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 505 records · Page 28Linked to original sources
PubMed2005

Myocardial late enhancement in contrast-enhanced cardiac MRI: distinction between infarction scar and non-infarction-related disease.

OBJECTIVE: Our objective was to assess and compare the patterns of late enhancement (LE) in contrast-enhanced cardiac MRI caused by myocardial infarction and different myocardial diseases that are not related to ischemic infarction. MATERIALS AND METHODS: A total of 811 consecutive contrast-enhanced cardiac MRI studies performed for different indications were reviewed for left ventricular myocardial LE after gadopentetate dimeglumine administration. MRI studies were performed on a 1.5-T scanner using an inversion recovery turbo FLASH sequence (TR/TE, 8/4 msec; flip angle, 25 degrees). The LE pattern of ischemic infarction scar was compared with that in nonischemic myocardial disease. RESULTS: LE was found in 421 (52%) patients. In all patients with myocardial infarction, LE included the subendocardial layer. Nineteen patients without history of myocardial infarction and angiographically excluded coronary artery disease showed different patterns of LE caused by myocarditis, sarcoidosis, arrhythmogenic right ventricular dysplasia, cardiomyopathy, endomyocardial fibrosis, and iatrogenic scars after biopsy, ablation of septal hypertrophy, and myocardial laser revascularization. CONCLUSION: LE in contrast-enhanced cardiac MRI is not specific for ischemic infarction. LE in ischemic infarction always involves the subendocardial layer, whereas it does not necessarily do so in other myocardial diseases. Therefore, if LE omit the subendocardial layer, different nonischemic myocardial diseases have to be considered. The pattern of LE might be helpful for the differential diagnosis of myocardial disease and in distinguishing it from ischemic disease.

Adult↗
PubMed2001

Impact of diabetes on long-term survival after acute myocardial infarction: comparability of risk with prior myocardial infarction.

OBJECTIVE: To determine the effect of diabetes on long-term survival after acute myocardial infarction and to compare its effect with that of a previous myocardial infarction. RESEARCH DESIGN AND METHODS: In a prospective cohort study, we followed 1,935 patients hospitalized with a confirmed acute myocardial infarction at 45 U.S. medical centers between 1989 and 1993, as part of the Determinants of Myocardial Infarction Onset Study. Trained interviewers performed chart reviews and face-to-face interviews with all patients. We analyzed survival using Cox proportional hazards regression to control for potentially confounding factors. RESULTS: Of the 1,935 patients, 320 (17%) died during a mean follow-up of 3.7 years. A total of 399 patients (21%) had previously diagnosed diabetes. Diabetes was associated with markedly higher total mortality in unadjusted (hazard ratio [HR] 2.4; 95% CI 1.9-3.0) and adjusted (1.7; 1.3-2.1) analyses. The magnitude of the effect of diabetes was identical to that of a previous myocardial infarction. The effect of diabetes was not significantly modified by age, smoking, household income, use of thrombolytic therapy, type of hypoglycemic treatment, or duration of diabetes, but the risk associated with diabetes was higher among women than men (adjusted HRs 2.7 vs. 1.3, P = 0.01). CONCLUSIONS: Diabetes is associated with markedly increased mortality after acute myocardial infarction, particularly in women. The increase in risk is of the same magnitude as a previous myocardial infarction and provides further support for aggressive treatment of coronary risk factors among diabetic patients.

Aged↗
PubMed2005

Terminal QRS complex distortion on the admission electrocardiogram in anterior acute myocardial infarction and association with residual flow and infarct size after primary angioplasty.

