Left auricular dilatation in calcified aortic stenosis in adults

Two groups of patients of comparable age, one comprising 12 subjects without detectable cardiac disease and the other comprising 38 patients with calcific aortic stenosis (CAS) underwent clinical, electrocardiographic, echocardiographic and haemodynamic studies to assess the degree and significance of left atrial hypertrophies in CAS. The volume of the left atrium (LA) was globally increased in CAS (maximum volume 68 per cent: 26/38) and LA ejection fraction was decreased in 60 per cent of patients (23/38). However, the maximum volume was only moderately greater than that of normal subjects (+38 per cent). The most specific non-invasive investigation for left atrial assessment is echocardiography. There was a linear relationship between LA angiographic volume and echocardiographic antero-posterior dimension (r = 0.43; p less than 1 x 10(-2)). The duration of the P wave in S2 was a specific (75 per cent) but relatively insensitive (27 per cent) sign of LA dilatation in pure CAS. On the other hand, the Morris index based on the surface of the P terminal force in V1 was quite sensitive (77 per cent) but not very specific (25 per cent). The maximum LA volume was not related to left ventricular volume, the severity of CAS, diastolic indices of compliance or left ventricular mass. However, the minimum LA volume (after atrial systole) was related to left ventricular end diastolic (r = 0.35, p less than 0.05) and end systolic volume (r = 0.34, p less than 0.05). The LA ejection fraction was inversely related to mean pulmonary capillary pressure (r = 0.34, p less than 5 x 10(-2).(ABSTRACT TRUNCATED AT 250 WORDS)     

Relation between mixed venous blood oxygen saturation and cardiac pumping function at the acute phase of myocardial infarction

In this study, we monitored changes in the mixed venous blood oxygen saturation (Sv-O2) level of 45 patients with acute myocardial infarction and compared these results to the traditional parameters. The Sv-O2 level was found to correlate well with the clinical course of patients and their hemodynamic conditions. The mean Sv-O2 level of the group having congestive heart failure (53.3 +/- 8.4%) was found to be statistically lower than those without (69.8 +/- 5.6). Furthermore, patients whose Sv-O2 level was lower than 60% were found to be at greater risk for heart failure and a very high mortality rate. Patients were classified into four subsets according to Forrester's hemodynamic classification; their Sv-O2 levels were 70.7 +/- 4.1% (I: 23 cases), 54.7 +/- 6.9% (II: 8 cases), 55.8 +/- 9.4% (III: 10 cases), and 47.0 +/- 8.0 (IV: 4 cases), respectively. A severe relationship between pulmonary capillary wedge pressure and Sv-O2 having a correlation coefficient of r = -0.64 was observed, and a logarithmic curvilinear relation between cardiac index approximately Sv-O2, stroke volume index approximately Sv-O2 and left ventricular stroke work index approximately Sv-O2 was also evident. When the decrease in the Sv-O2 level was more than 5%, it always showed a significant decrease in the cardiac index. This study suggested tht continuous monitoring of the Sv-O2 level revealed simultaneous changes in the hemodynamic state, which lead to the assistance and aid for treating patients with critical conditions of acute myocardial infarction. In such circumstances, it was noted that the Sv-O2 level should be maintained above 60% in order to stabilize the hemodynamic state.     

Isolated chronic mitral regurgitation with preserved systolic left ventricular function and severe pulmonary hypertension

Pulmonary hypertension in chronic mitral valve disease has been related most commonly to left ventricular dysfunction or mitral stenosis; its association with chronic, isolated mitral regurgitation and preserved left ventricular systolic function is unclear. In 41 catheterized patients with chronic mitral regurgitation (known history of mitral regurgitation for greater than 18 months) and preserved left ventricular systolic function (ejection fraction greater than 0.55), historic, electrocardiographic, echocardiographic and hemodynamic variables were analyzed. Ten patients (Group I) had normal pulmonary artery systolic pressure (less than 30 mm Hg), whereas 31 patients had pulmonary hypertension. Pulmonary artery systolic pressure was mildly increased (30 to 49 mm Hg) in 13 patients (Group II) and was greater than or equal to 50 mm Hg in 18 patients (Group III). Univariate analysis showed the more frequent occurrence of male gender and ruptured chordae tendineae in the groups with pulmonary hypertension. Mean pulmonary capillary wedge pressure, size of the V wave in pulmonary capillary wedge pressure and pulmonary arteriole resistance were higher, whereas cardiac index was lower in the hypertension groups. Multivariate stepwise analysis revealed higher mean pulmonary capillary wedge pressure and pulmonary arteriole resistance as the only variables independently differing among groups. In conclusion, pulmonary hypertension occurs frequently (76% of cases) in patients with chronic, isolated mitral regurgitation with preserved left ventricular systolic function. In these patients, a severe increase in pulmonary capillary wedge pressure is associated with elevation in pulmonary artery resistance, a finding similar to that in mitral stenosis.     

