Tachycardia exacerbates abnormal left ventricular–arterial coupling in heart failure

The purpose of this study was to assess the effect of heart rate on left ventricular (LV)–arterial coupling and LV mechanical efficiency before and after heart failure (CHF). The production of LV stroke work (SW) and mechanical efficiency depends on the coupling of the LV and arterial system. The response of LV–arterial coupling to tachycardia may be altered in heart failure. We compared the response of LV–arterial coupling to increased heart rate (HR) in six conscious, instrumented dogs before and after pacing-induced CHF. Coupling was quantified as E_ES/E_A, where E_ES is the slope of end-systolic pressure (P)–volume (V) relation, and E_A is arterial elastance. Mechanical efficiency was determined as the ratio of SW to a total P–V area (PVA). Before CHF, E_ES and E_A increased similarly with increased heart rate to 180min^–1. Thus, E_ES/E_A remained unaltered (0.96 ± 0.08 vs 0.94 ± 0.35), and SW/PVA was unchanged (0.62 ± 0.03 vs 0.59 ± 0.06). Compared with the results prior to CHF and after CHF the resting E_ES was decreased, thus both E_ES/E_A (0.58 ± 0.09) and SW/PVA (0.48 ± 0.06) were less (P 0.05) than baseline. After CHF, an increase in HR to 180min^–1 increased E_A but not E_ES, thus E_ES/E_A fell to 0.44 ± 0.06 (P 0.05) and SW/PVA fell to 0.41 ± 0.05 (P 0.05). Under normal conditions, LV–arterial coupling remains optimal during increases in HR. After CHF, tachycardia exacerbates the suboptimal baseline LV–arterial coupling, reducing the efficiency of producing SW.     

Altered left ventricular–arterial coupling precedes pump dysfunction in early heart failure

The objective of this study was to define alterations in ventricular–arterial (V-A) coupling early in the development of tachycardia-induced heart failure (HF). Although HF is characterized by impaired V-A coupling, the temporal relationship of these derangements to overt left ventricular (LV) dysfunction is unknown. Six anesthetized dogs instrumented with LV manometers and piezoelectric crystals were studied before and after 24 h of rapid ventricular pacing (RVP). V-A coupling was indexed by the ratio between the end-systolic pressure–volume relation slope (endsystolic elastance, E _ES) and effective arterial elastance (E _A), and mechanical efficiency by the ratio of stroke work (SW) to pressure–volume area (PVA). After RVP, there was no significant depression of LV function, but E _A and total peripheral resistance (R _T) were increased (P < 0.05), indicating increased arterial load. After RVP, E _ES/E _A and SW/PVA were maintained during unstressed conditions, but upon changes in load induced by phenylephrine, E _ES/E _A declined more precipitously with equivalent increases in R _T (slope E _ES/E _A–R _T relation −16.7 ± 4.6 vs −5.8 ± 4.0 ml/mmHg·min, P < 0.025). Furthermore, after RVP there was significant (P < 0.05) blunting of dobutamine-induced augmentation of E _ES, E _ES/E _A, and SW/PVA. Thus, after RVP there was a distinct loss of V-A coupling reserve during afterload and catecholamine stress. V-A coupling defects occur early in the development of tachycardia-induced HF prior to significant pump dysfunction, and are manifested primarily during hemodynamic and inotropic stress.     

Right Ventricular Pressure–Volume Analysis During Left Ventricular Assist Device Speed Optimization Studies: Insights Into Interventricular Interactions and Right Ventricular Failure

BackgroundInterventricular interaction, which refers to the impact of left ventricular (LV) function on right ventricular (RV) function and vice versa, has been implicated in the pathogenesis of RV failure in LV assist device (LVAD) recipients. We sought to understand more about interventricular interaction by quantifying changes in the RV systolic and diastolic function with varying LVAD speeds.Methods and ResultsFour patients (ages 22–69 years, 75% male, and 25% with ischemic cardiomyopathy) underwent a protocolized hemodynamic ramp test within 12 months of LVAD implantation where RV pressure–volume loops were recorded with a conductance catheter. The end-systolic PV relationship and end-diastolic PV relationship were compared using the V₂₀ and V₁₀ indices (volumes at which end-systolic PV relationship and end-diastolic PV relationship reach a pressure of 20 and 10 mm Hg, respectively). The ∆V₂₀ and ∆V₁₀ refer to the change in V₂₀ and V₁₀ from the minimum to maximum LVAD speeds. RV PV loops demonstrated variable changes in systolic and diastolic function with increasing LVAD speed. The end-systolic PV relationship changed in 1 patient (patient 2, ∆V₂₀ = 23.5 mL), reflecting a decrease in systolic function with increased speed, and was unchanged in 3 patients (average ∆V₂₀ = 7.4 mL). The end-diastolic PV relationship changed with increasing speed in 3 of 4 patients (average ∆V₁₀ = 12.5 mL), indicating an increase in ventricular compliance, and remained unchanged in one participant (patient 1; ∆V₁₀ = 4.0 mL).ConclusionsInterventricular interaction can improve RV compliance and impair systolic function, but the overall effect on RV performance in this pilot investigation is heterogeneous. Further research is required to understand which patient characteristics and hemodynamic parameters influence the net impact of interventricular interaction.     