BACKGROUND: Terminal QRS complex distortion on admission is a simple and reliable predictor of infarct size in patients with acute myocardial infarction (AMI). It is uncertain, however, whether this reflects reduced myocardial perfusion of the infarct area and a larger area of the myocardium at risk. This study was conducted to investigate whether terminal QRS distortion complex on admission is a reliable predictor of reduced residual flow and a larger area of the myocardium at risk compared to patients who are admitted without a terminal QRS distortion. METHODS: We evaluated the relationship between terminal QRS complex distortion and residual flow to the infarct zone and risk area in 46 anterior AMI patients undergoing primary angioplasty. (99m)Tc-sestamibi imaging was performed at baseline and 5-9 days after angioplasty. The study population was divided into those with (Group I, n=16) and without (Group II, n=30) terminal QRS complex distortion. RESULTS: Baseline characteristics were similar between the two groups. The area of the myocardium at risk was higher in Group I (59.9 +/- 15.3%) than in Group 11 (48.6 +/- 13.7%, p < 0.05; mean+SD) while the nadir measurement of the residual flow was lower in Group I (0.10 +/- 0.07) than in Group 11 (0.16 +/- 0.09, p < 0.05). Although the final infarct size was significantly higher in Group I (40.8 +/- 17.2%) than in Group 11 (27.1 +/- 18.1%, p < 0.05), the myocardial salvage index did not differ significantly between the two groups. CONCLUSION: Terminal QRS complex distortion seems to be associated with less residual flow to the infarct zone, a larger risk area and greater infarct size in patients with anterior AMI.

Angioplasty, Balloon↗
PubMed1991

Limitations of the electrocardiogram in estimating infarction size after acute reperfusion therapy for myocardial infarction.

OBJECTIVE: To assess the ability of the 12-lead electrocardiogram to estimate infarction size after reperfusion therapy for acute myocardial infarction. DESIGN: The presence or absence of Q waves and the Selvester QRS score obtained before and after hospital discharge were compared with radionuclide estimates of infarction size and ejection fraction at discharge and 6 weeks later, regional wall motion at discharge and 6 weeks later, and myocardial perfusion defect size quantitated with Tc-99m-sestamibi at discharge. SETTING: A tertiary referral center. PATIENTS: A consecutive series of 43 patients with acute myocardial infarction who received acute reperfusion therapy and were assessed using 12-lead electrocardiography, radionuclide angiography, and Tc-99m-sestamibi tomographic imaging before discharge. INTERVENTIONS: All 43 patients received acute reperfusion therapy: 21 patients received intravenous tissue plasminogen activator, and 22 patients underwent primary percutaneous transluminal coronary angioplasty. MAIN OUTCOME MEASURE: The correlation of QRS score and Q waves with three radionuclide estimates of infarction size. RESULTS: A significant correlation was found between myocardial perfusion defect size at discharge and both left ventricular ejection fraction and regional wall motion at discharge and 6 weeks later (r = -0.71 to -0.81; all comparisons, P less than 0.001). Little correlation was found between electrocardiographic findings and radionuclide measurements of left ventricular function and perfusion. Presence or absence of Q waves at discharge was not associated with any difference in ejection fraction, regional wall motion, or perfusion defect at discharge. No correlation was found between QRS score and ejection fraction or myocardial perfusion defect size at discharge. The QRS score at discharge correlated only weakly with regional wall motion at discharge and 6 weeks later. This lack of correlation was unchanged when electrocardiograms obtained after hospital discharge were analyzed. CONCLUSION: Although inexpensive and readily available, the 12-lead electrocardiogram does not appear to provide a reliable estimate of infarction size after reperfusion therapy for acute myocardial infarction.

Adult↗
PubMed1996

Recent age-related trends in the use of thrombolytic therapy in patients who have had acute myocardial infarction. National Registry of Myocardial Infarction.

