[The effects of nicardipine on hemodynamics, regional myocardial function and myocardial metabolism in the dog with coronary artery occlusion].
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Biomedical subjects
Publications and source records attributed to I Sotobata.
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Hemodynamic effects of isosorbide-5-mononitrate (ISMN) were studied in 14 patients with effort angina pectoris. Hemodynamic and echocardiographic data were obtained by angina-limited supine multistage bicycle ergometer exercise testing before and 120 minutes after single oral administration of 20 mg of ISMN. Compared with control exercise testing, the ST segment at peak exercise showed less depression after administration of ISMN (p less than 0.001). At rest, systolic and diastolic blood pressure decreased significantly after administration of ISMN (p less than 0.001 and p less than 0.01, respectively). At rest and at peak exercise, pulmonary artery wedge pressure (both p less than 0.001), left atrial volume (both p less than 0.001) and left ventricular end-diastolic volume (both p less than 0.05) decreased, whereas cardiac index, pressure-rate product and systemic vascular resistance did not change significantly after administration of ISMN. Average time to peak plasma ISMN concentration was 90 minutes and average peak plasma concentration was 460 ng/ml with an elimination half-life of 7 hours. These data suggest that the main mechanism of the antianginal action of ISMN is a reduction in left ventricular preload followed by diminution of myocardial oxygen requirements.
To evaluate the significance of the left atrial (LA) contribution to left ventricular (LV) filling in cardiac pacing, LV inflow velocity was recorded with pulsed Doppler echocardiography in 20 patients with a DDD pacemaker. The pacemaker was programmed to atrioventricular (AV) sequential pacing with AV intervals of 50, 100, 150, 200 and 250 ms, and then to VVI pacing at a fixed rate of 70 beats/min. To evaluate the relative changes of LV filling volume in individual patients, the percent change in time-velocity integral of LV inflow velocity in each pacing mode was calculated as the ratio to that of AV sequential pacing with an AV interval of 150 ms. To estimate the degree of LA contribution to LV filling, the ratio of time-velocity integral during LA ejection phase to that during total LV filling phase was measured at the optimal AV interval. The percent LV inflow volume in AV sequential pacing was 74% for an AV interval of 50 ms, 87% for 100 ms, 98% for 200 ms and 90% for 250 ms. The percent LV inflow volume in VVI pacing was 72%. The percent LV inflow volume at AV intervals of 150 ms was significantly greater than that at an AV interval of 50, 100 and 250 ms, and in VVI pacing (p less than 0.05). The degree of LA contribution to LV filling showed a positive correlation with the percent increase of LV inflow volume with mode conversion from VVI to AV sequential pacing (p less than 0.005) and also with age (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of diltiazem hydrochloride on exercise-induced changes in cardiovascular response, plasma renin activity, platelet function and blood coagulability were evaluated with multistage treadmill exercise in 20 patients who had systemic hypertension of stage 1 to 2 (World Health Organization classification). Heart rates, blood pressure, and pressure-rate product at rest, at peak exercise and in the recovery period were significantly reduced after 4 weeks of diltiazem administration, 180 mg/day. Plasma renin activity tended to increase after the medication. However, platelet adenosine diphosphate-induced aggregation sensitivity, prothrombin time, activated partial thromboplastin time, plasma fibrinogen concentration and antithrombin III activity did not change significantly. It is concluded that diltiazem could ameliorate the hyperresponsiveness of heart rate and BP to exercise in hypertensive patients without affecting blood coagulability.
Multistage bicycle ergometer exercise testings with Frank vectorcardiogram and M-mode echocardiogram were performed on 12 patients with effort angina pectoris. The left atrial and left ventricular end-diastolic volume (LAV and LVEDV) were calculated as a cube of the left atrial and left ventricular end-diastolic dimension. The mean pulmonary artery wedge pressure (mPAWP) was measured with a Swan-Ganz catheter during the testing. At peak exercise a statistically significant increase was observed in mPAWP (p less than 0.001), LAV (p less than 0.005), the maximal horizontal P-vector magnitude (Hmax) (p less than 0.05) and the percent change in Hmax (%Hmax). %Hmax showed a significant correlation with the increment of mPAWP (delta mPAWP) (r = 0.66, p less than 0.05), the increment of LVEDV (delta LVEDV) (r = 0.83, p less than 0.01) and the increment of LAV (delta LAV) (r = 0.81, p less than 0.001). Multiple regression analysis was performed on %Hmax as a dependent variable with delta LAV, delta mPAWP, and the increment of heart rate (delta HR) as independent variables (r = 0.84, p less than 0.05), but the partial correlation coefficients of delta mPAWP and delta HR were not significant. The present study demonstrated that the increase in Hmax had a close relationship with the increase in mPAWP and LVEDV and that the preload of the left ventricle during exercise-induced anginal attack could be predicted noninvasively by %Hmax. The increase in Hmax was thought to be due to the increase in LAV during anginal attack.
Near-maximal treadmill exercise testing was performed on 26 normal individuals (NL) and 78 patients with coronary artery disease (CAD) using a modified Bruce's protocol. Exercise-induced changes in orthogonal P wave measurements were made automatically, using an averaging technique, immediately before and 30 sec after treadmill exercise to assess their diagnostic significance in evaluation of left ventricular (LV) function in CAD patients. The maximal inferior and posterior components of the P wave and the maximal P-vector magnitude in the frontal and left sagittal planes showed a statistically significant increase after treadmill exercise both in NL and CAD patients. These changes were considered to be physiological responses of the P wave to dynamic exercise. The percent changes of the maximal horizontal P-vector magnitude (%Hmax) were significantly higher after treadmill exercise in CAD patients than in NL. In patients with effort angina pectoris and without a previous myocardial infarction, the %Hmax showed a highly significant negative correlation with the percent changes of the LV ejection fraction (r = 0.66, p less than 0.01), measured by exercise RI angiography. These results suggest that the exercise-induced increase in %Hmax reflects transient impairment of LV function during exercise. It was concluded that a %Hmax of more than 120% provided a useful, noninvasive index for assessing LV function in treadmill exercise testing.
