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Biomedical subjects

C A Visser

Publications and source records attributed to C A Visser.

At least 19 recordsLinked to original sources
PubMed2003

Type II secretory phospholipase A2 binds to ischemic flip-flopped cardiomyocytes and subsequently induces cell death.

Type II secretory phospholipase A2 (sPLA2) is a cardiovascular risk factor. We recently found depositions of sPLA2 in the necrotic center of infarcted human myocardium and normally appearing cardiomyocytes adjacent to the border zone. The consequences of binding of sPLA2 to ischemic cardiomyocytes are not known. To explore a potential effect of sPLA2 on ischemic cardiomyocytes at a cellular level we used an in vitro model. The cardiomyocyte cell line H9c2 or adult cardiomyocytes were isolated from rabbits that were incubated with sPLA2 in the presence of metabolic inhibitors to mimic ischemia-reperfusion conditions. Cell viability was established with the use of annexin V and propidium iodide or 7-aminoactinomycin D. Metabolic inhibition induced an increase of the number of flip-flopped cells, including a population that did not stain with propidium iodide and that was caspase-3 negative. sPLA2 bound to the flip-flopped cells, including those negative for caspase-3. sPLA2 binding induced cell death in these latter cells. In addition, sPLA2 potentiated the binding of C-reactive protein (CRP) to these cells. We conclude that by binding to flip-flopped cardiomyocytes, including those that are caspase-3 negative and presumably reversibly injured, sPLA2 may induce cell death and tag these cells with CRP.

Animals↗
PubMed2003

Utility and safety of prolonged temporary transvenous pacing using an active-fixation lead: comparison with a conventional lead.

Transvenous temporary pacing is associated with a substantial dislocation rate reported to range from 10 to 37%. The aim of the study was to assess the safety and utility of a recently introduced 3.5 Fr temporary pacing lead using active fixation in a consecutive series of 36 patients with prolonged (> or = 48 hours) transvenous temporary pacing (validation group). A group of 36 patients with prolonged transvenous pacing managed with a passive-fixation lead just prior to the introduction of the active-fixation lead served as a control group (reference group). Pacing related adverse events included dislocation, inappropriate pacing (i.e., two-fold or greater increase of initial pacing threshold), local infection, and thrombosis. There were no significant differences in patient characteristics or duration of pacing (5.84 +/- 2.4 days in the reference group vs 5.94 +/- 2.6 days in the validation group). Acute pacing threshold was significantly higher in the validation group as compared to the reference group (1.38 +/- 0.67 V vs. 0.7 +/- 0.21 V, P < 0.01). The dislocation rate was significantly lower in the validation group as compared to the reference group (5.5 vs 33.3%, P < 0.001). There were 11 (31%) pacing related adverse events in the validation group versus 21 (58%) in the reference group (P < 0.01). The vast majority of patients in the validation group (75%) had ambulatory temporary pacing. Thus, transvenous temporary pacing using active fixation is safe and is associated with a low dislocation rate and a reduction in pacing related adverse events.

Aged↗
PubMed2003

Successful percutaneous extraction of an inadvertently placed left ventricular pacing lead.

A 74-year-old patient was referred for a rapidly increasing pacing threshold 9 months after DDD pacemaker implantation because of symptomatic total atrioventricular (AV) block. She had a history of hypertension, diabetes with micro-angiopathy and a recent transient ischaemic attack. The paced electrocardiogram on admission had a right bundle branch block pattern and 3-dimensional transoesophageal echocardiography demonstrated passage of the lead through an atrial septal defect with a left ventricular position in addition to moderate atherosclerosis of the ascending aorta. No thrombus could be detected on the lead. Percutaneous extraction is usually not recommended because of the risk of mobilization of thrombus material. However, the risk of stroke during removal using cardiopulmonary bypass in this patient was considerably increased because of the presence of multiple independent risk factors. Therefore, percutaneous extraction using a locking device was selected and performed without complications: follow-up was uneventful.

Aged↗
PubMed2003

Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction.