Hemodynamic effects of intravenous flecainide relative to the level of ventricular function in patients with coronary artery disease

Flecainide, a new antiarrhythmic agent with poorly defined hemodynamic actions, was studied in 22 patients with coronary artery disease. Intravenous infusions of 1 mg/kg and 2 mg/kg resulted in respective increases in right atrial pressure (12%, p less than 0.05; 15%, p less than 0.01), mean pulmonary artery pressure (27%, p less than 0.01; 28%, p less than 0.01), and pulmonary capillary wedge pressure (44%, p less than 0.05; 33%, p less than 0.01). Cardiac index decreased 8% (p less than 0.05) after 1 mg/kg flecainide and 12% (p less than 0.05) after the 2 mg/kg dose. The mean left ventricular ejection fraction decreased by 15% (p less than 0.01) and 16% (p less than 0.01), respectively, 10 minutes after 1 mg/kg and 2 mg/kg of flecainide. Minimal increases in the heart rate (less than 5%) and no significant change in arterial pressure occurred 5 to 10 minutes after flecainide and were associated with borderline and variable increases in pulmonary and systemic vascular resistances. Flecainide diluent did not induce changes in pulmonary capillary wedge pressure or left ventricular ejection fraction. Thus, flecainide exerts a moderate but significant negative inotropic effect which may be clinically significant in patients with severely compromised ventricular function.     

Hemodynamic and volume correlates of left ventricular diastolic relaxation and filling in patients with aortic stenosis.

OBJECTIVE. The aim of the present study was to evaluate the hemodynamic and volume correlates of early diastolic filling and isovolumetric relaxation in patients with aortic stenosis. BACKGROUND. Left ventricular diastolic relaxation and filling have been found to be heterogeneous in patients with aortic stenosis. Potential mechanisms underlying this heterogeneity include individual differences in the severity of muscle hypertrophy or systolic dysfunction, or both, in the presence and severity of mitral regurgitation and in the level of left atrial pressure. METHODS. Right (fluid-filled) and left (high fidelity micromanometer) ventricular pressures, left ventricular volumes (contrast angiography) and transmitral inflow dynamics (Doppler echocardiography) were measured in 17 patients with isolated severe aortic stenosis (valve area less than 0.75 cm2). Measurements included left ventricular end-diastolic and end-systolic volumes, left ventricular ejection fraction, peak positive and negative first derivative of left ventricular pressure (dP/dt), the time constant of isovolumetric relaxation (tau), left ventricular end-diastolic pressure, left ventricular mass, left ventricular end-systolic stress, mean capillary wedge pressure and peak early (E) and late (A) transmitral filling velocities. Patients were subclassified according to left ventricular ejection performance at rest and mean capillary wedge pressure. RESULTS. Patients with normal ejection performance and normal mean capillary wedge pressure had a normal rate of isovolumetric left ventricular pressure decay and an abnormal diastolic filling pattern, with diastolic filling occurring primarily during atrial systole. In contrast, in patients with systolic dysfunction and elevated mean capillary wedge pressure, isovolumetric pressure decay was prolonged and diastolic filling occurred essentially during the rapid filling period, with reduced atrial contribution to left ventricular filling and a short isovolumetric relaxation period. Stepwise multiple linear regression analysis identified two variables as independent predictors of transmitral velocity profile and three variables independently predictive of the rate of left ventricular pressure decay. The single most important predictor of transmitral filling pattern was the pulmonary capillary wedge pressure (p less than 0.0001), followed by the left ventricular peak negative dP/dt (p = 0.002). The single most powerful predictor of the rate of reduction in left ventricular pressure was left ventricular mass index (p less than 0.0001), followed by end-systolic volume index (p = 0.0002) and left ventricular peak negative dP/dt (p = 0.0029). CONCLUSIONS. In patients with aortic stenosis, left ventricular filling is essentially determined by left atrial pressure, whereas isovolumetric relaxation more closely depends on the severity of muscle hypertrophy and chamber dilation.     

