Echocardiographic and Cardiac Magnetic Resonance Imaging-Derived Strains in Relation to Late Gadolinium Enhancement in Hypertrophic Cardiomyopathy.

We compared speckle tracking echocardiography (STE) and feature tracking cardiovascular magnetic resonance (FT-CMR) in patients with hypertrophic cardiomyopathy (HC) with a varying extent of fibrosis as defined by late gadolinium enhancement to look at the level of agreement between methods and their ability to relate those to myocardial fibrosis. At 2 reference centers, 79 patients with HC and 16 volunteers (the control group) underwent STE and CMR with late gadolinium enhancement and FT-CMR. Patients were classified into 3 categories: no detectable, limited, and extensive fibrosis. Global longitudinal strain (GLS) and global radial strain (GRS) were derived using FT-CMR and STE. STE-derived GRS was decreased in all HC categories compared with the control group (p <0.001), whereas FT-CMR GRS was reduced only in patients with HC with fibrosis (p <0.05). Reduced STE-derived GLS was associated with extensive fibrosis (p <0.05) and a value less than -15.2% identified those with extensive fibrosis (sensitivity 79%, specificity 92%, area under the curve 0.863, 95% confidence interval [CI] 0.76 to 0.97, p <0.001). Inter-modality agreement was moderate for STE versus CMR-GLS (overall population intra-class correlation coefficient = 0.615, 95% CI 0.42 to 0.75, p <0.001; patients with HC 0.63, 0.42 to 0.76, p <0.001) and GRS (overall population intra-class correlation coefficient = 0.601, 95% CI 0.397 to 0.735, p <0.001). A low level of agreement for GRS was seen between methods in patients with HC. In conclusion, strain indexes measured using echocardiography and CMR are reduced in patients with HC compared with the control group and correlate well with the burden of myocardial fibrosis. Reduced STE-GLS can identify patients with extensive fibrosis, but whether there is an added value for risk stratification for sudden cardiac death remains to be determined.

Left ventricular mass versus pulse wave velocity as predictors of coronary artery disease in hypertensive patients: data from a 6-year-follow-up study.

In treated hypertensive patients, there is a substantial residual cardiovascular (CV) risk that cannot be assessed by the available prediction models. This risk can be associated with subclinical organ damage, such as increased left ventricular mass (LVM) and arterial stiffness. However, it remains unknown which of these two CV markers better predicts coronary artery disease (CAD). A prospective cohort study was used to answer the above question. The study sample consisted of 1033 patients with hypertension (mean age 55.6 years, 538 males) free of CAD at baseline, who were followed for a mean period of 6 years. At baseline, all subjects underwent a complete echocardiographic study and pulse wave velocity (PWV) measurement. Hypertensive individuals who developed CAD (2.8%) compared to those without CAD at follow-up, had a higher baseline LVM index (by 16.7 g/m2, p < 0.001), higher prevalence of left ventricular hypertrophy (LVH) (21% greater, p = 0.027) and greater prevalence of high PWV levels at baseline (21% greater, p = 0.019). Multivariate Cox regression analysis revealed that baseline age >65 years (HR = 2.067, p = 0.001), male gender (HR = 3.664, p = 0.001), baseline chronic kidney disease (HR = 2.020, p = 0.026), baseline diabetes mellitus (HR = 1.952, p = 0.015) and baseline LVH (HR = 2.124 p = 0.001) turned out to be independent predictors of CAD, whereas high PWV levels were not. LVH proved to be an independent prognosticator of CAD in contrast to arterial stiffness that was not related to CAD after accounting for established confounders. Therefore, LVM can reliably help physicians to identify high-risk hypertensives in whom an intensified therapeutic management is warranted.

Multipoint left ventricular pacing effects on hemodynamic parameters and functional status: HUMVEE single-arm clinical trial (NCT03189368).