BACKGROUND/AIMS: Recent studies indicate the presence of reactive oxygen species (ROS) producing homologues of the enzymatic subunit (Nox2) of phagocytic NADPH oxidase in non-phagocytic cells. Interestingly, in these cells, ROS produced by the Nox2 homologue(s) was shown to play a role in various regulatory processes, including cell death, proliferation, and aging. The purpose of this study was to investigate whether human cardiomyocytes express Nox2. METHODS: The expression of Nox2 was studied in human cardiomyocytes using western blot and immunohistochemical analysis. To analyse the putative expression of Nox2 in human heart disease, cardiac samples from patients who had died subsequent to acute myocardial infarction (AMI) were studied. RESULTS: Both in western blot and immunohistochemical studies, Nox2 expression was found in normal human cardiomyocytes. In patients with AMI, a significant increase in Nox2 expression was found both in viable and in jeopardised cardiomyocytes in the infarcted area. In addition, in the "remote from infarction" area, Nox2 expression was present in cardiomyocytes, but was not increased. CONCLUSIONS: Nox2 or its homologue(s) is expressed in normal and jeopardised human cardiomyocytes. This expression is increased in patients with AMI, suggesting a role for this ROS producing Nox2 homologue(s) in the human heart after AMI.

Adult↗
PubMed2002

Assessment of the left atrial appendage mechanical function by three-dimensional echocardiography.

AIMS: We evaluated the feasibility of three-dimensional echocardiography, in the assessment of left atrial appendage (LAA) function. METHODS AND RESULTS: Forty-five patients underwent multiplane transoesophageal echocardiography. In addition to Doppler and two-dimensional echocardiography, data for three-dimensional echocardiography reconstruction were obtained during transoesophageal echocardiography. Left atrial appendage ejection fraction based on three-dimensional echocardiography volume measurements (EFv) and two-dimensional echocardiography area measurements (EFa), coupled with other echocardiographic data, were related to left atrial appendage late peak emptying velocity, a frequently used indicator of left atrial appendage function. Multiple regression analysis has revealed a significant association of peak emptying velocity with EFv (P<0.0001), spontaneous echocardiographic contrast (P=0.001), tricuspid regurgitation (P=0.03) and left ventricular hypertrophy (P=0.05). No significant relation was observed between peak emptying velocity and EFa, presence or absence of atrial fibrillation, left ventricular dysfunction, mitral stenosis and insufficiency, left atrial dilatation, pulmonary venous peak systolic, diastolic and peak reverse flow velocity at atrial contraction as well as left atrial appendage volumes derived from two-dimensional echocardiography and three-dimensional echocardiography. In a simple linear correlation, the degree of association between peak emptying velocity and EFv was higher as between peak emptying velocity and EFa (r=0.7 vs 0.4, both P<0.001). Observer variabilities for calculating EFv were considerably lower than for two-dimensional echocardiography derived EFa. Ejection fractions determined by two-dimensional echocardiography area measurements at 45 degrees, 90 degrees and 135 degrees cutplane angulations were related to EFv only at 135 degrees. CONCLUSIONS: Left atrial appendage ejection fraction calculation by three-dimensional echocardiography is feasible, more accurate than by two-dimensional echocardiography and has lower observer variability. Furthermore, an optimal cutplane angulation of the left atrial appendage view at 135 degrees has been demonstrated.

Adult↗
PubMed2002

Myocardial viability: impact on left ventricular dilatation after acute myocardial infarction.

