Impaired maximal rate of left ventricular relaxation in patients with coronary artery disease and left ventricular dysfunction.

It has been suggested that the rate of left ventricular (LV) relaxation is related to the inotropic state, end-systolic fiber length and peak LV pressure, but little information is available regarding the rate of LV relaxation in patients with coronary artery disease (CAD) and LV dysfunction. To assess the rate of LV relaxation we obtained high-fidelity LV pressure measurements with manometer-tip catheters in 39 patients. The signal was analyzed by a digital computer to yield the maximal rate of pressure rise (pos dP/dt) and the maximal rate of pressure fall (neg dP/dt). Selective coronary arteriography and biplane LV angiography with determination of LV volumes, ejection fraction (EF) and percent abnormally contracting segments (ACS) when present, were performed in all patients. In 10 patients with normal LV function (EF greater than 0.50, no asynergy) mean neg dP/dt (2074 +/- 121 mm Hg/sec) was significantly (p less than 0.01) greater than in 29 patients with CAD and LV dysfunction (1695 +/- 66 mm Hg/sec). In nine patients with LV dysfunction and EF less than 0.35, mean neg dP/dt was reduced to 1405 +/- 107 mm Hg/sec, significantly (p less than 0.01) lower than in patients with normal LV function. Neg dP/dt correlated well with pos dP/dt (r = 0.75), with EF (r = 0.74), and with ACS (r = -0.74), and less well with LV end-systolic volume (r = 0.67). There was very poor correlation between neg dP/dt and peak LV pressure (r = 0.30). These data suggest that the rate of LV relaxation, as assessed by neg dP/dt, is impaired in patients with CAD and LV dysfunction, and the extent of impairment is related to the severity of the dysfunction as determined hemodynamically by pos dP/dt, and angiographically by EF and ACS. In these patients the maximal rate of LV relaxation is inversely related to LV end-systolic volume, and is not related to peak LV pressure.     

Pressure of papillary sphincter zone and pancreatic main duct in patients with alcoholic and idiopathic chronic pancreatitis

Summary To determine the significance of manometric pressure of the pancreatic duct in patients with alcoholic and idiopathic chronic pancreatitis, we used a microtransducer inserted through a duodenoscope to measure pressures in the papillary sphincter zone and pancreatic main duct in 20 control subjects and 31 patients with chronic pancreatitis without papillary stenosis including 10 cases of alcoholic chronic pancreatitis (ALCP) and 21 cases of idiopathic chronic pancreatitis (ICP). The pancreatic main ductal pressure was significantly higher in the patients with ALCP (55.7±28.9 mm Hg) or ICP (44.5±25.8 mm Hg) than in the controls (16.2±8.7 mm Hg), but there was no significant difference between ALCP and ICP. There was no significant difference between control subjects and ICP in the motility of the sphincter of Oddi. In ICP there no were correlationships between pancreatic ductal pressure and the motility of papillary sphincter zone. In ALCP, the frequency of the papillary sphincter waves was significantly higher than in normal subjects and there was a correlation between the pancreatic ductal pressure and the motility of the papillary sphincter zone. These data suggest that increased pancreatic ductal pressure in ALCP may be in part due to papillary dysfunction, but not in ICP.     

Pressure of papillary sphincter zone and pancreatic main duct in patients with alcoholic and idiopathic chronic pancreatitis

To determine the significance of manometric pressure of the pancreatic duct in patients with alcoholic and idiopathic chronic pancreatitis, we used a microtransducer inserted through a duodenoscope to measure pressures in the papillary sphincter zone and pancreatic main duct in 20 control subjects and 31 patients with chronic pancreatitis without papillary stenosis including 10 cases of alcoholic chronic pancreatitis (ALCP) and 21 cases of idiopathic chronic pancreatitis (ICP). The pancreatic main ductal pressure was significantly higher in the patients with ALCP (55.7 +/- 28.9 mm Hg) or ICP (44.5 +/- 25.8 mm Hg) than in the controls (16.2 +/- 8.7 mm Hg), but there was no significant difference between ALCP and ICP. There was no significant difference between control subjects and ICP in the motility of the sphincter of Oddi. In ICP there were no correlationships between pancreatic ductal pressure and the motility of papillary sphincter zone. In ALCP, the frequency of the papillary sphincter waves was significantly higher than in normal subjects and there was a correlation between the pancreatic ductal pressure and the motility of the papillary sphincter zone. These data suggest that increased pancreatic ductal pressure in ALCP may be in part due to papillary dysfunction, but not in ICP.     