OBJECTIVE: To examine recent trends in the use of thrombolytic therapy in elderly patients who have had acute myocardial infarction and to determine whether failure to meet time-to-hospital presentation and electrocardiographic criteria might explain age-related differences in the use of thrombolytic therapy. DESIGN: A national registry of patients who have had acute myocardial infarction. SETTING: 1249 U.S. hospitals. PATIENTS: 350,755 patients who had an acute myocardial infarction from 1 July 1990 to 30 September 1994. MEASUREMENTS: Trends in the proportions of patients who received thrombolytic therapy were examined according to age and sex. The association between age and treatment with a thrombolytic agent was determined by crude and multivariable-adjusted analyses. RESULTS: Use of a thrombolytic agent was inversely related to patient age: Almost 51% of patients younger than age 55 years received a thrombolytic agent during hospitalization for acute myocardial infarction; this proportion decreased to 43.6% for patients aged 55 to 64 years, 33.0% for those aged 65 to 74 years, 19.0% for those aged 75 to 84 years, and 7.4% for those aged 85 years or older. However, relative increases in the use of thrombolytic therapy over time were greatest for patients in the oldest age groups. Between 1 July 1990 and 30 June 1991, 16.0% of patients aged 75 to 84 years received a thrombolytic agent compared with 21.4% between 1 June 1993 and 30 September 1994 (a 33.8% relative increase in use). Among persons aged 85 years or older, the proportion of treated patients increased from 5.3% to 9.1% over this same period (a 71.7% relative increase in use). Increases in thrombolytic use were most prominent for older women. After adjustment for sex, diagnosis by initial electrocardiogram, electrocardiogram-based infarction description, time from symptom onset to hospital presentation, and period of the acute myocardial infarction, the odds of receiving a thrombolytic agent were significantly reduced for patients in the older age groups compared with the odds for patients younger than age 55 years (for patients aged 75 to 84 years, the adjusted odds ratio was 0.27 [95% CI, 0.26 to 0.28]; for patients aged 85 years or older, the odds ratio was 0.09 [CI, 0.08 to 0.10]). CONCLUSIONS: Although older patients who have had acute myocardial infarction less commonly receive a thrombolytic agent, use of thrombolytic therapy in this population is expanding. However, substantial differences across age groups persist in the likelihood of receiving treatment, even after adjustment for potentially confounding factors. Age-related differences in thrombolytic use may not be completely explained by the degree to which older patients do not meet conventional eligibility criteria for thrombolytic therapy.

Age Factors↗
PubMed1998

Risk for intracranial hemorrhage after tissue plasminogen activator treatment for acute myocardial infarction. Participants in the National Registry of Myocardial Infarction 2.

BACKGROUND: The efficacy of thrombolytic therapy in reducing mortality from acute myocardial infarction has been unequivocally shown. However, thrombolysis is related to bleeding complications, including intracranial hemorrhage. OBJECTIVE: To determine the frequency of and risk factors for intracranial hemorrhage after recombinant tissue-type plasminogen activator (tPA) given for acute myocardial infarction in patients receiving usual care. DESIGN: Large national registry of patients who have had acute myocardial infarction. SETTING: 1484 U.S. hospitals. PATIENTS: 71073 patients who had had acute myocardial infarction from 1 June 1994 to 30 September 1996, received tPA as the initial reperfusion strategy, and did not receive a second dose of any thrombolytic agent. MEASUREMENT: Intracranial hemorrhage confirmed by computed tomography or magnetic resonance imaging. RESULTS: 673 patients (0.95%) were reported to have had intracranial hemorrhage during hospitalization for acute myocardial infarction; 625 patients (0.88%) had the event confirmed by computed tomography or magnetic resonance imaging. Of the 625 patients with confirmed intracranial hemorrhage, 331 (53%) died during hospitalization. An additional 158 patients (25.3%) who survived to hospital discharge had residual neurologic deficit. In multivariable models for the main effects of candidate risk factors, older age, female sex, black ethnicity, systolic blood pressure of 140 mm Hg or more, diastolic blood pressure of 100 mm Hg or more, history of stroke, tPA dose more than 1.5 mg/kg, and lower body weight were significantly associated with intracranial hemorrhage. CONCLUSIONS: Intracranial hemorrhage is a rare but serious complication of tPA in patients with acute myocardial infarction. Appropriate drug dosing may reduce the risk for this complication. Other therapies, such as primary coronary angioplasty, may be preferable in patients with acute myocardial infarction who have a history of stroke.

Age Factors↗
PubMed1992

[Hemorrhagic myocardial infarct. An analysis of the distribution of the hemorrhage and of the permeability of the artery related to the infarct].

