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
Difficulties in detection of acute coronary syndromes.
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.
Importance of iron for functioning and survival across all levels of complexity of living structures.
Major pools of utilized and stored iron in the body.
The concept of absolute and functional iron deficiency.
Tissues utilizing and/or storing iron and related biomarkers which are secreted by these tissues and can be detected in peripheral blood.
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).
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.
Role of brain and kidney in activation of the renin–angiotensin–aldosterone system in hypertension, and heart failure.
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.
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.