OBJECTIVE: To evaluate whether the presence of viable myocardium, detected by low dose dobutamine echocardiography, limits the likelihood of left ventricular dilatation in patients with acute myocardial infarction. PATIENTS: 107 patients were studied by low dose dobutamine echocardiography at (mean (SD)) 3 (1) days after acute myocardial infarction. Cross sectional echocardiography was repeated three months later. Patients were divided in two groups based on the presence (n = 47) or absence (n = 60) of myocardial viability. RESULTS: Baseline characteristics were comparable between the two groups, except for infarct location. Left ventricular end diastolic volume index (EDVI) was stable in patients with viability, but end systolic volume index (ESVI) decreased significantly (p = 0.006). Patients without viability had a significant increase in both EDVI (p < 0.0001) and ESVI (p = 0.0007). Subgroup analysis in patients with small and large infarcts (peak creatine kinase < or = 1000 v > 1000 IU/l) showed that ventricular dilatation occurred only in patients with large infarcts without viability. This resulted in larger ESVI values at three months in that group compared with patients with large infarcts plus viability (p < 0.05). Multivariate regression analysis identified myocardial viability as an independent predictor of left ventricular dilatation, along with wall motion score index on low dose dobutamine echocardiography and the number of pathological Q waves. CONCLUSIONS: The presence of viability early after acute myocardial infarction is associated with preservation of left ventricular size, whereas the absence of viability results in ventricular dilatation, particularly in large infarcts.

Cardiac Volume↗
PubMed2002

Early prediction of improvement in ejection fraction after acute myocardial infarction using low dose dobutamine echocardiography.

OBJECTIVE: To evaluate the relation between changes in ejection fraction during the first three months after acute myocardial infarction and myocardial viability. PATIENTS: Myocardial viability was assessed using low dose dobutamine echocardiography in 107 patients at mean (SD) 3 (1) days after acute myocardial infarction. Cross sectional echocardiography was repeated three months later. Left ventricular volumes and ejection fraction were determined from apical views using the Simpson biplane formula. RESULTS: In patients with viability, ejection fraction increased by 4.4 (4.3)%; in patients without viability it remained unchanged (0.04 (3.6)%; p < 0.001). A > or = 5% increase in ejection fraction was present in 21 of 107 patients (20%). Receiver operating characteristic analysis showed that myocardial viability in > or = 2 segments predicted this increase in ejection fraction with a sensitivity of 81% and a specificity of 65%. Multivariate logistic regression analysis was used to define which clinical and echocardiographic variables were related to > or = 5% improvement in ejection fraction. Myocardial viability, non-Q wave infarction, and anterior infarction all emerged as independent predictors, myocardial viability being the best (chi(2) = 14.5; p = 0.0001). Using the regression equation, the probability of > or = 5% improvement in ejection fraction for patients with a non-Q wave anterior infarct with viability was 73%, and for patients with a Q wave inferior infarct without viability, only 2%. CONCLUSIONS: Myocardial viability after acute myocardial infarction is the single best predictor of improvement in ejection fraction. In combination with infarct location and Q wave presence, the probability of > or = 5% improvement can be estimated in individual patients at the bedside.

Cardiotonic Agents↗
PubMed2002

Apoptosis in myocardial ischaemia and infarction.

Recent studies indicate that, in addition to necrosis, apoptosis also plays a role in the process of tissue damage after myocardial infarction, which has pathological and therapeutic implications. This review article will discuss studies in which the role and mechanisms of apoptosis in myocardial infarction were analysed in vivo and in vitro in humans and in animals.

Apoptosis↗
PubMed2001

Predictive value of markers of myocardial reperfusion in acute myocardial infarction for follow-up left ventricular function.

This study evaluated recently suggested invasive and noninvasive parameters of myocardial reperfusion after acute myocardial infarction (AMI), assessing their predictive value for left ventricular function 4 weeks after AMI and reperfusion defined by myocardial contrast echocardiography (MCE). In 38 patients, angiographic myocardial blush grade, corrected Thrombolysis In Myocardial Infarction frame count, ST-segment elevation index, and coronary flow reserve (n = 25) were determined immediately after primary percutaneous transluminal coronary angioplasty (PTCA) for first AMI, and intravenous MCE was determined before, and at 1 and 24 hours after PTCA to evaluate myocardial reperfusion. Results were related to global wall motion index (GWMI) at 4 weeks. MCE 1 hour after PTCA showed good correlation with GWMI at 4 weeks (r = 0.684, p <0.001) and was in an analysis of variance the best parameter to predict GWMI 4 weeks after AMI. The ST-segment elevation index was close in its predictive value. Considering only invasive parameters of reperfusion myocardial blush grade was the best predictor of GWMI at 4 weeks (R(2) = 0.3107, p <0.001). A MCE perfusion defect size at 24 hours of > or =50% of the MCE perfusion defect size before PTCA was used to define myocardial nonreperfusion. In a multivariate analysis, low myocardial blush grade class was the best predictor of nonreperfusion defined by MCE. Thus, intravenous MCE allows better prediction of left ventricular function 4 weeks after AMI than other evaluated parameters of myocardial reperfusion. Myocardial blush grade is the best predictor of nonreperfusion defined by MCE and is the invasive parameter with the greatest predictive value for left ventricular function after AMI. Coronary flow parameters are less predictive.