十二指肠乳头旁憩室对内镜十二指肠乳头切开术治疗胆总管结石及其并发症的影响

目的 探讨十二指肠乳头旁憩室（juxtapapillary duodenal diverticulum,JPDD）与胆总管结石的关系,以及对内镜乳头括约肌切开术（EST）治疗胆总管结石和术后并发症的影响.方法 回顾性分析513例ERCP病例,其中行EST治疗胆总管结石253例,合并JPDD的胆总管结石51例.分析JPDD与胆总管结石发生的关系;比较合并JPDD胆总管结石组与未合并JPDD胆总管结石组ERCP插管成功率、EST胆总管取石成功率及其并发症发生率的差异.结果 JPDD组原发性胆总管结石发生率显著高于无JPDD组（18.4％ VS 8.9％,P＜0.01）.与未合并JPDD胆总管结石组比较,合并JPDD胆总管结石组ERCP插管成功率无显著性差异（96.1％ VS 99.5％,P＞0.05）,而EST取石成功率明显降低（91.8％ VS 99.5％,P＜0.05）,EST术后创口出血显著增多（11.1％ VS 1.9％,P＜0.01）,其他近期并发症及远期并发症发生率均无显著性差异（P＞0.05）.结论 JPDD与原发性胆总管结石的发生相关;JPDD对EST治疗胆总管结石有一定影响;EST仍是治疗合并JPDD胆总管结石的一种相对安全、有效的治疗手段.     

Relation between exercise capacity and left ventricular systolic versus diastolic function during exercise in patients after myocardial infarction

BACKGROUND: It is known that left ventricular systolic function at rest does not correlate well with exercise capacity of patients with heart failure. However, the contribution of left ventricular diastolic dysfunction, especially during exercise, to exercise capacity of cardiac patients remains to be determined. OBJECTIVE: To determine the impact of left ventricular systolic and diastolic function during exercise on exercise capacity of patients with left ventricular dysfunction after myocardial infarction. METHODS: A symptom-limited exercise test was performed with measurements for hemodynamics and uptake of oxygen (Vo2) of 26 men who had previously suffered myocardial infarction. These patients were divided into two groups according to their peak Vo2 (group 1 with peak Vo2 > or = 16 ml/kg per min, n= 13; and group 2 with peak Vo2 < 16 ml/kg per min, n= 13). Pulmonary arterial pressure, left ventricular and systemic arterial pressure, and cardiac output were measured at rest and during exercise. RESULTS: At rest, there was no difference between the two groups in terms of hemodynamic parameters except for minimal dP/dt, minimal left ventricular pressure (LVP) and time constant for decay of left ventricular pressure (tau). During peak exercise, cardiac output, left ventricular end-diastolic pressure (EDP), minimal dP/dt, minimal LVP, and tau for the two groups were significantly different. Furthermore, peak Vo2 was significantly correlated with T, minimal LVP, minimal dP/dt, EDP, and maximal dP/dt during peak exercise for the whole group of patients. CONCLUSION: Left ventricular diastolic function during exercise, i.e. diastolic reserve, may be an important determinant of exercise capacity of patients with left ventricular dysfunction after myocardial infarction.     

Does intracoronary infusion of Fluosol-DA 20% prevent left ventricular diastolic dysfunction during coronary balloon angioplasty?

