Importance of regurgitant fraction for left ventricular end-systolic wall stress to end-systolic volume ratio in patients with chronic mitral regurgitation

End-systolic wall stress to end-systolic volume index (ESWS/ESVI) ratio is an index of myocardial contractility. In the presence of mitral regurgitation (MR), this ratio may be modified by the unloading effect of a leakage of flow into the low pressure left atrium. Therefore, to evaluate whether or not this ratio is an index of myocardial function in patients with MR, we compared the ratio with conventional measurements of myocardial performance in 11 patients with moderate to severe MR. The ESWS/ESVI ratio was 3.9 +/- 1.6 kdyn/cm5 per m2 in MR and slightly lower than the control value of 4.6 +/- 0.6 kdyn/cm5 per m2. The correlation between ESWS/ESVI ratio and ejection fraction was poor (r = 0.05, p:NS), while there was a close inverse correlation between the ratio and regurgitant fraction (r = 0.76, p less than 0.01). These results strongly suggest that ESWS/ESVI ratio is a better indicator of myocardial function than ejection fraction in MR; however, this ratio could be affected by not only the inotropic state of the ventricle, but also by the extent of mitral regurgitation.     

The immediate effects of isosorbide dinitrate on right ventricular function in patients with acute hypoxemic respiratory failure. A combined invasive and radionuclide study

We administered 20 mg of isosorbide dinitrate sublingually to 16 patients with acute hypoxemic respiratory failure (ARF) complicated by pulmonary artery hypertension (PAH) and evaluated its effects 20 to 30 min later using a combination of invasively measured pressures and flows and ECG-gated cardiac scintigraphy. We measured the right and left ventricular ejection fractions and a simultaneous thermodilution stroke volume index; we then calculated respective end-diastolic (EDVI) and end-systolic (ESVI) volume indexes. An initially depressed mean right ventricular ejection fraction (RVEF) increased modestly after the administration of isosorbide dinitrate (35 +/- 10 to 41 +/- 10%; p less than 0.02), whereas both the mean right ventricular end-diastolic (-27 +/- 50 ml/M2; p less than 0.04) and end-systolic (-27 +/- 44 ml/M2; p less than 0.03) volume indexes fell. The RVEF increased in 11 of 16 patients: within this subgroup, a decrease in the RVEDVI and RVESVI was associated with a decrease in both cardiac index (delta 0.3 L/min/M2) and LVEDVI (delta -15 +/- 21 ml/M2; p less than 0.01); hence, O2 delivery also fell (delta -36 +/- 56 ml/min/M2; p less than 0.05). In some patients with ARF complicated by PAH, sublingually administered nitrates may improve right ventricular systolic function when globally depressed. However, left ventricular "pump" function appears to be depressed when a concurrent depression in right ventricular "pump" function ensues.     

Quantitative evaluation of left ventricular systolic function using bidimensional echocardiography: comparison with cineangiography

The aim of the study was to compare the evaluation of the left ventricular systolic function performed both by angiography and 2D-echocardiography on 80 subjects (31 with coronary artery disease, 18 with left ventricular volume overload, 10 with left ventricular pressure overload, 14 with mitral valve disease and 7 normal controls). The 2D-echocardiograms of the left ventricle with simultaneous measurement of the right arm systolic blood pressure was performed within 24 hours of the angiographic examination. The following parameters were obtained using the two methods: end-diastolic volume index, end-systolic volume index, ejection fraction, left ventricular mass index, mass/volume ratio, end-systolic circumferential stress, contractility expressed as end-systolic circumferential stress/end-systolic volume ratio; the end-systolic circumferential stress/ejection fraction ratio was calculated only by 2D-echocardiography. The afterload and contractility were not calculated in subjects with coronary artery disease and left ventricular outflow gradient. No statistically significant differences were shown between the two methods, except a slight under-estimation by echocardiography of the angiographic end-diastolic volume index (93.1 +/- 38.9 ml/m2 vs 115 +/- 39.9 ml/m2; p less than 0.01) and over-estimation of the mass/volume ratio (1.38 +/- 0.33 g/ml vs 1.2 +/- 0.44 g/ml; p less than 0.01) was shown between the two methods for all parameters. A depressed contractile state was also demonstrated by the end-systolic circumferential stress/ejection fraction ratio. The inter and intraobserver variability was 6.6 +/- 4.4% (range 0.16%) and 4.2 +/- 3% (range 1.11%) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Maintenance of exercise stroke volume during ventricular versus atrial synchronous pacing: role of contractility

