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Inder S Anand

Publications and source records attributed to Inder S Anand.

At least 19 recordsLinked to original sources
PubMed2006

Influence of blood pressure on the effectiveness of a fixed-dose combination of isosorbide dinitrate and hydralazine in the African-American Heart Failure Trial.

OBJECTIVES: This study sought to assess the effect of baseline systolic blood pressure (SBP) and changes in SBP on the effectiveness of treatment with fixed-dose combination of isosorbide dinitrate and hydralazine (FDC I/H) in patients with heart failure (HF). BACKGROUND: Low SBP is a risk factor for adverse outcomes in patients with HF. However, FDC I/H lowered SBP in the A-HeFT (African-American Heart Failure Trial) and yet prolonged survival. Whether blood pressure (BP) lowering is critical to the efficacy of FDC I/H and whether a low BP limits its effectiveness is unclear. METHODS: The effects of FDC I/H on SBP and on mortality and hospitalization were compared in patients with a low or high baseline SBP using multivariable Cox regression models. The interaction between the effect of treatment and baseline SBP was examined. RESULTS: Mean +/- SD baseline SBP in all of the patients was 126 +/- 18 mm Hg. Patients with baseline SBP equal to or below the median (126 mm Hg) had features of more severe HF. Baseline SBP equal to or below the median was an independent risk factor for death (hazard ratio [HR] 2.09; 95% confidence interval [CI] 1.02 to 4.29) or first hospitalization for HF (HR 1.66; 95% CI 1.18 to 2.34). The FDC I/H treatment reduced BP in patients with SBP above the median but not in patients with SBP below 126 mm Hg. The FDC I/H treatment was associated with a similar decrease in mortality or hospitalization for HF in patients with SBP below the median and above the median. The effects of FDC I/H on mortality alone were also similar. CONCLUSIONS: In A-HeFT, patients with lower SBP had a greater risk but a similar relative benefit from the use of FDC I/H as those with higher SBP. The FDC I/H treatment did not reduce SBP in patients with low SBP. An asymptomatic low SBP should not be considered a contraindication to use of FDC I/H in patients with HF.

Adult↗
PubMed2006

Direct comparison of B-type natriuretic peptide (BNP) and amino-terminal proBNP in a large population of patients with chronic and symptomatic heart failure: the Valsartan Heart Failure (Val-HeFT) data.

BACKGROUND: The B-type or brain natriuretic peptides (BNP) and the amino-terminal probrain natriuretic peptide (NT-proBNP) are good markers of prognosis and diagnosis in chronic heart failure (HF). It is unclear, however, whether differences in their biological characteristics modify their clinical correlates and prognostic performance in HF. This work aimed to provide a direct comparison of the prognostic value of BNP and NT-proBNP in patients with chronic and stable HF. METHODS: We measured BNP and NT-proBNP at baseline in 3916 patients enrolled in the Valsartan Heart Failure Trial. To identify the variables associated with both peptides, we conducted simple and multivariable linear regression analyses. We used Cox multivariable regression models to evaluate the independent prognostic value for all-cause mortality, mortality and morbidity, and hospitalization for HF. Prognostic performance was assessed by pairwise comparisons of the area under the curve of receiver-operator characteristic curves. RESULTS: NT-proBNP and BNP had similar relationships with age, left ventrical ejection fraction, and internal diameter and creatinine clearance. Either peptide ranked as the first independent predictor of outcome after adjustment for major confounding clinical characteristics. ROC curves were almost superimposable for all-cause mortality (area under the curve (SE): BNP 0.665 (0.011) vs NT-proBNP 0.679 (0.011); P=0.0734), but NT-proBNP was superior to BNP for predicting mortality and morbidity (P=0.032) or hospitalization for HF (P=0.0143). Overall sensitivity and specificity ranged from 0.590 to 0.696. CONCLUSIONS: The natriuretic peptides BNP and NT-proBNP showed subtle differences in their relation to clinical characteristics and prognostic performance in a large population of patients with chronic and stable HF. They were the most powerful independent markers of outcome in HF.

Aged↗
PubMed2006

Incremental prognostic value of changes in B-type natriuretic peptide in heart failure.

