A compliant, banded outflow cannula for decreased afterload sensitivity of rotary right ventricular assist devices

Biventricular support with dual rotary ventricular assist devices (VADs) has been implemented clinically with restriction of the right VAD (RVAD) outflow cannula to artificially increase afterload and, therefore, operate within recommended design speed ranges. However, the low preload and high afterload sensitivity of these devices increase the susceptibility of suction events. Active control systems are prone to sensor drift or inaccurate inferred (sensor-less) data, therefore an alternative solution may be of benefit. This study presents the in vitro evaluation of a compliant outflow cannula designed to passively decrease the afterload sensitivity of rotary RVADs and minimize left-sided suction events. A one-way fluid-structure interaction model was initially used to produce a design with suitable flow dynamics and radial deformation. The resultant geometry was cast with different initial cross-sectional restrictions and concentrations of a softening diluent before evaluation in a mock circulation loop. Pulmonary vascular resistance (PVR) was increased from 50 dyne s/cm5 until left-sided suction events occurred with each compliant cannula and a rigid, 4.5 mm diameter outflow cannula for comparison. Early suction events (PVR ∼ 300 dyne s/cm5) were observed with the rigid outflow cannula. Addition of the compliant section with an initial 3 mm diameter restriction and 10% diluent expanded the outflow restriction as PVR increased, thus increasing RVAD flow rate and preventing left-sided suction events at PVR levels beyond 1000 dyne s/cm5. Therefore, the compliant, restricted outflow cannula provided a passive control system to assist in the prevention of suction events with rotary biventricular support while maintaining pump speeds within normal ranges of operation.

The rate of force generation by the myocardium is not influenced by afterload

The influence of afterload on the rate of force generation by the myocardium was investigated using two types of preparations: the in situ dog heart (dP/dt) and isolated papillary muscle of rats (dT/dt). Thirteen anesthetized, mechanically ventilated and thoracotomized dogs were submitted to pharmacological autonomic blockade (3.0 mg/kg oxprenolol plus 0.5 mg/kg atropine). A reservoir connected to the left atrium permitted the control of left ventricular end-diastolic pressure (LVEDP). A mechanical constriction of the descending thoracic aorta allowed to increase the systolic pressure in two steps of 20 mmHg (conditions H1 and H2) above control values (condition C). After arterial pressure elevations (systolic pressure C: 119 ± 8.1; H1: 142 ± 7.9; H2 166 ± 7.7 mmHg; P<0.01), there were no significant differences in heart rate (C: 125 ± 13.9; H1: 125 ± 13.5; H2: 123 ± 14.1 bpm; P>0.05) or LVEDP (C: 6.2 ± 2.48; H1: 6.3 ± 2.43; H2: 6.1 ± 2.51 mmHg; P>0.05). The values of dP/dt did not change after each elevation of arterial pressure (C: 3,068 ± 1,057; H1: 3,112 ± 996; H2: 3,086 ± 980 mmHg/s; P>0.05). In isolated rat papillary muscle, an afterload corresponding to 50% and 75% of the maximal developed tension did not alter the values of the maximum rate of tension development (100%: 78 ± 13; 75%: 80 ± 13; 50%: 79 ± 11 g mm-2 s-1, P>0.05). The results show that the rise in afterload per se does not cause changes in dP/dt or dT/dt

Evaluation of Vmax as an index of myocardial contractility during afterload and preload elevations

In order to test if the maximal velocity of shortening (V(max)TP) reflects the level of inotropism and is affected by preload and afterload, the behavior of this index was compared in two groups of anesthetized, atropinized dogs when preload and afterload were raised with an angiotensin II infusion. In seven dogs (group I), the arterial pressure elevation was allowed to inhibit reflectively the sympathetic tone and depress contractility. In eleven dogs (group II), the adrenergic activity was abolished by previous administration of reserpine. In group I, there was a significant decrease in V(max)TP during the angiotensin infusion. In group II, there was no significant change in the value of this index when the drug was infused. In six animals of this group, a further increase of arterial pressure was induced, but the values of V(max)TP remained similar to control. These results suggest that this index reflects the inotropic state of the myocardium and does not suffer significantly from the influence of preload and afterload elevations within our experimental limits.

