Late-onset doxorubicin-induced congestive heart failure in an elderly cancer survivor: A case report.

Background: Recently, the survival rate of patients with cancer has improved annually due to advancements in cancer diagnosis and treatment technologies. Meanwhile, late-onset complications associated with cancer treatment significantly affect survival and quality of life. However, different from pediatric cancer survivors, there is no unified view on the follow-up of late complications in elderly cancer survivors. We reported a case of congestive heart failure as a late-onset complication of doxorubicin (DXR) in an elderly cancer survivor. Case report: The patient is an 80-year-old woman with hypertension and chronic renal failure. She received six cycles of chemotherapy for Hodgkin's lymphoma that started in January 201X-2. The total dose of DXR was 300 mg/m2, and a transthoracic echocardiogram (TTE) performed in October 201X-2, showed good left ventricular wall motion (LVWM). In April 201X, she suddenly developed dyspnea. Upon arrival at the hospital, a physical examination revealed orthopnea, tachycardia, and leg edema. A chest radiograph showed cardiac enlargement and pleural effusion. A TTE showed diffusely reduced LVWM and a left ventricular ejection fraction in the 20% range. After close examination, the patient was diagnosed with congestive heart failure due to late-onset DXR-induced cardiomyopathy. Conclusion: Late-onset DXR-induced cardiotoxicity is considered high-risk from 250 mg/m2 or higher. Elderly cancer survivors are at higher risk of cardiotoxicity than non-elderly cancer survivors and may require closer follow-up.

Ability of Left Atrial Distensibility After Radiofrequency Catheter Ablation to Predict Recurrence of Atrial Fibrillation.

This study sought to assess the left atrial (LA) functional recovery after radiofrequency catheter ablation (RFCA) for atrial fibrillation (AF) and to evaluate the determining factor of procedural success of RFCA, using a novel preload stress echocardiography. A total of 111 patients with AF were prospectively recruited. The echocardiographic parameters were obtained during the leg-positive pressure (LPP) maneuver, both at baseline and midterm after RFCA. As an index of LA distensibility, the LA expansion index was calculated as (LAVmax - LAVmin) × 100 / LAVmin. During a median follow-up period of 14.2 months, AF recurrence was observed in 23 patients (20.7%). In LA functional parameters at baseline, only the Δ LA expansion index was significantly larger in the success group (16 ± 11% vs 4 ± 9%, p <0.05). At midterm follow-up, the Δ LA expansion index significantly increased to 32 ± 19% (p <0.05), together with structural LA reverse remodeling only in the success group. Moreover, the Δ stroke volume index during the LPP stress test significantly increased only in the success group (from 2.3 ± 1.3 ml/m2 to 3.1 ± 4.8 ml/m2, p <0.05). In a multivariate analysis, left ventricular ejection fraction (hazard ratio 0.911, p <0.05) and baseline Δ LA expansion index (hazard ratio 0.827, p <0.001) were independent predictors of AF recurrence. In conclusion, the baseline Δ LA expansion index during LPP stress is a reliable marker for predicting procedural success after RFCA. Moreover, maintenance of sinus rhythm resulted in an improvement of the preload reserve after RFCA.

Difficulty in Distinguishing Pulmonary Arterial Intimal Sarcoma from Pulmonary Thromboembolism Using FDG PET/CT.

