Search PubMed⌕ Search

Biomedical subjects

H Nonogi

Publications and source records attributed to H Nonogi.

At least 145 records · Page 8Linked to original sources
PubMed1988

Time course of regression of left ventricular hypertrophy after aortic valve replacement.

To assess the time course and extent of regression of myocardial hypertrophy after removal of the inciting hemodynamic stress, 21 patients with either aortic stenosis or aortic insufficiency were studied preoperatively, after an intermediate period (1.6 +/- 0.5 years), and late (8.1 +/- 2.9 years) after aortic valve replacement, and results were compared with those in 11 control patients. After aortic valve replacement there was significant hemodynamic improvement, with a fall in the left ventricular end-diastolic volume index (164 +/- 73 to 105 +/- 35 ml/m2, p less than .01), a fall in left heart filling pressure (19 +/- 9 to 12 +/- 5 mm Hg, p less than .01), and maintenance of the cardiac index (3.3 +/- 0.8 to 3.5 +/- 0.8 liters/min/m2, NS) and left ventricular ejection fraction (60 +/- 13% to 64 +/- 10%, NS). By the late study the cardiac index (4.0 +/- 0.6 liters/min/m2, p less than .01) and left ventricular ejection fraction (66 +/- 15%, p less than .05) had further increased and were significantly greater than before surgery. For the group as a whole, the left ventricular muscle mass index fell 31% after surgery by the time of the intermediate postoperative study (174 +/- 38 vs 120 +/- 29 g/m2, p less than .01), and a further 13% from the intermediate to the late study (105 +/- 32 g/m2, p less than .05). At the preoperative study left ventricular muscle mass index was greatest in those patients with aortic insufficiency (191 +/- 36 g/m2), and greater in those with aortic stenosis (158 +/- 33 g/m2) than in control subjects (85 +/- 9 g/m2, p less than .05). At the intermediate postoperative study left ventricular muscle mass index remained significantly higher in both those with preoperative aortic insufficiency (128 +/- 29 g/m2) and those with stenosis (114 +/- 27 g/m2) than in the control subjects (p less than .01). By the time of the late postoperative study there were no longer any significant differences in left ventricular muscle mass index. Thus, the regression of myocardial hypertrophy is a process that occurs over many years after correction of the primary hemodynamic abnormality. As this process of myocardial remodeling occurs, continued improvement in cardiac function may occur, and the improvement occurring between the intermediate and late postoperative studies at a slight but constant afterload excess (inherent in the relative stenosis of the aortic prosthesis) suggests that the hypertrophied myocardium is operating at a reduced level compared with normal myocardium.

Aortic Valve↗
PubMed1987

A multicenter study of a new inotropic agent, piperanometozine (OPC-8212) in congestive heart failure: clinical improvement during short-term treatment.

Piperanometozine (OPC-8212) is a new, orally effective inotropic agent. To evaluate the efficacy of this agent on systemic hemodynamics and clinical symptoms in patients with congestive heart failure, a multicenter study was performed. Thirty four patients with New York Heart Association (NYHA) functional classes II to IV and initially treated with digitalis were enrolled from ten centers. After a washout period of one or two weeks (placebo period), digitalis was replaced by piperanometozine (30 or 60 mg/day) for four weeks, while other drugs were continued. Clinical symptoms, routine physical findings, electrocardiogram, chest roentgenogram, echocardiogram, exercise tolerance time, and routine laboratory data were obtained in 34 patients. Four patients were withdrawn from the study before completion. After the withdrawal of digitalis, heart rate was increased and ejection fraction was decreased. Exercise tolerance time was increased while other parameters were unchanged. At the end of the treatment period with piperanometozine, ejection fraction significantly (p less than 0.05) increased with a decrease in LV end-systolic volume (p less than 0.05), whereas heart rate and blood pressure remained unchanged. Systolic blood pressure/LV end-systolic volume (P/V index) tended to decrease after the withdrawal of digitalis and increase during piperanometozine therapy. Exercise tolerance time was further increased (p less than 0.01) and NYHA functional class was improved in 11 patients, whereas it worsened in only one patient. No major adverse effects were observed. These results indicate that a short-term therapy of oral piperanometozine restored the depressed cardiac performance of the heart and improved clinical symptoms in patients with congestive heart failure. Thus, this promising agent deserves further clinical study in long-term trials.

