Yasushi Hayashi

High-sensitivity C-reactive protein and plaque composition in patients with stable angina pectoris: a virtual histology intravascular ultrasound study.

ObjectiveElevated high-sensitivity C-reactive protein (hs-CRP) is related to clinical outcome in coronary artery disease. We used virtual histology intravascular ultrasound to evaluate the relationship between serum hs-CRP level and coronary plaque composition in patients with stable angina pectoris. Methods and resultsOverall 113 consecutive patients with stable angina pectoris who had a de-novo culprit lesion were examined in this study. Patients were divided into an elevated hs-CRP group (>3 mg/l; n=40) or a normal hs-CRP group (n=73). Grayscale and virtual histology intravascular ultrasound analysis was performed across the entire culprit lesion. Mean plaque area was similar in both groups. Lesion length (18±5 vs. 16±6 mm, P<0.046) was significantly greater in the elevated hs-CRP group than that in the normal hs-CRP group. Although the percentage of dense calcium, fibrofatty tissue, and fibrous tissue was not different between the two groups, the percentage of necrotic core was significantly greater in the elevated hs-CRP group compared with the normal hs-CRP group (20±9 vs. 16±8%, P=0.014). The percentage of necrotic core was positively correlated with the serum hs-CRP level (r=0.20, P=0.037). A multivariate logistic regression model showed that the percentage of necrotic core was associated with elevated hs-CRP (P=0.019; odds ratio=1.1; 95% confidence interval=1.01–1.12). ConclusionElevated hs-CRP was related to the amount of necrotic core in the culprit lesion of stable angina pectoris. Our results suggest that elevated hs-CRP might reflect the inflammatory activity of the coronary atherosclerotic plaque even in the setting of stable angina pectoris.

Local Matrix Metalloproteinase 9 Level Determines Early Clinical Presentation of ST-Segment–Elevation Myocardial Infarction

Objective—Early clinical presentation of ST-segment–elevation myocardial infarction (STEMI) and non–ST-segment–elevation myocardial infarction affects patient management. Although local inflammatory activities are involved in the onset of MI, little is known about their impact on early clinical presentation. This study aimed to investigate whether local inflammatory activities affect early clinical presentation. Approach and Results—This study comprised 94 and 17 patients with MI (STEMI, 69; non-STEMI, 25) and stable angina pectoris, respectively. We simultaneously investigated the culprit lesion morphologies using optical coherence tomography and inflammatory activities assessed by shedding matrix metalloproteinase 9 (MMP-9) and myeloperoxidase into the coronary circulation before and after stenting. Prevalence of plaque rupture, thin-cap fibroatheroma, and lipid arc or macrophage count was higher in patients with STEMI and non-STEMI than in those with stable angina pectoris. Red thrombus was frequently observed in STEMI compared with others. Local MMP-9 levels were significantly higher than systemic levels (systemic, 42.0 [27.9–73.2] ng/mL versus prestent local, 69.1 [32.2–152.3] ng/mL versus poststent local, 68.0 [35.6–133.3] ng/mL; P<0.01). Poststent local MMP-9 level was significantly elevated in patients with STEMI (STEMI, 109.9 [54.5–197.8] ng/mL versus non-STEMI: 52.9 [33.0–79.5] ng/mL; stable angina pectoris, 28.3 [14.2–40.0] ng/mL; P<0.01), whereas no difference was observed in the myeloperoxidase level. Poststent local MMP-9 and the presence of red thrombus are the independent determinants for STEMI in multivariate analysis. Conclusions—Local MMP-9 level could determine the early clinical presentation in patients with MI. Local inflammatory activity for atherosclerosis needs increased attention.

Convulsive syncope on electroencephalogram

A 55yearold woman visited our hospital with repeated episodes of syncope. She had no memories around syncope, but she had incontinent of urine. Her family reported the process of syncope; she screamed suddenly and went into systemic clonic convulsions soon. She slowly returned to normal status over several minutes with lack of memories during attack without any neurological deficit. On arrival at our hospital, she could present her history fluently. We performed a physical examination, chest Xray pictures, blood chemistry, and electrocardiogram; however, no abnormal findings were revealed. We took a computed tomography (CT) of her brain; however, it also reveals no abnormal findings. She was suspected of having epilepsy. Thus, we decided to take emergency electroencephalogram (EEG). In the middle of EEG, she presented systemic clonic convulsion. After few minutes, she recovered her consciousness clearly. Fortunately, we could record attack through EEG (Figure 1). Her EEG pattern was suddenly changed into generalized high voltage with electromyogram artifacts, just after 13 seconds absence of electrocardiographic R wave. Systemic clonic convulsion was brought by wholebrain ischemia from temporary cardiac arrest. After transient R wave pausing, her systemic convulsion was terminated. She recovered her consciousness gradually. EEG also recovered at the same time (Figure 2). Echocardiography revealed no abnormal findings, such as cardiac valve diseases, cardiac myopathy, and focal asynergy. Of course,

Reply to “The electroencephalogram in syncope”

Thank you for your interest in our paper. As you mentioned, we did not reference Gastaut’s research in this report. We researched various reports in PubMed, many of which discussed EEG and wholebrain ischemia. However, a large portion of them discussed the relationship between relative brain ischemia, which was brought on by the headup tilt test and the Valsalva maneuver, and severe hypotension. As far as we could ascertain, few reports discuss EEG, convulsion, wholebrain ischemia, and cardiac arrest. We apologize for lacking information on Gastaut’s works. By searching “Author; Gastaut H” in PubMed, we found 418 reports. Eighteen reports examined the occurrence of syncope among patients with hypotension when the vasovagal reflex occurs or they perform the Valsalva maneuver.1 Additionally, Lempert et al2 reported on convulsive syncope with hypotension through videometric analysis. Apart from us, DiazCastro et al3 also reported a case in which cardiac arrest caused systemic epilepsy. It is still a curious phenomenon for many physicians. However, there are ethical issues in conducting experimental trials to reveal the mechanism of this phenomenon in humans. Therefore, it is very important to add new knowledge through case reports. I have confidence that this case report has enough value to be published, even if my description of the background of this case did not refer to Gastaut’s works, because the cause of brain ischemia in our case is quite different from Gastaut’s. CONFLIC T OF INTERE S T

Fatal necrotizing myositis from fulminant Streptococcus dysgalactiae subspecies equisimilis (SDSE) infection: A case report of autopsy images

Over the past few decades, Streptococcus dysgalactiae subspecies equisimilis (SDSE) have been considered as weak pathogenicity compared with S. pyogenes (GAS). Some recent reports argue that SDSE may bring severe soft tissue infection as same as GAS. No reports have been tried to reveal the clinical characteristics and autopsy images of fulminant SDSE infection. In this case report, we aimed to present a case of fatal necrotizing myositis from fulminant SDSE infection at iliopsoas, including autopsy appearance.

Brain Images in Fatal Methanol Intoxication

A 64-year-old man with no significant medical history was admitted to the intensive care unit with a progressive visual abnormality and he was also in a coma. Because of a rapid exacerbation of his symptoms and the onset of severe metabolic acidosis, we treated him with fomepizole due to suspected methanol intoxication, however, he never recovered from the coma. An extremely high concentration of methanol was found in his urine led to a definitive diagnosis of methanol intoxication associated with severe brain damage (1, 2). At five days after admission, diffusion-weighted magnetic resonance imaging (MRI), T2-weighted imaging and apparent diffusion coefficient (ADC) map revealed the symmetric and extensive range of deep white matter damage but sparing the cortex. Furthermore, T2* images suggested a