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Biomedical subjects

Peter Hanrath

Publications and source records attributed to Peter Hanrath.

At least 109 records · Page 6Linked to original sources
PubMed2002

Strain rate measurement by doppler echocardiography allows improved assessment of myocardial viability inpatients with depressed left ventricular function.

OBJECTIVES: This study sought to evaluate whether objective assessment of the myocardial functional reserve, using strain rate imaging (SRI), allows accurate detection of viable myocardium. BACKGROUND: Strain rate imaging is a new echocardiographic modality that allows quantitative assessment of segmental myocardial contractility. METHODS: In 37 patients (age 58 +/- 9 years) with ischemic left ventricular dysfunction, myocardial viability was assessed using low-dose (10 microg/kg body weight per min) two-dimensional dobutamine stress echocardiography (DSE), tissue Doppler imaging, SRI and (18)F-fluorodeoxyglucose ((18)FDG) positron emission tomography (PET). The peak systolic tissue Doppler velocity and peak systolic myocardial strain rate were determined at baseline and during low-dose dobutamine stress from the apical views. RESULTS: A total of 192 segments with dyssynergy at rest were classified by (18)FDG PET as viable in 94 and nonviable in 98. An increase of peak systolic strain rate from rest to dobutamine stimulation by more than -0.23 1/s allowed accurate discrimination of viable from nonviable myocardium, as determined by (18)FDG PET with a sensitivity of 83% and a specificity of 84%. Receiver operating characteristic (ROC) curve analysis showed an area under the curve for prediction of nonviable myocardium, as determined by (18)FDG PET using SRI, of 0.89 (95% confidence interval [CI] 0.88 to 0.90), whereas the area under the ROC curve using tissue Doppler imaging was 0.63 (95% CI 0.61 to 0.65). CONCLUSIONS: The increase in the peak systolic strain rate during low-dose dobutamine stimulation allows accurate discrimination between different myocardial viability states. Strain rate imaging is superior to two-dimensional DSE and tissue Doppler imaging for the assessment of myocardial viability.

Aged↗
PubMed2002

Expression patterns of integrins on quiescent and invasive smooth muscle cells and impact on cell locomotion.

Migration and invasion of human arterial smooth muscle cells (haSMCs) are essential steps during the development of atherosclerosis, restenosis, and transplant vasculopathy. The molecular mechanisms leading to these processes are only incompletely understood. Due to their contact to the surrounding extracellular matrix, integrins have been shown to be essentially involved in cell locomotion. Therefore, the function of integrins during this process was analyzed in an in vitro model which was based on the defined quiescent and invasive phenotypes of human haSMCs induced by cell culture conditions. Flow-cytometric analysis of integrin expression between both phenotypes showed a strong upregulation of alpha 5 beta 1 (13.1x) and a modest upregulation of alpha vs beta 3 (3.4x) and alpha IIb (3.0x) in invasive haSMCs in comparison to quiescent ones. Other integrins analyzed (alpha 2, alpha 3, alpha 4, beta 1) did not show differential regulation. Functional inhibition of alpha 5 beta 1 reduced cell migration (-29%+/-8), invasion (-49%+/-16), collagen contraction (-125%), and attachment to fibronectin. Although, there was a clear discrepancy between alpha 5 beta 1 and alpha vs beta 3 expression levels, inhibition of alpha vs beta 3 (-45%+/-9) reduced haSMC invasion equally. Interestingly, alpha vs beta 3 unlike alpha 5 beta 1 blockade caused a significant stimulation of collagen contraction (+52% vs 154%) with possible implications on vascular remodeling. In conclusion, alpha 5 beta 1 blockade or combined alpha 5 beta 1/alpha v beta 3 blockade by specific antibodies or selective RGD peptides together with local drug delivery strategies could be a promising strategy for the therapy of restenotic lesions or atheromatous plaques.

Antibodies, Monoclonal↗
PubMed2002

Thromboembolic complications after Fontan procedures: comparison of different therapeutic approaches.

