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Heart Failure

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Gender differences in heart failure: paving the way towards personalized medicine?

Eur. Heart J. (2010), 31 (10), 1165-1167; 10.1093/eurheartj/ehq073 - Click here to view abstract

Gender differences in heart failure are based on distinct characteristics in diagnosis, management, and prognosis in men and women. Molecular details of cardiac pathophysiology may influence the clinical phenotype. Genes differentially expressed (top) and phenotypic characteristics (bottom) are depicted relative to the other gender, where the left column represents genes and characteristics more prevalent in women, and the right column those more prevalent in men.

The Swedish paradox: or is there really no gender difference in acute coronary syndromes? - Figure 1

Eur. Heart J. (2011) 32 (24), 3070; 10.1093/eurheartj/ehr375 - Click here to view abstract

Difficulties in detection of acute coronary syndromes.

Novel insights on HIV/AIDS and cardiac disease: shedding light on the HAART of Darkness

Eur. Heart J. (2011) 33 (7), 813; 10.1093/eurheartj/ehr413 - Click here to view abstract

Disentangling the conundrum of aetiology, pathogenesis, and clinical manifestation of cardiac disease in human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS). HAART, highly active antiretroviral therapy; IRIS, immune reconstitution inflammatory syndrome; RHF, right heart failure.

Iron deficiency and heart failure: diagnostic dilemmas and therapeutic perspectives - Figure 1

Eur Heart J (2013) 34 (11): 816-829; 10.1093/eurheartj/ehs224 - Click here to view abstract

Importance of iron for functioning and survival across all levels of complexity of living structures.

Iron deficiency and heart failure: diagnostic dilemmas and therapeutic perspectives - Figure 2

Eur Heart J (2013) 34 (11): 816-829; 10.1093/eurheartj/ehs224 - Click here to view abstract 

Major pools of utilized and stored iron in the body.

Iron deficiency and heart failure: diagnostic dilemmas and therapeutic perspectives - Figure 3

Eur Heart J (2013) 34 (11): 816-829; 10.1093/eurheartj/ehs224 - Click here to view abstract 

The concept of absolute and functional iron deficiency.

Iron deficiency and heart failure: diagnostic dilemmas and therapeutic perspectives - Figure 4

Eur Heart J (2013) 34 (11): 816-829; 10.1093/eurheartj/ehs224 - Click here to view abstract

Tissues utilizing and/or storing iron and related biomarkers which are secreted by these tissues and can be detected in peripheral blood. 

What does the liver tell us about the failing heart - Figure 1

Eur Heart J (2013) 34 (10): 711-714; 10.1093/eurheartj/ehs440 - Click here to view abstract 

Haemodynamic disturbances in heart failure and mechanisms resulting in different patterns of elevated liver enzymes. Congestive hepatic injury (left panel) and ischaemic hepatic injury (right panel).

Reversing heart failure by CRT: how long do the effects last? - Figure 1

Eur Heart J (2013) 34 (33): 2582-2584; 10.1093/eurheartj/eht238 - Click here to view abstract 

Long-term impact of different ventricular activation patterns on regional load and hypertrophy. A, delayed LV activation in LBBB unloads the septum and increases the regional load in the delayed activated postero-lateral wall resulting in compensatory hypertrophy.8 B, Optimized CRT may normalize these pathologic relationships by simultaneous and more rapid ventricular activation. C, Hypothetical (and probably exaggerated) result of suboptimal CRT with early LV activation (reverse dyssynchrony). The early activated posterolateral wall is exposed to a lower regional load and the late activated opposing wall (i.e. the septum) responds with regional hypertrophy.

Non-pharmacological modulation of the autonomic tone to treat heart failure

Eur Heart J (2014) 35 (2): 77-85; 10.1093/eurheartj/eht436

Role of brain and kidney in activation of the renin–angiotensin–aldosterone system in hypertension, and heart failure.

Terminology and definition of changes renal function in heart failure

Eur Heart J (2014) 35 (48): 3413-3416 - 10.1093/eurheartj/ehu320

Factors involved in the cause and association with an outcome of changes in renal function in heart failure. (A) Organ-specific factors. The main determinants of decreased glomerular filtration rate are a decrease in renal blood flow and an increase in central and renal venous pressure. The latter can be caused by intravascular congestion, but also by an increase in intra-abdominal pressure. Owing to increased renal venous pressure, renal interstitial pressure rises, which results a ‘congested kidney’ since the kidney is encapsulated (B and C). Renal artery stenosis is present in ∼25% of heart failure patients, which can further compromise renal blood flow, especially in the presence of renin–angiotensin–aldosterone system inhibitors. (B) Glomerular factors. Decreased renal blood flow and low blood pressure trigger renal autoregulation, preserving glomerular filtration rate by increasing filtration fraction by increased efferent vasoconstriction. The use of renin–angiotensin–aldosterone system-inhibitors inhibits this process, which increases renal blood flow, but leads (in some patients) to a reduction in glomerular filtration rate (pseudo-worsening renal function). Non-steroidal anti-inflammatory drugs inhibit prostaglandin synthesis, thereby impairing prostaglandin associated increase/dependent renal blood flow. Increased interstitial pressure causes increased pressure in Bowman's capsule, which directly opposes filtration, in a glomerulus where the filtration gradient is already low due to a decreased renal blood flow and increased renal venous pressure. Concomitant diseases have direct, but differential effect on glomerular filtration, glomerular integrity and podocyte function, as well as autoregulation. (C) Nephronic factors. Different therapies have different renal effects and exert their action at specific sites as indicated in this diagram. Intravascular volume depletion (in the presence or absence of congestion) can lead to impaired renal perfusion and decreased glomerular filtration rate. The combination of increased interstitial pressure, reduced arterial perfusion, concomitant disease and therapies can cause tubular and glomerular injury. Increased renal venous pressure causes increased renal interstitial pressure, resulting in collapsing of renal tubules, which decreases glomerular filtration rate, and eventually leads to decreased urine output, sodium retention, and congestion. ACEi, angiotensin-converting enzyme inhibitor; ARB, angiotensin II receptor blocker; FF, filtration fraction; GFR, glomerular filtration rate; MRA, mineralocorticoid receptor antagonist; NSAIDs, non-steroidal anti-inflammatory drugs; RAAS, renin–angiotensin–aldosterone system; RBF, renal blood flow. 

