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Biomedical subjects

Thierry H Le Jemtel

Publications and source records attributed to Thierry H Le Jemtel.

16 recordsLinked to original sources
PubMed2006

Diagnostic and therapeutic challenges in patients with coexistent chronic obstructive pulmonary disease and chronic heart failure.

Chronic obstructive pulmonary disease (COPD) and heart failure (CHF) are common conditions. The prevalence of COPD ranges from 20% to 30% in patients with CHF. The diagnosis of CHF can remain unsuspected in patients with COPD, because shortness of breath is attributed to COPD. Measurement of plasma B-type natriuretic peptide (BNP) levels helps to uncover unsuspected CHF in patients with COPD and clinical deterioration. Noninvasive assessment of cardiac function may be preferable to BNP to uncover unsuspected left ventricular (LV) systolic dysfunction in patients with stable COPD. Patients with COPD or CHF develop skeletal muscle alterations that are strikingly similar. Functional intolerance correlates with severity of skeletal muscle alterations but not with severity of pulmonary or cardiac impairment in COPD and CHF, respectively. Improvement of pulmonary or cardiac function does not translate into relief of functional intolerance in patients with COPD or CHF unless skeletal muscle alterations concomitantly regress. The mechanisms responsible for skeletal muscle alterations are incompletely understood in COPD and in CHF. Disuse and low-level systemic inflammation leading to protein synthesis/degradation imbalance are likely to contribute. The presence of COPD impacts on the treatment of CHF, as COPD is still viewed as a contraindication to beta-blockade. Therefore, COPD often deprives patients with CHF due to LV systolic dysfunction of the most beneficial pharmacologic intervention. A large body of data indicates that patients with COPD tolerate well selective beta-blockade that should not be denied to CHF patients with concomitant COPD.

Adrenergic Antagonists↗
PubMed2006

Diagnostic usefulness of B-type natriuretic peptide and functional consequences of muscle alterations in COPD and chronic heart failure.

COPD affects up to one third of patients with chronic heart failure. The coexistence of COPD and chronic heart failure presents clinicians with diagnostic and therapeutic challenges. Measurement of B-type natriuretic peptide plasma levels facilitates the diagnosis of acute dyspnea in patients known to have both COPD and chronic heart failure. Patients with COPD or chronic heart failure have skeletal muscle abnormalities that limit functional capacity independently from primary organ failure. Exercise training reverses skeletal muscle abnormalities in patients with COPD or chronic heart failure and may be particularly indicated in patients with coexistent COPD and chronic heart failure.

Biomarkers↗
PubMed2005

Long-term effects of carvedilol or metoprolol on left ventricular function in ischemic and nonischemic cardiomyopathy.

Data regarding the effects of beta blockers on left ventricular (LV) function after 12 months are scarce in ischemic and nonischemic cardiomyopathy. Echocardiograms of 72 patients with ischemic and nonischemic cardiomyopathy, who were free of clinical events susceptible to alter LV function while receiving carvedilol or metoprolol for at least 24 months, were prospectively reanalyzed. Twelve months after beta-blocker initiation, LV ejection fraction (EF) increased by > or = 5% in 75% of patients, whereas EF failed to increase by 5% or decreased in the remaining 25%. Over the subsequent 32 months, LVEF increased further in patients who had experienced an initial EF increase by > or = 5%, whereas EF tended to further decrease in patients who had experienced an initial EF increase of <5% or a decrease. Thus, the benefits of carvedilol or metoprolol on LV function are long lasting in patients with ischemic or nonischemic cardiomyopathy who are free of events susceptible to alter LV function while receiving beta blockade.

Adrenergic beta-Antagonists↗
PubMed2004

Comparison of suppression of the circulating and vascular renin-angiotensin system by enalapril versus trandolapril in chronic heart failure.

Experimental studies suggest that angiotensin-converting enzyme (ACE) inhibitors with high tissue affinity confer a greater degree of vascular renin-angiotensin system suppression than those with low tissue affinity despite similar suppression of the circulating renin-angiotensin system. To test this hypothesis in a clinical setting, we randomized subjects with chronic heart failure to receive the low tissue affinity ACE inhibitor enalapril or the high tissue affinity ACE inhibitor trandolapril, and assessed the degree of circulating and vascular renin-angiotensin system suppression. Vascular renin-angiotensin system suppression was determined by measuring the pressor response to intravenous injections of angiotensin I. Circulating renin-angiotensin system suppression was determined by measuring plasma angiotensin II. Vascular and circulating renin-angiotensin system suppression, endothelial function (flow-mediated vasodilation), and maximal exercise capacity (peak oxygen uptake) were assessed after a 4-week run-in period on open-label enalapril 40 mg/day and after 8 weeks of randomized double-blind treatment with enalapril 40 mg/day or trandolapril 4 mg/day. Twenty-six men and 4 women (mean age 52 +/- 11 years; mean left ventricular ejection fraction 25 +/- 9%; New York Heart Association class II [n = 16] and III [n = 14]) were studied. After a 2-month randomized treatment period, vascular renin-angiotensin system suppression, circulating renin-angiotensin system suppression, endothelial function, and exercise capacity did not differ between subjects treated with enalapril and those treated with trandolapril. Despite substantial differences in the tissue affinity of enalapril and trandolapril, the degree of vascular renin-angiotensin system suppression achieved with these agents did not differ in subjects with chronic heart failure during long-term therapy.