BACKGROUND: Although patients after Fontan procedure have a high incidence of thromboembolic complications, anticoagulant therapy is not handled uniformly. We analyzed the frequency and clinical relevance of thromboembolism after Fontan procedure and compared different therapeutic approaches. METHODS: From 1986 to 1998, 101 patients (mean age, 7.3 +/- 8.1 years) underwent Fontan type procedure (modified Fontan, n = 40; total cavopulmonary connection, n = 61). In 85 of 87 survivors, transthoracic echocardiography was performed; and in 31 transesophageal echocardiography and/or angiography was performed. Mean follow-up was 5.7 +/- 3.5 years. Three groups with different anticoagulant regimen were compared: group I without medication (n = 45), group II with acetylsalicylic acid therapy (n = 14) and group III with Coumadin (n = 26). RESULTS: Thromboembolic events occurred in 13 of 85 patients (15.3%; 3.3 events/100 patient-years). Type of operation as well as other known risk factors had no influence on the rate of thromboembolism. Within the first postoperative year, seven of 13 events occurred. A second peak developed beyond 10 years of follow-up. Patients benefit significantly from Coumadin compared with those who did not receive any medication, with similar results in the entire population and the subgroup of patients with total cavopulmonary connection (log-rank, p = 0.031 and p = 0.033, respectively). With 4.2 events/100 patient-years, the cumulative event rate was substantially higher in group I than with 1.6 in group II and with 1.1 in group III. No relevant bleeding complications occurred. CONCLUSIONS: Thromboembolism is frequent after Fontan procedure with a peak during the first postoperative year and another peak beyond 10 years of follow-up. Coumadin is the most effective prophylactic therapy in preventing thromboembolism. Therefore, we suggest initial oral anticoagulation therapy in patients with Fontan type operation.

Anticoagulants↗
PubMed2002

Atrial fibrillation-induced atrial contractile dysfunction: a tachycardiomyopathy of a different sort.

OBJECTIVE: Although AF-induced atrial contractile dysfunction has significant clinical implications the underlying intracellular mechanisms are poorly understood. METHODS: From the right atrial appendages of 59 consecutive patients undergoing mitral valve surgery (31 in SR, 28 in chronic AF) thin muscle preparations (diameter<0.7 mm) were isolated. Isometric force of contraction was measured in the presence of different concentrations of Ca(2+) and isoprenaline. To assess the function of the sarcoplasmic reticulum, the force-frequency relationship and the post-rest potentiation were studied. The myocardial density of the ryanodine-sensitive calcium release channel (CRC) of the sarcoplasmic reticulum was determined by [3H]ryanodine binding. Myocardial content of SR-Ca(2+)-ATPase (SERCA), phospholamban (Plb), calsequestrin (Cals) and the Na(+)/Ca(2+)-exchanger (NCX) were analyzed by Western blot analysis. Adenylyl cyclase activity was measured with a radiolabeled bioassay using [32P]ATP as a tracer. RESULTS: In 72 muscle preparations of SR patients contractile force was 10.9+/-1.8 mN/mm(2) compared to 3.3+/-0.9 mN/mm(2) (n=48, P<0.01) in AF patients. The positive inotropic effect of isoprenaline was diminished but the stimulatory effect on relaxation and the adenylyl cyclase were not altered in AF patients. The force-frequency relation and the post-rest potentiation were enhanced in atrial myocardium of AF patients. The protein levels of CRC, SERCA, Plb, and Cals were not different between the two groups. In contrast, the Na(+)/Ca(2+)-exchanger was upregulated by 67% in atria of AF patients. CONCLUSIONS: AF-induced atrial contractile dysfunction is not due to beta-adrenergic desensitization or dysfunction of the sarcoplasmic reticulum and thus is based on different cellular mechanisms than a ventricular tachycardia-induced cardiomyopathy. Instead, downregulation or altered function of the L-type Ca(2+)-channel and an increased Ca(2+) extrusion via the Na(+)/Ca(2+)-exchanger seem to be responsible for the depressed contractility in remodeled atria.

Adenylyl Cyclases↗
PubMed2002

Upregulation of the cytoskeletal-associated protein Moesin in the neointima of coronary arteries after balloon angioplasty: a new marker of smooth muscle cell migration?

