Epidemiology Of Heart Failure Research Articles

Pulmonary Hypertension Due to Left Heart Disease

Pulmonary hypertension (PH) due to left heart disease, classified as group 2 according to the Dana Point 2008 classification, is believed to be the most common cause of PH and is associated with high morbidity and mortality. Epidemiological studies of group 2 PH are less exhaustive than for rarer causes of PH such as isolated pulmonary vasculopathies, but attention for this entity is growing rapidly. Group 2 PH may be caused by passive downstream elevation in left heart pressures or by a combination of the latter with pulmonary arteriolar pathologies. Improved understanding of the perturbations in pulmonary vascular structure and function that cause PH due to left heart disease is essential to reduce heart failure morbidity and mortality. In this review, epidemiology, mechanisms, diagnostic approaches, hemodynamic models, and clinical trials of heart failure complicated by group 2 PH are reviewed, along with a discussion of novel treatment strategies that are currently under investigation or hold promise for the future. Interest in group 2 PH has historically been confined to mitral valve disease and advanced stages of heart failure (HF), wherein clinical manifestations of right ventricular (RV) failure carry an extremely unfavorable prognosis.1⇓–3 Clinical recognition of group 2 PH has expanded, with recent studies demonstrating that increases in rest and exercise pulmonary arterial pressures may accompany normal aging4,5 and that patients with HF and preserved ejection fraction (HFpEF) frequently also display PH.6 Although left heart disease is believed to represent the most common form of PH, epidemiological data are less abundant in this group in comparison with others.7 The most recent European Guidelines define group 1 PH as a chronic elevation of a mean pulmonary arterial pressure ≥25 mm Hg in association with normal pulmonary capillary wedge pressure (PCWP; ≤15 mm Hg; …

Primary prevention of heart failure.

Most heart failure research and quality improvement efforts are targeted at treatment and secondary prevention of patients with manifest heart failure. This is distinct from coronary disease where primary prevention has been a focus for over three decades. Given the current importance and the projected worsening of heart failure epidemiology, a more focused effort on prevention is urgently needed.

Pharmaco-refractory chronic heart failure – The need for drug level tailored management

Pharmacorefractory chronic heart failure is a serious world-wide problem of systolic dysfunction not improving despite evidence based chronic heart failure pharmacotherapy. With the aim to reverse the poor pharmacorefractory chronic heart failure prognosis, severe sophisticated technical therapeutic approaches (from cardiac resynchronization usually with implantable cardioverter-defibrillator to heart transplantation) have been clinically adopted and detached at least for the most eligible pharmacorefractory chronic heart failure patients. However, both significant limitations of these highly specialised therapeutic techniques (cost, uncertain individual effect, complication, adverse effect, waiting list) and the pharmacorefractory chronic heart failure hopelessness for unfit patients make the effort to stop the pharmacorefractory chronic heart failure genesis never ending longing. Regarding growing knowledge on differences in pharmacokinetics, authors assume that the relative undertreatment despite fixed doses may explain the pharmacorefractory chronic heart failure genesis. If this hypothesis proves to be correct, the evidence based chronic heart failure pharmacotherapy innovatively personalized according to steady state drug serum level may reduce the pharmacorefractory chronic heart failure epidemiology with the lower need for cost-consuming techniques and be the promising strategy for patients left on individually ineffective evidence based chronic heart failure pharmacotherapy.

Global heart failure rates and erythropoietin

▸ Global variation in heart failure (HF) mortality rates is evident. ▸ Erythropoietin (EPO) has some cardioprotective properties. ▸ The release of EPO is stimulated by hypoxia. ▸ Hypoxia is caused by higher geographic elevation. ▸ Geographic landscape may help to explain epidemiology of HF. Global variation in heart failure (HF) prevalence and mortality rates is evident and multiple factors have been hypothesised to explain such non-random distribution. The author hypothesised that this non-random HF distribution could be attributed, in part, to individual variation in the level of erythropoietin (EPO), a hormone and a possible cardioprotectant. Such individual EPO variation can be explained by hypoxia resulting from regional differences in geographic elevation. This hypothesis was justified using results from various animal-based and clinical studies. In addition, data from the population-based Healthcare Cost and Utilization Project was used. The global distribution of HF can be explained, in part, by the geographic landscape. Prospective studies based on the author’s hypothesis may provide new treatment opportunities for such an important health issue as HF. In addition, this hypothesis may demonstrate new insights into the mechanism of HF.