PURPOSE: To study the extent of hemorrhagic myocardial infarction (HMI) and patency of the infarct related artery. METHODS: Forty seven cases of HMI diagnosed by necropsy (patient age range 30-81 years, mean 59) were studied retrospectively. Hemorrhagic extent was evaluated by microscopic analysis of myocardial sections of the infarcted areas and coronary patency was studied by angiography and by serial coronary sections at necropsy. RESULTS: In 12 cases hemorrhage extended outside the infarcted area and in the remaining cases it was restricted to the necrotic zone. Coronary patency was spontaneous in 8 of 24 cases, secondary to thrombolytic therapy or angioplasty in 8 and post coronary artery bypass in 15. Recent occlusive thrombus was diagnosed in 26 of 44 cases. Grouping all cases according to angiographic or macro and microscopic evidences of coronary patency, it was found that 35 of 47 studies cases (74.4%) had the infarct related coronary artery free of occlusion. In most cases of HMI myocardial hemorrhage restricted to the infarcted necrotic zone but in almost 25% it could reach areas beyond the infarcted necrotic zone probably resulting in deleterious consequences. CONCLUSION: Reperfusion is frequent and it plays a role in the hemorrhagic event but it was not seen in 25% of these studied cases. These findings suggest that other mechanisms could participate of the pathogenesis of HMI.

Adult↗
PubMed2003

Surgical techniques for emergent repair of post-infarction ventricular septal defect: compare endocardial patch and infarct exclusion method with traditional method.

BACKGROUND: The traditional surgical repair of post-infarction ventricular septal defect (VSD) includes excision of necrotic myocardium and approximation of the remaining of healthy ventricular wall and septal portion. The exclusion method emphasizes no excision of infarcted myocardium, preservation of the left ventricular geometry and exclusion of infarction area. We discuss our experiences in 13 patients and compared the results obtained from 2 different surgical methods. METHODS: From July 1996 to December 2001, 13 patients with post-infarction VSD received emergent repair. Seven patients were repaired in the traditional way and the other 6 with infarct exclusion method. There were 9 men and 4 women, ranging in age from 57 to 79. In the traditional group, all 7 patients were classified as NYHA IV and supported by intra-aortic balloon counter-pulsation (IABP) and 4 patients were for synchronous coronary bypass grafting. Patients using exclusion method were the 1 classified as NYHA III and 5 as IV with cardiogenic shock and supported by IABP. Coronary bypass grafting was performed concomitantly in 2 patients. RESULTS: Five patients died within 30 days after the surgery. Four patients (mortality rate = 57.1%) had reconstruction in traditional way and 1 (mortality rate = 16.6%) in exclusion way. The complication rate was higher in the traditional group (= 100%, n = 7, p = 0.005). In the traditional group, 1 patient received heart transplantation due to persistent severe pump failure and recovered well. Two received tracheostomy due to respiratory failure and 1 died 2 months later. In the group of exclusion method, 1 patient suffered recurrent VSD 2 days after the first surgery and died due to ventricular arrhythmia. CONCLUSIONS: The surgical mortality caused by acute post-infarction VSD has decreased with endocardial patch and infarction exclusion method. Rapid diagnosis, appropriate preoperative management and delicate surgical repair improve the overall results and help to attain long-term survival.

Aged↗
PubMed2004

[Immediate administration of mineralocorticoid receptor antagonist spironolactone prevents post-infarct left ventricular remodeling associated with suppression of a marker of myocardial collagen synthesis in patients with first anterior acute myocardial infarction].