Distal intracoronary infusion of the perfluorochemical Fluosol-DA 20% has been shown to prevent systolic dysfunction during coronary artery balloon occlusion in coronary angioplasty. To assess its effect on global diastolic dysfunction, a randomized, single-blind, crossover protocol comparing intracoronary infusion of Fluosol or no infusion (control) was performed during 60 s balloon inflations in 10 patients (mean age 67 years) undergoing coronary angioplasty. Assessment of global systolic and diastolic function was obtained with high fidelity micromanometer measurements of left ventricular pressure. Eighteen pairs of balloon inflations (Fluosol versus control) were analyzed. Patients reported significantly less severe chest pain during inflations accompanied by Fluosol compared with control. However, during coronary balloon occlusion, no significant differences in the changes from baseline values were observed between Fluosol and control with regard to ventricular relaxation, including the time constant of early ventricular relaxation (tau) and maximal rate of fall in left ventricular pressure (maximal negative dP/dt). No differences between Fluosol and control were observed in terms of the increase in end-diastolic pressure or minimal diastolic pressure during balloon inflation. Mean systolic pressure decrease from baseline values was greater during control than during Fluosol inflations (-9.0 +/- 3.3 mm Hg, p = 0.013), but no significant difference was observed in the change in maximal rate of rise in left ventricular pressure (maximal positive dP/dt). These results suggest that Fluosol does not preserve global left ventricular diastolic function during coronary balloon occlusion, possibly because of its limited oxygen delivery capability relative to arterial blood.     

Direct effects of hydralazine on cardiac contractile function, haemodynamics, and myocardial energetics in isolated myocardium

The direct cardiac effects of hydralazine were studied in isolated working rat heart, isolated cat right ventricular papillary muscle, and isolated rabbit right atrium. The haemodynamics, myocardial energetics, and contractility of isolated hearts were measured at hydralazine concentrations of 0.01, 0.1, 0.5, 1.0, 10 and 100 mumol.litre-1. Coronary flow was significantly increased (greater than or equal to 21%, p less than 0.01) in paced (325 beats.min-1) rat hearts at greater than or equal to 0.5 mumol.litre-1 hydralazine and in spontaneously beating hearts (greater than or equal to 37%; p less than 0.05) at greater than or equal to 1.0 mumol.litre-1 hydralazine. The increases in coronary flow occurred without significant increases in heart rate, contractility (dP/dtmax), or coronary perfusion pressure. Myocardial oxygen consumption was not significantly changed at any hydralazine concentration in spontaneously beating hearts and was unaltered in paced hearts except for a small significant increase (9.8%) at 10 mumol.litre-1. A negative inotropic effect was apparent at 100 mumol.litre-1 hydralazine as indicated by a significant reduction of dP/dtmax (paced and non-paced hearts), peak aortic flow rate (non-paced), and maximum left ventricular pressure (paced). In isolated cat papillary muscles and rabbit right atria, cumulative hydralazine log dose-response curves (0.1-1000 mumol.litre-1) were obtained. A positive inotropic effect that could be abolished by beta adrenergic blockade was produced in papillary muscles only at concentrations greater than or equal to 100 mumol.litre-1.(ABSTRACT TRUNCATED AT 250 WORDS)     

The relationship between juxtapapillary duodenal diverticula and disorders of the biliopancreatic system: analysis of 350 patients.

BACKGROUND: Data concerning the association of juxtapapillary duodenal diverticula (JPDD) with biliopancreatic disorders are inconsistent, but an association between bile duct stones and JPDD is widely accepted. The aim of this study was to investigate the frequency of JPDD and its association with biliopancreatic disorders in patients undergoing ERCP. METHODS: A retrospective analysis was conducted of 5497 consecutive ERCP procedures performed in 2925 patients. Matched-pair analysis yielded 350 pairs of patients with and without JPDD, matched for definite risk criteria such as age, gender, and indication for ERCP. RESULT: The incidence of JPDD was 12%. Patients with JPDD were significantly older than patients without JPDD (71 vs. 62 years; p < 0.0019) and had a significantly higher bleeding rate after endoscopic sphincterotomy (8.8% vs. 4.8%; p = 0.039). The presence of JPDD correlated with gallbladder stones (29.4% vs. 20.8%; p = 0.039), bile duct stones (46% vs. 33.1%; p < 0.001), and recurrence of bile duct stones (6.6% vs. 1.4%; p = 0.002). There were no significant differences in frequency of acute and chronic pancreatitis as well as pancreas divisum. After multivariate logistic regression analysis, technically difficult ERCP, bleeding after endoscopic sphincterotomy, and bile duct stones remained as independent risk factors. CONCLUSION: JPDD appears to be a risk factor for complications of endoscopic sphincterotomy and for gallbladder stones, bile duct stones, and their recurrence.     