PURPOSE: B-type natriuretic peptide is one of the most sensitive and specific biohumoral markers of heart failure. We hypothesized that B-type natriuretic peptide changes during treatment of heart failure may provide independent information on disease progression and outcome in patients enrolled in the Val-HeFT trial. METHODS: Patients were divided into four groups according to concentrations of B-type natriuretic peptide at baseline versus 4 months (n = 3740) or 12 months (n = 3343), with respect to the baseline median (97 pg/mL): low-->low (stable below median, 44%-46%), high-->high (stable above median, 32%-37%), high-->low (above to below median, 12%-14%), and low-->high (below to above median, 6%-9%). Cox multivariate regression analysis was used to assess the risk of death and morbidity, with adjustment for baseline B-type natriuretic peptide concentrations. RESULTS: Patients who improved their B-type natriuretic peptide at 4 months (high-->low) had a similar risk for mortality (hazard ratio = 1.191, 95% confidence interval [CI] 0.870-1.631, P =.2746) compared with the low-->low patients. Conversely, patients who worsened in their B-type natriuretic peptide (low-->high) had a risk for mortality (hazard ratio 2.578, CI, 1.861-3.571, P <.0001) higher than patients in the low-->low group, and indistinguishable from the high-->high group. Worsening of B-type natriuretic peptide (low-->high) was associated with 0.03 cm/m2 increase in left ventricular end-diastolic diameter, whereas it decreased by 0.10 cm/m2 in high-->low and low-->low groups (P <.001). CONCLUSIONS: Changes in B-type natriuretic peptide over time with respect to a threshold value of 97 pg/mL convey an independent and additional prognostic value compared with a single determination of B-type natriuretic peptide in a large population of patients with chronic symptomatic heart failure and might be helpful in the management of these patients.

Aged↗
PubMed2006

Relationships between clinical assessments and patients' perceptions of the effects of heart failure on their quality of life.

BACKGROUND: Hypothetically, most of the effects of heart failure on quality of life might be attributed to symptoms produced by the pathology. Relationships between measures of these concepts need to be quantified to test this conceptual model. METHODS AND RESULTS: Measurements of heart failure pathology and symptoms and quality of life as measured by the Minnesota Living with Heart Failure (MLHF) questionnaire at the 4-month visit in the Valsartan Heart Failure Trial were analyzed. Correlation and regression analyses corrected for estimated reliability of measurements were used to quantify relationships. The percentage of variance in dependent variables that was related to explanatory variables was summarized by the coefficient of determination (100 xR(2)) from regression models. Dyspnea at rest, dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, fatigue, and New York Heart Association class were significantly related to MLHF scores. Combined, these symptoms explained 41% of the variation in MLHF scores. Controlling for symptoms, age explained an additional 4.5% of the variation in MLHF scores, whereas race, gender, and available comorbidities each explained <1%. Pathologic measures including ejection fraction, B-type natriuretic peptide, jugular venous distension, rales, peripheral edema, systolic blood pressure, creatinine, and hemoglobin were not strongly related to symptom assessments (combined R(2) = 17%) or MLHF scores (combined R(2) = 7%). CONCLUSION: Symptoms of heart failure explain a substantial proportion of the variation in the effects of heart failure on patients' quality of life as measured by the MLHF score. The effects of heart failure on quality of life can vary with age independently of symptoms. Pathologic measures of heart failure including some well-known correlates of the risk of hospitalization and death are not strongly related to symptoms or quality of life. Further studies are needed to understand the relationships between heart failure pathology and symptoms and to identify determinants of the effects of heart failure on patients' quality of life that were not related to symptoms.

Age Factors↗
PubMed2006

Validation of a risk score for dying within 1 year of an admission for heart failure.

BACKGROUND: Development of heart failure greatly reduces life expectancy. Accurate estimates of the risk of dying are needed in clinical practice and for risk adjustment in observational studies. A relatively simple risk score has been developed to determine the risk of dying within 1-year of an admission for heart failure. We wanted to evaluate the risk score's predictive validity. METHODS AND RESULTS: Data were abstracted from the electronic medical records of 769 patients admitted to the Minneapolis Veterans Administration medical center with a primary diagnosis of heart failure. Mortality within 1 year of admission was 25%. The c-index for the risk score was 0.71 (95% confidence interval 0.67-0.76). Similar to the original derivation cohort, mortality in risk score groups was 7% for a score lower than 60 (n = 44), 14% for 61 to 90 (n = 246), 26% for 91 to 120 (n = 222), 51% for 121 to 150 (n = 106), and 50% for scores greater than 150 (n = 8). CONCLUSION: A previously developed risk score for 1-year mortality after an admission for heart failure provided a moderate degree of discrimination in a validation cohort from a different setting. Mortality in risk score groups was consistent with the original patient cohort. These results support the validity of the risk score and its application to a different patient population.

