This systematic review and meta-analysis included cluster randomized controlled trials that compared population-based sodium reduction interventions with usual care for blood pressure (BP) management. We searched PubMed, Cochrane Central Register of Controlled Trials, and IchuShi-Web and utilized a random-effects meta-analysis of the weighted mean difference (MD) in the comparison groups to collect data from the included trials. The primary outcome includes the pooled MD of office BP from baseline to each follow-up period. This meta-analysis considered 36 articles with 66,803 participants to be eligible. The population-based sodium reduction interventions decreased office systolic BP (SBP) compared with usual care in 36 studies (MD: -2.64 mmHg [95% confidence interval: -3.48- to 1.80]), with evidence of heterogeneity. Office SBP exhibited significant benefits among in adults (30 studies) and adults/children (1 study) but not in children (5 studies). Furthermore, office diastolic BP demonstrated comparable benefits with office SBP. Sensitivity analyses by cluster type in adults revealed that the workplace-based intervention exerted a greater SBP-lowering effect than the clinic/facility-based intervention. However, no significant difference was observed in the SBP-lowering effect by intervention type. The interventions were more effective in hypertensive cohorts compared with non-hypertensive cohorts and in Asian cohorts compared with non-Asian cohorts. Additionally, the benefits for secondary outcomes, including salt (sodium chloride) intake, were similar to those for office BP. In conclusion, population-based sodium reduction interventions improved BP management compared with usual care. The benefits along with the observed heterogeneity should be considered prudent for implementation in public health and clinical practices. This meta-analysis considered 36 studies with 66,803 participants to be eligible. The population-based sodium reduction interventions decreased office BP compared with usual care in 36 studies, with evidence of heterogeneity. Sensitivity analyses by cluster type in adults (30 studies) revealed that community-, family-, school-, and workplace-based interventions reduced office SBP. Concerning intervention type, sodium reduction counseling, salt substitution, and monitoring decreased office SBP. Interventions were more effective in hypertensive cohorts compared with non-hypertensive cohorts. The benefits for salt intake (22 studies) and urinary sodium excretion (17 studies) were comparable to those for office BP. BP: blood pressure; DBP: diastolic blood pressure; MD: mean difference; Na: sodium; RR: risk ratio; SBP: systolic blood pressure.

Objective: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a key mediator of inflammation and plays an important role in the pathogenesis of atherosclerosis. Both inflammation and atherosclerosis have been proposed as contributors to abdominal aortic aneurysm (AAA) pathogenesis. However, the role of LOX-1 in AAA pathogenesis remains unknown. We aimed to investigate effects of Olr1, which encodes LOX-1, deletion on angiotensin II (Ang II)-induced AAA in apolipoprotein E knockout (ApoE KO) mice to determine whether LOX-1 deficiency mitigates AAA development. Design and method: Either Ang II (1.44 mg/kg/day) or saline (control) was administered continuously through a subcutaneously implanted osmotic pump for 4 weeks in the following 8-week-old male mice: Apoe-/-Olr1+/+ mice (Ang II, n = 40; saline, n = 10), Apoe-/-Olr1+/- mice (Ang II, n = 30; saline, n = 9), and Apoe-/-Olr1-/- mice (Ang II, n = 39; saline, n = 9). Results: Ang II infusion raised systolic blood pressure by tail-cuff methods in all three groups. Serial non-invasive assessment with ultrasound demonstrated that Ang II gradually increased the maximum area of the suprarenal abdominal aortas leading to AAAs. Although the incidence and expansion rate of AAA were comparable among genotypes, Olr1 deletion significantly increased the severity and rupture rate of AAAs (p = 0.01; incidence of type IV and ruptured AAA was 25% in Apoe-/-Olr1-/- mice vs 5% in Apoe-/-Olr1+/+ mice). Since atherosclerosis is considered a major contributor to the development of AAAs, the extent of the atheroma burden localized in aneurysmal lesions was evaluated by Oil Red O staining. Olr1 deletion did not decrease atherosclerosis formation in the aneurysmal wall. Interestingly, further histopathological analysis revealed that aneurysmal lesions in LOX-1-deficient mice had fewer fibroblasts and myofibroblasts, as well as thinner adventitial collagen, although the degree of elastin fragmentation or disruption was similar between LOX-1-deficient and control mice. These in vivo data suggested that adventitial fibroblasts play a pivotal role in the increased severity of AAA in LOX-1-deficient mice. To further determine the effects of Olr1 deletion on fibroblast differentiation, fibroblasts were isolated from the adventitia of abdominal aortas harvested from 8-week-old Apoe-/-Olr1+/+ and Apoe-/-Olr1-/- mice, and then cultured with Ang II stimulation. An in vitro study confirmed that Olr1 deletion completely abolished the Ang II-induced proliferative activity in the aortic adventitial fibroblasts (p = 0.02). Conclusions: Olr1 deletion may not mitigate aneurysm development but rather increase the vulnerability to rupture by suppressing adventitial fibroblast proliferation and collagen.

