Duration of chest pain associated with acute myocardial infarction: a predictor of long-term prognosis.

This paper describes 109 patients who had their first myocardial infarction and were then followed up for 3 to 8 years. The following data were collected at the time of the infarction: duration and severity of chest pain, type of infarction and peak SGOT (serum glutamic oxaloacetic transaminase) level. The duration of chest pain has previously been shown to correlate with infarct size. Duration of chest pain, age and peak SGOT level were found to be the most important predictors of survival. None of the other independent variables contributed further to survival when the effects of duration of pain, age and SGOT level were taken into account. However, there was a significant association between pain duration and functional status. These data suggest that the duration of chest pain during first myocardial infarctions is a predictor of long-term prognosis and probably of functional status.     

Technetium pyrophosphate scanning in the detection of acute myocardial infarction: clinical experience.

Technetium-99m-stannous pyrophosphate (99mTc-PYP) accumulates in acutely infarcted myocardium and can be detected by scintiscanning. The clinical value of 99mTc-PYP scintiscanning was studied in 83 patients 6 hours to 21 days after the onset of acute chest pain. In 12 patients with normal electrocardiograms and serum enzyme values no uptake of 99mTc-PYP was detected on the scintigrams. Of 44 patients with electrocardiographic or enzyme evidence, or both, of acute myocardial infarction the scintigrams were positive in 31, "questionable" in 2 and negative in 11; no positive scan was obtained within 12 hours of the onset of pain, and the scans generally remained positive for up to 5 days. In 24 patients with evidence of prolonged myocardial ischemia the scans were positive in 2, questionable in 4 and negative in 18. The scans were negative in each of three patients with acute or constrictive pericarditis. Localization by electrocardiography and scintiscanning correlated nearly perfectly for transmural infarcts but subendocardial infarcts could not always be localized precisely by scintiscanning. The infarct area (total area of 99mTc-PYP uptake) correlated well with the peak serum value of creatine phosphokinase.     

Comparison of NOGA Endocardial Mapping and Cardiac Magnetic Resonance Imaging for Determining Infarct Size and Infarct Transmurality for Intramyocardial Injection Therapy Using Experimental Data

Objectives

We compared the accuracy of NOGA endocardial mapping for delineating transmural and non-transmural infarction to the results of cardiac magnetic resonance imaging (cMRI) with late gadolinium enhancement (LE) for guiding intramyocardial reparative substance delivery using data from experimental myocardial infarction studies.

Methods

Sixty domestic pigs underwent diagnostic NOGA endocardial mapping and cMRI-LE 60 days after induction of closed-chest reperfused myocardial infarction. The infarct size was determined by LE of cMRI and by delineation of the infarct core on the unipolar voltage polar map. The sizes of the transmural and non-transmural infarctions were calculated from the cMRI transmurality map using signal intensity (SI) cut-offs of>75% and>25% and from NOGA bipolar maps using bipolar voltage cut-off values of <0.8 mV and <1.9 mV. Linear regression analysis and Bland-Altman plots were used to determine correlations and systematic differences between the two images. The overlapping ratios of the transmural and non-transmural infarcted areas were calculated.

Results

Infarct size as determined by 2D NOGA unipolar voltage polar mapping correlated with the 3D cMRI-LE findings (r = 0.504, p<0.001) with a mean difference of 2.82% in the left ventricular (LV) surface between the two images. Polar maps of transmural cMRI and bipolar maps of NOGA showed significant association for determining of the extent of transmural infarction (r = 0.727, p<0.001, overlap ratio of 81.6±11.1%) and non-transmural infarction (r = 0.555, p<0.001, overlap ratio of 70.6±18.5%). NOGA overestimated the transmural scar size (6.81% of the LV surface) but slightly underestimated the size of the non-transmural infarction (−3.04% of the LV surface).

Conclusions

By combining unipolar and bipolar voltage maps, NOGA endocardial mapping is useful for accurate delineation of the targeted zone for intramyocardial therapy and is comparable to cMRI-LE. This may be useful in patients with contraindications for cMRI who require targeted intramyocardial regenerative therapy.     