Aged↗
PubMed1987

[Dynamics of cardiac output in patients with hypertrophic obstructive cardiomyopathy].

To characterise the duration of aortic flow velocity waveforms in hypertrophic obstructive cardiomyopathy (HOCM) the dynamics of aortic flow were investigated in 10 normals and 11 patients with hypertrophic obstructive cardiomyopathy performing 16-gated Doppler 2D-echocardiography of the ascending aorta. 16 flow velocities were recorded along the Doppler beam axis between the anterior and posterior aortic walls, and averaged over 8 beats. Flow times were derived from the flow curves and normalised by the ejection period as determined from the carotid pulse tracing. Thus, relative ejection time (% SEP) was calculated at the anterior (gate 4) and the posterior aortic wall (gate 13) as well as at the axis of the vessel (gate 9). In normals % SEP was 92 +/- 3% in gate 4, 95 +/- 4% in gate 9 and 93 +/- 3% in gate 13 (NS). In patients with HOCM % SEP was 92 +/- 5% in gate 4 and 83 +/- 4% (NS) in gate 9. At the posterior aortic wall (gate 13) % SEP amounted to 68 +/- 5% and was significantly lower than in gate 9 (P less than 0.05) and in gate 4 (P less than 0.001) respectively. It is concluded that in contrast to normals systolic flow time in hypertrophic obstructive cardiomyopathy varies along the sound beam in the ascending aorta. Flow time recorded at the posterior aortic wall is most abbreviated.

Blood Flow Velocity↗
PubMed1987

The relationship of afterload to ejection performance in chronic mitral regurgitation.

Simultaneous left ventricular micromanometry and biplane cineangiography were performed in nine control subjects (group 1), 14 patients with chronic mitral regurgitation and an ejection fraction of 57% or greater (group 2), and 13 patients with mitral regurgitation and an ejection fraction of less than 57% (group 3). End-diastolic volume index was increased in both groups with mitral regurgitation (p less than .001) compared with the control group. Left ventricular end-diastolic wall thickness did not differ among the three groups, but the left ventricular muscle mass index was greater in both groups with mitral regurgitation than in controls (p less than .001). End-diastolic pressure was elevated in both groups 2 and 3 compared with group 1 (p less than .05), but peak systolic, mean systolic, and incisural pressure were not different among the three groups. End-diastolic stress was larger in groups 2 and 3 than in group 1 (p less than .05). Muscle fiber stretch was greater in group 2 than in the control group (p less than .05) but was not different between the controls and group 3. End-systolic stress, determined as the circumferential stress at aortic valve closure, at the maximal pressure/volume ratio, or using a nonsimultaneous method, was larger in group 3 than in groups 1 and 2. Mean systolic stress was evaluated from aortic valve opening to aortic valve closure in all patients; mean stress from end-diastole to aortic valve closure and from end-diastole to minimum volume was assessed in mitral regurgitation alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Effects of pacing-induced ischemia on early left ventricular filling and regional myocardial dynamics and their modification by nifedipine.

The effect of pacing-induced ischemia on early left ventricular filling and regional myocardial lengthening was studied in 11 patients with coronary artery disease (CAD) and six control patients with normal coronary arteriograms. All of the 11 patients with CAD developed typical anginal pain during pacing tachycardia, and in the postpacing beat, the left ventricular end-diastolic pressure (LVEDP) rose from 13 +/- 4 to 26 +/- 4 mm Hg (mean +/- SD, p less than .01), the relaxation time constant increased from 43 +/- 9 to 59 +/- 7 msec (p less than .01), and the ejection fraction diminished from 62.1 +/- 6.7 to 51.6 +/- 10.6% (p less than .01). However, the peak rate of early left ventricular filling (LVPF) obtained from frame-by-frame analysis of left ventriculograms and the LVPF normalized for the stroke volume and for the end-diastolic volume did not change significantly. In the ischemic segment, the peak rate of lengthening (PL) decreased by 45% with ischemia, and the PL normalized for the end-diastolic segment length decreased by 42%. However, the PL normalized for the extent of systolic shortening did not change. In the control segment there was a tendency for these three variables to increase, but the changes were not statistically significant. The time difference from the PL to the LVPF increased significantly in the ischemic segment (31 +/- 28 vs 75 +/- 48 msec, p less than .05). Although the LVEDP rose slightly but significantly from 9 +/- 3 to 12 +/- 5 mm Hg (p less than .05) in the control patients in the postpacing beat, the other global hemodynamic variables and the variables of regional myocardial dynamics did not change. The administration of nifedipine in six patients with CAD resulted in the disappearance or diminution of anginal pain even with the same duration and rate of pacing and was associated with restoration of global systolic function and regional myocardial shortening and lengthening in the ischemic segment. In the control segment, the three variables of segmental lengthening increased with administration of nifedipine. Thus, the segmental myocardial lengthening rate decreased with ischemia due to a decrease in segmental shortening and impairment of myocardial distensibility. The LVPF did not decrease with ischemia despite impairment in isovolumetric relaxation, accentuation of asynchrony in left ventricular filling, and a decrease in the PL in the ischemic segment because of an increase in the PL in the nonischemic segment secondary to an increase in left ventricular filling pressure.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