Motility of the Sphincter of Oddi and Pancreatic Main Ductal Pressure in Patients with Alcoholic, Gallstone-Associated, and Idiopathic Chronic Pancreatitis

We endoscopically measured pressures of the pancreatic duct (PP) and the sphincter of Oddi (SO) in patients with alcoholic (ALCP, n = 10), gallstone-associated (GSCP, n = 7), and idiopathic chronic pancreatitis (ICP, n = 21), and in 20 controls. The PP was significantly higher in the patients with ALCP (55.7 +/- 28.9 mm Hg), GSCP (33.6 +/- 16.2 mm Hg), or ICP (44.5 +/- 25.8 mm Hg) than in the controls (16.2 +/- 8.7 mm Hg), but there was no significant difference between ALCP, GSCP, and ICP. There was no significant difference between control subjects and ICP in the motility of SO. In ICP, there was no correlation between the PP and the motility of SO. In ALCP and GSCP, the frequencies of the papillary sphincter waves were significantly higher than in normal subjects, and there were correlations between the PP and the motility of SO. These data suggest that increased pancreatic ductal pressure in GSCP with papillitis or ALCP may be due in part to papillary dysfunction, but not in ICP.     

A Novel Noninvasive Method to Assess Left Ventricular −dP/dt Using Diastolic Blood Pressure and Isovolumic Relaxation Time

Background: Left ventricular Doppler‐derived ?dP/dt determined from the continuous‐wave Doppler spectrum of the mitral regurgitation (MR) jet has been shown to be a valuable marker of diastolic function, but requires the presence of MR for its assessment. We sought to determine if a novel method of determining ?dP/dt using the diastolic blood pressure and isovolumic relaxation time (DBP‐IVRT method) correlates with Doppler‐derived ?dP/dt using the MR method (Doppler‐MR method). Methods: Thirty‐three patients with less than severe MR were enrolled. ?dP/dt was determined using the Doppler‐MR method from the continuous‐wave Doppler spectrum of the MR jet (32 mmHg/time from 3 to 1 m/sec). ?dP/dt was also determined using the DBP‐IVRT method using the following equation: ?dP/dt = (DBP ? LVEDP)/IVRT, where left ventricular end‐diastolic pressure (LVEDP) was estimated based on tissue Doppler and mitral inflow patterns. Results: Twenty‐five patients had adequate Doppler waveforms for analysis. The average amount of MR was mild‐to‐moderate severity. The mean ?dP/dt was 680 ± 201 mmHg by the Doppler‐MR method and 681 ± 237 mmHg by the DBP‐IVRT method. There was a significant correlation between the 2 methods of determining ?dP/dt (Pearson r = 0.574, P = 0.003). The Bland–Altman plot revealed almost no bias between the 2 methods; the difference in ?dP/dt between the 2 techniques was noted to be greater for patients with higher ?dP/dt, however. Conclusion: Diastolic blood pressure and isovolumic relaxation time may be used to noninvasively assess diastolic function in patients who do not have MR, especially in those with reduced diastolic function.     

Lack of inertia force of late systolic aortic flow is a cause of left ventricular isolated diastolic dysfunction in patients with coronary artery disease.

