[Severe pulmonary hypertension due to mitral regurgitation without overt sign of congestive heart failure: a case report].

A 49-year-old man was found to have a heart murmur at a local hospital and was referred to our hospital for further examination. Although he had no signs of congestive heart failure, echocardiography and cardiac catheterization showed severe pulmonary hypertension caused by severe mitral regurgitation. Mitral valve replacement was performed, followed by reduction of pulmonary artery pressure. This patient had an unusual combination of no signs of lung congestion despite severe mitral regurgitation with pulmonary hypertension.

Three-dimensional reconstruction of intravascular ultrasound images of coronary stents using an ECG-gated pull-back device.

Three-dimensional reconstruction (3D-R) of intravascular ultrasound (IVUS) images is not yet satisfactory because of artifacts caused by cardiac movement. This problem can be overcome with a new device, an electrocardiographic (ECG)-gated pull-back system. Using this device a catheter is pulled back stepwise gated by the ECG, and IVUS dynamic images of an entire cardiac cycle are acquired at each step. We performed 3D-R of IVUS images of stents using this new device in six patients with Palmaz-Schatz coronary stent implantation. We obtained precise 3D images in all cases, and stent structure was visualized in detail. In conclusion, use of an ECG-gated pull-back device enables precise 3D-R of IVUS images and provides useful information on the coronary artery.

[Left ventricular pseudoaneurysm recognized 9 years after mitral valve replacement and repeated heart failure of 3 years duration: a case report].

A 66-year-old woman had suffered from repeated heart failure beginning 6 years after mitral valve replacement. Left ventricular pseudoaneurysm was discovered 9 years after the replacement, while no evidence including histology was obtained for the cause of the pseudoaneurysm except the mitral valve replacement. The progression of aortic valve stenosis and the formation of the pseudoaneurysm may have contributed to the onset of congestive heart failure. Surgical treatment was successful. Although left ventricular pseudoaneurysm after mitral valve replacement is rare, careful echocardiographic examination is necessary for detecting such a complication in patients after surgery.

[Augmentation of left ventricular slow filling in hypertrophic cardiomyopathy].

To investigate the significance of augmentation of left ventricular slow filling, trans-mitral flow (TMF) was echocardiographically observed through pulsed Doppler method in 116 patients with hypertrophic cardiomyopathy (HCM), 74 with dilated cardiomyopathy (DCM), 27 with mitral regurgitation (MR), 86 with old myocardial infarction (OMI) and 80 normal controls (C). The slow filling-wave (SFW) in TMF was defined as the filling wave with obvious peak velocity during slow filling phase. The peak velocities (E, A, S) of the early filling, the atrial contraction and the slow filling waves were measured. The SFW was divided into two patterns according to the S and E ratio: large SFW (S/E greater than or equal to 1/2) and small SFW (S/E less than 1/2). 1) The small SFW was more frequently, but not significantly, observed patients with MR (37%) than in normal subjects (18%), patients with HCM (10%), DCM (4%) and OMI (7%). However large SFW was observed in 16 patients (14%) with HCM, but not in normal subjects and patients with other cardiac diseases excluding one patient with DCM. 2) In normal subjects and patients with DCM, OMI and MR, those with small SFW had larger E and smaller A/E than those without small SFW. However in patients with HCM, there was no difference in these indices (E and A/E) according to whether the patients were with or without SFW. 3) In HCM, patients with large SFW had significantly smaller E and significantly larger isovolumic relaxation time than those without SFW. Thus, appearance of the large slow filling wave, which might be caused by abnormal relaxation of the left ventricle, was frequently observed in patients with HCM.

[Effects of verapamil on the left ventricular diastolic function and diastolic asynchrony in patients with hypertrophic cardiomyopathy].

