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Biomedical subjects

H Asanoi

Publications and source records attributed to H Asanoi.

86 records · Page 5Linked to original sources
PubMed1988

[Effect of dobutamine on ventriculo-arterial coupling and ventricular work efficiency in patients with cardiac failure].

In nine patients with cardiac dysfunction (ejection fraction less than or equal to 50%), we evaluated the effects of dobutamine (5 micrograms/kg/min) on ventriculo-arterial coupling by monitoring direct arterial pressures and simultaneously-recorded M-mode echocardiograms guided with two-dimensional images. Left ventricular end-diastolic volume (EDV) and end-systolic volume (ESV) were calculated by the formula of Teichholz, and left ventricular end-systolic pressure (ESP) was approximately from the arterial dicrotic pressure. Arterial pressure was altered by phenylephrine or nitroprusside and the slope (Ees) and volume axis intercept (Vo) of the end-systolic pressure-volume relationship were determined as the contractile properties of the ventricle. The arterial system properties were expressed by the slope (Ea) of the end-systolic pressure-stroke volume relationships. Ees during dobutamine infusion was derived assuming that the Vo was unchanged from the baseline state. The left ventricular pressure-volume area (PVA), the sum of external work (EW) and end-systolic potential energy (PE), and ventricular work efficiency (EW/PVA) were determined from a time-varying elastance model. The EDV and ESV were significantly decreased by dobutamine (-4%, p less than 0.05; -22%, p less than 0.01), while the ESP and heart rate remained unchanged. Dobutamine increased the Ees markedly (+41%, p less than 0.01) and decreased the Ea (-23%, p less than 0.01). These changes resulted in a substantial decrease in the ratio of Ea to Ees (-44%, p less than 0.01). The EW was augmented (+22%, p less than 0.01), but the PE was reduced (-33%, p less than 0.01) by dobutamine, while the PVA remained the same as in the baseline state.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Importance of coronary collateral circulation for kinetics of serum creatine kinase in acute myocardial infarction.

The effect of coronary collateral perfusion on the kinetics of creatine kinase (CK) was examined in 32 patients undergoing intracoronary thrombolysis within 6 hours after the onset of a first acute myocardial infarction (AMI). Blood sampling for CK was performed every 2 to 4 hours for a period of 72 hours after AMI. The cumulative CK release was determined using the integrated appearance function curve with the individual disappearance rate. In 19 patients in whom thrombolysis was successful (group A), time to peak CK level was 11 +/- 1 (standard error of the mean) hours after AMI and cumulative CK release was 2,599 +/- 424 U/liter. In 6 patients who had a significant collateral circulation to the infarct-related coronary artery and unsuccessful reperfusion (group B), the time to peak CK was 16 +/- 1 hours (p less than 0.05 compared with group A) and cumulative CK release was 1,897 +/- 478 U/liter (difference not significant compared with group A). In the remaining 7 patients, with neither recanalization nor significant collateral perfusion group C, time to peak CK was 21 +/- 1 hours and significantly (p less than 0.05) longer than groups A and B. Cumulative CK release (2,707 +/- 776 U/liter) was not significantly different from groups A and B. Thus, collateral perfusion is an important determinant of the CK time-activity curve during AMI. Early peaking of CK levels does not reliably identify spontaneous or drug-induced recanalization of the infarct-related coronary artery.

Collateral Circulation↗
PubMed1987

Acute hemodynamic effects of a new inotropic agent (OPC-8212) in patients with congestive heart failure.

The acute effects of OPC-8212, a newly synthesized orally effective inotropic agent, were assessed clinically. Eleven patients with moderate congestive heart failure received a single mean dose of 6.5 mg/kg body weight of the drug. Eight hours after administration, the cardiac and stroke work indexes increased by 11% (p less than 0.01) and 20% (p less than 0.005), respectively, with concomitant decreases in the diastolic pulmonary artery (25%, p less than 0.005) and right atrial pressures (33%, p less than 0.01). There were no significant changes in blood pressure or heart rate. The contractile state of the left ventricle was also assessed by the shift of the Starling curve. To construct the function curve, lower body negative pressure was used to regulate the venous return to the heart. An inotropic effect of the agent was confirmed by the shift of this function curve upward and to the left, even when an augmentation of the cardiac output was masked by the marked reduction in preload. The hemodynamic and clinical effects of OPC-8212 were encouraging and the drug appears to be promising for the treatment of congestive heart failure.