An analysis of regional left ventricular function utilizing pressure-length relationship in patients with coronary artery disease.

Mechanisms related to increased left ventricular filling pressure associated with myocardial ischemia were studied in 13 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. All patients developed typical anginal pain during pacing tachycardia. Seven patients (group I) demonstrated no significant changes in ejection fraction (EF) and peak systolic pressure-end-systolic volume ratio (P/Ves) after rapid pacing. End-diastolic pressure (EDP), however, increased significantly from 14.9 +/- 4.9 to 24.4 +/- 8.5 mmHg (p less than 0.01). Six patients (group II) exhibited significant decreases in EF and P/Ves. Here again, EDP increased significantly from 14.0 +/- 7.6 to 28.0 +/- 7.7 mmHg (p less than 0.01). The regional myocardial function was expressed by a radial coordinate system with its origin at the center of gravity of the end-diastolic contour. In the normal segment, the end-diastolic length (EDL) was augmented by 13.6%, associated with a 22.4% increase in stroke excursion with pacing stress. In the ischemic segment, EDL remained unchanged, but stroke excursion was significantly reduced. The diastolic pressure-volume curve shifted directly upward or more to the right, while the diastolic pressure-length curve moved up on the single curve in the normal segment and shifted directly upward in the ischemic segment, so that pressure was higher at any given segment length in the ischemic segment, indicating regional alteration of the diastolic properties. Thus, an ischemic response to pacing tachycardia involves both systolic and diastolic impairment, but the latter is more sensitive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Relation between systolic and diastolic elastic muscle properties and the morphology of the hypertrophic pressure-loaded left ventricle].

According to Maxwell's model, left ventricular (LV) systolic elastic properties are characterized by a series-elastic element and LV diastolic properties by a parallel-elastic element. It is not known whether this functional concept is reflected by some morphological counterparts. In 12 patients with aortic stenosis (AS) before and 19 months after aortic valve replacement, and in ten controls, LV biplane volume and simultaneous high-fidelity pressure measurements were performed during diagnostic catheterization. The constant (k) of systolic myocardial stiffness was determined from LV peak wall stress, the maximum rate of systolic stress rise and instantaneous LV midwall circumferential fiber shortening rate at peak stress. The constant (k*; circ-1) of diastolic stiffness was assessed from the diastolic stress-stiffness relationship, using a viscoelastic model. In AS patients pre- and postoperative endomyocardial biopsies were taken to assess muscle fiber diameter, interstitial fibrosis and LV fibrous content. Systolic myocardial stiffness constant was 15 circ-1 in controls, 14 circ-1 in preoperative and 12 circ-1 in postoperative AS patients (P less than 0.01 vs. controls). Diastolic myocardial stiffness constant was 19 circ-1 in controls, 23 circ-1 in preoperative AS patients and increased slightly but not significantly to 33 circ-1 after valve replacement. Parallel to the postoperative decrease in systolic stiffness, muscle fiber diameter decreased significantly from 33 to 27 mu (P less than 0.05). The slight increase in diastolic stiffness was accompanied by a significant increase in interstitial fibrosis from 15% to 26% (P less than 0.05); LV fibrous content remained essentially unchanged after operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Stenosis↗
PubMed1986

Myocardial relaxation in atrial fibrillation.

