Biomedical subjects

Hendrik Tevaearai

Publications and source records attributed to Hendrik Tevaearai.

8 recordsLinked to original sources

PubMed2006

The effect of a myocardial infarction on the normalized time-varying elastance curve.

It has been suggested that the shape of the normalized time-varying elastance curve [E(n)(t(n))] is conserved in different cardiac pathologies. We hypothesize, however, that the E(n)(t(n)) differs quantitatively after myocardial infarction (MI). Sprague-Dawley rats (n = 9) were anesthetized, and the left anterior descending coronary artery was ligated to provoke the MI. A sham-operated control group (CTRL) (n = 10) was treated without the MI. Two months later, a conductance catheter was inserted into the left ventricle (LV). The LV pressure and volume were measured and the E(n)(t(n)) derived. Slopes of E(n)(t(n)) during the preejection period (alpha(PEP)), ejection period (alpha(EP)), and their ratio (beta = alpha(EP)/alpha(PEP)) were calculated, together with the characteristic decay time during isovolumic relaxation (tau) and the normalized elastance at end diastole (E(min)(n)). MI provoked significant LV chamber dilatation, thus a loss in cardiac output (-33%), ejection fraction (-40%), and stroke volume (-30%) (P < 0.05). Also, it caused significant calcium increase (17-fold), fibrosis (2-fold), and LV hypertrophy. End-systolic elastance dropped from 0.66 +/- 0.31 mmHg/microl (CTRL) to 0.34 +/- 0.11 mmHg/microl (MI) (P < 0.05). Normalized elastance was significantly reduced in the MI group during the preejection, ejection, and diastolic periods (P < 0.05). The slope of E(n)(t(n)) during the alpha(PEP) and beta were significantly altered after MI (P < 0.05). Furthermore, tau and end-diastolic E(min)(n) were both significantly augmented in the MI group. We conclude that the E(n)(t(n)) differs quantitatively in all phases of the heart cycle, between normal and hearts post-MI. This should be considered when utilizing the single-beat concept.

Animals↗

PubMed2006

Ventricular-arterial coupling in a rat model of reduced arterial compliance provoked by hypervitaminosis D and nicotine.

The vitamin D(3) and nicotine (VDN) model is one of isolated systolic hypertension (ISH) in which arterial calcification raises arterial stiffness and vascular impedance. The effects of VDN treatment on arterial and cardiac hemodynamics have been investigated; however, a complete analysis of ventricular-arterial interaction is lacking. Wistar rats were treated with VDN (VDN group, n = 9), and a control group (n = 10) was included without the VDN. At week 8, invasive indexes of cardiac function were obtained using a conductance catheter. Simultaneously, aortic pressure and flow were measured to derive vascular impedance and characterize ventricular-vascular interaction. VDN caused significant increases in systolic (138 +/- 6 vs. 116 +/- 13 mmHg, P < 0.01) and pulse (42 +/- 10 vs. 26 +/- 4 mmHg, P < 0.01) pressures with respect to control. Total arterial compliance decreased (0.12 +/- 0.08 vs. 0.21 +/- 0.04 ml/mmHg in control, P < 0.05), and pulse wave velocity increased significantly (8.8 +/- 2.5 vs. 5.1 +/- 2.0 m/s in control, P < 0.05). The arterial elastance and end-systolic elastance rose significantly in the VDN group (P < 0.05). Wave reflection was augmented in the VDN group, as reflected by the increase in the wave reflection coefficient (0.63 +/- 0.06 vs. 0.52 +/- 0.05 in control, P < 0.05) and the amplitude of the reflected pressure wave (13.3 +/- 3.1 vs. 8.4 +/- 1.0 mmHg in control, P < 0.05). We studied ventricular-arterial coupling in a VDN-induced rat model of reduced arterial compliance. The VDN treatment led to development of ISH and provoked alterations in cardiac function, arterial impedance, arterial function, and ventricular-arterial interaction, which in many aspects are similar to effects of an aged and stiffened arterial tree.

Animals↗

PubMed2005

Noninvasive Doppler-derived myocardial performance index in rats with myocardial infarction: validation and correlation by conductance catheter.

