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D Logeart

Publications and source records attributed to D Logeart.

At least 19 recordsLinked to original sources
PubMed2002

A non-invasively determined surrogate of cardiac power ('circulatory power') at peak exercise is a powerful prognostic factor in chronic heart failure.

OBJECTIVES: This study was designed to assess the prognostic value of a new variable derived from a cardiopulmonary exercise test, the circulatory power, a surrogate of cardiac power, at peak exercise, in patients with chronic heart failure. BACKGROUND: Peak exercise cardiac power and stroke work are invasive parameters with recently proven prognostic value. It is unclear whether these variables have better prognostic value than peak oxygen uptake (VO(2)). METHODS: The study population comprised 175 patients with chronic heart failure (ejection fraction <45%) who underwent a cardiopulmonary exercise test. Circulatory power and circulatory stroke work were defined as the product of systolic arterial pressure and VO(2) and oxygen pulse, respectively. Prognostic value was assessed by survival curves (Kaplan-Meier method) and uni- and multivariate Cox analyses. RESULTS: With a mean follow-up of 25+/-10 months, ejection fraction, heart rate, systolic arterial pressure, peak VO(2), VCO(2), the anaerobic threshold, minute ventilation, the ventilatory equivalents of oxygen and carbon dioxide, the half times of VO(2) and VCO(2) recoveries, and the circulatory stroke work and power predicted outcome. Multivariate analysis demonstrated that the peak circulatory power (chi-square=19.9, P<0.001) (but not peak circulatory stroke work) was the only variable predictive of prognosis. CONCLUSION: The prognostic value of cardiopulmonary exercise tests in heart failure patients can be improved by assessing a new variable, the circulatory power - a surrogate of cardiac power - at peak exercise.

Adult↗
PubMed2002

[Ultra-rapid measurement of brain natriuretic peptide].

B-type natriuretic peptide (BNP) is secreted by overloaded ventricles. Emerging of bedside dosages cause an increasing interest for this peptide as marker in various clinical situations with heart failure. At first, BNP dosage is a potential tool for detecting heart failure and left ventricular dysfunction. BNP has also a powerful and well-established prognosis value in chronic heart failure. In the emergency setting, and mainly about acute dyspnea, low blood BNP level could eliminate diagnosis of congestive heart failure. Moreover, serial measurement of BNP could allow non-invasive hemodynamic monitoring during decompensated heart failure and could also lead cares as need for intensifying treatment. Nevertheless, its daily use in various clinical situations require that cut-off values are refined.

Biomarkers↗
PubMed2002

Myocardial gene therapy.

Myocardial gene therapy was born at the beginning of the 90's from the marriage of well-defined pathophysiological mechanisms with recombinant adenovirus technology. Together with the development of relatively simple vector delivery procedures during the last few years, this made it possible to consider the possibility of treating diseases such as ischemic cardiomyopathies by the delivery of angiogenic factors and to bring the first proof, in rats, that myocardial gene therapy for experimental heart failure can improve cardiac performance and prolong life duration of the animals. It is now conceivable that such an approach will be applied to human heart failure within the next years. In contrast, regarding familial cardiomyopathies and channelopathies, because of the specificity of each disease type and complexity of the pathophysiology of each mutation, it is likely that much more time will be necessary. However, a number of barriers still exist before myocardial gene therapy can spread to the field of routine clinical cardiology, including finding a safe vector allowing good transduction efficiency rates to cardiac myocytes when delivered through coronary arteries. In contrast, it is conceivable that in the open chest setting, myocardial gene therapy will rapidly be used by surgeons, by itself or in association with the injection of "wild" cells or cells transfected with various types of genes. It can now be assumed that such biotherapies will soon offer patients suffering from myocardial diseases (and especially heart failure) the perspective of major therapeutic progresses.

Adenoviridae↗
PubMed2001

How to optimize in vivo gene transfer to cardiac myocytes: mechanical or pharmacological procedures?