Although atrial synchronous and rate-responsive ventricular pacing have been compared, the importance of maintaining synchronized atrial systole in addition to rate responsiveness has been incompletely defined. That is, the effects of these two pacing modes on cardiac volumes and contractility have not been studied. Accordingly, 16 patients with normal ventricular function were studied while in the upright position and at rest with gated radionuclide ventriculography during both atrial synchronous and ventricular pacing. Twelve of these patients were also studied during low-level upright exercise (300 kilopond-meters). Rest and exercise ventricular pacing heart rates were matched to those recorded with synchronous pacing. Ventricular volumes were determined with a counts-based method. The ejection fraction and peak systolic pressure/end-systolic volumes or contractility between the two pacing modes. However, during exercise to identical heart rates, blood pressures, and workloads, although stroke volume was the same during exercise with atrial synchronous and ventricular pacing (78 +/- 13 vs 75 +/- 12 ml), end-diastolic and end-systolic volumes were lower with ventricular pacing than with atrial synchronous pacing (end-diastolic volume 101 +/- 13 vs 113 +/- 16 ml, p less than .001; end-systolic volume 26 +/- 4 vs 35 +/- 7 ml, p less than .001). Stroke volume during ventricular paced exercise was maintained at atrial synchronous pacing levels by means of increased contractility (ejection fraction of 74 +/- 4% during ventricular pacing vs 69 +/- 5% during atrial synchronous pacing, p = .002; peak systolic pressure/end-systolic volume ratio of 6.51 +/- 1 during ventricular pacing vs 4.85 +/- 1 during atrial synchronous pacing, p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Preservation of left ventricular performance with reduced ischemic dysfunction by intravenous nisoldipine

The effect of intravenous nisoldipine on cardiac performance was examined during pacing-induced ischemia in 14 patients with coronary artery disease. The relative contributions of afterload reduction or prevention of myocardial ischemia were assessed using load-independent global (peak-systolic pressure/end-systolic volume) and regional (peak-systolic pressure/end-systolic radial length) "contractile" indexes. Nisoldipine decreased aortic pressure (predrug, 109 +/- 14 vs postdrug, 88 +/- 13 mm Hg, p less than 0.01) and prevented elevation of left ventricular end-diastolic pressure during rapid atrial pacing (predrug, 7.9 +/- 5.7 vs postdrug, -0.5 +/- 4.9 mm Hg, p less than 0.001). Resting cardiac index (predrug, 3.3 +/- 0.6 vs postdrug, 4.2 +/- 0.7 liters/min/m2, p less than 0.05), and left ventricular ejection fraction (predrug, 68.1 +/- 9.0 vs postdrug, 74.2 +/- 9.4%, p less than 0.05) increased after nisoldipine, which also prevented the deterioration in left ventricular ejection fraction (predrug, -8.1 +/- 7.9 vs postdrug, -1.0 +/- 3.7%, p less than 0.05) and fractional radial shortening (predrug, -8.7 +/- 13.1 vs postdrug, 3.7 +/- 16.4%, p less than 0.01) during rapid atrial pacing. Under these conditions, nisoldipine preserved myocardial function, as determined by global peak-systolic pressure/end-systolic volume (predrug, -0.82 +/- 0.39 vs postdrug, 0.17 +/- 1.54 mm Hg/ml, p less than 0.05) and regional (peak-systolic pressure/end-systolic radial length, predrug, -23.8 +/- 36.1 vs postdrug, 12.7 +/- 36.3 mm Hg/cm, p less than 0.01) "contractile" indexes. Intravenous nisoldipine maintains ventricular performance during rapid atrial pacing via a combination of systemic vasodilation and amelioration of ischemic myocardial dysfunction.     

