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[The Influence of the growth hormone in the profile of blood pressure. Results in adult patients with deficiency in this hormone].

INTRODUCTION AND OBJECTIVES: There is an increasing interest in the relationship between the growth hormone (GH) and the heart since the GH has an important inotropic effect and its use has been tested in patients with severe systolic dysfunction. However, cardiovascular diseases are the main cause of increased morbimortality observed in patients with acromegaly. Growth hormone deficiency has been related to different clinical findings depending on the age of onset. Recent studies have demonstrated that GH deficiency in adults is associated with alterations in blood pressure. The aim of our study was to assess the influence of GH in blood pressure. PATIENTS AND METHODS: We studied 14 adult patients with GH deficiency and 15 healthy subjects, matched for sex and age. The diagnosis of GH deficiency was based on GH response to intravenous insulin tolerance test < 5 ng/ml and IGF-1 levels lower than the normal limit for each age group. In all the patients 24-hour Holter blood pressure monitorization was performed in addition to a treadmill test and echographic evaluation. RESULTS: All patients showed normal systolic and diastolic function in the echocardiographic study. Only one patient had an increased left ventricular mass. Blood pressure was lower in the patients than in the control subjects (p < 0.05). Moreover, the difference remained significant when analysis was based on the time of day. However, the patients showed normal blood pressure response to the effort test with a mean increase of 60%. The length of the exercise on the treadmill test was shorter in the subgroup of GH deficient patients. CONCLUSIONS: Lower systolic blood pressure was observed in GH deficiency patients. The patients studied did not show structural heart alterations. Blood pressure and chronotrophic response to the effort test were similar in both groups.

Adolescent↗

Does continuous positive airway pressure by face mask improve patients with acute cardiogenic pulmonary edema due to left ventricular diastolic dysfunction?

OBJECTIVE: Continuous positive airway pressure (CPAP) by face mask is an effective method of treating severe cardiogenic pulmonary edema (CPE). However, to our knowledge, no study has provided a precise evaluation of the effects of CPAP on cardiac function in patients presenting with CPE and preserved left ventricular (LV) function. DESIGN: Prospective observational clinical study. SETTING: A 14-bed, medical ICU at a university hospital. PATIENTS: Nine consecutive patients presenting with hypoxemic acute CPE. INTERVENTIONS: All patients were selected for 30 min of CPAP with 10 cm H(2)O by mask with fraction of inspired oxygen adjusted for a cutaneous saturation > 90%. Doppler echocardiography was performed before CPAP application and during the last 10 min of breathing with CPAP. Two-tailed, paired t-tests were used to compare data recorded at baseline (oxygen alone) and after CPAP. MEASUREMENTS AND RESULTS: Four patients presented CPE with preserved left ventricular (LV) function (a preserved LV ejection fraction [LVEF] > 45%, and/or aortic velocity time integral > 17 cm in the absence of aortic stenosis or hypertrophic cardiomyopathy). Oxygenation and ventilatory parameters were improved by CPAP in all patients. Hemodynamic monitoring and Doppler echocardiographic analysis demonstrated that in patients with preserved LV systolic function, mean arterial pressure and LV end-diastolic volume were decreased significantly by CPAP (p < 0.04). In patients with LV systolic dysfunction, CPAP improved LVEF (p < 0.05) and decreased LV end-diastolic volume (p = 0.001) significantly. CONCLUSION: CPAP improves oxygenation and ventilatory parameters in all kinds of CPE. In patients with preserved LV contractility, the hemodynamic benefit of CPAP results from a decrease in LV end-diastolic volume (preload).

Acute Disease↗

Effect of antithrombotic therapy on risk of sudden coronary death in patients with congestive heart failure.

