Atrial, ventricular, or both cannulation sites to optimize left ventricular assistance?

The efficiency of left ventricular assist devices (LVADs) depends on the capacity of the inflow cannula to drain blood into the pump. Left atrial (LA) and left ventricular (LV) sites were compared in an animal model mimicking different hemodynamic conditions. Three calves (56.3+/-5.0 kg) were equipped with a Thoratec LVAD. A regular cardiopulmonary bypass (CPB) circuit was used as a right ventricular assist device (RVAD) (jugular vein/pulmonary artery), and preload conditions were adjusted by storage (or perfusion) of blood into (or from) the venous reservoir. LA and LV drainage, tested separately or simultaneously, was measured by its effect on the LVAD's performance. The LVAD was used alone on a beating heart or together with the RVAD (biVAD) on a beating and on a fibrillating heart. Increasing the central venous pressure (CVP) highlighted the differences between the LA and LV cannulation sites when the LVAD was tested either alone or together with the RVAD (biVAD) on a beating heart. Drainage through the LA or the LV was similar when CVP was set at 8 mm Hg, and increasing CVP to 14 mm Hg allowed for better drainage through the LV cannula. In contrast, after induction of fibrillation to mimic extreme heart failure, the drainage was better through the LA cannula. Using both LA and LV cannulae simultaneously did not improve the LVAD output in any of the conditions tested. LV cannulation provides better blood drainage when used on a normal beating heart and, therefore, allows for increased LVAD performance. However, in severe heart failure, blood drainage through the LV cannula decreases and the LA cannulation site is superior.     

The effects of asymmetric ventricular filling on left–right ventricular interaction in the normal rat heart

Heart failure is characterised by ventricular dysfunction and with the potential for changes to ventricular volumes constraining the mechanical performance of the heart. The contribution of this interaction from geometric changes rather than fibrosis or metabolic changes is unclear. Using the constant pressure Langendorff-perfused rat heart, the volume interaction between left ventricle (LV) and right ventricle (RV) was investigated. RV diastolic stiffness (P?<?0.001) and developed pressure (P?<?0.001) were significantly lower than LV. When the RV was fixed at the end-diastolic volume (EDV) or EDV?+?50?%, both LV systolic and diastolic performance were unaffected with increasing LV balloon volume. However, at fixed LV volume, RV systolic performance was significantly decreased when LV volume increased to EDV?+?50?% when RV volume was increased incrementally between 50 and 300?μl (P?<?0.001). Systolic interaction in RV was noted as declining RV peak systolic load with increasing LV systolic pressure (P?<?0.05) and diastolic interaction was noted for RV when LV volume was increased from EDV to EDV?+?50?% (P?<?0.05). RV diastolic wall stress was increased with increasing LV balloon volume (P?<?0.05), but LV wall stress was unaltered at fixed RV balloon volume. Taken together, increasing LV volume above EDV decreased systolic performance and triggered ventricular constraint in the RV but the RV itself had no effect on the performance of the LV. These results are consistent with overload of the LV impairing pulmonary perfusion by direct ventricular interaction with potential alteration to ventilation–perfusion characteristics within the lung.     

Left ventricular myxoma：a case report

Cardiac myxoma,the most common primary heart tumor,is located mainly in the left atrium.We reported a rare case of left ventricular myxoma incidentally found on echocardiography in an asymptomatic 60-year-old male.The tumor was carefully resected without fragmentation.The patient had an uneventful recovery and was discharged home on the 4th postoperative day.Surgical resection of this type of cardiac myxoma is recommended due to the rarity of tumor location.     

Arrhythmogenic right ventricular cardiomyopathy: use of a left ventricular assist device as a bridge to transplantation?

The principal characteristic of arrhythmogenic right ventricular cardiomyopathy (ARVC) is the tendency for ventricular arrhythmia and sudden death to occur without overt ventricular dysfunction. Current recommendations for management of patients with ARVC include insertion of an automated implantable cardioverter–defibrillator (AICD) to prevent sudden cardiac death. However, despite the use of AICD and/or anti-arrhythmic drugs some patients suffer recurrent ventricular arrhythmias unresponsive to optimum medical management. We present two cases of ARVC with refractory recurrent ventricular arrhythmias that were successfully managed by left ventricular assist device (LVAD) implantation, as a bridge to transplant (BTT). These two cases are unconventional examples of use of LVAD, given the predominant right ventricular pathology of ARVC and the arrhythmogenic nature of their presentation. The novelty of these cases should be taken in the context of increasing pressure to standardize indications for use of mechanical circulatory support.     

