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2.
Scand Cardiovasc J ; : 1-7, 2020 Mar 11.
Artigo em Inglês | MEDLINE | ID: mdl-32157906

RESUMO

Objectives. Infective endocarditis has potential for severe complications and high mortality. The number of patients with prosthetic valves has risen, and an increase in incidence of infective endocarditis has been suggested. We aimed to examine the epidemiology, etiology, treatment and outcome of patients admitted to Division of Cardiovascular and Pulmonary Diseases at Oslo University Hospital, and explore changes in incidence over the last four years. Design. We conducted a retrospective study including all patients admitted to a tertiary hospital in Oslo, Norway, and diagnosed with infective endocarditis according to ICD-10 between 2014 and 2017. Results. Two hundred and ninety-one patients ≥18 years were included (61.3 ± 13.8 years, 75.6% men). 36.4% had previous valve surgery and this proportion decreased during the period. The aortic valve was most commonly affected (51.9%). Streptococci were the most frequent microorganisms (35.1%), while staphylococci accounted for 26.8%. 81.8% were treated surgically, at a median of 6.5 (0-120) days after admission. Hemodynamic changes or instability was the primary surgical indication (51.5%). One-year mortality was 20.6%. Surgery within a week after admission resulted in poorer 1-year prognosis than surgery after one week. Also, surgically treated patients who died were significantly older than those who survived. Conclusions. In this cohort, streptococci were the most common causative microorganism. Approximately, one-third of the patients had prosthetic valves. Mortality remains high, underscoring the need for continuous medical awareness. A high number of streptococcus infections in this cohort suggest dental origin.

3.
Artigo em Inglês | MEDLINE | ID: mdl-31916922

RESUMO

Postcardiac arrest patients treated with hypothermia, frequently require vasopressors and inotropic medication. The aim of this experimental study was to investigate the effect of epinephrine on left ventricular (LV) function during hypothermia. In an open-chest porcine model, seven animals were equipped with LV micromanometer and epicardial ultrasound transducers to provide LV pressure, Tau, and wall thickness and thickening velocities in systole (S') and early diastole (e'). Arterial, central venous, and pulmonal artery pressures were recorded. Cardiac output (CO) was measured by transit-time flow probe on the ascending aorta. Hypothermia was induced using a cooling catheter through the femoral vein. Pacemaker leads were attached to the right atrium for pacing. LV volumes were obtained by two-dimensional echocardiography. Measurements were made at normothermia (38°C) and hypothermia (33°C), without and with epinephrine infusion (0.03 µg/kg/min), at spontaneous and paced heart rates (HRs) 120 and 140 beats/min. Hypothermia reduced LV stroke volume (SV). Epinephrine during hypothermia increased the SV with reduced end-systolic volumes. LV dP/dtmax and wall-thickening velocity increased. During normothermia, epinephrine increased CO mainly due to accelerated HR, but during hypothermia, the increased CO resulted from augmented SV and, to a lesser degree, elevated HR. The incomplete relaxation and shortened diastolic filling time and the following reduction in SV seen in hypothermic animals, was repealed by epinephrine. The CO remained elevated also due to a shortened systolic duration, which gave time for complete relaxation during higher HRs. Epinephrine infusion improved systolic and diastolic function during hypothermia, and thereby reversed the effects induced by hypothermia considerably. Epinephrine augmented CO at hypothermia through increases in both SV and HR, in contrast to a mainly HR-dependent effect during normothermia. Systolic duration was shortened, which gave sufficient diastolic duration for complete relaxation. This allowed diastolic filling and maintained CO at elevated HRs.