Data from epidemiologic, autopsy, Holter monitoring, and electrophysiologic studies support the hypothesis that acute myocardial ischemia, even in the absence of myocardial infarction, is a critical component of the pathophysiology of sudden coronary death. Acute myocardial ischemia superimposed upon ventricles damaged from previous infarctions has been demonstrated to enhance the generation of lethal ventricular arrhythmias. This is a retrospective analysis of 6,797 participants in the Studies of Left Ventricular Dysfunction prevention and treatment trials. Both univariate and multivariate Cox proportional-hazards modeling were used to study the association of anticoagulant and antiplatelet therapy with the risk for sudden cardiac death. The following covariates were adjusted for in the analysis: age, ejection fraction, gender, atrial fibrillation, diabetes, a history of angina, prior infarction, prior revascularization, and the regular use of beta blockers, diuretics, digoxin, antiarrhythmic agents, or enalapril. The overall incidence of sudden cardiac death per 100 patient-years of follow-up was 2.24%. In multivariate analysis, antiplatelet and anticoagulant monotherapy each remained independently associated with a reduction in the risk of sudden cardiac death: antiplatelet therapy with a 24% reduction (relative risk [RR] 0.76; 95% confidence interval [CI] 0.61-0.95) and antiplatelet monotherapy with a 32% reduction (RR 0.68; 95% CI 0.48-0.96). Thus, in patients with moderate to severe left ventricular systolic dysfunction resulting from coronary artery disease, antiplatelet and anticoagulant therapy are each associated with a reduction in the risk of sudden cardiac death.

Anticoagulants↗

[Dobutamine doppler echocardiography in severe aortic stenosis with left ventricular dysfunction. Comparison with postoperative examination].

The association of left ventricular dysfunction with aortic stenosis worsens the spontaneous prognosis and increases operative mortality. The aim of this prospective study was to assess the predictive value of dobutamine Doppler echocardiography on the indices of left ventricular contractile function in patients with aortic stenosis and left ventricular dysfunction (LVEF < 0.45) undergoing aortic valve replacement. Eighteen patients, including 9 with coronary artery disease, were included in a protocol consisting of analysis of left ventricular function and of the severity of aortic stenosis before, during dobutamine infusion, and after valvular replacement. The dobutamine was given in progressive increments of 5 micrograms/Kg up to a maximum of 20 micrograms/Kg. During pharmacological stress, the functional aortic valve area increased from 0.46 +/- 0.15 to 0.56 +/- 0.23 cm2. Tolerance of the procedure was good. All but 2 patients improved their postoperative ejection fraction with values equivalent to those observed during the last increment of dobutamine (r = 0.73; p < 0.003). The patients with initial mean pressure gradients > 50 mmHg normalised their LVEF after valve replacement. The authors conclude that dobutamine echocardiography is useful for predicting the values of postoperative left ventricular contractile indices when severe aortic stenosis is associated with systolic dysfunction. It allows evaluation of the expected short term benefits to these indices after aortic valve replacement.

Adult↗

Assessment of brain natriuretic peptide in patients with suspected heart failure: comparison with radionuclide ventriculography data.

BACKGROUND: The aim of the study was to prospectively evaluate patients with suspected or known heart disease using plasma brain natriuretic peptide (BNP) measurement and radionuclide ventriculography to examine whether left ventricular dysfunction is associated with an abnormal rise of BNP concentration. METHODS: Patients (n=153) and controls (n=14) underwent radionuclide ventriculography to determine Left ventricular Ejection Fraction (LVEF) and measurement of plasma BNP concentration using a commercial kit. RESULTS: Plasma BNP concentration in controls was significantly lower than that in patients whatever the stage of the disease, significantly lower than that of patients with normal LVEF (LVEF>55%); than that of patients with altered LVEF (LVEF< or =40%); and than that of patients with moderately reduced LVEF (40%<LVEF< or =5%). Comparisons between groups of patients showed that the more severe the disease, the higher the BNP level. From the ROC curve, a plasma BNP concentration of 52 pg/ml was attached to a 85% sensitivity and 82% specificity in identifying patients with LVEF< or =40%. CONCLUSIONS: Plasma BNP concentration provides a reliable and sensitive marker of LV systolic dysfunction evaluated by a nuclear medicine technique, and could be a potential screening test to identify patients for additional investigations.

