Objectives

We previously reported a higher left atrial volume index (LAVI) was independently associated with left atrial (LA) appendage (LAA) thrombus formation in 737 patients with non-valvular atrial fibrillation (NVAF) receiving appropriate oral anticoagulation therapy. Since our previous study was a retrospective single-center study, we designed and conducted a prospective multi-center study to verify our findings for LAVI as a predictor of LAA thrombus in patients with NVAF receiving appropriate oral anticoagulation therapy.

Methods

This prospective multi-center study comprised 746 consecutive patients with NVAF recruited between December 2021 and March 2023 from eight institutions in Japan, who were receiving appropriate oral anticoagulation therapy, had undergone transthoracic echocardiography and transesophageal echocardiography (TEE).

Results

LAA thrombi were observed in 21 patients (2.8%). The prevalence of LAA thrombus formation in patients with paroxysmal AF (PAF) was significantly lower than that in patients with non-PAF (0.7% vs. 4.1%, p = .006). LAA thrombus formation was detected in none (0/171) of the patients with normal size LA (LAVI ≤ 34 mL/m² ). The prevalence of LAA thrombus formation in patients with mildly dilated LA (LAVI: 34-49.9 mL/m² ) was 2.1% (6/283), but that in PAF patients was low at 1.0% (1/104). Furthermore, this prevalence in patients with severely dilated LA (LAVI ≥ 50 mL/m² ) was high at 5.1% (15/292).

Conclusions

The findings of this prospective multi-center study are consistent with those of our previous study. Thus, the need for TEE prior to catheter ablation or electrical cardioversion can be determined by the level of LAVI.

Acute myocarditis is a rare complication of Campylobacter jejuni enteritis. Herein, we report the case of a 20-year-old man who presented with chest pain that developed three days after the onset of enteritis. Electrocardiogram, echocardiogram, and cardiac enzyme levels suggested myocarditis. Cardiac magnetic resonance imaging revealed a late gadolinium enhancement in the inferior wall. Degeneration and necrosis of myocardial cells and lymphocyte-dominant inflammatory cell infiltration were found in the tissue obtained by endomyocardial biopsy. Acute myocarditis associated with C. jejuni enteritis was confirmed by these findings and C. jejuni detected in the stool culture. The symptoms of enteritis and myocarditis remitted 10 days after the onset. The left ventricular ejection fraction was improved from 40 % to 57 %.In previous cases, endomyocardial biopsy has not been performed because of mild myocarditis. The lack of pathological reports makes the mechanism of myocarditis associated with C. jejuni enteritis unknown. We report a case of myocarditis associated with C. jejuni enteritis, which was diagnosed using cardiac magnetic resonance imaging and endomyocardial biopsy.

Learning objective

Acute myocarditis is a rare but important complication of Campylobacter jejuni enteritis. Cardiac magnetic resonance imaging is useful for diagnosis. Most cases of myocarditis associated with C. jejuni enteritis were mild and remitted without specific treatment. In the present case, endomyocardial biopsy was performed and CD4-positive lymphocytes were predominantly detected in the myocardial tissue.

Thrombus formation in the microvessels and endocardium was suggestive of endothelial cell damage, myocardial ischemia, and a decreased coronary flow reserve. Sustained pulmonary hypertension due to thrombosis worsened the biventricular dysfunction.

Limited studies report on the status of surgical closure patches for atrial septal defect (ASD) in the remote period. In our case, transthoracic echocardiography revealed a fistula of ASD patch before pulmonary vein isolation for atrial fibrillation. Preoperative Imaging examinations aid in evaluating the effect of the needle puncture around the artificial material of the atrial septum and catheter manipulation for patients with a history of ASD closure.

Background

Transthyretin amyloid cardiomyopathy (ATTR-CM) is usually characterized by left ventricular (LV) hypertrophy or LV systolic dysfunction. However, right atrial (RA) amyloidosis without LV hypertrophy, leading to severe functional tricuspid regurgitation (FTR), is extremely rare.

Case summary

We present 75-year-old female with exertional dyspnoea and pre-syncope. Transthoracic echocardiography showed a normal LV function and no LV hypertrophy. A sick sinus syndrome and severe FTR due to right ventricular (RV) and RA dilatation were observed. A leadless cardiac pacemaker implantation was performed for sick sinus syndrome and the symptoms improved, but she complained of leg oedema and fatigue on effort again. A repeated transthoracic echocardiogram showed no notable changes in LV function, but progression of RV and RA dilatation was observed, with worsening FTR. Despite treatment of loop diuretics with 30 mg daily of azosemide, symptoms did not improve, and the patient underwent tricuspid valve annuloplasty. Pathological findings from right atrium led to a diagnosis of ATTR-CM, and deoxyribonucleic acid sequence analysis did not indicate any typical mutation, which supported a diagnosis of wild type of ATTR-CM (ATTRwt-CM). She has been asymptomatic after the surgical operation. She has also been treated with 80 mg daily of tafamidis meglumine to prevent further accumulation of transthyretin in the myocardium and potentially improve long-term outcomes.