Coronary–aortic interaction during ventricular isovolumic contraction

In earlier work, we suggested that the start of the isovolumic contraction period could be detected in arterial pressure waveforms as the start of a temporary pre-systolic pressure perturbation (AIC_start, start of the Arterially detected Isovolumic Contraction), and proposed the retrograde coronary blood volume flow in combination with a backwards traveling pressure wave as its most likely origin. In this study, we tested this hypothesis by means of a coronary artery occlusion protocol. In six Yorkshire × Landrace swine, we simultaneously occluded the left anterior descending (LAD) and left circumflex (LCx) artery for 5 s followed by a 20-s reperfusion period and repeated this sequence at least two more times. A similar procedure was used to occlude only the right coronary artery (RCA) and finally all three main coronary arteries simultaneously. None of the occlusion protocols caused a decrease in the arterial pressure perturbation in the aorta during occlusion (P > 0.20) nor an increase during reactive hyperemia (P > 0.22), despite a higher deceleration of coronary blood volume flow (P = 0.03) or increased coronary conductance (P = 0.04) during hyperemia. These results show that the pre-systolic aortic pressure perturbation does not originate from the coronary arteries.     

Sex differences in ventricular–vascular coupling following endurance training

Introduction

Ventricular and vascular coupling is defined as the ratio of arterial elastance (Ea) to ventricular elastance (Elv) and describes the interaction between the heart and arterial system. There are sex differences in both arterial and ventricular function in response to both acute exercise and aerobic exercise training.

Purpose

To examine the effects of aerobic exercise training on elastances and the coupling ratio in young adult men and women. We hypothesized a reduction in the coupling ratio in both sexes due to a decrease in Ea that would be more pronounced in men and an increase in Elv that would be larger in women.

Methods

Fifty-three healthy, young adults completed the study. Central pulse wave velocity and heart volumes were measured before and after an 8-week aerobic training intervention. Elastances were calculated as Ea = end-systolic pressure/stroke volume and Elv = end-systolic pressure/end-systolic volume and indexed to body surface area.

Results

After the intervention, women augmented indexed and un-indexed Elv from 2.09 ± 0.61 to 2.52 ± 0.80 mmHg/ml, p < 0.05, and reduced the coupling ratio from 0.72 ± 18 to 0.62 ± 15, p < 0.05, while men maintained their pre-training ratio (from 0.66 ± 0.20 to 0.74 ± 0.21, p > 0.05). Women also reduced end-systolic pressure (from 91 ± 10 to 87 ± 10 mmHg), and both groups reduced central pulse wave velocity (from 6.0 ± 1.0 to 5.6 ± 0.6 m/s, p < 0.05).

Conclusion

We conclude that after 8 weeks of aerobic training, only women reduced their coupling ratio due to an increase in Elv. This suggests that aerobic exercise training elicits sex-dependent changes in the coupling ratio in young, healthy individuals.     

Patient specific fluid–structure ventricular modelling for integrated cardiac care

Cardiac diseases represent one of the primary causes of mortality and result in a substantial decrease in quality of life. Optimal surgical planning and long-term treatment are crucial for a successful and cost-effective patient care. Recently developed state-of-the-art imaging techniques supply a wealth of detailed data to support diagnosis. This provides the foundations for a novel approach to clinical planning based on personalisation, which can lead to more tailored treatment plans when compared to strategies based on standard population metrics. The goal of this study is to develop and apply a methodology for creating personalised ventricular models of blood and tissue mechanics to assess patient-specific metrics. Fluid–structure interaction simulations are performed to analyse the diastolic function in hypoplastic left heart patients, who underwent the first stage of a three-step surgical palliation and whose condition must be accurately evaluated to plan further intervention. The kinetic energy changes generated by the blood propagation in early diastole are found to reflect the intraventricular pressure gradient, giving indications on the filling efficiency. This suggests good agreement between the 3D model and the Euler equation, which provides a simplified relationship between pressure and kinetic energy and could, therefore, be applied in the clinical context.     

Modeling ventricular function during cardiac assist: does time-varying elastance work?

