A highly unusual right atrial mass presented in two women.

Intravenous leiomyomatosis is a rare, benign neoplasm of the uterine, affecting adult women. We report two cases in whom intravenous leiomyomatosis extended through the inferior vena cava into the right heart chambers and the pulmonary artery. Both patients underwent staged operation with excision of the cardiac and primary tumour. The differential diagnosis of a right atrial mass in middle-aged women should include intravenous leiomyomatosis.

Impact of atrioventricular compliance on pulmonary artery pressure in mitral stenosis: an exercise echocardiographic study.

BACKGROUND: The decay of the pressure gradient across a stenotic mitral valve is determined by the size of the orifice and net AV compliance (C(n)). We have observed a group of symptomatic patients, usually in sinus rhythm, characterized by pulmonary hypertension (particularly during exercise) despite a relatively large mitral valve area by pressure half-time. We speculated that this discrepancy was due to low atrial compliance causing both pulmonary hypertension and a steep decay of the transmitral pressure gradient despite significant stenosis. We therefore tested the hypothesis that C(n) is an important physiological determinant of pulmonary artery pressure at rest and during exercise in mitral stenosis. METHODS AND RESULTS: Twenty patients with mitral stenosis were examined by Doppler echocardiography. C(n), calculated from the ratio of effective mitral valve area (continuity equation) and the E-wave downslope, ranged from 1.7 to 8.1 mL/mm Hg. Systolic pulmonary artery pressure (PAP) increased from 43+/-12 mm Hg at rest to 71+/-23 mm Hg (range, 40 to 110 mm Hg) during exercise. There was a particularly close correlation between C(n) and exercise PAP (r=-0.85). Patients with a low compliance were more symptomatic (P<0.025). Catheter- and Doppler-derived values for C(n), determined in 10 cases, correlated well (r=0.79). CONCLUSIONS: C(n), which can be noninvasively assessed, is an important physiological determinant of PAP in mitral stenosis. Patients with low C(n) represent an important clinical entity, with symptoms corresponding to severe increases in PAP during stress echocardiography.

L-NMMA (a nitric oxide synthase inhibitor) is effective in the treatment of cardiogenic shock.

BACKGROUND: The objective was to assess the safety and efficacy of L-NMMA in the treatment of cardiogenic shock. METHODS: We enrolled 11 consecutive patients with cardiogenic shock that persisted after >24 hours from admission, despite coronary catheterization and primary percutaneous transluminal coronary revascularization, when feasible, and treatment with mechanical ventilation, intraaortic balloon pump (IABP), and high doses of catecholamines. L-NMMA was administered as an IV bolus of 1 mg/kg and continuous drip of 1 mg. kg(-1). h(-1) for 5 hours. Treatment with catecholamines, mechanical ventilation, and IABP was kept constant throughout the study. RESULTS: Within 10 minutes of L-NMMA administration, mean arterial blood pressure (MAP) increased from 76+/-9 to 109+/-22 mm Hg (+43%). Urine output increased within 5 hours from 63+/-25 to 156+/-63 cc/h (+148%). Cardiac index decreased during the steep increase in MAP from 2. 0+/-0.5 to 1.7+/-0.4 L/(min. m(2)) (-15%); however, it gradually increased to 1.85+/-0.4 L/(min. m(2)) after 5 hours. The heart rate and the wedge pressure remained stable. Twenty-four hours after L-NMMA discontinuation, MAP (+36%) and urine output (+189%) remained increased; however, cardiac index returned to pretreatment level. No adverse events were detected. Ten out of eleven patients could be weaned off mechanical ventilation and IABP. Eight patients were discharged from the coronary intensive care unit, and seven (64%) were alive at 1-month follow-up. CONCLUSIONS: L-NMMA administration in patients with cardiogenic shock is safe and has favorable clinical and hemodynamic effects.

Myocardial viability as a determinant of the ejection fraction response to carvedilol in patients with heart failure (CHRISTMAS trial): randomised controlled trial.

