Radionuclide diagnosis of right ventricular myocardial infarction

The diagnostic capacities of 99mTc-pyrophosphate plane myocardial scintigraphy versus 99mTc-pyrophosphate single photon emission computed tomography (SPECT) were compared. Recording right precordial ECG leads showed that 26 patients had right ventricular myocardial infarction (MI)-typical changes as ST-segment evaluation, followed by abnormal Q wave. Plane scintigraphy indicated a characteristic inclusion of 99mTc-pyrophosphate into the right ventricular myocardium in 18.8% of the patients with acute lower MI and in one of 38 patients with acute MI of the anterior left ventricular wall. SPECT revealed a characteristic inclusion of 99mTc-pyrophosphate into the right ventricular myocardium much more frequently than did plane myocardial scintigraphy--in 34% of cases. Right ventricular myocardial inclusion of 99mTc-pyrophosphate was found in 50% of the patients with acute lower MI, including all 9 patients with positive 99mTc-pyrophosphate myocardial scintigraphy. Thus, the sensitivity of SPECT in the diagnosis of right ventricular MI is somewhat higher than that of precordial ECG and more than thrice higher than that of plane scintigraphy.     

Explorations cardiologiques nucléaires dans la cardiomyopathie de Takotsubo

Transient left ventricular apical ballooning syndrome, also known as Takotsubo cardiomyopathy (TTC) was described for the first time in Japan in the earliest nineties. It represents 1 to 2 % of acute cardiac events and mimics closely acute myocardial infarction. The aim of this study was to investigate ^99mTc-tetrofosmine or ²⁰¹Thallium myocardial Single Photon Emission Computed Tomography (SPECT), ¹²³I-metaIodoBenzylGuanidine (¹²³I-mIBG) myocardial SPECT and myocardial Positron Emission Tomography using ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) in patients with TTC, assessing respectively left ventricular perfusion, innervation and metabolism. We studied four patients (three females) with TTC. We performed two weeks after acute phase (subacute phase) myocardial perfusion SPECT and ¹²³I-mIBG myocardial SPECT for each patient. Two of them underwent myocardial PET with FDG. Then, we assessed left ventricular innervation and metabolism three months (chronic phase I) and more than six months (chronic phase II) after the acute phase. We compared the discrepancies between radionuclides uptake in the left ventricular apical region during a follow-up period of more than six months. In subacute phase, perfusion SPECT was normal for each patient. Conversely, ¹²³I-mIBG SPECT and FDG-PET showed concordant apical uptake defect. This perfusion-metabolism pattern called “inverse flow-metabolism mismatch” is the metabolic state of stunned myocardium. After three months, we found improvement of apical tracer uptake in both FDG-PET and ¹²³I-mIBG SPECT. These findings suggest that TTC is characterized by myocardial apical stunning which is related to a disturbance of cardiac sympathetic innervation. ¹²³I-mIBG SPECT might be useful to diagnose earlier this pathology and to rule out acute myocardial infarction.     

Contribution of endothelin to coronary vasomotor tone is abolished after myocardial infarction

Left ventricular dysfunction in swine with a recent myocardial infarction (MI) is associated with neurohumoral activation, including increased catecholamines and endothelin (ET). Although the increase in ET may serve to maintain blood pressure and, hence, perfusion of essential organs such as the heart and brain, it could also compromise myocardial perfusion by evoking coronary vasoconstriction. In the present study, we tested the hypothesis that endogenous ET contributes to perturbations in myocardial O2 balance during exercise in remodeled myocardium of swine with a recent MI. For this purpose, 26 chronically instrumented swine (10 with and 16 without MI) were studied at rest and while running on a treadmill at 1-4 km/h. After MI, plasma ET increased from 3.2 +/- 0.4 to 4.9 +/- 0.3 pM (P < 0.05). In normal swine, blockade of ETA (by EMD-122946) or ETA-ETB (by tezosentan) receptors resulted in an increase in coronary venous PO2, i.e., coronary vasodilation at rest, which decreased during exercise. In contrast, neither ETA nor ETA-ETB receptor blockade resulted in coronary vasodilation in swine with MI. Coronary vasoconstriction to intravenous ET-1 infusion in awake resting swine was blunted after MI. To investigate whether factors released by cardiac myocytes contributed to decreased vascular responsiveness to ET, we performed ET-1 dose-response curves in isolated coronary arterioles (70-200 microm). Vasoconstriction to ET-1 in isolated arterioles from MI swine was enhanced. In conclusion, the vasoconstrictor influence of endogenous as well as exogenous ET on coronary circulation in vivo is reduced. Because the response of isolated coronary arterioles to ET is increased after MI, the reduced vasoconstrictor influence in vivo suggests modulation of ET receptor sensitivity by cardiac myocytes, which may serve to maintain adequate myocardial perfusion.     