Prognostic importance of the immediate hemodynamic response to nifedipine in patients with severe left ventricular dysfunction

To determine the clinical significance of the occurrence of hemodynamic deterioration after the administration of calcium channel blocking drugs, nifedipine (20 mg orally) was administered to 29 patients with severe left ventricular dysfunction. Thirteen patients showed hemodynamic improvement with the drug (Group 1), as shown by a notable increase in cardiac index associated with a modest decrease in mean arterial pressure. The other 16 patients exhibited hemodynamic deterioration after nifedipine (Group 2), as reflected by a decline in right and left ventricular stroke work indexes accompanied by a marked hypotensive response. These differences were not related to differences in the peripheral vascular response to nifedipine, because both groups showed similar decreases in systemic and pulmonary vascular resistances. Groups 1 (hemodynamic improvement) and 2 (hemodynamic deterioration) were similar with respect to all demographic variables and pretreatment left ventricular performance (cardiac index, left ventricular filling pressure and systemic vascular resistance). Yet, the 1 year actuarial survival in patients in Group 1 was substantially better than that in patients in Group 2 (67 versus 23%, p = 0.009). Group 2, however, had higher values for plasma renin activity (17.7 +/- 6.0 versus 4.3 +/- 1.4 mg/ml per h, p less than 0.05), lower values for serum sodium concentration (134.6 +/- 1.2 versus 139.2 +/- 0.6 mEq/liter, p less than 0.05) and higher values for mean right atrial pressure (15.8 +/- 2.0 versus 7.9 +/- 1.4 mm Hg, p less than 0.01) than did patients in Group 1.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of propafenone in acute myocardial infarct

The hemodynamic effects of Propafenon were evaluated in 11 patients with acute myocardial infarction complicated by atrial and/or ventricular arrhythmias (atrial fibrillation in 4 cases, atrial premature beats in 3 cases, ventricular premature beats Class II-IVa in 4 and rapid sustained ventricular tachycardia in one case). Drug was administered as a bolus of 1-2 mg/kg in 5 min, followed by a 10-15 gamma/kg/min infusion for 24 hours in 7 patients. Serial measurements were taken of heart rate, systemic blood pressure, right atrial, pulmonary and capillary wedge pressure, cardiac output, cardiac index, total systemic resistances, left ventricular stroke work index, left ventricular ejection time and left ventricular mean ejection rate (LVMER) (8 cases) and PEP/LVET ratio (5 cases). After the intravenous bolus, a significant reduction of cardiac index (p less than 0.01) and LVMER (p less than 0.05) parallel to an increase of total systemic resistances and PEP/LVET ratio (p less than 0.01 and p less than 0.05 respectively); was observed no other parameter varied significantly. The peak hemodynamic effect was observed after 10 minutes and return to normal required from 30 minutes to 3-6 hours in the more severely affected patients. No late negative inotropic action was evident in 6 out of 7 patients who received long term infusion. Suppression or greater than 80% reduction of premature beats was evident in 9/12 cases. Sinus node function, atrioventricular and intraventricular conduction, and the QTc interval did not vary significantly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular effects of intracoronary atrial natriuretic peptide administration in man

An intracoronary drug infusion protocol was employed to assess the hemodynamic effects of synthetic atrial natriuretic peptide in normal subjects and to evaluate its actions on epicardial coronary artery dimensions. Increasing concentrations of synthetic atrial natriuretic peptide (1.75 to 84 micrograms/min) were infused at a constant rate directly into the left coronary artery in eight patients with normal left ventricular function and left coronary artery angiograms. Steady-state hemodynamic parameters and high-fidelity left ventricular pressure were recorded at each dose and indexes of left ventricular contractile and diastolic function were calculated. Coronary angiograms obtained at baseline and the highest dose of atrial natriuretic peptide were compared by quantitative image analysis techniques. At the highest dose administered, atrial natriuretic peptide decreased mean pulmonary artery pressure (-36%, p less than 0.01), pulmonary capillary wedge pressure (-80%, p less than 0.01), left ventricular end-diastolic pressure (-58%, p less than 0.01), left ventricular end-systolic pressure (-11%, p less than 0.01), mean arterial pressure (-8%, p less than 0.05), and pulmonary vascular resistance (-18%, p less than 0.05). Cardiac output and systemic vascular resistance were unchanged, and heart rate and peak positive dP/dt increased. Peak negative dP/dt and the time constant of early diastolic relaxation calculated by the logarithmic method both fell at the highest dose of atrial natriuretic peptide, although the time constants calculated by other less load-sensitive methods were unchanged. Doses of intracoronary atrial peptide that did not alter left ventricular load had no effect on indexes of left ventricular systolic or diastolic function despite a presumably high intramyocardial concentration of the agent.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left axis deviation and left anterior hemiblock in patients with essential hypertension during antihypertensive treatment (author's transl)

