Tsuyoshi Honda

Initial experience with X-ray CT based attenuation correction in myocardial perfusion SPECT imaging using a combined SPECT/CT system

Objective: Attenuation artifacts adversely affect the diagnostic accuracy of myocardial perfusion imaging. We assessed the clinical usefulness of X-ray CT based attenuation correction (AC) in patients undergoing myocardial perfusion imaging by comparing their myocardial AC- and non-corrected (NC) SPECT images with the coronary angiography (CAG).Methods: We retrospectively reviewed the myocardial SPECT images of 30 patients (18 men, 12 women; mean age 68 years). Thirteen of 30 patients with coronary artery disease (CAD) and 17 without CAD were confirmed by CAG. They underwent sequential CT and myocardial SPECT imaging with thallium-201 (111 MBq) under an exercise or pharmacological stress protocol using our combined SPECT/ CT system. Two readers reviewed the myocardial SPECT images for the presence of CAD on a 4-point scale where 1 = normal, 2 = probably normal, 3 = probably abnormal, and 4 = abnormal. Two reading sessions were held. First, non-corrected (NC)-SPECT and second, AC-SPECT images using X-ray CT images were interpreted. Interobserver variability was assessed with kappa statistics. Diagnostic performance (accuracy) of coronary arterial stenosis was compared between AC- and NC-images.Results: Interobserver agreement for visual assessment was substantial or almost perfect. For AC-images, the observer consensus for analysis was 0.84 for the LAD-, 0.87 for the LCX-, and 0.71 for the RCA-territory. For NC-images, it was 0.91, 0.71, and 0.78. AC resulted in statistically significant improvements in overall diagnostic accuracy (sensitivity/ specificity/accuracy = 76%/93%/89%, 67%/86%/81%, respectively, for AC- and NC-images).Conclusions: Because of an increase in the specificity, diagnostic accuracy was significantly increased on AC-images. These preliminary data suggest that X-ray CT based AC in myocardial SPECT imaging has the potential to develop into a reliable clinical technique.

Targeted Deletion of Class A Macrophage Scavenger Receptor Increases the Risk of Cardiac Rupture After Experimental Myocardial Infarction

Background— Class A macrophage scavenger receptor (SR-A) is a macrophage-restricted multifunctional molecule that optimizes the inflammatory response by modulation of the activity of inflammatory cytokines. This study was conducted with SR-A–deficient (SR-A−/−) mice to evaluate the relationship between SR-A and cardiac remodeling after myocardial infarction. Methods and Results— Experimental myocardial infarction (MI) was produced by ligation of the left coronary artery in SR-A−/− and wild-type (WT) male mice. The number of mice that died within 4 weeks after MI was significantly greater in SR-A−/− mice than in WT mice (P=0.03). Importantly, death caused by cardiac rupture within 1 week after MI was 31% (17 of 54 mice) in SR-A−/− mice and 12% (6 of 51 mice) in WT mice (P=0.01). In situ zymography demonstrated augmented gelatinolytic activity in the infarcted myocardium in SR-A−/− mice compared with WT mice. Real-time reverse transcription–polymerase chain reaction at day 3 after MI showed that the expression of matrix metalloproteinase-9 mRNA increased significantly in the infarcted myocardium in SR-A−/− mice compared with WT mice. Furthermore, SR-A−/− mice showed augmented expression of tumor necrosis factor-α and reduction of interleukin-10 in the infarcted myocardium at day 3 after MI. In vitro experiments also demonstrated increased tumor necrosis factor-α and decreased interleukin-10 expression in activated SR-A−/− macrophages. Conclusions— The present findings suggest that SR-A deficiency might cause impairment of infarct remodeling that results in cardiac rupture via insufficient production of interleukin-10 and enhanced expression of tumor necrosis factor-α and of matrix metalloproteinase-9. SR-A might contribute to the prevention of cardiac rupture after MI.