BACKGROUND/AIM: Pulmonary arterial intimal sarcoma (PAIS) is a rare malignant soft tissue tumor that is difficult to differentiate from pulmonary thromboembolism (PTE). Therefore, pre-operative diagnosis is often difficult. However, recent advances in fluorodeoxyglucose positron emission tomography (FDG-PET) have enabled the use of standardized uptake values (SUVs) for the differential diagnosis of PAIS from PTE, and the frequency of diagnosis of PAIS has increased. Here, we report a case of PAIS that was difficult to differentiate from PTE despite using FDG-PET. CASE REPORT: A 40-year-old woman presented with gradually worsening exertional dyspnea. Contrast-enhanced computed tomography (CT) revealed lesions with poor enhancement in the right lateral basal pulmonary artery. FDG-PET/CT did not reveal any tumor or thrombosis in other areas. Cytological evaluation using a right ventricular catheter did not lead to a definitive diagnosis. Because the patient did not respond to anticoagulation, we performed pulmonary artery endarterectomy. Pathological examination of the pulmonary artery tumor revealed a mucinous tumor with an edematous stroma and spindle-shaped tumor-cell proliferation, which confirmed the diagnosis of PAIS. However, FDG/PET demonstrated a low SUV of 3.4. CONCLUSION: Some PAISs with low cellular densities and high mucous tissue proportions have SUVs similar to those in PTE. In patients with low FDG uptake, if PAIS is suspected based on other objective findings, additional exploration using highly invasive tests or surgical procedures specific to PAIS is warranted.

Effect of hypertension on the optimal anthracycline cumulative dose for developing left ventricular dysfunction in patients with malignant lymphoma.

The most serious adverse effect of anthracycline chemotherapy is progressive dose-dependent left ventricular (LV) dysfunction, and a total cumulative doxorubicin dose ≥ 240 mg/m2 has been classified as putting patients at high risk for developing cardiac dysfunction. Hypertension is the single most important risk factor for heart failure and chemotherapy-induced LV dysfunction, but the effect of hypertension on the total cumulative doxorubicin dose to prevent the development of LV dysfunction in patients scheduled for anthracycline chemotherapy remains uncertain. The aim of this study was to investigate the effect of hypertension on the optimal total cumulative anthracycline dose to prevent the development of LV dysfunction in patients with malignant lymphoma. We retrospectively studied 92 patients with malignant lymphoma and preserved LV ejection fraction (LVEF) who underwent anthracycline chemotherapy. Echocardiography was performed before and 2 months after anthracycline chemotherapy. LV hypertrophy (LVH) was defined as concentric hypertrophy, and LV dysfunction after chemotherapy as a relative decrease in LVEF ≥ 5%. The cutoff value of the total cumulative doxorubicin dose for the development of LV dysfunction was lower for hypertensive patients (n = 23) than for non-hypertensive patients (n = 69) (259.3 mg/m2 vs. 358.9 mg/m2). Importantly, the cutoff value of the total cumulative doxorubicin dose to prevent the development of LV dysfunction in hypertensive patients with LVH was even lower at 40.1 mg/m2. A lower cumulative anthracycline dose can cause LV dysfunction in hypertensive patients with malignant lymphoma, especially when complicated by LVH. Our findings can thus be expected to have clinical implications for better management of such patients.

Easy-to-use preload stress echocardiography by using combined dynamic postural stress can identify high-risk patients with heart failure with reduced ejection fraction.

AIMS: Haemodynamic assessment during stress testing is not commonly performed in patients with heart failure with reduced ejection fraction (HFrEF) because of its invasiveness, lower feasibility, and safety concerns. This study aimed to assess the haemodynamic characteristics of patients with HFrEF in response to non-invasive preload stress during dynamic postural alterations achieved by combining both semi-sitting position and passive leg-lifting and to evaluate whether combined postural stress could be used for risk stratification in these patients. METHODS AND RESULTS: For this study, 101 patients with HFrEF and 35 age-matched and sex-matched healthy controls were prospectively recruited. After all standard echocardiographic measurements were obtained in the left decubitus position, all subjects underwent postural stress testing, which consisted of changing from semi-sitting position to passive leg-lifting. During a median follow-up period of 12.2 months, 21 (21%) patients developed adverse cardiovascular events. In patients without adverse cardiovascular events, the stroke volume index (SVi) significantly changed from 28 ± 8 to 35 ± 10 mL/m2 (P < 0.001) during combined postural stress. By contrast, ΔSVi during combined dynamic postural stress was significantly smaller in patients with cardiovascular events than in those without events (ΔSVi 3.4 ± 4.0 vs. 6.4 ± 3.8 mL/m2 , P = 0.002), which indicated severely diseased heart operated on a relatively flat portion of the Frank-Starling curve. In a multivariate Cox proportional hazard analysis, ΔSVi (hazard ratio 0.81, P = 0.02) was an independent predictor of future adverse cardiovascular events. CONCLUSIONS: The combined assessment of dynamic postural stress is a non-invasive, simple, quick, and easy-to-use clinical tool for assessing preload reserve and risk stratification in HFrEF patients.

