cost-conscious health care environment. Cathet. Cardiovasc. Intervent. 49:135-141, 2000.

Angioplasty, Balloon, Coronary↗
PubMed1988

Morbidity during five years after myocardial infarction and its relation to infarct size.

In 809 patients with a recent myocardial infarction, morbidity during 5-year follow-up was assessed. The overall 5-year mortality rate was 33% (39% in patients with larger infarcts and 26% in patients with smaller infarcts) as judged from maximum serum enzyme activity (p less than .001). In terms of morbidity, no significant association with estimated infarct size was observed. Patients with smaller infarcts tended to have a higher reinfarction rate and were rehospitalized more often, whereas a similar proportion of patients with large and small infarcts developed stroke. Among survivors, chest pain tended to be more common in patients having smaller infarcts, whereas symptoms of dyspnea and claudicatio intermittens were similar in both groups, as were smoking habits, work capability, and varying forms of medication. We thus conclude that during a 5-year follow-up after acute myocardial infarction, mortality, but not morbidity, was related to the original infarct size.

Electrocardiography↗
PubMed1995

In consecutive patients hospitalized with acute myocardial infarction, infarct location according to routine electrocardiogram is of minor importance for the outcome.

Most studies have suggested that patients with anterior myocardial infarction have an adverse prognosis compared with patients with inferior infarction. The objective of this study was to compare the mortality and morbidity in anterior versus inferior acute myocardial infarction (AMI) during 1 year in a consecutive series of patients hospitalized with AMI. All patients fulfilling the criteria for AMI who were admitted to a single hospital during 21 months (n = 921) participated in the study. Patients with anterior infarction (n = 312) had a 1-year mortality rate of 26% versus a rate of 24% for patients with inferior infarction (n = 269) (p > 0.2). The corresponding figures for patients with no previous infarction who developed Q waves were 27 and 21%, respectively (p > 0.2). Reinfarction, thromboembolic events, and other aspects of morbidity during long-term follow-up appeared with similar frequency in the two groups. Thus, in a nonselected group of patients admitted to a single hospital because of AMI, the prognosis was found to be similar among patients with inferior and those with anterior infarction. In the subset of patients with a first myocardial infarction who developed Q waves, there was a trend indicating higher mortality in anterior infarction.

Adrenergic beta-Antagonists↗
PubMed1993

Interstitial collagen is increased in the non-infarcted human myocardium after myocardial infarction.

In this study we report the changes of interstitial collagen in the human non-infarcted interventricular septum after a myocardial infarction as well as in hypertrophic human hearts with or without hypertension. The collagen amount was determined with the Sirius Red morphometry technique, which enabled us to perform these studies on routinely processed, paraffin embedded sections. The collagen amount was significantly increased in the septum of infarct patients as compared to non-infarcted controls (P < 0.001). The collagen amount in the septum of the hypertensive hypertrophy group (HH) was significantly increased as compared to the non-hypertensive hypertrophy group (NHH) (P < 0.01). The collagen content in the NHH was not significantly different from the controls in the infarct group, while the collagen amount in the HH showed no significant difference to the collagen content in the infarct group. The results indicate that collagen deposition is increased in the non-infarcted myocardium after a myocardial infarction, as well as in the hypertensive hypertrophied myocardium. The data suggest that the appearance of excessive collagen is not mediated by cardiac hypertrophy per se, but that the underlying cause, infarction or hypertension, is the significant factor.

Adult↗
PubMed1998

Impact of resting and ischemic blood flow on infarct probability in ischemic preconditioning--a new approach to infarct size-blood flow data by logistic regression.

The linear regression analysis of infarct size (IS) v ischemic myocardial blood flow (MBF) does not account for the heterogeneity of MBF and infarcted tissue; moreover, it cannot assess a blood flow threshold for infarction (MBFT) accurately, as with ischemic preconditioning (IP) the close relationship between ischemic MBF and IS otherwise observed is lost. Finally, the impact of resting blood flow on myocardial infarction cannot be considered in such analysis. Therefore, in a retrospective data analysis of 32 enflurane-anaesthetized swine undergoing 90 min severe ischemia and 120 min reperfusion without (CON, n = 12) or with IP induced by either 3 (IP3, n = 8) or 10 min ischemia (IP10, n = 12) and 15 min reperfusion, a MBFT was assessed by logistic regression (LR) in individual tissue pieces. MBFT was arbitrarily defined as that ischemic MBF (microspheres) at which infarct probability was 0.2, derived from the ratio of infarcted (n = 141, TTC) to all tissue samples (n = 684). The duration of the preconditioning ischemia and MBF both at rest and during the sustained ischemia were significant predictors of infarct probability. Ischemic MBFT at an infarct probability of 0.2, was 0.089 +/- 0.023 ml/min/g in CON. MBFT was decreased to 0.051 +/- 0.03 ml/min/g with IP3 (P < 0.05 v CON) and further to 0.004 +/- 0.037 ml/min/g with IP10 (P < 0.05 v CON, IP3). Corresponding to the leftward shift of MBFT, the relationships between infarct probability and MBF were shifted in parallel by IP with no change in their slopes.