Adult↗
PubMed1987

Importance of angina for development of collateral circulation.

The extent of collateral circulation in 46 patients who had intracoronary thrombolysis within six hours of the onset of acute myocardial infarction was evaluated. Patients who had had a previous myocardial infarction (4 cases) or who had spontaneously recanalized infarct related coronary arteries (5 cases) were excluded from the analysis. Collateral development was graded during coronary cineangiography according to the extent of opacification of the collateral and epicardial arteries distal to the site of occlusion (collateral index 0 to 3). Angina was considered to be present before myocardial infarction if it had occurred more than one week before acute myocardial infarction. Collateral channels were visible in only two of 19 patients without angina before infarction and nine of the 18 patients with angina before infarction. The prevalence of angina and the collateral index were not significantly influenced by the extent of coronary vessel disease. It is concluded that myocardial ischaemia is important in promoting collateral development in man as well as in laboratory animals.

Adult↗
PubMed1987

Effect of nicorandil on exercise performance in patients with effort angina: a multicenter trial using a treadmill exercise test.

The effects of a single oral dose (20 mg) of a new vasodilator, nicorandil, on exercise performance were assessed in 29 patients with stable effort angina using a symptom-limited treadmill exercise test. A single-blind, placebo-controlled, randomized, crossover design was employed. Compared with placebo, 20 mg of nicorandil significantly increased maximal exercise duration and time to 1 mm of ST-segment depression at 1, 3, and 6 h after administration. Systolic blood pressure was reduced both at rest and during exercise. Heart rate increase during exercise did not differ significantly compared with control, though resting heart rate was increased. The maximal pressure-rate product at peak exercise was increased in association with increased exercise time in about half of the patients, while it was unchanged or decreased in the others. It was suggested that nicorandil may act by either reducing myocardial oxygen demand and/or increasing myocardial oxygen supply.

Adult↗
PubMed1986

Acute hemodynamic effects of a new inotropic agent, OPC-8212, on severe congestive heart failure.

The hemodynamic and clinical effects of OPC-8212, a newly synthesized, orally effective inotropic agent, were assessed for the first time in ten patients with severe congestive heart failure by means of right heart catheterization with a Swan-Ganz catheter. Cardiac output was determined by the thermodilution technique. Patients received a single oral dose of 6 mg/kg. To determine the magnitude and time-course of the effects of OPC-8212, measurements were made during an observation period before and 2, 4, 8, and 12 h after administration. Blood was also taken at these times for measurement of the concentration of plasma OPC-8212. No large meals were allowed during the first 4 h. After the single oral dose of OPC-8212, plasma concentrations increased rapidly, reaching an effective level after 8 h and peaking at 12 h. Hemodynamic performance improved as the mean OPC-8212 plasma level increased, with the maximum effect being observed between 8 and 12 h after acute administration of the drug. At 8 h, the cardiac index was increased from the baseline value of 2.4 +/- 0.2 (SEM) to 2.8 +/- 0.3 1/min/m2 (P less than 0.01). The stroke work index rose from 26.2 +/- 5.1 to 31.7 +/- 60 g . m/m2. The excessive pulmonary artery diastolic pressure fell from 22 +/- 2 to 17 +/- 3 mmHg at 8 h (P less than 0.001) and to 16 +/- 2 mmHg (P less than 0.001) at 12 h. The incidence of ventricular premature beats was not increased and no other side effects were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1985

Modification of pacing-induced alterations in diastolic properties of the regional myocardium by nifedipine in patients with coronary artery disease.

