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PubMed1986

Prognostic significance of right ventricular ejection fraction for persistent complex ventricular arrhythmias and/or sudden cardiac death after first myocardial infarction: relation to infarct location, size and left ventricular function.

To assess the prognostic significance of right ventricular dysfunction after a first myocardial infarction for complex ventricular arrhythmias and or sudden cardiac death in relation to infarct location, size and left ventricular function, a series of 127 consecutive patients was prospectively studied and followed up for one year. Prior to hospital discharge, a 24-hour electrocardiographic recording and radionuclide angiocardiography were performed. Right ventricular ejection fraction was related to inferior infarct location and size (r = 0.45, P less than 0.01): similarly left ventricular ejection fraction was related to anterior infarct location and size (r = 0.76, P less than 0.001). The incidence of severe ventricular arrhythmias was significantly higher in patients with isolated right or left ventricular dysfunction compared to patients with normal function; it was highest in patients with severe depression of both ventricles. Patients with complex ventricular arrhythmia and/or sudden cardiac death had significantly reduced left and right ventricular ejection fractions. Detailed analysis in patients with left ventricular ejection fraction greater than 0.40 vs. less than or equal to 0.40 showed that presence of complex ventricular ectopic activity and/or sudden cardiac death after myocardial infarction was related not only to left, but also independently to right ventricular dysfunction. These results imply a significant prognostic contribution of right ventricular dysfunction to the occurrence of severe ventricular arrhythmias and/or sudden cardiac death after myocardial infarction independent of and additive to left ventricular dysfunction.

Adult↗
PubMed1988

Dipyridamole-thallium 201 scintigraphy in the early post-infarction period. (Safety and accuracy in predicting the extent of coronary disease and future recurrence of angina in patients suffering from their first myocardial infarction).

To evaluate the safety and usefulness of myocardial thallium-201 scintigraphy after intravenous dipyridamole during the early post-infarction period, 35 patients under 60 years of age and with recent first transmural uncomplicated myocardial infarction (27 inferior, 8 anterior) were examined between the 5th and 13th day of hospitalization. Although four patients experienced angina and transient ischemic ST depression during the test, there were no serious complications. Patients were followed for a mean period of 11.4 +/- 6.3 months after hospital discharge. None of the patients experienced recurrent infarction and there were no cardiac deaths. In 11 patients there were reversible perfusion defects in areas different from those of myocardial infarction. Of these patients, seven (one with infarct vessel stenosis only and six with multivessel coronary disease) developed angina during the follow-up: five underwent coronary surgery because of severe angina refractory to full medical therapy. Out of the 24 patients without reversible perfusion defects, only two (with multivessel coronary disease) showed typical angina symptoms. The presence of redistribution on thallium scans was significantly more frequent in patients who developed a recurrence of angina over a period of 11.4 +/- 6.3 months of follow-up (P less than 0.0005). Thus dipyridamole-thallium 201 scintigraphy is a safe, non-invasive stress test which may be used early following uncomplicated myocardial infarction in order to identify patients at risk for the recurrence of angina.

Adult↗
PubMed2004

In vivo transfer of soluble TNF-alpha receptor 1 gene improves cardiac function and reduces infarct size after myocardial infarction in rats.

