Non-uniform and non-linear end systolic pressure-length relations at low left ventricular pressures in anaesthetised cats

STUDY OBJECTIVE--The aims were (1) to establish a basis for measurements of regional inotropy using the slope (E) of the linear part of the end systolic pressure-length relation; (2) to investigate the range of end systolic pressure where linearity is valid, and particularly its lower pressure limit, called turning point pressure; (3) to determine whether local myocardial inotropy measured by normalised slope, E(n), varies with segment orientation DESIGN--Pressure and two cross oriented segment lengths were measured in the left ventricle. One pair of crystals measured a longitudinal segment, aligned with anterior midwall fibre direction; another pair measured a transverse segment, aligned with endocardial and epicardial fibre direction. Temporary obstruction of the inferior caval vein and descending aorta were performed to produce a wide pressure range of end systolic pressure-length relations during basal as well as high inotropic states (isoprenaline). SUBJECTS--Seven open chest cats anaesthetised with sodium pentobarbitone and nitrous oxide were used. MEASUREMENTS AND MAIN RESULTS - Turning point pressure for longitudinal segments showed lower values than for transverse segments (p less than 0.05). With isoprenaline, turning point pressure increased for all transverse segments, at 103(SEM 8) v 153(19) mm Hg (p less than 0.05), whereas no change occurred for longitudinal segments, at 82(4) v 87(7) mm Hg. In the basal state, E(n) showed lower values in all longitudinal segments compared to transverse segments, except for one pair. E(n) of all segments increased during isoprenaline infusion, except in one segment where no change occurred. CONCLUSIONS - There is a lower limit for linearity of end systolic pressure-length relations; this is affected by segment orientation as well as by the inotropic state of the heart. E(n) as a measure of regional inotropy varies with segment orientation, but offers a local measure of changes in inotropic state.     

Effects of changes in coronary stenosis on left ventricular diastolic filling assessed with pulsed Doppler echocardiography

To determine the effects of changes in coronary stenosis on left ventricular diastolic filling, diastolic filling was serially examined before and after percutaneous transluminal coronary angioplasty using pulsed Doppler echocardiography in 50 patients with stable exertional angina pectoris. Peak rapid filling velocity and the ratio of peak atrial filling to peak rapid filling velocities were measured from the transmitral flow velocity pattern before and 2 and 9 days after coronary angioplasty. Peak rapid filling velocity increased and the ratio of peak atrial filling to peak rapid filling velocities decreased gradually after coronary angioplasty. The improvement in left ventricular diastolic filling was greater in patients with severe (greater than 90%) coronary stenosis than in patients with mild (less than or equal to 90%) coronary stenosis. In the long-term follow-up period, the improved left ventricular diastolic filling worsened in only 11 patients with marked progression to greater than 90% coronary stenosis. Thus, left ventricular diastolic filling improved gradually after coronary angioplasty, possibly reflecting post-ischemic "stunned" myocardium. Serial examinations of left ventricular diastolic filling with pulsed Doppler echocardiography may be a means of noninvasively assessing the temporal changes in the coronary stenosis and predicting the occurrence of coronary restenosis after coronary angioplasty.     

Changes of left ventricular diastolic function in exercising dogs without and with ischemia