Direct photonic–plasmonic coupling and routing in single nanowires

Metallic nanoscale structures are capable of supporting surface plasmon polaritons (SPPs), propagating collective electron oscillations with tight spatial confinement at the metal surface. SPPs represent one of the most promising structures to beat the diffraction limit imposed by conventional dielectric optics. Ag nano wires have drawn increasing research attention due to 2D sub-100 nm mode confinement and lower losses as compared with fabricated metal structures. However, rational and versatile integration of Ag nanowires with other active and passive optical components, as well as Ag nanowire based optical routing networks, has yet to be achieved. Here, we demonstrate that SPPs can be excited simply by contacting a silver nanowire with a SnO₂ nanoribbon that serves both as an unpolarized light source and a dielectric waveguide. The efficient coupling makes it possible to measure the propagation-distance-dependent waveguide spectra and frequency-dependent propagation length on a single Ag nanowire. Furthermore, we have demonstrated prototypical photonic-plasmonic routing devices, which are essential for incorporating low-loss Ag nanowire waveguides as practical components into high-capacity photonic circuits.     

Left Ventricular Assist Device Therapy for Destination Therapy: Is Less Invasive Surgery a Safe Alternative?

Introduction and objectives

The number of older patients with congestive heart failure has dramatically increased. Because of stagnating cardiac transplantation, there is a need for an alternative therapy, which would solve the problem of insufficient donor organ supply. Left ventricular assist devices (LVADs) have recently become more commonly used as destination therapy (DT). Assuming that older patients show a higher risk-profile for LVAD surgery, it is expected that the increasing use of less invasive surgery (LIS) LVAD implantation will improve postoperative outcomes. Thus, this study aimed to assess the outcomes of LIS-LVAD implantation in DT patients.

Right heart remodeling induced by arterial hypertension: Could strain assessment be helpful?

Left ventricular structural and functional changes in patients with arterial hypertension are well established. However, the influence of arterial hypertension on right ventricular (RV) remodeling is still being investigated. The introduction of strain analysis provided an insight into RV function and mechanics. Previous research has demonstrated the predictive value of RV longitudinal strain in patients with various cardiovascular conditions, such as pulmonary hypertension, heart failure, congenital heart diseases, and valvular disease. Nowadays, we are aware of the fact that conventional echocardiographic methods usually do not provide necessary information about RV dysfunction in patients with arterial hypertension, which is why the evaluation of new parameters that could detect RV subtle changes in hypertension is essential. The present review article is an overview of the main principles of RV deformation and a summary of the current knowledge and clinical significance of RV strain in patients with arterial hypertension.     

Pulmonary Hypertension,Right Ventricular Failure,and Kidney: Different from Left Ventricular Failure?

