Evaluation of linear lesion formation and thermodynamics by dragging ablation with the third-generation laser balloon.

Background: The lesion formation properties of a motorized rotational delivery (RAPID) mode, third-generation laser balloon (LB3) ablation compared to point-by-point laser ablation in patients with atrial fibrillation remain unclear. Objective: The purpose of this study was to assess lesion characteristics and thermodynamics in LB3 ablation with a RAPID mode in vitro model. Methods: Chicken muscles were cauterized using LB3 in RAPID mode with 13 W and 15 W and 50% overlapped point-by-point fashion with 7 W/30 seconds, 8.5 W/20 seconds, 10 W/20 seconds, and 12 W/20 seconds. Lesion depth, width, and continuity were compared. Lesion continuity was classified by the visible gap degree categorized from 1 (perfect) to 3 (poor). Thermodynamics and maximum tissue temperatures were assessed under infrared thermographic monitoring. Fifteen and 5 lesions were evaluated per ablation protocol for measurement of lesion size and continuity and for thermographic assessment, respectively. Results: Lesion depth and width were smaller in RAPID mode laser ablation than point-by-point laser ablation (P <.001). However, RAPID mode laser ablation revealed sufficient mean lesion depth of 5 mm or more. Lesion continuity was 1 (perfect) in all samples in RAPID mode laser ablation and point-by-point laser ablation (P = 1). Infrared thermographic observation demonstrated fast and gapless linear lesion formation with thermal stacking in RAPID mode laser ablation. Maximum tissue temperature was lower in RAPID mode laser ablation than point-by-point laser ablation (P <.001). Conclusion: RAPID mode LB3 ablation could provide fast, gapless, and acceptable lesion formation with thermal stacking and moderate tissue temperature rise.

Combination Immunosuppressive Therapy for Giant Cell Myocarditis.

A 60-year-old woman with a history of hypothyroidism was referred to our hospital for shortness of breath and a left ventricular ejection fraction (LVEF) of 13%, which required continuous dobutamine injection with intra-aortic balloon pump support. An endomyocardial biopsy obtained from the right ventricle revealed an infiltration of giant cells and eosinophils, indicating giant cell myocarditis. In addition to heart failure treatment, combined immunotherapy with steroids, tacrolimus, and intravenous immunoglobulin was administered. Transthoracic echocardiography demonstrated a dramatic improvement in the LVEF after this therapy, and the patient was discharged home without symptoms on day 72.

Comparison of dragging ablation and point-by-point ablation with a laser balloon on linear lesion formation.

INTRODUCTION: Lesion size and continuity in dragging laser balloon (LB) ablation, which may enable fast and durable pulmonary vein isolation for atrial fibrillation, are unknown. We evaluated the differences in size and continuity of linear lesions formed by dragging ablation and conventional point-by-point ablation using an LB in vitro model. METHODS AND RESULTS: Chicken muscles were cauterized using the first-generation LB in dragging and point-by-point fashion. Dragging ablation was manually performed with different dragging speeds (0.5-2°/s) using an overlap ratio of the beginning and last site during one application at 12 W/20 s and 8.5 W/30 s. Point-by-point ablation was performed with 25% and 50% overlap ratios at six energy settings (5.5 W/30 s to 12 W/20 s). Lesion depth, width, and continuity were compared. Lesion continuity was assessed by the surface and deep visible gap degree categorized from 1 (perfect) to 3 (poor). Twenty lesions were evaluated for each ablation protocol. Lesion depth and width in dragging ablation at high power (12 W) were comparable with most measurements in point-by-point ablation. Lesion depth and width were smaller at faster-dragging speed and lower power (8.5 W) in dragging ablation. The surface visible gap degree was better in dragging ablation at all dragging speeds than a 25% overlapped point-by-point ablation (p < .001). CONCLUSION: Dragging LB ablation at high power provides deep and continuous linear lesion formation comparable with that of point-by-point LB ablation. However, lesion depth and width depending on the dragging speed and power.

Atrial fibrillation deteriorates tricuspid regurgitation following implantable cardioverter defibrillator lead placement in patient with hypertrophic obstructive cardiomyopathy.