Left ventricular (LV) diastolic function in the absence and presence of regional ischemia was examined in eight conscious dogs chronically instrumented with ultrasonic devices for measuring LV wall thickness and volume. During treadmill exercise, ischemia was induced (hydraulic occluder) to produce less than 10% systolic wall thickening in the ischemic zone. LV filling was assessed by the peak filling rate (PFR), mean filling rates in the first and second halves of filling (mFR1 and mFR2), an early filling index from mitral valve opening to minimal diastolic pressure (PDm), and the percentage of atrial filling. Also, LV relaxation (tau) and wall thinning rates during isovolumetric relaxation and the first and second halves of the filling phase were assessed. During control exercise without ischemia, PDm decreased by 2.61 mm Hg (p less than 0.05) to -1.1 mm Hg and there was a downward shift of the entire LV diastolic pressure-volume (P-V) curve. The LV relaxation rate, PFR, mFR1, and mFR2 were enhanced. Early filling was increased by 116%, the percentage of atrial filling by 118%, and overall diastolic filling by 23% despite a 63% decrease in the filling period. During ischemic exercise, systolic function was depressed compared with the resting state, PDm increased by 4.84 mm Hg (p less than 0.005) associated with a pronounced rightward and upward shift of the early portion of the P-V curve. LV relaxation rate, PFR, and mFR1 were reduced, the early filling index fell sharply by 62% but percentage of atrial filling was unchanged, while overall diastolic filling decreased by 30%. The thinning rate of the control wall was enhanced, whereas that of ischemic wall was depressed. Multiple factors contributed to the markedly impaired early and overall diastolic LV filling during ischemia, including impaired systolic function, reduced relaxation rate, nonuniformity of wall motion, an upward shift of the early diastolic P-V curve, and absence of a compensatory increase in late diastolic filling.     

Mitral stenosis with high left ventricular diastolic pressure.

Three patients with mitral stenosis are described, in whom the haemodynamic findings at cardiac catheterisation were more suggestive of left ventricular myocardial disease, in that the left ventricular diastolic pressure was high and the mitral valve gradient small. However, their echocardiograms showed abnormal wall movement during diastole characteristic of severe inflow obstruction, with slow and protracted filling, and at operation mitral stenosis was confirmed. Left ventricular wall stress was estimated throughout the cardiac cycle in one patient, and the diastolic stress-strain relation shown to be abnormal. The effects of mitral stenosis on left ventricular function are complex, and are not explicable simply by reduction in size of the mitral orifice.     

Mitral stenosis with high left ventricular diastolic pressure.

Three patients with mitral stenosis are described, in whom the haemodynamic findings at cardiac catheterisation were more suggestive of left ventricular myocardial disease, in that the left ventricular diastolic pressure was high and the mitral valve gradient small. However, their echocardiograms showed abnormal wall movement during diastole characteristic of severe inflow obstruction, with slow and protracted filling, and at operation mitral stenosis was confirmed. Left ventricular wall stress was estimated throughout the cardiac cycle in one patient, and the diastolic stress-strain relation shown to be abnormal. The effects of mitral stenosis on left ventricular function are complex, and are not explicable simply by reduction in size of the mitral orifice.     

Effects of isometric exercise on the diastolic function in patients with severe aortic stenosis with or without coronary lesion

BACKGROUND: There is no literature evaluating the effect of exercise on patients with aortic stenosis, in which patients with and without coronary artery disease were assessed separately. OBJECTIVE: To assess the effects of isometric exercise on the diastolic function in patients with aortic stenosis (AS). METHODS: 18 patients with AS, and 5 control patients were studied (group 1, G1). Patients with AS were divided in: group 2 (G2, n=10), without coronary lesion, and group 3 (G3, n=8), with coronary lesion. All patients underwent cardiac catheterization and performed isometric exercise until heart rate increased 32+/-9%. Left ventricular systolic pressure and end diastolic pressure (LVEDP), t1/2 (relaxation index), and the +dP/dt(max) were all measured. RESULTS: The +dP/dt(max) increased in G1, G2, and G3 during exercise returning to their basal values once exercise had concluded. While exercising, the LVEDP increased in G1, G2 and G3, returning to its original baseline value only in G1 and G2. The t1/2 increased, while exercising, in G2 and G3, and continued to be elevated after the exercise in both groups although it was only statistically significant in G3. The control group did not show significant changes. CONCLUSIONS: Isometric exercise decreases relaxation rate and increases LVEDP in patients with AS. After exercise, relaxation and LVEDP remained altered only in the patients with coronary lesion. The alteration in lusitropism and increased LVEDP after exercising suggest the presence of stunned myocardium.     