"Accelerated aging" of the heart as heart failure with preserved ejection fraction-analysis using leg-positive pressure stress echocardiography.

The aging process is a significant risk factor for heart failure. The incidence of heart failure with preserved ejection fraction (HFpEF) dramatically increases with age. Although HFpEF occurs along a continuum of aging of the cardiovascular system, the pathophysiology that differentiates overt HFpEF from physiological aging is not fully understood. A total of 102 subjects were prospectively recruited: 25 patients with HFpEF and 77 healthy controls. Controls were stratified into three age-groups: young (n = 27, 20-40 years), middle aged (n = 25, 40-65 years), and elderly (n = 25, > 65 years). All participants underwent preload stress echocardiography using a leg-positive pressure (LPP) maneuver. With an increase in age, progressive concentric left ventricular (LV) remodeling was observed in healthy controls, resulting in the hemodynamic consequences of an age-dependent increase in the E/e' ratio (ANOVA, P < 0.001). During LPP stress, the E/e' ratio significantly increased in the middle-aged and elderly groups (from 8 ± 2 to 9 ± 3, from 10 ± 2 to 12 ± 3, P < 0.05, respectively), and this was more pronounced in patients with HFpEF (from 16 ± 5 to 17 ± 7, P < 0.05). Forward stroke volume (SV) significantly increased in each healthy group during LPP stress (all P < 0.001) but failed to increase in the HFpEF group (from 43 ± 13 to 44 ± 14 mL/m2, P = 0.65). In a multivariate analysis, LV mass index (odds ratio [OR] 1.051, P < 0.05), E/e' ratio (OR 1.480; P < 0.05), and change in SV (OR 0.780; P < 0.05) were independent parameters that differentiated HFpEF from physiological aging. Structural remodeling and impaired preload reserve may both be critical features that characterize the pathophysiology of HFpEF.

Preoperative coupling between right ventricle and pulmonary vasculature is an important determinant of residual symptoms after the closure of atrial septal defect.

PURPOSES: The closure of atrial septal defect (ASD) is associated with a significant reduction in right ventricular (RV) overload and an improvement in functional capacity in most adults with ASD. However, a subset of patients remains symptomatic even after closure due to therapeutic delay. To date, no clinically robust preoperative predictor of postoperative residual symptoms has been clearly identified. METHODS: In this study, 120 adult patients with ASD and 39 controls were investigated. As an index of RV myocardial deformation, RV global longitudinal strain (RV-GLS) was evaluated. The degree of coupling between RV and pulmonary artery (PA) was quantified by the tricuspid annular plane systolic excursion (TAPSE) divided by the PA systolic pressure (PASP). RESULTS: Compared to controls, baseline RV-GLS was significantly greater (- 27 ± 7 vs. - 23 ± 5%, P = 0.02) and TAPSE/PASP ratio was severely impaired (0.8 ± 0.3 vs. 2.1 ± 1.6 mm/mmHg, P < 0.01) in ASD patients. At 6 months after closure, 15 patients (12.5%) remained symptomatic. In patients without residual symptoms, TAPSE/PASP ratio significantly improved from 0.9 ± 0.3 to 1.0 ± 0.6 mm/mmHg (P = 0.02), and RV-GLS normalized (from - 28 ± 11 to - 24 ± 7%, P < 0.01) after closure. However, RV-GLS and TAPSE/PASP ratio showed no significant change in ASD patients with residual symptoms. On multivariate analysis, preoperative TAPSE/PASP ratio (odds ratio [OR] 0.034, 95% confidence interval [CI] 0.000-0.604, P = 0.03) and pulmonary vascular resistance index ([PVRI], OR 1.011, 95% CI 1.000-1.021, P < 0.05) were associated with the postoperative symptomatic status. CONCLUSION: In terms of integrated assessment of the RV-PA unit, preoperative TAPSE/PASP ratio and PVRI were important determinants of residual symptoms after ASD closure.