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a key mediator of inflammation and plays an important role in the pathogenesis of atherosclerosis. Conversely, LOX-1 deficiency has been shown to decrease inflammation and atherosclerosis, both of which have been proposed to contribute to abdominal aortic aneurysm (AAA) pathogenesis. However, the role of LOX-1 in AAA pathogenesis remains unknown. Here, we investigated the effects of Olr1 (which encodes LOX-1) deletion on angiotensin II (Ang II)-induced AAA in apolipoprotein E knockout (ApoE KO) mice to determine whether LOX-1 deficiency mitigates AAA development. To accomplish this, we used serial, non-invasive ultrasound assessment, which revealed that the incidence and expansion rate of AAA were similar regardless of Olr1 deletion. However, Olr1 deletion significantly increased severe AAAs, including ruptured AAAs resulting in death. Oil Red O staining of the harvested aortas showed that the extent of atheroma burden localized in aneurysmal lesions did not differ between LOX-1-deficient and control mice, suggesting that Olr1 deletion did not decrease atheroma burden in the aneurysmal wall. Further histopathological analysis revealed that aneurysmal lesions in LOX-1-deficient mice had fewer fibroblasts and myofibroblasts, as well as thinner adventitial collagen, although the degree of elastin fragmentation or disruption was similar between LOX-1-deficient and control mice. An in vitro study confirmed that the proliferation of adventitial fibroblasts collected from LOX-1-deficient mice was significantly attenuated despite Ang II stimulation. In conclusion, Olr1 deletion may not mitigate aneurysm development but rather increases the vulnerability of rupture by suppressing adventitial fibroblast proliferation and collagen synthesis.

A 13-year-old girl was referred for closer examination of electrocardiographic abnormalities. She had a Levine 2/6 systolic murmur (SM) and a fourth heart sound. Electrocardiography findings showed poor R progression from V1 to V4 and negative T waves in the II, III, and aVF leads. Approximately 3.2 years later, her SM increased to Levine 3–4/6. Echocardiography indicated mitral regurgitation and left ventricular pressure gradient (LVPG) of 18.5 mmHg, together with a notch on the systolic wave in the apexcardiogram. We concluded that the electrocardiographic abnormalities were caused by hypertrophic cardiomyopathy. Approximately 6 months later, her SM further increased to Levine 4–5/6, and the voltage on the electrocardiogram increased. In carotid pulse tracing, steep upstroke and deflated percussion wave due to mitral regurgitation were noted. The LVPG was approximately 102 mmHg, and systolic anterior movement was confirmed. After the oral administration of 200 mg of cibenzoline, the LVPG decreased to approximately 48 mmHg. Subsequently, 300 mg/day of cibenzoline was administered. The LVPG further decreased, and her symptoms improved.Learning objectivesClinical symptoms and left ventricular pressure gradient decrease can be ameliorated by cibenzoline therapy in patients with hypertrophic obstructive cardiomyopathy. This finding applies not only to adult patients but also to teen-aged patients.

BACKGROUND:Our aim was to evaluate the ability of adenosine triphosphate (ATP)-stress myocardial computed tomography perfusion (CTP) imaging to detect myocardial ischemia in the left anterior descending artery (LAD) territory, and to compare this method with coronary flow velocity reserve (CFVR) measured by transthoracic Doppler echocardiography (TTDE). METHODS:ATP-stress CTP and CFVR were performed in 50 patients with stable angina pectoris. Myocardial ischemia assessed from CTP imaging was defined as qualitative visual perfusion defects and reduced myocardial blood flow (MBF) based on quantitative assessment. A cut-off value of CFVR of 2.0 was used. RESULTS:The mean CFVR was 1.9 ± 0.6 in ischemic regions by CTP, whereas it was 2.9 ± 0.8 in non-ischemic regions (p < 0.001). CTP imaging could accurately predict CFVR <2.0 with 84.0% diagnostic accuracy (94.7% sensitivity, 77.4% specificity, 72.0% positive predictive value, and 96.0% negative predictive value). When receiver operating characteristic curve analysis of the MBF data was performed to detect CFVR <2.0, the area under the curve was 0.89, and the optimal MBF cut-off value was 1.43 mL/g/min. CONCLUSIONS:This study suggests that qualitative and quantitative assessment of ATP-stress CTP exhibits a good correlation with CFVR for evaluation of myocardial ischemia.