The ECG's of 127 patients (81 men and 46 women) with uncomplicated essential hypertension were evaluated over a 4-year period of antihypertensive treatment. At the beginning of the study in 1973, 39 men (48%) showed ECG changes of left axis derivation (LAD) and 8 men (10%) a left anterior hemiblock (LAH), while 19 women (41) showed a LAD and 4 (9%) a LAH. During the course of the study no changes were noted in the 12 cases of LAH. However, two additional men developed signs of LAD in 1975/76 and one more in 1977/78. Men with LAH were somewhat older and women with LAH heavier in comparison to the total group. The combination of LAD and left ventricular hypertrophy (LVH) was evident in 9 men (11%) and 4 women (9%) at the beginning of the study, while 6 men (7%) and 1 woman showed a combination of LAH and LVH. Reversibility of LVH by ECG was observed in 10 patients (50%), but no concomitant changes in axis deviation were seen.     

Effect of nitroglycerin during hemodynamic estimation of valve orifice in patients with mitral stenosis

In patients with mitral stenosis, valve orifice calculations using pulmonary capillary wedge pressure as a substitute for left atrial pressure may overestimate the severity of disease. Previous studies have shown that mitral valve area determined from transseptal left atrial pressure measurements exceeds that area derived from pulmonary wedge pressure measurements. This is probably due to pulmonary venoconstriction, which is reversed by nitroglycerin. Nitroglycerin, 0.4 mg, was administered sublingually to 20 patients with mitral valve disease during preoperative cardiac catheterization using the pulmonary capillary wedge pressure as the proximal hydraulic variable. At the time of a peak hypotensive effect, 3 to 5 minutes after nitroglycerin administration, the mean pulmonary capillary wedge pressure decreased from 23 +/- 2 (mean +/- SEM) to 19 +/- 2 mm Hg (p less than 0.005). The mean diastolic transmitral pressure gradient (12.6 +/- 1.2 mm Hg before and 11.5 +/- 1.0 mm Hg after nitroglycerin; p = NS) and cardiac output (4.0 +/- 0.3 to 4.1 +/- 0.3 liters/min; p = NS) did not change significantly. Nevertheless, the hemodynamic mitral orifice area, calculated using the Gorlin formula, increased from 0.8 +/- 0.1 to 1.1 +/- 0.2 cm2 (p less than 0.05). In 12 patients with isolated mitral stenosis, without regurgitation, the mitral valve orifice area after nitroglycerin was 0.4 +/- 0.2 cm2 larger than it was before drug administration (p less than 0.05). Administration of nitroglycerin during evaluation of mitral stenosis eliminates pulmonary venoconstriction, which raises the pulmonary capillary wedge pressure above the left atrial pressure in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy and safety of sustained (48 hour) intravenous infusions of milrinone in patients with severe congestive heart failure: a multicenter study