Discussion

Isolated atrial amyloidosis, especially occurring predominantly in the right atrium and caused by ATTRwt-CM without LV hypertrophy, is extremely rare. However, differential diagnosis should be considered for patients with unexplained dilatation of the right-sided heart or bradyarrhythmia.

As the clinical manifestations of traumatic tricuspid valve regurgitation vary according to the extent of tricuspid valve injury, this condition can often go unnoticed and be incidentally discovered. Here, we report the case of a 40-year-old man with patent foramen ovale, in which severe tricuspid regurgitation due to tricuspid valve prolapse was incidentally discovered following blunt chest trauma. Further examination revealed that the prolapse had also caused active right ventricular mural infective endocarditis. The patient had no relevant past medical history of chronic debilitating disease or immunosuppression. After evaluation by the cardiology team, emergent surgical tricuspid valvular repair was successfully performed.

Learning objective

Tricuspid valve prolapses resulting from chest trauma may occasionally lead to severe tricuspid regurgitation. Furthermore, this may cause active right ventricular infective endocarditis. In the present case, Staphylococcus aureus was detected in blood cultures, which is usually rapidly progressive and often leads to devastating consequences. Early surgical approach should be considered in cases of infection in the left atrium via patent foramen ovale.

症例は71歳男性。特記すべき通院歴、既往歴なし。約1ヵ月前に他院で肺炎の診断で入院加療を行い、軽快し退院するも、徐々に増悪する全身倦怠感と発熱を主訴に当院救急外来を受診した。胸部単純CTで両側肺野に多発する小浸潤影を認め肺炎の再燃疑いで入院した。血液培養よりメチシリン感受性黄色ブドウ球菌が検出され、心エコー図検査で漏斗部型心室中隔欠損症に加えて、右室流出路に疣贅を疑う像と感染に続発したと思われるValsalva洞の穿孔、肺動脈弁穿孔が疑われた。また左室拡大と軽度から中等度の僧帽弁逆流も認めた。胸部X線画像で肺うっ血を認め右心カテーテル検査で肺体血流比が3.45であるも、肺血管抵抗の著明な上昇はなく体血圧は維持され左心不全症状は軽度であったことから、利尿薬の内服と抗生剤の点滴加療を先行した。第54病日にValsalva洞穿孔部と心室中隔欠損のパッチ閉鎖術および肺動脈弁尖穿孔部の縫合閉鎖術を施行し、術後経過は良好であったため第68病日に自宅退院した。敗血症性肺塞栓症が疑われる場合は、右心系の感染性心内膜炎および背景となる心疾患を疑い、入念に心エコー図検査を行うべきと考える。(著者抄録)

Hereditary protein C (PC) deficiency is a quantitative or qualitative abnormality of the coagulation regulator PC resulting in a decreased PC activity. It is caused by mutations in the PC gene (PROC) located on chromosome 2q13-q14. Although hereditary PC deficiency is an important risk factor for venous thromboembolism (VTE), it is often overlooked because of difficulties in genetic examination. The low prevalence of this disease has led to a lack of evidence for its treatment. We report the case of a 21-year-old male with VTE caused by hereditary PC deficiency due to a novel PROC gene mutation, c.566G>A, p.Arg 189 Gln. The patient was refractory to treatment with direct oral anticoagulants, but responded to catheter-directed thrombolysis. Further intrafamilial genetic survey revealed the presence of the same mutation in five of the six family members.

Learning objectives

Venous thromboembolism (VTE) caused by hereditary protein C deficiency that is refractory to direct oral anticoagulants may respond to catheter-directed thrombolysis. Furthermore, the first VTE in young patients with a strong family history and female family members of childbearing age should be considered for genetic testing. In addition, genetic examination will help establish evidence for the treatment of such patients.

Coral reef aorta is a stenosis of the aorta due to severe calcification. We report the case of a 74-year-old woman with coral reef aorta whose hemodynamics were physiologically similar to those found in patients with renovascular hypertension. The patient had resistant hypertension, refractory edema, and renal dysfunction. Bilateral renal artery stenosis and infrarenal aortic stenosis were suspected after a Doppler ultrasound examination. Evaluation by intravascular ultrasound and pressure wire revealed that the high blood flow caused by infrarenal aortic stenosis derived from the high-flow velocity in a renal artery without stenosis. Angioplasty with balloon improved the stenosis, and the patient was relieved from a spiral of uncontrollable hypertension, edema, and renal dysfunction. This rare case was a patient with coral reef aorta who was diagnosed with uncontrollable hypertension and angioplasty was performed effectively and minimally invasively. .