The effects of verapamil on the diastolic function and regional asynchrony of the left ventricle were echocardiographically investigated in 37 patients with hypertrophic non-obstructive cardiomyopathy (HCM). Before and 20 min after the intravenous administration of verapamil (0.1 mg/kg), blood pressure (BP), heart rate (HR), transmitral pulsed Doppler indices (R, A, A/R), M-mode echo indices (Dd, Ds, %FS) and the echo-phonocardiographic index (isovolumic relaxation time; IRT) were measured. We also measured the rapid extension times of the posterior walls at the chordae and papillary muscle level [Tc(pw), Tp(pw)] as the indices of regional diastolic function, and their difference [Tp-c(pw)] was used as the index of diastolic asynchrony. Before verapamil administration, the HCM patients had significantly larger A, A/R, IRT and Tp-c(pw) and smaller R than did 20 healthy controls, but showed no significant differences in HR, BP, Dd, Ds and %FS. After verapamil injection, R increased and A, A/R, IRT, Tp-c(pw) decreased significantly without any changes in BP and HR. The increment of R (delta R) correlated significantly with the decrement of Tp-c(pw) (r = -0.66, p less than 0.001). According to the value of delta R/R, 37 patients with HCM were categorized in 2 groups (19 responders with delta R/R greater than or equal to 10% and 18 non-responders with delta R/R less than 10%). The responders had smaller R and larger A/R, IRT and Tp-c(pw) before verapamil administration than did the non-responders. Verapamil increased R, Dd, Ds and decreased A, A/R and Tp-c(pw) in the responders, but not in the non-responders. These results suggested that verapamil might improve left ventricular diastolic function in HCM patients through the improvement of left ventricular diastolic asynchrony.

Mechanism of development of asymmetric septal hypertrophy in patients with essential systemic hypertension.

In order to understand the mechanism of development of asymmetric septal hypertrophy (ASH) in hypertension, 290 patients with essential hypertension (HT) were examined echocardiographically. Out of them 84 cases of advanced left ventricular hypertrophy (LVH) [37 cases of symmetric hypertrophy (HT-SH group) and 47 cases of ASH (HT-ASH group)] were compared in their clinical and echocardiographic findings with hypertrophic cardiomyopathy (HCM). In the 290 HT cases, the highest systolic pressure in each patient's history was found to correlate with left ventricular (LV) posterior wall thickness (PWT), but not with the septal wall thickness (IVST). There were no differences in LV thickness (IVST + PWT) among patients in the HT-ASH, HT-SH and HCM groups. While the HCM group patients showed no significant differences in IVST and PWT from those in the HT-ASH group, they did have greater IVST and smaller PWT than HT-SH group patients. The rapid filling rate (RFR) was also not much different in the HCM and HT-ASH groups, but was significantly lower in the HCM group than in the HT-SH group. Furthermore, HT-ASH group patients has a milder degree of hypertension and a higher incidence of familial occurrence of HCM than did those in the HT-SH group. After treatment for HT, the HT-SH group showed a significant decrease in wall thickness during long-term observation, while the HT-ASH and HCM groups, failed to exhibit such changes. Moreover, the degree of myocardial disarrangement in the HT-ASH group did not differ significantly from that in the HCM group. These results suggested that LVH in HT is related not only to pressure load but also to genetic factors similar to that in HCM.

Prognosis in hypertrophic cardiomyopathy--echocardiographic follow-up and histopathological study.

In 30 consecutive hypertrophic cardiomyopathy (HCM) patients who eventually died and 50 who survived, morphologic and functional changes in the heart during a follow-up period of an average of 3.9 years were echocardiographically evaluated. Echocardiographic indices were compared among 5 groups of patients with HCM, consisting of 4 groups of patients who eventually died (SD: 17 patients who suffered sudden death, ED: 4 who died of embolism, HF: 4 who died of congestive heart failure, NC: 5 who died of a noncardiac event) and 1 group of patients who survived with nondilated left ventricle (S: 50 patients). These indices at the last evaluation before death were compared with histopathological findings of left ventricles in 12 autopsied patients. At the initial evaluation ED and HF patients had a larger left ventricular end-diastolic dimension (LVDd), and HF patients had a smaller percent fractional shortening (%FS) and a slower normalized rapid filling rate (nRFR: mean rapid filling rate/LVEDV) than S patients, but these indices showed no differences between SD and S patients. During follow-up, no echocardiographic indices changed in S patients, but LVDd was increased and %FS and nRFR were decreased in SD and HF patients. Mean myocyte diameter and % area of disarray showed no differences among the 4 death groups. However, compared with NC, the other 3 groups, especially HF, had larger % area of massive fibrosis. The % area of massive fibrosis was correlated with LVDd (r = 0.80, p less than 0.005), %FS (r = -0.64, p less than 0.05), and nRFR (r = -0.95, p less than 0.001) at the last evaluation. These results suggested that echocardiographic follow-up was useful in predicting the progression of the myocardial lesion and the prognosis of HCM.

[Genesis of systolic anterior motion (SAM) of the mitral valve in patients with aortic regurgitation].

