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PubMed1991

Hypertrophy of surviving myocytes overlying the infarct in human old myocardial infarctions with abnormal Q waves.

The time course of hypertrophy of surviving myocytes overlying the infarct after the onset was examined and the hypertrophy was analyzed in relation to the transmural extent of infarct in 34 autopsied hearts with Q wave infarction. The 34 hearts were divided into 4 groups according to the length of time between the onset of infarction and death. This was less than 5 days in group 1 (n = 10), 20-30 days in group 2 (n = 7), 40-60 days in group 3 (n = 7), and 12-24 months in group 4 (n = 10). To clarify the regional hypertrophy of myocytes overlying the infarct, the size of the surviving myocytes in the outer third of the left ventricular wall in the 1-cm wide central zone of the infarct was compared with that of the myocytes in the outer third of the left ventricular wall without infarction (control wall) in the same heart. To exclude factors which stimulate the hypertrophy of the whole left ventricle, the ratio of the monocyte diameter in the infarcted wall to that in the control wall was examined. It was 1.0 +/- 0.0 (mean +/- SD) in group 1, 1.0 +/- 0.1 in group 2, 1.2 +/- 0.1 in group 3, and 1.3 +/- 0.1 in group 4. The ratio was significantly higher in group 3 than in group 1 and 2, and was highest in group 4. In group 4, the corrected percentage transmural extent of infarct indicating the original transmural extent of infarct at the acute stage was 63 + 8%, and this transmural extent correlated positively with the ratio of myocyte diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Effects of severity of the residual stenosis of the infarct-related coronary artery on left ventricular dilation and function after acute myocardial infarction.

OBJECTIVES: This study was designed to evaluate the relation between the severity of the residual stenosis of the infarct-related artery and changes in left ventricular volume and function after a first anterior myocardial infarction. BACKGROUND: Although thrombolytic therapy improves clinical outcome after acute myocardial infarction, the relations between the severity of the residual stenosis of the infarct-related artery and postinfarction left ventricular remodeling and function are unclear. METHODS: Fifty-eight patients with a first anterior myocardial infarction and significant disease only in the left anterior descending coronary artery on arteriography performed after 7 to 10 days were evaluated. All patients received thrombolytic therapy. Residual stenosis of the infarct-related artery was measured with quantitative coronary arteriography. Left ventricular volumes and ejection fraction were measured by echocardiography and radionuclide angiography, respectively, 7 to 10 days, 6 months and 1 year after infarction. End-diastolic and end-systolic left ventricular volumes were measured by two-dimensional echocardiography and normalized to body surface area. Patients were classified into three groups according to baseline residual stenosis severity: total occlusion (Group I), minimal lesion diameter less than 1.5 mm (Group II) and minimal diameter greater than or equal to 1.5 mm (Group III). RESULTS: Group I patients had significantly greater left ventricular end-diastolic and end-systolic volumes at 6 months and 1 year than did the other groups. Group II patients had greater end-diastolic and end-systolic volumes than did Group III patients at 1 year. In addition, Group I patients had a lower ejection fraction at 1 year than that of the other groups. The minimal lesion diameter was significantly correlated with percent change in end-diastolic volume at 1 year. CONCLUSIONS: The severity of the baseline residual stenosis of the infarct-related artery is an important predictor of change in left ventricular volumes in the 1st year after infarction. Total occlusion of the infarct-related artery is associated with greater left ventricular dilation and functional impairment.

Cardiac Catheterization↗
PubMed2004

Prehospital versus hospital fibrinolytic therapy using automated versus cardiologist electrocardiographic diagnosis of myocardial infarction: abortion of myocardial infarction and unjustified fibrinolytic therapy.