Changes in left ventricular diastolic function in coronary artery disease with and without angina pectoris assessed from exercise ventriculography

In 11 normals and 43 patients with coronary artery disease left ventricular (LV) diastolic pressure–volume (P–V) curves were obtained from biplane ventriculograms and simultaneous high fidelity pressure measurements. During exercise ventriculography 20 patients had angina pectoris (group B), and 16 patients were asymptomatic (group A). At rest there were no akinetic segments in 28 patients (group C), and an akinetic segment was found in 15 (group D). With different total work loads (951 ± 134 and 2100 ± 245 kpm in groups B and A), LV minimal and end-diastolic pressures and corresponding ventricular volumes increased to a similar extent in patients with and without angina during exercise ventriculography. With comparable work loads (1,296±221 and 1,494±195 kpm in groups C and D) the mean increase in diastolic pressure and volume was larger in group D, which corresponded to the more depressed LV resting function. Shifts in the diastolic P–V relationship with exercise were quantitated from the constants a and b of the linear log P–V relationship. In the control group, a and b did not change significantly, but in all CAD groups a significant decrease in a and a significant increase in b were observed during exercise. These changes were more pronounced in groups B and D, but were statistically significant in group A, too. While no patient with angina had an unchanged diastolic P–V relationship, as many as 12 patients had significant P–V shifts in the absence of angina. Eight of these were expected to develop myocardial ischemia with exercise as judged from their coronary artery stenosis and ventriculograms. A similar correlation was found for the diastolic P–V alterations and the exercise ECG. Fourteen patients without any ST-segment change during exercise showed significant P–V shifts, while no patient with signs of ischemia in the ECG had an unchanged P–V curve. We conclude that LV diastolic function is more sensitive to myocardial ischemia than both angina pectoris and the exercise ECG. An inappropriate increase in LV filling pressure with exercise probably reflects myocardial ischemia even in the absence of angina pectoris and ST-segment depression in the ECG.     

Effects of coronary venous pressure on left ventricular diastolic distensibility

Coronary arterial pressure and flow are known to influence left ventricular (LV) diastolic distensibility, but the influence of coronary venous pressure is unknown. To test the hypothesis that increased coronary venous pressure leads to an increase in LV wall volume and a decrease in LV diastolic distensibility, we studied excised, blood-perfused LV isovolumic dog hearts without the pericardium. In protocol I (n = 8), to raise coronary venous pressure the pressure of right atrium (RA) and right ventricle (RV) was increased by the height of a blood reservoir connected with a cannula that opened in both the RA and RV. In protocol II (n = 7), to isolate the effect of RV enlargement on LV diastolic distensibility (direct ventricular interaction), an isovolumic RV balloon was used with coronary venous pressure held constant at 0 mm Hg. Changes in LV diastolic distensibility were assessed by shifts of the LV end-diastolic pressure-volume relation. Changes in LV wall volume were detected by subepicardial segment length at end-diastole. The mean pressures of RA and RV (protocol I) and RV balloon only (protocol II) were increased from 0 to 15 and 30 mm Hg over a range of LV volume. In protocol I, when RA.RV pressure was increased from 0 to 30 mm Hg at three levels of LV volume (22 +/- 2, 31 +/- 3, and 40 +/- 3 ml), LV end-diastolic pressures increased significantly from 5.2 +/- 0.3 to 11.2 +/- 1.5, from 10.4 +/- 0.3 to 18.2 +/- 1.2, and from 20.2 +/- 1.0 to 28.8 +/- 1.2 mm Hg, respectively. In protocol II, when RV balloon pressure was increased from 0 to 30 mm Hg at the three LV volumes (21 +/- 3, 31 +/- 3, and 41 +/- 4 ml), LV end-diastolic pressures showed smaller increases from 5.2 +/- 0.2 to 6.6 +/- 0.2, from 9.8 +/- 0.3 to 11.6 +/- 0.6, and from 19.0 +/- 0.5 to 21.4 +/- 0.8 mm Hg, respectively. In both protocols, the LV end-diastolic pressure-volume relation shifted upward in a nearly parallel fashion, but the shift was much greater in protocol I than in protocol II. Despite constant LV volume, an increase in LV wall dimension in protocol I was significant and much greater than that in protocol II. From these results, we conclude that increased coronary venous pressure decreases LV diastolic distensibility with increasing LV wall volume, and this mechanism appears to act independently of diastolic ventricular interaction caused by RV enlargement.     