Response to Letter Regarding Article, “Mortality and Readmission of Patients With Heart Failure, Atrial Fibrillation, or Coronary Artery Disease Undergoing Noncardiac Surgery: An Analysis of 38 047 Patients”

We thank Drs Chatterjee and Chakraborty for their insightful comments. We acknowledge that studies on the general epidemiology of heart failure demonstrate that patients with an ischemic pathogenesis for heart failure have a worse prognosis than those with nonischemic heart failure; however, there are few publications that explore this relationship in the perioperative setting. A cohort from the United States …

Epidemiology and diagnosis of heart failure with preserved left ventricular ejection fraction: rationale and design of the study

Despite major advances in our understanding of 'systolic' heart failure, at present the epidemiology, pathophysiology, and therapy of heart failure with preserved left ventricular ejection fraction (HFpEF) is poorly understood, in large part because of the lack of robust and widely accepted diagnostic criteria. Although there is a good evidence base for the treatment of systolic heart failure, similar data are lacking for the treatment of HFpEF. Methods In our study, we will screen a consecutive series of 5000 subjects aged ≥60 from the community. Following symptom questionnaire and echocardiography, metabolic exercise testing will be used to confirm whether or not patients thought clinically to have HFpEF are in fact exercise limited and that this limitation is cardiac in origin. Blood samples for plasma brain natriuretic peptide (BNP) will be taken at rest and following exercise in symptomatic patients and matching controls. At the end of our study we will establish community prevalence and population characteristics of HFpEF, and also evaluate the diagnostic accuracy of current echocardiography parameters and BNP for the diagnosis of the condition.

Clinical Considerations of Heritable Factors in Common Heart Failure

Heart failure is a common condition responsible for at least 290 000 deaths each year in the United States alone.1 A small minority of heart failure cases are attributed to Mendelian or familial cardiomyopathies. The majority of systolic heart failure cases are not familial but represent the end result of 1 or many conditions that primarily injure the myocardium sufficiently to diminish cardiac output in the absence of compensatory mechanisms. Paradoxically, because they also injure the myocardium, it is the chronic actions of the compensatory mechanisms that in many instances contribute to the progression from simple cardiac injury to dilated cardiomyopathy and overt heart failure. Thus, the epidemiology of common heart failure appears to be just as sporadic as its major antecedent conditions (atherosclerosis, diabetes, hypertension, and viral myocarditis). Familial trends in preclinical cardiac remodeling2 and risk of developing heart failure3 reveal an important role for genetic modifiers in addition to clinical and environmental factors. Candidate gene studies performed over the past 10 years have identified a few polymorphic gene variants that modify risk or progression of common heart failure.4 Whole-genome sequencing will lead to the discovery of other genetic modifiers that were not candidates.5 The imminent availability of individual whole-genome sequences at a cost competitive with available genetic tests for familial cardiomyopathy will no doubt further expand the list of putative genetic heart failure modifiers. Heart failure risk alleles along with traditional clinical factors will need to be considered by clinical cardiologists in their design of optimal disease surveillance and prevention programs and in individually tailoring heart failure management. The use of individual genetic make-up is likely to have the earliest and greatest impact on managing patients with heart failure by tailoring available pharmacotherapeutics to optimize patient response and minimize adverse effects (ie, the …

Advances in the Epidemiology of Heart Failure and Left Ventricular Remodeling

Heart failure (HF) continues to impose a major public health burden.1 Whereas considerable improvements in HF treatment have resulted from clinical trials, epidemiological investigations complement clinical trials by enhancing our ability to identify individuals at risk and, in turn, facilitate the development of interventions aimed at the primary prevention of HF. Accordingly, there have been several noteworthy advances to date in the epidemiology of heart failure and subclinical myocardial disease, which are summarized below. Adverse left ventricular (LV) remodeling is considered an intermediate phenotype of HF, given the high incidence of HF events observed among individuals with subclinical abnormalities in LV structure or function (also known as stage B heart failure).2 Recent investigations have harnessed longitudinal data from large epidemiological cohorts to examine how the heart remodels over the adult life course and to characterize the factors that contribute to this remodeling. The most common form of adverse LV remodeling is increased LV mass, which has long been associated with incident HF; this association was originally demonstrated with the use of electrocardiography, followed by echocardiography, and then recently confirmed using cardiac MRI studies.3,4 Longitudinal data have now validated the results of previous cross-sectional studies indicating that LV mass progressively increases over the life course, and particularly in the presence of risk factors such as obesity, hypertension, and diabetes.5 However, increased LV mass can result from a variety of different remodeling patterns, including concentric or eccentric changes in geometry.6,7 The most common remodeling pattern observed in normally aging individuals over the life course is a concentric remodeling pattern, in which LV wall thickness progressively increases and LV cavity dimensions progressively decrease in the setting of preserved and increasing ejection fraction.3,8 Interestingly, the rate of increase in relative wall thickness …