OBJECTIVES: The aim of this study was to assess the capacity of optimized multipoint pacing (MPP) over optimized cardiac resynchronization therapy (CRT), in terms of clinical, functional, and echocardiographic parameters among patients with dyssynchronous heart failure (HF). METHODS: Eighty patients (Caucasian, 77.5% male, 68.4 ± 10.1 years, and 53.8% ischemic cardiomyopathy) sequentially received optimized CRT and optimized MPP over 6- and 12-month periods in a single-arm clinical trial. Clinical, laboratory, and echocardiographic assessment was conducted at baseline and after the completion of each step. RESULTS: Significant additive effects of optimized MPP over optimized CRT were noted with regard to 6-min walking distance (baseline/optCRT/optMPP: 293 ± 120 m vs 367 ± 94 m vs 405 ± 129 m and p < 0.001), NYHA class (2.36 vs 2.19 vs 1.45 and p < 0.001), VTIlvot (14.25 ± 3.2 cm vs 16.2 ± 4 cm vs 17.5 ± 3.4 cm and p < 0.001), stroke volume (48 ± 13.5 ml vs 55 ± 15 ml vs 59 ± 15 ml and p < 0.001), left ventricular ejection fraction (LVEF) (29% ± 7.1% vs 33% ± 7.3% vs 37% ± 7.7% and p < 0.001), maximal left atrial volume (77.2 ± 34.2 ml vs 74.2 ± 39.5 ml vs 67.7 ± 32 ml and p = 0.02), pulmonary artery systolic pressure (35.9 mmHg vs 33.5 mmHg vs 31 mmHg and p < 0.001), and right ventricular strain (-8.3% ± 6.9% vs -8.8% ± 6.6% vs -11.8% ± 6.1% and p = 0.022). With regard to VAC, stroke work (SW), and CP as percentages of maximal, there was a significant difference detected as compared to baseline for both CRT and MPP. Additive effects persisted only if suitable MPP dipoles were present. Exploratory analysis revealed that ischemic cardiomyopathy continued to exhibit significant differences that favor MPP, whereas nonischemic cardiomyopathy had similar findings with regard to total left atrial strain and quality of life. CONCLUSIONS: Optimized MPP showed significant improvements in hemodynamic parameters and ventricular function in patients with HF over optimized CRT. The beneficial effect was more prominent in men and in those with rather reduced LVEF, consistent with findings that suggest a beneficial trend in VAC and CP with more homogeneous depolarization offered by optimized MPP.

Multipoint left ventricular pacing as an addition to cardiac resynchronization therapy: a bridge to the holy grail?

Cardiac resynchronization therapy (CRT) constitutes a cornerstone to the treatment of advanced dyssynchronous heart failure (DyssHF); moreover it represents one of the few instances that a revolutionary approach was pursued, yielding previously unfathomable benefits to patients out of realistic therapeutic options. However, as is rather extensively established, nonresponse, or even negative response, to CRT continue to plague its course, precluding favourable effects in up to 40% of recipients, for a multitude of reasons. Given the scope of the issue of nonresponse, attempts to negate it by means of altering CRT delivery mode, and, more specifically, by introducing multipoint left ventricular pacing (MPP) have been focused on. Possible reasons for divergent trial results will be presented, as well as potential criteria for predicting whether MPP activation may reap additional benefits as compared to conventional biventricular pacing (BVP). Finally, an alternative framework for approaching CRT in general will be put forward, including advancements which in the (near) future may once more revolutionise heart failure treatment.

A Bayesian meta-analysis on early tobacco exposure and vascular health: From childhood to early adulthood.