In this article, the pathophysiology of left ventricular failure is reviewed. By contrast, the paucity of information about pulmonary arterial hypertension and right ventricular failure is acknowledged. The potential mechanisms whereby renal sodium and water retention in right ventricular failure secondary to pulmonary arterial hypertension can occur, despite normal left ventricular function, are discussed. With right ventricular failure as the primary cause of death in patients with pulmonary hypertension, more information about the mechanisms of renal sodium and water retention in these patients is direly needed. Specifically, studies to examine the activation of the neurohumoral axis at various stages of pulmonary arterial hypertension and right ventricular failure, including inhibition of mineralocorticoid and V2 vasopressin receptors, are indicated.The renal sodium and water retention that occurs with advanced left ventricular failure is associated with substantial morbidity and mortality. This sodium and water retention, which can lead to pulmonary edema, pleural effusion, and peripheral edema, occurs despite an increase in total blood volume. In normal individuals, a rise in total blood volume increases renal sodium and water excretion. The kidney is intrinsically intact with left ventricular failure, because the renal sodium and water retention does not persist after a successful heart transplant.This seeming paradox of increased blood volume yet renal sodium and water retention in cardiac failure has been explained by the body fluid volume regulation hypothesis (1–3). This hypothesis proposes that the kidney does not respond to changes in total blood volume but rather responds to what has been termed effective arterial blood volume. In general terms, approximately 85% of circulating blood volume is in the low-pressure venous side of the circulation, whereas only 15% is in the high-pressure arterial circulation. The integrity of the arterial circulation depends on cardiac output and systemic vascular resistance and is modulated by arterial stretch baroreceptors in the carotid sinus, aortic arch, and afferent arteriole of the glomerulus (4). Thus, despite an increase in total blood volume, arterial underfilling can occur secondary to a decrease in cardiac output in low-output heart failure or decreased systemic vascular resistance in high-output heart failure. With arterial underfilling secondary to either condition, arterial baroreceptor–mediated activation of the neurohumoral axis occurs. The resultant increase in renin-angiotensin-aldosterone system (RAAS) leads to sodium retention, and the increase in the nonosmotic release of arginine vasopressin (AVP) is associated with water retention and hyponatremia in advanced left ventricular failure, a known risk factor for increased mortality (5). This water retention is due to AVP activation of the V2 vasopressin receptors on the basolateral surface of the principal cells of the collecting duct, which increases aquaporin 2 water channel expression and trafficking to the apical membrane of the collecting duct (6–8).There is also evidence that increased plasma AVP concentration with left ventricular failure stimulates V1 vasopressin receptors on blood vessels, which contributes, along with angiotensin II and the sympathetic nervous system, to increasing systemic vascular resistance in low-cardiac output failure (9). This arterial baroreceptor–mediated neurohumoral activation maintains arterial pressure but at the expense of renal vasoconstriction and sodium and water retention. The pathophysiology of left ventricular cardiac failure is shown in Figure 1.These arterial baroreceptor pathways seem to override any of the low-pressure reflexes in the atria during left ventricular failure. An increase in transmural atrial pressure normally suppresses AVP and stimulates atrial natriuretic peptide (ANP), which leads to increased sodium and water excretion (10). With advanced left ventricular failure, however, left atrial pressure rises, yet sodium and water retention occurs. This suggests that activation of the arterial stretch receptors in cardiac failure predominates over any atrial pressure receptor reflex. There is also evidence that these normal atrial reflexes are blunted in patients with left ventricular failure (11).An increase in the ventricular synthesis of brain natriuretic peptide (BNP) and, thus, circulatory BNP concentration also occurs in left ventricular failure and may attenuate the degree of renal sodium and water retention. BNP may decrease the edema formation by both suppressing the RAAS and inhibiting tubular sodium reabsorption (12).     

Invasive opportunistic mycoses: Clinical trials review, 2007–2008

Invasive infections are important causes of morbidity and mortality in severely ill patients. The past decade has seen considerable expansion in the development of new antifungal compounds, and clinical trials continue to define their role in our antifungal armamentarium. This brief article summarizes the most pivotal clinical trials in the settings of treatment and prophylaxis of invasive opportunistic mycoses published between 2007 and 2008.     

Ventricular Tachycardia Burden and Mortality: Association or Causality?

Ventricular tachycardia (VT) is a potentially fatal cardiac rhythm disorder. Implantable cardioverter defibrillators (ICDs) are the primary management strategy for VT and have been shown to reduce the incidence of death but, ICDs do not reduce VT recurrences. Further, mounting evidence indicates that high VT burden, defined as the cumulative number of recurrent VTs or ICD shocks, is associated with an elevated risk of death; however, it is unclear if high VT burden is a cause of death or a marker of severe heart disease. Proposed mechanisms for a causal pathway suggest that multiple VT episodes or potential deleterious effects from ICDs might alter the myocardium of the ventricles to induce worsening heart disease, which might translate to an increased risk of mortality. In this review, we present the evidence to support association and causation hypotheses for the relationship between VT burden and risk of mortality and indicate potential gaps in evidence. Overall, there is insufficient evidence to prove causal hypotheses for the relationship between VT burden and mortality. Consistent definitions for VT burden, randomized controlled trials that assess the relationship between VT burden and mortality, and observational studies that capture VT burden are warranted to investigate if a potential causal relationship exists.