Cardiac Output, Low↗

Left ventricular diastolic dysfunction induced by cyclophosphamide in blood stem cell transplantation.

Cardiac complications are major limiting factors regarding the success of high-dose chemotherapy supported by blood stem cell transplantation (BSCT). The cardiotoxicity of cyclophosphamide remains obscure relative to that of anthracyclines. The aim of this study was to estimate noninvasively the cardiotoxicity of cyclophosphamide administered during the pretransplant conditioning of BSCT for patients with various hematological diseases. A total of 27 consecutive patients were divided into two groups depending on the conditioning regimen, ie, group A (n=15) which received cyclophosphamide (median dose of 120 mg/kg; range 100 to 200 mg/kg) and group B (n=12) which did not. Ultrasound cardiograms (UCG) and signal-averaged electrocardiograms (SAECG) were recorded in the two groups both preceding and following the BSCT. There were no statistical intergroup or intragroup differences in left ventricular (LV) dimensions or contractile function. Significant (P<0.01) posttransplant increases in interventricular septal wall thickness and Ap/Ep ratio were noted in group A. Moreover, the filtered QRS duration as estimated by SAECG was prolonged (P<0.05) whereas the summated LV voltage (S(V1)+R(V5)) was reduced in the posttransplant period only in group A. These results suggest that early cyclophosphamide cardiotoxicity was characterized by LV diastolic rather than systolic dysfunction. These findings may contribute to acute hemodynamic deterioration observed after cyclophosphamide-containing conditioning chemotherapy.

Adolescent↗

Impact of pregnancy on the systemic right ventricle after a Mustard operation for transposition of the great arteries.

OBJECTIVES: We sought to determine the impact of pregnancy on the systemic right ventricle (RV) after a Mustard operation for transposition of the great arteries. BACKGROUND: Dysfunction of the RV remains a continuing problem after a Mustard operation. Concerns exist about the potentially deleterious effects of pregnancy on this ventricle. METHODS: The records of 16 women who completed 28 pregnancies were reviewed for clinical status, echocardiographic evaluation of RV dimensions, RV function, and tricuspid regurgitation (TR) before, during, and after pregnancy. RESULTS: Women were in New York Heart Association functional class I (n = 21) and II (n = 7) before pregnancy. The functional class deteriorated in six women, with no return to the pre-pregnancy level after delivery in two. Data on RV dimensions were available in 18 pregnancies, on RV function in 21, and on TR in 20. Before pregnancy, RV dilation was absent (n = 4), mild/moderate (n = 12), or severe (n = 2) and progressed in five women (31%), with no recovery in all patients at the last follow-up. Right ventricular systolic dysfunction was absent (n = 16), mild/moderate (n = 4), or severe (n = 1) before pregnancy and progressed in four women (25%), with no recovery in three cases. Tricuspid regurgitation was absent (n = 8), mild (n = 9), or moderate (n = 3) before pregnancy and deteriorated in eight women (50%), with no recovery in three patients. CONCLUSIONS: Pregnancy after a Mustard operation is clinically well tolerated but carries a risk of RV dysfunction, which is sometimes irreversible.

Adult↗

Use of electrophysiological studies in the diagnosis and treatment of cardiac patients with left ventricular dysfunction and high grade ventricular ectopy.