BACKGROUND: Aldosterone has been shown to stimulate cardiac collagen synthesis and fibroblast proliferation via activation of local mineralocorticoid receptors. In patients with acute myocardial infarction, we demonstrated that aldosterone was extracted through the infarct-heart and extracting aldosterone stimulated post-infarct left ventricular remodeling. METHODS AND RESULTS: To evaluate the effect of mineralocorticoid receptor antagonist (MRA) spironolactone on post-infarct left ventricular remodeling. 134 patients with first anterior acute myocardial infarction were randomly divided into the MRA (n=65) or non MRA (n=69) group after revascularization. All patients were administrated angiotensin converting enzyme inhibitor (ACEI) and study drug just after revascularization. Left ventriculography with contrast medium was performed at acute and after 1 month to evaluate left ventricular remodeling. Aldosterone was measured at aortic root and coronary sinus. There was no difference in the baseline characteristics including infarct size and left ventricular performance between the two groups. However, left ventricular ejection fraction was significantly improved in MRA group compared with that in non MRA group (46.0 +/- 0.6% to 53.2 +/- 0.8% vs 46.5 +/- 0.8% to 51.0 +/- 0.8%, P interaction = 0.012). Left ventricular end-diastolic volume index was significantly suppressed in MRA group compared with that in non-MRA group (86.5 +/- 1.0 to 90.6 +/- 2.4 vs 87.5 +/- 1.3 to 106.8 +/- 3.5 ml/m2, P interaction = 0.002). Transcardiac extraction of aldosterone through the heart was significantly suppressed in MRA group (P interaction = 0.001) and plasma procollagen type III aminoterminal peptide, a biochemical marker of fibrosis, level was significant lower in MRA group compared with those in non-MRA group (P interaction + 0.002). CONCLUSIONS: These findings indicate that MRA combined with ACEI can prevent post-infarct left ventricular remodeling better than ACEI alone in association with the suppression of a marker collagen synthesis.

Biomarkers↗
PubMed2004

[Left ventricle hypertrophy following myocardial infarction. Morphometric evaluation of the infarcted region and the free wall of the left ventricle].

UNLABELLED: The aim of the study was to assess the relationship between the left ventricle (LV) hypertrophy and the effect of different morphological and clinical parameters in patients after Q-wave myocardial infarction (QMI). MATERIAL AND METHODS: A morphometric evaluation was performed in 21 patients after QMI (the mean age was 58.8 +/- 9.4). Samples from infarcted region and the free wall of LV obtained during autopsy were measured. Results were compared to parameters observed in the control group that comprised 10 patients who died due to non-cardiac causes (the mean age 52.4 +/- 11.2). The following morphological parameters were assessed: heart weight, LV mass, infarct scar extent, myocytes diameter, myocytes nuclei' diameter, myocytes nuclei' density, coronary capillaries density (immunohistochemical staining for CD34), LV fibrosis. Morphometric measurements were performed with the use of digital image analyser Leica Q500MC. Clinical characteristics such as patients age, duration of the disease, sex and prevalence of hypertension were also evaluated. RESULTS: Postmortem pathological studies showed significant increase in the LV mass in the investigated group when compared to control group (296.0 +/- 81.3 g vs. 150.2 +/- 18.6 g; p < 0.0003). LV hypertrophy was associated with different structural alterations: increase in the myocytes diameter both in the infarcted region (increase 61%) and free LV wall (increase 35%), increase in the myocytes nuclei diameter (increase 28.1% and 11.2%, respectively), reduction in the myocytes nuclei' density (decrease, 52.9% and 34.4%, respectively), reduction in the coronary capillaries density (decrease 48.6% and 4.1%; respectively) and the increase in fibrosis in the free wall of LV (increase 91%). Multiple regression analysis showed the increase in the myocytes' diameter in the infarcted region (beta = 0.355; p = 0.048) and the increase in the myocytes' diameter in the free LV wall (beta = 0.787; p = 0.015) as the only two factors affecting the degree of LV hypertrophy. A linear relationship between the LV mass and the increase in the myocytes' diameter was observed only in the free LV wall (r = 0.695; p < 0.001). Moreover, the increase in myocytes' diameter within the free wall of LV correlated to the infarct scar extent (r = 0.451; p = 0.046). CONCLUSIONS: (1) Compensatory increase in the LV mass following MI is proportionate to the loss of contractility of necrotic myocardium. (2) Increase in the LV mass that occurred after MI is mainly determined by the degree of myocytes' hypertrophy. The significance of correlations between the two parameters depends on the myocytes location (free wall of LV vs. infarcted region).

Aged↗
PubMed1988

Antigen preservation in infarcted lymphoid tissue. A novel approach to the infarcted lymph node using monoclonal antibodies effective in routinely processed tissues.