Objectives Although, endometrial cancer (EC) is commonly diagnosed at an early stage and has a favorable prognosis, recurrent disease usually shows poor prognosis. However, clinicopathological prognostic factors for recurrent EC have been still unclear. The current study aimed to identify clinicopathological prognostic factors, especially in long term survivors of recurrent EC. Methods We collected 2044 patients who underwent surgery including hysterectomy and were pathologically diagnosed as EC in our hospitals between 2001 and 2018. Clinicopathological information and survival data were retrospectively obtained by the review of medical record. Among 2044, 131 patients were included in this retrospective analysis. In recurrent cases, we analyzed the prognostic factors for long-term survivors of recurrent EC. Then we defined long-term and short-term survivors, as patients who survived &x2267; 3 years (n =53) and died within 3 years (n =78) after first recurrence, respectively. The correlation between prognosis and clinicopathological factors was statistically analyzed. Results In the multivariate analysis of long-term survivors, we identified that TTP &x2267; 1 year after surgery (P <0.01), surgical reduction of the first recurrence (P =0.03), non-peritoneal metastasis (P =0.045), were significantly associated with the long-term survivors of recurrent EC. Conclusion TTP &x2267; 1 year after surgery, non-peritoneal metastasis, surgical reduction of first recurrence were good prognostic factors of long-term survivors in recurrent EC.

Hypertensive disorders of pregnancy (HDP) represent a frequent disorder among pregnancies. Women with severe hypertension in pregnancy are at increased risk of maternal complications and require antihypertensive drug therapy. This study aimed to systematically review randomized control trials of antihypertensive drug(s) treating non-severe hypertension during pregnancy to estimate the effectiveness and safety of this intervention. On May 8, 2018, we searched PubMed, Cochrane Library, and Ichu-Shi with no restriction on publication year. We selected randomized control trials that involved women with HDP being treated with antihypertensive drug(s) as intervention. Fourteen trials (1804 women) were identified for meta-analysis. There were no significant differences in the risk of maternal death (373 women; risk ratio (RR) 0.70; 95% confidence interval (CI) 0.04 to 11.45), proteinuria (1214 women; RR 1.00; 95% CI 0.67 to 1.49), side effects (360 women; RR 2.69; 95% CI 0.32 to 22.64), cesarean section (1239 women; RR 0.97; 95% CI 0.82 to 1.15), neonatal and birth death (1548 women; RR 0.80; 95% CI 0.43 to 1.49), preterm birth (904 women; RR 0.86; 95% CI 0.53 to 1.39), or small for gestational age infants (1082 women; RR 1.04; 95% CI 0.66 to 1.63) with antihypertensive drug therapy versus placebo or no treatment. The current review suggests that antihypertensive drug therapy does not reduce or increase the risk of maternal or perinatal outcomes. Further studies are needed to build reliable estimates of the effectiveness and safety of antihypertensive drug therapy for women with HDP.

Background: The comparative tolerability, efficacy, and safety of bisoprolol and carvedilol have not been established in Japanese patients with heart failure and reduced ejection fraction (HFrEF). Methods and Results: The CIBIS-J trial is a multicenter, open-label, non-inferiority randomized controlled trial of bisoprolol vs. carvedilol in 217 patients with HFrEF (EF <= 40%). The primary endpoint was tolerability, defined as reaching and maintaining the maximum maintenance dose (bisoprolol 5 mg/day or carvedilol 20 mg/day) during 48 weeks of treatment. The primary endpoint was achieved in 41.4% of patients in bisoprolol (n=111) and 42.5% in carvedilol (n=106) groups. The non-inferiority of tolerability of bisoprolol compared with carvedilol was not supported, however, neither beta-blocker was superior with regard to tolerability. Heart rate (HR) decreased in both groups and its decrease from baseline was significantly greater in the bisoprolol group (20.3 vs. 15.4 beats/min at 24 week, P<0.05). Plasma B-type natriuretic peptide (BNP) levels decreased in both groups and the decrease was significantly greater in the carvedilol group (12.4 vs. 39.0 % at 24 weeks, P<0.05). Conclusions: There were no significant differences between bisoprolol and carvedilol in the tolerability of target doses in Japanese HFrEF patients. The clinical efficacy and safety were also similar despite the greater reduction in HR by bisoprolol and plasma BNP by carvedilol.