The clinical significance of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF-4) levels were evaluated in 26 patients with atrial fibrillation (af) complicated by valvular heart disease (VHD), 73 patients with af but without valvular heart disease and 57 normal subjects. The beta-TG level was significantly higher in af patients without VHD than in normal subjects (49.4 +/- 35.8 ng/ml vs 31.2 +/- 14.0 ng/ml, p less than 0.01) and in af patients with VHD than in normals (64.1 +/- 52.8 ng/ml vs 31.2 +/- 14.0 ng/ml, p less than 0.01). Af patients with or without VHD tended to show high levels of PF4 compared with normals (af patients without VHD: 34.1 +/- 45.5 ng/ml, af patients with VHD: 18.6 +/- 27.2 ng/ml, normals: 11.6 +/- 8.2 ng/ml). There was no correlation between beta-TG levels and age in af patients without VHD or in normals. There was also no correlation between beta-TG levels and heart rate in af patients without VHD. The activation of platelets was suggested in patients with atrial fibrillation on the basis of increased levels of platelet releasing substances, especially in those with VHD. The high levels of beta-TG and PF4 in patients with atrial fibrillation may be one explanation for the high incidence of thromboembolism in these patients, indicating the necessity of antiplatelet therapy.
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To investigate hemodynamic changes in ventricular premature contractions (VPCs), the blood flow velocities at the left ventricular (LV) outflow and inflow tracts were analyzed by pulsed Doppler echocardiography in 23 patients with VPCs and in two patients with ventricular parasystoles. Percent LV stroke volume of the ectopic and the postectopic sinus beats to the other sinus beats and %LV inflow volume of the sinus beats preceding ectopic beats to the other sinus beats were calculated from the time integral of the blood flow velocity. The following results were obtained. The %LV stroke volume of VPCs or %LV inflow volume of the preceding sinus beats correlated positively with the coupling interval of VPCs (r = 0.69, p less than 0.001 and r = 0.67, p less than 0.001, respectively). The %LV stroke volume of VPCs correlated positively with %LV inflow volume of the preceding sinus beats (r = 0.84, p less than 0.001). In some patients with VPCs of the RBBB pattern and in one patient with VPCs of the LBBB pattern associated with abnormal right axis deviation, the %LV stroke volume of VPC was much more reduced. In patients with depressed rapid filling and increased atrial filling, %LV stroke volume of the VPC or %LV inflow volume of the preceding sinus beat was smaller than in the other patients with the same coupling interval of VPCs. In VPCs of right ventricular (RV) origin, deterioration of RV hemodynamics was more prominent than in those of LV origin, and vice versa. Increased LV stroke volume was observed in postextrasystolic sinus beats, related to the coupling intervals of VPCs. However, the sum of %LV stroke volume of VPC and the postextrasystolic sinus beat decreased as the coupling intervals of VPC shortened. These results suggest that not only the coupling interval and the origin of VPCs but the LV diastolic behavior, as well, are important factors determining the hemodynamics in VPCs. They also suggest that the increment of stroke volume in postextrasystolic beats is more prominent in VPCs with shorter coupling intervals, but the LV performance as a whole is more depressed in VPCs with a shorter coupling intervals. In conclusion, pulsed Doppler echocardiography proved a useful noninvasive technique for evaluating the hemodynamics of VPCs.
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The clinical usefulness of thallium-201 myocardial emission computed tomography (ECT) for evaluating left ventricular myocardial fibrosis was assessed in 47 patients with Duchenne (MD), facioscapulo-humeral (FSH), limb-girdle (LG) and myotonic (MT) dystrophy. Trans-, long- and short-axial images were interpreted quantitatively by circumferential profile analysis, and the extent of fibrotic tissue (%FIB) was estimated by integrating hypoperfused areas in six to eight consecutive short-axial slices. Lung/mediastinum count ratio (L/M ratio), LV cavity dilatation, aneurysm formation and cardiac malrotation were also assessed with ECT. Distinct ECT defects were demonstrated in 95 of a total of 235 LV segments (40%) and in 37 of 47 cases (85% of DMD, 71% of FSH, 50% of MT and 60% of LG). They were observed specifically in the posterior wall (82%) and the apex (65%) in DMD, and were scattered in all LV wall segments in FSH, LG, and MT. There was a significant correlation between %FIB and the L/M ratio (r = 0.79, p less than 0.001), and the L/M ratio was significantly higher in DMD than in MT (0.67 +/- 0.36 vs 0.34 +/- 0.25, p less than 0.05). ECT showed marked LV dilatation in seven (15%), apical aneurysm in five (11%) and vertical heart in 12 (26%) of the 47 patients. There were no significant correlations between age or clinical stage scores and numbers of defect segments or %FIB in each group. During the one-year follow-up period of these patients, a DMD boy with the largest %FIB (54%) and the highest L/M ratio (1.4) together with LV dilatation had complications of refractory heart failure and he died eight months following the ECT examination. Thallium-201 planar imaging and standard 12-lead ECG underestimated the perfusion defects which were evaluated with ECT.