Increased circulating and cardiac TNF-alpha levels during myocardial ischemia have been found in both experimental animals and patients with ischemic heart disease and advanced heart failure. Soluble TNF-alpha receptor 1 (sTNFR1) is an antagonist to TNF-alpha. In the present study, we examined whether sTNFR1 improves cardiac function in rats after myocardial infarction. Male Wistar rats were subjected to left coronary artery (LCA) ligation. Immediately after the ligation, a total of 200 microg of either the sTNFR1 or LacZ plasmid was injected into three different sites in the left ventricular wall. From 1 to 21 days after LCA ligation, TNF-alpha bioactivity in the heart was higher in rats receiving LacZ plasmid than in sham-operated rats, whereas sTNFR1 plasmid significantly suppressed the increase. The LV diastolic dimension was significantly lower, and the fractional shortening was significantly higher in rats treated with the sTNFR1 plasmid than in those treated with the LacZ plasmid. At 21 days after LCA ligation, the LV end-diastolic pressure was also significantly lower in the rats treated with the sTNFR1 plasmid. In addition, the sTNFR1 expression plasmid had significantly reduced the infarct size. In conclusion, TNF-alpha bioactivity in the heart increased during the early stage of infarction and remained elevated. This elevation seemed partially responsible for the impairment of LV function and the increased infarct size. Suppression of TNF-alpha bioactivity from the early stage of infarction with the sTNFR1 plasmid improved cardiac function and reduced infarct size.

Animals↗
PubMedDate not supplied

Myeloperoxidase activity as a quantitative marker of polymorphonuclear leukocyte accumulation into an experimental myocardial infarct--the effect of ibuprofen on infarct size and polymorphonuclear leukocyte accumulation.

The accumulation of polymorphonuclear leukocytes (PMN) into a canine occlusion/reperfusion model of myocardial infarction (MI) has been quantitated using a spectrophotometric assay for the PMN-specific enzyme myeloperoxidase (MPO). In anaesthetized beagle dogs subjected to 1 h of occlusion of the left anterior descending coronary artery followed by coronary reperfusion for 1 h, MPO activity was found in fourfold greater amounts in infarcted myocardium as opposed to normal myocardium. MPO activity in infarcted myocardium increased with coronary reperfusion in a time-related manner, the greatest accumulation occurring at 5 h of coronary reperfusion. The time-related increase in MPO activity in ischemic myocardium was closely correlated with the observed accumulation of PMN as assessed by histological sectioning, thus supporting the specificity of the method. Pretreatment of dogs with ibuprofen (12.5 mg/kg i.v.) did not alter the MPO content and therefore PMN invasion of infarcted myocardium, a finding confirmed by light microscopy. However, pretreatment with ibuprofen increased myocardial infarct size (from 11.5 to 37.4%, p less than 0.01) and increased the incidence of haemorrhagic infarction and ventricular fibrillation. In conclusion, our studies demonstrate that MPO can be used as a sensitive and quantitative marker of PMN accumulation into an evolving MI. Furthermore, we have demonstrated that PMNs rapidly infiltrated injured myocardium in a time dependent manner and this accumulation was unaffected by ibuprofen pretreatment.

Animals↗
PubMed2004

Remifentanil limits infarct size but attenuates preconditioning-induced infarct limitation.

OBJECTIVES: We investigated the influence of the narcotic anesthetic remifentanil on irreversible myocardial ischemic injury. METHODS: New Zealand White rabbits were anesthetized with propofol (0.7-1.8 mg.kg.min) and then subjected to 30 min regional myocardial ischemia and 3 h reperfusion (CON). Some animals also underwent ischemic preconditioning, elicited by either one (IP1) or two (IP2) cycles of 5 min ischemia and 5 min reperfusion, and/or remifentanil, administered either as a transient infusion mimicking the preconditioning protocol (RP2, 10 microg x kg x min) or as a continuous infusion (R, 3-10 microg x kg x min). Rabbits were randomly assigned to experimental groups. Infarct size was assessed with tetrazolium. Results are reported as mean+/-SD. RESULTS: Non-preconditioned infarct size was approximately 50% of the area-at-risk (49.6+/-20.1% CON). Both one and two cycles of ischemic preconditioning markedly reduced infarct size (49.6+/-20.1% CON versus 18.6+/-8.6% IP and versus 7.5+/-7.6% IP2; both p<0.001). Preconditioning with remifentanil modestly reduced infarct size (49.6+/-20.1% CON versus 29.3+/-8.5% RP2; p<0.01). However, sustained administration of remifentanil did not provide protection (49.6+/-20.1% CON versus 43.9+/-16.2% R), and it attenuated the protection offered by preconditioning (49.6+/-20.1% CON versus 35.6+/-20.7% R+IP1, p=NS; and versus 14.5+/-14.5% R+IP2; p<0.05). CONCLUSION: Transient pre-ischemic administration of remifentanil modestly reduces infarct size in propofol-anesthetized rabbits, but continuous administration of remifentanil increases the threshold for ischemic preconditioning-induced infarct limitation.