An improved index of left ventricular function in chronic mitral regurgitation

The ratio of end-systolic wall stress (ESWS) to volume index (ESVI) has been proposed as a useful index of left ventricular (LV) function in chronic mitral regurgitation (MR). However, although this ratio reflects isometric contraction, the chronic changes in LV architecture caused by MR may affect its usefulness. An index was evaluated that incorporated the ejection fraction--(TVEF [tension-volume ejection fraction] = ESWS/ESVI X EF)--thus combining both isometric and ejection phase parameters. Forty patients with symptomatic MR but no other valvular or coronary disease had valve replacement between 1980 and 1984. Twenty-nine patients (group A) were in New York Heart Association class I or II postoperatively. The remaining patients (group B) were in class III or IV or died. Four preoperative LV function indexes were compared. The means of all indexes in groups A and B were significantly different, but only TVEF completely separated the groups. A TVEF of less than 1.47 uniformly predicted a poor operative outcome.     

Prognostic setting and bloodless hemodynamic evaluation of acute myocardial infarct with equilibrium radioisotopic ventriculography

Forty-four consecutive patients with acute myocardial infarction were studied with equilibrium radionuclide angiography (RNA) within 24 hours from the onset of symptoms, three days after admission and three days before hospital discharge (14 +/- 3 days). To assess the prognostic value of RNA derived parameters we assessed: the ejection fraction (EF), the left ventricular end-systolic volume index (ESVI), the left ventricular end-diastolic volume index (EDVI), the cardiac index (CI), the stroke volume index (SVI) and the peak systolic pressure/end-systolic volume index ratio (PSP/ESVI); we also determined Peel's prognostic index (PI) on admission and measured systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and cardiac frequency (CF) as the same time as the radioisotopic parameters were taken. Thirty-nine patients were discharged without signs of ventricular failure with and without medical treatment (group A), 5 died during hospitalization (group B). Using EF alone, we obtained a very clear distinction between the two groups (Group A 43 +/- 12%; Group B 22 +/- 3%; p less than 0.005). Stepwise, multivariate analysis showed that, by linking PSP/ESVI to EF, we can even obtain a function that correlate better with hospital survival (F = 0.09832 X EF - 0.32035 X PSP/ESVI - 3.12981; p less than 0.002). There was good exponential correlation between EF and PSP/ESVI (r = 0.781) and this would seem to confirm that PSP/ESVI is a more sensitive contractility index for patients with a not very depressed EF.     

Pulmonary hypertension and right ventricular function in patients with COPD

In 100 patients with chronic obstructive pulmonary disease (COPD), we found no significant correlation between simultaneous measurements of right ventricular ejection fraction, using radionuclide ventriculography, and pulmonary arterial pressure. There was, however, a weak but significant correlation between right ventricular ejection fraction and the pulmonary vascular resistance (r = 0.40, p less than 0.005). In 52 of these patients, 37 with pulmonary hypertension, right ventricular end-systolic volume index was 53 +/- 21 ml.m-2 and end-diastolic volume index was 86 +/- 27 ml.m-2, compared with a calculated mean of 33 ml.m-2 and 79 ml.m-2, respectively, for normal subjects. In 24 of these patients where the measurements were made at rest and on exercise, the mean right ventricular end-systolic volume increased from 66 +/- 20 ml.m-2 to 87 +/- 32 ml.m-2, with an increase in right ventricular systolic pressure from 28 +/- 9 mm Hg to 55 +/- 15 mm Hg. Analysis of the slope of the right ventricular end-systolic pressure volume relationship at rest and on exercise suggested relatively normal right ventricular contractility in the majority of patients. Thus, in these patients with stable COPD, despite the presence of pulmonary hypertension, right ventricular contractility remained relatively normal.     