We studied the sudden death occurrence in 28 patients (23 males, age 59.2 +/- 15.6 years) who had a documented cardiac disease with left ventricular dysfunction (ejection fraction < or = 0.4) and high grade ventricular ectopy. None had suffered from spontaneous sustained ventricular arrhythmia and/or syncope. Their diagnosis and treatment were guided by electrophysiological studies. Electrophysiological studies were performed in the antiarrhythmic drug-free state. In cases when sustained ventricular arrhythmias could be induced, antiarrhythmic treatment was prescribed according to the results of the electrophysiological studies. In cases of non-inducibility, no antiarrhythmic treatment was prescribed. The patients were followed up for a period of 20.6 +/- 11.2 months. The end points were occurrence of documented spontaneous sustained ventricular arrhythmia and sudden death. None of the 19 non-inducible patients experienced sudden death or spontaneous sustained ventricular arrhythmia. Two of the nine inducible patients died suddenly (P = 0.1). The 3-year sudden death mortality rate of the whole group was 7.5%. We conclude that when cardiac patients with high grade ventricular ectopy and left ventricular systolic dysfunction are treated according to the results of electrophysiological studies, it can be expected that their 3-year mortality rate will be low and significantly inferior to that reported for conventionally treated patients.

Adult↗

[Diagnostic and prognostic significance of homocysteine determined in acute phase of myocardial infarction].

THE AIM: Of this study was to assess the serum homocysteine concentration in subjects with acute myocardial infarction and its correlation with the course of infarction and further prognosis considering particularly left ventricle dysfunction, heart rate and conduction disorders as well as to assess the usefulness of metionin load test as a prognostic test in patients with myocardial infarction. MATERIAL AND METHODS: 66 patients were studied: 36 with recent myocardial infarction and 30 healthy individuals as a control group. Fasting serum homocysteine and its concentration two hours after metionin load were determined in all patients. They all underwent echocardiographic examination, stress test and 24-hour Holter monitoring. The study revealed a significant positive correlation between increased serum homocysteine concentration in patients with myocardial infarction and worsening of contractility parameters, extent of infarction area, and negative correlation between homocysteine concentration and ejection fraction. CONCLUSIONS: On the basis of the study outcome we can make a statement that increased homocysteine concentration in patients with acute phase of myocardial infarction indicates its more severe course, more extensive disorders of myocardium kinetics, more significant left ventricle diastolic and systolic dysfunction. Increased serum homocysteine in metionin load test indicates higher death risk in patients with myocardial infarction.

Adult↗

Impact of delayed reperfusion of myocardial hibernation on myocardial ultrastructure and function and their recoveries after reperfusion in a pig model of myocardial hibernation.