BACKGROUND: The improvement in left-ventricular ejection fraction (LVEF) in response to beta blockers is heterogeneous in patients with heart failure due to ischaemic heart disease, possibly indicating variations in the myocardial substrate underlying left-ventricular dysfunction. We investigated whether improvement in LVEF was associated with the volume of hibernating myocardium (viable myocardium with contractile failure). METHODS: We did a double-blind, randomised trial to compare placebo and carvedilol for 6 months in individuals with stable, chronic heart failure due to ischaemic left-ventricular systolic dysfunction. We enrolled 489 patients, of whom 387 were randomised. Patients were designated hibernators or non-hibernators according to the volume of hibernating myocardium. The primary endpoint was change in LVEF, measured by radionuclide ventriculography, in hibernators versus non-hibernators, on carvedilol compared with placebo. Analysis was by intention to treat. RESULTS: 82 patients dropped out of the study because of adverse events, withdrawal of consent, or failure to complete the investigation. Thus, 305 (79%) were analysed. LVEF was unchanged with placebo (mean change -0.4 [SE 0.9] and -0.4 [0.8] for non-hibernators and hibernators, respectively) but increased with carvedilol (2.5 [0.9] and 3.2 [0.8], respectively; p<0.0001 compared with baseline). Mean placebo-subtracted change in LVEF was 3.2% (95% CI 1.8-4.7; p=0.0001) overall, and 2.9% (0.7-5.1; p=0.011) and 3.6% (1.7-5.4; p=0.0002) in non-hibernators and hibernators, respectively. Effect of hibernator status on response of LVEF to carvedilol was not significant (0.7 [-2.2 to 3.5]; p=0.644). However, patients with more myocardium affected by hibernation or by hibernation and ischaemia had a greater increase in LVEF on carvedilol (p=0.0002 and p=0.009, respectively). INTERPRETATION: Some of the effect of carvedilol on LVEF might be mediated by improved function of hibernating or ischaemic myocardium, or both. Medical treatment might be an important adjunct or alternative to revascularisation for patients with hibernating myocardium.

Shortened Doppler-derived mitral A wave deceleration time: an important predictor of elevated left ventricular filling pressure.

OBJECTIVES: The aim of this study was to investigate whether a new variable of mitral inflow, A wave deceleration time, identifies patients with elevated left ventricular filling pressures. BACKGROUND: In patients with an elevated left ventricular end-diastolic pressure, the increase in left ventricular pressure after atrial contraction rapidly exceeds left atrial pressure, resulting in abrupt cessation of the A wave. Therefore, we postulated that a shortening of A wave deceleration time might be a marker for elevated end-diastolic pressure. METHODS: Adequate pulsed Doppler mitral inflow velocities could be recorded in 40 of 44 consecutive patients undergoing cardiac catheterization with capillary wedge pressure in 20 patients, and within 1 h after left ventricular end-diastolic pressure recording in 20. Fifteen healthy volunteers were also studied. RESULTS: Left ventricular end-diastolic pressure was 8 to 35 mm Hg, and mean pulmonary wedge pressure was 6 to 37 mm Hg. Close correlations were found between A wave deceleration time and mean pulmonary wedge pressure (r = -0.87) and left ventricular end-diastolic pressure (r = -0.74). There were modest correlations between both pressures and peak E/A, E wave deceleration time and A wave duration, respectively; r = 0.59, -0.30 and -0.58 for capillary wedge and r = 0.25, -0.38 and -0.49 for end-diastolic pressures. A wave deceleration time 18 mm Hg, respectively, with a sensitivity of 67% and 89% and specificity of 100% for both. CONCLUSIONS: A shortened Doppler mitral inflow A wave deceleration time is a useful index of elevated left ventricular filling pressure.

Improved posterobasal segment function after thrombolysis is associated with decreased incidence of significant mitral regurgitation in a first inferior myocardial infarction.