Thromboembolism and Antithrombotic Therapy in Patients With Heart Failure in Sinus Rhythm

Heart failure (HF) represents a major and growing public health problem because of its prevalence, incidence, morbidity, mortality, and economic costs. The prevalence of HF is 2% to 3% of the general population.1 Five million Americans are affected, with >550 000 cases diagnosed each year.2 The mortality rate from severe HF remains >60% within 5 years of diagnosis, and 50% of hospitalized patients with HF require readmission within 6 months of discharge. In the US estimated costs amount to > $35 billion per year.3 Although several therapies (eg, β-blockers, angiotensin-converting enzyme [ACE] inhibitors, and cardiac resynchronization therapy) have been proven effective in improving HF outcomes, many unanswered questions about optimal treatment remain. One area of ongoing uncertainty is the appropriate role for antithrombotic therapy in patients with HF. Observational data suggest that patients with HF have an increased venous thromboembolism (VTE) risk (deep venous thromboembolism [DVT], pulmonary embolism [PE], peripheral arterial thromboembolism, and stroke).4 These epidemiological findings are supported by multiple mechanisms that can contribute to a hypercoagulable state in patients with HF. Despite this increased risk of VTE, the role of antithrombotic therapy remains unclear. In this article, we provide an overview of epidemiology, pathophysiology, clinical trial data, and therapeutic recommendations for prevention of thromboembolism in HF. We searched PubMed for articles published between 1958 and 2010 using the following search terms: epidemiology of heart failure , thromboembolism and heart failure , thrombogenesis and heart failure , anticoagulation in heart failure , antiplatelet agent and heart failure , aspirin and heart failure , bleeding risk and anticoagulation , and aspirin and angiotensin-converting enzyme inhibitors . We also studied abstracts from national and international cardiovascular meetings to identify unpublished studies using the key words anticoagulation and dilated cardiomyopathy . Data from published observational studies and secondary …

Epidemiology and clinical course of heart failure with preserved ejection fraction

Heart failure with preserved ejection fraction (HFPEF) is increasingly recognized as a major public health problem worldwide. Significant advances have been made in our understanding of the epidemiology of HFPEF over the past two decades, with the publication of numerous population-based epidemiological studies, large heart failure registries, and randomized clinical trials. These recent studies have provided detailed characterization of larger numbers of patients with HFPEF than ever before. This review summarizes the state of current knowledge with regards to the disease burden, patient characteristics, clinical course, and outcomes of HFPEF. Despite the wealth of available data, substantive gaps in knowledge were identified. These gaps represent opportunities for further research in HFPEF, a syndrome that is clearly a rising societal burden and that is associated with substantial morbidity and mortality.

Diastology 2010: clinical approach to diastolic heart failure.

The role of echocardiography in the evaluation of left ventricular diastolic function is increasingly important in both systolic and diastolic heart failure. In routine clinical practice, the diastolic dysfunction associated with diastolic heart failure can mainly be evaluated by Doppler echocardiography. In order to use echocardiographic techniques for this purpose, one should recognize the definition, terminology, epidemiology, and pathophysiology of diastolic dysfunction and diastolic heart failure. There are various echocardiographic parameters for this purpose, including transmitral flow velocity, pulmonary venous flow velocity, mitral annular velocity, flow propagation velocity, left atrial size, strain, strain rate, twist, and so on. However, no single Doppler echocardiographic index has yielded a robust criterion for diastolic dysfunction and elevated left ventricular filling pressure. Thus, multiple indices are required to increase the sensitivity of the diagnosis. Clinicians who take care of heart failure patients should continue to make critical use of a current Doppler echocardiographic evaluation and utilize this information to improve survival and quality of life in these patients.

Trends in Heart Failure Epidemiology in a Midwestern State: Ruralness and Race over a Twelve Year Period

Trends in Heart Failure Epidemiology in a Midwestern State: Ruralness and Race over a Twelve Year Period

Section 5: Management of Asymptomatic Patients with Reduced Left Ventricular Ejection Fraction

Section 5: Management of Asymptomatic Patients with Reduced Left Ventricular Ejection Fraction

Advances in systolic heart failure

Heart failure due to systolic dysfunction has enormous global impact. Medical management based on an understanding of the pathophysiology of the disease as well as its neurohormonal mechanisms has greatly advanced over the past 25 years. Below is a review of recent and emerging data on epidemiology and diagnosis of heart failure due to systolic dysfunction and the current and future management techniques to ameliorate this disease. At the end, we will highlight three significant trials in the field in 2009 that will impact heart failure care: STICH, MADIT-CRT, and HeartMate II.