Aged↗
PubMed2006

The prognostic value of big endothelin-1 in more than 2,300 patients with heart failure enrolled in the Valsartan Heart Failure Trial (Val-HeFT).

BACKGROUND: Endothelin is elevated in heart failure and contributes to neurohormonal activation, hemodynamic deterioration, and cardiovascular remodeling. Here, we examined its prognostic value in a large population of patients with chronic heart failure. METHODS AND RESULTS: Big endothelin-1 (Big ET-1) and 4 other neurohormones were measured at study entry in 2359 patients enrolled in the Valsartan Heart Failure Trial (Val-HeFT) and their concentrations related to outcome over a median follow-up of 23 months. Baseline concentration of Big ET-1 (median 0.80 pmol/L) was proportional to severity of disease (New York Heart Association class, left ventricular structure and function). High circulating concentrations of brain natriuretic peptide (BNP), creatinine and bilirubin, advanced New York Heart Association class, elevated body mass index, and the presence of atrial fibrillation were independently associated to higher concentrations of Big ET-1. Big ET-1 (ranking second just behind BNP among neurohormonal factors) was an independent predictor of outcome defined as all-cause mortality (hazard ratio 1.49, 95% CI 1.20-1.84, P = .0003) or the combined endpoint of mortality and morbidity (hazard ratio 1.43, 95% CI 1.20-1.69, P < .0001) and provided incremental prognostic value compared with BNP. CONCLUSIONS: In a large population of patients with symptomatic heart failure, the circulating concentration of Big ET-1, a precursor of the paracrine and bioactive peptide ET-1, was an independent marker of mortality and morbidity. In this setting, BNP remained the strongest neurohormonal prognostic factor.

Aged↗
PubMed2005

Chronic heart failure with preserved left ventricular ejection fraction: diagnostic and prognostic value of left atrial size.

BACKGROUND: Almost 40% of patients with heart failure (HF) have preserved left ventricular (LV) ejection fraction (EF) and prognosis similar to those with reduced EF. Data on prognostic markers in such patients are limited. We analyzed the prevalence and prognostic value of left atrial (LA) size in this condition. METHODS: 89 normal subjects (Group I), 38 asymptomatic hypertensive patients (Group II) and 183 HF patients with preserved EF (EF >45%) (Group III) were studied. LA diameter (LAD), LV diastolic (LVD) and systolic (LVS) dimensions and mass (LVmass) and EF were measured. E and A wave velocities and E/A were measured. The primary end point was all cause mortality in group III patients. RESULTS: Groups did not differ in age, gender or EF. Group III patients had larger LAD (4.6+-1.0 cm) compared with both Group I (3.7+/-0.6) and Group II (3.7+/-0.5 cm) (p<0.0001). A markedly enlarged (arbitrarily defined as LAD higher or equal 5 cm) had an odds ratio of 34 (95% CI 8-144) in distinguishing HF patients from normals. After a mean follow-up period of 29+/-27 months, 40 patients (21.9%) died. In Cox univariate analysis, NYHA class (HR 2.8 95% C.I. 1.8-4.3; p<0.0001), diastolic blood pressure (DBP) (HR 0.92 95% C.I. 0.88-0.96; p<0.0001), age (HR 1.059 95% C.I. 1.01-1.11; p=0.02) and LAD (HR 1.72 95% C.I. 1.27-2.3; p=0.0005) were predictors of mortality. LAD predicted survival independently of other variables. CONCLUSION: The left atrium is frequently dilated in HF patients compared with controls despite similar EF. LAD showed powerful prognostic value independent of clinical variables.

Aged↗
PubMed2005

C-reactive protein in heart failure: prognostic value and the effect of valsartan.