Animals↗
PubMed1999

[Acute myocardial infarction in Germany between 1996 and 1998: therapy and intrahospital course. Results of the Myocardial Infarction Registry (MIR) in Germany].

The "Myocardial Infarction Registry" in Germany (MIR) is a multicenter and prospective registry of consecutively included, unselected patients with acute myocardial infarction. The purpose of MIR is to document the actual praxis of decision making and prescribing of an optimized infarction therapy in AMI patients. Optimized infarction therapy is defined as the combination of reperfusion therapy and ASS, betablocker, and ACE inhibitor.14,598 patients with acute myocardial infarction were included between 12/96 and 5/98 in 217 hospitals throughout Germany. 68% of the patients were male; mean age was 67 years. The prehospital delay time was 195 minutes in median, the first ECG was diagnostic in 66% of the patients. A reperfusion therapy was applied in 46.1% of the patients (thrombolysis 36.2%, primary PTCA 9.9%). During the acute phase, the following adjunctive therapy was used: ASS in 90.3%, betablockers in 53.8%, and ACE inhibitors in 52.5%. Intrahospital mortality was 15.4%. Compared to hospitals without cardiologists, the hospitals with cardiologist had a lower intrahospital mortality (13.8% versus 16.1%; p < 0.001). Reasons are the more frequent use of a reperfusion therapy by cardiologists (54.3% versus 42.3%; p < 0. 001) and the availability of a catheter laboratory with PTCA facilities.A lower intrahospital mortality was associated with each therapy of the optimized infarction therapy: reperfusion therapy (odds ratio 0.7; 95% CI: 0.5-0.8), ASS (odds ratio 0.6; 95% CI: 0. 5-0.8), betablocker (odds ratio 0.6; 95% CI: 0.5-0.7) and ACE inhibitor (odds ratio: 0.5; 95% CI: 0.4-0.7). However, patients with poor initial prognosis - such as cardiogenic shock, hypotension and/or bradycardia - could not benefit from the orally adjunctive therapy. This fact may have led to an overestimation of the influence on intrahospital mortality. In representative communal German hospitals, a reperfusion therapy in combination with an optimized adjunctive therapy in patients with acute myocardial infarction is associated with a reduction in intrahospital mortality. Compared to previous registries, the application of betablockers and ACE inhibitors was clearly increased. Reasons could be the participation in a quality registry, the obligation to document why a therapy has not been given and repeated and intensified education of the treating physicians.Thus, the mainly communal hospitals in Germany are increasingly following recommendations about the early treatment of acute myocardial infarction. Myocardial infarction registries such as MIR reflect daily prescribing habits in hospitals and describe the implementation of the results of randomized trials into daily routine.

Adrenergic beta-Antagonists↗
PubMed2005

Acute administration of angiotensin converting enzyme inhibitors in thrombolysed myocardial infarction patients is associated with a decreased incidence of heart failure, but an increased re-infarction risk.

INTRODUCTION: Ventricular remodeling starts very early after the onset of an acute myocardial infarction (AMI), and can be prevented by ACE-inhibitors. However, very limited data are available on the effect of acute (< 9 hours) treatment with angiotensin converting enzyme (ACE) inhibitors after an AMI on mortality, heart failure and re-infarction. The aim of the present study was to evaluate the effects of acute ACE-inhibitor treatment. METHODS: We performed a pooled analysis of three very similar randomized, placebo-controlled multi-center trials. In 845 thrombolysed patients with mainly first anterior MI, patients were randomised to acute ACE-inhibitor treatment (< 9 hours after MI) or placebo. RESULTS: After acute ACE-inhibitor treatment we observed similar 3-months mortality rates, and a significant reduction in the incidence of 3-months heart failure (26.1 vs. 19.3%; RR 0.67; 95% CI 0.45-1.0) as compared to placebo. In contrast, acute ACE-inhibitor treatment was associated with a significant 2.0 times increased 3-months re-infarction risk (7.0 vs. 3.6%; RR 2.0; 95% CI 1.1 to 3.8). Subgroup-analysis showed that patients with small infarct sizes treated with acute ACE-inhibitor (peak CPK < 1000 IU) had a 7.6 times higher re-infarction risk (95% CI 1.7 to 33) than patients with small infarctions treated with placebo. CONCLUSIONS: Acute ACE-inhibitor treatment in thrombolysed patients with mainly first anterior AMI resulted in a reduction of heart failure and similar mortality, but an increase in re-infarction rates, especially in patients with small infarct sizes. These results warrant caution for the very early use of ACE-inhibitors in smaller infarctions, although this needs to be confirmed in a larger prospective randomised clinical trial.