Anesthetics↗
PubMed2004

The assessment of infarct size in postmyocardial infarction patients undergoing thallium-201 tomographic imaging is improved using attenuation correction.

PURPOSE: Attenuation correction (ATC) has been shown to improve the accuracy of thallium-201 single photon emission computed tomography (SPECT) for the detection and evaluation of patients with coronary artery disease. The purpose of this study was to evaluate the value of ATC for the assessment of infarct size in patients after myocardial infarction (MI). MATERIALS AND METHODS: Tl-201 SPECT with ATC was performed on 39 patients with 49 previous MIs. This was followed by radionuclide ventriculography for the assessment of global and regional left ventricular function. Uncorrected and corrected 24-hour redistribution SPECT images were analyzed for regional perfusion using a 5-point segmental scoring scale from 0 (normal) to 4 (absent) thallium uptake. RESULTS: The mean number of segments with scores of >1 and 2 was significantly higher without ATC than with ATC (5.3 +/- 3.6 vs. 3.5 +/- 3.6, P = 0.0001 for scores >1; 3.8 +/- 3.6 vs. 2.5 +/- 3.0, P = 0.0001 for scores of >2, respectively). The mean total number of segments with scores of >1 assessed without ATC was significantly higher compared with that assessed with ATC (16.9 +/- 13.5 vs. 11.2 +/- 12.2, P = 0.0001). Evaluation without ATC demonstrated only a fair correlation between the SPECT parameters (number of segments with scores of >1 and >2, and total score of segments with scores of >1) and left ventricular regional and global function, whereas there was a clear improvement in all the parameters after ATC. With ATC, a decrease in infarct size was demonstrated in 27 of the 49 infarcts (55%). CONCLUSIONS: The improved correlation with left ventricular function indicates that SPECT imaging with ATC provides a more accurate assessment of infarct size in post-MI patients. The use of nonattenuation-corrected SPECT imaging overestimates infarct size in a majority of patients.

Adult↗
PubMed1981

Oesophageal dysfunction and ischaemic heart disease as origin of chest pain in non-infarction coronary care unit patients and patients with myocardial infarction.

Oesophageal dysfunction (OD), ischaemic heart disease (IHD) and their relation to chest pain were studied in two groups of patients. A group of 55 non-infarction coronary care unit patients were investigated within 6 months and at a three-year follow-up, and 52 male patients were studies within 6 months after an acute myocardial infarction. Oesophageal manometry, pH recording, acid perfusion test, ECG at rest and exercise, history by questionnaire and by interview were used as diagnostic tools. Non-infarction coronary care unit patients with unknown origin of their chest pain at discharge from hospital had a higher frequency of OD (58%) than patients with recent myocardial infarction (33%, p less than 0.05). In 7 of 55 (13%) non-infarction patients OD was regarded as the cause and in 17 (31%) IHD was regarded as the cause of pain on admission to the coronary care unit. OD was an uncommon cause of angina-like chest pain in patients with recent myocardial infarction (1 of 38 patients). Patients with OD had a higher frequency of oesophageally related questionnaire symptoms than patients with normal oesophageal function. For the differential diagnosis of chest pain a careful history is essential. Reproduction of the patient's chest pain during oesophageal acid perfusion test or exercise test offers additional valuable information.

Coronary Care Units↗
PubMed1984

Relationship between the enzymatically estimated infarct size and clinical findings in acute myocardial infarction.