The aim of this study was to investigate the association of type 2 diabetes mellitus (T2DM) with the development of new-onset atrial fibrillation (AF) for non-ischemic dilated cardiomyopathy (DCM) patients. We also tested the hypothesis that sodium glucose cotransporter type 2 (SGLT2) inhibitors reduce the risk of development of new-onset AF for non-ischemic DCM patients. We retrospectively studied 210 patients with non-ischemic DCM and sinus rhythm, mean age of 59.0 ± 16.7 years and left ventricular ejection fraction of 31.0 ± 8.2% (all < 45%). T2DM was identified in 60 patients (28.6%), and the remaining 150 patients (71.4%) were classified as non-T2DM patients. New-onset AF occurred in 21 patients (10.0%) over a median follow-up of 6.1 years. Kaplan-Meier curve analysis showed that non-ischemic DCM patients without T2DM experienced fewer occurrences of the development of new-onset AF compared with those with T2DM (log-rank p = 0.0003). Furthermore, global longitudinal strain in patients who showed development of new-onset AF was significantly lower than that in those whose sinus rhythm was preserved (6.4 ± 1.4% vs. 7.7 ± 2.2%, p = 0.01). Of the 60 non-ischemic DCM patients with T2DM, those treated with SGLT2 inhibitors experienced fewer occurrences of the development of new-onset AF than did those not treated with SGLT2 inhibitors (log-rank p = 0.040). T2DM is associated with the development of new-onset AF in non-ischemic DCM patients, and treatment with SGLT2 inhibitors can significantly reduce the development of new-onset AF. Our findings may thus offer a new insight into the management of non-ischemic DCM patients with T2DM.

This study aimed to clarify the effects of worsening renal function (WRF) during hospitalization on activities of daily living (ADL) at discharge of elderly heart failure (HF) patients. We included 323 consecutive patients hospitalized for HF who were prescribed phase I cardiac rehabilitation (CR) from November 2017 to April 2019. WRF was defined as a relative increase from baseline in serum creatinine of 25% or that in serum creatinine ≥ 0.3 mg/dL during hospitalization. The indices of ADL and physical function were the functional independence measure (FIM), short physical performance battery (SPPB) and 10-m comfortable gait speed as assessed at discharge. We compared background factors, clinical parameters, walking level before hospitalization, physical function, and FIM in two groups. Multiple regression analysis was performed with FIM at discharge as the dependent variable and items with P < 0.05 in bivariate correlation as independent variables. Ultimately, 160 patients were included and divided into the WRF group (n = 72) and non-WRF group (n = 88). FIM, SPPB, and 10-m comfortable walking speed were significantly lower in the WRF group. Moreover, even after adjustment for confounding factors (age, Hb, eGFR, CKD, GNRI, start day of standing), eGFR on admission (β = 0.12), WRF (β =  - 6.42) and walking level before hospitalization (β = - 10.00) were independent factors of ADL decline at discharge (adjusted R² = 0.46). WRF during hospitalization of elderly HF patients was a factor affecting ADL decline at discharge along with walking level before hospitalization and renal function at admission.

Background

Left ventricular (LV) longitudinal dysfunction has been identified in type 2 diabetes mellitus (T2DM) patients with preserved LV ejection fraction (LVEF). However, the impact of T2DM on LV longitudinal function or the association of LV longitudinal function with outcome for dilated cardiomyopathy (DCM) remains unclear.

Methods

We retrospectively studied 206 patients with non-ischemic DCM, mean age of 59 ± 17 years and LVEF of 31 ± 8% (all < 45%). All patients underwent a standard echocardiographic examination, and LV longitudinal function was assessed in terms of global longitudinal strain (GLS). Long-term outcomes were assessed, with a median follow-up period of 6.2 years, as primary endpoints of death from or hospitalization for deteriorating heart failure.

Results

GLS of DCM patients with T2DM (n = 55) was significantly lower than that in DCM patients without T2DM (n = 151) in spite of similar conventional LV function (7.0 ± 2.0% vs. 7.8 ± 2.2%, p = 0.03). Kaplan-Meier curves indicated that long-term outcomes for DCM patients without T2DM were better than for those with T2DM (log-rank p = 0.001). Subdividing the two groups into four with by using the median value of GLS (7.9%) showed long-term outcome was worst for DCM patients with T2DM and low GLS. Cox proportional hazards analyses demonstrated an independent association of T2DM, GLS and left atrial volume index with long-term outcome. Moreover, multiple regression analysis for the association of GLS showed that T2DM was the independent determinant parameter for GLS as well as for LVEF and left atrial volume index.

Conclusion

Management of DCM patients with T2DM may be improved by using GLS guidance.

Functional tricuspid regurgitation (FTR) is associated with prognosis for various heart diseases, but its association with pulmonary hypertension (PH) remains unclear. We studied 111 PH patients. Mid-term follow-up echocardiography was performed 7.1 ± 4.1 months after PH-specific therapy. The severity of FTR was graded as none or trace, mild, moderate, or severe, while more than moderate TR was defined as significant. Moreover, mid-term improvement in FTR after therapy was defined as an improvement in severity of FTR by a grade of 1 or more. Long-term follow-up to determine the primary endpoint of death or hospitalization for heart failure lasted 39 ± 14 months. Mid-term improvement in FTR after PH-specific treatment was observed in 25 patients (23%), and the primary end points occurred in 27 patients (24%) during the long-term follow-up. The Kaplan-Meier curve indicated that the non-FTR group showed more favorable long-term outcomes than the FTR group (log-rank P = 0.008). It further indicated that patients with mid-term improvement in FTR also had more favorable long-term outcomes than those without such improvement (log-rank P = 0.03). When divided into four sub-groups based on combined assessment of baseline FTR and mid-term improvement in FTR, long-term outcomes for patients without mid-term improvement in their baseline FTR were worse than for the other sub-groups (log-rank P = 0.02). Multiple regression analysis showed that a relative change in tricuspid annular diameter at the mid-term follow-up after PH-specific therapy was the only independent determinant parameters for mid-term improvement in FTR. FTR appears to be a valuable factor for predicting long-term outcomes for PH patients, and combined assessment of baseline FTR and mid-term improvement in FTR after PH-specific therapy may have clinical implications for better management of such patients.