Pioglitazone, a peroxisome proliferator-activated receptor-γ agonist, attenuates myocardial ischemia–reperfusion injury in mice with metabolic disorders

Although considerable attention has focused on obesity, insulin resistance and abnormal lipid metabolism as coronary risk factors, it remains unclear how these pathogenic factors affect the inflammatory response after myocardial ischemia-reperfusion. This study was conducted to evaluate whether these metabolic disorders exacerbate myocardial ischemia-reperfusion injury, and to determine if ischemia-reperfusion injury could be modified with the thiazolidinedione, pioglitazone. Experiments were performed in KK-A(y) and C57BL/6J mice subjected to 40 min of ischemia followed by reperfusion. Infiltration of inflammatory cells in ischemic myocardium, and infarct size 3 days after reperfusion were significantly higher in KK-A(y) than C57BL/6J mice (p<0.05 and p<0.001, respectively). Furthermore, expression of chemokines, inflammatory cytokines and extracellular matrix proteins in ischemic myocardium was significantly higher in KK-A(y) than C57BL/6J mice 1 day after reperfusion. Pioglitazone treatment of KK-A(y) mice for 14 days significantly reduced the accumulation of inflammatory cells in ischemic myocardium, and infarct size 3 days after reperfusion compared to vehicle treatment (p<0.05 and p<0.05, respectively). Pioglitazone also attenuated expression of chemokines, inflammatory cytokines and extracellular matrix proteins in ischemic myocardium 1 day after reperfusion. In vitro experiments demonstrated that tumor necrosis factor-alpha (TNF-alpha) was significantly higher in cultured peritoneal macrophages from KK-A(y) than C57BL/6J mice, and pioglitazone significantly reduced TNF-alpha in macrophages from both types of mice. These findings suggest that metabolic disorders exacerbate ischemia-reperfusion injury as a result of overexpression of inflammatory mediators, and this effect might be improved, in part by the anti-inflammatory effects of pioglitazone.

Three-Dimensional Cardiac Image Fusion Using New CT Angiography and SPECT Methods

OBJECTIVE The purpose of this study was to develop a method of fused images of coronary CT angiography and myocardial perfusion SPECT. CONCLUSION Four patients with ischemic heart disease underwent 3D volume-rendering fused images using a conversion program and volume-rendering fusion function of a computer workstation. The fusion images clearly showed the relationship of relevant coronary arteries and the abnormal perfusion territory in all patients and were useful for the evaluation of coronary artery disease.

Heart rate on admission is an independent risk factor for poor cardiac function and in-hospital death after acute myocardial infarction

BACKGROUND Increased resting heart rate (HR) due to sympathetic hyperactivity is associated with coronary risk factors and increased cardiovascular events. Acute myocardial infarction (AMI) is accompanied by autonomic imbalance, which is characterized by sympathetic activation and parasympathetic inactivation. Although an increased HR in patients with acute coronary syndrome has been reported to be associated with 30-day and 6-month mortality before the coronary intervention era, it is unclear if an increased HR on admission is associated with the prognosis of AMI in the coronary intervention era. METHODS We enrolled 200 consecutive patients with AMI within 24 h of symptom onset. All patients underwent coronary angiography. They were divided into quartiles based on resting HR on admission. RESULTS There was no difference in coronary risk factors and previous medical treatment among the four groups. Anterior AMI was significantly lower in the lowest quartile compared with other quartiles. There was no difference in peak creatine kinase value among the four groups, however left ventricular ejection fraction (LVEF) before discharge evaluated by echocardiography in the highest quartile group was significantly reduced compared to other quartiles. An increased HR was significantly associated with in-hospital death. Patients in the highest quartile of HR were about nine times more likely to have a poor prognosis after AMI compared to those in the lowest quartile. Multiple logistic analysis revealed that HR ≥93 was an independent risk factor for in-hospital death. HR was significantly associated with Killip class and LVEF on admission. CONCLUSIONS These findings indicate that increased HR on admission predicts for poor cardiac function and in-hospital death after AMI.

Changes in plasma Von Willebrand factor-cleaving protease (ADAMTS13) levels in patients with unstable angina

INTRODUCTION Increased plasma levels of von Willebrand factor (VWF) have been reported in acute myocardial infarction (AMI). Recently, we showed reduced activity of a VWF-cleaving protease (ADAMTS13) in AMI patients. However, there is no information as to whether ADAMTS13 affects the pathogenesis of unstable angina (UA). Thus, the purpose of this study was to examine changes in plasma VWF and ADAMTS13 levels in UA patients. MATERIALS AND METHODS Plasma VWF and ADAMTS13 levels (mU/ml) were measured in 45 patients with UA, 55 with stable exertional angina (SEA) and 47 with chest pain syndrome (CPS) at the time of coronary angiography. Levels were also measured in 15 UA patients after 6 months of follow-up. RESULTS VWF antigen levels (mU/ml) increased significantly in UA patients compared with SEA or CPS (2129.3+/-739.5, 1571.8+/-494.2 and 1569.5+/-487.0, respectively; P < 0.0001 in UA vs. SEA or CPS). ADAMTS13 antigen levels (mU/ml) were significantly lower in UA patients than SEA or CPS (737.3+/-149.5, 875.3+/-229.0 and 867.7+/-195.5, respectively; P < 0.01 in UA vs. SEA or CPS). Furthermore, there was a significant inverse correlation between VWF and ADAMTS13 antigen levels (r = -0.302, P = 0.0002). The antigen levels at 6 months of follow-up were not different compared to the acute phase in the 15 UA patients that had repeated blood sampling. CONCLUSIONS These findings suggest that there is prolonged thrombogenicity in UA patients represented as an imbalance between VWF and ADAMTS13 activity.