BACKGROUND: The role of C-reactive protein (CRP) in heart failure is not well studied. We assessed the prognostic value of CRP in patients randomized in Val-HeFT (Valsartan Heart Failure Trial) and studied changes in CRP that were associated with valsartan. METHODS AND RESULTS: Characteristics of patients with baseline CRP levels above and below the median value were compared. Univariable and multivariable Cox proportional hazards regression models were used to examine the relationship of CRP to mortality and morbidity. Interactions were tested to determine whether differences in CRP changes from baseline to 4 and 12 months between groups randomly assigned to valsartan or placebo depended on baseline ACE inhibitor use. Median plasma CRP was 3.23 mg/L (interquartile range 1.42 to 7.56 mg/L), which is higher than in the general population. Patients with CRP above the median had features of more severe heart failure than those with CRP levels below the median. The cumulative likelihood of death and first morbid event increased with increasing quartile of CRP. Relative to the lowest CRP quartile, the risk of mortality (hazard ratio 1.51, 95% CI 1.2 to 1.9) and first morbid event (hazard ratio 1.53, 95% CI 1.28 to 1.84) was increased in the highest CRP quartile in multivariable models. CRP added incremental prognostic information to that provided by brain natriuretic peptide alone. CRP did not change significantly over time in the placebo group; however, after 12 months, valsartan was associated with a decrease in CRP in patients not receiving ACE inhibitors but not in those receiving ACE inhibitors at 12 months. CONCLUSIONS: CRP is increased in heart failure. Higher levels are associated with features of more severe heart failure and are independently associated with mortality and morbidity. The ability of treatments to reduce CRP levels and the prognostic importance of reducing CRP require further study.

Aged↗
PubMed2005

Anemia and change in hemoglobin over time related to mortality and morbidity in patients with chronic heart failure: results from Val-HeFT.

BACKGROUND: Anemia is known to be a prognostic marker for patients with heart failure. However, little is known about the prognostic value of changes in hemoglobin (Hgb) over time or about the causes of anemia. METHODS AND RESULTS: Retrospective analysis of Valsartan Heart Failure Trial data indicated that the quartile of patients with the biggest average decrease in Hgb over 12 months (from 14.2 to 12.6 g/dL) had significantly (P< or =0.01) increased risk of subsequent hospitalization (hazard ratio [HR], 1.47), morbid events (HR, 1.41), and death (HR, 1.6) compared with the quartile that exhibited little change in Hgb over 12 months (from 13.7 to 13.8 g/dL). Increasing Hgb was significantly associated with lower mortality in patients with (HR, 0.78) and without (HR, 0.79) anemia at baseline. Anemia at baseline and the changes in Hgb were independently associated with serum albumin, blood pressure, glomerular filtration rate, B-type natriuretic peptide, and C-reactive protein. Lack of anemia at baseline and increases in Hgb over 12 months were not associated with smaller left ventricular diameters or higher ejection fractions. CONCLUSIONS: Changes in Hgb over 12 months were inversely associated with subsequent risk of mortality and morbidity, independently of the effects of baseline anemia and other important predictors. Several factors were independently related to anemia at baseline and changes in Hgb, suggesting multiple causes of anemia in patients with heart failure. These findings raise important questions about the optimal level of Hgb in patients with moderate to severe heart failure and how to achieve them.

Aged↗
PubMed2005

Pathogenesis of anemia in cardiorenal disease.

The link between chronic heart failure (CHF) and chronic kidney disease (CKD) is well known. Approximately 50% of patients with CHF have some renal dysfunction, and 25% of patients with CKD and serum creatinine levels ranging from 1.5 mg/dL to 6 mg/dL have CHF. The association of CHF with CKD is strong and may contribute to its long-term progression. Anemia is also common in patients with CKD and contributes to increased morbidity and mortality. More recently, anemia has been found to be frequently present in patients with CHF, and its presence is associated with worse long-term CHF outcomes. Thus, anemia, CHF, and CKD may be independently related to one another, and this relationship may have important implications for their management.

Anemia↗
PubMed2004

Critical stenosis of aortic and mitral valves after mediastinal irradiation.

Radiotherapy is used widely in cancer treatment. Mediastinal irradiation is associated with valvular regurgitation; however, stenosis is rare. We present a patient with critical aortic and mitral valve stenosis after mediastinal irradiation and discuss the natural history, treatment, and prognosis of radiation-associated valvular heart disease.

Aortic Valve Stenosis↗
PubMed2004

Is too much neurohormonal blockade harmful?