Background

The underlying mechanism of mitral regurgitation (MR) in atrial fibrillation (AF) is an isolated annulus dilation caused by left atrial (LA) remodeling. However, the association of mitral valve (MV) geometry with MR in AF patients remains unclear.Methods and Results:We studied 96 AF patients with preserved left ventricular ejection fraction (LVEF). MV geometry was evaluated with 3-dimensional transesophageal echocardiography (3D-TEE). Mitral annulus area of the MR group (n=11, ≥ moderate) was significantly larger (10.6±1.8 vs. 8.2±1.5 cm², P<0.0001), and relative posterior mitral leaflet (PML) area (PML area / mitral annulus area) was significantly smaller (0.51±0.06 vs. 0.57±0.01, P=0.002) than in the non-MR group (n=85, ConclusionsA relatively short PML plays an important role in the development of MR in AF patients. Assessment of MV geometry by 3D-TEE may thus have clinical implications for better surgical management of AF patients with significant MR.

Background

Left ventricular (LV) longitudinal myocardial systolic dysfunction (LVSD) has been identified in type 2 diabetes mellitus (T2DM) patients, and it should be considered the first marker of a preclinical form of DM-related cardiac dysfunction. Overweight has been postulated to contribute to the development of LVSD in T2DM patients, but the impact of amount of body fat mass on LVSD in T2DM patients remains uncertain.

Methods

We studied 71 asymptomatic T2DM patients with preserved LV ejection fraction (LVEF) (all ≥55%) without coronary artery disease. LVSD for T2DM patients with preserved LVEF was identified as global longitudinal strain (GLS) <18%. Body fat mass was measured with a commercially available body composition analyzer (In Body S-10, Biospace, Tokyo, Japan), and corrected by body surface area (BFI: body fat index).

Results

Univariate logistic regression analysis revealed that body weight, body mass index (BMI), and BFI were all associated with LVSD, whereas multivariate logistic regression analysis showed BFI was the only variable independently associated with LVSD (OR 1.147; 95% CI 1.001-1.314; p = 0.027). For sequential logistic regression models to predict LVSD, clinical variables including age, DM duration, and HbA1c tended to be improved by addition of BMI, but without statistical significance (p = 0.09), while it was significantly improved by addition of BFI (p = 0.047).

Conclusions

Using BFI for the control of body compression by means of a bioelectrical impedance assay is simple and easy-to-use, and this may have clinical implications for better management of T2DM patients with preserved LVEF to prevent future development of DM-related cardiac dysfunction.

OBJECTIVES:Our aim was to test the hypothesis that comprehensive simplified left atrial (LA) assessment derived from routine echocardiography may be more useful than assessment of LA volume alone for predicting atrial fibrillation (AF) recurrence after pulmonary vein isolation (PVI). METHODS:We studied 156 patients with paroxysmal AF (PAF) who had undergone PVI. Echocardiography was performed within two days before PVI. Maximum (Max-LAVi) and minimum LA volume index (Min-LAVi) were calculated with the biplane modified Simpson's method, and then normalized to the body surface area. On the basis of previous findings, the predefined cutoff value of Max-LAVi for AF recurrence was set at Max-LAVi ≥ 34 mL/m2 . ΔLA volume index (ΔLAVi) was also calculated as Max-LAVi minus Min-LAVi. The follow-up period after PVI was 24 months. RESULTS:AF recurrence was observed in 35 patients. Multivariate logistic regression analysis showed that ΔLAVi (odds ratio [OR]: 1.131; 95% confidence interval [CI]: 1.057-1.221; P < 0.001) was an independent predictor of AF recurrence. Sequential logistic regression models for predicting AF recurrence revealed that a model based on clinical variables including age, gender and AF duration (χ2  = 1.65) was improved by the addition of Max-LAVi ≥ 34 mL/m2 (χ2  = 13.8; P < 0.001), and further improved by the addition of ΔLAVi (χ2  = 18.2; P = 0.036). Of note is that only 1.02 ± 0.10 minutes per patient was needed to obtain a comprehensive LA assessment that included Max-LAVi, Min-LAVi, and ΔLAVi. CONCLUSION:This easy-to-use comprehensive simplified LA approach from routine echocardiography may well have clinical implications for better management of PAF patients.

Objectives

Pulmonary hypertension (PH) is characterized by marked and sustained elevation of pulmonary vascular resistance and pulmonary artery pressure, and subsequent right-sided heart failure. Right ventricular (RV) function and exercise capacity have been recognized as important prognostic factors for PH. Our aim was to investigate RV contractile reserve and exercise capacity during a leg-positive pressure (LPP) maneuver.