The rodent model of myocardial infarction (MI) is extensively used in heart failure studies. However, long-term follow-up of echocardiographic left ventricular (LV) function parameters such as the myocardial performance index (MPI) and its ratio with the fractional shortening (LVFS/MPI) has not been validated in conjunction with invasive indexes, such as those derived from the conductance catheter (CC). Sprague-Dawley rats with left anterior descending coronary artery ligation (MI group, n = 9) were compared with a sham-operated control group (n = 10) without MI. Transthoracic echocardiography (TTE) was performed every 2 wk over an 8-wk period, after which classic TTE parameters, especially MPI and LVFS/MPI, were compared with invasive indexes obtained by using a CC. Serial TTE data showed significant alterations in the majority of the noninvasive functional and structural parameters (classic and novel) studied in the presence of MI. Both MPI and LVFS/MPI significantly (P < 0.05 for all reported values) correlated with body weight (r = -0.58 and 0.76 for MPI and LVFS/MPI, respectively), preload recruitable stroke work (r = -0.61 and 0.63), LV end-diastolic pressure (LVEDP) (r = 0.82 and -0.80), end-diastolic volume (r = 0.61 and -0.58), and end-systolic volume (r = 0.46 and -0.48). Forward stepwise linear regression analysis revealed that, of all variables tested, LVEDP was the only independent determinant of MPI (r = 0.84) and LVFS/MPI (r = 0.83). We conclude that MPI and LVFS/MPI correlate strongly and better than the classic noninvasive TTE parameters with established, invasively assessed indexes of contractility, preload, and volumetry. These findings support the use of these two new noninvasive indexes for long-term analysis of the post-MI LV remodeling.

Animals↗

PubMed2005

Minimal versus conventional cardiopulmonary bypass: assessment of intraoperative myocardial damage in coronary bypass surgery.

OBJECTIVE: Minimal extracorporeal circulation (mini-ECC) is a new technology, consisting of a centrifugal pump, an oxygenator, and a modified suction system. The main advantage of mini-ECC is the reduction of tubing length (reduction of the priming volume). Additional beneficial effects are a decrease of coagulation cascade and a reduction of blood transfusion in patients undergoing coronary artery bypass grafting (CABG) surgery. We compared the intraoperative and early postoperative myocardial damage and outcome of patients who underwent CABG surgery with conventional cardiopulmonary bypass (CPB) or mini-ECC. METHODS: One hundred and thirty-six consecutive patients who underwent isolated CABG surgery at our institution were prospectively studied. Fifty-four patients (39.7%) were operated with mini-ECC. Patient characteristics were similar in both groups. The most interesting intraoperative details as well as in-hospital outcome were assessed. RESULTS: There was no difference in mortality between the two groups. Cross-clamping time was similar in both groups (p = 0.07). Defibrillation was required in one patient in the mini-ECC group (1.9%) and in 38 patients (46.3%) in the CPB group (p < 0.001). In the mini-ECC group, the requirement of inotropic support and incidence of atrial fibrillation was significantly lower than in the CPB group. Postoperative creatine kinase isoenzyme MB (CK-MB) and cardiac Troponin I (cTnI) were significantly lower in the mini-ECC group (p < 0.05). Duration of ventilation, length of stay in the intensive care unit and total hospitalization time were significantly shorter in patients operated with mini-ECC (p < 0.05). CONCLUSION: Mini-ECC is a safe procedure and is followed by a diminished release of CK-MB and cTnI than after CPB. Postoperative recovery is accelerated following mini-ECC and there is a significantly lower incidence of postoperative atrial fibrillation.

Aged↗

PubMed2005

Histo-blood group antigens as allo- and autoantigens.

The science of blood groups has made giant steps forward during the last decade. Blood-group typing of red blood cells (RBCs) is performed on more than 15 million samples per year in Europe, today much less often for forensic reasons than for clinical purposes such as transfusion and organ transplantation. Specific monoclonal antibodies are used with interpretation on the basis of RBC agglutination patterns, and mass genotyping may well be on its way to becoming a routine procedure. The discovery that most blood group systems, whose antigens are by definition found on RBCs, are also expressed in multiple other tissues has sparked the interest of transplantation medicine in immunohematology beyond the HLA system. The one and only "histo-blood group" (HBG) system that is routinely considered in transplantation medicine is ABO, because ABO antigen-incompatible donor/recipient constellations are preferably avoided. However, other HBG systems may also play a role, thus far underestimated. This paper is an up-to-date analysis of the importance of HBG systems in the alloimmunity of transplantation and autoimmune events, such as hemolytic anemia.

ABO Blood-Group System↗

PubMed2004

Early clinical experience with a new tubular equine pericardial stentless aortic valve.

BACKGROUND: This study details a single-center experience with the 3F Therapeutics stentless aortic bioprosthesis(investigational device) and is part of a prospective,nonrandomized worldwide multicenter study. We assessed the implantation procedure and the valve's efficacy in terms of early mortality and morbidity and early echocardiographic valve performance. METHODS: Between June 2001 and March 2004, 24 patients (14 men/10 women) underwent aortic valve replacement(AVR) with a 3F valve. Mean age was 72 +/- 13 years(range, 31-88 years). Combined revascularization was performed in 12 patients; 1 patient received biatrial ablation therapy, 1 patient a myectomy, and 3 patients combined carotid endarterectomy. Echocardiographic systolic gradient and valve performance were investigated intra- and postoperatively by Doppler echocardiography. RESULTS: There were 2 perioperative deaths, 1 non-valve related, due to aortic rupture in an 83-year-old woman, and 1 fatal cerebral embolism in a 77-year-old woman 5 days postoperatively. Cardiopulmonary bypass time was 102 +/- 32 minutes,aortic cross-clamp time was 79 +/- 24 minutes. Sizes for implanted 3F valves were 5 x 23 mm, 6 x 25 mm, 7 x 27 mm,and 6 x 29 mm. Follow-up systolic gradient results were 11.5 +/- 4.7 mm Hg at 30 days (n = 21), 11.4 +/- 4.5 mm Hg at 6 months (n = 18), and 13.3 +/- 4.4 mm Hg at 12 months (n =13). During the follow-up period trivial central aortic valve regurgitation was found in 6 patients. CONCLUSION: The 3F aortic valve shows favorable preliminary hemodynamic results. Owing to the new valve design,implantation technique is simplified compared with other stentless valves. Anticoagulation treatment is mandatory for the first 3 months postoperatively. Long-term observation is necessary to assess life span and durability.