Angiotensin II↗
PubMed2004

Therapeutic update: non-selective beta- and alpha-adrenergic blockade in patients with coexistent chronic obstructive pulmonary disease and chronic heart failure.

Patients with chronic heart failure (CHF) have a resting restrictive ventilatory defect. Any type of exercise requires patients with CHF to markedly increase their minute ventilation. Patients with chronic obstructive pulmonary disease (COPD) have airflow obstruction that leads to dynamic lung hyperinflation and reduced ventilatory response to exercise. Because exercise is associated with abnormally high minute ventilation in patients with CHF and with a limited minute ventilation increase in patients with COPD, functional capacity is severely impaired in patients with coexistent CHF and COPD. Optimal treatment of both conditions is a prerequisite to maximally improve functional capacity in patients with CHF and COPD. Unfortunately, beta-adrenergic blockade, the current cornerstone of CHF therapy, is frequently omitted in patients with CHF and COPD for fear of inducing bronchoconstriction. Furthermore, when prescribed, beta-adrenergic blockade is often attempted with a moderate dose of metoprolol tartrate, a beta-1-blocker that results in lesser clinical benefits than combined non-selective beta-blockade with carvedilol at the maximally recommended dose. Recent experience indicates that combined non-selective beta- and alpha-blockade with carvedilol is well tolerated in patients with COPD who do not have reversible airway obstruction. Alpha-adrenergic blockade may promote mild bronchodilation that offsets non-selective beta blockade-induced bronchoconstriction in patients with obstructive airway disease.

Adrenergic alpha-Antagonists↗
PubMed2004

Hospitalization for heart failure in the presence of a normal left ventricular ejection fraction: results of the New York Heart Failure Registry.

OBJECTIVES: We conducted a prospective multicenter registry in a large metropolitan area to define the clinical characteristics, hospital course, treatment, and factors precipitating decompensation in patients hospitalized for heart failure with a normal ejection fraction (HFNEF). BACKGROUND: The clinical profile of patients hospitalized for HFNEF has been characterized by retrospective analyses of hospital records and state data banks, with few prospective single-center studies. METHODS: Patients hospitalized for heart failure (HF) at 24 medical centers in the New York metropolitan area and found to have a left ventricular (LV) ejection fraction of > or 50% within seven days of admission were included in this registry. Patient demographics, signs and symptoms of HF, coexisting and exacerbating cardiovascular and medical conditions, treatment, laboratory tests, procedures, and hospital outcomes data were collected. Analysis by gender and race was prespecified. RESULTS: Of 619 patients, 73% were women, who were on average four years older than men (72.8 +/- 14.1 years vs. 68.6 +/- 13.8 years, p < 0.001). Black non-Hispanic patients comprised 30% of the study population. They were eight years younger than other patients (66.0 +/- 14.2 years vs. 74 +/- 13.5 years p < 0.001). Co-morbid conditions and their prevalence were: hypertension, 78%; increased LV mass, 82%; diabetes, 46%; and obesity, 46%. Before clinical decompensation that precipitated hospitalization, 86% of patients had chronic symptoms compatible with New York Heart Association functional classes II to IV. Factors precipitating clinical decompensation were identified in 53% of patients. In-hospital mortality was 4.2%. CONCLUSIONS: Patients hospitalized for HFNEF are most often chronically incapacitated elderly women with a history of hypertension and increased LV mass. Reasons for clinical decompensation are identified in only one-half of patients.

Adult↗
PubMed2004

Vasopressin antagonists in heart failure.

The recrudescence of interest in manipulation of the arginine vasopressin system and especially of V2 vasopressin receptor blockade in heart failure stems from the limited efficacy and possible detrimental effects of loop diuretics. The "braking phenomenon," hypertrophy of the collecting duct cells, and altered pharmacodynamics contribute to loop diuretic resistance in heart failure. Selective (tolvaptan) and nonselective (conivaptan) V2 vasopressin receptor antagonists now known as "vaptans" promote free-water excretion that is labeled aquaresis and correct hyponatremia in patients with severe heart failure. A large mortality study with tolvaptan in heart failure is presently ongoing.

Animals↗
PubMed2004

Inhibition of RAAS--when is it too much?