OBJECTIVES: This study was designed to investigate the association between wall motion abnormalities and the occurrence of ischemic mitral regurgitation in patients with a first inferior or posterior myocardial infarction and to reassess the role of thrombolytic treatment in these patients. BACKGROUND: We previously demonstrated that thrombolytic therapy reduces the incidence of significant mitral regurgitation in patients with a first inferior myocardial infarction, but the mechanisms responsible for this decrease were not clear. METHODS: Wall motion score on two-dimensional echocardiography (16 segments) and mitral regurgitation grade (0 to 3) on Doppler color flow imaging were assessed in 95 patients (in 47 after thrombolysis) at 24 h, 7 to 10 days and 1 month after myocardial infarction. Significant mitral regurgitation was defined as moderate or severe (grade 2 or 3). RESULTS: Multivariate analysis revealed that the presence of an advanced wall motion abnormality of the posterobasal segment of the left ventricle was the most significant independent variable associated with significant mitral regurgitation: odds ratio (OR) 15.0, 90% confidence interval (CI) 1.4 to 165.6 at 24 h; OR 2.8, CI 0.9 to 9.3 at 7 to 10 days; OR 4.2, CI 1.2 to 11.4 at 1 month. Thrombolysis reduced the prevalence of advanced wall motion abnormalities in the posterobasal segment at 24 h (55% vs. 75%, OR 0.5, CI 0.2 to 0.99), 7 to 10 days (44% vs. 73%, OR 0.3, CI 0.1 to 0.7) and 1 month (36% vs. 56%, OR 0.4, CI 0.2 to 0.9). CONCLUSIONS: There is a strong association between advanced wall motion abnormalities in the posterobasal segment and significant mitral regurgitation. In this study group, thrombolysis reduced the prevalence of advanced wall motion abnormalities in the posterobasal segment and thereby reduced the incidence of significant mitral regurgitation.

Left ventricular pseudohypertrophy in cardiac tamponade: an echocardiographic study in a canine model.

OBJECTIVES: This study was designed to establish whether left ventricular pseudohypertrophy in cardiac tamponade can be reproducibly induced in an experimental canine model and to investigate the mechanism of its production. BACKGROUND: Past experimental and clinical studies have shown reduction of ventricular volumes resulting from cardiac tamponade. Left ventricular pseudohypertrophy, a transient thickening of myocardial walls, was recently described as a new echocardiographic sign of cardiac tamponade. METHODS: Cardiac tamponade was induced in seven anesthetized open chest dogs with serial bolus injections of 50 ml each of 0.9% saline solution into the pericardial sac. Under hemodynamic monitoring, M-mode and two-dimensional echocardiographic measurements were performed from a right parasternal window at each stage of graded cardiac tamponade. RESULTS: There was a progressive increase of interventricular septal and posterior wall diastolic thickness. Mean wall thickness (interventricular septal thickness + posterior wall thickness divided by 2) was 9.8 +/- 1.3 mm at baseline, 14.3 +/- 0.9 mm at peak tamponade and 9.0 +/- 1.5 mm after fluid withdrawal (p < 0.0001). Mean wall thickness correlated directly with the severity of cardiac tamponade, as estimated from the level of right arterial pressures (r = 0.75 and p < 0.0001), and with the decrease of left ventricular cavity volume (r = -0.67 and p < 0.0001). Left ventricular mass did not change significantly. CONCLUSIONS: Left ventricular pseudohypertrophy is a constant manifestation of cardiac tamponade in a canine model. The degree of myocardial thickening correlates with the reduction of ventricular dimensions and with the severity of hemodynamic compromise, representing a constant facet of heart remodeling in cardiac tamponade.

Effect of thrombolytic therapy on the evolution of significant mitral regurgitation in patients with a first inferior myocardial infarction.