4.
J Appl Physiol (1985) ; 128(4): 729-738, 2020 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-31999529

RESUMO

We investigated whether tachycardia in left bundle branch block (LBBB) decreases left ventricular (LV) diastolic distensibility and increases diastolic pressures due to incomplete relaxation, and if cardiac resynchronization therapy (CRT) modifies this response. Thirteen canines were studied at baseline heart rate (120 beats/min) and atrial paced tachycardia (180 beats/min) before and after induction of LBBB and during CRT. LV and left atrial pressures (LAP) were measured by micromanometers and dimensions by sonomicrometry. The time constant τ of exponential pressure decay and degree of incomplete relaxation at mitral valve opening (MVO) and end diastole (ED) based on extrapolation of the exponential decay were assessed. Changes in LV diastolic distensibility were investigated using the LV transmural pressure-volume (PV) relation. LBBB caused prolongation of τ (P < 0.03) and increased the degree of incomplete relaxation during tachycardia at MVO (P < 0.001) and ED (P = 0.08) compared with normal electrical activation. This was associated with decreased diastolic distensibility seen as upward shift of the PV relation at MVO by 18.4 ± 7.0 versus 12.0 ± 5.0 mmHg, at ED by 9.8 ± 2.3 versus 4.7 ± 2.3 mmHg, and increased mean LAP to 11.4 ± 2.7 versus 8.5 ± 2.6 mmHg, all P < 0.006. CRT shifted the LV diastolic PV relation downwards during tachycardia, reducing LAP and LV diastolic pressures (P < 0.03). Tachycardia in LBBB reduced LV diastolic distensibility and increased LV diastolic pressures due to incomplete relaxation, whereas CRT normalized these effects. Clinical studies are needed to determine whether a similar mechanism contributes to dyspnea and exercise intolerance in LBBB and if effects of CRT are heart rate dependent.NEW & NOTEWORTHY Compared with normal electrical conduction, tachycardia in left bundle branch block resulted in incomplete relaxation during filling, particularly of the late activated left ventricular lateral wall. This further resulted in reduced left ventricular diastolic distensibility and elevated diastolic pressures and thus amplified the benefits of cardiac resynchronization therapy in this setting.

5.
JACC Cardiovasc Imaging ; 13(7): 1475-1484, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31954643

RESUMO

OBJECTIVES: The purpose of this study was to investigate how LBBB and CRT modify RV free wall function by direct ventricular interaction. BACKGROUND: Right ventricular (RV) function influences prognosis in patients with left bundle branch block (LBBB) and cardiac resynchronization therapy (CRT). There is, however, limited insight into how LBBB and CRT affect RV function. METHODS: In 24 patients with LBBB with nonischemic cardiomyopathy, RV and left ventricular (LV) strain by speckle-tracking echocardiography was measured before and after CRT. Underlying mechanisms were studied in 16 anesthetized dogs with ultrasonic dimension crystals and micromanometers. RESULTS: Patients with LBBB demonstrated distinct early systolic shortening in the RV free wall, which coincided with the typical abnormal early systolic septal shortening. In animals, this RV free wall contraction pattern resulted in reduced myocardial work as a large portion of the shortening occurred against low pressure during early systole, coinciding with abnormal leftward septal motion. RV systolic function was maintained by vigorous contraction in the late-activated LV lateral wall, which pushed the septum toward the RV. CRT reduced abnormal septal motion and increased RV free wall work because there was less inefficient shortening against low pressure. CONCLUSIONS: LBBB reduces workload on the RV free wall because of abnormal septal motion and delayed activation of the LV lateral wall. Restoring septal and LV function by CRT increases workload in RV free wall and may explain why patients with RV failure respond poorly to CRT. (Contractile Reserve in Dyssynchrony: A Novel Principle to Identify Candidates for Cardiac Resynchronization Therapy [CRID-CRT]; NCT02525185).