Effects of transluminal coronary angioplasty on left ventricular systolic and diastolic function at rest and during exercise

The left ventricular global and regional systolic function, ventricular volumes, and peak diastolic filling rate (PDFR) were studied in 30 patients with coronary artery disease, before and 2 to 5 days after transluminal coronary angioplasty (PTCA), utilizing equilibrium radionuclide angiography at rest and during exercise. At rest, the global ejection fraction (EF) was unchanged before (60 ± 9%) and after PTCA (62 ± 10%). During exercise, global EF increased from 59 ± 11% pre PTCA to 67 ± 10 post PTCA (p < 0.001). Twenty-two patients had abnormal EF response to exercise pre PTCA, versus seven post PTCA (p < 0.001). Improvements in exercise regional EF paralleled the changes in global EF. End-systolic volume was unchanged at rest but decreased significantly with exercise post PTCA (60 ± 36 ml pre vs 49 ± 32 ml post PTCA, p < 0.01). At rest, the PDFR was unchanged post PTCA (2.4 ± 0.9 end-diastolic volume (EDV)/sec pre vs 2.5 ± 0.8 EDV/sec post). During exercise, PDFR increased from 2.1 ± 0.7 EDV/sec pre PTCA to 2.5 ± 0.7 EDV/sec post PTCA (p < 0.02). In conclusion, in patients with coronary artery disease, successful PTCA improves global and regional systolic function during exercise. Diastolic function is improved during exercise, a fact not previously demonstrated.     

Load dependence of left ventricular diastolic pressure-volume relations during short-term coronary artery occlusion.

We evaluated the effect of altered loading conditions on left ventricular (LV) diastolic pressure-volume relations during acute coronary artery occlusion that was produced by inflation of an intracoronary balloon. Open-chest anesthetized dogs (n = 18) were instrumented so that LV pressure (micromanometer) and LV volume (conductance) could be measured without disturbing the pericardium. The effects of brief periods of occlusion (1-2 minutes) were assessed under steady-state conditions before and after dextran infusion with the pericardium present and absent and during vena caval occlusion. Under steady-state conditions before dextran infusion with the pericardium removed, at an LV end-diastolic pressure (EDP) of 8.4 +/- 1.4 mm Hg, occlusion resulted in a rightward shift in the diastolic portion of the LV pressure-volume loop (delta LVEDP, 2.7 +/- 2.3 mm Hg; delta LVEDV, 6.3 +/- 4.7 ml, both p less than 0.05 versus control). After dextran infusion (LVEDP, 20.9 +/- 6.0 mm Hg), occlusion resulted in a rightward and upward shift in the diastolic portion of the LV pressure-volume loop (delta LVEDP, 5.8 +/- 4.4 mm Hg; delta LVEDV, 4.2 +/- 3.0 ml, both p less than 0.05 versus control). At low cardiac volumes before dextran infusion, the intact pericardium did not affect the response to occlusion. By contrast, after dextran infusion in the presence of an intact pericardium, LVEDP significantly increased (delta, 6.4 +/- 3.6 mm Hg, p less than 0.05) but LVDEV did not (delta, 0.7 +/- 1.5 ml, p = NS). There was a parallel upward shift in the diastolic portion of the LV pressure-volume loop that was eliminated by removal of the pericardium. Thus, the change in LV diastolic pressure and volume during occlusion varied and depended on the baseline cardiac volume and presence of the pericardium. Before dextran infusion with the pericardium present and absent, coronary artery occlusion did not alter the LV diastolic chamber stiffness parameter, which was calculated from the diastolic interval of an averaged steady-state beat (0.040 +/- 0.019 versus 0.036 +/- 0.015 mm Hg/ml, p = NS). After dextran infusion with the pericardium present and absent, coronary artery occlusion increased the LV diastolic chamber stiffness parameter (0.057 +/- 0.034 and 0.074 +/- 0.034 mm Hg/ml, both p less than 0.05 versus controls, respectively). Vena caval occlusion eliminated the shifts in the diastolic portion of the LV pressure-volume loop with the pericardium present and absent.(ABSTRACT TRUNCATED AT 400 WORDS)     