Although atrial fibrillation (AF) often exists in patients with hypertrophic obstructive cardiomyopathy (HOCM), combination of tricuspid regurgitation (TR) and AF after implantation of pacemaker/implantable cardioverter defibrillator (ICD) lead and its optimal management have not been well discussed in this population. Herein, we present a patient with HOCM who subsequently died due to severe heart failure and deterioration of TR following ICD lead placement with AF. Autopsy findings demonstrated that ICD leads were entrapped by anomaly structure in the right atrium and ventricle, which might affect deterioration of TR.

Nardilysin is a promising biomarker for the early diagnosis of acute coronary syndrome.

BACKGROUND: Biomarkers for detection of transient myocardial ischemia in patients with unstable angina (UA) or for very early diagnosis of acute myocardial infarction (AMI) are not currently available. METHODS AND RESULTS: We performed two sequential screenings of autoantibodies elevated shortly after the onset of acute coronary syndrome (ACS), and focused on metalloendopeptidase nardilysin (NRDC) among 19 identified candidate antigens. In a retrospective analysis among 93 ACS and 117 non-ACS patients, the serum level of NRDC was significantly increased in patients with ACS compared with that in patients with non-ACS (2073.5±189.8pg/ml versus 775.7±63.4pg/ml, P<0.0001). The area under the curve of NRDC for the diagnosis of ACS was 0.822 by the receiver operating characteristic curves analysis. In the time course analysis in 43 consecutive ACS patients (AMI: N=35 and UA: N=8), serum concentration of NRDC was significantly increased even in UA patients with a peak serum NRDC levels reached at admission both in AMI and UA patients. In a mouse model of AMI, we found an acute increase in serum NRDC and reduced NRDC expression in ischemic regions shortly after coronary artery ligation. NRDC expression was also reduced in infarcted regions in human autopsy samples from AMI patients. Moreover, the short treatment of primary culture of rat cardiomyocytes with H2O2 or A23187 induced NRDC secretion without cell toxicity. CONCLUSION: NRDC is a promising biomarker for the early detection of ACS, even in UA patients without elevation of necrosis markers.

Clinicopathological features of bi-ventricular cardiac intimal sarcoma-Report of an autopsy case.

We present the clinicopathological characteristics of primary cardiac intimal sarcoma which was widely spread throughout bi-ventricles. The patient had a wide range of clinical manifestations starting with left-sided heart failure then finally developing refractory right-sided heart failure during 44 months of follow-up. .

Right ventricular free wall dissection as a rupture tract in left ventricular rupture during acute myocardial infarction.

Three rare cases of cardiac rupture with right ventricular wall dissection during acute myocardial infarction (AMI) were reported. The cases comprised 2% among our 148 previously reported postinfarction cardiac ruptures with sudden death. The dissections occurred in hearts with biventricular inferior wall AMI and developed between the superficial layers and the deeper layers of inferior wall of the right ventricle. All had an endocardial tear at the basal septum where it meets the inferior free wall of the left ventricle, and had an epicardial tear on the middle inferior wall of the right ventricle. Based on the evidence of the ages of the thrombi of the rupture tracts, delayed epicardial rupture was found besides that soon after the right ventricular dissection.

Autopsy finding of the Sapien XT valve from a patient who died suddenly after transcatheter aortic valve replacement.

An 89-year-old woman with severe aortic stenosis underwent transfemoral aortic valve replacement. The postoperative course was uneventful except transient bradycardia immediately after the procedure. Echocardiographic finding showed excellent valvular function. After discharge, the patient died suddenly. Autopsy findings showed compression of the atrioventricular conduction system region at the septum by the stent strut. Microscopic examination showed atrophy of the conduction fibers with eosinophilic degeneration of the cytoplasm or coagulation necrosis with pyknosis in the bundle of His and the left bundle branch. Compression by the stent strut triggering dysfunction of the conduction system could have caused fatal arrhythmic event.

Eosinophilic coronary periarteritis (vasospastic angina and sudden death), a new type of coronary arteritis: report of seven autopsy cases and a review of the literature.