Association between clinical risk factors and left ventricular function in patients with breast cancer following chemotherapy.

The sequential or concurrent use of two different types of agents such as anthracyclines and trastuzumab may increase myocardial injury and cancer therapeutics-related cardiac dysfunction (CTRCD), which is often the result of the combined detrimental effect of the two therapies for breast cancer patients. However, the association between clinical risk factors and left ventricular (LV) function in such patients is currently unclear. We studied 86 breast cancer patients with preserved LV ejection fraction (LVEF) and treated with anthracyclines, trastuzumab, or both. Echocardiography was performed before and 16 days after chemotherapy. In accordance with the current position paper, clinical risk factors for CTRCD were defined as: cumulative dose of doxorubicin > 240 mg/m2, age > 65-year-old, body mass index > 30 kg/m2, previous radiation therapy, B-type natriuretic peptide > 100 pg/mL, previous history of cardiovascular disease, atrial fibrillation, hypertension, diabetes, and smoking. The relative decrease in LVEF after chemotherapy for patients with more than four risk factors was significantly greater than that for patients without (- 9.3 ± 10.8% vs. - 2.2 ± 10.2%; p = 0.02). However, this finding did not apply to patients with more than one, two or three risk factors. Patients with more than four risk factors also tended to show a higher prevalence of CTRCD than those without (14.3% vs. 2.8%; p = 0.12). Moreover, the relative decrease in LVEF became greater as the number of risk factors increased. This study found multiple risk factors were associated with LV dysfunction following chemotherapy. Our findings can thus be expected to have clinical implications for better management of patients with breast cancer referred for chemotherapy.

Impact of hypertension on left ventricular function in patients after anthracycline chemotherapy for malignant lymphoma.

BACKGROUND: Hypertension is considered an important risk factors for cancer therapeutics-related cardiac dysfunction (CTRCD) as well as heart failure. However, the impact of hypertension and left ventricular (LV) hypertrophy (LVH), which is associated with hypertension, on LV function in patients treated with anthracycline chemotherapy for malignant lymphoma remains uncertain. METHOD: We studied 92 patients with malignant lymphoma and with preserved LV ejection fraction (LVEF). Echocardiography was performed before and two-month after anthracycline chemotherapy. CTRCD was defined as the presence of an absolute decrease in LVEF ≥10% to a final value <53%. LVH was defined as concentric hypertrophy, which was determined as relative wall thickness ≥ 0.42 and LV mass index >95 g/m2 for females and > 115 g/m2 for males. RESULTS: Relative decrease in LVEF after anthracycline chemotherapy in patients with hypertension (n = 23) was significantly higher than that in patients without hypertension (n = 69) (-5.8% [-9.4, -1.3]) vs. (-1.1% [-4.1, 2.5]); P = .005). Moreover, the prevalence of CTRCD in patients with hypertension tended to be higher than in those without hypertension (17% vs. 5%, p = .09). A sequential logistic model for predicting CTRCD, based on baseline clinical variables including major clinical risk factors, was improved by the addition of the complication of hypertension (P = .049), and further improved by the addition of the presence of LVH (P = .023). CONCLUSIONS: Hypertension, especially when complicated by LVH, was found to be associated with LV dysfunction after anthracycline chemotherapy in patients with malignant lymphoma and preserved LVEF. Watchful observation or early therapeutic intervention may thus be needed for such patients by the addition of the presence of LVH.

"The Heart Sound Quintet": A Case Report of Right-Sided Heart Failure Due to Free Pulmonary Regurgitation Long After Intracardiac Repair of Tetralogy of Fallot.