Methods

The study population comprised 43 PH patients and 17 normal controls. All patients underwent echocardiography at rest and during LPP stress. Exercise capacity was assessed by 6-minute walk distance for PH patients. RV relative wall thickness was calculated from dividing by RV free wall thickness by basal RV linear dimensions at end-diastole. RV function was calculated by averaging peak speckle-tracking longitudinal strain from the RV free wall. RV contractile reserve was assessed as the difference in RV free wall strain at rest and during LPP stress. Changes in left ventricular stroke volume (ΔSV) during LPP stress were also calculated.

Results

ΔSV and RV contractile reserve of PH patients were significantly lower than of controls (3.6 ± 6.0 mL vs 8.5 ± 2.3 mL, and 8.2 ± 11.9% vs 14.5 ± 6.6%; both P < 0.01). RV contractile reserve of PH patients with ΔSV <3.3 mL was significantly lower than of PH patients with ΔSV >3.3 mL (3.9 ± 13.2% vs 12.3 ± 8.9%; P = 0.02). ΔSV had also significant correlation with 6-minute walk distance (r = 0.42, P = 0.006). Multivariate regression analysis showed that RV relative wall thickness was an independent determinant parameter of ΔSV during LPP stress for PH patients (β = 3.2, P = 0.003).

Conclusions

Preload stress echocardiography in response to LPP maneuver, a noninvasive and easy-to-use procedure for routine clinical use, proved to be useful for the assessment of RV contractile reserve and exercise capacity of PH patients.

Background

Our aim was to investigate the baseline clinical and echocardiographic parameters for predicting left ventricular (LV) dysfunction after anthracycline chemotherapy and heart failure (HF) hospitalization in a single cancer disease. Methods and Results: We studied 73 patients with malignant lymphoma and preserved LV ejection fraction (LVEF). Echocardiography was performed before and after anthracycline chemotherapy. Global longitudinal strain (GLS) was determined from 3 standard apical views. LV dysfunction after anthracycline chemotherapy was defined according to the current definition of cancer therapeutics-related cardiac dysfunction. Long-term (50-month) unfavorable outcome was prespecified as hospitalization for HF. A total of 10 patients had LV dysfunction after anthracycline chemotherapy. Multivariate logistic regression analysis showed that baseline GLS was the only independent predictor of this dysfunction. Receiver-operating characteristic curve analysis identified the optimal GLS cutoff for predicting LV dysfunction after anthracycline chemotherapy as ≤19% (P=0.008). Furthermore, the Kaplan-Meier curve indicated that fewer patients with GLS >19% were hospitalized for HF than among those with GLS ≤19% (log-rank P=0.02). For sequential logistic models, a model based on baseline clinical variables (χ²=2.9) was improved by the addition of baseline LVEF (χ²=9.0; P=0.01), and further improved by the addition of baseline GLS (χ²=13.1, P=0.04).

Conclusions

Watchful observation or early therapeutic intervention with established cardioprotective medications may be necessary for patients with malignant lymphoma and preserved LVEF but with abnormal GLS.

BACKGROUND:The leg-positive pressure maneuver can safely and noninvasively apply preload stress without increase in total body fluid volume. The purpose of this study was to determine whether preload stress could be useful for risk stratification of patients with heart failure with reduced ejection fraction. METHODS AND RESULTS:For this study, 120 consecutive patients with heart failure with reduced ejection fraction were prospectively recruited. The stroke work index was estimated as product of stroke volume index and mean blood pressure, and the E/e' ratio was calculated to estimate ventricular filling pressure. The echocardiographic parameters were obtained both at rest and during leg-positive pressure stress. During the median follow-up period of 20 months, 30 patients developed adverse cardiovascular events. During preload stress, stroke work index increased significantly (from 3280±1371 to 3857±1581 mm Hg·mL/m2; P<0.001) along with minimal changes in ventricular filling pressure (E/e', from 16±10 to 17±9; P<0.05) in patients without cardiovascular events. However, patients with cardiovascular events showed impairment of Frank-Starling mechanism (stroke work index, from 2863±969 to 2903±1084 mm Hg·mL/m2; P=0.70) and a serious increase in E/e' ratio (from 19±11 to 25±14; P<0.001). Both the patients without contractile reserve and those without diastolic reserve exhibited worse event-free survival than the others (P<0.001). In a Cox proportional-hazards analysis, the changes in stroke work index (hazard ratio: 0.44 per 500 mm Hg·mL/m2 increase; P=0.001) and in E/e' (hazard ratio: 2.58 per 5-U increase; P<0.001) were predictors of cardiovascular events. CONCLUSION:Contractile reserve and diastolic reserve during leg-positive pressure stress are important determinants of cardiovascular outcomes for patients with heart failure with reduced ejection fraction.