Nuclear cardiac imaging for the assessment of myocardial viability

An important aspect of the diagnostic and prognostic work-up of patients with ischaemic cardiomyopathy is the assessment of myocardial viability. Patients with left ventricular dysfunction who have viable myocardium are the patients at highest risk because of the potential for ischaemia but at the same time benefit most from revascularisation. It is important to identify viable myocardium in these patients, and radionuclide myocardial scintigraphy is an excellent tool for this. Single-photon emission computed tomography perfusion scintigraphy (SPECT), whether using ²⁰¹thallium, ^99mTc-sestamibi, or ^99mTc- tetrofosmin, in stress and/or rest protocols, has consistently been shown to be an effective modality for identifying myocardial viability and guiding appropriate management.Metabolic and perfusion imaging with positron emission tomography radiotracers frequently adds additional information and is a powerful tool for predicting which patients will have an improved outcome from revascularisation. New techniques in the nuclear cardiology field, such as attenuation corrected SPECT, dual isotope simultaneous acquisition (DISA) SPECT and gated FDG PET are promising and will further improve the detection of myocardial viability. Also the combination of multislice computed tomography scanners with PET opens possibilities of adding coronary calcium scoring and noninvasive coronary angiography to myocardial perfusion imaging and quantification.     

Comparison of multislice spiral computed tomography and stress echocardiography in the evaluation of myocardial viability in patients with acute myocardial infarction

The purpose of the investigation was to analyze the data of 64-multislice spiral computed tomography (MSCT-64) versus those of low-dose dobutamine echocardiography (stress EchoCG) used to diagnose the viable myocardium in patients with acute myocardial infarction (AMI). The investigation enrolled 49 patients with AIM. Contrast-enhanced MSCT-64 and low-dose dubutamine stress EchoCG were performed in patients in the early periods of AMI. The viable myocardium was examined in 780 segments of the left ventricle (LV). The data of delayed MSCT and stress EchoCG agreed in 759 (97.3%) segments, did not in 21 (2.7%) segments; Cohen's kappa coefficient was 0.88. The affected segment index (As index) was introduced into the investigation, which is an integral indicator of the number of segments with perfusion defect and nonviable segments detected by MSCT. There was a statistically significant correlation of the As index with the asynergy index (r = 0.91; p = 0.000) and LV ejection fraction (r = -0.75; p = 0.000). Our previous study has demonstrated that MSCT-64 is an informative method to evaluate myocardial viability; the signs of myocardial perfusion and structural derangements can serve as predictors of diminished LV contractility.     

Migration of bone marrow-derived cells and improved perfusion after treatment with erythropoietin in a murine model of myocardial infarction

Erythropoietin (EPO) was shown to have protective effects after myocardial infarction (MI) by neovascularization and antiapoptotic mechanisms. Beside direct receptor-dependent mechanisms, mobilization and homing of bone marrow-derived cells (BMCs) may play a pivotal role in this regard. In this study, we intended to track different subpopulations of BMCs and to assess serially myocardial perfusion changes in EPO-treated mice after MI. To allow tracking of BMCs, we used a chimeric mouse model. Therefore, mice (C57BL/6J) were sublethally irradiated, and bone marrow (BM) from green fluorescent protein transgenic mice was transplanted. Ten weeks later coronary artery ligation was performed to induce MI. EPO was injected for 3 days with a total dose of 5000 IU/kg. Subpopulations (CD31, c-kit, CXCR-4 and Sca-1) of EGFP(+) cells were studied in peripheral blood, bone marrow and hearts by flow cytometry. Myocardial perfusion was serially investigated in vivo by pinhole single-photon emission computed tomography (SPECT) at days 6 and 30 after MI. EPO-treated animals revealed an enhanced mobilization of BMCs into peripheral blood. The numbers of these cells in BM remained unchanged. Homing of all BMCs subpopulations to the ischaemic myocardium was significantly increased in EPO-treated mice. Among the investigated subpopulations, EPO predominantly affected migration of CXCR-4(+) (4.3-fold increase). Repetitively SPECT analyses revealed a reduction of perfusion defects after EPO treatment over time. Our study shows that EPO treatment after MI enhances the migration capacity of BMCs into ischaemic tissue, which may attribute to an improved perfusion and reduced size of infarction, respectively.     