BACKGROUND: This study investigated the incidence of abortion of myocardial infarction and of unjustified fibrinolysis by using automated versus cardiologist-assisted diagnosis of acute ST-elevation myocardial infarction. The results of prehospital diagnosis and treatment (2 cities in the Netherlands) were compared with those of inhospital treatment. Unjustified fibrinolysis must be differentiated from justified thrombolysis resulting in aborted myocardial infarction. Both have the absence of a significant rise in cardiac enzymes in common. In aborted myocardial infarction, this is a result of timely reperfusion; in unjustified thrombolysis, this is the result of an incorrect diagnosis. METHODS: In the city of Rotterdam, 118 patients were treated before hospitalization for myocardial infarction, diagnosed through the use of a mobile computer electrocardiogram; in the city of Nijmegen, 132 patients were treated before hospitalization with the use of transtelephonic transmission of the electrocardiogram to the coronary care unit and judged by a cardiologist. Their data were compared with those of 269 patients treated inhospital in the city of Arnhem, using the same electrocardiographic criteria. Abortion of myocardial infarction was diagnosed as the absence of a significant rise in cardiac enzymes and the presence of resolution of chest pain and 50% of ST-segment deviation within 2 hours after onset of therapy. Lacking these, the diagnosis of unjustified fibrinolytic therapy was made. RESULTS: Unjustified treatment occurred in 8 (3.2%) prehospital-treated patients (4 in Rotterdam and 4 in Nijmegen). Of the inhospital-treated patients in Arnhem, 5 (1.9%) were treated unjustifiably (P =.49). Aborted myocardial infarction occurred in 15.3% and 18.2% in Rotterdam and Nijmegen, respectively, against 4.5% in inhospital treatment in Arnhem (P <.001). CONCLUSIONS: Abortion of myocardial infarction is associated with prehospital thrombolysis. Unjustified fibrinolysis for acute myocardial infarction occurs in prehospital fibrinolysis as frequently as in the inhospital setting. The use of different electrocardiographic methods for diagnosing acute myocardial infarction does not appear to make any difference.

Angina, Unstable↗
PubMed2006

Diabetes mellitus impairs myocardial oxygen metabolism even in non-infarct-related areas in patients with acute myocardial infarction.

BACKGROUND: Although diabetes is associated with poor clinical outcomes after acute myocardial infarction, to date there have been no reports focusing on the myocardial oxygen metabolism in these patients. Thus, we evaluated the myocardial oxygen metabolism in patients with and without diabetes suffering from acute myocardial infarction using carbon-11 acetate positron emission tomography. METHODS: 20 patients (13 diabetic patients [group A] and 7 non-diabetic patients [group B]) underwent carbon-11 acetate positron emission tomography soon after the onset of acute myocardial infarction. The myocardial oxygen metabolism was evaluated within the infarct-related area and in the non infarct-related area. 6 healthy volunteers (group C) and 6 diabetic patients without coronary artery disease (group D) also participated as controls. RESULTS: There were no significant differences in gender, age, infarct-related artery, peak level of serum creatine phosphokinase, left-ventricular ejection fraction at onset, or the defect severity on myocardial perfusion images between group A and group B. In group A, the clearance rate (Kmono) of carbon-11 acetate in infarct-related area (0.042+/-0.010) was not significantly different from that in group B (0.049+/-0.016). In contrast, Kmono in non infarct-related area in group A (0.059+/-0.010) was significantly lower than that in group B (0.076+/-0.009; p=0.002), group C (0.072+/-0.004; p=0.026) and group D (0.078+/-0.005; p=0.001). CONCLUSIONS: These data indicate that the myocardial oxygen metabolism even in non infarct-related area in diabetic patients was impaired after the onset of acute myocardial infarction.

Adult↗
PubMed1999

Recent aspirin use is associated with smaller myocardial infarct size and lower likelihood of Q-wave infarction.

BACKGROUND: Controversy exists about the effect of recent aspirin use on infarct size and the likelihood of Q-wave infarction in patients who sustain myocardial infarction. METHODS: We performed face-to-face interviews and chart reviews on 3665 patients with acute myocardial infarction for the Determinants of Myocardial Infarction Onset Study. For the 2206 patients who did not receive thrombolytic therapy, we assessed aspirin use, peak creatine kinase levels (in 1043 patients), and electrocardiographic interpretations (in 1447 patients). RESULTS: Of the initial 1043 patients, 317 (30. 3%) subjects reported aspirin use in the 4 days before their infarction. The mean +/- SD peak creatine kinase level for aspirin users was 701 +/- 570 IU/mL versus 851 +/- 727 IU/mL for nonusers, an 18% difference (95% confidence interval [CI], 8% to 26%; P <.001). After adjustment for confounding factors, the difference was 12% (95% CI, 2% to 21%; P =.03). Similarly, 38.9% of the aspirin users and 48.7% of the nonusers sustained a Q-wave infarction, an odds ratio of 0.67 (95% CI, 0.54 to 0.83, P <.001). The adjusted odds ratio was 0.77 (95% CI, 0.61 to 0.97, P =.03). CONCLUSIONS: Recent aspirin use was associated with smaller infarct size and fewer Q-wave infarctions among this population of early survivors of acute myocardial infarction who did not receive thrombolytic therapy.