Aged↗
PubMed2001

In-hospital and long-term prognostic value of viable myocardium detected by dobutamine echocardiography early after acute myocardial infarction and its relation to indicators of left ventricular systolic dysfunction.

The prognostic value of myocardial viability early after acute myocardial infarction (AMI) is still controversial, depending on the patient under study and the outcome end point considered. Furthermore, the relative prognostic importance of viability compared with indicators of systolic left ventricular (LV) dysfunction is not known. One hundred thirty-eight patients were studied with low-dose dobutamine echocardiography 3 +/- 1 days after AMI. Patients were divided in 2 groups based on presence (n = 55) or absence (n = 83) of myocardial viability and followed up for in-hospital and late cardiac events. During hospitalization, myocardial viability was the only independent predictor for recurrent ischemic events (chi-square 5.0, p = 0.025). End-systolic volume index and ejection fraction were both independent predictors of the occurrence of heart failure, whereas gender and end-systolic volume index emerged as independent predictors of hard cardiac events (death and sustained ventricular tachycardia). After hospital discharge, patients were followed for 19 +/- 7 months. Again, myocardial viability emerged as the only independent predictor of unstable angina (chi-square 7.7, p = 0.005). Age, hypertension, and ejection fraction were the most important independent predictors of hospitalization for heart failure, whereas ejection fraction was the only independent predictor of hard cardiac events. Presence of myocardial viability early after AMI is the single best predictor of recurrent in-hospital ischemic events and unstable angina after discharge. With respect to hard cardiac events and occurrence of heart failure, indicators of LV systolic dysfunction have a higher prognostic value than presence of myocardial viability.

Adrenergic beta-Agonists↗
PubMed2001

Time course of functional recovery of stunned and hibernating segments after surgical revascularization.

BACKGROUND: Recovery of function is possible in patients with ischemic cardiomyopathy when left ventricular dysfunction is caused by stunning or hibernation. It is plausible that recovery of function after revascularization may take a longer time in hibernating myocardium compared with stunned myocardium. Accordingly, the time courses of functional recovery in hibernating and stunned myocardium were compared. METHODS AND RESULTS: Patients (n=26) with ischemic cardiomyopathy undergoing surgical revascularization were studied; regional perfusion (resting (201)Tl single-photon emission CT), glucose utilization ((18)F-2-deoxyglucose single-photon emission CT), and contractile function (2D echocardiography) were assessed before revascularization. Dysfunctional segments with normal perfusion/glucose utilization were considered to be stunned, and dysfunctional segments with reduced perfusion/preserved glucose utilization were considered to be hibernating. Contractile function was reevaluated 3 months (early) and 14 months (late) after revascularization. Of the 266 dysfunctional segments, 57 (22%) were stunned, 62 (23%) were hibernating, and 147 (55%) were scar tissue. In stunned myocardium, contractile function improved significantly at 3 months, without further improvement at 14 months; 61% of the stunned segments improved at 3 months, and 9% improved at 14 months. In hibernating myocardium, contractile function improved at 3 months, with a further improvement at 14 months; 31% of the hibernating segments improved at 3 months, and 61% showed (additional) recovery at 14 months. CONCLUSIONS: Stunned myocardium is likely to demonstrate early recovery of function, whereas hibernating myocardium may take a longer time to (fully) recover in function after revascularization.

Cardiomyopathies↗
PubMed2001

Effects of calcium, inorganic phosphate, and pH on isometric force in single skinned cardiomyocytes from donor and failing human hearts.