The effects of nifedipine on regional dysfunction during pacing-induced ischemia were studied in eight patients with coronary artery disease. Single-plane left ventriculograms were obtained using a high-fidelity micromanometer-tipped catheter in the control and post-pacing periods both before and after pretreatment with nifedipine. All patients developed typical anginal pain during pacing tachycardia before but not after pretreatment with nifedipine. After pacing, left ventricular end-diastolic pressure (EDP) increased from 10 +/- 5 (SD) mmHg to 23 +/- 9 mmHg (P less than 0.01) with enlargement of the end-diastolic volume (EDV). The ejection fraction (EF) was reduced from 66 +/- 10% to 54 +/- 13% (P less than 0.05). With nifedipine, a post-pacing increase in EDP was markedly attenuated together with a 17% reduction in left ventricular systolic pressure (P less than 0.05). The regional myocardial function was expressed by a radial coordinate system with its origin at the center of gravity of the end-diastolic contour. Two representative radial grids for normal and ischemic segments were selected. In the normal segment, the end-diastolic length (EDL) was augmented by 14% (from 26.1 +/- 5.2 mm to 29.7 +/- 6.1 mm, P less than 0.01) associated with a 23% increase in stroke excursion (P less than 0.05) with pacing stress. In the ischemic segments, EDL remained unchanged in the post-pacing beat but stroke excursion was significantly reduced (from 11.4 +/- 5.2 mm to 4.3 +/- 1.8 mm, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Coronary angiographic findings in various types of unstable angina--study on the pathophysiology of unstable angina.

Coronary angiographic findings were studied in 129 patients with various types of unstable angina in order to clarify the pathophysiology of unstable angina. The subjects were divided into 3 types: effort angina (E), rest angina (R), and effort and rest angina (E+R), and each of these 3 types was subdivided into group I (new onset), II (recurrent) and III (changing pattern). 1) R had less severe coronary lesions than E or E+R. 2) Severity and distribution of coronary atherosclerotic lesions in unstable angina were similar to those in stable angina. 3) Incidence of coronary spasm is higher in unstable R and E+R than in stable R and E+R, respectively. 4) Unstable R and E+R with frequent attacks were associated with a higher frequency of coronary spasm and severe proximal coronary stenosis than those without frequent attacks, respectively. 5) Among unstable E+R-III (changing pattern), the patients who developed E+R from E showed significantly higher incidence of multiple vessel disease than those who developed E+R from R and significantly lower incidence of spontaneous spasm than those with E+R, who remained with the same pattern but in whom the frequency and/or the intensity of the attack increased, without any significant difference in the severity of coronary stenosis from other 2 subgroups. It is concluded that coronary spasm as well as severe coronary atherosclerotic lesions may be responsible for the unstable state of angina. Especially in R and E+R, coronary spasm is the most important factor responsible for the unstabilization of angina.

Adult↗
PubMed1981

Assessment of cardiac wall motion with the ejection fraction image: a comparison with contrast left ventriculography.

Twenty patients with ischemic heart disease were studied with biplane contrast left ventriculography and gated bloob pool scans. An ejection fraction (EF) image was calculated from each gated blood pool scan. The EF image and contrast ventriculograms were divided into three regions and seven segments respectively. The sites of asynergy observed in each study were compared. Segments two, three and six of the contrast ventriculogram corresponded to the anteroseptal and inferoapical regions of the EF image, but it was difficult to differentiate between these segments on the EF image. Segments three and four corresponded to the inferoapical region and segments five and seven corresponded to the posterolateral region. Diffuse asynergy with a low EF (less than 30%) causes a large defect on the EF image. The mean regional EF obtained from the EF image correlated well with the EF calculated from the left ventricular volume curve (n = 50, r = 0.94).

Angiocardiography↗
PubMed1981

Visualization of hypertrophied papillary muscle mimicking left ventricular mass on gated blood pool and T1-201 myocardial perfusion imaging.

A sixty-year old man with acute myocardial infarction was incidentally found to have a hypertrophied anterolateral papillary muscle (ALPPM) of the left ventricle on gated blood pool (GBP) and T1-201 myocardial perfusion images. Hypertrophy of the ALPPM was visualized as a movable defect in the lateral basal area on GBP imaging throughout the cardiac cycle and on the TI-201 study as a radionuclide accumulating structure, consistent with the defect in the GBP. A combination of these findings may suggest the presence of a hypertrophied papillary muscle of the left ventricle.

Cardiomyopathies↗