A previously reported autopsy case of eosinophilic coronary periarteritis (ECPA, or isolated eosinophilic coronary periarteritis, IECPA), and an additional six autopsy cases of ECPA are reported. In addition, another four autopsy cases of ECPA reported in the literature are discussed. Fifteen cases of ECPA with spontaneous coronary dissection (hematoma), which appeared in the literature from 1987 to 2011, are also reviewed. The characteristic clinico-pathological findings of ECPA are: (a) variant angina (Prinzmetal's vasospastic angina) appeared mainly from evening to early in the morning; (b) allergy or allergic history could be identified in only three of a total of 11 cases; (c) sudden unexpected death (sudden cardiac death) usually occurred early in the morning; (d) eosinophilic inflammation limited to the adventitia and periadventitial soft issue appeared in the epicardial large coronary arteries, chiefly in the left coronary anterior descending artery; (e) fibrinoid necrosis or granuloma could not be found in or around the inflammatory area; (f) no type of vasculitis could be found in any other tissues or organs (i.e., localized and non-systemic periarteritis); (g) ECPA was frequently accompanied by spontaneous coronary arterial dissection (SCAD) in the affected wall; and (h) ECPA without SCAD appeared mainly in men (male/female ratio was 8:3), while EPCA with SCAD appeared in almost all female cases (male/female ratio was 1:14). Although the etiology and pathogenesis are still unknown, we believe that ECPA (with or without SCAD) might be a distinct new type of coronary arteritis.

Aortic regurgitation caused by cusp bending of aortic valve leaflet.

Pure aortic regurgitation (AR) is caused by primary disease of the aortic leaflet and/or the aortic root. However, there are many patients with AR with unclear etiology and mechanism. The assessment of mechanism is critical to the decision of surgical modality for AR. Echocardiography, particularly a detailed analysis of the aortic leaflets and root by transesophageal echocardiography (TEE), could be an important diagnostic step to assess its mechanism. In this report, we present a case of AR in which the TEE images led to diagnosis of cusp bending of aortic leaflet without specific findings indicating this pathology.

Pathological evaluation of coronary lesions in cases of cardiac rupture during acute myocardial infarction: an autopsy study of 148 out-of-hospital sudden death cases.

We pathologically evaluated coronary artery lesions of left ventricular ruptures during acute myocardial infarctions (148 sudden out-of-hospital death cases; 93 men and 55 women; age range 42-94 years; mean age 68.9 years; 143 atherosclerotic and 5 non-atherosclerotic lesions). Among the 143 hearts with atherosclerotic coronary lesions, three-vessel disease was most frequent, and plaque rupture or erosion and occlusive thrombus were identified in most cases. Ages of the main component of the occlusive thrombus in the culprit coronary artery corresponded histopathologically to those of myocardial infarction. One of the most outstanding features in this pathological study is that acute thrombus in the culprit coronary artery was identified morphologically in most of the cases with advanced myocardial infarction (3 or more days). On the other hand, in cases of fresh myocardial infarction, a preceding mural non-occlusive organizing thrombus was observed mostly underneath the main component of the thrombus. It is suggested that, in most cases, cardiac rupture during acute myocardial infarction occurs at the time of a new ischemic event caused by a new thrombotic coronary lesion.

The effect of sivelestat sodium on post-cardiopulmonary bypass acute lung injury in a neonatal piglet model.

Cardiopulmonary bypass may cause acute lung injury and can seriously affect postoperative outcome, especially in younger patients. A synthesized neutrophil elastase inhibitor, sivelestat sodium, may be most effective when used during cardiopulmonary bypass. After anesthesia induction, sivelestat (2 mg/kg/h) was given to the SS group (n=7), and 0.9% saline solution to the placebo group (n=7). Piglets were placed on hypothermic cardiopulmonary bypass and subjected to myocardial ischemia (2 h) induced by cold crystalloid cardioplegia. At 24 h after surgery, PaO(2)/FiO(2) ratio and alveolar-arterial oxygen difference were significantly better in the SS group (379.1+/-93.9 mmHg and 250.5+/-89.3 mmHg) than the placebo group (232.4+/-105.3 mmHg, and 378.3+/-90.8 mmHg, P<0.05). Interleukin-8 level in the epithelial lining fluid was above the lowest standard in 6 out of 7 (4.5, 12.9, 24.6, 27.7, 37.7, and 159.8; mean=44.5+/-57.6 g/l) in the placebo group, and in 2 out of 7 (36.1 and 67.8 g/l) in the SS group (P<0.05). The median histological score of acute lung injury in the harvested lung was 3 (2-5) in the placebo group and 1 (1-5) in the SS group (P<0.05). Intraoperative administration of sivelestat effectively reduced neutrophil induction and activation in the lung and improved oxygenation after cardiopulmonary bypass in a piglet model.