Heterogeneous cardiac sympathetic innervation in heart failure after myocardial infarction of rats

We examined cardiac neuronal function and beta-receptor with a dual-tracer method of [(131)I]meta-iodobenzylguanidine (MIBG) and [(125)I]iodocyanopindolol (ICYP) in rat heart failure after myocardial infarction (MI). In rats with MI, left ventricular (LV) systolic function decreased, and LV dimension and right ventricular (RV) mass increased gradually. MIBG accumulations of the noninfarcted LV (remote region) and RV decreased by 15% at 1 wk compared with sham-operated rats, and these accumulations were restored by 71% and 56%, respectively, at 24 wk compared with age-matched sham rats despite sustained depletion of myocardial norepinephrine contents in these regions. ICYP accumulation of the remote region and of the RV did not decrease at any stages. Myocardial MIBG distribution was heterogeneous at 1 wk when it was lower in the peri-infarcted region than in the remote region, associated with reduced ICYP accumulation in the peri-infarcted region. The heterogeneous distribution of both isotopes disappeared at 12 wk. Thus cardiac sympathetic neuronal alteration was coupled with downregulation of beta-receptors in rat heart failure after MI. The abnormal adrenergic signaling occurred heterogeneously in terms of ventricular distribution and time course after MI.     

Étude de l’impact d’une correction d’atténuation par tomodensitométrie en scintigraphie myocardique

Myocardial perfusion SPECT is a routine for the assessment of patients with coronary artery disease (CAD). However, attenuation artifacts may decrease the specificity of the test. These artifacts can be corrected with an attenuation correction. We prospectively included 70 patients who underwent myocardial perfusion SPECT with (IRAC) and without (IRNC) attenuation correction using transmission CT imaging integrated in the acquisition system in patients with low prevalence of CAD. Automatic quantitative analysis with summed stress score (SSS) and rest (SRS) and summed difference score (SDS) was used as interpretation criteria. The results showed a specificity of 80% for IRAC and 56% for IRNC, a positive predictive value of 40% for IRAC and 23% for IRNC, without any significant change in sensitivity. An unpaired t-test showed no significant difference between the overall population and one where an artifact was corrected for heart rate and breath rate during the acquisition effort, the body mass index, chest and abdomen circumferences, and the ratio of these two parameters. Attenuation correction significantly improves the specificity of myocardial scintigraphy with no significant difference in sensitivity. The majority of corrections were for artifacts from the inferior wall in men. There is no correlation between the anthropomorphic and physiological parameters and the occurrence of an artifact of attenuation corrected with CT data.     

Clinical evaluation of four study protocols with 99mTc-methoxyisobutylisonitrile and SPECT for detecting diseased coronary vessels

Different techniques have been suggested for coronary artery disease (CAD) detection with single-photon emission computed tomography (SPECT) and 99mTc-methoxyisobutylisonitrile (99mTc-MIBI). We evaluated four protocols employing myocardial SPECT with 99mTc-MIBI in separate groups of patients. The first involved stress and rest studies performed on separate days, whereas the other three involved "same day" studies. Group 1 (n = 23) was examined in separate sessions, after ergometric exercise and at rest. Group 2 (n = 24) was first injected after dipyridamole infusion, then injected again at rest after completion of the stress study. Group 3 (n = 24) was first injected at rest and imaged one hour later. Afterwards an ergometric stress was performed, with injection at peak exercise. The inverse sequence was adopted for group 4 (n = 24). All patients underwent coronary angiography. For all groups and vessels, the sensitivity and specificity for diseased coronary artery identification were not statistically different. Studies using the new myocardial perfusion tracer 99mTc-MIBI may therefore be completed on the same day or on separate days according to laboratory and patient needs. Dipyridamole iv infusion proved to be as effective as ergometric exercise for diseased coronary artery identification.     