Aged↗
PubMed1998

Temporal induction of clusterin in the peri-infarct zone after experimental myocardial infarction in the rat.

Clusterin, a glycoprotein with potent cellular cohesive properties, is induced in many organs at times of tissue injury or remodeling. After renal infarction, for example, clusterin is localized to tubular epithelial cells in the peri-infarct zone. The purpose of this study was to examine the spatial and temporal expression of cardiac clusterin after myocardial infarction. Sprague-Dawley rats underwent permanent coronary ligation or sham operation. Hearts were harvested at 6 hours and at 2, 14, and 28 days after infarction. Cardiac clusterin expression was examined by immunohistochemistry and in situ hybridization. Left ventricular clusterin staining was evident at 6 hours and 2 days after myocardial infarction, although not at later time periods. Clusterin was localized to peri-infarct zone myocytes and endothelial cells of this region, and local synthesis of clusterin by myocytes was confirmed by in situ hybridization. Clusterin was not present in inflammatory cells or in left ventricular tissue distant from the infarct. The distribution of clusterin was different from the membrane attack complex of complement (C5b-9), with the latter being present diffusely throughout the infarct zone. Although the role of cardiac clusterin is not known, we speculate that clusterin's cohesive properties serve to promote myocyte interactions that are perturbed in the peri-infarct zone after myocardial infarction.

Animals↗
PubMed1986

Early thrombolysis in acute myocardial infarction: limitation of infarct size and improved survival.

The effect of thrombolysis in acute myocardial infarction on infarct size, left ventricular function, clinical course and patient survival was studied in a randomized trial comparing thrombolysis (269 patients) with conventional treatment (264 control patients). All 533 patients were admitted to the coronary care unit within 4 hours after the onset of symptoms related to the infarction. Baseline characteristics were similar in both groups. Informed consent was requested only of patients allocated to thrombolysis; no angiography was performed in 35. The infarct-related artery was patent in 65 patients and occluded in 169. Recanalization was achieved in 133 patients. The median time to angiographic documentation of vessel patency was 200 minutes after the onset of symptoms. The clinical course in the coronary care unit was more favorable after thrombolysis. Infarct size, estimated from myocardial enzyme release, was 30% lower after thrombolysis. In patients admitted within 1 hour after the onset of symptoms the reduction of infarct size was 51%, in those admitted between 1 and 2 hours it was 31% and in those admitted later than 2 hours it was 13%. Left ventricular function measured by radionuclide angiography before hospital discharge was better after thrombolysis (ejection fraction 48 +/- 15%) than in control patients (44 +/- 15%). Similar improvement was observed in patients with a first infarct only (thrombolysis 50 +/- 14%, control subjects 46 +/- 15%), in patients with anterior infarction (thrombolysis 44 +/- 16%, control subjects 35 +/- 14%) and in those with inferior infarction (thrombolysis 52 +/- 12%, control subjects 49 +/- 12%). Similar results were obtained by contrast angiography. Mortality was lower after thrombolysis. After 28 days 16 patients allocated to thrombolysis and 31 control patients had died. One year survival rates were 91 and 84%, respectively. On the other hand, nonfatal reinfarction occurred more frequently after thrombolysis (36 patients) than in control subjects (16 patients). Early thrombolysis by intracoronary streptokinase leads to a smaller infarct size estimated by enzyme release, preserves left ventricular function at the second week and leads to improved 1 year survival.