Milrinone is a new bipyridine inotrope that has shown promise in initial clinical testing when administered intravenously or orally. The present multicenter study was designed to evaluate the clinical effectiveness and safety of sustained (48 hour) intravenous infusions of different doses of milrinone, as would be used clinically, in a controlled fashion using invasive hemodynamic monitoring. Entry was limited to adult patients with chronic heart failure of functional class III or IV, with a cardiac index less than or equal to 2.5 liters/min per m2 or a pulmonary capillary wedge pressure greater than or equal to 15 mm Hg, or both. After stable baseline hemodynamic recordings were obtained, milrinone was given as loading (microgram/kg per 10 min) and maintenance infusions (microgram/kg per min) to 189 patients in one of four loading/maintenance dosage regimens: 37.5/0.375 (low dose, n = 26), 50/0.50 (intermediate dose, n = 95), 75/0.75 (high dose, n = 15) and 50/0.25 (lowest dose, n = 53). The lowest dose was shown to be ineffective for maintenance therapy. Effective individual patient responses were defined as greater than or equal to 20% increase in cardiac index or decrease in pulmonary capillary wedge pressure, or both. During early therapy (less than or equal to 3 hour), 99% of patients showed an effective maximal response, and 90% an effective mean response. An effective mean response was observed during days 1 and 2 in 80% of patients, with a positive dose-response trend (69% response, low dose; 80%, intermediate dose; 93%, high dose; day 1). Each loading regimen was effective, with maximal mean response occurring at 15 minutes. Cardiac index initially increased by an average of 24 to 42% for all patients in the three groups, whereas pulmonary capillary wedge pressure decreased by 24 to 33%. Initial decreases in systemic vascular resistance averaged 15 to 31%. Initial changes in heart rate (+4 to +13%) and mean arterial pressure (-2 to -13%) were modest. Significant mean hemodynamic responses were maintained over the 48 hours. Increases in cardiac index for days 1 and 2 averaged 38 and 39% for those completing constant low dose drug, 34 and 37% for intermediate dose and 73 and 44% for high dose. Decreases in pulmonary capillary wedge pressure for all patients averaged 18 to 32% on days 1 and 2, with little dose response. Heart rate changes were modest and variable, averaging -9 to 9%.(ABSTRACT TRUNCATED AT 400 WORDS)     

Acute hemodynamic effects of SIN-1 and isosorbide dinitrate in stable left ventricular failure: a comparative double-blind, cross-over study]

The acute hemodynamic effects of intravenous SIN-1 (1 mg) and sublingual isosorbide dinitrate (5 mg) were investigated in 12 patients (8 men and 4 women) between 38 and 80 years of age and suffering from stable chronic left ventricular failure (NYHA Classes III-IV) secondary to ischemic myocardiopathy (n = 5), hypertensive disease (n = 2) or idiopathic disorder (n = 5) corresponding to the following hemodynamic inclusion criteria: stable condition, cardiac index > or = 2 l/min/m2, mean capillary pressure > or = 18 mmHg and < or = 28 mmHg. Previous treatments were continued with the exception of vasodilators and diuretics which were stopped 24 hours earlier. The hemodynamic data from this cross-over, double-blind double-dummy trial were collected for two 60-hour periods separated by a washout period of 120 minutes. Simultaneously, venous samples were taken for the assay of plasma levels of SIN-1. The heart rate, cardiac output, pulmonary artery resistance and blood pressure were not affected by either SIN-1 or isosorbide dinitrate. An obvious reduction (> 15% of the basal value) in the mean capillary pressure, pulmonary artery pressure and mean right atrial pressure was observed in 10 subjects after SIN-1 and in 7 patients isosorbide dinitrate. A statistically non-significant trend towards a more marked effect (number of patients responding and maximum amplitude of pressure reduction) which occurred more rapidly and lasted longer was observed after SIN-1. Analysis of the relationship between the pharmacodynamics and pharmacokinetics of SIN-1 suggests that an active metabolites is involved. No adverse effects were reported.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic effects of a combination of vasopressin and ketanserin in patients with hepatitis b-related cirrhosis.

We measured the hemodynamic effects of intravenous vasopressin, ketanserin (a 5-hydroxytryptamine-2 receptor blocker), and vasopressin plus ketanserin in 33 patients with hepatitis B-related cirrhosis. Thirteen patients received vasopressin alone (0.66 units/min), ten patients ketanserin alone (10 mg), and ten patients vasopressin followed by vasopressin plus ketanserin. Vasopressin alone reduced the hepatic venous pressure gradient (from 18 +/- 5, mean +/- S.D., to 9 +/- 3 mmHg, p less than 0.0001) and cardiac output (p less than 0.0001), but increased mean arterial pressure (p less than 0.005), mean pulmonary arterial pressure (p less than 0.0001), pulmonary capillary wedge pressure (p less than 0.0001), and systemic vascular resistance (p less than 0.001). There was no significant change in heart rate. Ketanserin alone produced a significant fall in the hepatic venous pressure gradient (from 16 +/- 4 to 13 +/- 3 mmHg, p less than 0.0001), mean arterial pressure (p less than 0.005), mean pulmonary arterial pressure (p less than 0.005), and pulmonary capillary wedge pressure (p less than 0.005). Heart rate, cardiac output, and systemic vascular resistance were not significantly changed. The addition of ketanserin to vasopressin corrected most of the systemic hemodynamic disturbances produced by vasopressin. This combination did not lead to a further reduction in the hepatic venous pressure gradient. We conclude that intravenous ketanserin reduces portal pressure in patients with hepatitis B-related cirrhosis. The addition of ketanserin to vasopressin improves the detrimental systemic hemodynamic effects of vasopressin without further reducing the portal pressure.     