Myocardial infarct size measurement in the mouse chronic infarction model: comparison of area- and length-based approaches.

Efficacy of potential treatments for myocardial infarction (MI) is commonly assessed by histological measurement of infarct size in rodent models. In experiments involving an acute MI setting, measurement of the infarcted area in tissue sections of the left ventricle is a standard approach to determine infarct size. This approach has also been used in the chronic infarct setting to measure infarct area several weeks post-MI. We tested the hypothesis that, because wall thinning is known to occur in the chronic setting, the area measurement approach would be less appropriate. We compared infarct measurements in tissue sections based on 1) infarct area, 2) epicardial and endocardial infarct arc lengths, and 3) midline infarct arc length. Infarct sizes from all three measurement approaches correlated significantly with left ventricular ejection fraction and wall motion abnormality. However, the infarct size values derived from the area measurement approach were significantly smaller than those from the other two measurement approaches, and the range of values obtained was compressed 0.4-fold. The midline method allowed detection of the expected size differences between infarcts of variable severity resulting from proximal vs. distal ligation of the coronary artery. Segmental infarct size was correlated with segmental wall motion abnormality. We conclude that both area- and length-based measurements can be used to determine relative infarct size over a wide range of severity, although the area-based measurements are substantially more compressed due to wall thinning, and that the estimation of infarct midlines is a simple, reliable approach to infarct size assessment.     

Vomiting as a diagnostic aid in acute ischaemic cardiac pain.

The incidence of vomiting before the administration of analgesics was studied in 109 patients admitted to hospital as emergencies with prolonged ischaemic cardiac pain. In transmural myocardial infarction (58 patients) the incidence was 43% (anterior infarction 58%, inferior infarction 41%). Of the 23 patients with myocardial necrosis but without transmural infarction (that is, those with diffuse or subendocardial necrosis) and the 28 with coronary insufficiency but no necrosis, only one patient in each group experienced vomiting. When vomiting occurs early in association with cardiac pain transmural infarction may be expected in 90% of patients.     

The influence of rate of temperature change and peak stimulus duration on pain intensity and quality

An important aspect of experimental pain research is that the assessment methods can investigate the different aspects of pain perception. The aim of the present study was to investigate the influence of rate of temperature change and peak stimulus duration on heat evoked pain intensity and quality. All stimuli were applied within the medial aspect of the anterior forearm. The rate of temperature change was varied from 1 to 16 C/s without any effect on the pain threshold. The pain threshold decreased with an increasing peak stimulus duration from 0.1 to 2 s, but not from 2 to 3 s. The pain intensity for suprathreshold stimuli (46 C, 48 C, 50 C) increased for decreasing rates and increasing duration. The pain intensity was highly correlated with the energy of the stimulus. When the rates of temperature change (1-16 C/s) are varied, no differences between pricking and burning pain were present at either low stimulus intensity (46 C) or high stimulus intensity (50 C). At low stimulus intensity (46 C), the pricking pain was not influenced by the duration (0.1-3 s), but the burning pain was intensified when the duration was increased from 1.5 to 3 s. At high intensity stimuli (50 C), the pricking pain intensified with an increased duration, whereas burning pain did not. The heat pain threshold is influenced by the peak stimulus duration, and not by the rate of temperature change. If suprathreshold stimuli are used, both the rate of temperature change and the peak stimulus duration can strongly affect the pain intensity and the pain quality. Therefore, the same stimulus modality can be used to assess the modulation of different pain intensities and of the pricking and burning pain qualities simply by varying the stimulus configuration.     

