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Biomedical subjects

P Hanrath

Publications and source records attributed to P Hanrath.

At least 73 records · Page 4Linked to original sources
PubMed2001

Effect of volatile anesthetics on the force-frequency relation in human ventricular myocardium: the role of the sarcoplasmic reticulum calcium-release channel.

BACKGROUND: In human ventricular myocardium, contractile force increases at higher stimulation frequencies (positive force-frequency relation). In failing hearts, the force-frequency relation (FFR) is negative. Data on the effect of volatile anesthetics on FFR are very limited. METHODS: The authors obtained left ventricular tissue from 18 explanted hearts from patients undergoing cardiac transplantation and tissue of 8 organ donors. The negative inotropic effect of halothane, isoflurane, and sevoflurane on isometric force of contraction of isolated muscle preparations at a stimulation frequency of 1 and 3 Hz and the effect of each anesthetic on the FFR were studied. Ryanodine and verapamil were studied for comparison. In addition, the effect of the anesthetics on Ca(2+)-dependent (3)H-ryanodine binding was investigated. RESULTS: In nonfailing myocardium, halothane was the strongest negative inotropic compound, and the positive FFR was not affected by either drug. In failing myocardium, halothane also showed the strongest negative inotropic effect, but the positive shape of FFR was restored by halothane and ryanodine. In contrast, isoflurane, sevoflurane, and verapamil did not change FFR. Only halothane shifted the Ca(2+)-dependent (3)H-ryanodine binding curve toward lower Ca(2+) concentrations. CONCLUSION: In nonfailing human myocardium, none of the anesthetics affect FFR, but halothane is the strongest negative inotropic compound. In failing myocardium, halothane, but not isoflurane or sevoflurane, restores the positive shape of FFR. Both the more pronounced negative inotropic effect of halothane and the restoration of the positive shape of FFR in failing myocardium in the presence of halothane can be explained by its interaction with the myocardial sarcoplasmic reticulum calcium-release channel.

Anesthetics, Inhalation↗
PubMed2001

Infectious agents in coronary lesions obtained by endatherectomy: pattern of distribution, coinfection, and clinical findings.

BACKGROUND: Cytomegalovirus (CMV), Chlamydia pneumoniae (C. pneumoniae), and Helicobacter pylori (H. pylori) have been implicated in atherosclerosis and restenosis after angioplasty. The patterns of distribution within coronary lesions and possible coinfections of these pathogens in the coronary vasculature had not previously been evaluated. DESIGN: A prospective, observational clinical study. METHODS: Large coronary specimens (9-105 mm long) were obtained by endatherectomy of 53 patients undergoing aortocoronary bypass surgery. Samples were taken from two different sites of every lesion, resulting in a total of 106 probes. Presence of each pathogen was determined by polymerase chain reaction, subsequent hybridization, and DNA sequencing. RESULTS: Cytomegalovirus and C. pneumoniae were detected in 30 and 32% of the samples, respectively; H. pylori was not detectable. The pathogens were not homogeneously distributed. A concurrent infection with both pathogens was observed in five of 106 (5%) lesions and five of 53 (9%) patients. Restenotic lesions were more often found in specimens in which cytomegalovirus was detected (five of 16 versus two of 37). Patients with C. pneumoniae-positive coronary lesions more commonly presented with unstable angina. CONCLUSIONS: Inhomogeneous infections with cytomegalovirus and C. pneumoniae of coronary atherosclerotic lesions are found to be prevalent when serial analysis is performed. Concurrent infection with both pathogens occurs coincidentally; however, possible clinical implications of this new observation and the pathogenic impact on atherosclerosis need further investigation.

Aged↗
PubMed2001

A chymase gene variant is associated with atherosclerosis in venous coronary artery bypass grafts.