In 580 patients with a definite myocardial infarction (MI) and no previous MI, the enzymatically estimated infarct size was related to the clinical course including various complications. In all patients, heat-stable lactate dehydrogenase activity (EC 1.1.1.27, LD) was analyzed every 12 hours for 48-108 hours and in a subgroup (n = 170) creatine kinase activity (EC 2.7.3.2, CK) and creatinine kinase subunit B (CK B) were analyzed every 6 hours for 48 hours. The highest recorded enzyme activity was used as a rough estimate of infarct size. A positive correlation was found between serum enzyme activity and most of the clinical variables studied, such as incidence of congestive heart failure, treatment with furosemide, incidence of hypotension, cardiogenic shock, pericarditis, post myocardial infarction syndrome, AV block III, and the duration of hospitalization. We conclude that the enzymatically estimated infarct size determined by heat-stable LD, CK and CK B closely reflects the severity of the infarction.

Adrenergic beta-Antagonists↗
PubMed2004

Prevalence of right ventricular myocardial infarction in patients with acute inferior wall myocardial infarction.

The objective was to evaluate the prevalence of right ventricular myocardial infarction (RVMI) in patients with acute inferior wall myocardial infarction (IWMI) admitted to the National Institute of Cardiovascular Diseases, Karachi, Pakistan. Between August 2000 and May 2001, a total of 100 patients with acute IWMI were enrolled. History of all patients was taken, and thorough clinical examination was performed to asses the presence of signs of right ventricular infarction. Standard 12-lead electrocardiogram was recorded immediately on arrival of patients along with right precordial leads. All patients were considered for thrombolytic therapy in the absence of any contraindication and were managed with standard treatment strategies. Complications arising during the course of admission were recorded and compared between the two groups. There were 86 (86%) males and 14 (14%) females. Mean age was 56.3 +/- 13.13 years (range 33-83 years). The prevalence of RVMI in IWMI was 34%. Smoking and diabetes were more prevalent in RVMI group, while hypertension and family history of ischemic heart disease were more common in isolated IWMI. Ninety per cent of patients received thrombolytic therapy. In-hospital mortality (23.5%) was higher in RVMI group than isolated IWMI (18.1%). Other major complications were also higher in RVMI group than isolated IWMI. Right ventricular infarction was found in approximately one-third of IWMI. Right ventricular infarction was associated with considerable morbidity and mortality, and its presence defines a higher risk subgroup of patients with inferior wall left ventricular infarction.

Adult↗
PubMed1982

Effect of infarct size limitation by propranolol on ventricular arrhythmias after myocardial infarction.

These experiments show that pretreatment with propranolol was able to achieve significant infarct size reduction in this particular animal model of LAD occlusion followed by reperfusion through a critical stenosis. Despite infarct size reduction, the propranolol pretreatment prolonged the time course of spontaneous ventricular arrhythmias after acute myocardial infarction in the conscious dog. In contrast to this, propranolol pretreatment did not appear to protect against inducible ventricular arrhythmias in the late postinfarction period in the conscious dog. While it is, of course, impossible to extrapolate the results of animal studies to the clinical situation, future clinical studies designed to limit infarct size by pharmacologic intervention should specifically address the question of electrophysiologic instability after myocardial infarction, both in the early and late phases. The possibility exists that pharmacologic limitation of infarct size may preserve viable but potentially jeopardized areas of myocardium, leaving the risk of subsequent malignant arrhythmias and sudden death.

Animals↗
PubMed1996

Sex related differences in short and long-term prognosis after acute myocardial infarction: 10 year follow up of 3073 patients in database of first Danish Verapamil Infarction Trial.