We studied 11 cases of malignant lymphoma diagnosed concurrently with or following lymph node infarction. Cases included seven B-cell lymphomas, three T-cell lymphomas, and one case of Hodgkin's disease. Sections of viable and infarcted tissue were immunostained in parallel using a panel of antibodies effective in routinely processed, wax-embedded tissue. The panel included anti-leucocyte-common antigen (CD45), T-cell-associated antigens (UCHL1, MT1), B-cell-associated antigens (MB1, 4KB5 (CD45R), MT2, LN1), a B-cell-specific antigen (L26), C3D-1 (CD15), and BER-H2 (CD30). Antibodies to intermediate filament cytoskeletal proteins, epithelial membrane antigen, and Factor VIII-related antigen were also used. In eight cases, staining of the infarcted material gave evidence of a lymphoid proliferation of either T- or B-cell type; an in the case of Hodgkin's disease, the results supported this diagnosis. The immunophenotype derived in the infarcted tissue mirrored the findings in the viable material in these eight cases of non-Hodgkin's lymphoma. A case of testicular infarction with concurrent intraosseous lymphoma was also examined. Staining in this case provided evidence of infarcted lymphoma. Thus, immunostaining of infarcted lymphoid tissue with these novel antibodies provides valuable information that conventional light microscopy cannot offer.

Antibodies, Monoclonal↗
PubMed1986

In-hospital myocardial infarction. Pre-infarction features and their correlation with short-term prognosis.

A retrospective study of 107 patients who sustained an acute myocardial infarction (AMI) during hospitalization was undertaken to assess the early prognosis of Q wave AMI (55 patients, group 1) and no-Q wave AMI (52 patients, group 2). Forty-one patients in group 1 and 31 in group 2 had documented ischaemia at rest in the period preceding AMI. The incidence of pre-infarction ischaemic attacks was similar in Q wave AMI compared with non-Q wave AMI (average daily incidence per patient 3.1 +/- 4.3 vs 3.0 +/- 4.3). A 'crescendo' pattern of pre-infarction angina was rarely observed in both groups. The incidence of post-infarction ischaemia (documented in 28 patients of group 1 and in 28 of group 2) was greater, but not significantly, in group 2 (average daily incidence per patient 1.0 +/- 2.6 vs 1.4 +/- 3.2). All patients with pre-infarction ischaemia sustained infarction in the same territory. AMI in group 1 was always symptomatic while 12 AMIs in group 2 were totally asymptomatic. Fifty patients from group 1 and 27 from group 2 were on therapy while AMI developed. Twenty-one patients from group 1 showed life threatening arrhythmias (ventricular tachycardia, ventricular fibrillation, third degree AV block or asystole) during AMI; of these, 14 did not survive the arrhythmias; they all had signs of left ventricular failure. Only one patient from group 2 had runs of ventricular tachycardia, unrelated to AMI but during pre- and post-infarction ischaemia. The overall mortality rate of Q wave AMI was 29% while no deaths occurred in the non-Q wave AMI.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

The effect of intravenous nitroglycerin therapy on infarct size in patients with acute myocardial infarction.

The authors investigated the influence of glyceryl-trinitrate (NTG) given intravenously to the reduction of infarction size in 95 patients (71 men and 24 women) aged 36 to 75, with acute myocardial infarction (AIM) admitted to the Intensive Care Unit within six hours of the onset of pain. Infarction mass was calculated by mathematical model from the serial changes of CK and CK MB serum activities during 72 hours and expressed in CK and CK MB gEq. CK and CK MB were determined every four hours. The patients were divided into four groups according to the therapy they were receiving: I--NTG i.v. (n = 29); II SK + NTG i.v. (n = 29); III SK i.v. (n = 17) and IV ISDN per os (n = 20). Each group was divided into subgroups regarding the time interval from the onset of pain to the beginning of the therapy (within three hours and after three hours). Application of NTG i.v. in the early phase of AIM, 0-3 hours from the onset of pain, led to the significant reduction of infarction mass CK gEq and CK MB gEq (0-3 hours; middle rank = 11.35; 3-6 hours: middle rank = 17.7) (P < 0.05) and 0-3 hours: middle rank = 10.31; 3-6 hours: middle rank = 18.81 (P < 0.01). It was established that the "timing" factor was very important in the preservation of myocardial mass in AIM. It affirms the efficacy of NTG i.v., i.e., its direct effects on the coronary arteries and systemic effects that cause salvation of the myocardium. The influence of NTG iv to myocardial infarction size CK gEq did not depend on ECG localization. But it influenced the ECG localization when the infarction size was calculated from CK MB isoenzyme and expressed in CK MB gEq. Infarction mass CK MB gEq was statistically significantly smaller in the inferior than in the anterior localization (P < 0.05).

