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Biomedical subjects

S Laniado

Publications and source records attributed to S Laniado.

At least 37 records · Page 2Linked to original sources
PubMed1998

High anti-cytomegalovirus (CMV) IgG antibody titer is associated with coronary artery disease and may predict post-coronary balloon angioplasty restenosis.

Recent studies have demonstrated that cytomegalovirus (CMV) DNA was found in atherosclerotic coronary arteries in restenotic lesions, and prior infection with CMV could be a strong independent risk factor for restenosis after coronary atherectomy. We studied the correlation between anti-CMV antibody titer and coronary artery disease. Sixty-five patients (50 men and 15 women) with coronary artery disease were enrolled prospectively. All had symptomatic coronary artery disease with an angiographic documentation of a de novo single coronary lesion. All underwent balloon coronary angioplasty and were followed for 12 months with a thallium perfusion scan 3 months after angioplasty. Patients who had recurrent chest pain and/or a positive thallium scan had another coronary angiography. Blood samples were taken before angiography and 1 and 3 months later. Patients with high anti-CMV titer > or = 1:800 had a higher prevalence of coronary artery disease (p <0.001) than seropositive patients with a lower antibody titer (< or = 1:400); patients with high antibody titer (> or = 1:800) had a higher restenosis rate than seropositive patients with a low antibody titer (< or = 1:400) (p <0.05). High antibody titers against CMV (IgG) may be a strong marker for coronary artery disease, and might predict post-coronary angioplasty restenosis. These findings support the infectious theory of atherosclerosis (especially with prior CMV infection), and also suggest that a chronic immunologic response has a role in atherosclerosis and restenosis.

Adult↗
PubMed1998

Calcium channel blocking agents and risk of cancer in patients with coronary heart disease. Benzafibrate Infarction Prevention (BIP) Study Research Group.

OBJECTIVES: This analysis sought to estimate the risk ratio for cancer incidence and cancer-related mortality associated with the use of calcium channel blocking agents (CCBs) in a large group of patients with chronic coronary heart disease (CHD). BACKGROUND: Recent publications contend that the use of short-acting CCBs may double the risk of cancer incidence and possibly increase mortality in hypertensive patients. METHODS: Cancer incidence data were obtained for 11,575 patients screened for the Bezafibrate Infarction Prevention (BIP) study, one-half of whom were treated at the time of screening with CCBs, over a mean follow-up period of 2.8 years. Cause-specific mortality was available through September 1996 (mean follow-up 5.2 years). The statistical power of detecting an odds ratio > or = 1.5 (given the cancer incidence rate of 2.1 in the nonusers of CCBs) was 0.91. The power declined to 0.77, 0.54 and 0.41, with declining odds ratios of 1.4, 1.3 and 1.25, respectively. RESULTS: Of 246 incident cancer cases, 129 occurred among the users (2.3%) and 117 among nonusers of CCBs (2.1%). After adjustment for age, gender and smoking, the odds ratio estimates for all cancers combined was 1.07 (95% confidence interval [CI] 0.83 to 1.37) for CCB users relative to nonusers. The adjusted risk ratio for all-cause mortality for age, gender and smoking and pertinent prognostic clinical characteristics was estimated at 0.94 (95% CI 0.85 to 1.04). The adjusted risk ratio for cancer-related mortality was 1.03 (95% CI 0.75 to 1.41). CONCLUSIONS: Patients with CHD treated with CCBs exhibited a similar risk of cancer incidence and total and cancer-related mortality compared with nonusers of CCBs. This analysis provides a certain assurance that CCB use in middle-aged and elderly patients with CHD is not associated with a meaningful difference in cancer incidence and related mortality.

Aged↗
PubMed1998

Serum amyloid type A may be a predictor of restenosis.