OBJECTIVES: We investigated whether a lack of inertia force of late systolic aortic flow and/or apical asynergy provoke early diastolic dysfunction in patients with coronary artery disease (CAD). BACKGROUND: Left ventricular (LV) isolated diastolic dysfunction is a well-recognized cause of heart failure. METHODS: We evaluated LV apical wall motion and obtained left ventricular ejection fraction (LVEF) by left ventriculography in 101 patients who underwent cardiac catheterization to assess CAD. We also computed the LV relaxation time constant (Tp) and the inertia force of late systolic aortic flow from the LV pressure (P)-first derivative of left ventricular pressure (dP/dt) relation. Using color Doppler echocardiography, we measured the propagation velocity of LV early diastolic filling flow (Vp). Patients with LVEF > or =50% (preserved systolic function [PSF], n = 83) were divided into 2 subgroups: patients with inertia force (n = 53) and without inertia force (n = 30). No patient with systolic dysfunction (SDF) (LVEF <50%) had inertia force (n = 18). RESULTS: The Tp was significantly longer in patients with SDF (85.7 +/- 21.0 ms) and with PSF without inertia force (81.1 +/- 23.6 ms) than in those with PSF with inertia force (66.3 +/- 12.8 ms) (p< 0.001). The Vp was significantly less in the former 2 groups than in the last group. In patients with PSF, LV apical wall motion abnormality was less frequently observed in those with inertia force than in those without (p < 0.0001). CONCLUSIONS: An absence of inertia force in patients with PSF is one of the causes of isolated diastolic dysfunction in patients with CAD. Normal LV apical wall motion is substantial enough to give inertia to late systolic aortic flow.     

Mechanism of ischemic mitral regurgitation. An experimental evaluation

BACKGROUND. Papillary muscle dysfunction (PMD) has been implicated in the pathogenesis of ischemic mitral regurgitation (MR). We hypothesized that ischemic MR is not caused by PMD and/or dysfunction of the myocardial regions from where the papillary muscles arise but is related to reduction in global left ventricular (LV) function. To test this hypothesis, three groups of dogs were studied. METHODS AND RESULTS. In group 1 dogs (n = 8), varying degrees of regional and global LV dysfunction were produced. In group 2 dogs (n = 7), the circulation to the papillary muscles was isolated from that of the rest of the LV. Dysfunction of one or both papillary muscles was produced without producing global LV dysfunction. Global LV dysfunction was also produced while keeping papillary muscle function intact. The degree of MR (assessed using contrast echocardiography) was correlated in both groups of dogs with thickening of the papillary muscles and regional and global LV function. In the group 3 dogs (n = 6), the spatial distribution of blood flow within each papillary muscle was determined during ischemia by using radiolabeled microspheres. Thickening of the papillary muscles was assessed at three different levels along their lengths and was correlated with average blood flow at these levels. In group 1 dogs, MR was noted only when global LV function was affected and its severity correlated inversely with global LV function (r = -0.84 with peak positive LV dP/dt and r = -0.95 with global LV thickening, respectively). In comparison, there was poor correlation between MR and anterior and posterior papillary muscle thickening (r = -0.38 and r = -0.49, respectively). In group 2 dogs, MR did not occur in the presence of either PMD or akinesia of the immediately adjacent LV myocardium. MR occurred only when global LV dysfunction was produced (with the papillary muscle function intact), and its severity correlated inversely with global LV function (r = -0.92 with LV dP/dt and r = -0.86 with global LV thickening, respectively). There was poor correlation between the degree of MR and thickening of the anterior and posterior papillary muscles (r = -0.24 and r = -0.38, respectively). In both groups of dogs, MR was associated with incomplete mitral leaflet closure (IMLC), and the severity of MR correlated linearly with the degree of IMLC (r = 0.98). MR was never associated with mitral valve prolapse. In the group 3 dogs, despite more inhomogeneous flow during ischemia to the anterior compared with the posterior papillary muscle, mean thickening of these muscles was similar (3 +/- 10% and 3 +/- 4%, respectively). Furthermore, there was minimal variability in thickening between different parts of the muscles (3 +/- 2% and 5 +/- 3%, respectively). CONCLUSIONS. It is concluded that PMD and/or dysfunction of the immediately adjacent LV myocardium does not result in MR. MR occurs during ischemia only when global LV function is affected, even when thickening of the papillary muscles and the immediately adjacent LV remains intact. MR in this situation is related to IMLC; the greater the degree of IMLC, the greater the MR. These findings suggest that the mechanism of ischemic MR is not related to PMD. There may also be important therapeutic implications of these findings.     