BACKGROUND: Smoking has been consistently associated with increased cardiovascular risk in adults. Although exposure to tobacco products often starts in early life, evidence for the possible adverse effects on the cardiovascular system of the young is scarce. We sought to derive pooled estimates of smoking effects on indices of early vascular damage in children and adolescents. DESIGN AND METHODS: We performed a systematic review and meta-analysis of clinical studies involving young individuals up to 21 years old that provided data on smoking exposure (active or passive) and flow-mediated dilatation, carotid to femoral pulse wave velocity and maximum carotid intima-media thickness. We employed three distinct methodologies of random-effects data synthesis, including the Sidik-Jonkman estimator, the Hartung and Knapp correction and a Bayesian method with a well-informed prior on the level of between-study variance. RESULTS: In 12 studies and 5279 individuals in total, smoking exposure was related to deterioration in all three outcomes (mean adjusted flow-mediated dilatation decrease: -0.77%, 95% confidence interval -1.38--0.15, mean adjusted pulse wave velocity increase: 0.1 m/s, 95% confidence interval 0.02-0.17 and mean adjusted carotid intima-media thickness increase: 0.35 mm, 95% confidence interval 0.16-0.55, for the Sidik-Jonkman estimator). No difference was established between active and passive smoking on associations with arterial damage. CONCLUSIONS: Exposure to tobacco products is associated with subclinical vascular damage early in life, even from childhood. Public health initiatives should target these very young age groups to prevent early smoking exposure and associated arterial damage and its sequelae.

Aortic valve: anatomy and structure and the role of vasculature in the degenerative process.

Aortic valve stenosis is a degenerative disease affecting increasing number of individuals and characterised by thickening, calcification and fibrosis of the valve resulting in restricted valve motion. Degeneration of the aortic valve is no longer considered a passive deposition of calcium, but an active process that involves certain mechanisms, that is endothelial dysfunction, inflammation, increased oxidative stress, calcification, bone formation, lipid deposition, extracellular matrix (ECM) remodelling and neoangiogenesis. Accumulating evidence indicates an important role for neoangiogenesis (i.e. formation of new vessels) in the pathogenesis of aortic valve stenosis. The normal aortic valve is generally an avascular tissue supplied with oxygen and nutrients via diffusion from the circulating blood. In contrast, presence of intrinsic micro-vasculature has been demonstrated in stenotic and calcified valves. Importantly, presence and density of neovessels have been associated with inflammation, calcification and bone formation. It remains unclear whether neoangiogenesis is a compensatory mechanism aiming to counteract hypoxia and increased metabolic demands of the thickened tissue or represents an active contributor to disease progression. Data extracted mainly from animal studies are supportive of a direct detrimental effect of neoangiogenesis, however, robust evidence from human studies is lacking. Thus, there is inadequate knowledge to assess whether neoangiogenesis could serve as a future therapeutic target for a disease that no effective medical therapy exists. In this review, we present basic aspects of anatomy and structure of the normal and stenotic aortic valve and we focus on the role of valve vasculature in the natural course of valve calcification and stenosis.

Imaging predictors of incident heart failure: a systematic review and meta-analysis.

BACKGROUND: Preventing the evolution of subclinical cardiac disease into overt heart failure is of paramount importance. Imaging techniques, particularly transthoracic echocardiography (TTE), are well suited to identify abnormalities in cardiac structure and function that precede the development of heart failure. METHODS: This meta-analysis provides a comprehensive evaluation of 32 studies from 11 individual cohorts, which assessed cardiac indices from TTE (63%), cardiovascular magnetic resonance (CMR; 34%) or cardiac computed tomography (CCT; 16%). Eligible studies focused on measures of left ventricular geometry and function and were highly heterogeneous. RESULTS: Among the variables that could be assessed through a meta-analytic approach, left ventricular systolic dysfunction, defined as left ventricular ejection fraction (LVEF) lower than 50%, and left ventricular dilation were associated with a five-fold [hazard ratio (HR) 4.76, 95% confidence interval (95% CI) 1.85-12.26] and three-fold (HR 3.14, 95% CI 1.37 -7.19) increased risk of heart failure development, respectively. Any degree of diastolic dysfunction conveyed an independent, albeit weaker, association with heart failure (HR 1.48, 95% CI 1.11-1.96), although there was only a trend for left ventricular hypertrophy in predicting incident heart failure (hazard ratio 2.85, 95% CI 0.82-9.85). CONCLUSION: LVEF less than 50%, left ventricular dilation and diastolic dysfunction are independent predictors of incident heart failure among asymptomatic individuals, while left ventricular hypertrophy seems less predictive. These findings may serve as a framework for implementing imaging-based screening strategies in patients at risk of heart failure and inform future studies testing preventive or therapeutic approaches aiming at thwarting or halting the progression from asymptomatic (preclinical) to overt heart failure.