6.
Eur Heart J ; 41(14): 1401-1410, 2020 Apr 07.
Artigo em Inglês | MEDLINE | ID: mdl-31504415

RESUMO

AIMS: We aimed to assess structural progression in arrhythmogenic cardiomyopathy (AC) patients and mutation-positive family members and its impact on arrhythmic outcome in a longitudinal cohort study. METHODS AND RESULTS: Structural progression was defined as the development of new Task Force imaging criteria from inclusion to follow-up and progression rates as annual changes in imaging parameters. We included 144 AC patients and family members (48% female, 47% probands, 40 ± 16 years old). At genetic diagnosis and inclusion, 58% of family members had penetrant AC disease. During 7.0 [inter-quartile range (IQR) 4.5-9.4] years of follow-up, 47% of family members without AC at inclusion developed AC criteria, resulting in a yearly new AC penetrance of 8%. Probands and family members had a similar progression rate of right ventricular outflow tract diameter (0.5 mm/year vs. 0.6 mm/year, P = 0.28) by mixed model analysis of 598 echocardiographic examinations. Right ventricular fractional area change progression rate was even higher in family members (-0.6%/year vs. -0.8%/year, P < 0.01). Among 86 patients without overt structural disease or arrhythmic history at inclusion, a first severe ventricular arrhythmic event occurred in 8 (9%), of which 7 (88%) had concomitant structural progression. Structural progression was associated with higher incidence of severe ventricular arrhythmic events adjusted for age, sex, and proband status (HR 21.24, 95% CI 2.47-182.81, P < 0.01). CONCLUSION: More than half of family members had AC criteria at genetic diagnosis and yearly AC penetrance was 8%. Structural progression was similar in probands and family members and was associated with higher incidence of severe ventricular arrhythmic events.

7.
ASAIO J ; 66(1): 38-48, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-30688692

RESUMO

We have recently demonstrated that accelerometer-based pump thrombosis and thromboembolic events detection is feasible in vitro. This article focuses on detection of these conditions in vivo. In an open-chest porcine model (n = 7), an accelerometer was attached to the pump casing of an implanted HeartWare HVAD. Pump vibration was analyzed by Fast Fourier Transform of the accelerometer signals, and the spectrogram third harmonic amplitude quantified and compared with pump power. Interventions included injection of thrombi into the left atrium (sized 0.3-0.4 ml, total n = 35) and control interventions; pump speed change, graft obstruction, and saline bolus injections (total n = 47). Graft flow to cardiac output ratio was used to estimate the expected number of thrombi passing through the pump. Sensitivity/specificity was assessed by receiver operating characteristic curve. Graft flow to cardiac output ratio averaged 66%. Twenty-six of 35 (74%) thrombi caused notable accelerometer signal change. Accelerometer third harmonic amplitude was significantly increased in thromboembolic interventions compared with control interventions, 64.5 (interquartile range [IQR]: 18.8-107.1) and 5.45 (IQR: 4.2-6.6), respectively (p < 0.01). The corresponding difference in pump power was 3 W (IQR: 2.9-3.3) and 2.8 W (IQR: 2.4-2.9), respectively (p < 0.01). Sensitivity/specificity of the accelerometer and pump power to detect thromboembolic events was 0.74/1.00 (area under the curve [AUC]: 0.956) and 0.40/1.00 (AUC: 0.759), respectively. Persistent high third harmonic amplitude was evident at end of all experiments, and pump thrombosis was confirmed by visual inspection. The findings demonstrate that accelerometer-based detection of thromboembolic events and pump thrombosis is feasible in vivo and that the method is superior to detection based on pump power.

8.
PLoS One ; 14(6): e0218624, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31247004

RESUMO

INTRODUCTION: Right ventricular (RV) myocardial dysfunction is a common feature in septic shock. It can worsen outcome, but the etiology is poorly understood. Pulmonary artery hypertension (PAH) plays a part in the pathogenesis of the right heart dysfunction in sepsis but its importance is unknown. In pigs, PAH in sepsis is substantial and the translational value of porcine sepsis models therefore questioned. We hypothesized that porcine sepsis causes a myocardial inflammatory response which leads to myocardial dysfunction independent of PAH. MATERIALS AND METHODS: Sepsis was induced by Escherichia coli-infusion in 10 pigs resulting in PAH and increased right ventricular pressure (RVP). The same degree of RVP was achieved by external pulmonary artery banding (PAB) in a consecutive series of 6 animals. RESULTS: Sepsis, but not PAB, led to increase in endothelial damage marker PAI-1 and cytokines TNF and IL-6 (all p<0.05) in plasma. In myocardium, TNF and IL-6 were significantly elevated in sepsis, TNF in both ventricles and IL-6 mostly in RV, while IL-1ß, IL-18 and C5a were significantly higher in RV compared to LV after PAB (all p<0.05). Myocardial mRNA levels of IL-1ß, IL-6, IL-18, IP-10, E-selectin and PAI-1 were significantly elevated in RV and LV during sepsis compared to PAB, while Caspase-1 was decreased in septic compared to PAB animals (all p<0.05). Cathepsin L activity was increased in RV by PAB, while sepsis inhibited this response. Escherichia coli-induced sepsis caused myocardial inflammation independent of PAH. CONCLUSION: Prominent PAH should therefore not exclude porcine sepsis models to further our understanding of human sepsis.