UNLABELLED: This study examined the effect of delayed reperfusion of myocardial hibernation from 24 hours to 7 days on myocardial ultrastructural and functional changes and their recoveries after reperfusion. BACKGROUND: We have previously shown in pigs that after reperfusion the functional and structural alterations in short-term myocardial hibernation which was reperfused in 24 hours can recover in 7 days. The effect of delayed reperfusion of hibernating myocardium on the extent and severity of cellular and extracellular structural changes of hibernating myocardium, and their recoveries after reperfusion is not known. METHODS AND RESULTS: A severe LAD stenosis was created in 27 pigs, reducing resting flow by 30-40% immediately after placement of the stenosis and producing acute ischemia as evidenced by regional lactate production, a decrease in regional coronary venous pH, reduced regional wall thickening (from 38.5 +/- 5.1% to 10.4 +/- 8.0%) and a 33% reduction of regional oxygen consumption. The stenosis was maintained either for 24 hours in 9 pigs (group 1) with LAD flow of 0.65 +/- 0.13 ml/min/g (38% reduction), or for 7 days in 17 pigs (group 2) with LAD flow of 0.67 +/- 0.14 ml/min/g (36% reduction). There were no differences (p = NS) in the reduction of wall thickening, rate-pressure product, lactate production, or regional oxygen consumption between group 1 and group 2. Quantitative morphometric evaluation of the ultrastructure on electromicrographs revealed a greater decrease in sarcomere volume and a higher incidence of myocytes with reduced sarcomere volume in 7-day than in 24-hour hibernating regions (53 +/- 19% versus 33 +/- 14%, p < 0.05). Patchy myocardial necrosis with replacement fibrosis was common, but 6 of the 18 pigs had no myocardial necrosis or replacement fibrosis in the 7-day hibernating group, and 4 of 9 pigs had no patchy myocyte necrosis in the 24 hour hibernating group. In 6 pigs in group 1 in which the stenosis was then released and hibernating myocardium reperfused in 24 hours, regional wall thickening recovered to 30 +/- 6% (p = NS compared to baseline) after one week of reperfusion. In 12 pigs in group 2 in which the stenosis was released and hibernating myocardium reperfused in 7 days, regional wall thickening recovered slowly, from 10.1 +/- 7.2% to 18.1 +/- 8.3% at one week (n = 5) and to 28.0 +/- 3.6% at 3-4 weeks of reperfusion (n = 7, p < 0.05 compared to baseline). Similarly, the sarcomere volume or myofilament recovered significantly (p < 0.01) and was not different compared to the normal region (p = NS) in the 24-hour hibernating region of group 1, but the recovery was much slower and was incomplete at 4 weeks (p < 0.01) compared to baseline in the 7-day hibernating region of group 2. Recovery of regional wall thickening correlated with ultrstructural recovery (p < 0.01). By multivariate stepwise regression analysis, the degree of LAD flow reduction, the extent of fibrosis, and myofilament loss were independent predictors of the extent of functional recovery. CONCLUSIONS: In a porcine model of myocardial hibernation with myocardial hypoperfusion, systolic dysfunction, and metabolic adaptations, a longer period of myocardial hibernation with delayed reperfusion was associated with more severe abnormalities of myocytes. an increasing interstitial fibrosis, and more protracted myofibrillar and functional recoveries after reperfusion. The extent of functional recovery is related to the degree of coronary flow reduction, the severity of the ultrastructural changes, and the extent of interstitial fibrosis.

Animals↗

Beta-blockers for heart failure: why, which, when, and where.

Beta-blockers are a highly effective treatment for patients with all grades of heart failure secondary to LV systolic dysfunction. Beta-blockers are best deployed as a form of tertiary prevention in heart failure but have a very limited role for the treatment of a heart failure crisis. Physicians and patients need to understand the time course of the effects of beta-blocker therapy. The initial effects are often neutral or adverse, though the benefits, at least of carvedilol, may be apparent within days in patients with severe heart failure. Benefits accumulate gradually over a period of weeks to months. Some patience, perseverance, and education are required in order to allow patients to reap the full benefits of beta-blocker therapy for this malignant disease. Initiation of treatment early in the course of the disease maximizes the effectiveness and acceptance of therapy. Trials are under way to determine whether the benefits of beta-blockers extend to patients over 80 years of age and to those with preserved LV systolic function. It is likely that important differences exist between beta-blockers in terms of their clinical benefit, though whether differences exist between the agents that have been reported to be effective so far awaits the outcome of a large clinical trial. It is unclear whether the target doses of beta-blockers currently recommended are optimal.

Adrenergic beta-Antagonists↗

Does chronic ST segment elevation following Q wave myocardial infarction exclude tissue viability?