The Role of Antithrombotic Therapy in Heart Failure.

Heart failure is a major contributor to global morbidity and mortality burden affecting approximately 1-2% of adults in developed countries, mounting to over 10% in individuals aged >70 years old. Heart failure is characterized by a prothrombotic state and increased rates of stroke and thromboembolism have been reported in heart failure patients compared with the general population. However, the impact of antithrombotic therapy on heart failure remains controversial. Administration of antiplatelet or anticoagulant therapy is the obvious (and well-established) choice in heart failure patients with cardiovascular comorbidity that necessitates their use, such as coronary artery disease or atrial fibrillation. In contrast, antithrombotic therapy has not demonstrated any clear benefit when administered for heart failure per se, i.e. with heart failure being the sole indication. Randomized studies have reported decreased stroke rates with warfarin use in patients with heart failure with reduced left ventricular ejection fraction, but at the expense of excessive bleeding. Non-vitamin K oral anticoagulants have shown a better safety profile in heart failure patients with atrial fibrillation compared with warfarin, however, current evidence about their role in heart failure with sinus rhythm is inconclusive and further research is needed. In the present review, we discuss the role of antithrombotic therapy in heart failure (beyond coronary artery disease), aiming to summarize evidence regarding the thrombotic risk and the role of antiplatelet and anticoagulant agents in patients with heart failure.

Usefulness of F2-isoprostanes in early prognostication after cardiac arrest: a topical review of the literature and meta-analysis of preclinical data.

Prognostication after cardiac arrest (CA) represents a challenging issue, and several biomarkers have been proposed in the attempt to predict outcome. Among these, F2-isoprostanes stand out as potential biomarkers for early prognostication, providing information on the magnitude of global oxidative injury after return of spontaneous circulation (ROSC). We performed a topical review searching PubMed and Scopus databases to identify studies evaluating the modifications of F2-isoprostanes in the early period after CA, and a meta-analysis of studies providing curves of F2-isoprostanes plasma levels seeking to describe the biomarker's kinetics after CA. Evidence suggests that plasma levels of F2-isoprostanes increase in the early post-resuscitation period and seem well correlated with the burden of ischaemia-reperfusion injury. Our meta-analysis shows a possible increase as early as 5 minutes after ROSC, which persists at 2 hours and is attenuated at 4 hours. Clinical studies are warranted to evaluate the utility of this biomarker for prognostication purposes in CA survivors.

Comparison of left ventricular and biventricular pacing: Rationale and clinical implications.

Cardiac resynchronization therapy constitutes a cornerstone in advanced heart failure treatment, when there is evidence of dyssynchrony, especially by electrocardiography. However, it is plagued both by persistently high (~30%) rates of nonresponse and by deterioration of right ventricular function, owing to iatrogenic dyssynchrony in the context of persistent apical pacing to ensure delivery of biventricular pacing. Left ventricular pacing has long been considered an alternative to standard biventricular pacing and can be achieved as easily as inserting a single pacing electrode in the coronary sinus. Although monoventricular left ventricular pacing has been proven to yield comparable results with the standard biventricular modality, it is the advent of preferential left ventricular pacing, combining both the powerful resynchronization potential of multipolar coronary sinus and right-sided electrodes acting in concert and the ability to preserve intrinsic, physiological right ventricular activation. In this review, we aim to present the underlying principles and modes for delivering left ventricular pacing, as well as to highlight advantages of preferential over monoventricular configuration. Finally, current clinical evidence, following implementation of automated algorithms, regarding performance of left ventricular as compared with biventricular pacing will be discussed. It is expected that the field of preferential left ventricular pacing will grow significantly over the following years, and its combination with other advanced pacing modalities may promote clinical status and prognosis of patients with advanced dyssynchronous heart failure.