Assuntos
Miocardite/etiologia , Sepse/complicações , Disfunção Ventricular Direita/etiologia , Animais , Citocinas/sangue , Citocinas/genética , Modelos Animais de Doenças , Feminino , Hipertensão Pulmonar/complicações , Hipertrofia Ventricular Direita/etiologia , Hipertrofia Ventricular Direita/patologia , Masculino , Miocardite/genética , Miocardite/patologia , Miocárdio/metabolismo , Miocárdio/patologia , Inibidor 1 de Ativador de Plasminogênio/sangue , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Sepse/sangue , Sepse/genética , Sus scrofa , Disfunção Ventricular Direita/patologia
9.
Tidsskr Nor Laegeforen ; 139(6)2019 Mar 26.
Artigo em Norueguês | MEDLINE | ID: mdl-30917641

RESUMO

BACKGROUND: Approximately one half of all patients with heart failure have normal ejection fraction in the left ventricle, and heart failure is attributed to stiffness of the cardiac muscle. The most common cause is hypertension with ventricular hypertrophy. MATERIAL AND METHOD: Literature searches were conducted in PubMed. After we made our selection, a total of 15 articles on heart failure with normal ejection fraction were included. In addition, we included nine articles from our own literature archive. RESULTS: The diagnosis of heart failure with normal ejection fraction presupposes clinical findings consistent with heart failure and objective signs of diastolic dysfunction. The main objective sign is increased left ventricular filling pressure estimated by echocardiography. Ventricular hypertrophy and increased natriuretic peptides support the diagnosis. INTERPRETATION: Underlying conditions and symptoms are treated, and in general the same drugs are used as for heart failure with reduced ejection fraction.


Assuntos
Insuficiência Cardíaca , Volume Sistólico/fisiologia , Doenças Cardiovasculares/complicações , Doenças Cardiovasculares/tratamento farmacológico , Ecocardiografia , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/etiologia , Insuficiência Cardíaca/fisiopatologia , Humanos , Hipertensão/complicações , Hipertensão/tratamento farmacológico , Hipertrofia Ventricular Esquerda/complicações , Hipertrofia Ventricular Esquerda/tratamento farmacológico
10.
JACC Cardiovasc Imaging ; 12(12): 2402-2413, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-30772230

RESUMO

OBJECTIVES: This study sought to investigate how regional left ventricular (LV) function modifies septal motion in left bundle branch block (LBBB). BACKGROUND: In LBBB, the interventricular septum often has marked pre-ejection shortening, followed by immediate relengthening (rebound stretch). This motion, often referred to as septal flash, is associated with positive response to cardiac resynchronization therapy (CRT). METHODS: In 10 anesthetized dogs, we induced LBBB by radiofrequency ablation and occluded the circumflex (CX) (n = 10) and left anterior descending (LAD) (n = 6) coronary arteries, respectively. Myocardial dimensions were measured by sonomicrometry and myocardial work by pressure-segment length analysis. In 40 heart failure patients with LBBB, including 20 with post-infarct scar and 20 with nonischemic cardiomyopathy, myocardial strain was measured by speckle-tracking echocardiography and myocardial work by pressure-strain analysis. Scar was assessed by cardiac magnetic resonance imaging with late gadolinium enhancement. RESULTS: During LBBB, each animal showed typical septal flash with pre-ejection shortening and rebound stretch, followed by reduced septal systolic shortening (p < 0.01). CX occlusion caused LV lateral wall dysfunction and abolished septal flash due to loss of rebound stretch (p < 0.0001). Furthermore, CX occlusion restored septal systolic shortening to a similar level as before induction of LBBB and substantially improved septal work (p < 0.001). LAD occlusion, however, accentuated septal flash by increasing rebound stretch (p < 0.05). Consistent with the experimental findings, septal flash was absent in patients with LV lateral wall scar due to lack of rebound stretch (p < 0.001), and septal systolic shortening and septal work far exceeded values in nonischemic cardiomyopathy (p < 0.0001). Septal flash was present in most patients with anteroseptal scar. CONCLUSIONS: LV lateral wall dysfunction and scar abolished septal flash and markedly improved septal function in LBBB. Therefore, function and scar in the LV lateral wall should be taken into account when septal motion is used to evaluate dyssynchrony.

