Papillary fibroelastoma originating from the atrial septum touching the mitral valve leading to infective endocarditis: a case report.

BACKGROUND: Cardiac papillary fibroelastoma is a rare benign tumor, which is often mistaken for a vegetation. Predominantly asymptomatic, it can cause life-threatening complications. Although rare, mobile papillary fibroelastoma movement between affected valves may hamper valve closure and damage the valve, leading to valvular regurgitation. Endothelial damage increases the risk of developing infective endocarditis. We report a rare case of a highly mobile papillary fibroelastoma originating from the atrial septum touching the mitral valve, leading to mitral regurgitation and, eventually, infective endocarditis. CASE PRESENTATION: A 26-year-old woman with suspected infective endocarditis was referred to us from a previous hospital after having experienced intermittent fever for a month. Before the fever, she had been experiencing exertional dyspnea. In addition, she had undergone a cesarean section two weeks before this admission. A transthoracic echocardiogram showed a mobile mass originating from the atrial septum touching the mitral valve with severe mitral regurgitation. Computed tomography revealed an occluded right profunda femoris artery with an embolus. Infective endocarditis associated with a mobile vegetation with high embolic risk was diagnosed, and urgent surgery was performed. Following the surgery, examinations revealed papillary fibroelastoma originating from the atrial septum and infective endocarditis of the mitral valve. The histopathological examination confirmed that a mass initially thought to be a mobile vegetation was a papillary fibroelastoma. The postoperative course was uneventful except for pericarditis. There has been no recurrence of infective endocarditis or papillary fibroelastoma. CONCLUSIONS: The highly mobile papillary fibroelastoma was thought to have caused both chronic mitral regurgitation and infective endocarditis. Mobile papillary fibroelastomas can cause endothelial damage to nearby valves and predispose patients to infective endocarditis.

Differential Regulation of Plasma Copeptin Levels in Patients with Heart Failure: A Single-Center Prospective Study.

Elevated levels of arginine vasopressin (AVP) have been reported to be involved in the pathogenesis of heart failure (HF). Recent evidence has shown the role of copeptin, the C-terminal fragment of pro-AVP, as a biomarker in patients with HF. However, the relevant information is still limited. Therefore, we evaluated 39 Japanese patients admitted for HF between 2013 and 2015 (23 males and 16 females with an average age of 79.2 years). They were treated according to the Japanese acute HF guideline. Plasma copeptin levels were measured on admission and about 1 week later. The median plasma copeptin levels on admission were 0.5 (0.1-50.6) pmol/L, higher than the normal values (0.24 ± 0.06 pmol/L). Despite the similar clinical severity on admission, the patients showed great variability in plasma copeptin levels. They were divided into three groups (13 patients/group) according to plasma copeptin levels on admission: highest (> 30.8 pmol/L), midrange, and lowest (< 0.2 pmol/L) groups. Initial treatment improved HF symptoms in 37 of 39 patients, with the two unresponsive patients in the lowest group. Notably, plasma copeptin responses to initial treatment were different, depending on admission copeptin levels. The initial treatment significantly decreased copeptin levels in the highest group, but increased copeptin levels in the lowest group. By contrast, patients in the midrange group showed no significant changes. Thus, the treatment appears to restore the plasma copeptin levels. In conclusion, HF is a complex syndrome with the differential integration of stimulatory and inhibitory inputs to the AVP/copeptin secretory system.

Intravascular ultrasound predictors of side branch occlusion in bifurcation lesions after percutaneous coronary intervention.

BACKGROUND: Percutaneous coronary intervention (PCI) of bifurcation lesion has been associated with a low success rate and a high incidence of procedural complications, including side branch occlusion and myocardial infarction. It remains controversial whether preintervention intravascular ultrasound (IVUS) findings can help to identify side branches likely to occlude after PCI of bifurcation lesions. METHODS AND RESULTS: From our IVUS database we identified 81 bifurcation lesions in 72 patients. Side branches were classified into 2 groups: group 1 had ostial side branch stenosis due to atherosclerotic plaque only in the main vessel (n=61), and group 2 had plaque truly involved in the side branch ostium (n=20). There was no significant difference between the 2 groups in the extent of ostial stenosis as assessed by angiography. After PCI, 7 side branches occluded in group 2, compared with 5 side branches occluded in group 1 (35% vs 8%, p=0.003). CONCLUSION: Ostial plaque distribution as assessed by IVUS may be one of the consistent predictors of side branch occlusion after PCI.

Impact of peri-stent remodeling on in-stent neointimal proliferation in acute myocardial infarction.

Fifty stented lesions in 50 patients with acute myocardial infarction were studied by intravascular ultrasound (IVUS) before and just after stent implantation and at follow-up. Volumetric IVUS analyses revealed that greater peristent positive remodeling after stent implantation was associated with less neointimal proliferation and greater luminal gain at follow-up.

Relation of lateral ST-segment elevation pattern to myocardial salvage in patients with recanalized anterolateral acute myocardial infarction.