PURPOSE: Electrocardiographic (ECG) ST segment elevation lasting 2 or more weeks following Q wave myocardial infarction has been associated with 'ventricular aneurysm' and absence of tissue viability. Regional systolic dysfunction may reflect either viable myocardium or scar. Positron emission-tomographic (PET) imaging can distinguish viable from nonviable tissue. We hypothesized that patients with chronic ST segment elevation after Q wave infarction might demonstrate salvageable myocardium in the infarct region. METHODS: The ECGs of 1,229 sequential patients undergoing PET scans for viability assessment were reviewed by an electrocardiographer to identify individuals with chronic anteroseptal Q wave infarctions with persistent ST segment elevation exceeding 1 mV. Patients with QRS duration longer than 0.14 ms or rhythm other than sinus were excluded. Viability was considered present if either a reversible stress-induced perfusion defect (ischemia) or a resting perfusion-metabolism mismatch (hibernation) was identified. RESULTS: Anteroseptal ECG Q wave infarction was identified in 132 subjects (74% male, age 61 +/- 12 years). Chronic ST segment elevation was present in 84 subjects (64%) and absent in 48. Baseline clinical characteristics and left ventricular systolic function were similar in both groups. 63% of those with and 56% of those without chronic ST elevation had viable myocardium. No relationship was noted between chronic ST segment elevation and the presence or absence of myocardial viability. CONCLUSIONS: Chronic ST segment elevation after anteroseptal Q wave myocardial infarction does not exclude myocardial viability in the 'infarct zone'. Evaluation of residual tissue viability is indicated to assess the benefit of revascularization in patients with Q wave infarction and chronic ST segment elevation.

Aged↗

Temporal trends in survival and hospitalizations in outpatients with chronic systolic heart failure in 1995 and 1999.

Abstract Background Community and hospital studies have suggested that survival of patients with heart failure (HF) has increased; however, the causes of the improvement and the hospital readmission rates remain undetermined. Methods and Results We compared survival and hospital admission rates in 2 cohorts enrolled in a national registry of outpatients with HF secondary to left ventricular (LV) systolic dysfunction referred to cardiology centers in 1995 (n = 712) and 1999 (n = 603). One year after enrollment, 163 of 1315 patients (12%) were dead. Survival rates were 85% in the 1995 versus 91% in the 1999 cohort. Older age, New York Heart Association (NYHA) class III-IV, anemia, hyponatremia, hypotension, and a lower LV ejection fraction (LVEF) were associated to an increased risk of all-cause mortality by multivariate analysis. Furthermore a significant independent cohort effect was observed: the adjusted risk of death was 1.30 (95% CI 1.16-1.45) for the 1995 versus 1999 cohort (survival difference adjusted P = .0067). The proportion of patients admitted to hospital declined significantly in 1999 versus 1995, for all causes (20% versus 27%, P = .006), for cardiac causes (16% versus 22%, P = .002), and for worsening congestive heart failure (8% versus 15%, P = .0005). Survival free from HF admission was 69% in 1995 versus 84% in 1999 (adjusted P = .0001); NYHA class III-IV, hypotension, diuretics and a lower LVEF were associated to an increased risk of this combined end point by multivariate analysis, as well as the enrollment year (relative risk 1.38, 95% CI 1.22-1.56, P = .0039). Conclusion In a national cardiologic registry of outpatients with systolic HF, survival improved and hospital admissions decreased over a 4-year period. These results underscore the importance of networking and the careful implementation of practice guidelines to elevate standards of care.

Age Factors↗

Sensitive detection of myocardial contraction abnormality in chronic hemodialysis patients by ultrasonic tissue characterization with integrated backscatter.

Since acoustic properties of the myocardium are sensitive to the myocardial structure and the contractile conditions of myocyte, the authors evaluated cardiac dysfunction based on the integrated ultrasonic backscatter in 18 hemodialysis (HD) patients (duration: 102 +/- 84 months, mean age: 57.6 +/- 9.7 years) and 11 age-matched normals. The cyclic variation of integrated backscatter (CV-IB) at interventricular septum (IVS) and left ventricular posterior wall (PW) was measured and compared with percent fractional shortening (%FS) and percent wall thickening (%Th). The CV-IB of HD patients was smaller than that of control subjects (IVS: 6.2 +/- 1.1 dB vs 8.2 +/- 1.1 dB, p = 0.0003 and PW: 8.4 +/- 2.2 vs 10.3 +/- 1.3, p= 0.025). No significant difference was observed in %FS and %Th between HD patients and control subjects. In HD, the ratio of velocities of early diastolic inflow (E) to late atrial inflow was decreased (0.7 +/- 0.2 vs 1.1 +/- 0.7, p = 0.049) and deceleration time of E was prolonged significantly (200 +/- 28 msec vs 159 +/- 30 msec, p = 0.0082). In the absence of overt cardiac systolic dysfunction, myocardial damage indicated as a decrease in CV-IB and diastolic dysfunction identified on transmitral velocity waveform were detected, which may reflect from the myocardial fibrosis. As a mechanism, pressure overload, hyperparathyroidism, and anemia were neglected, and the other humoral factors may contribute to the myocardial damage in chronic renal failure.