The time-varying elastance theory of Suga et al. is widely used to simulate left ventricular function in mathematical models and in contemporary in vitro models. We investigated the validity of this theory in the presence of a left ventricular assist device. Left ventricular pressure and volume data are presented that demonstrate the heart-device interaction for a positive-displacement pump (Novacor) and a rotary blood pump (Medos). The Novacor was implanted in a calf and used in fixed-rate mode (85 BPM), whereas the Medos was used at several flow levels (0-3 l/min) in seven healthy sheep. The Novacor data display high beat-to-beat variations in the amplitude of the elastance curve, and the normalized curves deviate strongly from the typical bovine curve. The Medos data show how the maximum elastance depends on the pump flow level. We conclude that the original time-varying elastance theory insufficiently models the complex hemodynamic behavior of a left ventricle that is mechanically assisted, and that there is need for an updated ventricular model to simulate the heart-device interaction.     

Does left ventricular function improve with L-carnitine after acute myocardial infarction?

A double blind randomized placebo controlled clinical trial was carried out to assess the efficacy and safety of L-carnitine in patients suffering from acute anterior wall myocardial infarction with respect to left ventricular function. Sixty patients (34 men, 26 women, mean age 56+11 yr.) with acute anterior wall myocardial infarction were randomized to placebo and L-carnitine. All the patients were given intravenous L-carnitine / placebo in the dose of 6gm/day for the first seven days followed by oral L-carnitine / placebo 3 gm/day in three divided doses for a period of three months. Echocardiography was performed for regional wall motion abnormality, left ventricular end systolic volume (ESV), end diastolic volume (EDV) and ejection fraction (EF) on admission, after seven days and after three months of the infarction. Forty-four patients completed the study. There were three deaths, two in the placebo and one in the L-carnitine group (p>0.05). Thirteen patients were lost to follow up. Echo parameters in both groups were comparable (p>0.05). The duration of chest pain prior to initiation of the I.V. L-carnitine was 7.5 + 5.2 hrs in the L-carnitine group and 7 + 4 hrs in the placebo group (p>0.05). There was no statistical difference in the EF, ESV and EDV on admission, at discharge and after three months in the L-carnitine and the placebo groups (p>0.05). No significant adverse effects were noted. L-carnitine, though a safe drug, does not affect the left ventricular function in patients with myocardial infarction.     

Radiofrequency ablation can reverse the structural remodeling caused by frequent premature ventricular contractions originating from the right ventricular outflow tract even in a “normal heart”

OBJECTIVE:

The aim of this study was to evaluate whether frequent premature ventricular contractions originating from the right ventricular outflow tract remodel the cardiac structure and function in patients with a “seemingly normal heart” and whether radiofrequency ablation can reverse this remodeling.

METHODS:

Sixty-eight patients with idiopathic frequent premature ventricular contractions originating from the right ventricular outflow tract and normal heart structure and function were enrolled in this study. The patients were divided into three groups according to the therapeutic method: radiofrequency ablation group (24 cases), anti-arrhythmia drug group (26 cases), and control group (18 cases without any treatment). Clinical Registration number: ChiCTR-ONRC-12002834

RESULTS:

The basic patient characteristics were comparable between the three groups, except for the premature ventricular contraction rate, which was significantly lower in the control group. After six months of follow up, the premature ventricular contraction rate was significantly reduced in the radiofrequency ablation group, which was accompanied by a significant decrease in the following cardiac cavity inner diameters, as determined by echocardiography: right atrium (33.33±3.78 vs. 30.05±2.60 mm, p = 0.001), right ventricle (23.24±2.40 vs. 21.05±2.16 mm, p = 0.020), and left ventricle (44.76±4.33 vs. 41.71±3.44 mm, p = 0.025). These results were similar in the anti-arrhythmia drug group, although this group exhibited a smaller extent of change (right atrium: 33.94±3.25 vs. 31.27±3.11 mm, p = 0.024; right ventricle: 22.97±3.09 vs. 21.64±2.33 mm, p = 0.049; left ventricle: 45.92±6.38 vs. 43.84±5.67 mm, p = 0.039), but not in the control group (p>0.05). There was a tendency toward improvement in the cardiac functions in both the radiofrequency ablation and anti-arrhythmia drug groups. However, these differences were not statistically significant (p>0.05).

CONCLUSIONS:

These results indicate that radiofrequency ablation can potentially reverse the cardiac remodeling caused by frequent premature ventricular contractions even in structurally normal hearts and that frequent premature ventricular contractions should be abated even in structurally normal hearts.     

Can atrial vagal denervation influence ventricular function in a failing heart?