BACKGROUND: Elevation of acute phase proteins [C-reactive protein (CRP) and serum amyloid type A (SAA)] has been demonstrated in unstable angina with an adverse clinical prognosis. HYPOTHESIS: The study was undertaken to determine the effect of angioplasty on the levels of SAA and the correlation with postangioplasty restenosis. METHODS: In a university-affiliated tertiary medical center, a prospective case study was undertaken in 55 patients who underwent successful percutaneous transluminal coronary angioplasty (PTCA) of a single coronary lesion for angina pectoris. Three groups of patients were clinically characterized according to Braunwald's classification of anginal syndrome: Group A: class III; Group B: class I; Group C: stable angina. Serum amyloid type A was measured by an ELISA method before PTCA and after 24 h, 1, and 3 months. Patients were followed clinically for 12 months. A thallium stress perfusion scan was performed 3 months after PTCA and coronary angiography was repeated in patients with an abnormal thallium perfusion scan. RESULTS: Serum amyloid type A levels > 100 micrograms/ml could identify Group A patients with a high sensitivity and specificity (r = 0.85 and 0.86, respectively). Of the patients studied, 75% increased their SAA level 24 h after angioplasty. An increase of SAA by > 100% was associated with an increased risk of restenosis, with a relative risk of 6.4 (p < 0.05). CONCLUSION: Increased levels of SAA characterize patients with unstable angina pectoris with a high specificity and sensitivity. Levels of SAA that increase > 100% 24 h after angioplasty may serve as a marker of restenosis.

Adult↗
PubMed1998

Fractal organization of the pointwise correlation dimension of the heart rate.

OBJECTIVE: To depict and quantify the degree of organization of the heart rate variability (HRV) in normal subjects. METHODS: A modified algorithm was created to estimate series of 'point-dimensions' (PD2) from interbeat (R-R) interval series of 10 healthy subjects (21-56 years). Our innovation is twofold: (i) we quantified instances of low-dimensional chaos, random fluctuations, and those for which our method failed to provide either (due to poor statistics); (ii) consecutive subepochs of PD2s underwent a relative dispersion (RD) analysis, yielding an index (D) which quantifies the dynamical organization of the heart rate generator. RESULTS: The mean values of PD2 series varied between 4.58 and 5.88 (mean+/-SD= 5.21+/-0.41, n = 10). For group 1 (21-30 years, n = 6) we found an averaged PD2 of 5.49+/-0.27, while for group 2 (47-56 years, n = 4) PD2 averaged 4.79+/-0.17. The RD analysis performed for subepochs of PD2s yielded both instances obeying fractal scaling (D < 1.5) and stochasticity (D > 1.5). The average D for group 1 was 1.39+/-0.04 (14 subepochs) and for group 2, 1.20+/-0.008 (8 subepochs). Paired t-test and Hartley F-max test for comparison between D values and homogeneity of variance between the two groups were performed, yielding P-values 0.004 and 0.02, respectively. CONCLUSIONS: The complexity of the HRV seems to be modulated by a non-random fractal mechanism of a 'hyperchaotic' system, i.e. it can be hypothesized to contain more than one attractor. Also, our results support the 'chaos hypothesis' put forth recently, namely, the complexity of the cardiovascular dynamics is reduced with aging. The index of relative dispersion of the dimensional complexity has to be tested in various clinico-pathological settings, in order to corroborate its value as a potential new physiological measure.

Adult↗
PubMed1998

Angiographic Morphology Following Heparin and Aspirin Therapy in Patients with Acute Coronary Syndromes and Intracoronary Thrombus.