Influence of aortic stenosis on the hemodynamic importance of coronary artery narrowing in dogs without left ventricular hypertrophy

Coronary hemodynamic effects of controlled left ventricular outflow obstruction stimulating aortic valve stenosis were studied in 20 open-chest dogs, with and without graded coronary artery diameter narrowing. Aortic stenosis was regulated so that a mean left ventricular-aortic pressure gradient of 46 +/- 20 mm Hg (mean +/- standard deviation) was created as both heart rate and stroke volume were unchanged. In addition, during aortic stenosis, mean aortic pressure (105 +/- 17 to 84 +/- 15 mm Hg, p less than 0.05) and diastolic pressure time index/systolic pressure time index ratio (1.2 +/- 0.3 to 0.6 +/- 0.2, p less than 0.05) decreased and end-diastolic left ventricular pressure (7 +/- 4 to 14 +/- 6 mm Hg, p less than 0.05) increased. With no coronary narrowing, mean coronary flow increased during aortic stenosis (53 +/- 23 to 62 +/- 23 ml/min) as the percentage of diastolic flow increased (83 +/- 6 to 89 +/- 4) and endocardial/epicardial ratio decreased (1.14 +/- 0.16 to 0.95 +/- 0.24) (all p less than 0.05). Peak reactive hyperemic flow also decreased (168 +/- 85 to 125 +/- 73 ml/min, p less than 0.05). This value with no coronary narrowing was similar to peak hyperemic flow with 60% narrowing without aortic stenosis. With 90% coronary narrowing, mean coronary flow decreased with or without aortic stenosis. Transmural flow distribution also decreased but was lower during aortic stenosis (0.86 +/- 0.19 to 0.61 +/- 0.25, respectively; p less than 0.05). These data suggest that although mean coronary flow is increased during aortic stenosis, endocardial flow may be limited, and coronary reserve exposed during reactive hyperemia appears decreased. When a coronary artery is narrowed, aortic stenosis has an even more important hemodynamic influence on the coronary circulation.     

Influence of right ventricular hemodynamics on left ventricular diastolic pressure-volume relations in man.

To clarify the mechanism of displacement of the left ventricular diastolic pressure-volume function with alteration of loading conditions, the effects of nitroglycerin on pressure-volume relations in 13 patients were compared with those of amyl nitrite in 13 other patients during cardiac catheterization. After nitroglycerin, average systemic mean arterial pressure declined by 15.1 mm Hg (17%) and left ventricular end-diastolic pressure by 9.4 mm Hg (49%); right ventricular systolic and end-diastolic pressures fell 11.6 mm Hg (36%) and 5 mm Hg (41%), respectively. In all patients diastolic pressure-volume curves were significantly displaced downward and leftward. After amyl nitrite, average systemic mean arterial pressure fell 20.1 mm Hg (22%), but left ventricular end-diastolic pressure and right ventricular systolic and end-diastolic pressures were not significantly reduced. No significant displacement of diastolic pressure-volume curves occurred. Both the rate constant of the exponentially fit diastolic pressure-volume curve, and the rate of diastolic isovolumic relaxation (T) were unchanged after each drug. Thus downward displacement of diastolic pressure-volume functions after nitroglycerin appears to be dependent more upon reduction of right ventricular filling dynamics than coronary perfusion pressures. More favorable effects upon left ventricular function may be associated with reduction of both left ventricular filling pressures and systemic impedance (reflecting both "preload" and "afterload") than of systemic arterial pressures ("afterload") alone.     

Systemic and left ventricular responses to exercise stress in asymptomatic patients with valvular aortic stenosis.