An efficient gene delivery system is a prerequisite for myocardial gene therapy. Among the various procedures studied so far, catheter-based percutaneous gene delivery to the myocardium through the coronary vessels seems the most relevant to routine clinical practice; however, the optimal conditions remain to be determined. We selectively infused adenoviral vectors encoding luciferase (1 x 10(9) PFU) or beta-galactosidase (1 x 10(10) PFU) into coronary arteries of adult rabbits in various experimental conditions. Coronary artery occlusion for 30 sec, during and after adenovirus delivery, was required to observe luciferase activity in the target area of the circumflex artery (4.0 +/- 1.0 x 10(5) vs. 1.1 +/- 0.2 x 10(4) RLU/mg with and without coronary occlusion, respectively, p < 0.01, and 1.0 +/- 0.1 x 10(3) RLU/mg using nonselective infusion). When adenoviruses were delivered using high-pressure infusion (82 +/- 12 vs. 415 +/- 25 mmHg before and during infusion, respectively, p < 0.01), luciferase activity increased to 8.5 +/- 2.5 x 10(5) RLU/mg (p < 0.05 vs coronary occlusion alone). Coronary venous sinus occlusion with saline buffer retroinfusion starting before and during anterograde adenovirus delivery resulted in a further 4.7-fold increase in luciferase activity (4.4 +/- 0.8 x 10(6) RLU/mg, p < 0.01) with 5-25% blue-stained myocytes in the target area, compared with 0-5% with the other procedures. Histamine or VEGF-A(165) pretreatment, used to increase vascular permeability, slightly increased gene transfer efficiency (8.5 +/- 2.0 x 10(5) and 9.0 +/- 2.5 x 10(5) RLU/mg respectively, p < 0.05 vs. coronary occlusion alone). We conclude that catheter-mediated adenoviral gene transfer to cardiac myocytes through coronary vessels can be a very efficient procedure for myocardial gene therapy, particularly when the vector residence time and perfusion pressure in the vessels are increased.

Adenoviridae↗
PubMed2001

Adenoviral SERCA1a gene transfer to adult rat ventricular myocytes induces physiological changes in calcium handling.

OBJECTIVE: We examined the functional consequences of expressing adult rabbit fast skeletal sarcoplasmic reticulum (SR) Ca(2+)-ATPase (SERCA1a) in isolated adult rat ventricular myocytes. METHODS: Myocytes were infected with a recombinant adenovirus harboring SERCA1a. Then 2 days after myocyte infection, protein expression was estimated using Western blot and SDS-PAGE analysis. We also measured the ATP-dependent oxalate-facilitated Ca(2+) uptake of myocyte homogenates and monitored Ca(2+) transient in myocytes loaded with the Ca(2+) dye, indo-1. RESULTS: SERCA1a gene expression resulted in a 36% increase in the total SERCA protein level in infected myocytes compared to controls (P<0.01), while SERCA2 and phospholamban levels did not change. This increase was associated with a 42% rise in SR Ca(2+) uptake (P<0.01), while tau (the time constant of Ca(2+) transient decay), and the time to peak fell by 32% (P<0.01) and 38% (P<0.001), respectively. Increasing the frequency of stimulation from 0.2 to 2 Hz decreased tau in both cell types (P<0.01). However, the decrease was much smaller in infected (P<0.01) than in uninfected cells (P<0.001). Isoproterenol (1 microM) further decreased tau in infected myocytes by 23% (P<0.05). In these cells, the diastolic [Ca(2+)](i) decreased by 50% (P<0.05) while the systolic [Ca(2+)](i) increased by 19% (P<0.05). No difference was found in the speed of SR Ca(2+) reloading after caffeine washout between the two cell types. CONCLUSION: Adenovirus-mediated SERCA1a gene transfer to adult rat ventricular myocytes enhances SR Ca(2+) handling to a degree similar to that observed following physiological stimulation.

Adenoviridae↗
PubMed2001

[Drug prospects in the treatment of heart insufficiency].

Pharmacological and validated treatment of chronic heart failure (HF) includes successively angiotensin converting enzyme inhibitors (ACEi), beta-blockers and antialdosterone, which is associated with diuretics. The effectiveness of this manner in which to block more and more hormonal systems demonstrate the validity of the "hormonal" paradigm to explain heart failure. Therefore broader educational means are required to increase the prescription of these drugs for HF. Several questions about these drugs remain unresolved: HF with preserved systolic function and elderly patients, class effect, and the role of antagonists of angiotensin II receptors (as an alternative or associated with ACEi). Other short- and mid-term pharmacological perspectives target target hormonal systems and cytokines: endothelin-receptor antagonists, inhibition of natriuretic peptide degradation (via neutral endopeptidase), and newer drugs acting against TNF such as etanercept. Moreover, recent knowledge about molecular mechanisms of myocardium remodeling allows new drug strategies with target more specifically remodeling such as metalloproteinases. Finally, these perspectives should be largely modified by on-going research in the field of genomics.