Dobutamine stress magnetic resonance imaging suffices for the demonstration of myocardial ischaemia and viability

We report three patients in whom dobutamine stress magnetic imaging (DS-MRI) was essential in assessing myocardial ischaemia. Two patients were referred to the cardiologist because of chest pain. Patient A had typical exertional angina and a normal resting electrocardiogram (ECG). Patient B had typical exercise-induced angina and had recently experienced an attack of severe chest pain at rest for 15 minutes. The ECG showed a complete left bundle branch block (LBBB). Patient C was referred for heart failure of unknown origin. There were no symptoms of chest pain during rest or exercise. Echocardiography in this patient demonstrated global left ventricular (LV) dilatation, systolic dysfunction and a small dyskinetic segment in the inferior wall. In all these patients exercise stress testing had failed to demonstrate myocardial ischaemia. Patients A and C produced normal findings whereas in patient B the abnormal repolarisation due to pre-existent LBBB precluded a diagnosis of ischaemia.Breath-hold DS-MRI was performed to study LV wall motion and wall thickening at rest through increasing doses of dobutamine. A test was considered positive for myocardial ischaemia if wall motion abnormalities developed at high-dose levels of the drug (20 μg/kg/min or more with a maximum of 40 μg/kg/min) in previously normal vascular territories or worsened in a segment that was normal at baseline. Recovery of wall thickening in a previously hypokinetic or akinetic segment at a low dose of dobutamine (5-10 μg/kg/min) was taken as proof of viability.Patients A and B developed hypokinesia progressing into akinesia at high-dose dobutamine in the anteroseptal area of the LV indicative of ischaemia. These findings were corroborated by coronary angiography demonstrating severe coronary artery disease which led to coronary artery bypass grafting (CABG) in patient A and balloon angioplasty in patient B. In patient C global recovery of LV contractions during low-dose dobutamine was followed by hypokinesia in the inferoseptal area during high-dose dobutamine. This biphasic response indicates myocardial viability as well as ischaemia. CABG was carried out because of multiple stenoses in the left coronary artery. Post-operatively LV function normalised.DS-MRI is a valuable method for detecting myocardial ischaemia and viability in patients with suspected coronary artery, and can be applied in every hospital with MRI equipment at its disposal.     

Comparison of contrast enhanced three dimensional echocardiography with MIBI gated SPECT for the evaluation of left ventricular function

Background

Real-time perfusion (RTP) contrast echocardiography can be used during adenosine stress echocardiography (ASE) to evaluate myocardial ischemia. We compared two different types of RTP power modulation techniques, angiomode (AM) and high-resolution grayscale (HR), with^99mTc-tetrofosmin single-photon emission computed tomography (SPECT) for the detection of myocardial ischemia.

Methods

Patients with known or suspected coronary artery disease (CAD), admitted to SPECT, were prospectively invited to participate. Patients underwent RTP imaging (SONOS 5500) using AM and HR during Sonovue^® infusion, before and throughout the adenosine stress, also used for SPECT. Analysis of myocardial perfusion and wall motion by RTP-ASE were done for AM and HR at different time points, blinded to one another and to SPECT. Each segment was attributed to one of the three main coronary vessel areas of interest.

Results

In 50 patients, 150 coronary areas were analyzed by SPECT and RTP-ASE AM and HR. SPECT showed evidence of ischemia in 13 out of 50 patients. There was no significant difference between AM and HR in detecting ischemia (p = 0.08). The agreement for AM and HR, compared to SPECT, was 93% and 96%, with Kappa values of 0.67 and 0.75, respectively (p < 0.001).

Conclusion

There was no significant difference between AM and HR in correctly detecting myocardial ischemia as judged by SPECT. This suggests that different types of RTP modalities give comparable data during RTP-ASE in patients with known or suspected CAD.     