Administration, Oral↗
PubMed1995

Cocaine-associated myocardial infarction. Mortality and complications. Cocaine-Associated Myocardial Infarction Study Group.

BACKGROUND: The frequency of complications in patients with cocaine-associated myocardial infarction is unknown. This study was performed to determine the short-term morbidity and mortality secondary to cocaine-associated myocardial infarction. METHODS: We performed a retrospective cohort study at 29 hospital centers throughout the United States. Patients with cocaine-associated myocardial infarction that occurred between 1987 and 1993 were identified through record review. The primary outcome measures were in-hospital mortality and the incidence and timing of major cardiovascular complications. RESULTS: Cocaine-associated myocardial infarction was identified 136 times in 130 patients. Patients were generally young (mean age, 38 years), nonwhite (72%), tobacco smokers (91%) with a history of cocaine use in the past 24 hours (88%). The initial electrocardiogram disclosed infarction in 44% and ischemia in an additional 18% of patients. Myocardial infarctions were evenly distributed between anterior (45%) and inferior (44%) and were most often non-Q-wave (61%). Complications occurred 64 times in 49 patients (36%; 95% confidence interval, 28% to 44%), including congestive heart failure in nine patients, ventricular tachycardia in 23 patients, supraventricular tachycardia in six patients, and brady-dysrhythmias in 26 patients. Most patients who had complications (90%) had them within 12 hours of presentation. Acute in-hospital mortality was 0% (95% confidence interval, 0% to 2%). CONCLUSIONS: The mortality of patients hospitalized with cocaine-associated myocardial infarction was low. The majority of complications occurred within 12 hours of presentation.

Adult↗
PubMed1975

Results of long-term administration of anticoagulants in patients with myocardial infarction and coronary heart disease without infarction.

Long-term treatment with anticoagulants (Sintrom, Suncumar) was applied in 300 cases of myocardial infarction and 106 cases of coronary heart disease without infarction aged 31 to 70 years over periods ranging from one to six years. The control group comprised 347 patients with myocardial infarction and 195 patients with coronary heart disease without infarction in the same age range who were not treated with Syncumar because of contraindications. Treatment with Syncumar was started on the first day at hospital and was continued after discharge from the hospital on an outpatient basis. The level of prothrombin was kept within the range of 35-45%. In the Syncumar treated group the mortality in patients with myocardial infarction was 8.0% and in the control group it was 20.5%. In the Syncumar treated group the incidence of repeated infarctions was 12.7% and in the controls it was 33.1%. On the other hand, no effects of Syncumar on the mortality of patients with chronic coronary heart disease without infarction was observed.

Adult↗
PubMed1993

[Late onset seizures in cerebral infarction--clinical study of late onset seizures in cortical branch infarction].

We retrospectively analyzed the clinical features, prognosis, CT scans and electroencephalograms in 527 patients with cerebral infarction in the Toranomon hospital between 1983 and 1990. CT scans revealed cortical involvement in 130 cases and subcortical infarcts in the territory of the perforating branch arteries in 397 cases. The mean duration of the follow up was 38.5 +/- 27 months (M +/- SD). Of these, late onset seizures developed in 5.69% (30/527). The incidence of seizures after cortical branch infarcts was 20% (26/130), which was significantly higher than that after subcortical infarcts (1%; 4/397) (p < 0.05). These late seizures could be either generalized or partial seizures. The interval between stroke and the onset of seizures was 2.4 years (mean), and 78% of late onset seizures developed within 3 years after the stroke. CT scans of the patients with late seizures showed that infarcted area was located mainly in the territory of the left middle cerebral artery. The incidence of late seizures was significantly higher in patients with left cortical infarction (12/41, 29.3%) than those with right one (6/29, 15.4%, p < 0.05). These results suggest that left-sided cortical involvement may have some liability to late onset seizures in patients with cerebral infarction. Further study on indication of prophylactic use of anticonvulsants might be requested in patients with right hemiparesis and aphasia.