Heart Failure↗
PubMed2001

[Papillary fibroelastoma: a rare but treatable cause of cerebral infarction].

INTRODUCTION: Papillary fibroelastoma is a benign cardiac tumor which can be associated with serious embolic complications. EXEGESIS: We report on a 42-year-old man admitted for an ischemic stroke in the left middle cerebral artery region. Transesophageal echocardiography revealed a mitral valve tumor. Surgical excision and histological examination showed a papillary fibroelastoma. Clinical course was uneventful. CONCLUSION: We consider the high embolic potential of this tumor, which represents a surgically treatable cause of ischemic stroke.

Adult↗
PubMed2001

Evidence of cardiac myolysis in severe nonischemic heart failure and the potential role of increased wall strain.

BACKGROUND: Myocyte death could play a role in heart failure (HF) irrespective of the presence of coronary artery disease. The study aimed to assess this hypothesis by use of the cardiac troponin I (cTnI) assay. METHODS AND RESULTS: Seventy-one patients with nonischemic HF, New York Heart Association (NYHA) class II-IV, with a normal coronary angiogram and after exclusion of myocardiopathies were evaluated in the study. The control group included 9 healthy subjects and 15 patients hospitalized for severe noncardiac dyspnea. Cardiac TnI concentrations were determined at admission with a research reagent (cTnIus) characterized by a detection limit of 0.026 ng/mL and a high analytic sensitivity of 0.002 ng/mL. cTnIus levels were more than 0.026 ng/mL in 19 HF patients, ranging between 0.027 and 0.463 ng/mL, whereas no cTnIus level was detectable in the control group. With use of a reference assay, only 2 HF patients had abnormal cTnI values. Severe HF was observed in 17 of these 19 patients, assessed by NYHA class IV or by the presence of pulmonary edema. Patients with an increased cTnIus level had a more restrictive mitral Doppler pattern (P <.001) and a more distinctive left ventricular (LV) concentric remodeling (P <.0001), whereas LV ejection fraction was similar in both HF groups. The increased cTnIus level was also associated with a LV wall strain biologic marker (ie, an increased brain natriuretic peptide plasma level) (P <.001). CONCLUSIONS: cTnI assay is a promising biochemical method for detecting cardiac myolysis in HF, independent of the presence of coronary artery disease. This subtle myolysis could be in part related to the severely increased LV wall strain.

Adult↗
PubMed2001

[Functional mitral insufficiency: a neglected vascular lesion?].

Functional mitral regurgitation is usually neglected during the course of dilated cardiomyopathies. However, functional mitral regurgitation is a sensitive marker of decreased survival. Recent development of treatments such as new surgical approach, permanent biventricular pacing and beta-blockade therapy lead to assess and treat more specifically the accompanying functional mitral regurgitation in congestive heart failure.

Adrenergic beta-Antagonists↗
PubMed2000

[Diastolic heart failure. Physiopathology].

BACKGROUND: Systolic dysfunction of the left ventricle is not the only mechanism of heart failure. An increasing number of patients are found to have heart failure with an ejection fraction > or = 40%. The proportion of heart failure patients with "diastolic" (or more appropriately preserved systolic function) heart failure increases with age. This clinical entity currently accounts for 30 to 40% of all hospitalizations for heart failure and in patients over 80 is found in more patients than is systolic dysfunction. PATHOPHYSIOLOGY: Diastolic heart failure generally associates prolonged ventricular relaxation with reduced left ventricular capacity for distention. The main causes are ischemic, hypertensive and age-related heart disease. Concentric remodeling of the left ventricle, with or without hypertrophy, always leads to diastolic functional disorders. A triggering factor is almost always found for episodes of acute congestion. CONCLUSION: The incidence of "diastolic" heart failure increases with age. Physicians should be aware of the complex underlying pathophysiological mechanisms.

Adult↗
PubMed2000

[Diastolic heart failure. Signs and diagnosis].