High-soy diet decreases infarct size after permanent middle cerebral artery occlusion in female rats

Estrogen is a powerful neuroprotective agent in rodent models of ischemic stroke. However, in humans, estrogen treatment can increase risk of stroke. Health risks associated with hormone replacement have led many women to consider alternative therapies including high-soy diets or supplements containing soy isoflavones, which act as estrogen receptor ligands to selectively mimic some of estrogen's actions. We hypothesized that a high-soy diet would share the neuroprotective actions of estrogen in focal cerebral ischemia. Female Sprague-Dawley rats were ovariectomized and divided into three groups: isoflavone-free diet + placebo (IF-P), isoflavone-free diet + estradiol (IF-E), or high-soy diet + placebo (S-P). Two weeks after being placed on diets, rats underwent left permanent middle cerebral artery occlusion (MCAO). Reductions in ipsilateral cerebral blood flow were equivalent across groups ( approximately 50%). Twenty-four hours later neurological deficit was determined, and brains were collected for assay of cerebral infarct by TTC staining. In the IF-P rats MCAO produced a 50 +/- 4% cerebral infarct. Estrogen and high-soy diet both significantly reduced the size of the infarcts to 26 +/- 5% in IF-E rats and to 37 +/- 5% in S-P rats. Analysis at five rostro-caudal levels revealed that estrogen treatment was slightly more effective at reducing infarct size than high soy diet. Overall neurological deficit scores at 24 h correlated with infarct size; however, there were no statistically significant differences among the treatment groups. These data show that 2 wk of a high-soy diet is an effective prophylactic strategy for reducing stroke size in a rat model of focal cerebral ischemia.     

Beta-adrenoceptor and adenylate cyclase function in the infarct model of rat heart failure.

In order to determine the possible etiology for diminished inotropic responsiveness to catecholamines in the infarction model of chronic congestive heart failure in rats, we studied beta-adrenoceptor number and site-specific stimulated adenylate cyclase activity in noninfarcted left ventricular tissue of rats at 3 months after ligation of the left coronary artery. Rats were divided into sham, small infarct, and large infarct groups according to infarct size. The large infarct groups showed increased right ventricle to body weight ratio (0.93 +/- 0.07 mg/g for the large infarcts vs 0.52 +/- 0.02 and 0.54 +/- 0.02 mg/g for the shams and small infarcts, respectively). Beta-Adrenoceptor number among the groups was similar (shams, 27 +/- 1 fmol/mg; small infarcts, 26 +/- 1 fmol/mg; and large infarcts, 29 +/- 1 fmol/mg), as was Kd (20 +/- 1 pmol, 18 +/- 2 pmol, and 18 +/- 2 pmol, respectively). Site-specific stimulation of adenylate cyclase using isoproterenol, Gpp(NH)p, forskolin, and MnCl2 revealed no significant differences among the groups. We conclude that this system is not responsible for the altered inotropic responsiveness to catecholamines seen in this model.     

Factors Related to Executive Dysfunction after Acute Infarct

Aim

The aim of this study was to investigate the association of infarct location with post-stroke executive dysfunction.

Methods

One hundred seventy-seven patients hospitalized with acute infarction were enrolled. General information and NIHSS score at admission were recorded. The infarct site was recorded from magnetic resonance T2-W1 and FLAIR images, and the extent of white matter disease was assessed using the Fazekas score. Seven days after symptoms, executive function was assessed using the validated Chinese version of Mattis Dementia Rating Scale (MDRS) Initiation/Perseveration (I/P) [MDRS I/P].

Results

The average MDRS I/P score of the 177 infarction patients was 24.16±5.21, considerably lower than the average score (32.7±3.1) of a control group of normal individuals. Patients with infarcts in the corona radiata or basal ganglia had significantly lower MDRS I/P scores that those without infarcts at these locations. The number of infarcts in the basal ganglia was also significantly associated with low MDRS I/P scores. Male gender and low NIHSS score were significantly associated with low MDRS I/P score, and high-density lipoprotein cholesterol was significantly associated with high MDRS I/P score. The number of infarcts in areas other than the basal ganglia as well as corona radiata and the extent of white matter disease had no influence on this score.

Conclusions

The number of infarcts in the basal ganglia corona radiata, low NIHSS score, and male gender are significantly and independently related to poor executive function (that is, low MDRS I/P score) after acute infarct.     