OBJECTIVES:The closure of atrial septal defect (ASD) results in normalized left ventricular (LV) and right ventricular (RV) geometry, and can increase LV stroke volume (LVSV), but the parameters associated with this increase after the closure of ASD remain uncertain. METHODS:Seventy ASD patients, who underwent transcatheter closure, were studied. Their mean age was 57.80 ± 16.88 years, 42 (60%) were female, and LV ejection fraction (LVEF) was 66.76% ± 7.91% (all ≥55%). Transthoracic echocardiography was performed before and 3 months after the procedure. Global longitudinal strain (GLS) was determined as the average peak speckle tracking strain of 18 segments from the 3 standard apical views, LV dispersion was defined as standard deviation of time-to-peak strain from the same views, and RV systolic function was calculated by averaging the 3-regional peak speckle tracking longitudinal strains from the RV free wall. A significant relative increase in LVSV between before and 3 months after the closure was defined as ∆LVSV ≥15%. Twenty age-, gender-, and LVEF-matched controls served as the control group. RESULTS:Global longitudinal strain (GLS) and RV free wall strain were similar for ASD patients and controls, but LV dispersion in ASD patients was significantly larger. Global longitudinal strain (GLS) remained unchanged after transcatheter closure, whereas RV free wall strain and LV dispersion decreased significantly. An important finding of the multivariate logistic regression analysis showed that ∆LV dispersion was the only independent determinant of increased LVSV after the closure (OR 1.023; 95% CI 1.001-1.046; P < .01). CONCLUSIONS:The assessment of LV dispersion may well have clinical implications for better management of ASD patients after transcatheter closure.

BACKGROUND:Coexistence of left ventricular (LV) longitudinal myocardial systolic dysfunction with LV diastolic dysfunction could lead to heart failure with preserved ejection fraction (HFpEF). Diabetes mellitus (DM) is known as a significant factor associated with HFpEF. Although the mechanisms of DM-related LV myocardial injury are complex, it has been postulated that overweight contributes to the development of LV myocardial injury in type 2 diabetes mellitus (T2DM) patients. However, the precise impact of overweight on LV longitudinal myocardial systolic function in T2DM patients remains unclear. METHODS:We studied 145 asymptomatic T2DM patients with preserved LV ejection fraction (LVEF) without coronary artery disease. LV longitudinal myocardial systolic function was assessed by global longitudinal strain (GLS), which was defined as the average peak strain of 18-segments obtained from standard apical views. Overweight was defined as body mass index (BMI) ≥ 25 kg/m2. Ninety age-, gender- and LVEF-matched healthy volunteers served as controls. RESULTS:GLS of overweight T2DM patients was significantly lower than that of non-overweight patients (17.9 ± 2.4% vs. 18.9 ± 2.6%, p < 0.05), whereas GLS of both overweight and non-overweight controls was similar (19.8 ± 1.3% vs. 20.4 ± 2.1%, p = 0.38). Furthermore, multiple regression analysis revealed that for T2DM patients, BMI was the independent determinant parameters for GLS as well as LV mass index. CONCLUSIONS:Overweight has a greater effect on LV longitudinal myocardial systolic function in T2DM patients than on that in non-DM healthy subjects. Our finding further suggests that the strict control of overweight in T2DM patients may be associated with prevention of the development of HFpEF.

This report concerns an 83-year-old woman with aortic stenosis (AS) who had a history of repetitive hospitalization due to decompensated heart failure. Although her clinical history was compatible with significant AS, findings for aortic valve area, hemodynamics, and valvular calcium burden were discrepant. Multiplanar reconstruction images revealed the membranous structures attached to a subcommissural lesion, which resulted in severe stenosis. The patient had a favorable clinical course after transcatheter aortic valve replacement. This is the first reported case of severe AS due to the subcommissural adhesions, which were successfully visualized by means of echocardiography and computed tomography.

Although right ventricular (RV) pacing is the only effective treatment for patients with symptomatic bradycardia, it creates left ventricular (LV) dyssynchrony, which can induce LV dysfunction and heart failure. The current criterion for consideration of cardiac resynchronization therapy (CRT) is LV ejection fraction (LVEF) ≤ 35%, but indication for CRT in patients required for RV pacing with LVEF > 35% remains unclear.We studied 40 patients, all LVEF ≥ 35%, who had undergone implantable cardioverter-defibrillator implantation with RV pacing < 5%. Echocardiography was performed at baseline and during RV pacing. LV dyssynchrony was defined as anteroseptal-to-posterior wall delay from the mid-LV short-axis view using two-dimensional speckle-tracking radial strain (significant: ≥ 130 ms). Patients were divided into two groups based on baseline LVEF: normal LVEF ( ≥ 50%; n = 20) and mildly reduced LVEF (35-50%; n = 20).LVEF and LV dyssynchrony in patients with mildly reduced LVEF deteriorated significantly during RV pacing compared to those in patients with normal LVEF. Moreover, changes in LV dyssynchrony during RV pacing significantly correlated with changes in LVEF (r = -0.44, P < 0.01). Multivariate logistic regression analysis showed that baseline LVEF was the only independent predictor and baseline LVEF < 48% predictive of significant LV dyssynchrony during RV pacing.The extent of RV pacing-induced LV dysfunction may be associated with baseline LV function. These adverse effects on patients with mildly reduced LVEF of 35-50% and indications for RV pacing due to bradycardia can thus be prevented by CRT.