BACKGROUND: Although anterior acute myocardial infarction (AMI) with ST-segment elevation in lateral leads is associated with a poor prognosis, the significance of the pattern of lateral ST-segment elevation has not been examined. HYPOTHESIS: The aim of the study was to examine the relation of the pattern of lateral ST-segment elevation to myocardial reperfusion and infarct size in patients with AMI. METHODS: We studied 111 patients who had a first AMI presenting with anterolateral ST-segment elevation and Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow of the left anterior descending coronary artery within 6 h from symptom onset. Patients were classified into two groups according to the pattern of lateral ST-segment elevation on the admission electrocardiogram: Group 1, 42 patients with equivalent or greater ST-segment elevation in lead I than in lead aVL, and Group 2, 69 patients with lesser ST-segment elevation in lead I in than in lead aVL. Left ventricular ejection fraction (LVEF) was measured by predischarge left ventriculography. RESULTS: There were no differences between the two groups in age, gender, time from onset to recanalization, culprit lesion, or collateral development. Group 1 patients had a higher probability of impaired myocardial reperfusion as indicated by a myocardial blush grade of 0 or 1 after recanalization, a higher peak creatine kinase level, and a lower LVEF than Group 2 patients (p = 0.0001, respectively). CONCLUSIONS: We conclude that equivalent or greater ST-segment elevation in lead I than in lead aVL is associated with impaired myocardial reperfusion and less myocardial salvage in patients with recanalized AMI who present with anterolateral ST-segment elevation on the admission electrocardiogram.

Significance of thrombolysis in myocardial infarction (TIMI) grade 2 flow early after thrombolysis followed by immediate percutaneous coronary intervention in patients with acute myocardial infarction.

Although pre-interventional thrombolysis has recently been shown to restore early patency and preserve left ventricular function in patients with acute myocardial infarction, the significance of Thrombolysis in Myocardial Infarction (TIMI) grade flow early after thrombolysis remains unclear. Patients were classified into 3 groups according to TIMI grade flow 45 min after thrombolysis; 38 patients with TIMI grade 0 or 1 flow (group T0) and 46 with TIMI grade 2 flow (group T2) additionally received immediate percutaneous coronary intervention (PCI) and 50 patients with TIMI grade 3 flow (group T3) were treated conservatively after thrombolysis. Although the door-to-balloon times did not differ in groups T0 and T2, group T2 had lower peak creatine kinase, a higher rate of complete (>/=70%) ST resolution and better regional wall motion at discharge as compared with group T0, similar to group T3 (group T2, group T3 vs group T0; 2,857+/-1,756, 2,314+/-1,948 vs 3,779 +/-2,214 mU/ml; 57, 72 vs 34%; -1.5+/-1.6, -1.2+/-1.6 vs -2.2+/-1.6; all p<0.01, respectively). These results suggest TIMI grade 2 flow at 45 min after thrombolysis followed by immediate PCI, as well as TIMI grade 3 flow, is associated with greater myocardial salvage than TIMI grade 0 or 1 flow.

Relation between the timing of the last preinfarction angina and microvascular reperfusion in patients with recanalized acute myocardial infarction.

In patients with recanalized acute myocardial infarction (AMI), the relation between the timing of preinfarction angina (PA) and microvascular reperfusion remains unclear. A total of 186 patients (114 with anterior and 72 with inferior AMI) who had total occlusion and TIMI 3 recanalization < or = 6 hours from the onset of AMI were divided into 4 groups according to the time interval between the last episode of PA and the onset of AMI: < or = 2 hours (group A, n = 52); 2 to 48 hours (group B, n = 43), > or = 48 hours (group C, n = 33), and no PA (group D, n = 58). The angiographic myocardial blush grade, a marker of microvascular reperfusion, was retrospectively assessed immediately after recanalization. There were no differences in baseline characteristics, except for sex among the 4 groups. Myocardial blush grade 3 was more frequent (42% vs 21%, 9%, and 14%) and peak creatine kinase was lower (2659 vs 3455, 4422, and 4622 mU/mL) in group A than in groups B, C, and D (all P < 0.05). Multivariate analysis showed that PA occurring < or = 2 hours before AMI (OR 3.88, P < 0.05), a smaller summed ST-segment elevation before recanalization (OR 0.84, P < 0.01), earlier time to recanalization (OR 0.52, P < 0.05), and interior AMI (OR 4.87, P < 0.05) were independently associated with adequate microvascular reperfusion. We conclude that PA < or = 2 hours before the onset of AMI is independently associated with adequate microvascular reperfusion after recanalization in patients with AMI.

Reliability of resolution of ST-segment elevation after coronary reperfusion in predicting myocardial salvage in anterior wall acute myocardial infarction.

Resolution of ST-segment elevation (ST resolution) after reperfusion therapy has been shown to correlate with improved left ventricular (LV) function in patients with acute myocardial infarction (AMI). However, not all patients with ST resolution have preserved LV function. We evaluated the clinical significance of ST resolution in 129 patients with anterior wall AMI who underwent successful coronary recanalization within 6 hours after symptom onset by studying the relation to myocardial blush grade, another angiographic marker of myocardial reperfusion. A reduction of > or =50% in ST-segment elevation after recanalization was defined as ST resolution. Ninety-eight patients had ST resolution and 31 patients did not. Patients with ST resolution were subdivided into 2 groups according to myocardial blush grade after recanalization: 67 patients with blush grade 2 or 3, and 31 with blush grade 0 or 1. The QRS score after recanalization was higher (5.9 +/- 1.9 vs 3.4 +/- 2.0, p <0.01) and predischarge LV ejection fraction was lower (39 +/- 8% vs 57 +/- 9%, p <0.01) in patients with blush grade 0 or 1 than in those with blush grade 2 or 3. However, the QRS score after recanalization and the predischarge LV ejection fraction were similar in patients who had ST resolution with blush grade 0 or 1 and in those without ST resolution. Our findings suggest that ST resolution after recanalization does not consistently predict myocardial salvage in patients with anterior AMI.