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A 77-year-old Japanese woman underwent bioprosthetic aortic valve replacement (AVR) and the Maze procedure for severe aortic valve disease and paroxysmal atrial fibrillation (AF), and one year after the AVR, she also underwent a permanent pacemaker implantation for sick sinus syndrome. At two postoperative years, a large mural mass happened to be detected in her left atrium on routine trans-thoracic echocardiography. The cardiac rhythm records produced by the implanted pacemaker demonstrated the recurrence of AF. As anticoagulant therapy was not effective at reducing the size of the mass, surgery was performed and organized thrombus was detected on the ablation line made at the Maze procedure. < Learning objective: The formation of large mural thrombi in the left atrium after the Maze procedure is rare in patients without mitral valve disease. The thrombus was considered to have been caused by several complex factors, including atrial wall damage brought by the Maze procedure and the recurrence of atrial fibrillation (AF). It is important to be aware that the recurrence of AF after the Maze procedure can carry a risk of unexpected mural thrombus formation in the left atrium.> [ABSTRACT FROM AUTHOR]

Summary: Background: Prolonged pre-hospital time for acute myocardial infarction (AMI) is associated with decreased indication for primary percutaneous coronary intervention (PCI). However, the efficacy of primary PCI in AMI patients with prolonged pre-hospital time has not been fully investigated in Japan. Methods and results: A total of 3010 consecutive AMI patients admitted to AMI-Kyoto Multi-Center Risk Study Group hospitals were retrospectively analyzed, and the clinical characteristics and in-hospital prognosis of these patients were reviewed. Patients with pre-hospital delay [elapsed time (ET)>12h] had a lower frequency of Killip≥3 (9.3%) and less frequently received primary PCI (77.7%) compared with patients with ET≤12h. In the ET>12h group, older patients or patients with MI history tended to be complicated by heart failure. Primary PCI was performed for patients with ET>12h, irrespective of the severity of heart failure [Killip 1 (78.7%) vs Killip≥2 (74.0%); p =0.3827]. On multivariate logistic regression analysis, age [odds ratio (OR) 1.053], MI history (OR 2.860), Killip≥2 (OR 10.235), and multi-vessels or left main coronary artery as culprit (OR 11.712) were significant independent positive predictors of in-hospital mortality for patients with ET>12h. Practice of primary PCI was not a significant negative predictor for patients with ET>12h (OR 0.812), but it was for patients with ET≤12h (OR 0.425). Conclusions: These findings indicate that patients with ET>12h have a less severe condition and less frequently receive primary PCI compared with patients with ET≤12h. Although primary PCI is often performed for these patients irrespective of the severity of heart failure, no preferable effect of primary PCI on the in-hospital mortality is demonstrated. In contrary, practice of primary PCI is a significant negative predictor of in-hospital mortality for patients with ET≤12h. [Copyright &y& Elsevier]

Summary: A 64-year-old man complaining of resting angina underwent emergent coronary angiogram and significant stenosis in the mid-left anterior descending artery was discovered. Although deployment of the drug-eluting Cypher stent relieved the stenosis, the guiding catheter accidentally induced coronary dissection in the left main coronary artery (LMCA). Then, deployment of another Cypher stent at the lesion successfully managed the complication. 20 days later, although asymptomatic, extensive aortic dissection was detected from the coronary sinus of Valsalva to the femoral artery. 64-Row multidetector computed tomography demonstrated that the dissection originated from the LMCA and retrogradely expanded to the aorta. This type of dissection is a rare complication related to coronary intervention and even in such a clinical setting, asymptomatic delayed progression of retrograde aortic dissection has not previously been reported to our knowledge. [Copyright &y& Elsevier]