Migrating cells like coronary smooth muscle cells in restenosis change their cell shape and form cellular protrusions called filopodia. A prerequisite for filopodia formation is the rearrangement of the actin cytoskeleton. An essential role of the 78-kDa protein Moesin is described for Rho- and Rac-dependent assembly of actin filaments. In vivo Moesin is not observed in mature smooth muscle cells. The objective of this study was to demonstrate that Moesin is upregulated in migrating coronary smooth muscle cells during restenosis development. In vivo expression of Moesin was upregulated in neointimal coronary smooth muscle cells of dilated porcine coronary arteries compared to the undilated left circumflex coronary artery of the same swine. Concordant to these results Moesin expression was upregulated in migrating and invading human arterial smooth muscle cells in vitro analyzed by FACS, Western blotting and RT-PCR. In addition, the invasive potential of Moesin-positive Mel Im cells transfected with Moesin sense DNA increased by 28% as compared to mock-transfected control, whereas antisense transfected cells had a decreased invasive potential of 32%. Transfection of Moesin-negative HepG2 with Moesin sense cDNA increased the invasive potential by 43%. Finally, transfection of human arterial smooth muscle cells with Moesin sense cDNA caused an increased invasive potential of 30%. Transfection of haSMCs with antisense cDNA decreased the invasive potential by 37% in comparison to mock-transfected control. These results demonstrate for the first time an upregulation of Moesin expression in coronary smooth muscle cells of the neointima after arterial injury. The increased migrative and invasive potential of cells transfected with Moesin confirmed the functional role of Moesin in cell migration. This indicates an important role of Moesin during restenosis development.

Actins↗
PubMed2002

Analysis of several hundred genetic polymorphisms may improve assessment of the individual genetic burden for coronary artery disease.

BACKGROUND: Single polymorphisms of different genes have been associated with coronary artery disease (CAD). The aim of this study was to evaluate the benefit of analyzing multiple genetic polymorphisms as a compound unit to assess the individual genetic burden for CAD. METHODS AND RESULTS: The study population consisted of 100 case patients with, and 100 control patients without, angiographically proven CAD. The patients were matched for age, sex, and numbers of standard cardiac risk factors. Sixteen different genetic polymorphisms were analyzed using polymerase chain reaction-based technologies. None of these polymorphisms showed a significant difference in the allele frequency between case and control patients. Eight genes with a higher allele frequency in the case group (delta allele frequency >0.05) were defined as risk alleles (RA) and subsequently tested as a compound unit. A risk stratification for 64.5% of all patients was possible when eight genes with their 16 RA were included in the analysis. With more than eight RA per individual, the odds ratio for developing CAD was 3.21 (95% CI 1.77-5.82, P<0.001). However, there was still an overlap in the number of RA in case and control patients. A computer simulation estimated that more than 200 polymorphisms were needed for a reasonable genetic discrimination for patients at risk for CAD. CONCLUSIONS: An increasing number of risk alleles are associated with an elevated risk for CAD. An analysis of multiple polymorphisms, some several hundred, each with a small impact, may allow improved assessment of the individual genetic burden for CAD. Larger studies are needed to prove this hypothesis.

Journal Article↗
PubMed2002

Rationale and design of the carvedilol or metoprolol European trial in patients with chronic heart failure: COMET.

In large clinical trials both carvedilol and metoprolol have been shown to reduce mortality and morbidity in patients with chronic heart failure. Carvedilol is an adrenoceptor antagonist, which inhibits beta(1)-, beta(2)-, and alpha(1)-adrenergic receptors. Carvedilol has additional metabolic and antioxidant properties. Metoprolol is a selective antagonist of beta(1)-adrenergic receptors. The carvedilol or metoprolol European trial (COMET) is the first study to investigate whether beta-blocking agents with differing pharmacological profiles exert different effects on morbidity and mortality in patients with chronic heart failure. 3029 patients from 15 different European countries were enrolled into COMET and will be followed until 1020 fatal events have been observed, unless the data and safety monitoring committee (DSMC) recommends early termination. The target dose for carvedilol is 25 mg bid and for metoprolol tartrate 50 mg bid. This manuscript outlines the rationale, design and possible outcomes of COMET.