Aged↗

Hemodynamic effects of sildenafil in patients with congestive heart failure and pulmonary hypertension: combined administration with inhaled nitric oxide.

STUDY OBJECTIVES: In patients with pulmonary hypertension (PH) secondary to congestive heart failure, inhaled nitric oxide (NO) increases pulmonary vascular smooth-muscle intracellular cyclic guanosine monophosphate (cGMP) concentration, thereby decreasing pulmonary vascular resistance (PVR) and increasing cardiac index (CI). However, these beneficial effects of inhaled NO are limited in magnitude and duration, at least in part due to cGMP hydrolysis by the type 5 isoform of phosphodiesterase (PDE5). The goal of this study was to determine the acute pulmonary and systemic hemodynamic effects of the selective PDE5 inhibitor, sildenafil, administered alone or in combination with inhaled NO in patients with congestive heart failure and PH. DESIGN: Single center, case series, pharmacohemodynamic study. SETTING: Cardiac catheterization laboratory of a tertiary care academic teaching hospital. PATIENTS: We studied 11 patients with left ventricular systolic dysfunction due to coronary artery disease or idiopathic dilated cardiomyopathy who had PH. INTERVENTIONS: We administered oral sildenafil (50 mg), inhaled NO (80 ppm), and the combination of sildenafil and inhaled NO during right-heart and micromanometer left-heart catheterization. MEASUREMENTS AND RESULTS: Sildenafil administered alone decreased mean pulmonary artery pressure by 12 +/- 5%, PVR by 12 +/- 5%, systemic vascular resistance (SVR) by 13 +/- 6%, and pulmonary capillary wedge pressure by 12 +/- 7%, and increased CI by 14 +/- 5% (all p < 0.05) [+/- SEM]. The combination of inhaled NO and sildenafil decreased PVR by 50 +/- 4%, decreased SVR by 24 +/- 3%, and increased CI by 30 +/- 4% (all p < 0.01). These effects were greater than those observed with either agent alone (p < 0.05). In addition, sildenafil prolonged the pulmonary vasodilator effect of inhaled NO. Administration of sildenafil alone or in combination with inhaled NO did not change systemic arterial pressure or indexes of myocardial systolic or diastolic function. CONCLUSIONS: PDE5 inhibition with sildenafil improves cardiac output by balanced pulmonary and systemic vasodilation, and augments and prolongs the hemodynamic effects of inhaled NO in patients with chronic congestive heart failure and PH.

Adult↗

Uric acid--a marker for systemic inflammatory response in patients with congestive heart failure?

Congestive heart failure is associated with hyperuricemia and elevations in the levels of circulating markers for inflammation. The purpose of this study was to assess the relationship between levels of serum uric acid, activity of the renin-angiotensin-aldosterone system and TNF-alpha in heart failure patients with respect to the extent of left ventricular dysfunction. Circulating uric acid, TNF-alpha, plasma renin activity and concentrations of aldosterone were measured in 30 patients with congestive heart failure, divided into subgroups according to their NYHA class (II-IV). We found a significant step-by-step increase in TNF-alpha among the subgroups. Significant differences among the subgroups were found for the values of uric acid and the values of plasma renin and aldosterone. Serum uric acid correlated significantly with TNF-alpha concentrations (r = 0.36, P < 0.05) leukocytes (r = 0.38, P = 0.03) and ejection fraction (r = 0.64, P < 0.01). No significant correlation was found between the activity of the renin-angiotensin-aldosterone system and uricemia (r = 0.34). In a multivariate model, uric acid concentration was predicted significantly by the ejection fraction and blood leukocytes, this relationship being independent of serum creatinine, treatment modality, age and gender. We conclude that serum uric acid may reflect the severity of systolic dysfunction and the activation of an inflammatory reaction in patients with congestive heart failure.