Effects of intravenous isradipine on left ventricular performance during rapid atrial pacing in coronary artery disease

The effects of isradipine, a new dihydropyridine calcium antagonist, were evaluated in 24 patients referred for elective cardiac catheterization because of suspected coronary artery disease. Hemodynamics and left ventricular (LV) function (by digital subtraction angiography) were measured at baseline and during rapid atrial pacing (mean peak heart rate 135 beats/min), which induced chest pain or electrocardiographic changes in all patients. After a control pacing period, intravenous isradipine (0.01 mg/kg, n = 16) or placebo (n = 8) was administered in a double-blind fashion and all variables were measured again at baseline and during pacing to the same maximum heart rate. Before isradipine was given, pacing had no effect on systolic blood pressure, while increasing diastolic blood pressure (68 +/- 8 to 87 +/- 11 mm Hg, p less than 0.0001) and LV end-diastolic pressure measured in the immediate postpacing period (13 +/- 5 to 18 +/- 6 mm Hg, p less than 0.03) and decreasing LV end-diastolic volume index (59 +/- 18 to 40 +/- 12 ml/m2, p less than 0.001), stroke volume index (37 +/- 11 to 23 +/- 10 ml/m2, p less than 0.0001), ejection fraction (0.64 +/- 0.07 to 0.53 +/- 0.12, p less than 0.0003) and percent regional shortening in 4 of 5 myocardial wall segments. During pacing after isradipine, systolic and diastolic blood pressures were lower, ejection fraction was higher and percent regional shortening decreased in only 2 of 5 myocardial segments. In comparison to placebo, isradipine increased baseline heart rate, ejection fraction and stroke volume index while it decreased arterial pressure and end-systolic volume index before the second pacing period.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of rapid atrial pacing on left ventricular ejection fraction in patients without organic heart disease

Pacing-induced decrease of left ventricular ejection fraction (LVEF) in patients with coronary artery disease has been proposed as a sign of myocardial ischemia, whereas a slight increase or no change is speculated to be the normal response to rapid atrial pacing. The studies of the pacing-induced effects in normals, however, are of limited value, because of either inhomogeneous patient population or different, mainly non-invasive, methods for determination of LVEF. It was therefore the aim of the present study to assess the pacing-induced changes of left ventricular ejection fraction in a homogeneous group of patients. In 10 patients (mean age: 48 +/- 2 years) with normal coronary arteriograms and normal LV-function at rest, rapid atrial pacing was performed stepwise to a maximal pacing rate of 150 beats per minute. In all patients left ventricular end-diastolic pressure LVEDP and time constant of relaxation period tau decreased, while the parameter of contractility Max Dp/dt increased due to increase in heart rate. Furthermore, there was no limited coronary reserve or myocardial lactate production during atrial stimulation as a sign of pacing-induced ischemia. In all patients biplane ventriculography was performed at rest and during maximal stimulation. While end-diastolic volume index EDVI decreased in every patient (71 +/- 5----42 +/- 4 ml/m2, p less than 0.005) and systolic volume index did not change (17 +/- 2----14 +/- 2 ml/m2, N.S.), there was a significant decrease of ejection fraction from 75 +/- 2 to 66 +/- 3% (p less than 0.005). Basal heart rate, age, sex or basal ejection fraction did not influence the response of ejection fraction to rapid atrial pacing. Even after drug-induce afterload reduction there was a significant pacing induced decrease of ejection fraction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular performance in patients with coexistent mitral stenosis and aortic insufficiency