Patients with heart disease may have myocardial ischemia or left ventricular (LV) dysfunction without symptoms. The exercise responses of 14 asymptomatic patients with valvular aortic stenosis (AS) were studied using treadmill testing, thallium-201 scintigraphy and radionuclide angiography. Compared with age- and gender-matched control subjects, patients with AS demonstrated reduced exercise tolerance (10.7 +/- 2.5 vs 13.3 +/- 4.2 min; p = 0.06) and maximal oxygen consumption (26.7 +/- 6.3 vs 36.3 +/- 9.5 ml O2/min/kg; p = 0.004) associated with decreased peak systolic blood pressure response to exercise (177 +/- 18 vs 214 +/- 42 mm Hg; p less than 0.004). Ten of 14 patients developed ST-segment depression during exercise, only 3 of whom had reversible thallium defects. Patients with AS tended to have greater LV ejection fractions at rest (65 +/- 11 vs 58 +/- 7; p = 0.08) and significantly decreased early peak filling rates (4.8 +/- 1.3 vs 6.1 +/- 0.6 stroke volume/s; p = 0.003) compared with those of control subjects. During maximal supine exercise, patients with AS had less of an increase in ejection fraction (2 +/- 9 vs 15 +/- 7%; p less than 0.001) associated with a decrease in end-diastolic (-7 +/- 15 vs +5 +/- 16%; p = 0.06) and stroke (-6 +/- 17 vs +30 +/- 13%; p less than 0.001) volumes from baseline measurements.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impaired regional diastolic distensibility in coronary artery disease: relations with dynamic left ventricular compliance

The regional left ventricular distensibility and its relations with the dynamic left ventricular chamber compliance were studied in 11 normal subjects and in 30 patients with coronary artery disease. The regional peak filling rates were calculated from angiographic data in eight ventricular segments and used as an index of regional distensibility. A depressed global peak filling rate was observed in only 30% of the patients with angina pectoris, but regional abnormalities in peak filling rate were detected in 75% of these patients. A relation between alterations in regional peak filling rate and left ventricular compliance was evident in these patients. Despite comparable end diastolic volume and pressure (10 +/- 2 mm Hg vs. 10 +/- 3 in normal subjects; not significant), the patients with angina pectoris, whose ventricle had at least three segments with a reduced peak filling rate, had indeed significant increases in mean left ventricular filling pressure (14 +/- 4 mm Hg vs. 8 +/- 3 in normal subjects; p less than 0.01) and upward shifts of their left ventricular pressure-volume relation during rapid filling. Conversely, an increase in regional peak filling rate produced by intravenous administration of the calcium antagonist nicardipine in a subgroup of patients with poor diastolic function was accompanied by a reduction in mean left ventricular filling pressure and by a downward shift of the early diastolic left ventricular pressure-volume relation. It is concluded that even in the absence of clinical signs of ischemia and of a previous myocardial infarction, large areas with impaired distensibility are frequently present in patients with angina pectoris.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of critical coronary stenosis on global systolic left ventricular function quantified by pressure-volume relations during dobutamine stress in the canine heart

Objectives. In this study we quantified the effects of a critical coronary stenosis on global systolic function using pressure-volume relations at baseline and during incremental dobutamine stress.Background. The effects of coronary stenosis have previously been analyzed mainly in terms of regional (dys)function. Global hemodynamics are generally considered normal until coronary flow is substantially reduced. However, pressure-volume analysis might reveal mechanisms not fully exposed by potentially load-dependent single-beat parameters. Moreover, no systematic analysis by pressure-volume relations of the effects of dobutamine over a wide dose range has previously been presented.Methods. In 14 dogs left ventricular volume and pressure were measured by conductance and micromanometer catheters, and left circumflex coronary flow by Doppler probes. Measurements in control and with left circumflex stenosis were performed at baseline and at five levels of dobutamine (2.5 to 20 μg/kg/min). The end-systolic pressure-volume relation (ESPVR) dP/dt_MAX− vs. end-diastolic volume (dP/dt_MAX− V_ED) and the relation between stroke work and end-diastolic volume (preload recruitable stroke work [PRSW]) were derived from data obtained during gradual caval occlusion.Results. In control, dobutamine gradually increased heart rate up to 20 μg/kg/min, the inotropic effect blunted at 15 μg/kg/min. With stenosis, the chronotropic effect was similar, however, contractile state was optimal at approximately 10 μg/kg/min and tended to go down at higher levels. At baseline, the positions of ESPVR and PRSW, but not of dP/dt_MAX− V_ED, showed a significant decrease in function with stenosis. No differences between control and stenosis were present at 2.5 μg/kg/min; the differences were largest at 15 μg/kg/min.Conclusions. Pressure-volume relations and incremental dobutamine may be used to quantify the effects of critical coronary stenosis. The positions of these relations are more consistent and more useful indices than the slopes. The positions of the ESPVR and PRSW show a reduced systolic function at baseline, normalization at 2.5 μg/kg/min and a consistent significant difference between control and stenosis at dobutamine levels of 5 μg/kg/min and higher.     