Sleep apnoea in acute heart failure: fluid in flux

Eur Heart J (2014) - 10.1093/eurheartj/ehv084 [In Press]

Fluid shift in the pathogenesis of obstructive (OSA) and central sleep apnoea (CSA) in heart failure. Upper panel: chronic stable heart failure. Fluid accumulation in the leg and splanchnic veins while upright during the day shifts to the neck and thorax during recumbent sleep. Jugular fluid distention and fluid accumulation in peri-pharyngeal tissue decreases upper airway cross-sectional area (UA-XSA) and increases the likelihood of upper airway (UA) obstruction and OSA. An increase in pulmonary capillary wedge pressure (PCWP) and pulmonary congestion stimulates irritant receptors, causing reflex hyperventilation. An acute reduction in PCO<sub>2</sub> below the apnoea threshold triggers central apnoea. Metabolic CO<sub>2</sub> production causes PCO<sub>2</sub> to rise during apnoea until it reaches the ventilator threshold, provokes hyperventilation, and initiates Cheyne–Stokes respiration. Augmented chemoreflex gain increases risk for CSA. As indicated by the bottom double-headed arrow, the predominant type of sleep apnoea can change over time in response to changes in PCWP. Lower panel: with acute decompensation, fluid reserved in capacitance vessels of the splanchic circulation and legs redistributes rapidly to the neck and thorax in response to an inciting event, increasing the likelihood of both OSA and CSA, and their severity.

Cachexia and right ventricular dysfunction in chronic heart failure: what is the chicken and what the egg?

Eur. Heart J. (2016) 37(21) doi: 10.1093/eurheartj/ehw118 - Click here to view the abstract

Intestinal congestion as a potential cause of cardiac cachexia in advanced heart failure. This diagram illustrates the consequences of ventricular backward failure in heart failure with a consecutive increase in right atrial pressure (RAP) which induces venous congestion, intestinal damage, and release of proinflammatory cytokines.

After TOPCAT: What to do now in Heart Failure with Preserved Ejection Fraction

Eur. Heart J. (2016) 37(41) doi: 10.1093/eurheartj/ehw114 - Click here to view the abstract

Differential diagnosis of heart failure in the setting of preserved left ventricular ejection fraction.

Left ventricular heart failure and pulmonary hypertension

Eur. Heart J. (2016) 37(12) doi: 10.1093/eurheartj/ehv512 - Click here to view the abstract

Cardiopulmonary interaction and pathobiology of pulmonary hypertension (PH) in left ventricular heart failure. Shown is (i) the backward transmission of elevated left ventricular filling pressures into the pulmonary circulation (post-capillary haemodynamic profile), (ii) potential superimposed components contributing to the extent of PH (leading to a pre-capillary component),11 which may be associated with (iii) pulmonary vascular remodelling in some patients, thus leading to (iv) right ventricular strain and dysfunction over time. Right ventricular (RV) dilation and increase in wall stress/tension (internal RV afterload) result in elevated myocardial oxygen consumption, which with concomitant reduction in coronary perfusion gradient leads to RV ischaemia and progressive RV failure.

Left ventricular heart failure and pulmonary hypertension

Eur. Heart J. (2016) 37(12) doi: 10.1093/eurheartj/ehv512 - Click here to view the abstract

Left atrial (LA) remodelling and dysfunction in heart failure. (A) Phases of LA function. PEV, passive empting volume = Vmax – Vp; CV, conduit volume = LV stroke volume – (Vmax– Vmin); AEV, active emptying volume = Vp – Vmin (modified from Rossi et al.25). (B) Left atrial pressure–volume loops in normal LA function (left) and LA dysfunction (right). (C) Left atrial imaging by cardiac magnetic resonance imaging (cMRI) in a patient with pulmonary arterial hypertension and normal LA function (left) vs. LA enlargement and dysfunction in a patient with left heart disease (right) (cMRI movies may be downloaded from the Supplementary material online).

Left ventricular heart failure and pulmonary hypertension

Eur. Heart J. (2016) 37(12) doi: 10.1093/eurheartj/ehv512 - Click here to view the abstract


Sequence of pathophysiological factors contributing to pulmonary hypertension in left ventricular heart failure. Backward transmission of left- to right-sided pathological features at the level of the ventricles, atrioventricular valves, and atria. Data derived from Tedford et al.33 showing that in left heart failure related pulmonary hypertension with increased wedge pressure the RC time is constant, but slightly decreased (leftward shift) (images containing video loops may be downloaded from the Supplementary material online).

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