OBJECTIVES: This study was designed to test the hypothesis that reperfusion therapy with thrombolysis will prevent the development of significant mitral regurgitation in patients with inferior myocardial infarction. BACKGROUND: The value of thrombolytic therapy in patients with inferior or posterior wall myocardial infarction has been controversial. We hypothesized that successful reperfusion therapy with intravenous thrombolysis may reduce the incidence and severity of postinfarction mitral regurgitation in this patient group. METHODS: We prospectively studied 104 patients with a first inferior myocardial infarction. Thrombolytic therapy was administered to 55 patients (treatment group) 3.2 +/- 2.1 h after the onset of symptoms. The other 49 patients formed the control group. Doppler echocardiographic color flow imaging was performed in all patients within 24 h, at 7 to 10 days and at 28 to 30 days after myocardial infarction. Significant mitral regurgitation was defined as moderate or severe (grade 2 or 3). RESULTS: No significant differences in baseline clinical characteristics were observed between the treatment and control groups. The overall incidence rates of significant mitral regurgitation at 24 h, 7 to 10 days and at 28 to 30 days were 10 (10%) of 104 patients, 18 (17%) of 104 patients and 11 (11%) of 100 patients, respectively. Multivariate analysis reveals the following independent predictors of the occurrence of significant mitral regurgitation: female gender (at 7 to 10 days, odds ratio 5.3, 90% confidence interval [CI] 1.8 to 15.5; at 28 to 30 days, odds ratio 3.7, 90% CI 1.1 to 12.7), heart failure (at 7 to 10 days, odds ratio 7.7, 90% CI 2.2 to 26.9) and transient complete atrioventricular block (at 24 h of myocardial infarction, odds ratio 5.8, 90% CI 1.2 to 27). Compared with the control group, the treatment group exhibited marked reduction in the incidence of significant mitral regurgitation at 24 h (16% vs. 4%; odds ratio 0.1, 90% CI 0.0 to 0.7); at 7 to 10 days (24% vs. 11%; odds ratio 0.3, 90% CI 0.1 to 0.9) and at 28 to 30 days (15% vs. 7%; odds ratio 0.4, 90% CI 0.1 to 1.6). Severe (grade 3) mitral regurgitation developed in five patients in the control group but in no patient in the treatment group. CONCLUSIONS: Thrombolytic therapy in the patients with a first inferior myocardial infarction was associated with a reduced incidence of significant mitral regurgitation. These results support the use of such therapy in patients with inferior myocardial infarction.

Intracoronary injection of basic fibroblast growth factor enhances angiogenesis in infarcted swine myocardium.

OBJECTIVES: This study was performed to examine the effect of intracoronary exogenous basic fibroblast growth factor (bFGF) on angiogenesis in infarcted myocardial regions. BACKGROUND: Exogenous bFGF is a potent promoter of angiogenesis. Little information is available on its effect on myocardial angiogenesis. METHODS: Myocardial infarction was induced in 10 pigs by intracoronary injection of microscopic beads. Four pigs served as a control group; in six pigs slow-release bFGF was delivered by the beads. Cardiac performance was evaluated by repeated echocardiographic measurement and angiogenesis was evaluated by immunohistochemical studies 14 days later. RESULTS: As compared with control pigs, pigs treated with bFGF had higher microvessel counts (mean +/- SEM) in both viable tissue (141 +/- 27 per field vs. 39 +/- 4, p = 0.01) and nonviable tissue (329 +/- 26 per field vs. 95 +/- 7, p < 0.001) within the infarct area. No significant differences in total regional left ventricular wall motion were noted between the two groups throughout the 14-day study period. CONCLUSIONS: In the swine, direct intracoronary application of bFGF to infarcted myocardium enhances myocardial neovascularization within 2 weeks.

Ultrasound integrated backscatter tissue characterization of remote myocardial infarction in human subjects.

To determine whether quantitative ultrasound tissue characterization differentiates normal myocardial regions from segments of remote infarction, 32 consecutive patients with a diagnosis of previous myocardial infarction were evaluated. Images were obtained in real time with a modified two-dimensional ultrasound system capable of providing continuous signals in proportion to the logarithm of integrated backscatter along each A line. In 15 patients, adequate parasternal long-axis images that delineated both normal and infarct segments were obtained with standard time-gain compensation. Image data were analyzed to yield both magnitude and delay (electrocardiographic R wave to nadir normalized for the QT interval) of the cyclic variation of backscatter. Cyclic variation was present in 55 of 56 normal myocardial sites, averaging (mean +/- SEM) 3.2 +/- 0.2 dB in magnitude and exhibiting a mean normalized delay of 0.87 +/- 0.03. The magnitude of cyclic variation in infarct segments was significantly reduced to 1.1 +/- 0.2 dB (42 sites), and the delay was markedly increased to 1.47 +/- 0.12 (21 sites) (p less than 0.0001 for both). In 20 of 42 infarct sites, no cyclic variation was detectable. Thus, ultrasound tissue characterization quantitatively differentiated infarct segments from normal myocardium in patients with remote myocardial infarction.