Cardiac Resynchronisation Therapy and Cellular Bioenergetics: Effects Beyond Chamber Mechanics.

Cardiac resynchronisation therapy is a cornerstone in the treatment of advanced dyssynchronous heart failure. However, despite its widespread clinical application, precise mechanisms through which it exerts its beneficial effects remain elusive. Several studies have pointed to a metabolic component suggesting that, both in concert with alterations in chamber mechanics and independently of them, resynchronisation reverses detrimental changes to cellular metabolism, increasing energy efficiency and metabolic reserve. These actions could partially account for the existence of responders that improve functionally but not echocardiographically. This article will attempt to summarise key components of cardiomyocyte metabolism in health and heart failure, with a focus on the dyssynchronous variant. Both chamber mechanics-related and -unrelated pathways of resynchronisation effects on bioenergetics - stemming from the ultramicroscopic level - and a possible common underlying mechanism relating mechanosensing to metabolism through the cytoskeleton will be presented. Improved insights regarding the cellular and molecular effects of resynchronisation on bioenergetics will promote our understanding of non-response, optimal device programming and lead to better patient care.

Pharmacotherapeutic strategies for atrial fibrillation in pregnancy.

Introduction: Atrial fibrillation (AF) is rare during pregnancy but its incidence is expected to rise in parallel to increasing age of women in pregnancy and fraction of pregnant women with structural heart disease. Areas covered: The authors provide a review of the contemporary evidence on diagnostic work-up and optimal pharmacotherapeutic management of AF in pregnancy. The authors have performed a systematic search for relevant articles using MEDLINE, the COCHRANE LIBRARY, and ClinicalTrials.gov. Expert opinion: New-onset AF during pregnancy is usually an indication of underlying heart disease and should lead to hospital admission. Patients should be evaluated by an experienced cardiologist or an electrophysiologist. Direct cardioversion is highly effective and safe in pregnant women and should be prioritized over pharmacologic cardioversion with intravenous ibutilide or flecainide. Amiodarone should be avoided if possible. Digoxin and beta-blockers are the rate-control pharmaceutic agents with the widest experience of use. Catheter ablation during pregnancy should be considered in selected cases of atrial flutter refractory to medication and only performed using fluoroless techniques, preferably during the second trimester. Vitamin K antagonists (VKAs) can be used after the first trimester, while low molecular weight heparin should be accompanied by periodic evaluation of anti-Xa factor. Non-VKA oral anticoagulants should be avoided because of limited experience in pregnancy.

Orthostatic hypotension: From pathophysiology to clinical applications and therapeutic considerations.

Orthostatic hypotension (OH), that is blood pressure fall when standing from the supine to the erect position, is a common cardiovascular disorder, highly prevalent in elderly and frail individuals and in patients with multiple comorbidities. Orthostatic hypotension is considered a manifestation of dysfunction of the autonomic nervous system, caused or facilitated by several neurological or non-neurological diseases and conditions, while its clinical significance is increasingly recognized as a cause of impairment of quality of life and potentially of worse outcomes. Indeed, OH has been extensively studied and numerous prospective cohort studies support its association with adverse events, including coronary artery disease, heart failure, stroke, cognitive dysfunction, and, most importantly, mortality rates. Specific pharmacological and non-pharmacological interventions have been established for the treatment of OH. However, randomized data evaluating the impact of therapeutic interventions on morbidity and mortality outcomes are lacking. Thus, despite that OH seems to have important prognostic implications indicated by several reported associations with adverse events, it remains unclear whether OH treatment could improve prognosis. In the present review, we discuss the clinical applications associated with ΟΗ by outlining the current perspectives on ΟΗ definition, diagnosis, pathophysiology, prognostic role, and treatment.

The Role of Arterial Hypertension in Mitral Valve Regurgitation.