This series included 26 patients with acute myocardial infarction (15 patients) or unstable angina (11 patients), with thrombotic lesions identified by angiography and treated with intravenous heparin (mean 8 +/- 3 days, aPTT 1.5-2.5 times baseline) and aspirin (250 mg/day). A quantitative angiographic analysis was performed, and comparison of the lesion morphology before and after the antithrombotic treatment was conducted, using a computer-based analysis of the lesion contour. On average, minimal lumen diameter increased by 15.6% (1.15 +/- 0.5mm to 1.33 +/- 0.5mm, P = 0.02), percent diameter stenosis decreased by 10.7% (60.0 +/- 18% to 53.6 +/- 19%, P = 0.009), percent area stenosis decreased by 6.5% (80.0 +/- 14% to 74.8 +/- 16%, P = 0.05), and TIMI flow increased by 8% (2.5 +/- 0.9 to 2.7 +/- 0.7, P = 0.02). A significant improvement in the lesion morphology was more often observed in the right coronary artery (n = 9), than the left coronary artery (n = 16). We conclude that heparin and aspirin therapy improves the angiographic morphology and TIMI flow of thrombotic lesions in patients sustaining the acute coronary syndrome. This improvement was primarily found when the lesion was located in the right coronary artery.

Journal Article↗
PubMed1998

Hemodynamic changes determine the efficacy of thrombolysis: results from an in-vitro flow model.

BACKGROUND: The efficacy of thrombolytic therapy might be influenced by changes in the hemodynamic status. The aim of the study was to examine whether changes in perfusion pressure could affect the time to reflow in an in-vitro model. METHODS: The in-vitro flow system comprised flexible plastic tubes that enclosed a blood clot formed in one of the circuit arms. Streptokinase (125,000 U) or saline (control) was injected from a proximal side branch to induce thrombolysis. The protocol comprised four treatments: A, perfusion pressure 150/90 mmHg with streptokinase infusion; B, perfusion pressure 150/90 mmHg with saline; C, perfusion pressure 120/60 mmHg with streptokinase; D, perfusion pressure 120/60 mmHg with saline. Reflow was defined as flow restoration determined by the ultrasonic flowmeter. RESULTS: Successful recanalization was obtained in six of six samples subjected to treatment A (100%), two of seven samples subjected to treatment B (28%), three of five samples subjected to treatment C (60%) and none of six samples subjected to treatment D (0%). Time to reflow was 23 +/- 11 min with treatment A, 76 +/- 24 min with treatment B, 66 +/- 25 min with treatment C, and > 90 min with treatment D. CONCLUSIONS: Our data suggest that the hemodynamic status determines the efficacy of streptokinase-induced thrombolysis, and that spontaneous clot lysis is more likely to occur at greater perfusion pressures. It is conceivable that the hypotensive reaction induced by streptokinase in the clinical setting may adversely affect angiographic patency, compared with that observed with other lytic agents such as tissue-type plasminogen activator.

Blood Pressure↗
PubMed1998

Transient bradycardia induced by carotid sinus pressure increases outflow obstruction in hypertrophic obstructive cardiomyopathy but not in valvular aortic stenosis.

BACKGROUND: The murmur of hypertrophic obstructive cardiomyopathy (HOCM) increases in intensity in about 80% of those patients in whom carotid sinus pressure (CSP) slows the heart rate. This does not occur in valvular aortic stenosis (AS). STUDY OBJECTIVES, DESIGN, AND PATIENTS: It was hypothesized that left ventricular (LV) obstruction increases with CSP in HOCM and not in AS. Furthermore, it was not clear whether it was the sudden bradycardia or CSP itself that was responsible for the effect noted. Therefore, studies were performed using two different interventions: (1) Doppler echocardiography was performed before and during CSP in 36 HOCM patients and 21 AS patients; (2) two patients with DDD pacemakers and HOCM were examined before and after pacemaker rate slowing. Finally, atrial pacing was performed in three HOCM patients at catheterization, and atrial pacing was either slowed or stopped (without CSP). RESULTS: LV outflow velocity and pressure gradient increased in 28 of 30 HOCM patients (92%) in whom heart rate decreased with CSP. The peak instantaneous pressure gradient increased from 45+/-37 to 77+/-53 mm Hg (p<0.005), and the velocity contour became more typical of HOCM. The pressure gradient increased from 30 mm Hg to 64 and 81 mm Hg, respectively, in the two patients with DDD pacemakers after pacemaker rate slowing. Similar results were seen with slowing or cessation of atrial pacing at catheterization. In contrast, the pressure gradient increased in only three of 21 AS patients (14%), to 44+/-28 from 41+/-25 mm Hg, and remained unchanged in the other 18. CONCLUSION: This study shows that LV outflow velocity and pressure gradient increase markedly in most HOCM patients (92%) if CSP succeeds in slowing the heart rate, but not in patients with valvular AS. A similar effect is obtained by simply decreasing the atrial rate in patients with DDD or atrial pacemakers. This increase in outflow tract obstruction is sufficient to account for the increase in murmur intensity. Decreased afterload (secondary to greater aortic decompression with the longer diastole), increased intrinsic force of contraction with the bradycardia (the Woodworth effect), and Starling's law may play independent roles in the dynamic increase in obstruction observed during CSP in patients with HOCM. Worsening of mitral regurgitation was not clearly shown to contribute to the increase in murmur, but it cannot readily be ruled out.