Adrenergic beta-Antagonists↗
PubMed2002

Preserved parasympathetic cardiac innervation after atrioventricular node modification: evidence from circle maps of respiratory sinus arrhythmia.

INTRODUCTION: Respiratory sinus arrhythmia (RSA) and heart rate variability (HRV) are parameters of autonomic cardiac innervation. They decrease with age and after atrioventricular nodal modification (AVNM) suggesting vagal denervation in both situations. We hypothesized, however, that AVNM causes only a transient, functional decline in vagal activity, whereas aging causes permanent vagal denervation. A new method of analyzing RSA phase dynamics based on circle maps (CM) can potentially differentiate between both forms of reduced vagal activity. METHODS: In 18 younger and 14 older healthy control subjects 24-hour Holter ECGs were recorded for HRV analysis. Repeated measurements of RSA were acquired during paced breathing (PB). In 16 consecutive patients undergoing AVNM the same measurements were applied before, 1 day and 3 months after the procedure. CM were calculated from consecutive RR intervals and the similarity between different CM quantified by the Kullback information gain (KIG). RESULTS: HRV analysis revealed lower HF bands, LF bands and RSA amplitudes in older vs. younger control subjects. KIG revealed less similarity between younger and older control subjects than within the respective age groups. After AVNM a decrease in HF bands was noted in HRV analysis. Three months after AVNM, HF bands returned to pre-ablation values. CM obtained before and 1 day after AVNM displayed comparable similarity to CM acquired 1 day before and 3 months after ablation. CONCLUSIONS: In contrast to conventional HRV parameters, CM of RSA are not altered by ablation in the posteroseptal space but by aging. Thus, this new method appears to differentiate between transient autonomic modification and chronic denervation.

Adult↗
PubMed2002

Temporary disturbances of the QT interval precede the onset of ventricular tachyarrhythmias in patients with structural heart diseases.

An increase in sinus rate prior to ventricular tachyarrhythmias has been demonstrated in previous studies. There is no clear data available concerning changes in ventricular de- and repolarization prior to ventricular tachyarrhythmias, especially in patients with structural heart disease. Therefore, the aim of this study was to analyze the QT and QTc interval (Bazett's formula immediately before the onset of ventricular tachyarrhythmias in stored electrograms of patients with ICDs. The study analyzed 228 spontaneous ventricular tachyarrhythmia episodes in 52 patients (mean age 64 +/- 10 years, 49 men, 3 women) and compared them with 146 electrograms of baseline rhythm recorded during regular ICD follow-up. Mean ventricular cycle length (CL), QT interval, and QTc were measured before the onset of ventricular tachyarrhythmia and during baseline rhythm. Prior to ventricular tachyarrhythmias onset, CL was significantly shorter than during baseline rhythm (714 +/- 139 vs 828 +/- 149 ms, P < 0.0001). By contrast, the QT interval (430 +/- 67 ms) and QTc interval (518 +/- 67 ms) were significantly prolonged before the onset of ventricular tachyarrhythmias as compared to baseline rhythm (QT 406 +/- 67 ms, QTc 450 +/- 61 ms; P < 0.0001). CL, QT, and QTc changes were independent of concomitant treatment with antiarrhythmic drugs. Ventricular tachyarrhythmias are preceded by a significant prolongation of the QT and QTc intervals. This phenomenon may represent a greater than normal disparity of repolarization recovery times possibly facilitating the development of ventricular tachyarrhythmias.

Cardiomyopathies↗
PubMed2002

Intravenous myocardial contrast echocardiography predicts left ventricular remodeling in patients with acute myocardial infarction.