BACKGROUND: Angiotensin II is known to stimulate proliferation of fibroblasts and smooth muscle cells and enhance the atherosclerotic process in native coronary arteries. The impact of genetic polymorphisms of the renin-angiotensin-aldosterone system on coronary bypass graft degeneration is unknown. METHODS: We examined polymorphisms of four genes (AGTR1, CYP11B2, ACE, CMA) in 101 patients who had follow-up coronary angiography due to symptoms 88 +/- 52 months after coronary artery bypass graft surgery. Bypass degeneration was determined with quantitative coronary angiography and an adjusted Gensini score. RESULTS: Homozygosity for the G allele of the CMA-1905 polymorphism was associated with a higher degree of bypass degeneration (Bypass Gensini score CMA AA 21.4 +/- 39; AG 24.2 +/- 39.8; GG 27.8 +/- 42.3; NS-time adjusted Gensini bypass scores CMA AA 0.25 +/- 0.68; AG 0.57 +/- 1.82; GG 3.25 +/- 13.2; P = 0.005). No association could be detected for the AGTR1, CYP11B2 or ACE polymorphism. CONCLUSION: The CMA allele G is a genetic risk factor for atherosclerosis in venous coronary artery bypass grafts. Its importance has to be shown in further studies. Other polymorphisms of the renin-angiotensin-aldosterone system do not seem to play a role in bypass degeneration.

Aged↗
PubMed2001

The vitamin D receptor genotype predisposes to the development of calcific aortic valve stenosis.

OBJECTIVE: To test the hypothesis that vitamin D receptor polymorphism is associated with calcific aortic valve stenosis. DESIGN: The distribution of one polymorphism of the vitamin D receptor (BsmI B/b) was examined in 100 consecutive patients with calcific valvar aortic stenosis and compared with a control group of 100 patients (paired match for age, sex, and the presence of coronary artery disease from a total of 630 patients without calcified aortic valves). Polymerase chain reaction and restriction fragment length polymorphism were used to determine genotypes. RESULTS: There was a significant difference in vitamin D receptor allele and genotype frequencies between the two groups. The allele B had a higher prevalence in patients with calcific aortic stenosis (B = 0.56, b = 0.44) than in the control cohort (B = 0.40, b = 0.60) (p = 0.001). CONCLUSIONS: There is a significant association of vitamin D receptor polymorphism with calcific aortic valve stenosis. The B allele of the vitamin D receptor is more common in patients with calcific aortic valve stenosis. It now needs to be evaluated whether other genes that control calcium homeostasis are involved in the pathogenesis of this disorder.

Aged↗
PubMed2001

Activation of ATP-sensitive potassium channels in hypoxic cardiac failure is not mediated by adenosine-1 receptors in the isolated rat heart.

BACKGROUND: Hypoxic cardiac failure is accompanied by action potential shortening, which in part might be a consequence of opening of cardiac ATP-sensitive potassium channels (K(ATP) channels). Coupling of the adenosine-1 receptor (A-1 receptor) to these channels has been described; however, the interaction of A-1-receptors and K(ATP) channels in different models of ischemia is still under debate. The hypothesis as to whether A-1 receptors are involved in hypoxic K(ATP) channel-activation in the saline-perfused rat heart was tested. METHODS AND RESULTS: Pharmacologic modulation of the K(ATP) channel by Glibenclamide (inhibitor) and Rimalkalim (activator) and of the A-1 receptor by R(-)-N6-(1-methyl-2-phenylethyl)-adenosine (R(-)-PIA, agonist) and 1,3-diethyl-3,7-dihydro-8-phenyl-purine-2,6-dione (DPX, antagonist) at different oxygen tensions (95% O2 and 20% O2) was performed in isolated Langendorff-rat hearts. Peak systolic pressure (PSP, intraventricular balloon), duration of monophasic action potential (epicardial suction electrode, time to 67% of repolarization: MAP(67%)), coronary flow, and heart rate (HR) were registered. Hypoxic perfusion resulted in a significant reduction of PSP (from 106 +/-11 to 56 +/-8 mmHg, P < 0.005) and shortening of MAP(67%) (from 37 +/-3 to 25 +/-4 ms, P < 0.005). With application of 1 microM Glibenclamide, MAP(67%) returned to normoxic values and PSP increased to 78 +/-9 mmHg (P < 0.005 vs hypoxia). In normoxia, 2 microM Rimalkalin resulted in reduction of MAP(67%) and PSP, which was reversed by Glibenclamide. Application of 0.1 microM R(-)-PIA in normoxia resulted in a decrease of HR (from 235 +/-36/min to 75 +/-41/min, P < 0.005), which was accompanied by an increase of PSP from 96 +/-7 to 126 +/-9 mmHg (P < 0.05) without changes in MAP(67%). These effects were reversible by 1 microM DPX and remained unaffected by application of 1 microM Glibenclamide. Application of 1 microM DPX in hypoxia had no effect on the measured parameters. CONCLUSION: In isolated rat hearts, the K(ATP) channel-system is activated in hypoxic cardiac failure and contributes to action potential shortening and reduced contractile performance. These effects seem to be independent of the A-1 receptor in this model.

