Myocardial blood volume reserve by intravenous contrast echocardiography predicts improvement in left ventricular function in patients with nonischemic dilated cardiomyopathy.

BACKGROUND: Impaired myocardial perfusion has been shown in nonischemic dilated cardiomyopathy (DCM). Intravenous myocardial contrast echocardiography (MCE) has been introduced to examine myocardial blood volume (MBV) noninvasively. This study was designed to evaluate if MBV reserve assessed by intravenous MCE with adenosine triphosphate (ATP) can predict efficacy of optimal medical therapy in patients with DCM. METHODS AND RESULTS: Fifteen DCM patients and 8 control subjects underwent conventional echocardiography and intravenous MCE. We obtained the change in peak contrast integrated backscatter intensity (∆PI) by ATP on the left ventricular (LV) anteroseptal myocardium. After 3 months of optimal medical therapy in DCM patients, we reperformed conventional echocardiography. A good responder to therapy was defined as a decrease in LVDd >5 mm to final LVDd <55 mm and increase in LVEF >20 % to final LVEF >45 %. In DCM patients, ∆PI was lower compared to controls (p < 0.001). Good responders to therapy (n = 6) had higher ∆PI than poor responders (n = 9) (p < 0.05). CONCLUSIONS: The present study demonstrates that the response to the medical therapy in DCM is predicted by the assessment of dilator reserve in MBV. Intravenous MCE with ATP may provide useful information to evaluate MBV reserve.

Echocardiographic evaluation of iatrogenic atrial septal defect after catheter-based mitral valve clip insertion.

The geometries and sizes of persistent iatrogenic atrial septal defects (IASDs) after transseptal puncture during catheter-based mitral valve clip insertion (MVCI) have not been detailed. In this study, 11 IASDs were investigated in 10 patients who underwent MVCI using a guide catheter (24Fr proximally and 22Fr at the atrial septum). The diameters of the long and short axes and the area at maximum and minimum during a cardiac cycle were measured after MVCI using real-time 3-dimensional (RT3D) transesophageal echocardiography (TEE). A circular shape was assumed on 2-dimensional TEE, resulting in an area calculation of π × (dimension/2)(2). The anatomic geometries of IASDs were visualized in a 3-dimensional en face view of the atrial septum. Furthermore, 1 month after MVCI, IASDs were evaluated using echocardiography. The IASDs had a variety of irregular geometries. The mean long-axis diameter was 1.0 ± 0.24 cm, the mean short-axis diameter was 0.51 ± 0.22 cm, and the mean area was 0.40 ± 0.24 cm(2) on RT3D TEE. The diameters and area changed significantly between the maximal and minimal values during the cardiac cycle. Importantly, 2-dimensional TEE underestimated the maximal diameters of IASDs (0.54 ± 0.17 vs 1.0 ± 0.24 cm by RT3D TEE, p <0.01) and the maximal areas of IASDs (0.25 ± 0.15 vs 0.40 ± 0.23 cm(2) by RT3D TEE, p <0.05). One month after MVCI, the smallest and the second smallest IASDs had closed, and the other 9 remained open. In conclusion, RT3D TEE is useful to assess the irregular geometries of IASDs created during MVCI.

Left atrial size and function are related to pulmonary hypertension in coronary artery disease.

BACKGROUND: Left atrial (LA) size reflects diastolic burden and is a prognostic parameter of common cardiovascular death. However, the association between LA size and function and pulmonary hypertension (PH) in coronary artery disease (CAD) has not been well investigated. We hypothesized that LA size and function are associated with PH in CAD. METHODS: One hundred seven patients with CAD were studied. LA size was determined in three different methods; namely, LA volume index (LAV), LA area index, and LA dimension. LAV total emptying fraction was also determined. Pulsed Doppler E, A, E/A, DT, tissue Doppler E', A', and E/E' were measured. Pulmonary artery systolic pressure (PASP) was estimated. RESULTS: All LA size parameters are significantly associated with PH. LAV emptying fraction, age, E, E/A, E/E', and A' were also associated with PH significantly. CAD patients with PH showed larger LA size, higher E, E/A, and E/E' and lower LAV emptying fraction, A and A' than CAD patients without PH. Multivariate regression analysis revealed that maximum LAV, E, E/A ratio, and age were independent predictors of PH. Maximum LAV > 35.6 mL/m(2) predicted PASP > 40 mmHg with a sensitivity of 83.9% and specificity of 62.2%. CONCLUSION: LAV is associated with PH in CAD patients.

Pathophysiological characteristics and responsiveness to neurohormonal antagonism in idiopathic dilated cardiomyopathy patients with antihepatitis C virus antibody.

A high prevalence of hepatitis C virus (HCV) infection has been reported among idiopathic dilated cardiomyopathy (DCM) patients. We examined the prevalence of DCM patients with HCV antibody, and the pathophysiological characteristics and responsiveness to neurohormonal antagonism in DCM with HCV. HCV antibodies were determined in 540 patients with cardiac diseases. In 117 DCM patients, clinicopathologic data were evaluated before and 1 year after angiotensin converting enzyme inhibitor and/or beta-blocker (ACE-inhibitor/BB) administration and their prognosis was followed-up for a mean of 72 +/- 41 months. HCV antibodies were found in 12 of 135 DCM patients (8.9%) and in 37 of 405 patients without DCM (9.1%) (P = NS). At baseline, contrary to DCM without HCV, DCM with HCV was associated (P < 0.05) with greater left ventricular (LV) end-diastolic and end-systolic dimension, LV mass, and myocardial diameter in endomyocardial biopsy, and lower % fractional shortening. By multivariate analysis, HCV infection was independently associated with larger LV end-systolic dimension among DCM patients (P = 0.005). The advanced LV dilatation and hypertrophy in DCM with HCV decreased more in response to the ACE-inhibitor/BB therapy compared to DCM without HCV. There were no differences between DCM patients with and without HCV in survival and cardiac event-free rates. In summary, although HCV infection appears not to be the specific cause of DCM, HCV may enhance ventricular remodeling leading to heart failure among DCM patients. Nevertheless, the advanced ventricular remodeling with HCV was adequately reversed by neurohormonal antagonism, and did not lead to an unfavorable outcome.