BACKGROUND: This study evaluated the ability of intravenous myocardial contrast echocardiography (MCE) performed in the setting of acute myocardial infarction for prediction of left ventricular (LV) remodeling. METHODS: Intravenous MCE was performed immediately before, 1 hour, and 24 hours after primary percutaneous transluminal coronary angioplasty (PTCA) in 35 patients with a first myocardial infarction. The MCE was used to define the relative perfusion defect size (in %; relMCD). Two-dimensional echocardiography was performed directly after angioplasty and after 4 weeks to determine LV end-diastolic volumes (LVEDV). The increase in LVEDV at 4 weeks defined a remodeling (> 15% increase) and a nonremodeling group (< or = 15% increase). RESULTS: Patients with remodeling had larger relMCD before (22.0 +/- 16.1 vs 8.0 +/- 11.9, P =.015), 1 hour (20.0 +/- 13.0 vs 4.9 +/- 11.6, P =.001), and 24 hours after PTCA (22.9 +/- 14.1 vs 1.2 +/- 2.8, P <.001). There was a significant correlation between relMCD 24 hours after PTCA and the increase in LVEDV at 4 weeks (r = 0.648; P <.001). Receiver operating characteristic (ROC) curve analysis revealed a relMCD at 24 hours of 5.1% or more to predict remodeling with a sensitivity of 94% and a specificity of 87% (area under ROC curve = 0.917; SE = 0.054). Multivariate analysis demonstrated relMCD at 24 hours to be the only predictor of remodeling (odds ratio = 173.4; P =.022). CONCLUSION: The size of the persistent MCE perfusion defect after revascularization for acute myocardial infarction has a high predictive value for LV remodeling during a 4-week follow-up period.

Aged↗
PubMed2002

Xenon does not impair the responsiveness of cardiac muscle bundles to positive inotropic and chronotropic stimulation.

BACKGROUND: Most volatile anesthetics exhibit a direct myocardial depressant effect. This side effect often limits their applicability in patients with impaired cardiac function. Xenon is a new gaseous anesthetic that did not show any adverse cardiovascular effects in clinical and experimental studies. The authors tested the hypothesis that xenon does not affect myocardial contractility or the positive inotropic effect of isoproterenol, calcium, and increase in pacing rate in isolated guinea pig ventricular muscle bundles. METHODS: Thin ventricular muscle bundles from guinea pig hearts with a mean diameter of 0.4-0.45 mm were prepared under stereomicroscopic control. Force of contraction and contraction times were studied in muscles superfused with medium equilibrated with either 65% xenon and 35% oxygen (xenon group), 1.2% isoflurane in oxygen (isoflurane group), or 65% nitrogen and 35% oxygen (control group). In addition, the positive inotropic effects of calcium, isoproterenol (10(-10)-3 x 10(-8) M) and increasing frequency (0.5-2 Hz) were studied during xenon and isoflurane exposure. RESULTS: In contrast to isoflurane, xenon did not alter myocardial force of contraction or contraction times. The positive inotropic effect of isoproterenol, calcium, and increasing pacing frequencies did not differ between the muscles exposed to xenon and the control group. Isoflurane elicited the expected negative inotropic effect (30% reduction of force of contraction) but did not impair the response to inotropic stimuli. CONCLUSIONS: Xenon does not alter myocardial contractility and the response to inotropic stimuli such as calcium, isoproterenol, or increase in pacing frequency in isolated guinea pig ventricular muscle bundles.

Adrenergic beta-Agonists↗
PubMed2002

Decrease of vascular smooth muscle cell locomotion by abciximab, but not tirofiban: a possible role of different affinity to alpha v beta 3 integrins.

AIM: The EPISTENT and EPIC studies demonstrated a reduction of clinically driven re-interventions after percutaneous transluminal coronary angioplasty (PTCA) and stent implantation in patients treated with abciximab, while for tirofiban no similar effects could be demonstrated. This may be explained by the different effects on the migratory and invasive potential of vascular smooth muscle cells (VSMCs) by integrin alpha v beta 3 blockade. Therefore, the objective of this study was to compare the effectiveness of abciximab and tirofiban to affect VSMC migration and invasion. METHODS: Vascular smooth muscle cells were treated with abciximab (0.1-1 microg/ml), tirofiban (0.1-1 microg/ml), and the alpha v beta 3 specific antibody LM609 (1-5 microg/ml), that was used as a positive control during the assay (treatment) over 24 h before the assay (pre-treatment), or before and during the assay (combined treatment). Sodium 3'-[1-(phenylaminocarbonyl)-3,4-tetrazolium]-bis (4-methoxyy-6-nitro) benzene sulfonic acid (XTT)-assay and cell counting measured the influence of the substances on VSMC proliferation. Using a Boyden Chamber model, the capability of VSMCs for migration and invasion was tested with different chemo-attractants and barriers. RESULTS: Any influence of the platelet glycoprotein (GP) IIb/IIIa receptor (integrin alpha IIb beta 3) antagonists on VSMC proliferation could be excluded. After combined treatment, abciximab demonstrated a dose-dependent inhibition of migration (IC50 = 33 microg/ml) and invasion (IC50 = 0.5 microg/ml) of VSMCs. Administration during the assay without pre-treatment inhibited migration similarly (IC50 = 32 microg/ml) but invasion to a significant lower extent (IC50 = 44 microg/ml). Administration of tirofiban during the assay with or without pre-treatment had no inhibitory effect on VSMC migration and invasion. Pre-treatment alone with one of the substances also did not alter VSMC migration or invasion. CONCLUSION: Abciximab administration in physiological concentrations was capable of significantly inhibiting the migratory and invasive potential of VSMCs, while for tirofiban no similar effect could be demonstrated.