A number of neurohormones and cytokines are activated in heart failure and their activity is related to the progression of heart failure. Inhibiting the deleterious effects of the activated sympathetic and the renin-angiotensin-aldosterone systems with b-blockers, angiotensin-converting enzyme inhibitors, and aldosterone blockers has been remarkably successful in improving the survival of patients with heart failure. However, inhibition of the other neurohormones and cytokines has not provided the expected incremental benefit, and in some cases has been deleterious, suggesting a ceiling effect of further neurohormonal blockade. This article reviews some of these studies and analyzes the possible causes of these observations.

Angiotensin Receptor Antagonists↗
PubMed2004

Syndromes of subacute mountain sickness.

Two clinical syndromes, acute and chronic mountain sickness, have traditionally been associated with high altitude. Recently, two separate entities of subacute nature have been described in infants and adults. In this paper, we review the published literature on these conditions. Subacute infantile mountain sickness is a condition seen predominantly in Han Chinese infants living in Tibet, although it has been described in other high altitude communities as well. It came into prominence only after the large-scale migration of Chinese population from the low altitude of mainland China to the high altitudes of the Qinghai-Tibetan plateau. The condition is characterized by features of severe hypoxic pulmonary hypertension and heart failure. Pulmonary histology is consistent with muscularization of the pulmonary arterioles, but no intimal proliferation or plexiform lesions are seen. The second syndrome, adult subacute mountain sickness, has been described almost exclusively in Indian soldiers living at extreme altitude for prolonged periods of time. In this condition also, hypoxic pulmonary hypertension appears to be the dominant factor responsible for severe congestive heart failure. Both these conditions have several similarities with brisket disease in cattle; hypoxic pulmonary vasoconstriction plays an important role in the pathogenesis, and removal from high altitude results in complete resolution. Thus, it appears that both these syndromes are human counterparts of brisket disease in cattle.

Adaptation, Physiological↗
PubMed2003

Sustained reduction of aldosterone in response to the angiotensin receptor blocker valsartan in patients with chronic heart failure: results from the Valsartan Heart Failure Trial.

BACKGROUND: Aldosterone has been implicated in the progression of heart failure. The Valsartan Heart Failure Trial (Val-HeFT) provided the first opportunity to examine the long-term effects of an angiotensin receptor blocker on plasma aldosterone levels in patients with NYHA class II through IV heart failure. METHODS AND RESULTS: Plasma aldosterone was measured by radioimmunoassay in core laboratories at baseline and during follow-up in patients assigned to valsartan at a target dose of 160 mg twice daily or placebo. In the placebo group, aldosterone (baseline, 150+/-160 pg/mL, mean+/-SD; n=2025) increased at 4, 12, and 24 months. In the valsartan group, aldosterone (baseline, 137+/-124 pg/mL, mean+/-SD; n=2023) decreased at 4 months and remained suppressed for up to 2 years. At end point (last measurement in each patient), mean aldosterone increased by 17.8+/-3.0 pg/mL (SEM) (11.9%) in the placebo group and decreased by 23.8+/-3.0 pg/mL (SEM) (-17.4%) in the valsartan group (P<0.00001). The effect of valsartan was similar in all subgroups, including those receiving neither ACE inhibitors (ACE-I) nor beta-blockers (BB) at baseline and those receiving concomitant ACE-I or BB. In contrast, outcome effects varied in the 4 subgroups, with a statistically significant reduction in the combined mortality/morbidity end point in those receiving neither neurohormonal inhibitor and an adverse trend in those treated with both drugs. CONCLUSIONS: Valsartan added to background therapy for heart failure produces sustained reduction in plasma aldosterone, consistent with the observed significant reduction in the combined mortality/morbidity end point. A similar reduction in all subgroups based on ACE-I or BB therapy, despite differing clinical outcomes in these subgroups, suggests that aldosterone plasma levels may not be a critical marker of the progression of heart failure.

Aldosterone↗
PubMed2003

Changes in brain natriuretic peptide and norepinephrine over time and mortality and morbidity in the Valsartan Heart Failure Trial (Val-HeFT).