Aortic Valve↗

PubMed2002

An alternative to left ventricular volume reduction.

BACKGROUND: Left ventricular (LV) remodeling leading to ventricular dilatation is ultimately a maladaptative process according to the law of Laplace. To counteract the wall stress increase, a new concept of reducing the LV cavity radius by changing the LV globular shape to a bilobular one through the insertion of transventricular splints has emerged. This procedure is tested in a model of congestive heart failure. METHODS: A bovine model was used (n = 9). Following splint insertion through a sternotomy, boluses of 2 liters of crystalloid were injected. After every bolus, hemodynamic measurements were performed without and with the splints tightened to a 10% and 20% stress level reduction, respectively. Comparisons between the 3 measurements were performed with analysis of variance test (p < 0.05). RESULTS: Splint tightening significantly reduced right and left heart pressures for central venous pressure (CVP) >10 mm Hg (CVP: 14.7 +/- 5.2, 12.1 +/- 5, 10.6 +/- 4.7 mm Hg, p < 0.001 for baseline, 10% and 20% stress level reduction, respectively; mean pulmonary artery pressure: 33.5 +/- 4.7, 31 +/- 4.4, 29.4 +/- 5.1 mm Hg, p < 0.001; pulmonary capillary wedge pressure: 20.5 +/- 2.8, 18.9 +/- 3.3, 17.5 +/- 3.1 mm Hg, p < 0.001). The same holds true for cardiac output (6.5 +/- 1.6, 6.7 +/- 1.4, 6.8 +/- 1.7 liter/minute, p < 0.001), whereas heart rate and mean arterial pressure were not affected. The systemic and pulmonary resistances did not vary significantly throughout the procedure. Importantly, none of the hemodynamic parameters worsened at any stage with the splints. CONCLUSIONS: In this model, hemodynamic parameters are improved with the splints for higher values of CVP, supporting the concept of reshaping the remodeled LV. This technique has the potential to improve patients with congestive heart failure.

Animals↗

PubMed2002

Vascular-targeted overexpression of G protein-coupled receptor kinase-2 in transgenic mice attenuates beta-adrenergic receptor signaling and increases resting blood pressure.

Cardiovascular regulation is tightly controlled by signaling through G protein-coupled receptors (GPCRs). beta-Adrenergic receptors (ARs) are GPCRs that regulate inotropy and chronotropy in the heart and mediate vasodilation, which critically influences systemic vascular resistance. GPCR kinases (GRKs), including GRK2 (or betaARK1), phosphorylate and desensitize agonist-activated betaARs. Myocardial GRK2 levels are increased in heart failure and data suggest that vascular levels may also be elevated in hypertension. Therefore, we generated transgenic mice with vascular smooth muscle (VSM) targeted overexpression of GRK2, using a portion of the SM22alpha promoter, to determine its impact on vascular betaAR regulation. VSM betaAR signaling, as determined by adenylyl cyclase and mitogen-activated protein (MAP) kinase activation assays, was attenuated when GRK2 was overexpressed 2- to 3-fold. In vivo vasodilation in response to betaAR stimulation using isoproterenol was attenuated and conscious resting mean arterial blood pressure was elevated from 96 +/- 2 mm Hg in nontransgenic littermate control (NLC) mice (n = 9) to 112 +/- 3 mm Hg and 117 +/- 2 mm Hg in two different lines of SM22alpha-GRK2 transgenic mice (n = 7 and n = 5, respectively; p < 0.05). Interestingly, medial VSM thickness was increased 30% from 29.8 +/- 1.6 microm in NLC mice (n = 6) to 39.4 +/- 1.6 microm in SM22alpha-GRK2 mice (n = 7) (p < 0.05) and vascular GRK2 overexpression was sufficient to cause cardiac hypertrophy. These data indicate that we have developed a unique mouse model of hypertension, providing insight into the contribution that vascular betaAR signaling makes toward resting blood pressure and overall cardiovascular regulation. Moreover, they suggest that GRK2 plays an important role in vascular control and may represent a novel therapeutic target for hypertension.

Animals↗