Background and aims: Abdominal aortic aneurysm (AAA) is a common disease; however, its exact pathogenesis remains unknown, and no specific medical therapies are available. Interleukin (IL)-18 plays a crucial role in atherosclerotic plaque destabilization and is a strong predictor of cardiovascular death. Here, we investigated the role of IL-18 in AAA pathogenesis using an experimental mouse model. Methods and results: After infusion of angiotensin II (Ang II) for 4 weeks and beta-aminopropionitrile (BAPN) for 2 weeks, 58% of C57/6J wild-type (WT) mice developed AAA associated with enhanced expression of IL-18; however, disease incidence was significantly lower in IL-18(-/-) mice than in WT mice (p < 0.01), although no significant difference was found in systolic blood pressure between WT mice and IL-18(-/-) mice in this model. Additionally, IL-18 deletion significantly attenuated Ang II/BAPN-induced macrophage infiltration, macrophage polarization into inflammatory M1 phenotype, and matrix metalloproteinase (MMP) activation in abdominal aortas, which is associated with reduced expression of osteopontin (OPN). Conclusions: These findings indicate that IL-18 plays an important role in the development of AAA by enhancing OPN expression, macrophage recruitment, and MMP activation. Moreover, IL-18 represents a previously unrecognized therapeutic target for the prevention of AAA formation.

The cardiac phenotype of laminopathies is characterized by cardiac conduction disorders (CCDs) and dilated cardiomyopathy (DCM). Although laminopathies have been considered monogenic, they exhibit a remarkable degree of clinical variability. This case series aimed to detect the causal mutation and to investigate the causes of clinical variability in a Japanese family with inherited CCD and DCM.Of the five family members investigated, four had either CCD/DCM or CCD alone, while one subject had no cardiovascular disease and acted as a normal control. We performed targeted resequencing of 174 inherited cardiovascular disease-associated genes in this family and pathological mutations were confirmed using Sanger sequencing. The degree of clinical severity and variability were also evaluated using long-term medical records. We discovered a novel heterozygous truncating lamin A/C (LMNA) mutation (c.774delG) in all four subjects with CCD. Because this mutation was predicted to cause a frameshift mutation and premature termination (p.Gln258HisfsTer222) in LMNA, we believe that this LMNA mutation was the causal mutation in this family with CCD and laminopathies. In addition, gender-specific intra-familiar clinical variability was observed in this Japanese family where affected males exhibited an earlier onset of CCD and more severe DCM compared to affected females. Using targeted resequencing, we discovered a novel truncating LMNA mutation associated with CCD and DCM in this family characterized by gender differences in clinical severity in LMNA carriers. Our results suggest that in patients with laminopathy, clinical severity may be the result of multiple factors.

ABSTRACT Calcification of bioprosthetic valves (BVs) implanted in aortic position can result in gradual deterioration and necessitate aortic valve replacement. The molecular mechanism of calcium deposition on BV leaflets has been investigated, but remains to be fully elucidated. The present study aimed to identify explanted bioprosthetic valve (eBV)-specific proteins using a proteomics approach and to unveil their biochemical and histological involvements in calcium deposition on BV leaflets. Calcification, fibrosis, and glycosylation of the valves were histologically assessed using Von Kossa, Masson's Trichrome and Alcian Blue staining, as well as immunostaining. Protein expression in the explanted biological valves was analysed using proteomics and western blotting. In a histological evaluation, αSMA-positive myofibroblasts were not observed in eBV, whereas severe fibrosis occurred around calcified areas. SDS-PAGE revealed three major bands with considerably increased intensity in BV leaflets that were identified as plasminogen and fibrinogen gamma chain (100 kDa), and fibrinogen beta chain (50 and 37 kDa) by mass analysis. Immunohistochemistry showed that fibrinogen β-chain was distributed throughout the valve tissue. On the contrary, plasminogen was strongly stained in CD68-positive macrophages, as evidenced by immunofluorescence. The results suggest that two important blood coagulation-related proteins, plasminogen and fibrinogen, might affect the progression of BV degeneration.