Abciximab↗
PubMed2002

Intravascular ultrasound evaluating coronary stents for patients with coronary artery disease: compared old with new multilink stents.

OBJECTIVE: It was suggested that coronary stent design and coating may affect stent performance and hence induce varying degrees of thrombogenesis and neointimal hyperplasia. The purpose of this study is to compare the 6-month follow-up results between old and new Multilink stents with the method of intravascular ultrasound (IVUS) imaging. METHODS: We have performed old (n = 40) and new (n = 35) Multilink stent implantations on 75 patients with coronary artery disease. Coronary angiography was performed before, immediately after, and 6 months after the in-stent procedure respectively. Six-month follow-up IVUS imaging was performed and analyzed off-line. RESULTS: Minimal lumen cross sectional area (CSA) of new Multilink stents was significantly larger than that of old Multilink stents (P = 0.0053). Mean stent lumen area of new Multilink stents was significantly larger than that of old Multilink stents (P = 0.040). Similarly, minimal lumen diameter (MLD) of new Multilink stents was larger than that of old Multilink stents (P = 0.011). Old Multilink stents had a higher percentage of plaque area than new Multilink stents. CONCLUSION: The new Multilink stent is obviously superior to old Multilink stents, in particular, in the stent MLD and lumen CSA--major determinants of the restenosis.

Adult↗
PubMed1998

Clinical Determinations of Volumes of Normal and Aneurysmatic Left Ventricles by Three-Dimensional Transesophageal Echocardiography.

Biplane methods of determining left ventricular volumes are inaccurate in the presence of aneurysmal distortions. Multiplane transesophageal echocardiography, which provides multiple, unobstructed cross-sectional views of the heart from a single, stable position, has the potential for more accurate determinations of volumes of irregular cavity forms than the biplane methods. The aim of the study was to determine the feasibility of three-dimensional measurements of ventricular volumes in patients with normal and aneurysmatic left ventricles by using multiplane transesophageal echocardiography. With the echotransducer in the mid-esophageal (transesophageal) position, nine echo cross-sectional images of the left ventricle in approximately 20 degrees angular increments were obtained from each of 29 patients with coronary artery disease who had undergone biplane ventriculography during diagnostic cardiac catheterization. In 17 of these 29 patients, echo cross-sectional images of the left ventricle with the echotransducer in transgastric position were also obtained. End-diastolic volume, end-systolic volume, and ejection fraction were determined from multiplane transesophageal echocardiographic images and biplane ventriculographic images by the disc-summation method and compared with each other. In another ten patients with indwelling pulmonary artery catheters, stroke volumes calculated from multiplane transesophageal echocardiographic images were compared with those derived from thermodilution cardiac output measurements. Correlations between biplane ventriculographic and multiplane transesophageal echocardiographic measurements were higher in the ten patients with normal ventricular shape [for end-diastolic volumes, r = 0.91, SEE = 19 ml; for end-systolic volumes, r = 0.98, SEE = 9.3 ml; for ejection fractions (EFs), r = 0.91, SEE = 5.4%] than in the 19 patients with ventricular aneurysms (for end-diastolic volumes, r = 0.61, SEE = 31.5 ml; for end-systolic volumes, r = 0.66, SEE = 32.5 ml; for EFs, r = 0.79, SEE = 8%). Correlations between echocardiographic volumes from the transesophageal and transgastric transducer positions were high independent of left ventricular geometry (for end-diastolic volumes, r = 0.84, SEE = 13.1 ml; for end-systolic volumes, r = 0.98, SEE = 9.6 ml; for EFs, r = 0.97, SEE = 3.4%). In 12 observations (4 normal and 8 aneurysmal) from the ten patients with indwelling pulmonary artery catheters, correlation between stroke volumes determined from thermodilution cardiac output measurements and those derived from multiplane transesophageal echocardiographic images was high (r = 0.91, SEE = 6 ml). The results indicate that three-dimensional measurements of volumes of irregular and distorted left ventricles are feasible with multiplane transesophageal echocardiography. This method may be more accurate than biplane methods, especially in the presence of left ventricular aneurysms.