Aged↗
PubMed2001

Sex differences in survival after myocardial infarction in Sweden; data from the Swedish National Acute Myocardial Infarction Register.

AIMS: Women, particularly younger women, hospitalized with acute myocardial infarction have been found to have poorer prognosis than men. A large proportion of deaths due to myocardial infarction, however, occur in the pre-hospital phase. We set out to analyse age-specific sex differences in survival after myocardial infarction at different time intervals from the onset of acute myocardial infarction, including pre-hospital deaths and 1-year overall survival. METHODS AND RESULTS: The National Acute Myocardial Infarction Register in Sweden was used to analyse age-specific sex differences in mortality outside hospital, 28-day mortality and 1-year mortality in 353 905 cases occurring between 1987 and 1995 in Swedish men and women aged 30 to 89 years. Overall, one in four of all myocardial infarction victims died outside hospital. At all ages, except in individuals younger than 50 years, men had higher pre-hospital mortality. The odds of dying within 28 days for women below 50 years of age, compared to men, was 1.84 (1.56--2.18) in hospitalized patients and 1.31 (1.18--1.46) in all infarction patients. Above the age of 65, in the total population with myocardial infarction, women had a better prognosis, with odds ratios ranging from 0.83 to 0.89. In patients surviving the first 28 days, 4.0% of the women and 2.9% of the men below the age of 50 were dead within a year after the infarction, odds ratio 1.37 (1.06--1.76). This excess mortality was mainly due to diabetes and non-cardiac causes. Only women younger than 50 years had a significantly poorer overall 1-year survival than men of the same age. At the age of 70 or more, women had a small survival advantage. CONCLUSION: In the total acute myocardial infarction population, only women under 50 years of age have a consistently worse prognosis than men. Much of the excess mortality in young women seems to be associated with diabetes.

Aged↗
PubMed1993

Physical exertion as a trigger of acute myocardial infarction. Triggers and Mechanisms of Myocardial Infarction Study Group.

BACKGROUND: It is controversial whether the onset of myocardial infarction occurs randomly or is precipitated by identifiable stimuli. Previous studies have suggested a higher risk of cardiac events in association with exertion. METHODS: Consecutive patients with acute myocardial infarction were identified by recording all admissions to our hospital in Berlin and by monitoring a general population of 330,000 residents in Augsburg, Germany. Information on the circumstances of each infarction was obtained by means of standardized interviews. The data analysis included a comparison of patients with matched controls and a case-crossover comparison (one in which each patient serves as his or her own control) of the patient's usual frequency of exertion with the last episode of exertion before the onset of myocardial infarction. RESULTS: From January 1989 through December 1991, 1194 patients (74 percent of whom were men; mean age [+/- SD], 61 +/- 9 years) completed the interview 13 +/- 6 days after infarction. We found that 7.1 percent of the case patients had engaged in physical exertion (> or = 6 metabolic equivalents) at the onset of infarction, as compared with 3.9 percent of the controls at the onset of the control event. For the patients as compared with the matched controls, the adjusted relative risk of having engaged in strenuous physical activity at the onset of infarction or the control event was 2.1 (95 percent confidence interval, 1.1 to 3.6). The case-crossover comparison yielded a similar relative risk of 2.1 (95 percent confidence interval, 1.6 to 3.1) for having engaged in strenuous physical activity within one hour before myocardial infarction. Patients whose frequency of regular exercise was less than four and four or more times per week had relative risks of 6.9 and 1.3, respectively (P < 0.01). CONCLUSIONS: A period of strenuous physical activity is associated with a temporary increase in the risk of having a myocardial infarction, particularly among patients who exercise infrequently. These findings should aid in the identification of the triggering mechanisms for myocardial infarction and improve prevention of this common and serious disorder.

Aged↗
PubMed2003

Mechanism of higher incidence of ischemic mitral regurgitation in patients with inferior myocardial infarction: quantitative analysis of left ventricular and mitral valve geometry in 103 patients with prior myocardial infarction.