High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema.

OBJECTIVE: To determine the feasibility, safety and efficacy of bilevel positive airway ventilation (BiPAP) in the treatment of severe pulmonary edema compared to high dose nitrate therapy. BACKGROUND: Although noninvasive ventilation is increasingly used in the treatment of pulmonary edema, its efficacy has not been compared prospectively with newer treatment modalities. METHODS: We enrolled 40 consecutive patients with severe pulmonary edema (oxygen saturation <90% on room air prior to treatment). All patients received oxygen at a rate of 10 liter/min, intravenous (IV) furosemide 80 mg and IV morphine 3 mg. Thereafter patients were randomly allocated to receive 1) repeated boluses of IV isosorbide-dinitrate (ISDN) 4 mg every 4 min (n = 20), and 2) BiPAP ventilation and standard dose nitrate therapy (n = 20). Treatment was administered until oxygen saturation increased above 96% or systolic blood pressure decreased to below 110 mm Hg or by more than 30%. Patients whose conditions deteriorated despite therapy were intubated and mechanically ventilated. All treatment was delivered by mobile intensive care units prior to hospital arrival. RESULTS: Patients treated by BiPAP had significantly more adverse events. Two BiPAP treated patients died versus zero in the high dose ISDN group. Sixteen BiPAP treated patients (80%) required intubation and mechanical ventilation compared to four (20%) in the high dose ISDN group (p = 0.0004). Myocardial infarction (MI) occurred in 11 (55%) and 2 (10%) patients, respectively (p = 0.006). The combined primary end point (death, mechanical ventilation or MI) was observed in 17 (85%) versus 5 (25%) patients, respectively (p = 0.0003). After 1 h of treatment, oxygen saturation increased to 96 +/- 4% in the high dose ISDN group as compared to 89 +/- 7% in the BiPAP group (p = 0.017). Due to the significant deterioration observed in patients enrolled in the BiPAP arm, the study was prematurely terminated by the safety committee. CONCLUSIONS: High dose ISDN is safer and better than BiPAP ventilation combined with conventional therapy in patients with severe pulmonary edema.

Normal left ventricular performance in children with X-linked hypophosphatemic rickets: a Doppler echocardiography study.

To determine if chronic hypophosphatemia causes myocardial dysfunction, we explored one model for this metabolic derangement by prospectively investigating 11 patients (aged 5-18 years) with X-linked hypophosphatemic rickets (XLH) by M-mode, two-dimensional, and Doppler echocardiography. Inorganic phosphate and calcitriol (1,25-dihydroxyvitamin D3) treatment was withheld 72 h prior to study. None of the patients had cardiovascular symptoms. Fasting serum inorganic phosphate concentrations were subnormal in all: 2.6 +/- 0.5 mg/dl (SD). Serum total and ionized calcium, magnesium, sodium, potassium, and creatine kinase myocardial fraction (CK-MB) levels were unremarkable. Electrocardiograms revealed early repolarization abnormalities in 3 of the 11 patients: 1 had significant QT prolongation (corrected for heart rate), and 2 had T wave abnormalities. Exaggerated U waves occurred in 4 subjects. Resting echocardiograms were normal in 9 patients. In 1 subject there was mitral valve prolapse, and 1 patient possibly had an atrial septal defect (these findings were considered unrelated to hypophosphatemia). All M-mode measurements were normal. The two-dimensionally derived end-diastolic and end-systolic left ventricular volumes were 60.3 +/- 18.0 and 20.5 +/- 6.9 ml, respectively. Left ventricular ejection fraction was 66.1 +/- 4.7%, and the cardiac index by Doppler study was 4.1 +/- 0.8 liters/min per m2 (both values were within normal limits). Although the precise pathogenesis of XLH is unknown and our findings suggest that some electrocardiographic abnormalities may be common in this disorder, we found no evidence for left ventricular dysfunction in this human model of clinically significant long-standing hypophosphatemia.