PURPOSE OF REVIEW: To review medical literature for evidence of association between hypertension and mitral regurgitation (MR) and summarize potential favorable effects of antihypertensive drugs on MR natural history and treatment. RECENT FINDINGS: Hypertension and MR are common diseases affecting a large proportion of the general population. Contemporary evidence suggests that hypertension may worsen the progression and prognosis of MR through augmented mechanical stress and increased regurgitation volume. Renin-angiotensin axis inhibitors, beta-blockers, and vasodilators have been tested in order to prevent or decrease primary or secondary MR. Although antihypertensive agents may improve hemodynamic parameters and left ventricular remodeling in primary MR, there is no strong evidence of benefit on clinical outcomes. On the other hand, a beneficial effect of these drugs on secondary MR is better established. Moreover, there are no studies evaluating a possible benefit of lower blood pressure targets in MR. Randomized controlled trials are warranted to elucidate the precise role of antihypertensive therapy on treatment of MR.

Orthostatic hypertension: From pathophysiology to clinical applications and therapeutic considerations.

Orthostatic hypertension (OHT), that is, sustained increase in blood pressure after standing, is an increasingly recognized cardiovascular disorder having been examined in much fewer studies compared with orthostatic hypotension (OH). However, in both OHT and OH, dysfunction of the autonomous nervous system is considered to be the primary pathophysiological disturbance, while significant associations with essential hypertension have been observed. Although in many studies OHT has been related to subclinical or clinical target organ damage, there is also evidence denying such an association. Because OHT is defined variably across different studies, the comparison of relevant outcomes is at least problematic. Since evidence about OHT treatment is exclusively based on limited non-randomized studies, no specific recommendations have been developed. Therefore, both the prognostic role and the clinical significance of OHT remain largely undefined. The aim of the present review is to summarize the available evidence regarding the definition, diagnosis, pathophysiology, prognostic role and treatment of OHT and highlight potential clinical implications of this underestimated condition.

Arterial hypertension in patients under antineoplastic therapy: a systematic review.

BACKGROUND: Cardio-oncology aims to mitigate adverse cardiovascular manifestations in cancer survivors, but treatment-induced hypertension or aggravated hypertension has received less attention in these high cardiovascular risk patients. METHODS: In this systematic review, we searched literature for contemporary data on the prevalence, pathophysiologic mechanisms, treatment implications and preventive strategies of hypertension in patients under antineoplastic therapy. RESULTS: Several classes of antineoplastic drugs, including mainly vascular endothelial growth factor inhibitors, proteasome inhibitors, cisplatin derivatives, corticosteroids or radiation therapy were consistently associated with increased odds for new-onset hypertension or labile hypertensive status in previous controlled patients. Moreover, hypertension constitutes a major risk factor for chemotherapy-induced cardiotoxicity, which is the most serious cardiovascular adverse effect of antineoplastic therapy. Despite the heterogeneity of pooled studies, the pro-hypertensive profile of examined drug classes could be attributed to common structural and functional disorders. Importantly, certain antihypertensive drugs are considered to be more effective in the management of hypertension in this population and may partially attenuate indirect complications of cancer treatment, such as progressive development of cardiomyopathy and/or cardiovascular death. Nonpharmacological approaches to alleviate hypertension in cancer patients are also described, albeit adjudicated as less effective in general. CONCLUSION: A growing body of evidence suggests that multiple antineoplastic agents increase the rate of progression of hypertension. Physicians need to balance the life-saving cancer treatment and the inflated risk of adverse cardiovascular events due to suboptimal management of hypertension in order to achieve improved clinical outcomes and sustained survival for their patients.

Vitamins in Heart Failure: Friend or Enemy?