A novel model of cryoinjury-induced myocardial infarction in the mouse: a comparison with coronary artery ligation

Mouse myocardial infarction (MI) models are frequently used research tools. The most commonly applied model is coronary artery ligation. However, coronary ligation often gives rise to apical aneurysmatic infarcts of variable size. Other infarct models include cryoinfarction, which produces reproducible infarcts of the anterior wall. Thus far, this model has not been extensively described in mice. Therefore, we developed a murine cryoinfarction model and compared it with coronary ligation. Studies were performed under isoflurane anesthesia with a follow-up of 4 and 8 wk. Cryoinfarction was induced using a 2- or 3-mm cryoprobe. Two-dimensional guided M-mode echocardiography was used to assess fractional shortening and left ventricular (LV) dimensions at baseline and end point. At end point, hemodynamics were assessed using a 1.4-Fr Millar catheter. Pressure-diameter relations were constructed by combining echocardiography and hemodynamic data. Histological and morphometric analyses of infarct and remote areas were performed. At 4 wk, 3-mm cryoinfarction resulted in decreased LV fractional shortening as well as decreased global LV contractility and relaxation, which was comparable with coronary ligation. No adverse remodeling was observed at this time point, in contrast with the ligation model. However, progressive LV remodeling occured between 4 and 8 wk after cryoinfarction with a further decline in hemodynamic parameters and LV pump function. Histologically, cryoinfarction resulted in highly reproducible, transmural, cone-shaped infarcts with reperfusion at the macrovascular level. These results indicate that the cryoinfarction model represents the anterior myocardial infarct with modest adverse remodeling and may thus be representative for infarcts encountered in clinical practice.     

Effect of Rifampicin and Isoniazid on Liver Function

The effects of rifampicin and isoniazid on liver function have been studied in 63 patients with pulmonary tuberculosis; 29% showed abnormalities of serum aspartate aminotransferase (SGOT) and a similar percentage abnormalities of serum bilirubin. These usually occurred during the first 12 weeks of therapy. The average duration of the abnormalities was 14½ days, irrespective of whether treatment was interrupted or not.The relationship between raised SGOT and acetylator phenotype in a small number of patients suggests that those with raised SGOT are usually slow acetylator phenotypes. It seems that hepatic reactions in patients with previously normal liver function are usually mild and non-specific. However, patients who continue with rifampicin should be kept under close biochemical observation.     

Substance P and Acute Pain in Patients Undergoing Orthopedic Surgery

Objective

There is a limited information about the role of Substance P (SP) in acute pain nociception following surgical stimulation in patients with a chronic inflammatory state not to mention the link between this neuropeptide level changes and intensity of pain. The goal of the research was to find the correlation between SP level changes and acute pain intensity in patients with rheumatoid arthritis undergoing elective orthopedic surgery.

Material and Methods

Patients with rheumatoid arthritis (RA) were enrolled in the study. The correlation between acute pain intensity and concentration of SP in serum as well as in drainage fluid from postoperative wound was assessed in patients with RA who underwent Total Knee Replacement (TKA) under spinal anesthesia.

Results

In patients with RA a correlation between intensity of acute pain and serum SP was found postoperatively, whereas there was no correlation between intensity of acute pain and concentration of SP in drainage fluid.

Conclusions

1. The correlation between acute pain intensity and SP serum concentration was found postoperatively in patients with RA. 2. The correlation between acute pain intensity and SP concentration in drainage fluid was not found postoperatively in patients with RA.     

Characterization of a new double-filament model of focal cerebral ischemia in heme oxygenase-2-deficient mice