Bedside hemodynamic monitoring in the management of acute cardiac patients

Hemodynamic monitoring was performed in 100 acutely ill patients admitted to a Coronary Care Unit, 72 of whom had sustained an acute myocardial infarction (AMI). In patients with AMI, the initial pulmonary capillary wedge (PCW) pressure was related to prognosis, with a mortality of 68% in those with elevated pressures. The mean PCW pressure was 25 mmHg in those who died as compared with 17 mmHg (p less than 0.01) in the survivors. Cardiac catheterization confirmed the clinical impression of high risk in the majority of cases but also identified those in whom the clinical signs were misleading; 9 of those with AMI (12.5%) had high PCW pressures in the absence of clinical or radiological heart failure. The diagnosis of serious hemodynamic complications of AMI (right ventricular infarction, ventricular septal defect, and mitral regurgitation) was established in 14 cases (19%). There were no serious complications related to catheterization, and we conclude that pulmonary artery catheterization is safe and of clinical value in acutely ill cardiac patients.     

Serum uric acid levels correlate with filling pressures in systolic heart failure

The authors studied the relationship between liver function tests and serum uric acid level with clinical and hemodynamic profiles in heart failure. Fifty patients (aged 44±15 years; 74.5% men) with an ejection fraction (EF) <35% were enrolled and clinical assessment was performed. Hemodynamic indices (including pulmonary arterial pressure [PAP], pulmonary capillary wedge pressure [PCWP], and cardiac index were studied by standard Edwards Lifesciences Swan-Ganz catheters, and liver function tests and serum uric acid level were measured simultaneously. Fifty age- and sex-matched controls with normal EF were also studied. A total of 73% of patients had ischemic cardiomyopathy. Mean uric acid level was 7.2±3.8 mg/dL and was significantly higher than in the control group (P value<.001). In multivariate analysis, uric acid correlated significantly with PAP (r=.5, P<.001) and PCWP (r=.4, P=.002) and was also associated with clinical signs of rales, edema, paroxysmal nocturnal dyspnea (r=.5, P=.01), and New York Heart Association class (r=.4, P=.005). Uric acid level was also correlated inversely with left ventricular EF (r=.27, P=.006). Elevated uric acid levels in patients with systolic heart failure is associated with impaired clinical and hemodynamic profile and might be used as a noninvasive indicator of elevated left ventricular filling pressures.     

Effect of nasal continuous positive airway pressure on cardiac output and oxygen delivery in patients with congestive heart failure.

We studied the acute hemodynamic effects of increasing nasal continuous positive airway pressure (CPAP) in 13 patients with acute decompensation of congestive heart failure. Heart rate, respiratory rate, pulmonary capillary wedge pressure, right atrial pressure, systemic blood pressure, and thermodilution cardiac outputs were measured at baseline, during, and after application of nasal CPAP at increasing pressures of 5, 10, and 15 cm H2O. Cardiac index, stroke volume, and oxygen delivery were calculated. Based on a significant change in cardiac output greater than or equal to 400 ml, seven patients were classified as responders, whereas six patients were considered to be nonresponders. In responders, significant increases were noted in cardiac index (2.5 +/- 0.7 to 2.9 +/- 0.9 L/min/m2), stroke volume (49 +/- 15 to 57 +/- 16 ml), and oxygen delivery (10.3 +/- 5.1 to 12.3 +/- 6.0 ml/min/kg) without a change in pulmonary capillary wedge pressure. In contrast, the nonresponders showed no significant change in any of the hemodynamic parameters. Improvement in cardiac output could not be predicted by any of the baseline hemodynamic or clinical variables, nor was it related to random variations since all variables returned to baseline after cessation of CPAP. Increase in stroke volume without a change in pulmonary capillary wedge pressure (preload) suggests either improved inotropic function of the left ventricle or reduced left ventricular afterload with CPAP. Thus, CPAP may offer a new noninvasive adjunct to improving left ventricular function and augmenting cardiac performance in a subset of patients with congestive heart failure.     