BACKGROUND: The failing heart is characterized by a depleted metabolic energy reserve and the upregulation of several molecular mechanisms leading to cardiac hypertrophy, inflammation, fibrosis, angiogenesis, and apoptosis. Dietary or non-dietary supplementation of vitamins could potentially benefit energy balance. OBJECTIVE: The objective of the present study was to evaluate all available information on vitamins supplementation in patients with chronic HF for possible beneficial effect on metabolic, inotropic, chronotropic and hemodynamic indices. METHOD: We searched MEDLINE via Pubmed by using the following terms: "chronic heart failure" OR "cardiomyopathy" AND "vitamins", "vitamin A", "B complex vitamins", "vitamin C", "ascorbic acid", "vitamin D", "retinol", "vitamin E", "thiamine", "riboflavin", "niacin", "pyridoxine", "cobalamin", "folate", "pantothenic acid", "biotin", "tocopherol" and combinations of them. RESULTS: Data regarding supplementation of micronutrients in HF for most vitamins were sparse, and the inference about cardiovascular outcomes was obscured by the heterogeneity of studies, high inherent morbidity, and mortality of this group of high-risk patients, limited sample sizes in certain studies, unclear design and lack of head to head comparisons. Most vitamins in human trials failed to offer survival, or robust beneficial effect. Mostly indirect favorable evidence is derived from patients with deficiencies of certain micronutrients rather than their ad hoc supplementation. CONCLUSION: While vitamins and micronutrients are promising compounds for optimizing myocardial metabolism and homeostasis in HF, additional randomized clinical trials of larger scale are warranted to demonstrate the benefits of their supplementation in this high risk group of patients.

QT Prolongation and Malignant Arrhythmia: How Serious a Problem?

QT prolongation constitutes one of the most frequently encountered electrical disorders of the myocardium. This is due not only to the presence of several associated congenital syndrome but also, and mainly, due to the QT-prolonging effects of several acquired conditions, such as ischaemia and heart failure, as well as multiple medications from widely different categories. Propensity of repolarization disturbances to arrhythmia appears to be inherent in the function of and electrophysiology of the myocardium. In the present review the issue of QT prolongation will be addressed in terms of pathophysiology, arrhythmogenesis, treatment and risk stratification approaches. Although already discussed in literature, it is hoped that the mechanistic approach of the present review will assist in improved understanding of the underlying changes in electrophysiology, as well as the rationale for current diagnostic and therapeutic approaches.

Short term omega-3 polyunsaturated fatty acid supplementation induces favorable changes in right ventricle function and diastolic filling pressure in patients with chronic heart failure; A randomized clinical trial.

INTRODUCTION: Omega-3 polyunsaturated fatty acids (omega 3-PUFAs) seem to favorably affect cardiac hemodynamics and may benefit the clinical course of heart failure patients. The role of omega 3-PUFAs supplementation on the left and right ventricular function of patients with chronic compensated systolic heart failure, under optimal treatment, was studied. METHODS: 205 consecutive patients with chronic compensated heart failure, due to ischemic (IHF) or dilated cardiomyopathy (DCM)-NYHA classification I-III, under optimal medical treatment, were enrolled. Participants were 1-to-1 randomized on 1000 mg omega 3-PUFA supplementation or no supplementation, in a non-blinded fashion. Echocardiographic assessment was performed at first visit and 6 months after. Plasma BNP and serum creatinine levels were also measured. RESULTS: As compared with the control group, BNP levels in omega 3-PUFA intervention group were 34.6% lower (p=0.001); end-diastolic and end-systolic left ventricle dimensions were decreased by 2.5% (p=0.047) and 3.7% (p=0.01), maximum diameter of left atrium was decreased by 8.4% (p=0.004), left atrium ejection fraction was ameliorated by 6.03% (p=0.021) and as regards tissue Doppler parameters, TDI_Etv/Atv was decreased in omega 3-PUFA intervention group by 6.3% (p=0.038). Moreover, improvement in diastolic indices was more prominent in subjects with DCM as compared to IHF patients. CONCLUSION: Omega 3-PUFA supplementation was associated with improved left diastolic function and decreased BNP levels in patients with chronic heart failure. These findings suggest a beneficial role of omega 3-PUFAs on the hemodynamic course of patients with systolic heart failure.