Atrial fibrillation (AF) and congestive heart failure (CHF) often coexist (AF-CHF), and each adversely affects the other with respect to management and prognosis. Therapy with antiarrhythmic drugs to maintain sinus rhythm was disappointing. Ablation is more successful than antiarrhythmic drug therapy for the prevention of AF with few complications, although in patients with AF-CHF it is noted. Ablating autonomic nerves and ganglia on the large vessels and the heart can result in AF suppression with little damage to healthy myocardium. Our study in patients with AF-CHF found that cardiac function aggravation was more frequent in patients with AF recurrence than that of those who successfully maintain sinus rhythm. The autonomic nervous system is a fine network spreading throughout the myocytes; hence the elimination of atrial vagal with radiofrequency catheter ablation can influence the innervation in sinus and AV nodes even in the ventricular region. Thus we propose that atrial vagal denervation may result in paratherapeutic sympathovagal imbalance in the ventricular region, which has a negative effect in a failing heart, although it is neutralized by the benefit accrued from sinus rhythm after successful ablation.     

Left ventricular assist device-related infections: does the time of onset matter?

Journal of Artificial Organs - A frequent complication of left ventricular assist devices (LVAD) is the LVAD-associated infections (LVADIs). Contamination may occur during initial surgery/admission...     

Left ventricular flow propagation velocity measurement: Is it cast in stone?

This study aims to investigate the measurement of left ventricular flow propagation velocity, V _p, using phase contrast magnetic resonance imaging and to assess the discrepancies resulting from inflow jet direction and individual left ventricular size. Three V _p measuring techniques, namely non-adaptive (NA), adaptive positions (AP) and adaptive vectors (AV) method, were suggested and compared. We performed the comparison on nine healthy volunteers and nine post-infarct patients at four measurement positions, respectively, at one-third, one-half, two-thirds and the conventional 4 cm distances from the mitral valve leaflet into the left ventricle. We found that the V _p measurement was affected by both the inflow jet direction and measurement positions. Both NA and AP methods overestimated V _p, especially in dilated left ventricles, while the AV method showed the strongest correlation with the isovolumic relaxation myocardial strain rate (r = 0.53, p < 0.05). Using the AV method, notable difference in mean V _p was also observed between healthy volunteers and post-infarct patients at positions of: one-half (81 ± 31 vs. 58 ± 25 cm/s), two-thirds (89 ± 32 vs. 45 ± 15 cm/s) and 4 cm (98 ± 23 vs. 47 ± 13 cm/s) distances. The use of AV method and measurement position at one-half distance was found to be the most suitable method for assessing diastolic dysfunction given varying left ventricular sizes and inflow jet directions.     

The effect of 18 h of simulated high altitude on left ventricular function

High altitude produces increased pulmonary capillary pressure by hypoxia induced pulmonary vasoconstriction. It is also possible that hypoxia results in mildly elevated left ventricular (LV) filling pressures that may contribute to the elevated capillary pressures. This study investigates the impact of simulated high altitude on global and regional echocardiographic measures of LV performance and filling pressure. Seventeen healthy individuals underwent transthoracic echocardiography, including tissue Doppler of the septal mitral annulus and basal segments before and after an 18-h overnight stay in a high altitude simulation tent with a FiO₂ of 12%, simulating an altitude of approximately 4,000 m above sea level. In simulated high altitude, the ratio of early transmitral flow velocity to early myocardial relaxation velocity increased 22%, P < 0.001, and the Index of Myocardial Performance increased 30%, P < 0.01 due to an 58% increase in the isovolumic relaxation time (IVRT), P < 0.001. Simulated high altitude leads to a reduction in LV performance with an accompanying increase in markers of LV filling pressure. The significant changes in filling pattern and IVRT in the setting of normal and unchanged systolic function, indicates that hypoxia induces mild diastolic dysfunction in young healthy individuals.     

Cerebral lateral ventricular asymmetry on CT: how much asymmetry is representing pathology?