Multimodal functional cardiac MRI in creatine kinase-deficient mice reveals subtle abnormalities in myocardial perfusion and mechanics

A decrease in the supply of ATP from the creatine kinase (CK) system is thought to contribute to the evolution of heart failure. However, previous studies on mice with a combined knockout of the mitochondrial and cytosolic CK (CK(-/-)) have not revealed overt left ventricular dysfunction. The aim of this study was to employ novel MRI techniques to measure maximal myocardial velocity (V(max)) and myocardial perfusion and thus determine whether abnormalities in the myocardial phenotype existed in CK(-/-) mice, both at baseline and 4 wk after myocardial infarction (MI). As a result, myocardial hypertrophy was seen in all CK(-/-) mice, but ejection fraction (EF) remained normal. V(max), however, was significantly reduced in the CK(-/-) mice [wild-type, 2.32 +/- 0.09 vs. CK(-/-), 1.43 +/- 0.16 cm/s, P < 0.05; and wild-type MI, 1.53 +/- 0.11 vs. CK(-/-) MI, 1.26 +/- 0.11 cm/s, P = not significant (NS), P < 0.05 vs. baseline]. Myocardial perfusion was also lower in the CK(-/-) mice (wild-type, 6.68 +/- 0.27 vs. CK(-/-), 4.12 +/- 0.63 ml/g.min, P < 0.05; and wild-type MI, 3.97 +/- 0.65 vs. CK(-/-) MI, 3.71 +/- 0.57 ml/g.min, P = NS, P < 0.05 vs. baseline), paralleled by a significantly reduced capillary density (histology). In conclusion, myocardial function in transgenic mice may appear normal when only gross indexes of performance such as EF are assessed. However, the use of a combination of novel MRI techniques to measure myocardial perfusion and mechanics allowed the abnormalities in the CK(-/-) phenotype to be detected. The myocardium in CK-deficient mice is characterized by reduced perfusion and reduced maximal contraction velocity, suggesting that the myocardial hypertrophy seen in these mice cannot fully compensate for the absence of the CK system.     

Repairing chronic myocardial infarction with autologous mesenchymal stem cells engineered tissue in rat promotes angiogenesis and limits ventricular remodeling

Background

Tissue engineering scaffold constitutes a new strategy of myocardial repair. Here, we studied the contribution of a patch using autologous mesenchymal stem cells (MSCs) seeded on collagen-1 scaffold on the cardiac reconstruction in rat model of chronic myocardial infarction (MI).

Methods

Patches were cultured with controlled MSCs (growth, phenotype and potentiality). Twenty coronary ligated rats with tomoscingraphy (SPECT)-authenticated transmural chronic MI were referred into a control group (n = 10) and a treated group (n = 10) which beneficiated an epicardial MSC-patch engraftment. Contribution of MSC-patch was tested 1-mo after using non-invasive SPECT cardiac imaging, invasive hemodynamic assessment and immunohistochemistry.

Results

3D-collagen environment affected the cell growth but not the cell phenotype and potentiality. MSC-patch integrates well the epicardial side of chronic MI scar. In treated rats, one-month SPECT data have documented an improvement of perfusion in MI segments compared to control (64 ± 4% vs 49 ± 3% p = 0.02) and a reduced infarction. Contractile parameter dp/dtmax and dp/dtmin were improved (p & 0.01). Histology showed an increase of ventricular wall thickness (1.75 ± 0.24 vs 1.35 ± 0.32 mm, p &0.05) and immunochemistry of the repaired tissue displayed enhanced angiogenesis and myofibroblast-like tissue.

Conclusion

3D-MSC-collagen epicardial patch engraftment contributes to reverse remodeling of chronic MI.     

Tomographic methods in the assessment of myocardial perfusion

Myocardium visualization using the most up-to-date tomographic techniques is extremely important in clinical cardiology. Myocardial viability assessment is of particular importance in management of patients with Ischemic Heart Disease (IHD). Although rest echocardiography is the most common in assessment of heart function, nuclear cardiology (SPECT and PET), and recently cardiac computed tomography and magnetic resonance become playing important clinical roles. Determining and understanding of real capabilities of these methods is of great necessity in this regard. This review examines the current abilities of current cardiac tomographic modalities for the assessment of myocardial perfusion in patients with known IHD.     