A controller for a miniature intra-aortic ventricular assist device.

Two control algorithms have been developed for a minimally invasive axial-flow ventricular assist device (VAD) for placement in the descending aorta. The purpose of the device is to offload the left ventricle and to augment lower body perfusion in patients with moderate congestive heart failure. The VAD consists of an intra-aortic impeller with a built-in permanent magnet rotor and an extra-aortic stator. The control algorithms, which use pressure readings upstream and downstream of the VAD to determine the pump status, have been tested in a mock circulatory system under two conditions, namely with or without afterload sensitivity. The results give an insight into controller design for an intra-aortic blood pump working in series with the heart.

PulseCath iVAC 3LTM hemodynamic performance for simple assisted flow.

The PulseCath iVAC 3L? left ventricular assist device is an option to treat transitory left heart failure or dysfunction post-cardiac surgery. Assisted blood flow should reach up to 3 l/min. In the present in vitro model exact pump flow, depending on various frequencies and afterload was examined. Optimal flow was achieved with inflation/deflation frequencies of about 70-80/min. The maximal flow rate was achieved at about 2.5 l/min with a minimal afterload of 22 mmHg. Handling of the device was easy due to the connection to a standard intra-aortic balloon pump console. With increasing afterload (up to a simulated mean systemic pressure of 66 mmHg) flow rate and cardiac support are in some extent limited.

Coronary reserve impairment prevents the improvement of left ventricular dysfunction and adversely affects the long-term outcome of patients with hypertensive dilated cardiomyopathy

In hypertension, left ventricular (LV) hypertrophy develops as an adaptive mechanism to compensate for increased afterload and thus preserve systolic function. Associated structural changes such as microvascular disease might potentially interfere with this mechanism, producing pathological hypertrophy. A poorer outcome is expected to occur when LV function is put in jeopardy by impaired coronary reserve. The aim of this study was to evaluate the role of coronary reserve in the long-term outcome of patients with hypertensive dilated cardiomyopathy. Between 1996 and 2000, 45 patients, 30 of them male, with 52 +/- 11 years and LV fractional shortening <30% were enrolled and followed until 2006. Coronary flow velocity reserve was assessed by transesophageal Doppler of the left anterior descending coronary artery. Sixteen patients showed >= 10% improvement in LV fractional shortening after 17 +/- 6 months. Coronary reserve was the only variable independently related to this improvement. Total mortality was 38% in 10 years. The Cox model identified coronary reserve (hazard ratio = 0.814; 95% CI = 0.72-0.92), LV mass, low diastolic blood pressure, and male gender as independent predictors of mortality. In hypertensive dilated cardiomyopathy, coronary reserve impairment adversely affects survival, possibly by interfering with the improvement of LV dysfunction. J Am Soc Hypertens 2010;4(1):14-21. (C) 2010 American Society of Hypertension. All rights reserved.

Effect of physiological overload on pregnancy in women with mitral regurgitation

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cardiac remodeling in a rat model of diet-induced obesity

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Influência da pós-carga sobre a taxa de variação da tensão desenvolvida (dT/dt). Estudo em músculo cardíaco isolado.

PURPOSE: To evaluate the effects of afterload on peak rate of tension rise (dT/dt) in the isolated muscle. METHODS: Left ventricular papillary muscles from Wistar rats were studied in isometric and isotonic afterloaded contractions. Muscles were analised in Krebs-Henseleit solution with calcium concentration of 2.52mM at 28 degrees C. The resting muscle length (preload) was maintained constant. The peak isometric developed tension (DT) and dT/dt were measured during increases of afterload (25, 50, 75 and 100% from DT). RESULTS: A rise in afterload corresponding to 50, 75 and 100% of DT, did not cause an increase in dT/dt values (p > 0.05). The dT/dt value decreased (p < 0.05) when afterload was changed from 75% to 25% of DT. CONCLUSION: The data suggest that an increase in the afterload from 50% of the DT did not promote changes in the dT/dt.