Action Potentials↗
PubMed2001

Diagnosis of pulmonary arterial hypertension and pulmonary embolism with magnetic resonance angiography.

BACKGROUND: Pulmonary magnetic resonance angiography (PMRA) has been proven to be accurate for the diagnosis of suspected acute or chronic pulmonary embolism (PE). Only limited data exist on the reliability of PMRA for the diagnosis of acute and chronic pulmonary artery hypertension (PAH). The aim of this study was to determine the accuracy of PMRA in the differentiation between patients suffering from PAH of varying etiologies. METHODS: Fifty patients (21 women; mean [+/- SD] age, 52 +/- 16 years) were examined with gadolinium-enhanced PMRA for the evaluation of pulmonary artery (PA) disease. The diagnosis of PAH (ie, systolic PA pressure of > 35 mm Hg) was determined by Doppler echocardiography. The criteria for the diagnosis of chronic PAH by PMRA were dilated central PAs (diameter > 28 mm) and abnormal proximal-to-distal tapering of the PAs. The diagnostic criterion for acute and chronic PE was the presence of an intravascular filling defect. RESULTS: Chronic PAH was present in 18 patients, which was correctly identified by PMRA in 16 patients (sensitivity, 89%). All patients without PAH had normal findings on PMRA (specificity, 100%). Only 1 of 18 patients with normal findings on PMRA showed moderate chronic PAH (negative predictive value, 94%). PAH due to acute/subacute pulmonary thromboembolism (15 patients) was identified in all patients (sensitivity, 100%). Acute PAH was differentiated from chronic PAH in all cases by the detection of intravascular filling defects and the lack of abnormal proximal-to-distal tapering of PAs. CONCLUSIONS: PMRA is a promising noninvasive imaging modality for the identification of patients with acute or chronic PAH. This technique should be considered a sensitive and highly specific screening tool for suspected chronic PAH.

Acute Disease↗
PubMed2000

Echocardiographic evidence of hemodynamic and clinical improvement in patients paced for heart failure.

Dilated cardiomyopathy is frequently associated with electrical conduction disturbances. Development of left bundle-branch block with discoordinated ventricular contraction pattern further contributes to impaired hemodynamic performance. Biventricular pacing has evolved as a new treatment option for patients with dilated cardiomyopathy and conduction disturbances. The "electrical" approach aims to normalize the disturbed contraction pattern, thereby improving hemodynamic function by simultaneous stimulation at different ventricular sites. Acute hemodynamic improvement with biventricular pacing has been demonstrated in patients with depressed left ventricular function and delayed intraventricular conduction. Due to the variations in optimal pacing site and atrioventricular delay, individual optimization to achieve optimal hemodynamic benefit is necessary. Echocardiography has the potential to provide hemodynamic data by Doppler techniques and combine these with geometric information about ventricular volumes, ejection fraction, and contraction patterns. This article focuses on the use of echocardiographic techniques for noninvasive optimization in cardiac pacing and presents preliminary experience from the initial trials on multisite pacing in heart failure.

Arrhythmias, Cardiac↗
PubMed2000

[Ischemic preconditioning. Does this animal experiment phenomenon have clinical relevance?].