Adult↗
PubMed1997

Analysis of coronary ultrasound thrombolysis endpoints in acute myocardial infarction (ACUTE trial). Results of the feasibility phase.

BACKGROUND: It has been demonstrated that therapeutic ultrasound effects ultrasound thrombolysis by selectively disrupting the fibrin matrix of the thrombus. This study was conducted to evaluate the clinical feasibility of percutaneous transluminal coronary ultrasound thrombolysis in acute myocardial infarction (AMI). METHODS AND RESULTS: Consecutive patients (n = 15) with evidence of anterior AMI and Thrombolysis in Myocardial Infarction (TIMI) grade 0 or 1 flow in the left anterior descending artery underwent coronary ultrasound thrombolysis. Angiographic follow-up was performed after 10 minutes and 12 to 24 hours. Ultrasound induced successful reperfusion (TIMI grade 3 flow) in 87% of the patients. Adjunct percutaneous transluminal coronary angioplasty (PTCA) after ultrasound thrombolysis produced a final residual stenosis of 20 +/- 12% as determined by quantitative coronary angiographic analysis. There were no adverse angiographic signs or clinical effects during the procedure. There was no change in the degree of flow in any of the patients at the 12- to 24-hour angiograms. During hospitalization, 1 patient had recurrent ischemia on the fifth day after the procedure, and emergent catheterization revealed occlusion at the treatment site. The patient was successfully treated with PTCA. CONCLUSIONS: These results suggest that ultrasound thrombolysis has the potential to be a safe and effective catheter-based therapeutic modality in reperfusion therapy for patients with AMI and other clinical conditions associated with intracoronary thrombosis.

Adult↗
PubMed1997

Usefulness of self-administration of intramuscular lidocaine in the prehospital setting for ventricular tachyarrhythmias unassociated with acute myocardial infarction (the "Shahal" experience in Israel).

We report on the experience accumulated by the subscribers of SHAHAL cardiac services who self-injected intramuscular lidocaine (using an automatic injector "LidoPen") for documented ventricular tachyarrhythmias which were not associated with an acute myocardial infarction. SHAHAL provides professional care to its subscribers who telephone a monitor center and describe their symptoms, whereupon therapeutic measures are decided upon. Patient data are stored in a central computer, and the center can dispatch mobile intensive care units. All subscribers carry a portable transtelephonic electrocardiographic transmitter and are provided with the LidoPen. Indications for self-injection were: transmission of a wide-QRS tachycardia (rate > 100 beats/min), symptomatic multiple or complex ventricular premature complexes in association with chest discomfort, and when the time of arrival of a medical team to the patient was estimated to be at least 8 to 10 minutes. Successful usage of the LidoPen was reported in 137 cases (123 patients). An additional 11 patients failed to use the injector properly. There was a success rate in abolishing rapid sustained ventricular tachycardia (27 of 76 patients) and nonsustained ventricular tachycardia and/or multiple and complex ventricular ectopic activity (8 of 30 patients) of 33% (total 35 of 106 patients). In another 9%, those arrhythmias were slowed markedly. The remaining 31 cases were eventually interpreted as being of supraventricular origin. No complications attributed to the use of the injector were reported and its use was found to be both feasible and effective in the prehospital setting.