Understanding changing patterns of survival and hospitalization for heart failure over two decades in New Zealand: utility of ‘days alive and out of hospital’ from epidemiological data

To describe changes in heart failure (HF) epidemiology in New Zealand between 1988 and 2008 using the number of days alive and out of hospital after a first hospitalization for HF, and to use these data to evaluate the overall impact of changing patterns of hospitalization and survival. We performed a population analysis of all HF hospitalization and mortality data from 1 January 1988 to 31 December 2008 in New Zealand. The main outcome measures were: days alive and out of hospital, age standardized hospitalization rates, and mortality after an index hospitalization for HF. The number of days alive and out of hospital at 2 years increased by 2 months over the two decades of the study (from 448.8 to 511.3 days). Age standardized index HF hospitalization rates increased from 1988 to 1999, and declined thereafter, current rates are 106.9/100 000 for women and 174.3/100 000 for men. Patient age at index admission progressively increased, and hospital length of stay decreased. Mortality rates progressively decreased until 2000, but there has been no further decrease since then. Total hospital days have decreased up to 2008. There have been major changes in the epidemiology of HF in New Zealand between 1988 and 2008, during which time there have been important changes in HF management. Despite increasing age, hospitalization rates are now declining and patients with HF are surviving longer out of hospital and with fewer hospital days. These results support the need for continued emphasis on delivery of effective community-based care for patients with this long-term condition.

Heart Failure: the Commonest Reason for Hospitalization in Germany—Medical and Economic Perspectives: Limitations of the Between-Sex Comparison

We read the important article on the epidemiology of heart failure in Germany with great interest. The conclusions resulting from figures 1 to 3 and the discussion with regard to how the risk of morbidity and mortality differ by sex are misleading, however (1). The data source used by the authors (2) reveals that for almost all categories themorbidity and mortality rates are higher in men than in women up to a very old age. Up to the age of 70, women have a 50–56% lower risk of death or hospitalization than men. This difference evens out slowly by about the age of 90. Women are slightly more affected only at an older age. The reason for the apparent discrepancy in findings is that the use of the standard population of Germany 1987 for age standardization leads to different reference groups for men and women: The age standardized rates for men derived from federal health monitoring data (2) were applied to the male population of 1987 and the female rates to the female population of 1987 (3). The rates for men and women are therefore suitable for comparisons within the sexes (for example, between federal states or over time) but not between them. A correct analysis of sex differences would therefore require the use of a standard population with identical age structure in men and women (for example, the Old European Standard Population). Alternatively, it is possible to use the same reference population for both sexes. Correct age standardization reveals that the standardized death and hospitalization rates of women, shown by the authors in figures 1 to 3, are not higher but lower than those in men.

Therapeutic approaches to diastolic dysfunction

Progressive abnormalities of passive stiffness or active relaxation of the myocardium that impair ventricular filling during diastole may be an important contributor to the development of heart failure in patients with preserved ejection fraction. In this review, we discuss the epidemiology and pathophysiology of diastolic dysfunction and heart failure with preserved ejection fraction, highlighting potential therapeutic approaches and exploring the limited available evidence base for improving clinical outcomes in patients with these challenging entities.

Irbesartan did not reduce all-cause death or CV hospitalization in heart failure and preserved ejection fraction