Isolated mitral stenosis and isolated aortic insufficiency impose unique and opposite loading conditions on the left ventricle. To assess these combined effects, hemodynamic and angiographic factors were compared among normal subjects and patients with isolated mitral stenosis, isolated aortic insufficiency or combined mitral stenosis and aortic insufficiency. Left ventricular end-diastolic volume index was lower in patients with combined lesions and severe or moderate aortic insufficiency than in patients with isolated severe or moderate aortic insufficiency (138 +/- 19 versus 206 +/- 20 cc/m2 and 87 +/- 5 versus 145 +/- 22 cc/m2, respectively) (p less than 0.05 for both). Left ventricular end-diastolic and end-systolic volume indexes were normal in two-thirds of patients with combined lesions and moderate or severe aortic insufficiency, whereas these indexes were high in all but one patient with isolated moderate or severe aortic insufficiency. Among patients with moderate or severe aortic insufficiency, 8 of 14 with isolated insufficiency had a reduced ejection fraction or circumferential fiber shortening rate compared with 5 of the 9 patients with combined lesions. Among patients with isolated aortic insufficiency, left ventricular end-systolic wall stress and end-diastolic and end-systolic volume indexes were higher (p less than 0.05) in those with reduced ejection performance than in those with normal ejection performance. These variables did not differ between patients with reduced or normal ejection performance in the group with combined lesions. The contractile index (ratio of end-systolic wall stress to end-systolic volume index) was significantly depressed in patients with severe aortic insufficiency in the groups with isolated aortic insufficiency or combined lesions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular adaptations to intense swim training in sedentary middle-aged men and women

Central and peripheral cardiovascular adaptations to 12 weeks of intense swim training were characterized in 12 previously sedentary middle-aged men and women. Peak oxygen uptake (VO2) during upright bicycle exercise improved from 29.2 +/- 5.6 to 34.7 +/- 6.7 ml/kg/min (mean +/- SD, p less than .01) because of similar increases in peak cardiac output (CO) and calculated arteriovenous oxygen difference (both p = .02). Peak supine VO2 was 10% higher after training (p less than .005) solely because of enhanced CO (p = .005). Peak heart rate decreased in both postures; therefore stroke volume at peak exercise was greater by 10% and 18% in the upright and supine postures, respectively (p = .05 and p = .005). There was an identical 18% rise (p = .01) in peak supine left ventricular end-diastolic volume index by radionuclide ventriculography but no change in left ventricular ejection fraction or end-systolic volume index (ESVI). Peak systolic blood pressure (SBP) was unchanged in the upright posture but was 8% higher (p = .002) during recumbency despite a similar total peripheral resistance and SBP/ESVI ratio. Maximal calf conductance (Gmax), assessed separately by venous occlusion plethysmography after local ischemic exercise to fatigue, was augmented 20% (p less than .02) by training, resulting in an 18% greater hyperemic blood flow (p = .05). Peak VO2, CO, and Gmax were unchanged in five nonexercising control subjects. We conclude that in middle-aged humans, intense swim training for 12 weeks produces adaptations that include a greater capacity for vasodilatation in skeletal muscle and an enhanced cardiac pump capacity.     

Left ventricular myocardial remodeling and contractile state in chronic aortic regurgitation