Clinical evaluation of the cause of left ventricular dysfunction in type 2 diabetes without significant cardiac disease

OBJECTIVES: The relationship between left ventricular dysfunction and hypertension or proteinuria was evaluated in type 2 diabetic patients without significant cardiac disease to investigate the cause of diabetic cardiac dysfunction. METHODS: Twenty-one patients with type 2 diabetes mellitus (mean age 63.8 +/- 7.4 years) underwent left ventriculography and Doppler echocardiography to calculate the ejection fraction and E/A ratio (E/A). RESULTS: Thirteen patients had hypertension (61.9%) and six patients had proteinuria (28.6%). The E/A was 0.82 +/- 0.21 in all patients. The E/A in patients with hypertension or proteinuria was significantly less than in those without these diseases (0.74 +/- 0.18 vs 0.97 +/- 0.18, p = 0.011; 0.65 +/- 0.10 vs 0.89 +/- 0.20, p = 0.010, respectively). The ejection fraction was 73.3 +/- 7.2% in all patients. The ejection fraction in patients with proteinuria was significantly less than in those without proteinuria (67.6 +/- 10.0% vs 75.5 +/- 4.4%, p = 0.019), but there was no significant difference in ejection fraction between patients with and without hypertension. The duration of diabetes was significantly related to the ejection fraction (r = -0.436, p = 0.048) but not to the E/A. CONCLUSIONS: In patients with type 2 diabetes without significant cardiac disease, left ventricular diastolic function may be related to both hypertension and proteinuria and left ventricular systolic function may be related to proteinuria and duration of diabetes. Therefore, in addition to hypertension, complications of nephropathy or long duration of diabetes may be related to the cause of the diabetic cardiac dysfunction.     

Effects of a cardioselective beta 1 partial agonist (corwin) on left ventricular function and myocardial metabolism in patients with previous myocardial infarction

Corwin is a new selective beta 1 partial agonist, able to stabilize the beta 1 adrenoceptors at approximately 43% of their maximal activity. The aim of the study was to determine the effects of this agent in patients with coronary artery disease (CAD) and previous myocardial infarction (MI). In a first group of 14 patients, corwin increased significantly the peak (+)dP/dt (+35%; p less than 0.005), the global ejection fraction, and the ejection fraction of abnormally contracting segments (from 20 +/- 18 to 26 +/- 19%; p less than 0.02). Corwin also induced significant decreases in mean systolic (-8%; p less than 0.05) and mean diastolic (-38%; p less than 0.001) wall stress and accelerated the relaxation rate. In a second group of 11 patients, a metabolic study indicated that neither myocardial oxygen consumption (15 +/- 7 versus 15 +/- 7 ml/min; difference not significant) nor lactate extraction was modified by the drug. In this group, increases in peak (+)dP/dt, acceleration in ventricular relaxation (-8 ms in time constant of isovolumic pressure decrease; p less than 0.01), and decreases in left ventricular end-diastolic pressure also were noted after administration of corwin, both under basal conditions and during a cold pressor test. In conclusion, corwin is a positive inotrope which, in patients with CAD and left ventricular dysfunction, improves left ventricular systolic and diastolic function without inducing myocardial ischemia.     