Adult↗
PubMed1997

Changes in hemostatic function at times of cyclic variation in occupational stress.

In this study we demonstrated, in the same healthy subjects, a significant elevation in coagulation factors VII and VIII, fibrinogen, thrombocyte count, and thrombin and adenosine diphosphate-induced platelet aggregation during a period of increased workload compared with a calm work period. These findings may add to the understanding of the mechanism that links mental stress to coronary disease.

Adult↗
PubMed1997

The CB-12L: a new device for transtelephonic transmission of a 12-lead electrocardiogram.

The value of transtelephonic transmission of ECG information is well established, and technological advances have continuously provided improved state-of-the-art equipment. Shahal Medical Services provides professional care to subscribers who call the medical center and describe their symptoms, whereupon therapeutic measures are decided upon. A new 12-lead patient controlled device for telephonically transmitting an ECG (GB-12L) has become available; the aim of this study was to evaluate its accuracy and practicability. Forty tracings (20 standard ECG tracings obtained under medical supervision in the physician's office and 20 by the patient in his home using the new CB-12L ECG device and transmitted by telephone to the center) from 20 subjects with various electrocardiographic pathologies were reviewed by 19 experienced physicians who were asked to interpret the results and identify the recording device. In 82% of the possibilities, the interpretation of the tracings was identical for both those recorded by the standard ECG recorder and the CB-12L ECG. An equal number of physicians could not identify the means by which device the tracings were taken. Proper placement of the electrodes did not prove to be a problem for the patient. Thus, the CB-12L ECG was found to be an easily operable and reliable tool which may be of value for early and prompt diagnosis of threatening cardiac situations in the prehospital setting.

Electrocardiography↗
PubMed1997

Mode of onset of malignant ventricular arrhythmias in idiopathic ventricular fibrillation.

INTRODUCTION: The mode of onset of malignant ventricular arrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF]) has been well described in patients with organic heart disease and in patients with the long QT syndromes. Less is known about the mode of onset of VF in patients with out-of-hospital VF who have no evidence of organic heart disease or identifiable etiology. METHODS AND RESULTS: We reviewed the ECGs of all our patients with idiopathic VF. Documentation of the onset of spontaneous arrhythmias was available for 22 VF episodes in 9 patients (6 men and 3 women; age 41 +/- 16 years). In all instances, spontaneous VF followed a rapid polymorphic VT, which was initiated by premature ventricular complexes (PVCs) with very short coupling intervals. The PVC initiating VF had a coupling interval of 302 +/- 52 msec and a prematurity index of 0.4 +/- 0.07. These PVCs occurred within 40 msec of the peak of the preceding T wave. Pause-dependent arrhythmias were never observed. CONCLUSION: Cardiac arrest among patients with idiopathic VF has a very distinctive mode of onset. Documentation of a polymorphic VT that is not pause dependent is of diagnostic value.

Adult↗
PubMed1996

Reduction of reinfarction and angina with use of low-molecular-weight heparin therapy after streptokinase (and heparin) in acute myocardial infarction.