This study was performed to evaluate the incidence and genesis of systolic anterior motion (SAM) of the mitral valve apparatus in patients with aortic regurgitation (AR). The study population consisted of 44 patients with non-rheumatic AR, without significant aortic stenosis or mitral regurgitation. The presence and location of SAM in the short-axis view were determined by M-mode echocardiography guided by two-dimensional echocardiography. The extent and direction of the regurgitant jet were decided by pulsed or two-dimensional Doppler echocardiography. SAM was observed in 21 (48%) of the 44 patients, and it was more frequently observed in patients with an etiology of aortic valve prolapse or annuloaortic ectasia than in those of other etiology (10/14 vs 10/30; p less than 0.05). Twenty-eight patients whose regurgitant jet was directed posteriorly and impinged on the mitral valve apparatus had a significantly higher incidence of SAM than did the other 16 patients (18/28 vs 3/16; p less than 0.01). In eight of 10 patients in whom the direction of the regurgitant jet could be precisely observed by two-dimensional Doppler echocardiography. SAM was observed at the place where a regurgitant jet was directed along the anterior mitral valve in the short-axis view. M-mode measurements (LVDd, LVDs, %FS, LVDd-LVDs) of the patients with SAM had greater values than those of patients without SAM.(ABSTRACT TRUNCATED AT 250 WORDS)

[Observations of dilated cardiomyopathy with marked clinical improvement].

Although the prognosis of dilated cardiomyopathy (DCM) is poor, some patients occasionally follow favorable clinical courses and have significant improvement in cardiac function. To elucidate the mechanism of such improvement, we compared the clinical and pathological findings of 54 cases with DCM, including 12 cases with significant improvement (Dd less than 55 mm, %FS greater than 22%) during two years' follow-up (improved group), 26 without significant improvement (unimproved group), and 16 who died within two years (decreased group). Percent fractional shortening (%FS) in the deceased group was less than that in the unimproved group (12.4 +/- 3.9 vs 17.2 +/- 6.2, p less than 0.01). Pulmonary capillary pressure (PC) and % fibrosis in the deceased group were greater than those in the unimproved group [(22.7 +/- 9.5 vs 11.4 +/- 4.2 mmHg, p less than 0.001), (21.7 +/- 9.9 vs 13.4 +/- 3.6, p less than 0.01)], respectively. Although Dd, Ds, %FS, end-diastolic wall thickness (Thd), and PC in the improved group were not different from those in the unimproved group. End-systolic wall stress (WSes) in the improved group was greater than that in the unimproved group (376 +/- 73 vs 319 +/- 60 g/cm2, p less than 0.02), but % fibrosis was less in the improved group (7.6 +/- 3.4 vs 13.4 +/- 3.6, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

[Comparison of regional contractile dynamics and pathological findings of the left ventricular wall in patients with hypertrophic cardiomyopathy].

To investigate the relationship between regional contractile dynamics and regional myocardial lesions of the left ventricular wall in patients with hypertrophic cardiomyopathy (HCM), autopsy findings of 11 patients were compared with their ante mortem echocardiographic findings. The regional systolic wall thickenings (%RWT) of the interventricular septum (IVS) and left ventricular posterior wall (LVPW) obtained using M-mode echocardiography were converted into % normalized RWT (%NRWT) by the averaged %RWT in 15 normal subjects. The %NRWT was compared with the wall thickness obtained by echocardiography and/or autopsy, and histological findings, such as the myocardial fibrosis ratio, disarray area ratio, and mean myocyte diameter. 1. There were no significant correlations among wall thickness of the left ventricle, the myocardial fibrosis ratio, the disarray area ratio, and the mean myocyte diameter of each segment. 2. The %NRWT in 22 segments of the 11 patients with HCM was not significantly related to the echocardiographic wall thickness at end-systole, the autopsy wall thickness, the mean myocyte diameter and the disarray area ratio, but that correlated significantly with the echocardiographically-determined wall thickness at end-diastole (r = -0.53, p less than 0.02), and with the myocardial fibrosis ratios (r = -0.59, p less than 0.005). 3. The %NRWT in the IVS was significantly less than that in the LVPW. The %NRWT in all segments of the LVPW was significantly related to the myocardial fibrosis ratios (r = -0.80, p less than 0.005), but was not related to the wall thicknesses or the disarray area ratios.(ABSTRACT TRUNCATED AT 250 WORDS)

[Prognosis of hypertrophic cardiomyopathy: echocardiographic and postmortem histopathologic study of 30 patients].