11.
Europace ; 21(2): 347-355, 2019 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-30418572

RESUMO

Aims: There are conflicting data and no consensus on how to measure acute response to cardiac resynchronization therapy (CRT). This study investigates, which contractility indices are best markers of acute CRT response. Methods and results: In eight anaesthetized dogs with left bundle branch block, we measured left ventricular (LV) pressure by micromanometer and end-diastolic volume (EDV) and end-systolic volume (ESV) by sonomicrometry. Systolic function was measured as LV ejection fraction (EF), peak rate of LV pressure rise (LV dP/dtmax) and as a gold standard of contractility, LV end-systolic elastance (Ees), and volume axis intercept (V0) calculated from end-systolic pressure-volume relations (ESPVR). Responses to CRT were compared with inotropic stimulation by dobutamine. Both CRT and dobutamine caused reduction in ESV (P < 0.01) and increase in LV dP/dtmax (P < 0.05). Both interventions shifted the ESPVR upwards indicating increased contractility, but CRT which reduced V0 (P < 0.01), caused no change in Ees. Dobutamine markedly increased Ees, which is the typical response to inotropic stimulation. Preload (EDV) was decreased (P < 0.01) by CRT, and there was no change in EF. When adjusting for the reduction in preload, CRT increased EF (P = 0.02) and caused a more marked increase in LV dP/dtmax (P < 0.01). Conclusion: Increased contractility by CRT could not be identified by Ees, which is a widely used reference method for contractility. Furthermore, reduction in preload by CRT attenuated improvement in contractility indices such as EF and LV dP/dtmax. These results suggest that changes in LV volume may be more sensitive markers of acute CRT response than conventional contractility indices.

13.
JACC Cardiovasc Imaging ; 12(6): 967-977, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-29361486

RESUMO

OBJECTIVES: This study sought to investigate the hypothesis that patients with left bundle branch block (LBBB) are hypersensitive to elevated afterload. BACKGROUND: Epidemiological data suggest that LBBB can provoke heart failure in patients with hypertension. METHODS: In 11 asymptomatic patients with isolated LBBB and 11 age-matched control subjects, left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) were measured by echocardiography. Systolic arterial pressure was increased by combining pneumatic extremity constrictors and handgrip exercise. To obtain more insight into mechanisms of afterload response, 8 anesthetized dogs with left ventricular (LV) micromanometer and dimension crystals were studied during acutely induced LBBB and aortic constriction. Regional myocardial work was assessed by LV pressure-dimension analysis. RESULTS: Consistent with normal afterload dependency, elevation of systolic arterial pressure by 38 ± 12 mm Hg moderately reduced LVEF from 60 ± 4% to 54 ± 6% (p < 0.01) in control subjects. In LBBB patients, however, a similar blood pressure increase caused substantially larger reduction in LVEF (p < 0.01), from 56 ± 6% to 42 ± 7% (p < 0.01). There were similar findings for GLS. In the dog model, aortic constriction abolished septal shortening (p < 0.02), and septal work decreased to negative values (p < 0.01). Therefore, during elevated systolic pressure, the septum made no contribution to global LV work, as indicated by net negative work, and instead absorbed energy from work done by the LV lateral wall. CONCLUSIONS: Moderate elevation of arterial pressure caused marked reductions in LVEF and GLS in patients with LBBB. This reflects a cardiodepressive effect of elevated afterload in the dyssynchronous ventricle and was attributed to loss of septal function.