BACKGROUND Intracardiac repair of tetralogy of Fallot (TOF) is generally performed during childhood. However, the majority of patients develop the sequelae long after surgical repair, which results in significant right ventricular (RV) dilation, RV myocardial dysfunction, and, ultimately, in right-sided heart failure. CASE REPORT A 52-year-old man was referred to our institution for the evaluation of sudden-onset ventricular tachycardia. His medical history included RV outflow tract reconstruction at 5 years of age. Auscultation revealed a harsh diastolic regurgitant murmur, widely split first heart sound (S1), and a single second heart sound (S2), indicating a severely dilated RV due to severe pulmonary regurgitation (PR) and the presence of a non-functioning pulmonary valve. Moreover, the right-sided third heart sound (S3) and fourth heart sound (S4) were present, consistent with elevated RV filling pressure and the presence of a non-compliant RV. Eventually, the aforementioned "heart sound quintet" was confirmed using multimodal evaluation as right-sided heart failure with a concomitant severely dilated RV because of complete regression of the pulmonary valve and resultant free PR. CONCLUSIONS We encountered a case with a "heart sound quintet" that was composed of a widely split S1, single S2 with a harsh diastolic regurgitant murmur, and right-sided S3 and S4 The logical interpretation of the findings from physical examination will contribute to understanding the pathophysiology and aid clinical decision-making.

Severe pulmonary regurgitation mimicking constrictive pericarditis: a case report-the sac or the content? That is the question.

BACKGROUND: Constrictive pericarditis (CP) is a pathological condition of the pericardium, resulting from fibrosis, scarring, and calcification of the pericardium. Other conditions have been reported to mimic 'constrictive physiology' despite the presence of an intact pericardium. However, there has been no report of pulmonary regurgitation (PR) mimicking the haemodynamic characteristics of CP. CASE SUMMARY: A 51-year-old woman was admitted to our institute because of severe right-sided heart failure. Transthoracic echocardiography revealed severe PR concomitant with significant dilatation of the right-sided heart. Septal bounce and the respiratory reciprocation of the transmitral and transtricuspid inflow velocities were also observed, indicating exacerbated ventricular interdependence. Cardiac catheter examination demonstrated elevated right atrial pressure with a prominent y descent, dip, and plateau waveform in the right ventricular pressure, and equalization of the diastolic pressure of all cardiac chambers, which are quite consistent with CP. On surgical inspection, however, there was no pericardial thickening or adhesion, indicating no obvious signs of CP. DISCUSSION: Pericardial constriction results from the relative relationship between intrapericardial volume and pericardial reserve. When the intrapericardial volume exceeds the physiological limit, the cardiac chambers compete with each other in a fixed pericardial space. In this case, prominent dilation of the right-sided chambers caused by severe PR resulted in overstretching of the pericardium above the pericardial reserve, which led to a characteristic haemodynamic picture that resembled CP. Thus, it is important to recognize the diagnostic pitfall in the preoperative evaluation of a 'CP mimic physiology'.

Noninvasive Leg-Positive Pressure Stress Echocardiography Reveals Preload Reserve in Adult Patients after Complete Repair of Tetralogy of Fallot.

