Additional file 2: of A comparative study of time-specific oxidative stress after acute myocardial infarction in patients with and without diabetes mellitus

d-ROM levels in stable CAD patient with DM and without DM. These data were collected from stable CAD patients with DM and without DM, who had undergone coronary stenting for stable CAD except ACS more than 8 months before data collection. Values are expressed as mean Âą SD, and boxes show median and interquartile ranges between the 25th and the 75th percentiles. d-ROM, derivatives of reactive oxygen metabolites; CAD, coronary artery disease; DM, diabetes mellitus; ACS, acute coronary syndrome. (DOCX 385 kb

The Spatial Distribution of Plaque Vulnerabilities in Patients with Acute Myocardial Infarction.

OBJECTIVE:Although the plaque characteristics have been recognized in patients with acute myocardial infarction (AMI), the plaque spatial distribution is not well clarified. Using color-mapping intravascular ultrasound (iMAP-IVUS), we examined culprit lesions to clarify plaque morphology, composition and spatial distribution of the sites of potential vulnerability. METHODS:Sixty-eight culprit lesions in 64 consecutive AMI patients who underwent angiography and IVUS examinations before intervention were analyzed. Plaque morphology and composition were quantified with iMAP-IVUS. The spatial distribution of the sites of potential vulnerability was assessed with longitudinal reconstruction of the consecutive IVUS images. The plaque characteristics were also compared between ruptured and non-ruptured lesions, and between totally occlusive (TO) and non-TO lesions. RESULTS:The sites with maximum necrotic area (maxNA), maximum plaque burden (maxPB) and most severely narrowed (minimal luminal area, MLA) were recognized vulnerability. In the majority of cases, maxNA sites were proximal to the maxPB sites, and MLA sites were distal to the maxNA and maxPB sites. Ruptures usually occurred close to maxNA sites and proximal to maxPB and MLA sites. The average distance from the site of rupture to the maxNA site was 0.33 ± 4.04 mm. Ruptured lesions showed significant vessel remodeling, greater plaque volume, and greater lipidic volume compared to those of non-ruptured lesions. Both the length and plaque burden (PB) of TO lesions were greater than those of non-TO lesions. CONCLUSIONS:Instead of overlapping on maxPB sites, most maxNA sites are proximal to the maxPB sites and are the sites most likely to rupture. Plaque morphology and composition play critical roles in plaque rupture and coronary occlusion

Catheter Ablation for Three Focal Atrial Tachycardias in a Patient with Prior Fontan Surgery for Tricuspid Atresia

A 28-year-old woman who had undergone Fontan surgery for tricuspid atresia at 6 years of age was admitted to Nihon University Hospital due to syncope. Supraventricular tachycardia at 141 beats/min was induced with isoproterenol infusion during a tilt table test. The patient showed atresia of the right atrial orifice of the coronary sinus with persistent drainage into the left superior vena cava. Electrophysiological study was performed. Atrial tachycardia (AT) was induced by rapid atrial pacing. The AT originated in the lower lateral right atrium and electroanatomical mapping showed a focal origin. After successful ablation of the AT, two additional ATs were induced. These ATs were also shown to be of focal origin and were successfully ablated without recurrence during follow-up

A case of cardiac sarcoidosis presenting with double tachycardia

Although the most feared cardiac manifestation in cardiac sarcoidosis is the onset of ventricular arrhythmia, some patients may present with supraventricular arrhythmias. We present a rare case of cardiac sarcoidosis associated with double tachycardia manifesting as atrial flutter and ventricular tachycardia

Clinical characteristics of the total patients, patients with ruptured versus non-ruptured plaques, and patients with TO versus non-TO lesions.

<p>Clinical characteristics of the total patients, patients with ruptured versus non-ruptured plaques, and patients with TO versus non-TO lesions.</p

Angiographically determined distribution of the culprit lesions.

<p>Angiographically determined distribution of the culprit lesions.</p

Distance from the maxNA site to the maxPB site in all lesions.

<p>Distance from the maxNA site to the maxPB site in all lesions.</p

Spatial relations between the sites of rupture, maxNA, maxPB and MLA sites.

<p>Spatial relations between the sites of rupture, maxNA, maxPB and MLA sites.</p

Overall spatial relations between the maxNA and maxPB sites and the MLA site.

<p>Overall spatial relations between the maxNA and maxPB sites and the MLA site.</p