Purpose: Hypertrophic cardiomyopathy (HCM) impairs left ventricular (LV) diastolic function leading to left atrial (LA) dilatation. Because Doppler echocardiography cannot accurately assess LV diastolic function in hearts with heterogeneous hypertrophy, assessment of LA function might be useful for risk stratification of patients with HCM. This study aimed to elucidate the impact of LA function on outcome in patients with patients. Methods: Seventy-six patients with HCM who underwent echocardiographic and cardiac magnetic resonance imaging were retrospectively enrolled. Twenty-six control subjects were also included. Using speckle tracking echocardiography, LA function was divided into active and passive strain indices based on the timing of the second positive peak of LA strain rate that occurred during LV systole. Results: Left atrial strain indices of active and passive function were significantly impaired concomitantly with increased LA volume index in HCM patients compared with controls. During follow-up (2.6 +/- 1.7 years), 14 patients with HCM developed cardiac events (heart failure hospitalization or atrial fibrillation). The association of LA active strain with cardiac events was independent of and incremental to clinical and echocardiographic parameters (age, gender, E/e', LV global longitudinal strain, and LA volume index) in sequential models. Cardiac events were more frequent in HCM patients with LA active strain <20.3% than with active strain >= 20.3% (P = .01). Conclusion: Loss of LA active function was associated with increased cardiac events in patients with HCM.

BACKGROUND Fractional flow reserve (FFR) is widely used for the assessment of myocardial ischemia. Intravascular ultrasound (IVUS) is an intracoronary imaging method that provides information about lumen and vessel morphology. Previous studies on the expanded use of IVUS to identify functional ischemia have noted an association between anatomy and physiology, but IVUS-derived minimum lumen area (MLA) has a weak-moderate correlation with myocardial ischemia compared with FFR. We developed a method to calculate FFR using IVUS-derived anatomical information for the assessment of myocardial ischemia. The aims of this study were to investigate the relationship between wire-based FFR and IVUS-derived FFR (IVUS-FFR) and to compare the usefulness of IVUS-FFR and IVUS-derived MLA for functional assessment.Methods and Results:We retrospectively analyzed 50 lesions in 48 patients with coronary stenosis who underwent IVUS and FFR simultaneously. IVUS-FFR was calculated using our original algorithm and fluid dynamics. Mean percent diameter stenosis determined on quantitative coronary angiography and on FFR was 56.4±10.7 and 0.69±0.08, respectively. IVUS-FFR had a stronger linear correlation with FFR (R=0.78, P<0.001; root mean square error, 0.057 FFR units) than with IVUS-derived MLA (R=0.43, P=0.002). CONCLUSIONS IVUS-FFR may be a more valuable method to identify myocardial ischemia, compared with IVUS-derived MLA.

Fractional flow reserve (FFR) is widely used for the assessment of myocardial ischemia. Optical coherence tomography (OCT) provides accurate visualization of coronary artery morphology. The aim of this study was to investigate the relation between FFR and OCT-derived FFR. We retrospectively analyzed 31 lesions (25 left anterior descending arteries, 2 left circumflex arteries, and 4 right coronary arteries) in 31 patients with moderate-to severe coronary stenosis, who underwent OCT and FFR measurements simultaneously. OCT-derived FFR was calculated by the original algorithm, which was calculated using the following equation based on fluid dynamics: Delta P = FV + SV2, where V is the flow velocity, F is the coefficient of pressure loss because of viscous friction (Poiseuille resistance), and S is the coefficient of local pressure loss because of abrupt enhancement (flow separation). Mean values of % diameter stenosis by quantitative coronary angiography and FFR were 55.2 +/- 14.0% and 0.70 +/- 0.14, respectively. OCT-derived FFR showed a stronger linear correlation with FFR measurements (r = 0.89, p <0.001; root mean square error = 0.062 FFR units) than quantitative coronary angiography % diameter stenosis (r = 0.65, p <0.001), OCT measurements of minimum lumen area (r = 0.68, p <0.001), and % area stenosis (r = 0.70, p <0.001). OCT-derived FFR has the potential to become an alternative method for the assessment of functional myocardial ischemia, and may elucidate the relation between coronary morphology and FFR. (C) 2017 Elsevier Inc. All rights reserved.