OBJECTIVE: The mechanism of higher incidence of ischemic mitral regurgitation in patients with inferior compared with anterior myocardial infarction despite less global left ventricular remodeling and dysfunction is controversial. We hypothesized that inferior myocardial infarction causes left ventricular remodeling, which displaces posterior papillary muscle away from its normal position, leading to ischemic mitral regurgitation. METHODS: In 103 patients with prior myocardial infarction (61 anterior and 42 inferior) and 20 normal control subjects, we evaluated the grade of ischemic mitral regurgitation on the basis of the percentage of Doppler jet area, left ventricular end-diastolic and end-systolic volumes, midsystolic mitral annular area, and midsystolic leaflet-tethering distance between papillary muscle tips and the contralateral anterior mitral annulus, which were determined by means of quantitative echocardiography. RESULTS: Global left ventricular dilatation and dysfunction were significantly less pronounced in patients with inferior myocardial infarction (left ventricular end-systolic volume: 52 +/- 18 vs 60 +/- 24 mL, inferior vs anterior infarction, P<.05; left ventricular ejection fraction: 51% +/- 9% vs 42% +/- 7%, P <.0001). However, the percentage of mitral regurgitation jet area and the incidence of significant regurgitation (percentage of jet area of 10% or greater) was greater in inferior infarction (percentage of jet area: 10.1% +/- 7.5% vs 4.4% +/- 7.0%, P =.0002; incidence: 16/42 (38%) vs 6/61 (10%), P <.0001). The mitral annulus (area = 8.2 +/- 1.2 cm2 in control subjects) was similarly dilated in both inferior and anterior myocardial infarction (9.7 +/- 1.7 vs. 9.5 +/- 2.3 cm2, no significant difference), and the anterior papillary muscle-tethering distance (33.8 +/- 2.6 mm in control subjects) was also similarly and mildly increased in both groups (35.2 +/- 2.4 vs 35.2 +/- 2.8 mm, no significant difference). However, the posterior papillary muscle-tethering distance (33.3 +/- 2.3 mm in control subjects) was significantly greater in inferior compared with anterior myocardial infarction (38.3 +/- 4.1 vs 34.7 +/- 2.9 mm, P =.0001). Multiple stepwise regression analysis identified the increase in posterior papillary muscle-tethering distance divided by body surface area as an independent contributing factor to the percentage of mitral regurgitation jet area (r2 = 0.70, P <.0001). CONCLUSIONS: It is suggested that the higher incidence and greater severity of ischemic mitral regurgitation in patients with inferior compared with anterior myocardial infarction can be related to more severe geometric changes in the mitral valve apparatus with greater displacement of posterior papillary muscle caused by localized inferior basal left ventricular remodeling, which results in therapeutic implications for potential benefit of procedures, such as infarct plication and leaflet or chordal elongation, to reduce leaflet tethering.

Aged↗
PubMed1997

'Expected infarct size without thrombolysis', a concept that predicts immediate and long-term benefit from thrombolysis for evolving myocardial infarction.

BACKGROUND: Thrombolytic therapy should only be used when expected benefits outweigh the risks. In order to obtain a precise estimation of prognosis, with and without thrombolytic therapy, we postulated that mortality reduction by thrombolytic therapy is a function of the area of myocardium at risk for necrosis. We developed a model to estimate the myocardial area at risk for necrosis from clinical parameters readily available upon hospital admission. This model was validated in relation to long-term prognosis and benefits of thrombolytic therapy. METHODS: Enzymatic infarct size with and without thrombolysis was predicted from the haemodynamic state and the electrocardiogram on hospital admission by multivariate regression analysis in 885 patients in the rt-PA placebo and rt-PA/PTCA trial of the European Cooperative Study Group. This multivariate function was used to validate the 'expected infarct size without thrombolytic treatment' in a test population of 533 patients from the Intracoronary Streptokinase trial of the Interuniversity Cardiology Institute of The Netherlands (ICIN) and 1741 patients from the Intravenous Streptokinase in Acute Myocardial Infarction (ISAM) study, both trials with a non-thrombolysed control group. RESULTS: Expected infarct size correlated well with the actual enzymatic infarct size in the non-thrombolysed patients of the latter two series. Limitation of infarct size by thrombolytic therapy was greatest in patients with a large 'expected infarct size' and absent in patients with a small area at risk. Similarly, one year mortality reduction was greatest in patients with a large 'expected infarct size without thrombolysis'; four deaths were prevented per hundred (95% confidence interval 0 to 9) if the area at risk was large, vs one death (95% confidence interval -2 to 3) in patients with a small area at risk. Benefit was most pronounced in patients with a large area at risk who were treated early within 3 h of symptom onset. A score for the determination of 1 year mortality with and without thrombolytic therapy is presented to help the clinician determine who to treat with thrombolytic therapy. CONCLUSION: 'Expected infarct size without thrombolysis' is a useful tool for clinicians to estimate the amount of myocardium at risk of necrosis in individual patients and to decide whether thrombolytic therapy is warranted. It is the only validated parameter of myocardium at risk for necrosis that is readily available for all patients with myocardial infarction and does not need high-tech equipment.