Although myocardial contractility has been known to vary from beat to beat in atrial fibrillation, myocardial relaxation in this arrhythmia has not been investigated. In this study, left ventricular relaxation was examined in seven patients with atrial fibrillation (four with mitral valve disease, one with aortic regurgitation, one with secundum type atrial septal defect and one with apical left ventricular hypertrophy). The left ventricular pressure was measured with a micromanometer-tipped catheter and the time constant of isovolumic left ventricular pressure decline (the relaxation time constant) was calculated by means of exponential curve fitting from more than 20 consecutive beats in each patient. The maximal rate of rise of left ventricular pressure (dP/dt) and the relaxation time constant were examined in relation to the preceding RR interval (RR2) and to the ratio of the RR2 interval to the pre-preceding RR interval (RR2/RR1), and the correlation coefficients were obtained. The dP/dt correlated better with RR2/RR1 than with the RR2 interval (0.82 +/- 0.05 versus 0.48 +/- 0.2), but the relaxation time constant did not show any correlation with RR2/RR1 or the RR2 interval (0.03 +/- 0.21 and 0.06 +/- 0.21, respectively). The relaxation time constant was fairly constant in each patient even when the RR2 interval and RR2/RR1 varied greatly. Thus, relaxation in atrial fibrillation is independent of changes in contractility as seen in the relation between postextrasystolic relaxation and postextrasystolic potentiation of contractility.

Adult↗
PubMed1986

Altered platelet alpha 2 adrenoreceptor in acute myocardial infarction and its relation to plasma catecholamine concentrations.

Changes in platelet alpha 2 adrenoreceptors and their relation to plasma catecholamine concentrations were studied in 11 patients with acute transmural myocardial infarction. A radiolabelled alpha 2 adrenoreceptor antagonist, [3H]-yohimbine, was used to assay alpha 2 adrenoreceptors on platelet membranes, and plasma catecholamine concentrations were measured by high performance liquid chromatography. The number of platelet alpha 2 adrenoreceptors, the dissociation constant, and plasma noradrenaline and adrenaline concentrations were studied 6.6 (3.3) (mean (SD)) hours after the onset of acute myocardial infarction and one month later. The mean (SD) number of adrenoreceptors increased significantly from 94.5 (50.5) fmol/mg protein immediately after infarction to 157.0 (65.7) fmol/mg protein one month later. The dissociation constant, however, did not change significantly (4.33 (1.40) nmol/l vs 4.37 (1.22) nmol/l). Raised noradrenaline (5.60 (4.37) nmol/l) and adrenaline (0.28 (0.14) nmol/l) concentrations had fallen significantly to normal values (1.21 (0.67) and 0.09 (0.05) nmol/l respectively) a month after infarction. The decrease in the number of alpha 2 adrenoreceptors soon after infarction may be beneficial because such a change will reduce the strength of various reactions to catecholamines, such as vasoconstriction.

Aged↗
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↗
PubMed1985

Changes in diastolic properties of the regional myocardium during pacing-induced ischemia in human subjects.

Mechanisms related to alterations in the diastolic properties of the left ventricle during angina were studied in seven patients with coronary artery disease. Single plane left ventriculograms were obtained using a high fidelity micromanometer-tipped catheter in both the resting state and immediately after rapid cardiac pacing. In all patients, typical anginal pain developed with pacing stress. After atrial pacing, the left ventricular end-diastolic pressure increased from 10 +/- 3 to 21 +/- 7 mm Hg (+/- standard deviation) (p less than 0.005) regardless of the changes in the end-diastolic volume. The ejection fraction was reduced from 59 +/- 10 to 48 +/- 13% (p less than 0.05). The diastolic pressure-volume curves shifted upward in post-pacing beats in four patients, while in three the curves shifted more to the right. The regional myocardial function was expressed in quantitative terms by a radial coordinate system with the origin at the center of gravity of the end-diastolic silhouette. Two representative radial grids for normal and ischemic segments were selected. In the normal segment, the end-diastolic length was augmented by 15% (p less than 0.005) and was associated with a 24% increase in stroke excursion with pacing stress (p less than 0.05). The increase in diastolic pressure was accompanied by comparable increases in end-diastolic length, and the diastolic pressure-length relation moved up to the higher portion of the single curve. In the ischemic segment, the end-diastolic length remained unchanged in the post-pacing beat, but segment shortening was significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

[Interventricular septal configurations and motions in patients with hypertrophic cardiomyopathy by angled biventriculography].