A WELL-RECOGNIZED ENTITY: Diastolic heart failure is an increasingly common diagnosis. Signs may be misleading and positive etiological diagnosis remains difficult. CLINICAL SIGNS AND COMPLEMENTARY INVESTIGATIONS: Fatigue, and most importantly dyspnea, are the cardinal signs of diastolic heart failure. Cor pulmonale is often the inaugural sign. The physical examination contributes little to diagnosis. The chest x-ray shows a small heart. Electrocardiographic anomalies are almost always found. A hemodynamic exploration of the right heart, the key diagnostic tool not always performed in routine work-ups, evidences increased filling pressure of the left ventricle. Doppler-echocardiography is used widely. It demonstrates preservation of the left ventricle function (normal ejection fraction) and visualizes the anatomic subtratum of the diastolic dysfunction, quantifying filling and relaxation disorders and allowing an indirect estimation of pulmonary pressures. In the future, it will be possible to assay atrial natriuretic peptide which will provide a most useful tool for the positive diagnosis of this type of heart failure. CONCLUSION: The diagnosis of diastolic heart failure is complex, warranting rigorous, and critical, evaluation of left ventricular filling using noninvasive methods, particularly Doppler-echocardiography.

Adult↗
PubMed2000

[Diastolic heart failure. Treatment].

THERAPEUTIC OPTIONS: Many therapeutic options are proposed for the treatment of diastolic heart failure although no consensus has been established. In experimental trials, several drugs have demonstrated a potentially beneficial effect on ventricular diastolic dysfunction and could be used for diastolic heart failure: nitrate derivatives, converting enzyme inhibitors, angiotensin II antagonists, spirolactones and bradycardia agents. CLINICAL PRACTICE: In everyday clinical practice, low-dose diuretics and treatments aimed at reducing the triggering factor leading to episodes of heart failure are used alone or in combination with treatments aimed at the underlying cause of the diastolic dysfunction: betablockers, calcium inhibitors or nitrate derivatives for ischemic heart disease, drug therapy for hypertension, anti-diabetes agents, anti-arrhythmic agents for atrial fibrillation. Digitalics are not indicated. In experimental trials, converting enzyme inhibitors and angiotensin II antagonists have demonstrated interesting properties for the left ventricle but to date are not warranted for diastolic heart failure. TREATMENT OF THE CAUSE: Due to the lack of consensus on the optimal treatment for diastolic heart failure, most clinicians rely on treating the underlying heart disease and triggering factors.

Adrenergic beta-Antagonists↗
PubMed2000

Highly efficient adenovirus-mediated gene transfer to cardiac myocytes after single-pass coronary delivery.

Efficient and homogeneous gene transfer to cardiac myocytes is a major target in myocardial gene therapy. The aim of this study was to determine the conditions permitting efficient, homogeneous, adenovirus-mediated gene transfer to cardiac myocytes, with a view to application during coronary artery catheterization. Gene transfer to adult rat ventricular myocytes was conducted using type 5 adenoviruses carrying the lacZ reporter gene. Adenovirus delivery via coronary arteries was performed on isolated perfused rat hearts, and gene transfer efficiency was analyzed on whole ventricles, freshly isolated myocytes, and cultured myocytes. Single-pass delivery of 1 X 10(9) PFU associated with 1 min of no-flow yielded only 1 +/- 0.5% of positive myocytes. Pretreatment by histamine perfusion (10(-5) M final concentration) increased this value to 30 +/- 9% (p < 0.001), and pretreatment by Ca2+-free buffer perfusion increased it to 67 +/- 8% (p < 0.001). Combination of the two pretreatments had no additional effect. Increasing the viral dose to 3 X 10(9) PFU increased transfection efficiency only in permeabilized vessels. The 1-min no-flow period after adenovirus delivery was crucial for efficient gene transfer: despite histamine pretreatment, only 2 +/- 1% positive myocytes were observed without flow interruption (p < 0.05 versus 1 min of no-flow). Gene transfer was shown to occur in situ during cardiac perfusion, rather than during heart digestion or myocyte isolation. This study shows that highly efficient adenovirus-mediated gene transfer to cardiac myocytes in situ can be achieved by single-pass intracoronary vector delivery, provided that vascular permeability is first increased and coronary flow is briefly interrupted.