Aged↗

Beta-blockers: the new standard of therapy for mild heart failure.

Many physicians are reluctant to prescribe beta-blockers to patients with mild heart failure, especially when standard therapy (diuretics and an angiotensin-converting enzyme inhibitor, with or without digitalis glycosides) seems to be effective at relieving symptoms. However, current first-line medications for heart failure either ignore or incompletely inhibit adrenergic activation, one of the primary contributors to progressive left ventricular systolic dysfunction. Thus, even effective standard "triple" therapy does not safeguard the patient against further catastrophic deterioration of cardiac performance. Clinical trials have shown that the use of beta-blockers in addition to standard therapy improves left ventricular function, reduces hospitalizations, and-in the cases of bisoprolol, long-acting metoprolol, and carvedilol-improves survival in patients with chronic heart failure. In addition, carvedilol has been found to significantly slow disease progression even in mildly symptomatic patients. Though achieving beta-blockade in patients with heart failure requires extra effort by the clinician (appropriate patient selection, optimization of background therapy, initiating drug treatment at low doses, and titrating slowly with careful vigilance for early signs of clinical instability), the cost is small compared with the consequence of postponing adrenergic intervention. The educational objective of this article is to provide the primary care physician with a review of the current understanding of the pathophysiological characteristics underlying chronic systolic heart failure, the clinical benefits of administering beta-blockers during the early stages of heart failure, and the practical considerations of initiating therapy.

Adrenergic beta-Antagonists↗

How well can the chest radiograph diagnose left ventricular dysfunction?

OBJECTIVES: To review the diagnostic utility of the chest radiograph for left ventricular dysfunction. DATA SOURCES: Structured MEDLINE searches, citation reviews of relevant primary research, review articles, and textbooks, personal files, and data from experts. STUDY SELECTION: Studies of patients without valvular disease that allowed calculation of the sensitivity and specificity of selected radiographic signs compared with a criterion standard of increased left ventricular preload or reduced ejection fraction. DATA EXTRACTION: Two independent readers reviewed 29 studies. Studies were pooled after stratification by radiographic finding, criterion standard, and clinical setting. MAIN RESULTS: Redistribution best diagnosed increased preload with a sensitivity of 65% (95% confidence interval [CI] 55%, 75%) and specificity 67% (95% CI 53%, 79%). Cardiomegaly best diagnosed decreased ejection fraction with a sensitivity of of 51% (95% CI 43%, 60%) and specificity of 79% (95% CI 71%, 85%). Interrater reliability was fair to moderate for redistribution and moderate for cardiomegaly. The clinical setting affected results by decreasing the specificity of cardiomegaly to 8% in detecting increased preload in patients with severe systolic dysfunction. The absence of redistribution could only exclude increased preload in situations in which the suspicion (pretest probability) of disease was less than 9%, whereas redistribution could confirm increased preload when the pretest probability was greater than 91%. The absence of cardiomegaly could only exclude a reduced ejection fraction if the pretest probability was less than 8%, whereas cardiomegaly could confirm a reduced ejection fraction if the pretest probability was greater than 87%. CONCLUSIONS: Redistribution and cardiomegaly are the best chest radiographic findings for diagnosing increased preload and reduced ejection fraction, respectively. Unfortunately, neither finding alone can adequately exclude or confirm left ventricular dysfunction in usual clinical settings. Redistribution is not always reliably interpreted.

Confidence Intervals↗