Normal left ventricular performance documented by Doppler echocardiography in patients with long-standing hypocalcemia.

INTRODUCTION: Several reports suggest significantly reduced left ventricular performance in subjects with chronic hypocalcemia. We prospectively investigated eight patients, aged 13 to 31 years, with long-standing hypocalcemia due to idiopathic hypoparathyroidism or pseudohypoparathyroidism by echocardiography. PATIENTS AND METHODS: Six subjects had symptomatic hypocalcemia manifested as recurrent tetany (four), seizures (four), mental retardation (three), behavior disorder (one), and skeletal abnormalities (four); three subjects were untreated when studied. None had cardiovascular symptoms. Each patient underwent clinical, biochemical, and cardiac studies, including Doppler, two-dimensional, and M-mode echocardiography, on the same day. RESULTS: In serum, both total and ionized calcium concentrations were reduced and averaged 7.2 mg/dl (range: 5.3 to 8.5 mg/dl; normal: 9.0 to 10.3 mg/dl) and 3.6 mg/dl (range: 3.0 to 3.9 mg/dl; normal: 4.5 to 5.3 mg/dl), respectively. Electrocardiograms revealed prolonged QTc intervals in six patients. Also noted were prominent U waves (five), T-wave abnormalities (four), and right-axis deviation (one). Resting echocardiography, however, demonstrated normal left ventricular function in all subjects. All M-mode measurements were normal. Two-dimensional-derived left ventricular end-diastolic and end-systolic volumes were 87.1 +/- 20.1 ml and 30.2 +/- 9.7 ml (mean +/- SD), respectively. Left ventricular ejection fraction was 65 percent (61.2 to 74.7 percent). Doppler-derived cardiac output and cardiac index averaged 5.1 liters/minute (2.9 to 6.7 liters/minute) and 3.0 liters/minute/m2 (1.7 to 4.3 liters/minute/m2), respectively. CONCLUSION: Our prospective study of eight subjects with functional hypoparathyroidism demonstrated that, despite electrocardiographic abnormalities, long-standing hypocalcemia was not associated with left ventricular dysfunction.

Thiamine deficiency in patients with congestive heart failure receiving long-term furosemide therapy: a pilot study.

PURPOSE: To test the hypothesis that long-term furosemide therapy in patients with congestive heart failure (CHF) is associated with clinically significant thiamine deficiency via urinary loss. DESIGN: (1) Biochemical evaluation of thiamine status in hospitalized patients with CHF treated with long-term furosemide and in age-matched control patients. (2) Uncontrolled trial of the effect of intravenous thiamine on cardiac performance in a subset of six patients with CHF. SETTING: General medical ward of a teaching community hospital. PATIENTS: Twenty-three patients with chronic CHF receiving furosemide, and 16 age-matched control patients without heart failure and not taking diuretics. Daily furosemide doses were 80 to 240 mg, and duration of furosemide therapy was 3 to 14 months. Patients with identifiable causes of inadequate thiamine intake, absorption, or utilization or increased metabolic requirements were excluded. INTERVENTION: A 7-day course of intravenous thiamine, 100 mg twice daily, in six consenting patients with CHF. RESULTS: A high thiamine pyrophosphate effect (TPPE), indicating thiamine deficiency, was found in 21 of 23 furosemide-treated patients and in two of 16 controls (p less than 0.001). The mean (+/- SE) TPPE (normal: 0% to 15%) in furosemide-treated and control patients was 27.7 +/- 2.5% and 7.1 +/- 1.6%, respectively (p less than 0.001). Despite the high TPPE, the mean (+/- SE) urinary thiamine excretion in the furosemide-treated patients (n = 18) was inappropriately high (defined as greater than 130 micrograms/g creatinine), 410 +/- 95 micrograms/g creatinine, even in comparison with that in the controls (n = 14): 236 +/- 69 micrograms/g creatinine. In six patients treated with intravenous thiamine, the elevated TPPE decreased to normal, from a mean (+/- SE) of 27.0 +/- 3.8% to 4.5 +/- 1.3% (p less than 0.001), indicating normal thiamine utilization capacity. Left ventricular ejection fraction increased in four of five of these patients studied by echocardiography. CONCLUSIONS: These preliminary findings suggest that long-term furosemide therapy may be associated with clinically significant thiamine deficiency due to urinary loss and contribute to impaired cardiac performance in patients with CHF. This deficit may be prevented or corrected by appropriate thiamine supplements.

Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy.

PURPOSE: We have previously found thiamine (vitamin B1) deficiency in patients with congestive heart failure (CHF) who had received long-term furosemide therapy. In the present study, we assessed the effect of thiamine repletion on thiamine status, functional capacity, and left ventricular ejection fraction (LVEF) in patients with moderate to severe CHF who had received furosemide in doses of 80 mg/d or more for at least 3 months. PATIENTS AND METHODS: Thirty patients were randomized to 1 week of double-blind inpatient therapy with either i.v. thiamine 200 mg/d or placebo (n = 15 each). All previous drugs were continued. Following discharge, all 30 patients received oral thiamine 200 mg/d as outpatients for 6 weeks. Thiamine status was determined by the erythrocyte thiamine-pyrophosphate effect (TPPE). LVEF was determined by echocardiography. RESULTS: TPPE, diuresis, and LVEF were unchanged with i.v. placebo. After i.v. thiamine, TPPE decreased (11.7% +/- 6.5% to 5.4% +/- 3.2%; P < 0.01). LVEF increased (0.28 +/- 0.11 to 0.32 +/- 0.09; P < 0.05), as did diuresis (1,731 +/- 800 mL/d to 2,389 +/- 752 mL/d; P < 0.02), and sodium excretion (84 +/- 52 mEq/d to 116 +/- 83 mEq/d, P < 0.05). In the 27 patients completing the full 7-week intervention, LVEF rose by 22% (0.27 +/- 0.10 to 0.33 +/- 0.11, P < 0.01). CONCLUSIONS: Thiamine repletion can improve left ventricular function and biochemical evidence of thiamine deficiency in some patients with moderate-to-severe CHF who are receiving longterm furosemide therapy.

Systematic analysis of contrast echocardiograms.

Contrast echocardiography was first described in 1968. Since then, many reports have described clinical and experimental uses for the technique. Contrast echocardiography is performed at least occasionally in most echocardiography laboratories, but most physicians use this technique merely to determine the presence of a shunt or, more rarely, for structure identification. Contrast echocardiography can provide much more information. Some different types of information available from contrast echocardiographic records are discussed, including timing of contrast appearance within the cardiac cycle, relative timing of appearance in different cardiac structures, relative intensity of contrast opacification, cyclical changes in contrast opacification, negative contrast effect, slope of contrast trajectories on M-mode contrast echocardiography, and clearance times.

Two-dimensional echocardiography in discrete subaortic stenosis.

Thirty-seven patients with discrete subaortic stenosis (DSS) underwent 2-dimensional echocardiography (2-D echo) and cardiac catheterization. The peak systolic pressure gradients ranged from 0 to 150 mm Hg. Thirty-two patients had membranous DSS and 5 had fibromuscular DSS. Of 37 patients with DSS, 2-D echo diagnosed the presence and type in 35; in 2, a membrane was demonstrated by angiography. Of the 35 patients accurately diagnosed by 2-D echo, angiography corroborated the diagnosis in 33, but failed to show the membrane in 2. Subsequent cardiac surgery confirmed the accuracy of the echocardiographic diagnosis in these 2 patients. In all patients with membranous DSS, the anterior insertion of the membrane was demonstrated. In 9 of them the posterior insertion was demonstrated by tilt of the transducer but the anterior insertion disappeared. In 4 patients both insertions were demonstrated simultaneously and in 3 patients the membrane was demonstrated as a continuous line. In 4 of the 5 patients with fibromuscular DSS, both insertions of the lesion were demonstrated simultaneously. However, 2-D echo was unsuccessful in assessing the severity of obstruction. In only 1 patient did demonstration of the whole subaortic membrane as a continuous line below the aortic valve correlate with severe obstruction. Thus, the presence and type of DSS, but not the degree and severity, can be accurately and reliably diagnosed by means of 2-D echo.