To clarify the influence of cardiac function of myocardial histologic lesions on the prognosis of hypertrophic cardiomyopathy (HCM), most recent echocardiographic findings of 30 deceased patients were reviewed. In 12 patients, histological sections from the left ventricular transverse plane made at necropsy were examined. According to the main causes of death, patients were categorized into four groups as sudden death (17 cases), heart failure death (four cases), embolic death (four cases), and non-cardiac death (five cases). 1. Clinically, atrial fibrillation and heart failure (NYHA III, IV) were frequently observed in heart failure and embolic groups. 2. Echocardiographically, left ventricular wall thickness did not differ among the four groups, but percent fractional shortening was significantly smaller in heart failure group than in non-cardiac group, and left ventricular end-diastolic dimension (LVDd) and left atrial dimension were significantly greater in heart failure group than in non-cardiac group. The normalized rapid filling rate was less in heart failure, embolic, sudden death and non-cardiac groups in that order. 3. Histopathologically, the mean myocyte diameter (MD) and percent area of disarray (%D) did not differ among the four groups, but % area of massive fibrosis (MF) greater than 2 mm2 was larger in heart failure, embolic, sudden death and non-cardiac groups in that order, especially in heart failure group. 4. Comparison of echocardiographic and histopathological findings: Though MD and %D did not correlate with any echocardiographic indices, %MF correlated significantly with LVDd (r = 0.83, p less than 0.005), and correlated inversely with the normalized rapid filling rate (r = -0.80, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

[Pulsed Doppler echocardiographic findings in 117 professional cyclists].

To investigate the effect of long-term athletic training on the heart, pulsed Doppler echocardiography was performed in 117 male professional cyclists (Group C: 20-59 years of age), and 40 age- and sex-matched untrained normal controls (Group N). According to age, the subjects in each group were categorized in two subgroups: 74 cyclists (Group CI), 20-39 years of age and 43 cyclists (Group CII), 40-59 years of age; 24 control subjects (Group NI), 20-39 years of age and 16 control subjects (Group NII), 40-59 years of age. The average durations as professional cyclists were eight years in Group CI and 29 years in Group CII. The ratios of pre-ejection period to ejection time (LV-PEP/ET, RV-PEP/ET) as obtained from Doppler flow velocity patterns of the left and right ventricles (LV, RV) were used as parameters of systolic function. The peak flow velocities during rapid filling (LV-R, RV-R) and atrial systole (LV-A, RV-A), and the ratio of A to R (LV-A/R, RV-A/R) were used as parameters of diastolic filling dynamics. The parameters of systolic function of both ventricles and those of diastolic filling dynamics of the RV did not differ between Group C and Group N, Group CI and Group NI, and Group CII and Group NII. Study of the diastolic filling dynamics of the LV disclosed that Group C had a significantly higher LV-A/R (p less than 0.05) than did Group N; therefore, no significant differences between Group CI and Group NI, and Group CII had a significantly lower LV-R (p less than 0.005) and a higher LV-A/R (p less than 0.005) than did Group NII. Twenty-four hour ambulatory ECG monitoring was performed for 49 cyclists. Thirty cyclists aged 20-39 years were categorized in two groups according to their LV-A/R values: eight cyclists (Group A) with the LV-A/R greater than the mean + SD value (0.69) in Group NI and 22 cyclists (Group B) with the LV-A/R lower than or equal to 0.69. Nineteen cyclists aged 40-59 years were separated into two groups according to the LV-A/R value: 11 cyclists (Group A) with the LV-A/R values greater than the mean + SD value (0.89) in Group NII, and eight cyclists (Group B) with the LV-A/R equal to or less than 0.89.(ABSTRACT TRUNCATED AT 400 WORDS)

[A trial diagnosis of latent dilated cardiomyopathy].

To diagnose latent dilated cardiomyopathy (latent DCM), we performed loading echocardiography with Angiotensin II and ergometer exercise in 41 patients. Twenty-one patients were suspected of having latent DCM because of histories, of heart failure of myocarditis; 10 patients had DCM; and 10 normal persons served as controls. On angiotensin II loading, cardiac function deteriorated in the DCM group, but it was maintained in the normal controls. Nine patients in the latent DCM group showed the same pattern as normals (L1-group), and 12 did as the DCM group (L2-group). Although % fractional shortening, end-diastolic and end-systolic dimensions of the left ventricle did not differ between the L1 and L2-groups, the A/R, the ratio of the pulsed Doppler echocardiogram at the left ventricular inflow tract, was larger and the exercise change of the % fractional shortening and exercise tolerance were less in the L2-group than in the L1-group. Furthermore, the biopsy findings of the L2-group were similar to those of the DCM group in terms of myocardial degeneration, myocardial hypertrophy and interstitial fibrosis. Thus, patients in the L2-group were thought to have a risk for DCM, and were cases of latent DCM. Angiotensin II loading is thought to be useful for diagnosing such cases.