Electrocardiography↗
PubMedDate not supplied

Time-dependent increases in syndecan-1 and fibroglycan messenger RNA expression in the infarct zone after experimentally induced myocardial infarction in rats.

BACKGROUND: Syndecan-1 and fibroglycan, heparan sulphate proteoglycans, play important roles in extracellular matrix formation via their biological functions. OBJECTIVE: To examine experimentally the sequential changes in syndecan-1 and fibroglycan messenger RNA (mRNA) expression after acute myocardial infarction. MATERIALS AND METHODS: The left coronary arteries of male Sprague-Dawley rats were ligated and the hearts were excised on days 1-14, 28 and 42. Syndecan-1 and fibroglycan mRNA expression in the infarct and non-infarct zones and in sham-operated hearts was determined by reverse transcriptase-polymerase chain reaction. Amplified products were quantified by densitometry of the electrophoresed bands stained with ethidium bromide and standardized relative to the glyceraldehyde 3-phosphate dehydrogenase or beta-actin mRNA expression. Northern hybridization was also performed in the infarct and non-infarct zones on day 3. RESULTS: Expression both of syndecan-1 and of fibroglycan mRNA began to increase on day 2. The expression attained maximum levels on day 3. The maximum levels of syndecan-1 and fibroglycan expression were, respectively, sevenfold and fivefold the preligation level and the level in the sham-operated hearts. The levels remained elevated until day 14, whereupon they declined gradually, returning to the control levels by around day 42. Northern blotting also demonstrated that there was an increased expression both of syndecan-1 and of fibroglycan mRNA in the infarct compared with that in the non-infarct zone on day 3. CONCLUSION: Our results demonstrated that there are sequential increases in the expression both of syndecan-1 and of fibroglycan mRNA in the infarct zone after experimentally induced myocardial infarction in rats, suggesting that these proteoglycans play some role in the pathological course of infarction.

Animals↗
PubMed2006

Treatment with the gap junction modifier rotigaptide (ZP123) reduces infarct size in rats with chronic myocardial infarction.

Treatment with non-selective drugs (eg, long-chain alcohols, halothane) that reduce gap junction intercellular communication (GJIC) is associated with reduced infarct size after myocardial infarction (MI). Therefore, it has been suggested that gap junction intercellular communication stimulating compounds may increase infarct size. The antiarrhythmic peptide analogue rotigaptide (ZP123) increases cardiac gap junction intercellular communication and the purpose of the present study was to examine the effects of rotigaptide treatment on infarct size. Myocardial infarction was induced in male rats by ligation of the left anterior descending artery (LAD). Rats (n = 156) were treated with rotigaptide at three dose levels or vehicle from the onset of ischemia and for 3 weeks following LAD occlusion. Infarct size was determined using histomorphometry after 3 weeks treatment. Rotigaptide treatment producing steady state plasma levels of 0.8 +/- 0.1, 5.5 +/- 0.5, and 86 +/- 8 nmol/L had no effect on mortality, but reduced infarct size to 90 +/- 10% (P = 0.41), 67 +/- 7% (P = 0.005), and 82 +/- 7% (P = 0.13), respectively relative to vehicle-treated myocardial infarction rats (100 +/- 12%). In contrast to what was predicted, our data demonstrates that rotigaptide treatment was associated with a significant infarct size reduction. We conclude that whereas treatment with non-selective inhibitors of gap junction intercellular communication cause a reduction in infarct size, this information cannot be extrapolated to the effects of compounds that selectively increase gap junction intercellular communication.