Assuntos
Pressão Arterial , Bloqueio de Ramo/fisiopatologia , Insuficiência Cardíaca/fisiopatologia , Hipertensão/fisiopatologia , Volume Sistólico , Disfunção Ventricular Esquerda/fisiopatologia , Função Ventricular Esquerda , Idoso , Animais , Bloqueio de Ramo/complicações , Bloqueio de Ramo/diagnóstico por imagem , Estudos de Casos e Controles , Modelos Animais de Doenças , Cães , Ecocardiografia Doppler , Feminino , Insuficiência Cardíaca/diagnóstico por imagem , Insuficiência Cardíaca/etiologia , Humanos , Hipertensão/complicações , Hipertensão/diagnóstico , Masculino , Pessoa de Meia-Idade , Disfunção Ventricular Esquerda/diagnóstico por imagem , Disfunção Ventricular Esquerda/etiologia
14.
Open Heart ; 5(2): e000902, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30364544

RESUMO

Objective: Patients with univentricular hearts (UVH) have high mortality despite modern treatment, and better methods to identify patients at highest risk are needed. We wanted to improve risk stratification in patients with UVH by focusing on the prognostic significance of single right versus single left ventricular morphology (SRV vs SLV). Methods: All 395 patients with UVH operated at our centre were prospectively included from 1972 to 2016 (195 SRV, 166 SLV, 34 mixed or indeterminate ventricular morphology). Diagnoses, UVH morphology, types of all operations and time and causes of death or heart transplantation (HTX) were recorded. The primary endpoint was death or HTX. Results: Among the 111 non-Fontan patients, 88 died (SRV 62 vs SLV 20; p<0.0001), 32 due to heart failure (SRV 23 vs SLV 5; p=0.0012). Twenty-five years of cumulative SRV versus SLV survival among the 284 Fontan patients (41 deaths/HTX) was 66.9% vs 87.9% (p=0.0027), partly explained by more deaths/HTX due to heart failure among patients with SRV (p=0.0006). Survival in patients with SRV with and without hypoplastic left heart syndrome (HLHS) was similar. SRV versus SLV was a strong predictor of death/HTX in multivariable proportional hazards analyses (RR 3.3, 95% CI 1.6 to 6.6). Conclusion: SRV versus SLV is a strong short-term and long-term predictor of survival among patients with UVH, mainly explained by higher rates of death/HTX due to heart failure in the SRV group. Our findings apply to patients with SRV both with and without HLHS.

16.
J Appl Physiol (1985) ; 125(5): 1482-1489, 2018 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-30188795

RESUMO

Atrial switch operation in patients with transposition of the great arteries (TGA) leads to leftward shift and changes the geometry of the interventricular septum. By including the implications of regional work and septal curvature, this study investigates if changes in septal function and geometry contribute to reduced function of the systemic right ventricle (RV) in adult TGA patients. Regional myocardial work estimation has been possible by applying a recently developed method for noninvasive work calculation based on echocardiography. In 14 TGA patients (32 ± 6 yr, means ± SD) and 14 healthy controls, systemic ventricular systolic strains were measured by speckle tracking echocardiography and regional work was calculated by pressure-strain analysis. In TGA patients, septal longitudinal strain was reduced to -14 ± 2 vs. -20 ± 2% in controls ( P < 0.01) and septal work was reduced from 2,046 ± 318 to 1,146 ± 260 mmHg·% ( P < 0.01). Septal circumferential strain measured in a subgroup of patients was reduced to -11 ± 3 vs. -27 ± 3% in controls ( P < 0.01), and a reduction of septal work (540 ± 273 vs. 2,663 ± 459 mmHg·%) was seen ( P < 0.01). These reductions were in part attributed to elevated afterload due to increased radius of curvature of the leftward shifted septum. To conclude, in this mechanistic study we demonstrate that septal dysfunction contributes to failure of the systemic RV after atrial switch in TGA patients. This is potentially a long-term response to increased afterload due to a flatter septum and suggests that medical therapy that counteracts septal flattening may improve function of the systemic RV. NEW & NOTEWORTHY We have demonstrated that transposition of the great arteries patients with systemic right ventricles (RVs) have reduced function of the interventricular septum (IVS). Since the IVS is constructed to eject into the systemic circulation, it may seem unexpected that it does not maintain function when being part of the systemic RV. By applying the principles of regional work, wall tension, and geometry, we have identified unfavorable working conditions for the IVS when the RV adapts to systemic pressures.