BACKGROUND: Neurohormones are considered markers of heart failure progression. We examined whether changes in brain natriuretic peptide (BNP) and norepinephrine (NE) over time are associated with corresponding changes in mortality and morbidity in the Valsartan Heart Failure Trial. METHODS AND RESULTS: Plasma BNP and NE were measured before randomization and during follow-up in approximately 4300 patients in the Valsartan Heart Failure Trial. The relation between baseline BNP and NE and all-cause mortality and first morbid event (M&M) was analyzed in subgroups, with values above and below the median, and by quartiles. The change and percent change from baseline to 4 and 12 months in BNP and NE were also analyzed by quartiles for subsequent M&M. Risk ratios for M&M were calculated using a Cox proportional hazard model. Risk ratio of M&M for patients with baseline BNP or NE above the median was significantly higher than that for patients with values below the median. Baseline BNP and NE in quartiles also showed a quartile-dependent increase in M&M. BNP had a stronger association with M&M than NE. Patients with the greatest percent decrease in BNP and NE from baseline to 4 and 12 months had the lowest whereas patients with greatest percent increase in BNP and NE had the highest M&M. CONCLUSIONS: Not only are plasma BNP and NE important predictors of heart failure M&M, but changes in these neurohormones over time are associated with corresponding changes in M&M. These data further reinforce their role as significant surrogate markers in HF and underscore the importance of including their measurement in HF trials.

Biomarkers↗
PubMed2003

The role of arginine vasopressin and its receptors in the normal and failing rat heart.

OBJECTIVE: To evaluate the role of arginine vasopressin (AVP) in the normal and post-myocardial infarction (post-MI) hearts, and to investigate whether chronic AVP receptor antagonism can attenuate post-infarct ventricular remodeling. BACKGROUND: A number of neurohormones, like norepinephrine and angiotensin II, have detrimental effects in heart failure (HF) and inhibiting them is beneficial. AVP shares some important properties with these hormones and is activated in HF. However, its role in the syndrome of HF, especially the effect of AVP inhibition, is largely undefined. METHODS AND RESULTS: Effects of AVP-V1a and AVP-V2 receptor stimulation on normal rat cardiomyocyte contractile function, intracellular calcium [Ca2+]i, inositol 3 phosphate (IP3) generation and cell survival were studied. In post-MI rats, AVP receptor function was assessed in cardiomyocytes as well as isolated working hearts. AVP receptor total number (ligand binding) and mRNA levels (RT-PCR) were measured in myocytes. Finally, the effects of chronic AVP-V1a blockade were assessed in post-MI rats using echo and morphometry to measure ventricular remodeling. Normal cardiomyocytes showed a dose-dependent increase in myocyte contractile function, [Ca2+]i, and IP3 generation in response to AVP-V1a receptor stimulation. AVP-V2 agonists had no effect. Cells from MI hearts showed reduced inotropic response to AVP-V1a stimulation. Myocyte AVP-V1a receptor number and receptor mRNA were decreased. Prolonged exposure to AVP reduced cellular viability. However, chronic AVP-V1a blockade did not attenuate structural remodeling or improve function in post-MI hearts. CONCLUSIONS: Isolated adult rat cardiomyocytes bear AVP-V1a receptors that mediate inotropic effects through the IP3 pathway. These receptors are functionally and numerically downregulated in the post-MI remodeled hearts. Despite evidence that AVP is cytotoxic to cells, chronic AVP-V1a receptor blockade does not attenuate post-MI ventricular remodeling in this model. Thus, AVP may not play a major role in the structural progression of HF.

Animals↗
PubMed2002

Surrogate end points in heart failure.

Because of the increasing number of pharmacologic strategies available for treatment of heart failure (HF), the time has come to reassess the adequacy of end points used to evaluate therapeutic efficacy. Interest in the use of surrogate end points in clinical studies is increasing. A surrogate end point is defined as a measurement that can substitute for a true end point for the purpose of comparing specific interventions or treatments in a clinical trial. A true end point is one that is of clinical importance to the patient (e.g., mortality or quality of life), whereas a surrogate end point is one biologically closer to the disease process (e.g., ejection fraction or left ventricular volume in HF). The prime motivation for the use of a surrogate end point concerns the possible reduction in sample size or trial duration. Such reductions have important cost implications and in some cases may influence trial feasibility. Another, perhaps more important, aspect of measuring surrogate end points is that they increase our understanding of the mechanism of action of drugs and thus may help physicians to take a more enlightened approach in managing their patients. In this article we have analyzed the possible potentials of the surrogate end points in clinical studies of patients with chronic HF. Other uses of possible surrogates are discussed, and the limitations in finding true surrogates are mentioned. At this time we conclude there is no well established surrogate in HF.

Biomarkers↗