Deactivation of the renin-angiotensin-aldosterone system (RAAS) is clearly beneficial in patients with recent myocardial infarction and chronic heart failure. Most of the experience with deactivation of the RAAS has been collected in placebo-controlled randomized trials of angiotensin- converting enzyme inhibition (ACEI). The hypothesis that angiotensin receptor blockade may be a better approach to deactivate the RAAS has not survived the test of time. Despite the extensive experience with ACEI and aldosterone receptor blockade in patients with recent myocardial infarction and chronic heart failure, several issues remain unanswered. These are addressed in this review.

Angiotensin Receptor Antagonists↗
PubMed2002

Elevated plasma aldosterone levels despite complete inhibition of the vascular angiotensin-converting enzyme in chronic heart failure.

BACKGROUND: Plasma aldosterone levels are elevated in patients with chronic heart failure (CHF) taking angiotensin-converting enzyme (ACE) inhibitors. Elevated aldosterone levels may reflect incomplete inhibition of the vascular converting enzyme during long-term ACE inhibition. We simultaneously measured plasma aldosterone levels and the degree of inhibition of the vascular converting enzyme in patients with CHF. METHODS AND RESULTS: Thirty-four subjects with CHF receiving the maximum recommended doses of ACE inhibitors for a duration of 3 to 105 months were studied. The pressor response to exogenous angiotensin I (AI) was measured and normalized for the pressor response to angiotensin II (AII) to assess inhibition of the vascular converting enzyme (AII/AI ratio). Aldosterone levels were determined by solid-phase radioimmunoassay. Eleven of the 34 subjects had plasma aldosterone levels above the upper limit of normal, ie, >15.0 ng/dL. Seven of these 11 subjects (64%) had an AII/AI ratio < or =0.05, indicating complete inhibition of the vascular converting enzyme. In the entire cohort, the AII/AI ratio did not correlate with the duration of ACE inhibitor therapy. CONCLUSIONS: Plasma aldosterone levels are elevated in patients with CHF during long-term ACE inhibitor therapy despite complete inhibition of the vascular converting enzyme. Complete inhibition of the vascular converting enzyme does not obviate the need for aldosterone receptor blockade in patients with CHF.

Aldosterone↗
PubMed2002

Biopsy coupled to quantitative immunofluorescence: a new method to study the human vascular endothelium.

Limited availability of endothelial tissue is a major constraint when investigating the cellular mechanisms of endothelial dysfunction in patients with metabolic and cardiovascular diseases. We propose a novel approach that combines collection of 200-1,000 endothelial cells from a superficial forearm vein or the radial artery, with reliable measurements of protein expression by quantitative immunofluorescence analysis. This method was validated against immunoblot analysis in cultured endothelial cells. Levels of vascular endothelial cell activation, oxidative stress, and nitric oxide synthase expression were measured and compared in five patients with severe chronic heart failure and in four healthy age-matched subjects. In summary, vascular endothelial biopsy coupled with measurement of protein expression by quantitative immunofluorescence analysis provides a novel approach to the study of the vascular endothelium in humans.

Aged↗
PubMedDate not supplied

Clinical profile of chronic heart failure in elderly women.

The pathogenesis, clinical course, and treatment of chronic heart failure (HF) are different in elderly women from those of patients recruited in the landmark trials of chronic HF. Patients included in these landmark trials were predominantly men whose age was 10-15 years younger than the average age of patients with chronic HF in the United States. Diastolic dysfunction resulting in impaired left ventricular (LV) filling is the preponderant LV functional alteration that leads to chronic HF in elderly women. Gender differences in the LV remodeling process that accompanies chronic cardiac pressure are likely to be responsible for the preponderance of LV diastolic dysfunction over systolic dysfunction in elderly women. In response to chronic pressure overload, the LV wall becomes thicker in women than in men. Consequently, in response to chronic pressure overload, women are able to normalize LV wall stress and preserve LV systolic function to a greater extent than men. However, impaired LV filling is an undesirable consequence of the greater increase in LV wall thickness in women. Thus, clinical observations and therapeutic guidelines derived from data collected in the landmark trials of chronic HF may not apply to elderly women with chronic HF. In view of the lack of evidence-based information needed to guide the management of elderly women with chronic HF, special attention should be given to include a substantial number of elderly women in future therapeutic trials recruiting patients with chronic HF.

Age Factors↗
PubMedDate not supplied

Serum brain natriuretic peptide level in a patient with chronic obstructive pulmonary disease and chronic heart failure.

A 52-year-old woman with chronic obstructive pulmonary disease (COPD) and chronic heart failure presented in respiratory distress. Physical examination could not differentiate COPD exacerbation from chronic heart failure decompensation. As her serum B-type natriuretic peptide level was 1030 pg/mL, she was initially treated for chronic heart failure decompensation. Serum B-type natriuretic peptide level fell to 308 pg/mL, but respiratory distress persisted. She was then treated with intravenous solumedrol for COPD exacerbation. Respiratory distress rapidly resolved. Serum B-type natriuretic peptide level is useful to detect heart failure in the presence of COPD but does not substitute for clinical judgment to initiate proper management.

Albuterol↗