Assuntos
Transposição das Grandes Artérias/efeitos adversos , Septos Cardíacos/fisiopatologia , Transposição dos Grandes Vasos/fisiopatologia , Disfunção Ventricular Direita/etiologia , Adulto , Fenômenos Biomecânicos , Estudos de Casos e Controles , Feminino , Humanos , Masculino , Transposição dos Grandes Vasos/cirurgia , Disfunção Ventricular Direita/fisiopatologia , Função Ventricular Esquerda , Adulto Jovem
17.
Ther Hypothermia Temp Manag ; 8(3): 156-164, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-29394143

RESUMO

Therapeutic hypothermia is an established treatment in patients resuscitated from cardiac arrest. It is usually well-tolerated circulatory, but hypothermia negatively effects myocardial contraction and relaxation velocities and increases diastolic filling restrictions. A significant proportion of resuscitated patients are treated with long-acting beta-receptor blocking agents' prearrest, but the combined effects of hypothermia and beta-blockade on left ventricle (LV) function are not previously investigated. We hypothesized that beta1-adrenergic receptor blockade (esmolol infusion) exacerbates the negative effects of hypothermia on active myocardial motions, affecting both systolic and diastolic LV function. A pig (n = 10) study was performed to evaluate the myocardial effects of esmolol during hypothermia (33°C) and during normothermia, at spontaneous and pacing-increased heart rates (HRs). LV function was assessed by a LV pressure transducer, an epicardial ultrasonic transducer (wall thickness, wall thickening/thinning velocity) and an aortic ultrasonic flow-probe (stroke volume, cardiac output). The data were compared using a paired two-tailed Students t-test, and also analyzed using a linear mixed model to handle dependencies introduced by repeated measurements within each subject. The significance level was p ≤ 0.05. The effects of hypothermia and beta blockade were distinct and additive. Hypothermia reduced myocardial motion velocities and increased diastolic filling restrictions, but end-systolic wall thickness increased, and stroke volume and dP/dtmax (pumping function) were maintained. In contrast, esmolol predominantly affected systolic pumping function, by a negative inotropic effect. In combination, hypothermia and esmolol reduced myocardial velocities in systole and diastole by ∼40%, compared with normothermia without esmolol, inducing in combination both systolic and diastolic LV function impairment. The cardiac dysfunction deteriorated at increased HRs during hypothermia. Beta1-adrenergic receptor blockade (esmolol) exacerbates the negative effects of hypothermia on active myocardial contraction and relaxation. The combination of hypothermia with beta-blockade induces both systolic and diastolic LV function impairment.


Assuntos
Antagonistas de Receptores Adrenérgicos beta 1/uso terapêutico , Hipotermia Induzida , Propanolaminas/uso terapêutico , Função Ventricular Esquerda/efeitos dos fármacos , Antagonistas de Receptores Adrenérgicos beta 1/farmacologia , Animais , Frequência Cardíaca , Propanolaminas/farmacologia , Suínos
19.
Interact Cardiovasc Thorac Surg ; 24(2): 188-195, 2017 02 01.
Artigo em Inglês | MEDLINE | ID: mdl-28364479

RESUMO

OBJECTIVES: Myocardial dysfunction may occur during weaning from cardiopulmonary bypass (CPB). Epicardial accelerometers have been shown to be useful in continuous monitoring of myocardial ischaemia during beating-heart surgery. We aimed to investigate whether an accelerometer can detect myocardial dysfunction during weaning from CPB. METHODS: In 23 patients undergoing isolated aortic valve replacement (AVR), a three-axis accelerometer was attached to the left ventricle and 3D velocity was calculated from the signals. Peak early systolic velocity (Vsys) and velocity at aortic valve closure (Vavc) were measured. Measurements were undertaken during normothermia with 50% bypass flow and atrial pacing (90 beats/min) before aortic cross-clamping and after cross-clamp removal. Myocardial dysfunction was defined as Vsys < Vavc, and patients were classified as having normal function or dysfunction. Left ventricular (LV) stroke work via pulmonary artery catheter and systolic velocity by echocardiography were compared between groups and used as reference methods. RESULTS: The accelerometer identified a substantial proportion of patients with myocardial dysfunction during weaning from CPB, 56% of patients compared with 11% before aortic cross-clamping. Patients classified with normal myocardial function during weaning significantly improved their LV stroke work and systolic velocity by echocardiography in response to AVR, whereas those classified with dysfunction did not. Accelerometer classification of normal function predicted an increase in echocardiographic systolic velocity [r = 0.63, regression coefficient 1.98, 95% CI (0.57, 3.40) (P < 0.01)]. CONCLUSIONS: The accelerometer detected myocardial dysfunction during weaning from CPB in accordance with measures obtained by echocardiography and pulmonary artery catheter. Clinical Trials identifier: NCT01926067. https://clinicaltrials.gov/.