Aphasia↗
PubMed1995

[Dobutamine stress echocardiography in patients after an acute myocardial infarct: what is the significance of arterial patency related to the infarct?].

BACKGROUND: Dobutamine stress echocardiography is a very promising technique for assessing myocardial viability, ischemia and prognosis in patients with a recent acute myocardial infarction. Recent studies have shown that the type of perfusion in the infarct-related artery also plays a role in the prognosis of these patients. PURPOSE: To evaluated in patients with non complicated infarction the ability of low-dose and high-dose dobutamine stress echocardiography to assess the presence of both viability and inducible ischemia and correlate the results with the patency of the infarct related artery and the accuracy to predict cardiac events during one year follow-up. PATIENTS AND METHODS: Fifty one consecutive in-hospital patients (47 male and four female, mean age 52 +/- 11 years, range 31-75 years) with acute myocardial infarction were evaluated both by dobutamine stress echocardiography and by coronary angiography and followed-up for a mean of 12 +/- 8 months. RESULTS: With low-doses of dobutamine, the incidence of myocardial viability was 33% and with high-doses, the incidence of residual inducible ischemia was 41%. The patency of infarct-related artery showed significant correlation with score wall motion index for viability and for myocardial ischemia. Twenty four (47%) patients suffered cardiac events. Dobutamine stress echocardiography showed a positive predictive value of 67% and a negative of 70% and identified high and low risk patients. CONCLUSIONS: Dobutamine stress echocardiography in patients with acute myocardial infarction is a safe and well tolerated test, and provides in a single test useful information regarding viability, ischemia and prognosis.

Adult↗
PubMed1998

[New computerized tomography sign of intestinal infarction: isolated pneumoretroperitoneum or associated with pneumoperitoneum or late findings of intestinal infarction].

INTRODUCTION: We retrospectively reviewed the CT findings of the acute abdomen patients examined in the last two years to investigate the frequency of a new CT sign of intestinal infarction, the pneumoretroperitoneum, and its association with other CT findings highly suggestive of this condition. MATERIAL AND METHODS: The CT findings of 60 patients with diagnostic confirmation of intestinal infarction were retrospectively reviewed. CT was performed without (no. = 55) and with (no. = 5) oral administration of contrast material and without (no. = 3) and with (no. = 57) the i.v. injection of nonionic contrast agents in repeated 50 mL boluses. To assess the specificity of this sign, we selected a control group of 400 patients submitted to CT for acute abdomen, but not blunt trauma; 19 of these patients had pneumoretroperitoneum. RESULTS: Pneumoperitoneum was found in five patients with intestinal infarction; it was an isolated sign in two cases and it was associated with few small perihepatic air bubbles in one case. Finally, it was associated with highly suggestive findings of late intestinal infarction in the other two cases. All cases of pneumoretroperitoneum in the control group had been correctly referred to other diseases by previous plain film and/or CT findings and surgery and/or endoscopy confirmed this diagnosis. DISCUSSION AND CONCLUSIONS: Pneumoretroperitoneum has been described as a complication of different benign or severe disorders; prompt recognition of its origin is essential since surgical and/or septic conditions may be involved. However, if the patient's history is negative for abdominal trauma, gastroduodenal ulcer or sepsis, pneumoretroperitoneum is generally cured with conservative treatment. Intestinal infarction or severe ischemia, a usually surgical conditions, should be considered among the different causes of pneumoretroperitoneum alone or associated with pneumoperitoneum or with highly suggestive late findings of infarction such as portal venous gas or pneumatosis intestinalis. This sign had a non-negligible incidence in intestinal infarction in our review (8.5%), but it should be known of and sought with specific window setting to enhance gas depiction on CT images to avoid false negatives.

Aged↗