Summary: A 45-year-old woman complaining of consciousness disturbance demonstrated multiple brain infarctions. Echocardiogram showed vegetation on the posterior mitral leaflet. Infectious endocarditis was initially suspected and we started empirical antibiotics. However, mitral vegetation grew rapidly and caused severe mitral regurgitation. Acute heart failure was so poorly controlled by conservative treatment that we concluded cardiac surgery was indicated. Mitral valve replacement was safely performed, and there was no sign of heart failure or recurrent thromboembolism during the postoperative course. Thereafter, multiple hepatic masses and a solid lesion in the pancreatic head were detected by computed tomography. The patient finally died of multiple organ failure that presumably resulted from malignancy in the terminal stage. The clinical course of this case can be explained by the pathology of nonbacterial thrombotic endocarditis (NBTE). The standard treatment for NBTE consists of systemic anticoagulation as well as controlling the underlying malignancy. However, we could not diagnose this case as NBTE before surgery. Although mitral valve replacement was finally effective to control acute heart failure in this case, NBTE should be exactly diagnosed as quickly as possible and the treatment policy should be deliberated. [ABSTRACT FROM AUTHOR]

Summary: A 49-year-old woman complaining of anterior chest pain underwent emergent coronary angiogram and thrombotic obstruction in the proximal left anterior descending artery was discovered. Deployment of a bare metal stent recovered good coronary flow and congestive heart failure was soon relieved. However, on day 3 of hospitalization, chest radiography suddenly showed newly emergent bilateral pulmonary infiltration shadow mimicking congestive heart failure. Chest computed tomography and clinical findings suggested bilateral alveolar hemorrhage. The patient received dual antiplatelet therapy, aspirin 100mg/day and clopidogrel 75mg/day and continuous 15,000U/day heparin infusion, after percutaneous coronary intervention. Therapies that minimize bleeding risk while maintaining an antithrombotic effect are required for patients with acute coronary syndrome (ACS). Due to concern about the increased risk of early stent thrombosis induced by discontinuation of antiplatelet therapy, we continued to administer dual antiplatelet therapy. Pulmonary hemorrhage complicated with ACS without abciximab is a rare clinical entity, and we successfully overcame this potentially life-threatening complication with conservative therapy. [Copyright &y& Elsevier]

: ObjectivesWe examined whether amlodipine, a calcium channel antagonist with potent antioxidant activity, inhibits doxorubicin-induced apoptosis in cultured neonatal rat cardiac myocytes.: BackgroundRecent studies have shown that doxorubicin induces apoptosis as well as necrosis in myocytes through generation of reactive oxygen species.: MethodsThe effects of amlodipine and several other antioxidants on doxorubicin-induced oxidative stress and mitochondria-mediated apoptosis were examined.: ResultsTreatment of myocytes with doxorubicin (10−6 mol/l) for 14 h increased the number of cells with elevated peroxides, as histochemically estimated by 2′,7′-dichlorofluorescin (DCF) diacetate, and the percentage of apoptotic myocytes, as estimated by Hoechst 33258 nuclear staining, compared with control myocytes (25.0 ± 1.6% vs. 5.2 ± 1.2%). Moreover, doxorubicin-induced myocyte apoptosis was also confirmed by annexin V–fluorescein isothiocyanate binding assay. Doxorubicin induced a reduction in myocyte adenosine 5′-triphosphate content, a loss of mitochondrial membrane potential, cytochrome c release from the mitochondria into the cytosol, and caspase-3 activation to 1.9-fold of control. Amlodipine significantly attenuated increased DCF fluorescence, inhibited the mitochondria-mediated apoptotic responses described earlier, and decreased apoptosis in the doxorubicin-treated myocytes in a dose-dependent fashion. Amlodipine at 10−6 mol/l significantly decreased apoptosis to 15.4 ± 0.7%, and this antiapoptotic action was more effective than that seen with other antioxidants, including probucol, ascorbic acid, and alpha-tocopherol. In contrast, the calcium channel antagonist nifedipine (10−6 mol/l) did not inhibit apoptosis. Catalase, glutathione, and N-acetylcysteine, but not mannitol or superoxide dismutase, significantly decreased DCF fluorescence and attenuated myocyte apoptosis induced by doxorubicin to 18.7 ± 1.2%, 19.1 ± 1.7%, and 18.7 ± 0.6%, respectively.: ConclusionsAmlodipine significantly inhibits doxorubicin-induced myocyte apoptosis by suppressing the mitochondrial apoptotic pathway. This effect is attributed to the antioxidant properties of amlodipine, affecting mainly hydrogen peroxide. [Copyright &y& Elsevier]