Assuntos
Acelerometria , Estenose da Valva Aórtica/cirurgia , Ponte Cardiopulmonar/efeitos adversos , Implante de Prótese de Valva Cardíaca/efeitos adversos , Complicações Intraoperatórias/diagnóstico , Isquemia Miocárdica/diagnóstico , Idoso , Idoso de 80 Anos ou mais , Ecocardiografia , Estudos de Viabilidade , Feminino , Humanos , Complicações Intraoperatórias/etiologia , Masculino , Pessoa de Meia-Idade , Isquemia Miocárdica/etiologia , Sístole , Função Ventricular Esquerda/fisiologia
20.
J Transl Med ; 14(1): 345, 2016 12 20.
Artigo em Inglês | MEDLINE | ID: mdl-27998282

RESUMO

BACKGROUND: Extracorporeal cardiopulmonary resuscitation (E-CPR) is increasingly used as a rescue method in the management of cardiac arrest and provides the opportunity to rapidly induce therapeutic hypothermia. The survival after a cardiac arrest is related to post-arrest cardiac function, and the application of therapeutic hypothermia post-arrest is hypothesized to improve cardiac outcome. The present animal study compares normothermic and hypothermic E-CPR considering resuscitation success, post-arrest left ventricular function and magnitude of myocardial injury. METHODS: After a 15-min untreated ventricular fibrillation, the pigs (n = 20) were randomized to either normothermic (38 °C) or hypothermic (32-33 °C) E-CPR. Defibrillation terminated ventricular fibrillation after 5 min of E-CPR, and extracorporeal support continued for 2 h, followed by warming, weaning and a stabilization period. Magnetic resonance imaging and left ventricle pressure measurements were used to assess left ventricular function pre-arrest and 5 h post-arrest. Myocardial injury was estimated by serum concentrations of cardiac TroponinT and Aspartate transaminase (ASAT). RESULTS: E-CPR resuscitated all animals and the hypothermic strategy induced therapeutic hypothermia within minutes without impairment of the resuscitation success rate. All animals suffered a severe global systolic left ventricular dysfunction post-arrest with 50-70% reductions in stroke volume, ejection fraction, wall thickening, strain and mitral annular plane systolic excursion. Serum concentrations of cardiac TroponinT and ASAT increased considerably post-arrest. No significant differences were found between the two groups. CONCLUSIONS: Two-hour therapeutic hypothermia during E-CPR offers an equal resuscitation success rate, but does not preserve the post-arrest cardiac function nor reduce the magnitude of myocardial injury, compared to normothermic E-CPR. Trial registration FOTS 4611/13 registered 25 October 2012.


Assuntos
Reanimação Cardiopulmonar , Coração/fisiopatologia , Hipotermia Induzida , Animais , Aspartato Aminotransferases/sangue , Gasometria , Pressão Sanguínea/efeitos dos fármacos , Pressão Sanguínea/fisiologia , Temperatura Corporal/efeitos dos fármacos , Cardiotônicos/farmacologia , Cardioversão Elétrica , Coração/efeitos dos fármacos , Frequência Cardíaca/efeitos dos fármacos , Frequência Cardíaca/fisiologia , Hemodinâmica/efeitos dos fármacos , Imagem por Ressonância Magnética , Coloração e Rotulagem , Sus scrofa , Troponina T/sangue , Fibrilação Ventricular/sangue , Fibrilação Ventricular/fisiopatologia , Fibrilação Ventricular/terapia
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