Non-invasive assessment of the peak pressure gradient between the aorta and pulmonary artery in patent ductus arteriosus

The validity of continuous wave Doppler ultrasound estimation of the peak pressure gradient between the aorta (Ao) and pulmonary artery (PA) in patients with patent ductus arteriosus (PDA) was evaluated. Ten patients, all without other anomalies, underwent cardiac catheterization and cine-angiography, and the peak pressure gradient between the Ao and PA (dP(C)) was measured during catheterization. In all cases the mean PA pressure was less than 35 mmHg. According to the angiographic findings, the patients were categorized as Group A, consisting of seven patients whose features of the ductus were wedge- or tube-like in configuration; Group B, consisting of two patients whose features were termed "orifice-like" stenosis including one with abrupt narrowing on the PA side of the ductus and the other with a short segmental ductus. Group C consisted of one patient who had a long curved segmental ductus. The maximum velocity of ductus flow was measured by continuous wave Doppler ultrasonography, and the estimated peak pressure gradient between the Ao and PA by Doppler (dP(D] was calculated using the simplified Bernoulli equation (dP = 4V2). In group A, dP(D) was overestimated compared to dP(C) in all patients by 19 to 51 mmHg (mean 34 mmHg). However, in group B, the difference between dP(D) and dP(C) was small, 5 mmHg and 7 mmHg, respectively. In group C, dP(D) was underestimated as opposed to dP(C). Thus, in the limited cases, the simplified Bernoulli equation could be used in estimating the peak pressure gradient between the Ao and PA. However, this equation leads to overestimation in many cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects on hemodynamics and left ventricular ejection fraction of intravenous bepridil for impaired left ventricular function secondary to coronary artery disease

To define the hemodynamic effects of bepridil in patients with depressed left ventricular (LV) function, 22 patients with an LV ejection fraction (EF) of 0.45 or less were studied before and after 2 mg/kg (n = 11) and 4 mg/kg (n = 11) of intravenous bepridil. Maximal hemodynamic effects were evident between 15 and 30 minutes after drug infusion. After 2 mg/kg, heart rate decreased 9% (p less than 0.01), cardiac index 17% (p less than 0.01), LV dP/dt max 16% (p less than 0.01), stroke work index 14% (p less than 0.01) and mean aortic pressure 8% (difference not significant). Right atrial pressure increased 8% (not significant), pulmonary arterial wedge pressure 24% (p less than 0.01) and systemic vascular resistance 17% (p less than 0.01). After administering 4 mg/kg of bepridil the changes in heart rate, cardiac index, right atrial pressure, LV dP/dt max, mean aortic pressure and systemic vascular resistance were almost identical to those after the smaller dose. The larger dose produced a 40% (p less than 0.01) increase in pulmonary arterial wedge pressure and a 22% decrease in stroke work index (p less than 0.01), but only the change in wedge pressure was significantly greater (p less than 0.01) than that produced by the lower dose. Radionuclide-determined LVEF decreased 6% (p less than 0.05), from 0.33 +/- 0.14 after 2 mg/kg and 11% (p less than 0.05) from 0.27 +/- 0.11 after 4 mg/kg of bepridil. The data indicate that bepridil exerts significant negative inotropic and chronotropic effects in patients with impaired LV function.     

Changes in left ventricular function with effort in the coronary patient. l.]

The altered haemodynamics of the coronary patient have been investigated in 30 patients both at rest and under conditions of maximal effort as carried out on the bicycle ergometer under the usual conditions for an exercise electrocardiogram. Patients with angina of effort but no previous infarction have normal left ventricular function at rest; under the ischaemia induced by exercise there is acute dysfunction of the left ventricle as witnessed by a reduction in maximal cardiac output, a raised end-diastolic pressure, and changes in compliance which are more marked than those in contractility. Patients with a healed infarct but without sequelae have a rigid left ventricle, but it is not failing; they show normal changes in dP/dt max and in the indices of left ventricular work, but a pathological form of negative peak of dP/dt, of end-diastolic pressure, and of deltaP/deltaV (which reflects myocardial compliance). Patients who have had an infarction with sequelae such as angina or attacks of left ventricular failure have filling pressures which are already elevated at rest, and cardiac failure, which becomes evident on exercise.     