A 38 years-old man was referred to our hospital for further cardiac examination of atrial tachycardia and poor left ventricular (LV) function. ECG showed atrial fibrillation (AF) tachycardia (130 beats/min), transthoracic echocardiography revealed LV dilation, diffuse hypokinesis (LVEF 35%) and no significant valvular heart disease. He had diagnosed as a tachycardia-induced cardiomyopathy, because he had no significant coronary stenosis and structural heart disease. After administration, he recovered sinus rhythm by DC shock and maintained with amiodarone administration. In addition, sleep study reveled mild sleep apnea syndrome. Therefore, adaptive servo-ventilation therapy had also performed. Optimal medical therapy (OMT), including angiotensin converting enzyme inhibitors and β blockers, and non-pharmacological treatments were started. Three months after first administration, LVEF and BNP were dramatically improved, from 35 to 49%, and from 752 to 16 pg/ml, respectively. However, He had sometimes palpitations and Holter ECG showed paroxysmal AF recurrence with short duration. Therefore, pulmonary vein (PV) isolation by radiofrequency catheter ablation was performed. Four years after PV isolation, he had never administration for heart failure worsening and AF recurrence. In conclusion, total management is very important for heart failure patients. In especially, OMT and catheter ablation are useful and safety treatment for patients with tachycardia-induced cardiomyopathy.

Perivascular adipose tissue exhibits characteristics of active local inflammation, which contributes to the development of atherosclerotic disease as a complication of obesity/metabolic syndrome. However, the precise role of perivascular adipose tissue in the progression of abdominal aortic aneurysm remains unclear. To test the hypothesis that genetic deletion of angiotensin II type 1a (AT1a) receptor in perivascular visceral adipose tissue (VAT) can attenuate aortic aneurysm formation in apolipoprotein E–deficient (ApoE−/−) mice, we performed adipose tissue transplantation experiments by using an angiotensin II–induced aneurysm murine model, in which we transplanted VAT from ApoE−/− or ApoE−/− AT1a−/− donor mice onto the abdominal aorta of ApoE−/− recipient mice. Compared with ApoE−/− VAT transplantation, ApoE−/− AT1a−/− VAT transplantation markedly attenuated aortic aneurysm formation, macrophage infiltration, and gelatinolytic activity in the abdominal aorta. AT1a receptor activation led to the polarization of macrophages in perivascular VAT toward the proinflammatory phenotype. Moreover, osteopontin expression and gelatinolytic activity were considerably lower in ApoE−/− AT1a−/− perivascular VAT than in ApoE−/− perivascular VAT, and angiotensin II–induced osteopontin secretion from adipocytes was eliminated after deletion of AT1a receptor in adipocytes. Notably, induction of macrophage migration by conditioned medium from angiotensin II–stimulated wild-type adipocytes was suppressed by treatment with an osteopontin-neutralizing antibody, and ApoE−/− OPN−/− VAT transplantation more potently attenuated aortic aneurysm formation than ApoE−/− VAT transplantation. Our findings indicate a previously unrecognized effect of AT1a receptor in perivascular VAT on the pathogenesis of abdominal aortic aneurysm.

【背景】植込みデバイス治療の安全性向上のためには，心臓解剖の習熟と手術手技の修練が不可欠である．本邦でも，手術手技習得を目的としたカダバートレーニング（死体を使った手術研修）が始まっており，今回デバイス植込み手技習得のためのカダバートレーニングを施行したため，報告する．【方法】Thiel固定液で固定された献体を対象とした．解剖室に放射線管理区域を設定し，X線透視を使用できる環境を整えた．実際のデバイス植込みと同様に鎖骨下静脈から心房•心室リードを留置し，その後解剖を行った．【結果】実臨床と同様に鎖骨下静脈からのリード留置が可能であった．しかしながら，非拍動下では心耳の同定が難しく，右心耳へのリード留置は困難であった．リード留置後の解剖では，解剖学的に組織が薄い部位を確認することができた．また，透視では心尖部と思われたリードは実際には心尖部近傍中隔に留置されており，透視上と解剖上の留置部位が異なっていた．真の解剖学的心尖部は，透視のみでは把握困難と考えられた．【結語】カダバートレーニングは心臓の構造を理解し，手技の安全性を向上させるうえで有用であると考えられた．