Transthoracic echocardiographic parameters in the estimation of pulmonary capillary wedge pressure in patients with present or previous heart failure

Multiple echocardiographic criteria are routinely used for the estimation of left heart filling pressures. We assessed the predictive value of various echocardiographic parameters to estimate the left heart filling pressure and proposed a simplified approach for its evaluation. We collected the clinical, echocardiographic, and invasive hemodynamic data from 93 patients with heart failure who underwent right-sided heart catheterization and transthoracic echocardiography within a 24-hour period. Of these 93 patients, 57% had a left ventricular ejection fraction <50% and 69% had an elevated mean pulmonary capillary wedge pressure of ≥15 mm Hg. A mitral E/E' of ≥15 had a sensitivity of 55% but a specificity of 96%. A left atrial area of ≥20 cm(2) had a sensitivity of 66% and specificity of 89%. A deceleration time <140 ms had a sensitivity of 51% and specificity of 93% to predict a pulmonary capillary wedge pressure of ≥15 mm Hg. The combination of E/E' ≥15 ± left atrial area of ≥20 cm(2) ± deceleration time <140 ms provided a sensitivity of 92% and specificity of 85%. On multivariate analysis, the combination of E/E' ≥15, left atrial area of ≥20 cm(2), and deceleration time <140 ms was the most significant predictor of a pulmonary capillary wedge pressure of ≥15 mm Hg (odds ratio 48, 95% confidence interval 10 to 289, p <0.001). In conclusion, this simplified approach using 3 echocardiographic parameters provides an accurate and a practical approach for the routine estimation of the elevated left heart filling pressure.     

急性心肌梗塞并发室内传导障碍与近期预后

本文分析127例急性心肌梗塞(AMI)病例,其中无室内传导障碍(NIVCD)91例,并发室内传导障爵(IVCD)36例(28%)。住院期(6～8周)病死率:NIVCD者15.4%,IVCD者33.3%,差异显著(P<0.025),合并IVCD者的病死率高于NIVCD者两倍。     

急性下壁心肌梗塞发生左前分支阻滞的意义

为探讨急性下壁心肌梗塞发生左前分支阻滞的意义,根据心电图把52例首次急性下壁心肌梗塞的病人分成发生左前分支阻滞组(A组)和未发生左前分支阻滞组(B组),并对两组的临床资料及冠脉造影结果对照分析.结果发现17.3%的急性下壁心肌梗塞病人发生左前分支阻滞,两组的临床特点及冠脉造影结果无显著性差异.提示在急性下壁心肌梗塞发生左前分支阻滞不能作为前降支病变及多支血管病变的标志.     

Milrinone in congestive heart failure: acute and chronic hemodynamic and clinical evaluation

Acute and chronic hemodynamic and clinical responses to milrinone, a new oral inotrope-vasodilator agent, were evaluated prospectively in 37 patients with severe congestive heart failure. The majority of patients (n = 31) had not responded to prior vasodilator therapy, with a substantial number (n = 8) requiring intravenous inotropic support at the time of initial study. All patients showed acute hemodynamic improvement with oral milrinone, and an optimal maintenance dose was chosen for each patient during dose-ranging studies (average dose 48 mg/day). Milrinone was discontinued before follow-up hemodynamic study in 12 patients (because of worsening congestive heart failure in 6 patients, sudden death in 3 patients, arrhythmia in 1 patient and refusal by 2 patients). Hemodynamic effects of milrinone both acutely and after chronic therapy (average 37 days) were compared in the remaining 25 patients. Acutely, mean cardiac index increased from 1.9 +/- 0.5 to 2.5 +/- 0.5 liters/min per m2 (p less than 0.001), and mean pulmonary capillary wedge pressure decreased from 28 +/- 9 to 18 +/- 8 mm Hg (p less than 0.001). When oral milrinone was readministered after chronic therapy, mean cardiac index increased from 1.9 +/- 0.5 to 2.5 +/- 1.7 liters/min per m2 (p less than 0.001), and pulmonary capillary wedge pressure decreased from 27 +/- 8 to 20 +/- 8 mm Hg (p less than 0.001) at 1 hour. New York Heart Association functional class improved in 18 of the 25 patients treated over a long-term period (mean 5.5 +/- 2.3 months).(ABSTRACT TRUNCATED AT 250 WORDS)