Gender differences in detecting coronary artery disease with dipyridamole stress myocardial perfusion imaging using 99m-Tc sestamibi gated SPECT

There are some specifics in the presentation of coronary artery disease (CAD) in women compared with men that may cause diagnostic pitfalls. The accuracy of noninvasive diagnostic testing in women tends to be lower than that in men. Stress myocardial perfusion imaging with 99m-Tc sestamibi gated SPECT is an accurate technique for detecting CAD. Only a few studies have compared dipyridamole stress imaging according to gender. The aim of the study was to compare the diagnostic value of dipyridamole myocardial perfusion imaging with 99m-Tc sestamibi gated SPECT in detecting CAD among patients of both sexes. We studied 62 consecutive patients (38 men, 24 women) using 99m-Tc sestamibi gated SPECT and dipyridamole stress to detect CAD. All the patients also underwent coronary angiography. Overall regional sensitivity was significantly lower in women compared with men (71.4% vs. 92.7%, p=0.039). There were no significant differences for detecting CAD in individual coronary arteries, although regional sensitivity in all three vascular territories was higher in men compared to women. The lowest sensitivity in women was found in the LAD territory (66.6%). Overall regional specificity in men and women was similar and did not reach statistical significance (88.7% vs. 94.7%). Significantly lower specificity in men was found only in the RCA territory (79.1%), compared with that in women (100%). Our results confirmed that there are certain gender differences in the diagnostic performance of dipyridamole stress myocardial perfusion imaging with 99-Tc sestamibi gated SPECT which are assigned to the characteristics of the female population. However, the diagnostic accuracy is also quite high in women, which makes this technique efficient enough in detecting CAD among this population.     

HindIII polymorphism of lipoprotein lipase gene and risk of myocardial infarction

The purpose of this study was to determine whether HindIII restriction polymorphism found in intron 8 of lipoprotein lipase gene is associated with the onset of myocardial infarction (MI) in Russians and Tartars living in Bashkortostan. HindIII polymorphism was investigated by the polymerase chain reaction in myocardial infarction survivors (males aged under 55 years (98 Russians and 68 Tartars) and in controls (53 Russians and 80 Tartars). The distribution of genotypes and allele frequencies in the controls were as follows: the frequencies of genotypes HindIII(-/-), HindIII(+/-), and HindIII(+/+) in Russians (3.77, 49.06, and 47.17%, respectively) did not differ from those in Tartars (7.50, 51.24, and 41.25%, respectively), while the frequency of HindIII(-) allele was 28.30% in Russians and 33.13% in Tartars. Among Tartars, the HindIII(+/+) genotype was more common in myocardial infarction survivors than in controls (OR 2.03). In the Russians this genotype was not associated with the risk of MI. The frequencies of HindIII(+/+) genotype and allele HindIII(+) were significantly higher (OR 8.96 and 6.71, respectively) and frequencies of HindIII(+/-) genotype and allele HindIII(-) were lower (OR 0.13 and 0.15) in Russian patients with repeated MI. These findings indicate that HindIII polymorphism may be a genetic risk factor for MI before 55 years of age in the Tartars and for repeated MI in Russians. This association prompts genotyping of HindIII polymorphism for predicting MI recurrence in Russian survivors after MI.     

C-reactive protein and vulnerability to mental stress-induced myocardial ischemia

Myocardial ischemia provoked in the laboratory during mental stress (MSI) in patients with stable coronary artery disease (CAD) predicts subsequent clinical events. The pathophysiology of MSI differs from that of exercise ischemia, and the mechanisms tying MSI to poor prognosis are not known. C-reactive protein (CRP) is a risk marker for cardiovascular events in patients with CAD, but little is known regarding the relationship of CRP to MSI. The purpose of this study was to examine the association of CRP to risk of MSI in CAD patients. Eighty-three patients with stable CAD underwent simultaneous single-photon emission computed tomography (SPECT) imaging with technetium-99m tetrofosmin myocardial perfusion imaging (MPI) and transthoracic echocardiography (TTE), at rest and during MS induced by laboratory mental stress. Serum CRP levels were measured 24 h after MS. MSI was defined by the presence of a new perfusion defect on SPECT and/or new regional wall motion abnormality on TTE during MS. Of the 83 patients, 30 (36%) developed MSI. There was no difference in gender, sex, BMI, histories of diabetes, hypertension, smoking, lipid profile, medications used (including statins, beta-blockers, ACE inhibitors, and aspirin), or hemodynamic response during MS between those with and without MSI. In univariate logistic regression analysis, each unit (1 mg/L) increase in CRP level was associated with 20% higher risk of MSI (OR 1.2, 95% CI 1.01-1.39, P=.04). This relationship remained in multivariate models. These data suggest that levels of CRP may be a risk marker for MSI in patients with CAD.     