BACKGROUND: In chronic aortic regurgitation, eccentric hypertrophy, with combined concentric hypertrophy of the left ventricle, is an important adaptive response to volume overload, which in itself is a compensatory mechanism for permitting the ventricle to normalize its afterload and to maintain normal ejection performance (physiologic hypertrophy). However, progressive dilatation of the left ventricle leads to depressed left ventricular (LV) contractility and myocardial structural changes, including cellular hypertrophy and interstitial fibrosis (pathological hypertrophy). HYPOTHESIS: The study was undertaken to determine the relationship between left ventricular myocardial structure and contractile function in 14 patients with chronic aortic regurgitation by cardiac catheterization and endomyocardial biopsies. METHODS: Myocardial cell diameter and percent interstitial fibrosis were obtained from biopsy samples. Contractile function was evaluated from the ratio of end-systolic wall stress to end-systolic volume index (ESS/ESVI) and the ejection fraction-end-systolic stress (EF-ESS) relationship, which was obtained from 30 normal control subjects. RESULTS: Myocardial cell diameter correlated significantly with the ESVI (r = 0.72, p < 0.005), ejection fraction (r = -0.58, p < 0.05), and ESS/ESVI (r = -0.58, p < 0.05). The percent interstitial fibrosis also correlated inversely with ESS/ESVI (r = -0.71, p < 0.005). Compared with very few patients with an ESVI < 70 ml/m2, the majority of patients with ESVI > or = 70 ml/m2 had a cell diameter of > or = 30 microns and a percent interstitial fibrosis of > or = 10%. The nine patients who had depressed contractile function, as assessed from the EF-ESS relationship, had a higher percent interstitial fibrosis (p < 0.05) than five patients showing a normal EF-ESS relationship, despite the fact that there was no significant difference in myocardial cell diameter between them. Thus, advanced cellular hypertrophy and excessive interstitial fibrosis were significantly and independently associated with myocardial contractile dysfunction and appeared to be responsible for ventricular remodeling. CONCLUSION: Our findings suggest that in many patients with aortic regurgitation, eccentric hypertrophy changes its nature from physiologic to nonphysiologic during the earlier stages in the course of the disease rather than during the stage described previously.     

Myocardial contractility and left ventricular function in obese patients with essential hypertension

Although the risk of developing congestive heart failure increases in parallel with the degree of obesity, load-dependent indexes of left ventricular function are found to be reduced in patients with morbid obesity only. We used the ratio of end-systolic wall stress to end-systolic volume index, which is load-independent, to assess myocardial contractility in 23 nonobese, 28 mildly obese and 26 moderately obese patients with mild to moderate essential hypertension. Although load-dependent indexes (i.e., ejection fraction, fractional fiber shortening and velocity of circumferential fiber shortening) were similar in the 3 groups, end-systolic wall stress to end-systolic volume index was lower in the moderately obese group (2.63 +/- 0.4, p less than 0.002) and even in the mildly obese group (2.88 +/- 0.8, p less than 0.05) than in the nonobese group (3.27 +/- 0.7). Further, there was a significant inverse relation between end-systolic wall stress to end-systolic volume index and body mass index (r = -0.34, p less than 0.005), diastolic diameter (r = -0.56, p less than 0.001) and left ventricular mass index (r = -0.55, p less than 0.001). Some obese patients have depressed myocardial contractility when compared with lean patients despite well-preserved pump function.     

Impaired left ventricular functional reserve in hypertensive patients with left ventricular hypertrophy

To determine whether patients with hypertension and especially those with left ventricular hypertrophy have subtle changes in cardiac function, we measured the increase in left ventricular ejection fraction and in systolic blood pressure to end-systolic volume index ratio with exercise in 40 hypertensive patients and 16 age-matched normotensive volunteers. Twenty-two hypertensive patients without hypertrophy had normal end-systolic wall stress at rest and exercise responses. In contrast, the 18 patients with echocardiographic criteria for left ventricular hypertrophy demonstrated a significant increase in end-systolic wall stress at rest compared with normal subjects (69 +/- 16 vs. 55 +/- 15 10(3) x dyne/cm2, p less than 0.05) despite having normal resting left ventricular size and ejection fraction. In patients with left ventricular hypertrophy, the increase in ejection fraction with exercise was less than in the normotensive control subjects (7 +/- 7 vs. 12 +/- 8 units, p less than 0.05), and delta systolic blood pressure to end-systolic volume with exercise was reduced (3.3 +/- 3.8 vs. 8.3 +/- 7.7 mm Hg/ml/m2, p less than 0.05). The hypertensive patients with hypertrophy displayed a shift downward and to the right in the relation between systolic blood pressure to end-systolic volume ratio and end-systolic wall stress compared with control subjects and hypertensive patients without left ventricular hypertrophy. Thus, hypertensive patients with left ventricular hypertrophy by echocardiography and normal resting ejection fraction exhibit abnormal ventricular functional responses to exercise. This finding may have implications in identifying patients at higher risk for developing heart failure.     