Angiocardiographic evaluation of the left ventricular function in adult and pediatric subjects with interatrial defect of the ostium secundum type]

In order to assess left ventricular function in adults and children with ostium secundum atrial septal defect (ASD), 42 patients were examined by hemodynamic and angiocardiographic techniques. Patients were divided into three groups: Group I, 18 patients (mean age 42 years) with ASD; Group II, 14 patients (mean age 9 years) with ASD; Group III, 10 patients without cardiopathies who represented the control group. The following parameters of ventricular function were assessed: left ventricular end diastolic volume, global and regional left ventricular ejection fraction, left ventricular telediastolic pressure, mean pulmonary artery pressure, the ratio between pulmonary flow and systemic flow (QP/QS). Group I patients showed higher values of left ventricular end diastolic pressure and mean pulmonary artery pressure (16 +/- 0.6 mmHg; 33 +/- 1.5 mmHg) in relation to those of Group II (5.1 +/- 0.4 mmHg; 14 +/- 1.4 mmHg) and Group III (8.1 +/- 0.5 mmHg; 18 +/- 1.6 mmHg). In both cases the difference was statistically significant (p less than 0.001). A significant difference (p less than 0.05) was also noted in the incidence of mitral valve prolapse between patients in Group I and II. There was no significant difference (p = NS) however, between overall ejection fraction values in the three groups of patients; a lower regional ejection fraction (postero-basal segment) was recorded in Group I patients with mitral valve prolapse in comparison to patients in the other two groups (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of coronary collateral vessels during transient coronary occlusion during angioplasty assessed by hemodynamic, electrocardiographic and metabolic changes

The clinical role of collateral vessels was evaluated during transient coronary occlusion by percutaneous transluminal coronary angioplasty in 22 patients with (8) and without (14) collateral vessels. Coronary occlusion pressure, the ratio of mean coronary occlusion pressure to mean aortic pressure and myocardial perfusion pressure at 40 s of balloon inflation were significantly higher in patients with than in patients without collateral vessels. The changes in left ventricular systolic and end-diastolic pressure, maximal rate of rise of left ventricular pressure (peak dP/dt) and maximal rate of fall of left ventricular pressure (negative peak dP/dt) during balloon inflation were less in patients with than in patients without collateral vessels. Myocardial lactate was produced in patients without collateral vessels but not in those with such vessels. Marked ST segment elevation in the electrocardiogram occurred in patients without collateral vessels but either ST segment depression or mild ST segment elevation was observed in patients with collateral vessels. This study indicates that collateral vessels limit myocardial ischemia during coronary occlusion, probably as a result of increased myocardial perfusion pressure.     

Right ventricular contractile function in children with congenital heart disease

Indexes of right ventricular (RV) systolic function were evaluated in 41 patients undergoing cardiac catheterization. High-fidelity tracings were used to determine RV pressure, maximal RV dP/dt and the velocity of contractile element shortening at a developed pressure of 10 mm Hg (VCE10). In 14 children with an RV systolic pressure less than 35 mm Hg, normal RV volume, pulmonary vascular resistance (PVR) less than 3 units X m2 and no shunts (our normal group), mean (+/- standard deviation) RV dP/dt was 437 +/- 116 mm Hg X s-1 and VCE10 was 1.15 +/- 0.33 muscle length X s-1. In patients with RV systolic hypertension due to valvular pulmonary stenosis or isolated increases in PVR, mean values for RV dP/dt and VCE10 were significantly (p less than 0.05) greater than the normal values. In patients with a ventricular septal defect, RV hypertension and normal PVR, VCE10 was normal but RV dP/dt was significantly elevated. Children with chronic RV volume overload had normal RV contractile indexes. No patient in any group had values for RV dP/dt or VCE10 that were less than normal (mean normal - 2 standard deviations). This study establishes for the first time the indexes of RV isovolumic systole in children. It also shows that RV contractile function is preserved in young patients with chronic RV pressure or volume overload who do not have overt congestive heart failure.