This study examined whether extending the anticoagulation effect of heparin by low-molecular-weight heparin (clexane) can prevent recurrent myocardial infarction (AMI) treated by streptokinase. On the fifth day after AMI and after heparin therapy cessation, 103 patients were randomly assigned to either treatment with low-molecular-weight heparin (40 mg subcutaneously per day for 25 days, n=43) or control (no treatment, n=60). All patients were followed carefully for 6 months after the infarction date. A total of 32 patients (31%) sustained a cardiac event during the 6-month observation period. There were 12 patients (20%) with reinfarction in the control group versus 2 patients (4.6%) in the low-molecular-weight heparin group during the first 30 days of the study (p=0.02). One additional patient sustained reinfarction at 3 months of followup in the control group, which yielded a total of 13 patients (21.6%) sustaining reinfarction in the control group versus 2 patients (4.6%) in the low-molecular-weight heparin group during 6 months of followup (p=0.01). Angina pectoris after AMI was diagnosed in 13 control patients (21.6%) versus 4 low-molecular-weight heparin-treated patients (9.3%) (p=0.078) during the study period. No major bleeding events were reported in either low-molecular-weight heparin-treated or control patients. Among patients with recently diagnosed AMI treated by streptokinase, extending the anticoagulant effect of heparin for 25 days may prevent recurrent coronary events for at least one month.

Adult↗
PubMed1996

Calcium antagonists and mortality in patients with coronary artery disease: a cohort study of 11,575 patients.

OBJECTIVES: This study sought to establish the risk ratio for mortality associated with calcium antagonists in a large population of patients with chronic coronary artery disease. BACKGROUND: Recent reports have suggested that the use of short-acting nifedipine may cause an increase in overall mortality in patients with coronary artery disease and that a similar effect may be produced by other calcium antagonists, in particular those of the dihydropyridine type. METHODS: Mortality data were obtained for 11,575 patients screened for the Bezafibrate Infarction Prevention study (5,843 with and 5,732 without calcium antagonists) after a mean follow-up period of 3.2 years. RESULTS: There were 495 deaths (8.5%) in the calcium antagonist group compared with 410 in the control group (7.2%). The age-adjusted risk ratio for mortality was 1.08 (95% confidence interval [CI] 0.95 to 1.24). After adjustment for the differences between the groups in age and gender and the prevalence of previous myocardial infarction, angina pectoris, hypertension, New York Heart Association functional class, peripheral vascular disease, chronic obstructive pulmonary disease, diabetes and current smoking, the adjusted risk ratio declined to 0.97 (95% CI 0.84 to 1.11). After further adjustment for concomitant medication, the risk ratio was estimated at 0.94 (95% CI 0.82 to 1.08). CONCLUSIONS: The current analysis does not support the claim that calcium antagonist therapy in patients with chronic coronary artery disease, whether myocardial infarction survivors or others harbors an increased risk of mortality.

Calcium Channel Blockers↗
PubMed1996

High-dose intravenous magnesium attenuates complement consumption after acute myocardial infarction treated by streptokinase.

OBJECTIVE: This study was designed to detect changes in complement levels following acute myocardial infarction and to test whether magnesium sulphate (MgSO4) administration interferes with the complement response that follows acute myocardial infarction. DESIGN: Twenty-nine patients with acute myocardial infarction treated with streptokinase were included and randomly assigned to three treatment groups. In groups A and B, a bolus of 1 g MgSO4 was infused intravenously followed by 4 g (group A) and 14 g (group B) MgSO4 for 24 h while normal saline was administered in group C (control). Blood samples for C3, C4 and CH-100 were obtained at baseline and repeatedly during the 48 h following the initiation of magnesium infusion. RESULTS: In groups A and C, a remarkable decrease in the levels of C3, C4 and CH-100 was observed when measured 1 h after the end of streptokinase infusion and thereafter for the ensuing 48 h compared to baseline values (P < 0.05). In group B, the decrease in these complement elements was attenuated, and a significant (P < 0.05) delayed decrease of C3 and C4 was observed only at 24 h and later up to 48 h. The mean level of CH-100 in group B was significantly depressed compared to baseline from 3 h and thereafter up to 48 h. Mean C3 values plotted against observation time differed between the three groups (P = 0.021). A similar trend was observed for C4 (P = 0.133) but not for CH-100 (P = 0.46). CONCLUSION: (1) Complement elements are being consumed following acute myocardial infarction treated by streptokinase. (2) High-dose intravenous magnesium attenuates the complement process following acute myocardial infarction. (3) These results might signify that magnesium modulates the inflammatory response that follows infarction.