Precise configurations and motions of the interventricular septum (IVS) in hypertrophied hearts were assessed using angled biventriculography (BVG) for eight patients with apical hypertrophic cardiomyopathy (AH), three with hypertrophic obstructive cardiomyopathy (HOCM), six with hypertrophic non-obstructive cardiomyopathy (HNCM) and four with hypertensive heart disease (HHD). Analysis was by the computer system, OSCON. The configurations of the IVS differed among the four groups: the thickness of the IVS increased gradually towards the apex in patients with AH; that of the upper IVS increased abnormally in patients with HOCM; that of the mid-IVS increased in patients with HNCM; and that of the IVS increased uniformly in patients with HHD. The segmental thickening of the IVS also differed in each of the four groups. Among them, a characteristic pattern of the segmental thickening of the IVS was evident in patients with HNCM. In addition, the relative contributions of the IVS to right and left ventricular contractions in patients with AH and HHD differed from those in patients with HOCM and HNCM. Briefly, IVS contractions contributed more to the left than to the right ventricle in patients with AH and HHD, but not in those with HOCM and HNCM. Although further study is necessary, it can be concluded that AH can be regarded as one type of hypertrophic cardiomyopathy, according to its IVS configuration and motion.

Adult↗
PubMed1984

Three-dimensional analysis of regional myocardial function in response to nitroglycerin in patients with coronary artery disease.

Biplane cineventriculography was performed at rest and after sublingual nitroglycerin in 13 patients with coronary artery disease. In six patients (responders), there was a significant increase in ejection fraction [40 +/- 5 to 52 +/- 4% (p less than 0.001)], while in the other seven (nonresponders), there was no alteration in ejection fraction. To evaluate the extent of regional myocardial response to nitroglycerin, the contractile pattern of the regional myocardium over the entire ventricular surface was analyzed using a computer-generated three-dimensional model. The spatial coordinates that define the elliptic ventricular surface on a given horizontal plane cross section of the chamber were determined by four counter values in the two orthogonal silhouettes. Then, 32 points at equal angles around the center of gravity of the end-diastolic cavity were generated to form the border image. Repetition of this process for 16 successive cross sections allowed for reconstruction of the ventricular surface by the sequence of 32 X 16 (512) points. The regional wall motion was expressed as the percent change of the radial length, drawn from the center of gravity to each surface point. There was significant heterogeneity in regional response to nitroglycerin. In the responders, the normally contracting area was significantly increased (from 16.5 +/- 16.0 to 36.2 +/- 14.9% of the total surface area, p less than 0.001), largely mediated by the greater improvement in segmental shortening of each graded contractile pattern relative to its deterioration. In the nonresponders, a lessening of the severe dysfunction of the given area was associated with significant deterioration of segmental shortening of the other normally contracting area (49.1 +/- 19.7% of the area with a contractile pattern of grade 5 had deteriorated, p less than 0.05). Thus, the ratio of the area with respective graded segmental shortening was virtually unchanged. These differences in response of the ischemic ventricle to nitroglycerin appeared to be related to the development of adequate coronary collateral vessels as well as to an interaction of changes in preload and afterload.

Cineradiography↗
PubMed1984

Analysis of asynchronous wall motion by regional pressure-length loops in patients with coronary artery disease.

The progression of regional dysfunction during angina pectoris was studied in eight patients with coronary artery disease. Single plane left ventriculograms were obtained using a high fidelity micromanometer-tipped catheter both at rest and immediately after rapid cardiac pacing. Each image of the left ventriculogram was digitized and transferred to a computer. The boundary of the ventricular cavity was automatically determined and sequentially superimposed. Regional shortening was quantified by a radial coordinate system originating at the center of gravity of the end-diastolic silhouette. Thirty-two radial grids were drawn around the center of gravity, and the length of each radial grid was measured to characterize the centripetal motion of a given surface point. Each radial length was then plotted simultaneously and continuously against left ventricular pressure to generate a pressure-length loop. The area of the pressure-length loop provided an index of regional myocardial work. In the ischemic ventricle, the loops exhibited a striking deformity in configuration. Prolonged relaxation of ischemic segments was associated with outward motion of the normal segments. Shortening of the normal segment occurred earlier than that of the ischemic segment associated with its stretch. Thus, the loops of the two areas inclined in opposite directions. Pacing stress increased the magnitude of hypofunction in the potentially ischemic area, the average extent of shortening being reduced by 30% and the segmental work by 25% (p less than 0.005). In the normal area, contrary to the significant increase in segmental shortening (20% above control values [p less than 0.005]), the average segmental work remained at 7% below control values because of an augmented deformation of the loop.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1984

Unusual vasomotor coronary arterial responses after reversal of ergonovine induced spasm with glyceryl trinitrate.