Variations in vascular anatomy in knockout mouse strains can influence infarct volume after middle cerebral artery (MCA) occlusion (MCAO). In wild-type (WT) and heme oxygenase-2 gene-deleted (HO2-/-) mice, infarcts were not reproducibly achieved with the standard intraluminal filament technique. The present study characterizes a double-filament model of MCAO, which was developed to produce consistent infarcts in both WT and HO2-/- mice. Diameters of most cerebral arteries were similar in WT and HO2-/- mice, although the posterior communicating artery size was variable. In halothane-anesthetized mice, two 6-0 monofilaments with blunted tips were inserted into the left internal carotid artery 6.0 and 4.5 mm past the pterygopalatine artery junction to reside distal and proximal to the origin of the MCA. The tissue "volume at risk" determined by brief dye perfusion in WT (59 +/- 2% of hemisphere; +/-SE) was similar to HO2-/- (62 +/- 4%). The volume of tissue with cerebral blood flow <50 ml.min(-1).100 g(-1) was similar in WT (35 +/- 9%) and HO2-/- (36 +/- 11%) during MCAO and at 3 h of reperfusion (<2%). After 1 h MCAO, infarct volume was greater in HO2-/- (44 +/- 6%) than WT (25 +/- 3%). After increasing MCAO duration to 2 h, the difference between HO2-/- (47 +/- 4%) and WT (36 +/- 3%) diminished, but infarct volume remained substantially less than the volume at risk. Infusion of tin protoporphyrin IX, an HO inhibitor, during reperfusion after 1 h MCAO increased infarct volume in WT but not significantly in HO2-/- mice, although infarct volume remained less than the volume at risk. Thus greater infarct volume in HO2-/- mice is not attributable to a greater volume at risk, lower intraischemic blood flow, or poor reflow, but rather to a neuroprotective effect of HO2 activity. The double-filament model may be of use as an alternative in other murine knockout strains in which the standard filament model does not yield consistent infarcts.     

Mechanism of Protection by Soluble Epoxide Hydrolase Inhibition in Type 2 Diabetic Stroke

Inhibition of soluble epoxide hydrolase (sEH) is a potential target of therapy for ischemic injury. sEH metabolizes neuroprotective epoxyeicosatrienoic acids (EETs). We recently demonstrated that sEH inhibition reduces infarct size after middle cerebral artery occlusion (MCAO) in type 1 diabetic mice. We hypothesized that inhibition of sEH would protect against ischemic injury in type 2 diabetic mice. Type 2 diabetes was produced by combined high-fat diet, nicotinamide and streptozotocin in male mice. Diabetic and control mice were treated with vehicle or the sEH inhibitor t-AUCB then subjected to 60-min MCAO. Compared to chow-fed mice, high fat diet-fed mice exhibited an upregulation of sEH mRNA and protein in brain, but no differences in brain EETs levels were observed between groups. Type 2 diabetic mice had increased blood glucose levels at baseline and throughout ischemia, decreased laser-Doppler perfusion of the MCA territory after reperfusion, and sustained larger cortical infarcts compared to control mice. t-AUCB decreased fasting glucose levels at baseline and throughout ischemia, improved cortical perfusion after MCAO and significantly reduced infarct size in diabetic mice. We conclude that sEH inhibition, as a preventative treatment, improves glycemic status, post-ischemic reperfusion in the ischemic territory, and stroke outcome in type 2 diabetic mice.     

Post-stroke memory impairment among patients with vascular mild cognitive impairment

Background

The American Stroke Association/American Heart Association recommended the criteria for diagnosis of vascular cognitive impairment and memory impairment (MI) is a feature in the classification of vascular mild cognitive impairment (VaMCI). VaMCI patients with MI may differ in terms of infarct location or demographic features, so we evaluated the clinical characteristics associated with MI in patients with VaMCI.

Methods

A prospective multicenter study enrolled 353 acute ischemic stroke patients who underwent evaluation using the Korean Vascular Cognitive Impairment Harmonization Standard Neuropsychological Protocol at three months after onset. The association between MI and demographic features, stroke risk factors, and infarct location was assessed.

Results

VaMCI was diagnosed in 141 patients, and 58 (41.1%) exhibited MI. Proportions of men and of left side infarcts were higher in VaMCI with MI than those without (75.9 vs. 57.8%, P?=?0.03, 66.7 vs. 47%, P?=?0.02). Multiple logistic analyses revealed that male sex (odds ratio [OR] 3.07, 95% confidence interval [95% CI] 1.12-8.42), left-side infarcts (OR 3.14, 95% CI 1.37-7.20), and basal ganglia/internal capsule infarcts (OR 4.53, 95% CI 1.55-13.22) were associated with MI after adjusting other demographic variables, vascular risk factors, and subtypes of stroke.

Conclusions

MI is associated with sex and infarct location in VaMCI patients.