Adult↗
PubMed1996

Enhancement of recombinant tissue-type plasminogen activator thrombolysis with a selective factor Xa inhibitor derived from the leech Hirudo medicinalis: comparison with heparin and hirudin in a rabbit thrombosis model.

OBJECTIVE: To compare the efficacy of Yagin, a factor Xa inhibitor derived from the leech Hirudo medicinalis, with those of heparin and hirudin as adjuncts to recombinant tissue-type plasminogen activator (rTPA) thrombolysis in a rabbit thrombosis model. METHODS: Thirty-one animals were allocated randomly to three groups, all administered four boluses of 0.25 mg/kg rTPA every 10 min for 30 min, 17 mg/kg aspirin intravenously, and heparin (as a 100 IU/kg bolus followed by infusion of 50 IU/kg heparin per h), hirudin (as a 2 mg/kg bolus followed by infusion of 1 mg/kg hirudin per h), or Yagin (as an 80 micrograms/kg bolus followed by infusion of 43 micrograms/kg Yagin per h). RESULTS: Administration of Yagin was associated with a significant acceleration of the reflow time, this time being 14.5 +/- 1.2 min with Yagin, 25.8 +/- 5.2 min with heparin (P < 0.0001, versus Yagin), and 28.7 +/- 16.0 min with hirudin (P = 0.012, versus Yagin). Overall patency did not differ significantly among the three groups. CONCLUSIONS: At the indicated single doses, inhibition of factor Xa by a relatively low concentration of Yagin was found to be superior than that with either heparin or hirudin for accelerating rTPA thrombolysis.

Animals↗
PubMed1995

Improvement of cardiac performance by intravenous infusion of L-arginine in patients with moderate congestive heart failure.

OBJECTIVES: The aim of this study was to evaluate the hemodynamic effect of L-arginine infusion in patients with congestive heart failure. BACKGROUND: Endothelium-dependent vasodilation is impaired in patients with congestive heart failure. Nitric oxide, which was identified as endothelium-derived relaxing factor, is generated by nitric oxide synthase from L-arginine. Our hypothesis was that administration of L-arginine in patients with congestive heart failure may increase nitric oxide production and have a beneficial hemodynamic effect. METHODS: Twelve patients with congestive heart failure (New York Heart Association class II or III) due to coronary artery disease (left ventricular ejection fraction < 35%) were given 20 g of L-arginine by intravenous infusion over 1 h at a constant rate. Stroke volume, cardiac output and left ventricular ejection fraction were determined with Doppler echocardiography at baseline and at 30 and 60 min and 1 h after the end of infusion. Blood and urinary levels of nitrite/nitrate (NO2/NO3), stable metabolites of nitric oxide, were measured and clearance was calculated. RESULTS: One hour of infusion of L-arginine resulted in a significant increase in stroke volume (from 68 +/- 18 ml to 76 +/- 23 ml [mean +/- SD], p = 0.014) and cardiac output (from 4.07 +/- 1.22 liters/min to 4.7 +/- 1.42 liters/min, p = 0.006) without a change in heart rate. Mean arterial blood pressure decreased (from 102 +/- 11 mm Hg to 89 +/- 9.5 mm Hg, p < 0.002), and systemic vascular resistance decreased significantly. Within 1 h after cessation of L-arginine infusion, blood pressure, stroke volume, cardiac output and systemic vascular resistance were statistically not different from baseline values. Clearance of NO2/NO3 increased significantly during L-arginine administration (from 13.28 +/- 0.42 ml/min to 29.97 +/- 1.09 ml/min, p < 0.001). CONCLUSIONS: Infusion of L-arginine in patients with congestive heart failure results in increased production of nitric oxide, peripheral vasodilation and increased cardiac output, suggesting a beneficial hemodynamic and possibly therapeutic profile.

Aged↗