ACP Journal Club19 May 2009Irbesartan did not reduce all-cause death or CV hospitalization in heart failure and preserved ejection fractionJustin A. Ezekowitz, MD, Finlay A. McAlister, MDJustin A. Ezekowitz, MDUniversity of Alberta,, Edmonton, Alberta, Canada (J.A.E., F.A.M.)Search for more papers by this author, Finlay A. McAlister, MDUniversity of Alberta,, Edmonton, Alberta, Canada (J.A.E., F.A.M.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-150-10-200905190-02010 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationMassie BM, Carson PE, McMurray JJ, et al. Irbesartan in patients with heart failure and preserved ejection fraction. N Engl J Med. 2008;359:2456-67. https://pubmed.ncbi.nlm.nih.gov/19001508Clinical Impact RatingsGIM/FP/GP: Cardiology: References1 McAlister FA, Teo KK, Taher M, et al. Insights into the contemporary epidemiology and outpatient management of congestive heart failure. Am Heart J. 1999;138:87-94. [PMID: 10385769] Google Scholar2 Ezekowitz JA, Lee DS, Tu JV, Newman AM, McAlister FA. Comparison of one-year outcome (death and rehospitalization) in hospitalized heart failure patients with left ventricular ejection fraction >50% versus those with ejection fraction <50%. Am J Cardiol. 2008;102:79-83. [PMID: 18572040] Google Scholar3 Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial. Lancet. 2003;362:777-81. [PMID: 13678871] Google Scholar4 Cleland JG, Tendera M, Adamus J, et al. The perindopril in elderly people with chronic heart failure (PEP-CHF) study. Eur Heart J. 2006;27:2338-45. [PMID: 16963472] Google Scholar Author, Article, and Disclosure InformationAffiliations: University of Alberta,, Edmonton, Alberta, Canada (J.A.E., F.A.M.)This article was published at Annals.org on 5 May 2009. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byBeta-blockers and inhibitors of the renin-angiotensin aldosterone system for chronic heart failure with preserved ejection fractionBeta-blockers and inhibitors of the renin-angiotensin aldosterone system for chronic heart failure with preserved ejection fraction 19 May 2009Volume 150, Issue 10Page: JC5-10KeywordsACE inhibitorsEjection fractionHeart failureHospitalizationsHypertensionLongitudinal studiesMorbidityMyocardial infarction ePublished: 19 May 2009 Issue Published: 19 May 2009 Copyright & PermissionsCopyright © 2009 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...

Understanding the ‘epidemic of heart failure’: a systematic review of trends in determinants of heart failure

We conducted a systematic review of recent studies investigating trends in the epidemiology of heart failure (HF). We fitted simple linear regression models of rates against calendar year for mortality and hospital admission. Based on Population Attributable Fractions (PAFs) from the NHANES I Epidemiological Follow-up Study and self-reported prevalences of risk factors for HF, the estimated changes in numbers of new cases of HF in Australia were calculated from 1995 to 2005. A clear decline in mortality from HF and some data on decreases in admissions to hospitals for HF, as well as the lack of reports showing an increase in the incidence of HF, all argue against the existence of an 'epidemic' of HF. However, most reports on trends in HF survival have shown a secular improvement. The latter, together with population aging, are major factors that may increase the caseload of HF. Against this background of conflicting influences, we estimate that in Australia, the inflow into the caseload of HF decreased by 1.6% among people aged > or =55 years in 2005 relative to 1995. Available evidence does not support an increase in the caseload of HF over recent years. Taking all of the influences on the epidemiology of HF together, it is likely that the number of new cases of HF will rise over the next few years, even if the incidence rate falls, chiefly because the elderly population is expanding so quickly.

Epidemiology of Incident Heart Failure in a Contemporary Elderly Cohort

The race- and sex-specific epidemiology of incident heart failure (HF) among a contemporary elderly cohort are not well described. We studied 2934 participants without HF enrolled in the Health, Aging, and Body Composition Study (mean [SD] age, 73.6 [2.9] years; 47.9% men; 58.6% white; and 41.4% black) and assessed the incidence of HF, population-attributable risk (PAR) of independent risk factors for HF, and outcomes of incident HF. During a median follow-up of 7.1 years, 258 participants (8.8%) developed HF (13.6 cases per 1000 person-years; 95% confidence interval, 12.1-15.4). Men and black participants were more likely to develop HF. No significant sex-based differences were observed in risk factors. Coronary heart disease (PAR, 23.9% for white participants and 29.5% for black participants) and uncontrolled blood pressure (PAR, 21.3% for white participants and 30.1% for black participants) carried the highest PAR in both races. Among black participants, 6 of 8 risk factors assessed (smoking, increased heart rate, coronary heart disease, left ventricular hypertrophy, uncontrolled blood pressure, and reduced glomerular filtration rate) had more than 5% higher PAR compared with that among white participants, leading to a higher overall proportion of HF attributable to modifiable risk factors in black participants vs white participants (67.8% vs 48.9%). Participants who developed HF had higher annual mortality (18.0% vs 2.7%). No racial difference in survival after HF was noted; however, rehospitalization rates were higher among black participants (62.1 vs 30.3 hospitalizations per 100 person-years, P < .001). Incident HF is common in older persons; a large proportion of HF risk is attributed to modifiable risk factors. Racial differences in risk factors for HF and in hospitalization rates after HF need to be considered in prevention and treatment efforts.