Animals↗
PubMed1988

Relation of infarct site to 15 year prognosis in patients who survived for 28 days after a first myocardial infarction.

Six hundred and eighty four patients (629 men), all aged under 60 years, who had survived for 28 days after a first acute myocardial infarction were studied to determine the influence of the site of infarction on long term prognosis. The infarct site was not significantly related to age nor to extent of infarct at the time of the acute episode. Mechanical complications were more common in patients with anteroseptal infarctions, while atrioventricular conduction disturbances were more commonly found in those with inferior infarction. The site of infarction was not related to smoking habits or angina before the infarction or at 2 year follow up. Life table methods did not show any relation between infarction site and morbidity or mortality either two years or 15 years after the initial infarction.

Age Factors↗
PubMed1997

Thrombolytic treatment for myocardial infarction: an examination of practice in 39 United Kingdom hospitals. Myocardial Infarction Audit Group.

OBJECTIVE: To examine use of thrombolytic drugs for myocardial infarction and use of contraindications to treatment in the United Kingdom. DESIGN: Observational study, based on a continuing audit. SETTING: 39 hospitals in the United Kingdom. PATIENTS: 30,029 patients admitted between November 1992 and June 1995 with suspected myocardial infarction. RESULTS: Of 13,628 patients with a final diagnosis of definite myocardial infarction 10,316 (75.7%) were considered eligible for thrombolytic treatment on the basis of typical cardiographic changes or new left bundle branch block. Of these, 8139 (59.7%) were diagnosed at admission to hospital and 6991 (85.9%) were administered thrombolytic drugs; 14.1% were considered too late for treatment or had a clinical contraindication. In 2177 patients (16% of 13,628)-thrombolytic treatment was given in the absence of contraindications and after the diagnosis of infarction had been confirmed by further electrocardiographic evidence. A further 591 (4.3%) with a final diagnosis of definite infarction without typical cardiographic changes also received thrombolytic treatment as did 1018 patients without a final diagnosis of definite infarction. In total, 9459 of 13,628 patients (71.6%) received thrombolytic treatment. The range of use of treatment between hospitals for a final diagnosis of infarction was 49.1-85.4%. This variation reflected differences in the frequency with which a diagnosis of definite myocardial infarction was made at admission, and the subsequent use of clinical contraindications to thrombolytic treatment. CONCLUSIONS: 75.7% of patients with a final diagnosis of definite myocardial infarction were eligible for thrombolytic treatment on the basis of cardiographic changes. Differences between hospitals in the frequency with which a diagnosis of infarction was made on admission, and differences in subsequent use of thrombolytic drugs, results in wide variation in treatment rates. Differences in use of thrombolytic treatment mainly reflect different thresholds for the use of clinical contraindications relating to haemorrhagic risk.

Aged↗
PubMed1982

Estimation of infarct size by myocardial emission computed tomography with thallium-201 and its relation to creatine kinase-MB release after myocardial infarction in man.

We evaluated emission computed tomography (ECT) for thallium-201 (201TI) myocardial imaging in estimating infarct size (IS). In 18 patients in whom IS was estimated enzymatically at the time of the acute episode, planar 201TI perfusion scintigraphy and ECT with a rotating gamma camera were performed 4 weeks after the first myocardial infarction. From the size of 201TI perfusion defects, the infarct area in planar images and the infarct volume in reconstructed ECT images were measured by computerized planimetry. When scintigraphic IS was compared with the accumulated creatine kinase-MB isoenzyme release (CK-MBr), infarct volume determined from ECT correlated closely with CK-MBr (r = 0.89), whereas infarct area measured from planar images correlated less satisfactorily with the enzymatic IS (for an average infarct area from three views, r = 0.69; for the largest infarct area, r = 0.73). Although conventional scintigraphic evaluation is useful for detecting and localizing infarction, quantification of ischemic injury with this two-dimensional technique has a significant inherent limitation. The ECT approach can provide a more accurate three-dimensional quantitative estimate of infarction, and can corroborate the enzymatic estimate of IS.