BACKGROUND: Infarct size following coronary artery occlusion can be markedly reduced by brief preceding periods of ischemia in several animal models. This phenomenon is called "ischemic preconditioning" and is one of the most powerful mechanisms of cardioprotection known to date. PRECONDITIONING IN HUMANS: There is increasing evidence that preconditioning effects exist in humans as well. The occurrence of angina prior to myocardial infarction might result in reduction of infarct size depending on the time pattern of preinfarct-angina. Similarly, "walking-through-angina", i.e., the relief of exercise-induced anginal symptoms with continuing exercise, is attributed to cardioprotection by ischemic preconditioning. During coronary angioplasty, a lesser shift of ST segments in the intracardial ECG and reduced anginal symptoms are registered during a second balloon inflation in comparison with the first balloon inflation. These findings might represent a "preconditioning-like" effect of the first balloon inflation. THERAPEUTICAL IMPLICATIONS: With respect to the mechanisms of ischemic preconditioning identified in animal models some pharmacological agents that exhibit a "preconditioning-like" cardioprotective effect have been intensively investigated. In clinical studies it was demonstrated that application of adenosine, adenosine-receptor-agonists, and dipyridamole--a nucleoside-transport inhibitor--prior to coronary angioplasty results in reduced ischemia during the subsequent balloon inflation. In a randomized trial the treatment with nicorandil, an activator of the ATP-sensitive potassium channel (K-ATP channel) in patients with unstable angina resulted in a marked reduction of myocardial ischemia which also can be attributed to a "preconditioning-like" effect. Therapeutical applications of ischemic preconditioning have been developed in different clinical settings: brief periods of ischemia and "pharmacologic preconditioning" prior to coronary angioplasty, prior to cardiac surgery, and for protection of donor heart for cardiac transplantation were performed to induce cardioprotection. Moreover, possible "anti-preconditioning effects" of several drugs have to be carefully considered for the treatment of patients with coronary artery disease. In particular, patients treated for acute myocardial infarction by coronary angioplasty with concomitant sulfonylurea drug therapy using glibenclamide demonstrated an increased early mortality. CONCLUSION: To raise the step from "laboratory-based protection" to "evidence-based medicine" further research should focus on clinical studies transferring the results from animal models to the clinical setting.

Angina Pectoris↗
PubMed2000

Assessment of myocardial reperfusion by intravenous myocardial contrast echocardiography and coronary flow reserve after primary percutaneous transluminal coronary angioplasty [correction of angiography] in patients with acute myocardial infarction.

BACKGROUND: This study investigated whether the extent of perfusion defect determined by intravenous myocardial contrast echocardiography (MCE) in patients with acute myocardial infarction (AMI) treated by primary percutaneous transluminal coronary angioplasty (PTCA) relates to coronary flow reserve (CRF) for assessment of myocardial reperfusion and is predictive for left ventricular recovery. METHODS AND RESULTS: Twenty-five patients with first AMI underwent intravenous MCE with NC100100 with intermittent harmonic imaging before PTCA and after 24 hours. MCE before PTCA defined the risk region and MCE at 24 hours the "no-reflow" region. The no-reflow region divided by the risk region determined the ratio to the risk region. CFR was assessed immediately after PTCA and 24 hours later. Left ventricular wall motion score indexes were calculated before PTCA and after 4 weeks. CFR at 24 hours defined a recovery (CFR >/=1.6; n=17) and a nonrecovery group (CFR <1.6; n=8). Baseline CFR did not differ between groups. MCE ratio to the risk region was smaller in the recovery group compared with the nonrecovery group (34+/-49% vs 81+/-46%, P=0.009). A ratio to the risk region of </=50% defined an MCE reperfusion group. It was associated with improvement of CFR from 1.67+/-0.47 at baseline to 2. 15+/-0.53 at 24 hours (P<0.001) and of regional wall motion score index from 2.6+/-0.5 to 1.9+/-0.5 at 4 weeks (P<0.001). CONCLUSIONS: Intravenous MCE can be used to define perfusion defects after AMI. Assessment of microcirculation by MCE corresponds to evaluation by CFR. Serial intravenous MCE has the potential to identify patients likely to have improved left ventricular function after AMI.

Aged↗
PubMed2000

Lesion-to-lesion relationship of the restenosis process after placement of coronary stents.