BACKGROUND: Long-term sequelae such as right ventricular dysfunction and reduced hemodynamic reserve are the main determinants of cardiovascular outcomes after repair of tetralogy of Fallot (TOF). Echocardiographic parameters at rest offer only partial information on impaired hemodynamics in these patients, and data during stress testing are lacking. The leg-positive pressure (LPP) maneuver has recently been reported to be able to apply acute preload stress. The aim of this study was to test the hypothesis that preload reserve is impaired and ventricular interaction is exacerbated in patients with TOF. METHODS: In this prospective cross-sectional study, we recruited 44 consecutive patients with TOF and 30 normal control subjects. Echocardiography was performed both at rest and during LPP stress, and preload reserve was defined as the change between baseline stroke volume (SV) and that obtained during LPP stress. The eccentricity index was calculated as the ratio of the left ventricular anteroposterior to septal-lateral dimensions to quantify ventricular interaction. RESULTS: LPP stress significantly increased SV from 73 ± 14 to 83 ± 16 mL (P < .01) in control subjects, while the increase in SV was significantly blunted (from 75 ± 19 to 79 ± 18 mL; P < .01 for interaction) in patients with TOF. The eccentricity index significantly changed during LPP stress in patients with TOF only from 1.07 ± 0.13 to 1.13 ± 0.14 (P < .01 for interaction). Patients with TOF were subdivided into two subgroups on the basis of the median value of increased response in SV (22 with sufficient and 22 with insufficient preload reserve). Multivariate analysis identified significant pulmonary regurgitation as the only independent determinant factor for insufficient preload reserve (odds ratio, 4.57; 95% CI, 1.048-19.90; P = .04). CONCLUSIONS: In patients after repair of TOF, ventricular interaction was exacerbated and preload reserve was impaired, especially in patients with significant pulmonary regurgitation. LPP stress testing may direct tailored treatment approaches, risk stratification, and clinical decision-making, such as more aggressive pharmacologic therapy, meticulous outpatient follow-up, or earlier reintervention.

Associations between functional tricuspid regurgitation and long-term outcomes for patients with pulmonary hypertension.

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.

Cardiac resynchronization therapy improves left atrial reservoir function through resynchronization of the left atrium in patients with heart failure with reduced ejection fraction.

This study aimed to test the hypothesis that left ventricular dyssynchrony may negatively affect left atrial (LA) dyssynchrony and reservoir function, and cardiac resynchronization therapy (CRT) may improve LA function. It also assessed, whether residual LA dyssynchrony affects the prognosis in patients with heart failure with reduced ejection fraction (HFrEF). Ninety subjects were included: 40 HFrEF patients with a wide-QRS complex (≧130 ms), 28 HFrEF patients with a narrow-QRS, and 22 normal controls. LA global longitudinal strain (LA-GLS) and LA dyssynchrony were quantified by speckle-tracking strain analysis. LA dyssynchrony was defined as the maximal difference of time-to-peak strain (LA time-diff). All patients with a wide-QRS underwent CRT, and event-free survival was tracked for 24 months. At baseline, LA dyssynchrony was significantly more pronounced in patients with a wide-QRS HFrEF (342 ± 126 ms) than that in patients with a narrow-QRS (236 ± 127 ms, P < 0.001) and controls (186 ± 78 ms, P < 0.001). Six months after CRT, LA-GLS significantly improved from 11.9 ± 4.7 to 19.6 ± 10.1% (P < 0.05) and LA time-diff was reduced from 338 ± 123 to 245 ± 141 ms (P < 0.05) in responders only. Patients with an LA time-diff < 202 ms and those with an LA-GLS ≧14.6% six months after CRT showed significantly better outcomes than the others (P < 0.05, respectively). Among the responders, those with an LA time-diff < 202 ms after CRT showed a better prognosis than others (P < 0.05). CRT improved LA dyssynchrony and reservoir function through the improved left ventricular coordination. Reduced LA dyssynchrony and improved LA reservoir function after CRT lead to better outcomes.

Effects of balloon pulmonary angioplasty for chronic thromboembolic pulmonary hypertension on remodeling in right-sided heart.