BACKGROUND: During ischemia, the intracellular calcium and inorganic phosphate (P(i)) concentrations rise and pH falls. We investigated the effects of these changes on force development in donor and failing human hearts to determine if altered contractile protein composition during heart failure changes the myocardial response to Ca(2+), P(i), and pH. METHODS AND RESULTS: Isometric force was studied in mechanically isolated Triton-skinned single myocytes from left ventricular myocardium. Force declined with added P(i) to 0.33+/-0.02 of the control force (pH 7.1, 0 mmol/L P(i)) at 30 mmol/L P(i) and increased with pH from 0.64+/-0.03 at pH 6.2 to 1.27+/-0.02 at pH 7.4. Force dependency on P(i) and pH did not differ between donor and failing hearts. Incubation of myocytes in a P(i)-containing activating solution caused a potentiation of force, which was larger at submaximal than at maximal [Ca(2+)]. Ca(2+) sensitivity of force was similar in donor hearts and hearts with moderate cardiac disease, but in end-stage failing myocardium it was significantly increased. The degree of myosin light chain 2 phosphorylation was significantly decreased in end-stage failing compared with donor myocardium, resulting in an inverse correlation between Ca(2+) responsiveness of force and myosin light chain 2 phosphorylation. CONCLUSIONS: Our results indicate that contractile protein alterations in human end-stage heart failure alter Ca(2+) responsiveness of force but do not affect the force-generating capacity of the cross-bridges or its P(i) and pH dependence. In end-stage failing myocardium, the reduction in force by changes in pH and [P(i)] at submaximal [Ca(2+)] may even be less than in donor hearts because of the increased Ca(2+) responsiveness.

Adult↗
PubMed2001

Quantification of regional contractile function after infarction: strain analysis superior to wall thickening analysis in discriminating infarct from remote myocardium.

OBJECTIVES: Using two-dimensional wall thickening (WT) (expressed as percentage) and strain analysis, regional contractile myocardial function was quantified and compared in 13 control subjects and 13 patients with a first myocardial infarction (MI). The findings in the patient group were related to global ventricular function and infarct size. BACKGROUND: In patients with coronary artery disease, regions with dysfunctional myocardium cannot be differentiated easily from regions with normal function by planar WT analysis. Physiologic factors, in combination with limitations of conventional imaging techniques, affect the calculation of WT. Quantitative assessment of contractile function by magnetic resonance (MR) tissue tagging and strain analysis may be less affected by these factors. METHODS: Two-dimensional regional WT and strain were calculated in three short-axis MR cine and tagged images, respectively. Left ventricular volumes and ejection fraction (EF) were obtained from a series of contiguous short-axis cine images. RESULTS: In patients with infarct-related ventricles, WT and strain analysis both revealed reduced myocardial function, as compared with control subjects (p < 0.005 and p < 0.001, respectively). However, WT analysis yielded no significant regional differences in function between infarct-related and remote myocardium (p = 0.064), whereas strain analysis did (p < 0.005). For detecting dysfunctional myocardium of electrocardiographically and angiographically defined infarct areas, WT analysis had a sensitivity of 69% and a specificity of 92%, whereas strain analysis demonstrated a sensitivity of 92% and a specificity of 99%. The EF correlated with WT (r = 0.76, p < 0.005) and strain (r = 0.89, p < 0.001). CONCLUSIONS: Two-dimensional strain analysis is more accurate than planar WT analysis in discriminating dysfunctional from functional myocardium, and it provides a strong correlation between regional myocardial and global ventricular function.

Aged↗
PubMed2001

Carbon-11 acetate as a tracer of myocardial oxygen consumption.

Estimation of myocardial oxygen consumption (MVO2) and myocardial blood flow (MBF) is important for the understanding of various (patho)physiological mechanisms and diseases. Clearance rates of carbon-11 labelled acetate, determined with positron emission tomography, allow estimation of MVO2 on a segmental level and non-invasively. In addition, MBF can be determined from uptake rates. In this review, the background to estimation of MVO2 and MBF is discussed, as well as the currently available literature that has used 11C-acetate to estimate MVO2 and MBF.

Acetates↗