Unusual vasomotor responses in the coronary arteries occurred in two patients after the administration of glyceryl trinitrate to relieve spasm induced by ergonovine maleate. In one patient after treatment with glyceryl trinitrate and despite dilatation of the adjoining segments a new severe reduction in diameter occurred distally to the segments of the right coronary artery where the ergonovine induced spasm developed. In the other patient the left anterior descending artery filled very slowly after the completely occlusive spasm of the right coronary artery had resolved with glyceryl trinitrate though the circumflex did not. These vasomotor changes were associated with chest discomfort and electrocardiographic abnormalities in both cases. These findings indicate that caution is needed when performing provocative tests even after the ergonovine induced spasm has been reversed with glyceryl trinitrate.

Adult↗
PubMed1984

Intravenous left ventriculography utilizing digital subtraction technique.

To detect the left ventricular boundary in the intravenous ventriculography, we used a subtraction technique for background suppression. Images containing contrast medium and reference mask images were transferred to a computer through a flying spot scanner and stored on the digital disc. Stored reference mask images were subtracted from the digitized contrast images. The resulting images were then electronically enhanced to extract the left ventricular (LV) image. The LV boundary was delineated with an algorithm we have developed and the volume of the LV cavity was calculated automatically. The validity of this method was compared with data obtained from conventional left ventriculogram (LVG). In 11 patients, values for end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (EF) calculated from the intravenous LVG were correlated closely with those from the conventional LVG (128 +/- 38 (SD) vs 133 +/- 39 ml, r = 0.95; 50 +/- 28 vs 53 +/- 30 ml, r = 0.98; 63 +/- 10 vs 62 +/- 12%, r = 0.96, respectively). Nine patients with valvular regurgitation were followed up serially after valve replacement. EDV index fell significantly after corrective surgery (145 +/- 50 to 81 +/- 33 ml/m2, p less than 0.02), whereas, EF was affected variably depending upon the preoperative state (58 +/- 13 to 61 +/- 11%, not significant). Thus, this method is less invasive than conventional LVG and has successfully allowed for sequential determination of ventricular function on an outpatient basis.

Adult↗
PubMed1984

[Assessment of cardiac function by left heart catheterization: an analysis of left ventricular pressure-volume (length) loops].

The mechanical property of the cardiac muscle has been classically analyzed in two ways; shortening of muscle fiber, and the development of tension within the muscle. In the ejecting ventricle, left ventricular (LV) function can be analyzed by the analogous two-dimensional framework of pressure-volume loops, which are provided by plotting the instantaneous volume against corresponding LV pressure. The integral pressure with respect to volume allows to assess a total external ventricular work during ejection. The diastolic pressure-volume relations reflect a chamber stiffness of the ventricle. Force-velocity relations also provide an useful conceptual framework for understanding how the ventricle contracts under given afterload, with modification of preload. In the presence of coronary artery disease, the regional nature of left ventricular contractile function should be defined as well as the global ventricular function as described above, because the latter is determined by the complex interaction of dysfunction of the ischemic myocardium and of compensatory augmentation of shortening of the normally perfused myocardium. We utilized a computer technique to analyze the local wall motion of the ischemic heart by cineventriculography. The boundaries of serial ventricular images are automatically traced and superimposed using the external reference system. Radial grids are drawn from the center of gravity of the end-diastolic image. Measurement of length of each radial grid throughout cardiac cycle provides the analysis of movement of the ventricle at a particular point on the circumference. Using phasic pressure obtained simultaneously with opacification as the common parameter, segmental pressure-length loops are constructed simultaneously at various segments. The loops are similar over the entire circumference in the normal heart, being rectangular in morphology and with synchronous behavior during contraction and relaxation. However, the marked distortion of pressure-length loops with clockwise rotation or figure of eight inscription is observed in the ischemic segments. Systolic work of the ischemic segment diminishes dramatically, and the loops exhibit varying degrees of inclination. The control segment loops also show an inclination to the opposite direction of the ischemic loops. These differences are presumably related to the local redistribution of the myocardial tension during systole in the ischemic ventricle. Thus, the method described should be of particular value in assessing the regional myocardial function in the ischemic ventricle and effects of various interventions which modify ischemia.

Cardiac Catheterization↗