Adenoviridae↗
PubMed2000

Comparison of the prognostic value of left ventricular filling and peak oxygen uptake in patients with systolic heart failure.

AIM: The aim of this prospective study was to compare the prognostic value of the mitral inflow pattern and peak oxygen uptake in patients with systolic heart failure. BACKGROUND: Peak oxygen uptake is a major prognostic parameter in heart failure. It is not known whether a restrictive mitral inflow pattern has similar prognostic value. METHODS: One hundred heart failure patients (ejection fraction <45%) underwent exercise testing after Doppler evaluation; prognosis was assessed after a mean follow-up of 17 months. RESULTS: The ejection fraction was larger in group 1 (non-restrictive pattern: E/A mitral wave ratio <1 or between 1 and 2 with E wave deceleration time >/=140 ms, n=45) than in group 2 (restrictive pattern: E/A ratio >2 or between 1 and 2 with E deceleration time <140 ms, n=40) (29+/-9 vs 22+/-10%, P<0.05). Peak oxygen uptake was lower in group 2 (17+/-4 vs 22+/-5 ml. min(-1). kg(-1)57+/-11 vs 75+/-15% of predicted values;P<0.05 for both comparisons). Univariate analysis showed that the deceleration time (r=0.65), E/A ratio (r=-0.50) and heart rate increment (r=0.47) correlated best with peak oxygen uptake. A third group of patients with persistent fusion of the E and A waves (n=15) had exercise responses similar to those of group 2 patients. A short deceleration time (P=0.006), a restrictive or a fusion pattern (P=0.04) were associated with a poor outcome; the prognostic value of these Doppler variables was greater than that of ejection fraction, but remained less than peak oxygen uptake indexed by predicted values (P=0.0004). CONCLUSION: The left ventricular filling pattern is a strong predictor of exercise capacity, and outcome, in patients with systolic heart failure and is independent of the left ventricular ejection fraction. Peak oxygen uptake remains a more powerful prognostic variable.

Aged↗
PubMed2000

[Ambulatory management of chronic cardiac failure. Possible value of health networking].

Cardiac failure is one of the commonest medical conditions. It usually affects the elderly and is responsible for repeated hospital admission with its high cost for the social security. Several attempts at ambulatory management in certain countries have been successful. Their application may be possible in France. The setting up of health systems like the ones which exist for diabetes, could be a solution to the problem.

Ambulatory Care↗
PubMed1999

Cardiac metaiodobenzylguanidine uptake in patients with moderate chronic heart failure: relationship with peak oxygen uptake and prognosis.

OBJECTIVES: This prospective study was undertaken to correlate early and late metaiodobenzylguanidine (MIBG) cardiac uptake with cardiac hemodynamics and exercise capacity in patients with heart failure and to compare their prognostic values with that of peak oxygen uptake (VO2). BACKGROUND: The cardiac fixation of MIBG reflects presynaptic uptake and is reduced in heart failure. Whether it is related to exercise capacity and has better prognostic value than peak VO2 is unknown. METHODS: Ninety-three patients with heart failure (ejection fraction <45%) were studied with planar MIBG imaging, cardiopulmonary exercise tests and hemodynamics (n = 44). Early (20 min) and late (4 h) MIBG acquisition, as well as their ratio (washout, WO) were determined. Prognostic value was assessed by survival curves (Kaplan-Meier method) and uni- and multivariate Cox analyses. RESULTS: Late cardiac MIBG uptake was reduced (131+/-20%, normal values 192+/-42%) and correlated with ejection fraction (r = 0.49), cardiac index (r = 0.40) and pulmonary wedge pressure (r = -0.35). There was a significant correlation between peak VO2 and MIBG uptake (r = 0.41, p < 0.0001). With a mean follow-up of 10+/-8 months, both late MIBG uptake (p = 0.04) and peak VO2 (p < 0.0001) were predictive of death or heart transplantation, but only peak VO2 emerged by multivariate analysis. Neither early MIBG uptake nor WO yielded significant insights beyond those provided by late MIBG uptake. CONCLUSIONS: Metaiodobenzylguanidine uptake has prognostic value in patients with wide ranges of heart failure, but peak VO2 remains the most powerful prognostic index.

3-Iodobenzylguanidine↗