OBJECTIVE: To re-examine the prevailing hypothesis that women fare worse than men after acute myocardial infarction. DESIGN: 10 year follow up of all patients with confirmed acute myocardial infarction registered in the database of the Danish verapamil infarction trial in 1979-81. SETTING: 16 coronary care units, covering a fifth of the total Danish population. PATIENTS: 3073 consecutive patients with acute myocardial infarction, 738 (24%) women and 2335 (76%) men. MAIN OUTCOME MEASURES: Early mortality (before day 15). For patients alive on day 15: mortality, cause of death, admission with recurrent infarction, and mortality after reinfarction. RESULTS: Early mortality increased significantly with age (P < 0.0001) but was not significantly related to sex, with a 15 day mortality of 17% in women and 16% in men. Adjustment for age and sex simultaneously revealed a significant interaction (P = 0.02) between these variables, with a greater increase with age in early mortality for men than for women (early mortality was equal for the two sexes at age 64 years). Ten year mortality in patients alive on day 15 was 58.8%. The overall age adjusted hazard ratio (95% confidence interval) for women versus men was 0.90 (0.80 to 1.01); 0.90 (0.78 to 1.04) for 10 year reinfarction (48.8%); and 0.98 (0.82 to 1.16) for 10 year mortality after reinfarction (82.3%). No difference in cause of death was found between the sexes. With a follow up of up to 10 years for patients alive on day 15 mortality, rate of reinfarction, and mortality after reinfarction increased with increasing age (P < 0.0001). CONCLUSION: Sex by itself is not a risk factor after acute myocardial infarction.

Aged↗
PubMed1986

Long term improvement in global left ventricular function after early thrombolytic treatment in acute myocardial infarction. Report of a randomised multicentre trial of intracoronary streptokinase in acute myocardial infarction.

The effect of reperfusion achieved by early intracoronary streptokinase in acute myocardial infarction on left ventricular function was studied in 533 patients enrolled in a prospective randomised multicentre study. Two hundred and sixty four patients were allocated to conventional treatment and 269 patients to thrombolysis. At the end of the procedure patency of the infarct related vessel was achieved in 198 (85%) of 234 patients in whom coronary angiography was performed. The median interval from onset of symptoms till the angiographic documentation of patency was 200 minutes. Data were analysed according to the original treatment allocation. Global left ventricular ejection fraction was determined by radionuclide angiography in 418 patients within two days of admission, in 361 patients after two weeks, and in 307 patients after three months. Global left ventricular function remained unchanged throughout the observation period in the control group, whereas it improved during the first two weeks in patients allocated to thrombolytic treatment. Improved function in these patients persisted up to three months after the infarction. Global left ventricular ejection fraction was significantly better in the thrombolysis group than in the control group at two days, two weeks, and at three months. In patients with anterior myocardial infarction the left ventricular ejection fraction was 9% better than in the control group at two weeks and at three months. In the patients with inferior myocardial infarction differences between the two treatment groups were smaller because of photon attenuation within the body. Angiographic evidence suggested that the improvement in function seen after thrombolysis is indeed associated with the patency of the infarct related artery.

Aged↗
PubMed1988

Effect of nifedipine on enzymatically estimated infarct size in the early phase of acute myocardial infarction.

In a double blind placebo controlled trial, 434 patients with suspected myocardial infarction were randomised to treatment with nifedipine (n = 217) or placebo (n = 217) within six hours from the onset of chest pain. During the treatment period of 48 hours, a 10 mg capsule containing nifedipine or placebo was given sublingually every four hours for 24 hours, then orally every four hours for the next 24 hours. Acute myocardial infarction was confirmed in 295 patients (146 in the nifedipine group and 149 in the placebo group). The median delay time to intervention with nifedipine in patients with acute myocardial infarction was 111 minutes. Infarct size was assessed by the estimation of release of creatine kinase isoenzyme MB and creatine kinase from blood samples taken every four hours for 48 hours. The total mean (SEM) creatine kinase MB released was 406.4 (27.2) IU/l in the nifedipine group and 345.7 (20.5) IU/l in the placebo group. Total mean (SEM) creatine kinase released was 2749.6 (165.1) IU/l in the nifedipine group and 2698.4 (145.9) IU/l in the placebo group. In hospital mortality was similar for both the nifedipine and placebo groups (6.6% and 5.8% respectively). Treatment with nifedipine in the early phase of acute myocardial infarction seems to have no effect on enzymatically measured infarct size.