Preprocedural recognition of the segment of latest mechanical contraction along with the anatomy of the coronary venous system is important for successful and effective cardiac resynchronization therapy. We present a case of ischemic cardiomyopathy who underwent implantation of a cardiac resynchronization therapy device with a defibrillator, which was facilitated by preprocedural computed tomographic images reconstructed to visualize the left ventricular slab and the coronary venous system simultaneously on the cardiac contour. The present reconstruction method using computed tomography is optimal and feasible method to incorporate the echocardiographic findings into the procedure performed under fluoroscopy appropriately.

Background

Although aortic valve intervention is recommended for virtually all symptomatic patients with aortic stenosis (AS), how urgently the intervention should be performed remains controversial. The aim of this study was thus to determine whether the preload reserve in response to leg-positive pressure (LPP) maneuver could serve for decision-making for AS patients awaiting aortic valve intervention.Methods and Results:Sixty-eight patients with symptomatic AS, who were referred for aortic valve intervention, were recruited. Stroke volume (SV) was assessed by means of pulsed-wave Doppler, and the ratio between transmitral E wave and mitral annular velocity (e') was calculated to estimate ventricular filling pressure. While waiting for intervention, 11 patients experienced preoperative cardiac events. During acute preload stress, forward SV for patients without cardiac events increased significantly (from 43±9 to 49±10 mL/m², P<0.01) along with a minimal change in filling pressure (E/e': from 20±8 to 21±9, NS). For patients with cardiac events, the Frank-Starling mechanism was significantly impaired (SVi: from 40±9 to 38±7 mL/m², NS), while filling pressure increased to the critical level (E/e': from 24±8 to 31±8, P<0.001). Both the patients without flow reserve (∆SVi <4.5 mL/m²) and those without diastolic reserve (∆E/e' ≥2.9) exhibited significantly worse event-free survival than the others (P<0.05, respectively).

Conclusions

Assessment of preload reserve during LPP stress could facilitate risk stratification of patients with severe AS waiting for aortic valve intervention.

Mid-term right ventricular (RV) reverse remodeling after treatment in patients with pulmonary hypertension (PH) is associated with long-term outcome as well as baseline RV remodeling. However, baseline factors influencing mid-term RV reverse remodeling after treatment and its prognostic capability remain unclear. We studied 54 PH patients. Mid-term RV remodeling was assessed in terms of the RV area, which was traced planimetrically at the end-systole (RVESA). RV reverse remodeling was defined as a relative decrease in the RVESA of at least 15% at 10.2 ± 9.4 months after treatment. Long-term follow-up was 5 years. Adverse events occurred in ten patients (19%) and mid-term RV reverse remodeling after treatment was observed in 37 (69%). Patients with mid-term RV reverse remodeling had more favorable long-term outcomes than those without (log-rank: p = 0.01). Multivariate logistic regression analysis showed that RV relative wall thickness (RV-RWT), as calculated as RV free-wall thickness/RV basal linear dimension at end-diastole, was an independent predictor of mid-term RV reverse remodeling (OR 1.334; 95% CI, 1.039-1.713; p = 0.03). Moreover, patients with RV-RWT ≥0.21 showed better long-term outcomes than did those without (log-rank p = 0.03), while those with RV-RWT ≥0.21 and mid-term RV reverse remodeling had the best long-term outcomes. Patients with RV-RWT <0.21 and without mid-term RV reverse remodeling, on the other hand, had worse long-term outcomes than other sub-groups. In conclusions, RV-RWT could predict mid-term RV reverse remodeling after treatment in PH patients, and was associated with long-term outcomes. Our finding may have clinical implications for better management of PH patients.

Left ventricular (LV) hypertrophy (LVH) is an independent cardiovascular risk factor for heart failure (HF) patients. The renin-angiotensin system plays a key role in LVH, and since olmesartan increases plasma angiotensin-(1-7) through an increase in angiotensin-converting enzyme-related carboxypeptidase (ACE2) expression, it was hypothesized to reduce LVH, unlike other angiotensin II receptor blockers (ARBs). The objective of this study was therefore to investigate the effects of a changeover from other ARBs to olmesartan on LVH in HF patients. Participants enrolled in this prospective trial were 64 outpatients with stable HF who had received ARBs other than olmesartan for more than 1 year (age: 59 ± 13 years). Transthoracic echocardiography and laboratory tests were performed before and 6 months after administration of olmesartan. Other drugs were not changed during follow-up. The primary end point was defined as a change in LV mass index (LVMI) from baseline up to 6 months after administration of olmesartan. No significant changes were observed in blood pressures and heart rate after administration of olmesartan. LVMI showed a significant decrease from 119 ± 38 to 110 ± 24 g/m² (p = 0.007) 6 months after administration of olmesartan, and further decreased from 110 ± 24 to 103 ± 35 g/m² (p = 0.0003) after 12 months. Moreover, this reduction tended to be more prominent in patients with LVH. In conclusions, LVH in HF patients was reduced by the changeover to olmesartan. This finding may well have clinical implications for better management of HF patients.

Aims

Current guidelines recommend implantation of prophylactic implantable cardioverter-defibrillators (ICD) in patients with left ventricular (LV) ejection fraction (EF) <35%. We explored the prognostic factors of fatal ventricular arrhythmias for heart failure (HF) patients with LVEF ≥35%.