Adaptation in properties of skeletal muscle to coronary artery occlusion/reperfusion in rats

The present study was designed to determine if changes in function and metabolism of heart muscle induce alterations in characteristics of skeletal muscle. We investigated the histochemical and biochemical properties of soleus (SOL) and extensor digitorum longus (EDL) muscles in Wistar rats at the chronic phase after coronary artery occlusion/reperfusion. The size of myocardial infarct region was evaluated using a high resolution pinhole single photo emission computed tomography (SPECT) system. 4 wk after left coronary artery occlusion/reperfusion, the SOL and EDL of hindlimb were dissected out and immersed in isopentane cooled with liquid nitrogen for subsequent histochemical and biochemical analysis. From SPECT imaging, the blood circulation was recovered, but the recovery of fatty acid metabolism was not observed in infarct region of heart. Citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD) activities in infarct region of heart were lower in the myocardial infarction (MI, n = 6) group compared with that of age-matched sham-operated (Sham, n = 6) group. In addition, heart muscle hypertrophy caused by the dysfunction in MI group was observed. In skeletal muscle, the atrophy and transition of fiber type distribution in MI group, reported in previous studies of heart failure, were not observed. However, the succinate dehydrogenase (SDH) activity in the slow twitch oxidative (SO) from SOL of MI group decreased by 9.8% and in the fast twitch oxidative glycolytic fibers (FOG), 8.0% as compared with sham group. Capillary density of the SO fibers from SOL of MI group also reduced by 18.5% and in the FOG fibers, 18.2% as compared with Sham group. Decreased capillary density in this study related significantly to decreased SDH activity of single muscle fibers in chronic phase of perfusion after surgical infarction. Our results make it clear that there is a difference in the reaction of skeletal muscle to coronary artery occlusion/reperfusion compared with chronic heart failure. However, our data would support the notion that there is a linkage between the function of heart and physiological properties of skeletal muscle.     

Interstitial K+ concentration in active muscle after myocardial infarction

Previous work demonstrated that Na(+)-K(+) pump activity within skeletal muscle is attenuated in myocardial infarction (MI). This may lead to enhanced interstitial K(+) concentration ([K(+)](o)) in the muscle. We tested the hypothesis that [K(+)](o) rises with muscle contraction and that, in rats with MI, the rate of rise in [K(+)](o) is greater than it is in control animals. Microdialysis probes were inserted in the skeletal muscle of six healthy control and six MI rats. The ends of the probes were then attached to the K(+) electrodes, and [K(+)](o) was continuously measured. Muscle contraction was induced by electrical stimulation of the sciatic nerves for 1 min. Stimulation at 1 and 3 Hz increased muscle [K(+)](o) by 14.2% and 44.7% in controls and by 22.9% and 62.8% in MI rats (P < 0.05 vs. controls), respectively. When ouabain, an inhibitor of Na(+)-K(+) pump, was added to the perfusate, muscle [K(+)](o) rose significantly. This effect of ouabain was significantly attenuated in MI animals. In conclusion, when compared with that in control animals, an increase of [K(+)](o) in exercising muscle is augmented in MI rats, likely due to an attenuation of Na(+)-K(+) pump activity.     

The interleukin-1 receptor antagonist gene and the inhibitor of kappa B-like protein gene polymorphisms are not associated with myocardial infarction in Slovene population with type 2 diabetes

In this study we investigated the association of the interleukin-1 receptor antagonist gene variable number tandem repeat (IL1RN VNTR) polymorphism and of the inhibitor of kappa B-like protein (IKBL) gene polymorphism with myocardial infarction (MI) in a group of patients with type 2 diabetes. The IL1RN VNTR and the IKBL+ 738T > C gene polymorphisms were tested in 374 Caucasians: 151 cases with MI and 223 subjects with no history of coronary artery disease. The IL1RN VNTR polymorphism was not a risk factor for MI in Caucasians with type 2 diabetes (genotype 22 vs. the rest: odds ratio (OR) 1.6; 95% confidence interval (CI) = 0.8-3.5; p = 0.2). We also failed to demonstrate that IKBL+ 738T > C gene polymorphism was associated with MI in patients with type 2 diabetes (OR = 0.9; 95% CI = 0.3-2.6; p = 0.9). We provide evidence that the IL1RN VNTR and the IKBL + 738T > C gene polymorphisms are not risk factors for MI in Caucasians with type 2 diabetes.