     

The Changes in Fluorescence of Acridine Orange-Stained Hela Cells During Ultraviolet Illumination

HeLa cells were stained with a 1/12,000 concentration of acridine orange at pH 7.2 for 3 min and the fluorescence emission was measured quantitatively for effects of ultraviolet illumination with durations including intervals between 5 and 210 min. The total photometric fluorescence intensity increased for the first 30 min, then decreased with illumination time. The initial maximum fluorescence intensity occurred at 525 nm and shifted progressively to shorter wavelengths. Fluorescence intensity above 580 nm decreased with increasing duration of illumination time while that below 580 nm showed an initial increase in intensity followed by a gradual fading.     

Twitch interpolation technique in testing of maximal muscle strength: Influence of potentiation, force level, stimulus intensity and preload

The aim was to study the methodological aspects of the muscle twitch interpolation technique in estimating the maximal force of contraction in the quadriceps muscle utilizing commercial muscle testing equipment. Six healthy subjects participated in seven sets of experiments testing the effects on twitch size of potentiation, time lag after potentiation, magnitude of voluntary force, stimulus amplitude, stimulus duration, angle of the knee, and angle of the hip. In addition, the consequences of submaximal potentiation on the estimation of maximal force from twitch sizes were studied in five healthy subjects. We found an increase in twitch size with increasing levels of potentiation and twitch size decreased exponentially following potentiation. We found a curvilinear relationship between twitch size and voluntary force, and these properties were more obvious when the stimulation intensity of the preload was reduced. The relationship between twitch size and force was only linear, for force levels greater than 25% of maximum. It was concluded that to achieve an accurate estimate of true maximal force of muscle contraction, it would be necessary for the subject to be able to perform at least 75% of the true maximal force.     

Chinese medicinal formula Guan-Xin-Er-Hao protects the heart against oxidative stress induced by acute ischemic myocardial injury in rats

Guan-Xin-Er-Hao (GXEH) is a Chinese medicine formula for treating ischemic heart diseases (IHD) and has a favorable effect. Our aim was to examine whether or not acute oral GXEH could protect the heart against myocardial infarction and apoptosis in acute myocardial ischemic rats. If so, we would explain the antioxidative mechanism involved. The left anterior descending coronary artery was occluded to induce myocardial ischemia in hearts of Sprague-Dawley rats. At the end of the 3 h ischemic period (or 24 h for infarct size), we measured the myocardial infarct size, myocardial apoptosis and the activities of antioxidative enzymes. GXEH reduced infarct size, myocardial apoptosis and the serum level of malondialdehyde (MDA), increased the activities of total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and GSH-peroxidase (GPX) activities and the serum level of glutathione (GSH). GXEH exerts significant cardioprotective effects against acute ischemic myocardial injury in rats, likely through its antioxidation and antilipid peroxidative properties, and thus may be used as a promising agent for both prophylaxis and treatment of IHD.     

Early interventions in the management of acute uncomplicated myocardial infarction.

The demonstration that the vast majority of acute transmural myocardial infarctions are caused by an occlusive thrombus in the coronary artery, together with the concept that myocardium can be salvaged for a period of time after the onset of such occlusion, has heralded a new era of management of this disorder. This involves an aggressive interventional approach aimed at restoring coronary artery patency early while decreasing myocardial oxygen demands. Abundant data show that coronary flow can be reestablished using either intravenous chemical thrombolytic agents (tissue-type plasminogen activator and streptokinase), percutaneous transluminal coronary angioplasty, or coronary artery bypass grafting. Conjunctive aspirin or heparin therapy (or both) is effective in maintaining vessel patency once perfusion is restored. Myocardial oxygen demand can be reduced, where feasible, by pharmacotherapy and control of the patient''s associated pain and anxiety. The beta-adrenergic blockers and nitrates are particularly suitable in this regard, and angiotensin-converting enzyme inhibitors favorably affect infarct expansion and ventricular remodeling. With such an approach, infarct size can be reduced, leading to improved left ventricular function--the prime determinant of morbidity and mortality in patients with acute infarction. The in-hospital mortality has fallen from about 30% three decades ago to less than 8% in many coronary care units.