Diagnosing tricuspid regurgitation by direct imaging of the regurgitant flow in the right atrium using contrast echocardiography.

To determine whether tricuspid regurgitation (TR) can be diagnosed by direct imaging of regurgitant flow in the right atrium (RA) using contrast echocardiography, echocardiography was performed in 35 patients using peripheral intravenous injections of 5% dextrose solution. Fifteen patients had TR judged by v-wave synchronous contrast appearance on the inferior vena cava echogram (a previously validated method for diagnosing TR), 5 of whom had clinically obvious TR. Twenty patients had no TR on inferior vena cava contrast echocardiography, 9 of whom were normal volunteers. On subsequent blind review, 13 of the 15 patients with TR were correctly identified on the basis of the regurgitant contrast flow just posterior to the tricuspid valve in the RA. Of the 20 without TR, 19 were correctly identified and there was 1 false-positive result. Using different criteria for the diagnosis (insisting on imaging of flow across the tricuspid valve in systole), another blinded observer correctly diagnosed only 8 of the 15 patients as having TR, but had no false-positive results. To avoid false-positive results, it is important to realize that there are 2 regions where retrograde flow can normally be seen in the RA: (1) briefly at the onset of systole coincident with tricuspid valve closure, and (2) in the posterior RA, as distinct from the anterior RA area just behind the tricuspid valve where TR is diagnosed in this study.(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of losartan, captopril, and furosemide in preventing nitrate tolerance and improving control of unstable angina pectoris.

Sixty consecutive normotensive patients with unstable angina pectoris, who were on continuous intravenous isosorbide dinitrate (ISDN) treatment and had not previously received angiotensin II receptor antagonists, angiotensin-converting enzyme (ACE) inhibitors, or diuretics were randomly assigned to treatment groups receiving intravenous ISDN for 72 hours. No additional treatment was given to group A (n = 15). Captopril, in a test dose of 6.25 mg, and followed by 12.5 mg 3 times daily for 24 hours and 25 mg 3 times daily for the next 24 hours, was given to group B (n = 15). The same dose of captopril plus 40 mg of furosemide in the morning were given to group C (n = 15). Losartan, in a single dose of 25 mg/day and increased to 50 mg after 24 hours was given to group D (n = 15). Nitrate tolerance was evaluated at 24-hour intervals at trough levels of each of the drugs by administering intravenous ISDN (1 mg bolus dose every 4 minutes) and recording the total ISDN test dose required to decrease the mean arterial blood pressure by > or =10%. Treatment with continuous ISDN only (group A) induced nitrate tolerance. The ISDN (mean +/- SD) test dose was 3.5 +/- 1.8 mg at baseline, increasing to 4.9 +/- 2.4 mg at 24 hours, and 8.0 +/- 3.0 mg at 48 hours. The addition of increasing doses of captopril to the continuous ISDN treatment (group B) completely prevented nitrate tolerance. Losartan, however, did not attenuate nitrate tolerance at 24 hours and attenuated it only partially at 48 hours. The addition of furosemide to captopril had no further effect on nitrate tolerance. Of 15 patients in group A (ISDN only), 4 (27%) experienced recurrent ischemic events requiring urgent coronary catheterization. No such events were recorded in group B (captopril), but did occur in 1 patient in each of group C (captopril plus furosemide) and D (losartan) (p = 0.083). Thus, the addition of captopril to the ISDN treatment regimen prevented tolerance to nitrates and improved angina control with apparent safety. Losartan also decreased nitrate tolerance, although to a lesser extent, and also improved angina control. The addition of furosemide to captopril conferred no further benefit.