Effects of direct-current electrical shocks on systolic and diastolic left ventricular function in dogs

Although direct-current (DC) electrical shocks do not significantly alter left ventricular systolic performance, their effects on ventricular diastolic properties and the role of sympathetic stimulation in maintaining postshock contractility are unknown. Accordingly, we studied both diastolic and systolic left ventricular performance in seven open-chest dogs before and after three consecutive 50 joule DC shocks applied directly to the heart. High-fidelity left ventricular pressure and segmental dimensions were recorded as pressure was varied systematically under conditions of beta-adrenergic blockade. The exponential left ventricular end-diastolic pressure-segment length relationship was not significantly altered by electrical shocks. Likewise, pre- and postshock beats matched for loading conditions did not differ in peak positive dP/dt, end-systolic segment length, or percentage of segment shortening, although mean normalized shortening rate decreased by approximately 11% (p less than 0.05). However, the time constant (T) for isovolumic pressure fall, an index of the rate of left ventricular relaxation, increased after shocks in all animals (T = 42.2 +/- 5.3 and 51.1 +/- 7.0 msec before and after shock, respectively; (p less than 0.01). We conclude that high-energy electrical shocks applied directly to the heart cause modest slowing of left ventricular relaxation but do not have important effects on left ventricular compliance or on systolic myocardial performance. These data suggest that DC shocks have only minor functional consequences when applied to normal hearts, even when sympathetic compensation is prevented.     

Relation between left ventricular diastolic function and exercise tolerance in patients with left ventricular dysfunction

Previous studies show no correlation between resting systolic left ventricular performance assessed as the ejection fraction and exercise tolerance. This study examined the relation between left ventricular diastolic performance and exercise tolerance in 63 patients with left ventricular dysfunction (ejection fraction less than 50%) due to known or suspected coronary artery disease. The 51 men and 12 women, aged 54 +/- 8 years (mean +/- standard deviation), underwent symptom-limited upright exercise testing on a bicycle ergometer. The exercise end-points were angina (n:5), dyspnea (n:16), and fatigue (n:42). The patients were divided into three groups: group 1 (n:28) with normal exercise tolerance (9.5 +/- 2.4 minutes), group 2 (n:18) with mild exercise intolerance (5.8 +/- 0.5 minutes), and group 3 (n:17) had severe exercise intolerance (3.7 +/- 0.9 minutes). The three groups did not differ in age, ejection fraction, end-diastolic volume, exercise end-point, exercise heart rate, and left ventricular peak filling rate at rest. The exercise peak filling rate was, however, significantly higher in group 1 (p = 0.03). Stepwise multivariate discriminant analysis of important variables identified the exercise peak filling rate as the only predictor of exercise tolerance (F = 6.0). Thus, variation in exercise peak filling rate may in part explain the variability of exercise tolerance in patients with left ventricular dysfunction; patients with preserved exercise capacity have higher exercise peak filling rate than those with exercise intolerance.     

左室造影时左室舒张末期压力的改变与左室功能状态的关系 50例冠状动脉造影分析

本文分析了50例冠状动脉造影病人左室造影前后左室舒张末期压力的变化与室壁运动、左室功能、冠状动脉病变程度之间的关系。发现左室舒张末期压力的变化与左室电影造影时观察到的室壁运动障碍的程度密切相关;与双维超声心动图所见的室壁节段性运动异常有一定的相关性;与冠状动脉病变无直接关系;与超声射血分数之间无正相关,本文还探讨了左室舒张末期压力改变的直接影响因素是左室收缩顺应性障碍,这可从左室dp/dt的变化得到证实。