Methods and results

We retrospectively studied 72 patients with LVEF of 52 ± 12% (all ≥35%) who had undergone ICD implantation. Heterogeneity of LV regional myocardial contraction was defined as standard deviation of peak strain (dyssynergy index) and time-to-peak strain (dispersion index) from 18 LV segments determined by speckle tracking. Fatal ventricular arrhythmias with appropriate ICD therapy occurred in 34 patients (47%) during a median follow-up of 17 months. Receiver operating characteristic curve analysis identified dispersion index ≥101 ms and dyssynergy index ≥6.1% as predictors of fatal ventricular arrhythmias (P = 0.004 and P = 0.0001, respectively). In addition, the combination of dispersion index ≥101 ms and dyssynergy index ≥6.1% was the most predictive of fatal ventricular arrhythmias with a sensitivity of 77%, specificity of 79%, and area under the curve of 0.795 (P < 0.0001). A sequential Cox model based on clinical and conventional echocardiographic variables including age, gender, HF aetiology, and LVEF (χ(2) = 4.8) was improved, but not statistically significant (χ(2) = 4.9; P = 0.82), by addition of global longitudinal strain, whereas improvement by the addition of the dispersion index (χ(2) = 8.9; P = 0.04) and further improvement by the addition of the dyssynergy index (χ(2) = 20.2; P < 0.005).

Conclusion

Combined assessment of LV dyssynergy and dispersion can enhance predictive capability for fatal ventricular arrhythmias in patients with LVEF ≥35% and may have potential for better management of such patients.

症例1 : 30歳代, 女性. アルコール依存症, 神経性食思不振症にて精神科外来加療中であったが1 年前より通院を中断していた. 2012年5 月下旬の夕食後, 突然の痙攣様発作で救急要請. 救急隊到着時, 心室細動波形で心肺蘇生を開始, 合計3 回の電気的除細動が施行され当院搬入となった. び漫性左室壁運動低下を認め, 血清カリウム2.2mEq/L, 血清リン1.1mg/dLと電解質異常を認めていた. 入院後電解質補正を行い不整脈は消失したが, 低酸素脳症のため意識レベルの改善なく経過した. 症例2 : 40歳代, 男性. 2012年5 月下旬より下肢筋力低下, 起立困難から脳梗塞を疑われ近医で頭部精査入院となったが, 明らかな脳神経疾患は認めなかった. 前医第2 病日の朝食後, 突然心室細動が出現し心肺蘇生が施行されるも, 難治性心室頻拍となり某院救急センターへ搬送. 冠動脈造影にて有意狭窄はなかったが, 薬剤的, 電気的にもコントロール困難で経皮的心肺補助装置 (percutaneous cardiopulmonary support ; PCPS) 挿入下に当院に紹介搬送となった. 当院では多形性心室頻拍 (torsades de pointes ; TdP) を認め, び漫性に左室壁運動が低下しており, 血清カリウム : 1.6mEq/L, 血清リン : 1.6mg/dLと電解質異常を認めた. 入院後電解質補正によりTdPは消失, PCPS抜去にいたるも低酸素脳症から意識障害が遷延し第10病日に死亡退院となった. 両症例ともアルコール依存症を背景に持ち, カロリー摂取後の致死的不整脈出現からrefeeding症候群の関与が疑われた. 慢性低栄養患者に発症した若年性心肺停止患者ではrefeeding症候群の可能性を常に考慮する必要があると考えられた.

症例は，37歳，女性．3回経妊3回経産，某院産婦人科にて妊娠管理中36週より血圧上昇と尿蛋白を認め，重症妊娠高血圧症候群と診断された．38週4日に分娩誘発中，胎児心拍低下し緊急帝王切開で女児出産，産褥後，高血圧は改善した．産褥18日目より夜間呼吸困難が出現，産褥36日目に増悪を認め救急搬送され，胸部X線写真で肺うっ血と心胸郭比拡大と，心エコー図上，左室駆出率24％と高度低下を認め，心不全の診断で入院となった．入院後，通常の心不全治療とともに抗プロラクチン療法併用により心不全は改善し，左室壁運動の改善が得られた．妊娠関連の心筋症は本邦においてはいまだ実態が把握されておらず，確立された治療法がない．従来の心不全加療に加え，抗プロラクチン療法の有効性が少数例ながら報告されており，今後症例数を増やした検討が待たれる．

120名の心不全患者および20名の正常者に対して下肢陽圧負荷エコー検査を施行した。正常者では、下肢陽圧に対して充満圧の上昇なしに20%の駆出血流の増大が得られた。一方心不全患者では、負荷に対して充満圧の上昇といった犠牲を払いながら駆出量の10%の増大反応を示した。経過観察期間の20ヶ月間において、120名の心不全患者のうち、30名の患者において心血管イベントが発生した。イベントを起こさなかった心不全群では、下肢陽圧負荷により軽度の左室充満圧上昇はあるものの、前方駆出量の有意な増大反応が見られた。一方、イベントを起こした群では、左室充満圧の著明な上昇と、前方駆出量増大反応の低下が認められた。