Aged↗
PubMed1999

Spontaneous late improvement of myocardial viability in the chronic infarct zone is possible, depending on persistent TIMI 3 flow and a low grade stenosis of the infarct artery.

OBJECTIVE: In the chronic phase of myocardial infarction, the relation between myocardial recovery and infarct related artery status remains unclear. The spontaneous changes in rest-redistribution thallium defect size were prospectively studied over six months in 52 patients with chronic Q wave myocardial infarction. DESIGN: Changes in rest thallium defect size, thallium uptake in the infarct area, and radionuclide left ventricular ejection fraction were compared to the quantitative coronary angiogram data. Two groups of patients were considered: patients with a percentage of stenosis below 100% (group 1, n = 31); and patients with an occluded artery (group 2, n = 21). RESULTS: In the overall population, the mean (SD) defect size decreased from 28.2 (17.2)% to 24.9 (19.3)% of the whole myocardium (p = 0.01), while, in this area, the thallium uptake increased from 62.9 (13.7)% to 66. 9 (15.6)% (p < 0.001). At the time of inclusion, the defect size, thallium uptake, and ejection fraction were similar in both groups. In group 1 patients only, the reduction in defect size correlated with the improvement in ejection fraction (r = 0.41, p = 0.02) and was related to the percentage of coronary artery stenosis. TIMI 3 patients reduced the defect size while other patients increased this defect (-5.1 (7.0)% v +11.0 (14.4)%, p < 0.001). In contrast, no significant relations were found in group 2 patients. CONCLUSION: Late spontaneous recovery in thallium defect can occur in patients with a patent infarct related artery, depending on the TIMI flow grade and a low grade stenosis of the infarct related artery, and is associated with functional improvement.

Aged↗
PubMed2005

Late defect on delayed contrast-enhanced multi-detector row CT scans in the prediction of SPECT infarct size after reperfused acute myocardial infarction: initial experience.

PURPOSE: To prospectively assess the accuracy of multi-detector row computed tomography (CT) in the prediction of infarct size after successful reperfusion of acute myocardial infarction (MI) by using single photon emission computed tomography (SPECT) images obtained 6 weeks later as the reference standard. MATERIALS AND METHODS: Institutional review board approval and informed consent were obtained. A total of 34 patients (29 men and five women; mean age, 56 years +/- 13) underwent dual-phase 16-detector row CT within 3 days +/- 3 after successful reperfusion of acute MI. Iodinated contrast medium (1.5 mL per kilogram of body weight) was injected at a flow rate of 3.5 mL/sec. A first arterial phase acquisition was followed 5 minutes later by a late acquisition, without reinjection of contrast medium. A radiologist and a cardiologist used a 17-segment model in a blind analysis of images obtained during late acquisition. For each segment, presence of late defect or late enhancement was recorded. Findings were compared with SPECT studies analyzed by a nuclear medicine physician and a cardiologist 6 weeks after the acute event. CT defects were compared with SPECT defects on a segmental and per-patient basis. Mean number of segments with late defects on multi-detector row CT scans was compared with infarct size on SPECT images by using the t test. RESULTS: All patients had late enhancement in the infarcted myocardium. In 27 of 34 patients, a late defect surrounded by a subepicardial late enhancement was detected. Segments with late defect on CT scans were predictive of residual perfusion defects at 6-week follow-up, with sensitivity of 78%, specificity of 91%, and accuracy of 90%. On a per-patient basis, sensitivity was 93%, specificity was 100%, and accuracy was 94%. Mean number of segments with late defects on multi-detector row CT scans (ie, 3.1 segments) was not significantly different from infarct size on SPECT images (eg, 2.5 segments) (P = .2). CONCLUSION: Late defect on multi-detector row CT scans indicates residual perfusion SPECT defect and infarct size after successfully reperfused MI, with sensitivity of 93%, specificity of 100%, and accuracy of 94%.