The interrelation between multiple stented lesions within one patient in the restenosis process is only partially understood. From 492 patients with follow-up angiograms after coronary stent placement, 115 patients underwent multilesion procedures involving 233 lesions. In randomly chosen 39 patients with 79 lesions, additional intravascular ultrasound (IVUS) studies were performed to measure intimal hyperplasia cross-sectional area (CSA) and thickness. A general linear model with intraclass correlation was used to calculate the coefficient of correlation rho (rho = 1.0 indicates perfect correlation; rho = 0.0 indicates no correlation) of late loss, late loss index, intimal hyperplasia CSA, and intimal hyperplasia thickness. Multivariate analysis showed restenosis in the companion lesion (odds ratio 4.68, 95% confidence interval 1. 68-12.92, P = 0.003) and small minimal lumen diameter preintervention (odds ratio 0.28, 95% confidence interval 0.11-0.73, P = 0.009) to be predictors of restenosis. There was a weak correlation between multiple lesions within the same patient for late lumen loss rho = 0.28 (95% confidence interval 0.10-0.46, P < 0. 001) and late loss index. IVUS analysis demonstrated correlation of intimal hyperplasia CSA rho = 0.40 (95% confidence interval 0.06-0. 74, P = 0.009) and of intimal hyperplasia thickness. In conclusion, late loss and intimal hyperplasia demonstrate a correlation between multiple stented lesions within one patient. In addition to known lesion related factors, restenosis in a companion lesion is a predictor for restenosis. Cathet. Cardiovasc. Intervent. 51:266-272, 2000.

Aged↗
PubMed2000

Abciximab inhibits the migration and invasion potential of human coronary artery smooth muscle cells.

In the EPIC trial, high-risk patients received the integrin receptor antagonist abciximab v placebo during and for 12 h following percutaneous coronary intervention with a significant 23% decrease of repeat revascularisation at 6 months. However, EPILOG and CAPTURE trials could not confirm these promising long-term results. Recently presented data from the EPISTENT trial suggested a beneficial effect of abciximab on restenosis in patients with diabetes. Based on these divergent results the aim of this study was to test whether alpha v beta 3 receptor blockade by abciximab could cause inhibition of human coronary smooth muscle cell (hcSMC) proliferation, migration, and invasion which represent crucial steps during restenosis development. In contrast to quiescent hcSMCs, proliferating cells were capable to migrate towards chemoattractive stimuli and even capable to invade through a basement membrane equivalent. Abciximab and LM609, an alpha v beta 3 specific inhibiting antibody, caused only a modest dose-dependent inhibition of hcSMC proliferation. On the contrary, the chemotactic and invasive potential of hcSMCs was significantly inhibited by abciximab administration 24 h prior to and during migration. (IC(50)=33.0 microg/ml for chemotaxis and IC(50)=0.5 microg/ml for invasion). For LM609 similar results were obtained. Administration of the drugs just during migration without pretreatment inhibited migration equally but invasion to a lower extent (abciximab: IC(50)=32.6 microg/ml for chemotaxis and IC(50)=44.9 microg/ml for invasion; LM609 IC(50)=3.1 microg/ml for chemotaxis and IC(50)=2.0 microg/ml for invasion). The attachment to the extracellular matrix proteins collagen I, collagen IV, laminin and vitronectin was not influenced. Pretreatment for 24 h with abciximab or LM609 did not cause a downregulation of the alpha v beta 3-integrin receptor. The results of this study indicate that the alpha v beta 3 antagonist abciximab is a potent inhibitor of hcSMC migration and invasion which could explain the observed lower reintervention rate after PTCA and stent implantation.

Abciximab↗
PubMed2000

Evaluation of the SOFA score: a single-center experience of a medical intensive care unit in 303 consecutive patients with predominantly cardiovascular disorders. Sequential Organ Failure Assessment.