Effect of coronary artery bypass grafting on left ventricular response to isometric exercise

The left ventricular (LV) response to isometric exercise was evaluated in 20 patients who performed handgrip exercise tests before and 3 months after coronary artery bypass grafting. Preoperative LV ejection fraction (EF) decreased during the handgrip test from 0.57 +/- 0.08 to 0.49 +/- 0.09 (p less than 0.001); the ratio between the LV peak systolic pressure (PSP) and end-systolic volume index (ESVI) did not change. In 12 patients with patent grafts, the LVEF after operation did not change (0.54 +/- 0.06 at rest and 0.56 +/- 0.06 during handgrip exercise) and PSP/ESVI ratio increased from 4.5 +/- 1.5 to 5.6 +/- 2.1 mm Hg/ml X m-2 (p less than 0.001) during exercise. In 8 patients with occluded grafts, the LVEF after operation decreased from 0.56 +/- 0.10 to 0.48 +/- 0.06 (p less than 0.02), whereas PSP/ESVI did not change during handgrip exercise. Thus, the LV response to isometric handgrip exercise appears to improve after coronary artery bypass grafting in patients with patent grafts, but not in patients with 1 or more occluded grafts.     

Preoperative left ventricular function: minimal requirement for successful late results of valve replacement for aortic regurgitation

Postoperative survival and left ventricular function were studied in 62 patients who underwent aortic valve replacement for isolated, chronic aortic regurgitation between 1978 and 1985. The average follow-up period was 3.8 years. There were three in-hospital and six late deaths. Five (56%) of the nine postoperative deaths were of cardiac-related causes. The mean 7 year survival rate was 83 +/- 5%. Preoperative left ventricular end-systolic volume index was the most important indicator (p less than 0.001) for subsequent cardiac death. The 6.5 year survival rate was 92 +/- 4% for patients with an end-systolic volume index less than 200 ml/m2 compared with 51 +/- 16% for those whose index was greater than 200 ml/m2. None of the 48 patients with an end-systolic volume index less than 200 ml/m2 died of cardiac-related causes. Twenty-three of the 48 patients with an end-systolic volume index less than 200 ml/m2 (Group 1) and 6 of the 12 patients with a higher index (Group 2) underwent repeat catheterization 26 months postoperatively. Preoperative afterload, assessed by end-systolic wall stress, was elevated in both groups, but decreased postoperatively, becoming identical to the afterload in 20 normal control subjects. Although the preoperative ejection fraction was depressed in both groups, the great majority of patients in Group 1, compared with none in Group 2, exhibited normal ejection fraction postoperatively. Thus, in patients who recently underwent surgery for aortic regurgitation, satisfactory late results in both long-term survival and reversal of left ventricular dysfunction were obtained when the preoperative end-systolic volume index was less than 200 ml/m2.     

Effect of positive end-expiratory pressure on right ventricular performance. Importance of baseline right ventricular function