Endocardial tears and rupture tracts of left ventricular ruptures during acute myocardial infarction: an autopsy study of 50 out-of-hospital sudden death cases.

We pathologically evaluated endocardial tears and rupture tracts of left ventricular ruptures during acute myocardial infarctions (50 sudden out-of-hospital death cases; 28 men and 22 women; age range 42-88 years; mean age 68.4 years). Endocardial tears were frequently seen at or near the base of the papillary muscles (54%) or in the area where the septum meets the free wall (42%). The endocardial tear was longer in the adjacent septum (mean 2.1+/-1.0cm) than at the papillary muscle base (mean 1.0+/-0.8cm). Accessory tears were observed near the main endocardial tear in about half of the cases (44%). The rupture tract was located well within the infarcted area in 88% and at the border of the infarcted and normal myocardium in 12%. Mature fresh thrombus was found on most main endocardial tears. In most rupture tracts, the thrombus was more mature in the subendocardial than in the subepicardial zone. Morphologically, this study confirmed that most cardiac ruptures start with an endocardial tear at or near the base of the papillary muscles or in the area where the septum meets the free wall, and rapidly progress independent of the histopathologic age of the infarction.

Simultaneous determination of flunitrazepam and 7-aminoflunitrazepam in human serum by ion trap gas chromatography-tandem mass spectrometry.

A method for the determination of flunitrazepam (FNZ) and 7-aminoflunitrazepam (7-AFNZ) in human serum was developed with ion trap gas chromatography (GC)-tandem mass spectrometry. The 7-AFNZ was derivatizated with 50 microl trifluoroacetic anhydride (TFAA), 60 degrees C-20 min. EI mass spectra and tandem mass spectra of FNZ and 7-AFNZ-TFA were m/z 238, 239, 266, 286, 294, 312, 313(M(+)), m/z 350, 351, 360, 378, 379(M(+)), m/z 238, 239, 240 (precursor ion m/z 286, collision energy 1.5 V), and m/z 239, 254, 264, 336 (precursor ion m/z 351, collision energy 1.8 V), respectively. The detection limits of full scan EI mass spectrometry and tandem mass spectrometry for FNZ and 7-AFNZ in human serum were ca. 200 ng/ml, 60 ng/ml, 15 ng/ml and 1 ng/ml, respectively.

Acute coronary syndrome as a cause of sudden death in patients with old myocardial infarction: a pathological analysis.

Old myocardial infarction (OMI) is one of the most important pathological manifestations in sudden cardiac death. Fatal arrhythmia arising from a fibrotic scar has been determined as the cause of death in most cases with old myocardial infarction. However, the significance of acute plaque disruption/thrombosis of the coronary arteries in those patients has not been investigated. We examined a series of 33 hearts from individuals with OMI who died suddenly during the period from 1998 to 2001. Detailed coronary pathological findings on these hearts indicated fresh or recent rupture of the coronary plaque with thrombosis in 18 cases (55%). As a result of comprehensive analysis, the sudden deaths were explained by acute coronary syndrome in 18 cases (55%), fatal arrhythmia in eight (24%), cardiac pump failure in five (14%), and other causes in two (6%) cases. Our findings revealed that a new coronary plaque rupture independent of the old infarct was a major cause of sudden cardiac death with OMI.

Histopathological study of pulmonary arteries in 14 autopsy cases with massive pulmonary thromboembolism.

As the pathological features of acute massive pulmonary thromboembolism (PTE) remain unclear, early diagnosis is difficult. We examined 14 autopsy cases of sudden death by massive PTE. Eight cases were male and six female, with a mean age of 57+/-18 years. While none of the cases were diagnosed with PTE during their lifetime, 12 cases had predicting factors for thrombosis. Deep vein thrombosis was found at autopsy in 11 cases. Cross sections of each segmental pulmonary artery were dissected for histological examination. The distribution of fresh thrombi and organized thrombi in the pulmonary arteries was investigated. Results revealed that 13 cases contained both fresh and organized thrombi. More detailed examination indicated that as the organized thrombi were spread in all lobes, the distribution of thrombi extended from the proximal to peripheral arteries. Our findings indicated that most cases of fatal PTE had a subclinical recurrent history. Thus, proper diagnosis and treatment of prior emboli may be vital for the prophylaxis of sudden death by PTE.