OBJECTIVE: To evaluate the use of the Sequential Organ Failure Assessment (SOFA) score, the total maximum SOFA (TMS) score, and a derived variable, the deltaSOFA (TMS score minus total SOFA score on day 1) in medical, cardiovascular patients as a means for describing the incidence and severity of organ dysfunction and the prognostic value regarding outcome. DESIGN: Prospective, clinical study. SETTING: Medical intensive care unit in a university hospital. PATIENTS: A total of 303 consecutive patients were included (216 men, 87 women; mean age 62 +/- 12.6 years; SAPS II 26.2 +/- 12.7). They were evaluated 24 h after admission and thereafter every 24 h until ICU discharge or death between November 1997 and March 1998. Readmissions and patients with an ICU stay shorter than 12 h were excluded. MAIN OUTCOME MEASURE: Survival status at hospital discharge, incidence of organ dysfunction/failure. INTERVENTIONS: Collection of clinical and demographic data and raw data for the computation of the SOFA score every 24 h until ICU discharge. MEASUREMENTS AND MAIN RESULTS: Length of ICU stay was 3.7 +/- 4.7 days. ICU mortality was 8.3% and hospital mortality 14.5%. Nonsurvivors had a higher total SOFA score on day 1 (5.9 +/- 3.7 vs. 1.9 +/- 2.3, p < 0.001) and thereafter until day 8. High SOFA scores for any organ system and increasing number of organ failures (SOFA score > or = 3) were associated with increased mortality. Cardiovascular and neurological systems (day 1) were related to outcome and cardiovascular and respiratory systems, and admission from another ICU to length of ICU stay. TMS score was higher in nonsurvivors (1.76 +/- 2.55 vs. 0.58 +/- 1.39, p < 0.01), and deltaSOFA/total SOFA on day 1 was independently related to outcome. The area under the receiver-operating characteristic curve was 0.86 for TMS, 0.82 for SOFA on day 1, and 0.77 for SAPS II. CONCLUSIONS: The SOFA, TMS, and deltaSOFA scores provide the clinician with important information on degree and progression of organ dysfunction in medical, cardiovascular patients. On day 1 both SOFA score and TMS score had a better prognostic value than SAPS II score. The model is closely related to outcome and identifies patients who are at increased risk for prolonged ICU stay.

Cardiovascular Diseases↗
PubMed2000

[Imaging techniques in cardiology: three-dimensional echocardiography].

UNLABELLED: Three-dimensional echocardiography offers new opportunities for clinical cardiology and the solution of scientific questions. Data acquisition is possible using different techniques: (1) Realtime 3D echocardiography with matrix-array transducers is the most promising approach, but is still limited by several difficulties; (2) 3D reconstruction is based on a number of sequentially acquired 2D image planes (like in multiplane TEE), which are put together afterwards. There are 2 ways of data analysis. 1. Morphological analysis. Surface rendering of the endocardial border can create perspectives not achievable with conventional methods such as the "en face" view of atrial septal defects or the atrial view of the mitral valve. Prolapsing leaflets and the spatial relationship can be identified much easier than using 2D methods. In complex congenital heart disease 3D echo may provide better spatial orientation and easier communication with the cardiothoracic surgeons. 2. Quantitative analysis of volumes, masses, and surfaces is only possible after manual contour tracing with several cut planes generated from the 3D data set. This procedure is time consuming and limits the use in clinical routine, even though validation studies demonstrated that 3D echo determination of masses and volumes is superior to one- or two-dimensional techniques which are based on geometric assumptions. Furthermore, quantitative 3D analysis has a unique pre- and postinterventional diagnostic potential. FUTURE PERSPECTIVES: Combination with color Doppler data may lead to a more precise quantitation of valve regurgitations. Improvements of hard- and software will allow faster acquisition, reconstruction, and quantitative analysis. Assessment of regional myocardial perfusion may be possible in combination with left heart contrast agents. CONCLUSION: 3D echocardiography allows perspectives not achievable conventionally and has a great potential for precise quantitative and reproducible analysis of cardiac morphology which overcomes the limitations of 2D echocardiography.

Angiography↗
PubMed2000

Three-dimensional reconstructions of normal and aneurysmatic left ventricles in vivo using transesophageal echocardiography.