Aged↗
PubMed1986

Relationship between changes in ST segment elevation and patency of the infarct-related coronary artery in acute myocardial infarction.

Forty-one patients with acute myocardial infarction and ST segment elevation were studied to determine the relationship between early changes in ST segment elevation, time to peak serum creatine kinase (CK), peak serum CK, left ventricular function, and patency of the infarct-related artery. ST segment elevation decreased by more than 40% within 8 hours of peak sigma ST in all patients with inferior infarction and in 10 of the 13 patients with anterior infarction and subtotal occlusion, but in none of the patients with anterior infarction and total occlusion (p = 0.003). The time to peak serum CK was related to the rate of decrease of ST segment elevation in patients with anterior (r = 0.59) and inferior (r = 0.71) infarction. In patients with anterior infarction, peak serum CK tended to be lower and left ventricular ejection fraction (EF) higher in those with rapid resolution of ST segment elevation than in those with persistent ST elevation (1721 +/- 1422 U/L vs 3285 +/- 1148 U/L, p less than 0.10, for peak CK; and 50.3 +/- 18.5% vs 41.2 +/- 12.8%, p = NS, for EF), but there was no difference in the patients with inferior infarction. Early resolution of ST segment elevation is an index of early spontaneous antegrade or collateral reperfusion in patients with acute myocardial infarction.

Adult↗
PubMed1992

Reduced infarct size in nonreperfused myocardial infarction by combined infusion of isosorbide dinitrate and streptokinase.

The value of thrombolytic therapy in myocardial infarction is well established, while any beneficial effect of adjunct therapy is more uncertain. In a double-blind, randomized, parallel-group study the effect of combined intravenous infusions of streptokinase and isosorbide dinitrate (ISDN) on enzyme-estimated infarct size was investigated. One hundred consecutive patients with strong clinical and electrocardiographic suspicion of myocardial infarction, admitted to the coronary care unit within 8 hours after the onset of symptoms, were given a streptokinase infusion of 1.5 million units for 1 hour and a titrated dose of ISDN or placebo for 48 hours. From isoenzyme B of creatine kinase (CK-B) values measured every 4 hours, the infarct size was calculated and the possible presence of reperfusion was evaluated. The infarct size in patients receiving ISDN infusion was reduced (p = 0.04, one-sided test) compared with placebo. By subdividing the patients according to whether or not reperfusion had occurred, the infarct size appeared to be similar following ISDN and placebo in patients with reperfusion (419 versus 369 U/L), whereas the infarct size in patients not reperfused was markedly reduced after treatment with ISDN (223 versus 1320 U/L, p = 0.003). In conclusion, the present study demonstrates that the infarct size may be reduced by other means than reperfusion and it supports the use of combined infusion of thrombolytic agents and nitrates in patients with suspected myocardial infarction.

Adult↗
PubMed1992

Ventricular tachycardia after infarction: sources of coronary blood flow to the infarct zone.

The purpose of this study was to determine the sources of coronary blood flow to infarct scars in patients with sustained ventricular tachycardia occurring late after myocardial infarction, which is necessary for transcoronary sclerosis or embolization. Angiograms of 32 consecutive patients (age 63 +/- 8 years, ejection fraction 0.30 +/- 0.10) were reviewed. Sources of blood flow to the infarct zone were identified as coming from a recanalized infarct-related artery, side branch, collateral, or coronary bypass graft. Eighty-four percent of patients in the study had an identifiable blood supply to the area of previous infarction. More than one source of blood flow to anterior infarct locations were observed more often than to inferior infarct locations (53% vs 17%, p = 0.03). Transcoronary mapping for possible chemical ablation should be technically feasible in the majority of patients with ventricular tachycardia. Infarct zone blood flow arises from any of several sources and varies somewhat depending on infarct location.

Collateral Circulation↗