Adult↗
PubMedDate not supplied

Prognostic significance of infarction location in patients with recurrent myocardial infarction. SPRINT Study Group. Secondary Prevention Reinfarction Israel Nifedipine Trial.

This study assesses the impact of infarct location on immediate (in-hospital) and 1- and 5-year mortality among patients with reinfarction during the year following discharge from the initial episode of myocardial infarction. The analysis included 192 patients with a second myocardial infarction who were compared in four infarction location groups. The in-hospital mortality associated with reinfarction was higher in patients with a second anterior (32%) than with a second inferior (18%) location, irrespective of the first infarction location (p = 0.03). At 5 years of follow-up, the mortality (65%) tended to be higher in patients with a first anterior-second anterior infarction as compared with patients with all other combinations of location.

Age Factors↗
PubMedDate not supplied

Infarct size measured by single photon emission computed tomographic imaging with (99m)Tc-sestamibi: A measure of the efficacy of therapy in acute myocardial infarction.

BACKGROUND: Use of mortality as an end point in randomized trials of reperfusion therapy requires increasingly large sample sizes to test advances compared with existing therapy, which is already highly effective. There has been a growing interest in infarct size measurements by (99m)Tc-sestamibi SPECT (single photon emission computed tomographic) imaging as a surrogate end point. METHODS AND RESULTS: We reviewed the reports published in English regarding infarct size measurements by (99m)Tc-sestamibi. Four separate lines of published evidence support the validity of SPECT imaging with (99m)Tc-sestamibi for determination of infarct size. This end point has been used in a total of 7 randomized trials-1 single center and 6 multicenter. The end point compares favorably with left ventricular function and infarct size measurements with the use of other radiopharmaceuticals. The most important limitation of this approach is the absence thus far of a randomized trial that has shown a corresponding decrease in mortality in association with a therapy that reduces infarct size. CONCLUSIONS: SPECT imaging with (99m)Tc-sestamibi is the best available measurement tool for infarct size. It has already served as an end point in early pilot studies to evaluate potential efficacy and in dose-ranging studies. It has the potential to serve as a surrogate end point to uncover advantages of new therapies that may be equivalent to existing therapies with respect to early mortality.

Heart↗
PubMed1982

Effect of infarct location on the in-hospital prognosis of patients with first transmural myocardial infarction.

We studied the in-hospital prognosis of 1105 patients who had their first transmural myocardial infarction; 611 patients (55.3%) had anterior myocardial infarction (AMI) and 494 (44.7%) had inferior myocardial infarction (IMI). Patients with IMI had a significantly lower in-hospital mortality rate (9.1% vs 15.6%, p = 0.0014) and significantly lower prevalences of congestive heart failure (39.4% vs 47.6%, p = 0.0066), cardiogenic shock ( 8.7% vs 12.6%, p = 0.0384) and conduction defects (left anterior hemiblock, right bundle branch block and intraventricular conduction defect). The patients with AMI had significantly higher peak enzyme levels, and a greater percentage of them (40.1% vs 25.9%) had SGOT greater than 240 IU/l, whereas more patients with IMI (34.6% vs 27.8%) had SGOT less than 120 IU/l (p = 0.0001). When the parallel subgroups were compared according to the peak SGOT levels (less than 120, 120-240, and greater than 240 IU/l, the differences in the mortality and morbidity between the two infarct locations diminished. However, patients with AMI still had a less favorable outcome. Logistic regression analysis demonstrated that both the peak enzyme level and the infarct location had an independent influence on the in-hospital prognosis of patients with first transmural infarction.

Aged↗