OBJECTIVE: To perform three-dimensional surface reconstructions to provide spatial delineations of a normal and an aneurysmatic left ventricle, using transesophageal echocardiography. DESIGN: Prospective study. SETTING: University hospital. PARTICIPANTS: Eight patients in cardiogenic shock admitted to the intensive care unit and two patients undergoing surgery with general anesthesia. INTERVENTIONS: Using a multiplane transesophageal echocardiography probe, nine echocardiographic cross-sectional images of the heart at approximately 20 degrees angular increments were obtained from midesophageal level in each patient for three-dimensional surface reconstructions. Multiple determinations of cardiac output using the thermodilution principle were also made in each patient to verify the accuracy of three-dimensional data sets. MEASUREMENTS AND MAIN RESULTS: End-diastolic and end-systolic volumes were determined from three-dimensional data sets using the disc-summation method. Stroke volume was derived as the difference between end-diastolic and end-systolic volumes. Stroke volume was also calculated from thermodilution cardiac output measurements and heart rate. Correlation and limits of agreement between stroke volumes derived by the two methods were determined. Three-dimensional wire-frame models of a normal and an aneurysmatic left ventricle at end-systole were constructed from the nine echocardiographic cross-sectional images. Correlation coefficient between stroke volume derived from three-dimensional data sets using the disc-summation method and that measured by the thermodilution method was 0.91 (p < 0.001). Wire-frame models reveal a normal symmetric cavity and an aneurysmal cavity in sharp relief. CONCLUSIONS: Three-dimensional surface reconstruction can be performed from multiple cross-sectional images obtained using an unmodified commercially available multiplane transesophageal echocardiography probe, to reveal the left ventricular cavity in sharp relief. High correlation between stroke volume calculated from three-dimensional data sets and that measured by the thermodilution method attests to the accuracy of the three-dimensional data sets.

Adult↗
PubMed2000

MIC trial: metoprolol in patients with mild to moderate heart failure: effects on ventricular function and cardiopulmonary exercise testing.

UNLABELLED: Beta-blocker therapy results in a functional benefit in patients with heart failure (CHF) due to idiopathic dilated cardiomyopathy (DCM). This study assessed if similar effects were observed in patients with ischemic heart disease (CAD), NYHA II-III after 6 months of therapy with metoprolol. METHODS AND RESULTS: Fifty-two patients with CHF secondary to DCM (26 patients) and CAD (26 patients) and a left ventricular ejection fraction (EF)<40% were enrolled in the placebo-controlled study. The study medication was titrated over 6 weeks, the mean final dosage was 135 mg/day. Three patients died due to cardiogenic shock, two received placebo and one metoprolol. Eight patients did not complete the study due to non-compliance. Metoprolol significantly reduced heart rate at rest and after submaximal and maximal exercise. Vo(2)-max and Vo(2)-AT as well as the 6-min walk test improved significantly after metoprolol treatment. There was a significant increase in EF at rest (27.3-35. 2%), submaximal (28.5-37.7%) and maximal exercise (28.7-40.9%) in the metoprolol-treated patients. No differences were found between patients with CAD and DCM. We also observed reduced left ventricular volumes. CONCLUSION: The additional therapy with metoprolol improved cardiac function and the cardiopulmonary exercise capacity in patients with CHF.

Adrenergic beta-Antagonists↗
PubMed2000

A metabolic syndrome of hypertension, hyperinsulinaemia and hypercholesterolaemia in the New Zealand obese mouse.

BACKGROUND: New Zealand obese (NZO) mice exhibit a polygenic obesity associated with hyperinsulinaemia and hyperglycaemia. Here we show that the strain presents additional features of a metabolic syndrome, i.e. elevated blood pressure, serum cholesterol and serum triglyceride levels. MATERIALS AND METHODS: A back-cross model of NZO mice with the lean Swiss Jackson Laboratory (SJL) strain was established in order to investigate further the correlation between hypertension, obesity, serum insulin and hyperglycaemia. RESULTS: Systolic blood pressure was significantly elevated at 6 weeks of age and appeared to parallel the weight gain of the animals. Serum insulin levels, presumably reflecting insulin resistance, and systolic blood pressure values were significantly correlated with the body mass index (r2 = 0.707 and 0.486, respectively) in the back-cross mice. In contrast, blood pressure was only weakly correlated with serum insulin (r2 = 0.288) in non-diabetic mice, and was independent of serum insulin levels in diabetic animals. CONCLUSION: The data are consistent with the concept that hypertension and insulin resistance are a characteristic consequence of the genetic constellation leading to obesity in the NZO strain, and that these traits reflect related mechanisms. It appears unlikely, however, that hypertension is a direct consequence of hyperinsulinaemia.

Animals↗