Purpose The purpose of this study was to evaluate the association of asymmetric lateral ventricle (ALV) with clinical and structural pathologies and assess its clinical importance. Materials and methods We analyzed 170 consecutive ALV cases on computed tomography (CT) and 170 control group patients with normal head CT. Patients who had apparent etiologic causes for ALV were excluded. The differential diagnosis of ALV and unilateral hydrocephalus (UH) was made by using three different ventricle-brain ratios (VBRs). The measurements of the ALV were made at the frontal horn level. Patients with asymmetry were divided into three subgroups including mild, moderate and severe groups to eloborate the grade of the ventricular asymmetry. Additional CT findings including septal deviation, diffuse enlargement, atrophy and the densities of constant sites were also recorded systematically for each patient. Clinical and handedness data were collected and analyzed. Results The prevalence of ALV in the study population was 6.1%. Headache was the most common reason for head CT examination and was significantly more common in the asymmetry group (61.7% in group A, 42.9% in group B, P = 0.001). Transient ischemic attack, focal neurologic findings, vertigo, ataxia, visual and hearing disturbances were similar in both groups (P > 0.5). There was no difference in smoking and alcohol habits in both patient groups. Ten (5.8%) patients in group A and 16 (9.4%) patients in group B had neuropsychiatric disorders, which did not achieve statistical significance. In group A patients, the larger ventricle was more common in the left side than in the right (left = 70.0%, right = 30.0%). Group A consisted of 57.0% mild (grade 1, n = 97), 26.5% moderate (grade II, n = 45) and 16.5% severe (grade III, n = 28) patients. There was no significant correlation between handedness and ALV. The density of different brain sites was found close similar on both sides in ALV and control group (P > 0.5). Choroidal cystic or solid neoplasm or periventricular dysplasia was detected in six ALV patients in group A (3.5%), on their additional MR examinations. Conclusion The physician should not overlook an ALV finding on unenhanced CT, particularly in cases with severe degree of asymmetry or diffuse ventricular enlargement, and search for possible accompanying disorders.     

β-Adrenergic modulation of prepulse facilitation of L-type calcium channels in rabbit ventricular myocytes

It is reported that strong depolarization augments cardiac L-type Ca currents by inducing the special gating mode with long-lasting openings (mode 2) (Pietrobon and Hess Nature 346:651-655, 1990). However, a prepulse to +90 mV did not obviously facilitate the current at 0 mV in rabbit ventricular myocytes as measured in the whole-cell configuration of the patch-clamp method in the presence of 2 mM BaCl(2) in the external solution. In the presence of isoproterenol (1 microM), the inactivation during the prepulse was attenuated, and the prepulse evoked facilitation. However, the current at 0 mV whose amplitude was normalized to the extent of the inactivation at +90 mV still exhibited greater facilitation in the presence than in the absence of isoproterenol. In the cell-attached configuration with 110 mM BaCl(2) in pipettes, repolarization from +110 to +20 mV yielded mainly blank sweeps (mode 0) and only occasionally mode 2, leading to no facilitation of the average current. Isoproterenol augmented the prepulse-induced increase in mode 2, reciprocally inhibited that in mode 0, and increased the fraction of mode 2 in non-blank sweeps after the prepulse. Therefore, beta-adrenergic stimulation favors mode 2 rather than mode 0 at strongly depolarized potentials, thereby promoting the prepulse facilitation and attenuating the inactivation of cardiac L-type Ca currents.     

Anion and cation modulation of the guinea-pig ventricular action potential during β-adrenoceptor stimulation

Modulation of the ventricular action potential by -adrenergic activation of Ca²⁺, K⁺ and cyclic adenosine monophosphate (cAMP)-dependent Cl^– channels was assessed in enzymatically isolated guinea-pig ventricular myocytes. The effectiveness and relative selectivity of 9-anthracene carboxylic acid (9-AC), as an antagonist of cAMP-dependent Cl^– channels was also tested. Membrane currents and action potentials were recorded using the conventional whole-cell variant of the patch-clamp technique or with the amphotericin B perforated-patch technique. The -adrenergic agonist isoproterenol either increased or decreased action potential duration depending on whether the dominant effect was on inward Ca²⁺ currents or on outward K⁺ or Cl^– currents. When Ca²⁺ and K⁺ channel modulation was prevented by nisoldipine and low temperature respectively, -adrenergic activation of Cl^– channels caused a significant reduction in action potential duration and a slight depolarization of the membrane potential. The -adrenergic-mediated effects were reversed by the Cl^– channel blocker, 9-AC. In the absence of -adrenergic stimulation, 9-AC had no detectable effects on action potentials or Ca²⁺ currents. These results suggest that -adrenergic activation of Cl^– channels is a potent mechanism for regulation of action potential duration and that 9-AC may be a useful, relatively specific, pharmacological tool for evaluating the physiological role of cAMP-activated Cl^– channels in heart. 9-AC also reversed the ability of isoproterenol to antagonize prolongation of action potential duration by the class III antiarrhythmic agent E-4031.