Adult↗
PubMed1988

Quantification of infarct size by 201Tl single-photon emission computed tomography during acute myocardial infarction in humans. Comparison with enzymatic estimates.

We prospectively investigated whether 201Tl single-photon emission computed tomography (SPECT) could accurately diagnose the presence and quantify the extent of acute myocardial infarction when compared with infarct size assessed by plasma MB-creatine kinase activity. Thirty patients with enzymatic evidence of infarction were imaged within 12-36 hours of chest pain (mean, 23.4 hours). No patient had a previous infarction, and none underwent intervention seeking to restore coronary patency. Infarct size was quantified with computer-generated polar maps of the myocardial radioactivity and expressed as a percentage of the total left ventricular volume. To assess left and right ventricular performance, blood-pool gated radionuclide angiography was performed immediately after SPECT. All 30 patients had perfusion defects consistent with myocardial infarction. Scintigraphic and enzymatic estimates of infarct size correlated well for the group as a whole (r = 0.78, p less than 0.001, SEE = 9.1) but especially for those patients with anterior infarction (r = 0.91, p less than 0.001, SEE = 7.9). The poor correlation observed in patients with inferior infarction (r = 0.50, p less than 0.05, SEE = 10.0) was believed to be related to the frequent occurrence of right ventricular involvement because SPECT assessed only left ventricular damage, whereas the enzymatic method estimated the myocardial injury in both ventricles. A quantitative index of right ventricular infarct size, derived from the relation between the scintigraphic and enzymatic estimates, had a strong inverse correlation with right ventricular ejection fraction (r = -0.89, p less than 0.001, SEE = 3.6).(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗
PubMed1988

Intravenous nitroglycerin therapy to limit myocardial infarct size, expansion, and complications. Effect of timing, dosage, and infarct location.

To determine 1) whether the effect of intravenous nitroglycerin (NG) therapy during acute myocardial infarction on creatine kinase infarct size is influenced by infarct location (anterior vs. inferior), timing (therapy less than 4 hours vs. greater than or equal to 4 hours after onset of pain), and dose response (mean blood pressure greater than or equal to 80 mm Hg vs. less than 80 mm Hg during the first 12 hours) and 2) whether NG therapy modifies infarct expansion, 310 patients were randomly allocated to NG (n = 154) and control (n = 156) groups. NG infusion was titrated to lower mean blood pressure by 10% in normotensive and 30% in hypertensive patients, but not below 80 mm Hg, and was maintained for 39 hours. Measurements included clinical variables, creatine kinase infarct size (geq) as well as left ventricular (LV) asynergy, LV ejection fraction, expansion index, and thinning ratio on serial two-dimensional echocardiography. Compared with controls, creatine kinase infarct size was less in the NG group (41 vs. 55 geq, p less than 0.001), in anterior (44 vs. 58 geq, p less than 0.05), and inferior (39 vs. 53 geq, p less than 0.025) NG subgroups, and in early than late NG subgroups (43% vs. 22% decrease). Other indexes of infarct size also improved (p less than or equal to 0.05) with NG compared with controls. Thus, by 10 days, LV asynergy was 40% less, LV ejection fraction was 22% more, and Killip class score was 41% less. A negative effect of mean blood pressure less than 80 mm Hg with NG was reflected in these indexes. In addition, expansion index increased (p less than 0.001) by 31% and thinning ratio decreased (p less than 0.001) by 17% in controls by 10 days but remained unchanged with NG. Infarct-related major complications were less frequent in the NG than the control groups: infarct expansion syndrome (2% vs. 15%, p less than 0.0005), LV thrombus (5% vs. 22%, p less than 0.0005), cardiogenic shock (5% vs. 15%, p less than 0.005), and infarct extension (11% vs. 22%, p less than 0.025). Mortality was less in NG than in control groups in-hospital (14% vs. 26%, p less than 0.01), at 3 months (16% vs. 28%, p less than 0.025) and 12 months (21% vs. 31%, p less than 0.05), but this advantage was only found in the anterior subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