Remodeling in the right-sided heart plays an important role in the management of pulmonary hypertension (PH) patients. However, the effect of balloon pulmonary angioplasty (BPA) on right ventricular (RV) and right atrial (RA) morphology of patients with chronic thromboembolic pulmonary hypertension (CTEPH) remains uncertain. This study involved 45 CTEPH patients who underwent BPA with mean pulmonary artery pressure (mPAP) of 37.0 mmHg (all ≥ 25 mmHg). All patients underwent echocardiography and right-heart catheterization at baseline and 3 months after BPA. RV and RA remodeling was assessed as RV and the RA area, and RV systolic function was calculated by averaging peak speckle-tracking longitudinal strain of the RV free-wall (RV free-wall strain). Significant reverse remodeling in the right-sided heart was observed after BPA, resulting in improvement of mPAP and pulmonary vascular resistance (RV area: from 15.0 ± 5.3 to 9.6 ± 3.0 cm2, p < 0.0001; RA area: from 17.3 ± 6.6 to 13.4 ± 3.8 cm2, p = 0.0002; RV free-wall strain: from 15.9 ± 5.6 to 21.2 ± 4.9%, p < 0.0001). Furthermore, multiple regression analysis showed that the baseline RV area was an independent predictor of post-BPA normalization of RV systolic function defined as RV free-wall strain ≥ 20% (odds ratio = 1.16, p = 0.0305). Interestingly, significant RV reverse remodeling was also observed after additional BPA even in 18 CTEPH patients with residual pulmonary arterial stenosis, whose mPAP was normalized after BPA (RV area: from 11.5 ± 3.8 to 9.2 ± 3.8 cm2, p = 0.0045; RV free-wall strain: from 17.2 ± 4.8 to 22.8 ± 7.4%, p = 0.0216). Significant reverse remodeling in the right-sided heart, as well as hemodynamic improvement, was observed in CTEPH patients after BPA.

Transcatheter Atrial Septal Defect Closure in a 'Nonagenarian' with Intractable Heart Failure.

A 92-year-old man was referred to our hospital with decompensated heart failure. He was treated with diuretics and inotropic agents, but the clinical response was unsatisfactory. Echocardiography incidentally revealed an atrial septal defect (ASD) with a significant left-to-right shunt and pulmonary-to-systemic-blood-flow ratio of 2.36. Because the ASD was considered to be the primary cause of his treatment-resistant heart failure, the patient underwent transcatheter ASD closure. Shortly after shunt closure, his hemodynamics significantly improved, and he was discharged nine days later. This is an extremely rare case of a nonagenarian who showed an excellent clinical course after transcatheter ASD closure.

Association of body fat mass with left ventricular longitudinal myocardial systolic function in type 2 diabetes mellitus.

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.

Association of glycemic variability with left ventricular diastolic function in type 2 diabetes mellitus.

BACKGROUND: Type 2 diabetes mellitus (T2DM) is a major cause of heart failure (HF) with preserved ejection fraction (HFpEF), usually presenting as left ventricular (LV) diastolic dysfunction. Thus, LV diastolic function should be considered a crucial marker of a preclinical form of DM-related cardiac dysfunction. However, the impact of glycemic variability (GV) on LV diastolic function in such patients remains unclear. METHODS: We studied 100 asymptomatic T2DM patients with preserved LV ejection fraction (LVEF) without coronary artery disease (age: 60 ± 14 years, female: 45%). GV was evaluated as standard deviation of blood glucose level using continuous glucose monitoring system for at least 72 consecutive hours. LV diastolic function was defined as mitral inflow E and mitral e' annular velocities (E/e'), and > 14 was determined as abnormal. RESULTS: E/e' in patients with high GV (≥ 35.9 mg/dL) was significantly higher than that in patients with low GV (11.3 ± 3.9 vs. 9.8 ± 2.8, p = 0.03) despite similar age, gender-distribution, and hemoglobin A1c (HbA1c). Multivariate logistic regression analysis showed that GV ≥ 35.9 mg/dL (odds ratio: 3.67; 95% confidence interval: 1.02-13.22; p < 0.05) was an independently associated factor, as was age, of E/e' > 14. In sequential logistic models for the associations of LV diastolic dysfunction, one model based on clinical variables including age, gender and hypertension was not improved by addition of HbA1c (p = 0.67) but was improved by addition of high GV (p = 0.04). CONCLUSION: Since HFpEF is a syndrome caused by diverse agents, reducing GV may represent a potential new therapeutic strategy for the prevention of the development of HFpEF in T2DM patients.