Fusion Imaging Between Myocardial Perfusion Single Photon Emission Computed Tomography and Cardiac Computed Tomography

A 68-year-old woman with an acute myocardial infarction with left anterior descending artery stenosis had undergone percutaneous transluminal coronary angioplasty and coronary stenting, (Figure 1). Three weeks later, ECG-gated cardiac 8-slice CT angiography and thallium stress test were performed in a …

Influence of weather conditions on the frequent onset of acute myocardial infarction

BACKGROUND This study was conducted to clarify the influence of weather conditions on the onset of acute myocardial infarction (AMI) in Kumamoto. METHODS We studied 642 consecutive patients (males 433, females 209; 71±13 years) who were admitted with AMI. Days of frequent onset (F-days) were defined as days on which ≥2 patients had been admitted for AMI, whereas days of non-frequent onset (N-days) indicated those with fewer than 2 admissions for AMI. Meteorological factors, including the mean atmospheric pressure and rainfall, the mean, maximum, and minimum temperature, intra-day temperature difference, humidity, wind speed, and the number of sunlight hours, were analyzed. All variables were measured on the day of onset of AMI and on each of the 2 days immediately prior to the day of onset. RESULTS There were 86 F-days and 1740 N-days. F-days were significantly associated with lower air temperature (mean, maximum, and minimum), higher intra-day temperature difference, lower humidity, and longer daily duration of sunlight compared with N-days. In addition, meteorological factors for frequent onset of AMI affected older subjects to a greater extent than either young or female subjects. Multiple logistic regression analysis showed that minimum temperature two days before onset was associated with the frequent onset of AMI (odds ratio, 0.805; p<0.05). CONCLUSION Lower minimum temperature on the 2nd day preceding the onset is an independent risk factor for the frequent onset of AMI. The association between low ambient temperature and frequent onset of AMI was stronger in elderly and female subjects.

Potassium Concentration on Admission Is an Independent Risk Factor for Target Lesion Revascularization in Acute Myocardial Infarction

Background. Acute myocardial infarction (AMI) is accompanied by excessive production of catecholamines, which is characterized by a hypokalemic dip. A polymorphism of the adrenergic receptor has also been reported to be associated with target lesion revascularization (TLR) after coronary intervention. Subjects and Methods. We enrolled 276 consecutive patients with AMI within 24 hours of symptom onset, who underwent emergency coronary intervention using bare metal stents and had examinations over a 5–10-month follow-up period. The patients were divided into tertiles based on their serum potassium level on admission (low K, <3.9; mid K, ≥3.9, <4.3; and high K, ≥4.3). Results. Sixty-four TLRs were observed in the study. Increased potassium concentration was associated significantly with TLR. Patients in the high K group were about two and a half times more likely to have a TLR after AMI compared to those in the low K group. Multiple logistic analysis showed that potassium level on admission was an independent risk factor for TLR (odds ratio 1.69; confidence interval 1.04 to 2.74; P = 0.036). Conclusions. These findings indicated that increased potassium levels on admission might predict TLRs in AMI patients treated with bare metal stents.

Markedly high b-type natriuretic peptide level in a patient with duchenne muscular dystrophy and left ventricular non-compaction

A boy with Duchenne muscular dystrophy was admitted to our hospital due to a transient loss of consciousness. Transthoracic echocardiography revealed left ventricular (LV) dilatation and diffuse hypokinesis of the LV wall. The LV wall was thin, and both non-compaction of the LV wall and marked thinning of the posterior LV wall resulting from a lesion were observed. The plasma B-type natriuretic peptide (BNP) level ultimately increased to 7,795 pg/mL, and the patient died of cardiac arrest following ventricular tachycardia. Severe heart failure, a critical condition, and thinning of the LV wall may have contributed to the markedly high plasma BNP level in this case.