Influencia da elevacao sustentada da pressao arterial sobre a dP/dt do ventriculo esquerdo mantendo-se constante a pressao diastolica do ventriculo esquerdo

Purpose - To evaluate the influence of sustained elevations of arterial pressure on dP/dt values, which the left ventricular end diastolic pressure was kept constant. Methods - Thirteen anesthetized dogs, mechanically ventilated and submitted to thoracotomy and pharmacological autonomic block (atropine - 0.5 mg/kg IV + oxprenolol - 3 mg/kg IV) were studied. The arterial pressure elevation was obtained by mechanical constriction of the descending thoracic aorta. Analyses were made in control (C) situation and after two successives increments of arterial pressure, sustained for 10min, called hypertension 1 (H1) and hypertension 2 (H2), respectively. The end diastolic left ventricular pressure was kept constant by utilization of a perfusion system connected to the left atria. Results - Heart rate did not change (C: 125 ± 13.9bpm; H1: 125 ± 13.5bpm; H2: 123 ± 14.1bpm; p > 0.05); the LVSP increased (C: 119 ± 8.1mmHg; H1: 142 ± 7.9mmHg; H2: 166 ± 7.7mmHg; p < 0.01); the AoDP increased (C: 89 ± 11.6mmHg; H1: 99 ± 9.5mmHg; H2: 120 ± 11.8mmHg; p < 0.01); the LVEDP (C: 6.2 ± 2.48mmHg; H1: 6.3 ± 2.43mmHg; H2: 6.1 ± 2.51mmHg; p > 0.05) and the dP/dt (C: 3068 ± 1057.1mmHg/s; 3112 ± 995.7mmHg/s; H2: 3086 ± 979.5mmHg/s; p > 0.05) did not change. Conclusion - dP/dt values are not influenced by a sustained elevation of arterial pressure, when the end diastolic left ventricular pressure is kept constant.

Ventricular systolic reserve in asymptomatic children previously treated with low doses of anthracyclines: A longitudinal, prospective exercise echocardiography study

Background: The time course of mild cardiotoxicity induced by anthracycline remains unknown. The aim of this study was to evaluate the long-term evolution of decreased myocardial reserve in children previously treated with a cumulative dose of anthracycline up to 100mg/m 2. Patients and Methods: Twenty-seven asymptomatic cancer survival patients (25 with lymphoblastic leukemia), in continuous remission and off treatment for >12 months with no alterations in conventional echocardiograms were evaluated by exercise echocardiography at 37±15.4 months (T1) and 101±24 months (T2) after finishing treatment (ADRIA group). This group was compared with 25 healthy individuals (control group) similar to the ADRIA group with respect to age and body surface area (BSA). All individuals underwent treadmill exercise testing according to Bruce protocol. Echocardiograms were performed before and immediately after exercise. Results: The groups were similar regarding cardiac structure and left ventricular (LV) systolic function at rest at T1 and T2. The growth of LV posterior wall thickness related to BSA was lower in the ADRIA group at T2. Post exercise, smaller LV ejection indexes and attenuated changes in the afterload in ADRIA group were observed at T1 and T2. Conclusion: The decreased systolic reserve induced by a low dose of anthracycline in asymptomatic children and adolescents remains unaffected over a 5-year period, suggesting that positive outcomes in chronic cardiotoxicity would be expected in patients with mild impairment after anthracycline treatment. © 2011 Wiley Periodicals, Inc.

Comportamento dos níveis plasmáticos do Peptídeo Natriurético tipo-B em idosos com função sistólica do ventrículo esquerdo preservada

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Estudo da variabilidade da frequência cardíaca em cães

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)