Thirty-six patients with diverse baseline right ventricular function were evaluated during incremental positive end-expiratory pressure (PEEP) application. Right heart pressures, cardiac output, right ventricular ejection fractions, and ventricular volumes were obtained at each PEEP level. Right ventricular peak systolic pressure-end-systolic volume relations were analyzed as an index of contractile function. Patients with severely depressed baseline right ventricular ejection fractions (30 percent or less) had an increase in end-diastolic (270 +/- 74 to 391 +/- 76 ml, 0 to 20 cm water (H2O) PEEP, p less than 0.05) and end-systolic volumes (210 +/- 70 to 321 +/- 70 ml, 0 to 20 cm H2O PEEP, p less than 0.05). These patients also had a decline in estimated right ventricular contractile function at 20 cm H2O PEEP as estimated by the slope of systolic pressure-volume relations (0.12 to 0.04 mm Hg/ml, 0 to 15 and 15 to 20 cm H2O PEEP, respectively, p less than 0.05). Patients with normal (40 percent or more) or moderately depressed (31 to 40 percent) baseline right ventricular ejection fractions had no change in right ventricular volumes or estimated contractile function. Therefore, the effect of PEEP on right ventricular function differs depending on the baseline right ventricular ejection fraction.     

Left ventricular pressure/volume relationship in aortic regurgitation

In this study we examined the left ventricular pressure/volume relationship in 39 patients with moderate or severe aortic regurgitation (AR) and 15 normal subjects. The patients with AR were divided into two groups; patients with normal resting ejection fraction (EF greater than or equal to 50%, group I, n = 21) and patients with abnormal EF (group II, n = 18). The patients in group I were younger (p less than 0.005), exercised to a higher workload, and had better exercise tolerance than patients in group II (p less than 0.01). The patients' exercise heart rate and blood pressure were not significantly different between the two groups. During exercise tests nine patients in group I and seven patients in group II had normal EF response (greater than or equal to 5% increase) (p = NS). The peak systolic blood pressure to end-systolic volume index ratio (SBP/ESVI) was higher in normal subjects than in patients in groups I and II, at rest it was (4.3 +/- 1.0 vs 2.6 +/- 1.2 vs 1.6 +/- 0.8, respectively, p less than 0.0001) and during exercise it was (7.6 +/- 1.8 vs 4.2 +/- 1.4 vs 2.6 +/- 1.3, respectively, p less than 0.0001). The resting SBP/ESVI ratio was below the lower normal limit in 12 patients (57%) in group I and in 16 patients (89%) in group II. Also, the exercise SBP/ESVI ratio was below the lower normal limit in 17 patients (81%) in group I and all of the patients (100%) in group II. Multivariate discriminant analysis identified the change in SBP/ESVI (F = 34.8) and resting end-diastolic volume (F = 6.7) as independent predictors of the EF response to exercise. Thus, most patients with AR, including those with normal resting EF or normal EF response to exercise, have abnormal SBP/ESVI at rest or during exercise.     

Noninvasive measurement of the rest and exercise peak systolic pressure/end-systolic volume ratio: a sensitive two-dimensional echocardiographic indicator of left ventricular function

Thirty-five patients with previous myocardial infarction and 25 normal subjects underwent subcostal view two-dimensional echocardiography at rest and at peak up-right bicycle exercise. The purpose was to assess changes in left ventricular volume with maximal upright bicycle exercise and to compare the utility of the peak systolic pressure/end-systolic volume index ratio and ejection fraction as indicators of left ventricular function. With exercise, normal subjects had a decrease in end-systolic volume index (22 +/- 8 to 11 +/- 3 ml/m2) (p less than 0.001); the normal ejection fraction (59 +/- 9 to 72 +/- 8%, p less than 0.001) and the pressure/volume ratio (6 +/- 3 to 18 +/- 6, p less than 0.001) increased. In patients with prior myocardial infarction there was no change in end-systolic volume index, ejection fraction or pressure/volume ratio with exercise. Although at peak exercise significant differences between normal subjects and patients with prior infarction were demonstrated in end-systolic volume index (p less than 0.001), ejection fraction (p less than 0.001) and pressure/volume ratio (p less than 0.001), the pressure/volume ratio provided sharper delineation between the two groups than did ejection fraction. The exponential relation of the pressure/volume ratio and ejection fraction at peak exercise demonstrates that the pressure/volume ratio is more sensitive as an indicator of normal or borderline left ventricular function and that ejection fraction is more sensitive in quantifying the degree of left ventricular dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)