Journal Article↗
PubMed1997

Quantitative Stress Echocardiography in Chronic Aortic and Mitral Regurgitation.

It was the purpose of the present study to prove the feasibility and reliability of quantitative stress-echocardiography as an alternative method to radionuclide angiography (RNA) in chronic regurgitant valvular lesions. Echocardiography and RNA are most commonly used to obtain various left ventricular (LV) morphometric and functional parameters that have been postulated to predict long-term prognosis in patients with aortic and mitral valvular regurgitation. Supine bicycle ergometry with a workload ranging from 25-250 Watts was used to evaluate stress dependent LV volumes and ejection fractions (EFs) in patients with pure aortic (n = 18) and mitral regurgitation (n = 14). Most patients (23/32) underwent simultaneous right heart catheterization. Echocardiographic EFs were validated by RNA with good correlations (r = 0.81, P < 0.01). Patients with aortic regurgitation and functional class I/II (9), had a significant increase in EF during exercise (60%-67%, P < 0.001) and a reduction in end-systolic volume (71-52 mL, P < 0.01). In comparison, patients with class III symptoms (9), had a drop in EF (53%-49%, P < 0.01), had larger baseline end-systolic volume (104 mL, P = NS), which did not decrease during stress (104 vs 107 mL, P = NS). In patients with chronic mitral regurgitation baseline and exercise EF did not differ between class I/II (6) and class III (8), however, mildly symptomatic patients increased from 57%-67%, (P < 0.01) versus patients in class III (65% vs 69%, P = NS). Stroke volume index was not different at baseline (44 vs 33 mL/m(2), P = NS); however, there were significant differences during exercise (70 vs 41 mL/m(2), P = 0.05). Quantitative stress-echocardiography is a noninvasive and safe alternative method to RNA, which allows reliable calculation of stress dependent LV volumes and EF. Determination of end-systolic volumes may be of additional prognostic value. The combination of a high baseline EF and low stroke volume index with the inability to improve during exercise might reflect early stages of impaired LV function in patients with severe mitral regurgitation.

Journal Article↗
PubMedDate not supplied

Mechanisms of myocardial hypoperfusion during rotational atherectomy of de novo coronary artery lesions and stenosed coronary stents: insights from serial myocardial scintigraphy.

BACKGROUND: Rotational atherectomy (rotablation) frequently results in transient myocardial hypoperfusion due to peripheral vessel obstruction. This study compares the incidence, extent, and severity of perfusion defects induced by rotablation of de novo coronary lesions with rotablation of in-stent restenosis. METHODS AND RESULTS: Twenty-five patients undergoing rotablation for restenosed stents (group A) were studied by technetium 99m sestamibi single photon emission computed scintigraphy at rest before rotablation, during rotablation, and 2 days after the procedure. For semiquantitative analysis, perfusion in 24 left ventricular regions was expressed as percentage of maximal sestamibi uptake. The results were compared with those of 25 patients treated for de novo coronary lesions (group B). Transient perfusion defects were observed in 22 (88%) of 25 patients in group A and, similarly, in 23 (92%) of 25 in group B. Perfusion was significantly reduced during rotablation in 3.1 +/- 2.6 (mean +/- SD) regions in group A and in 3.3 +/- 2.5 regions in group B. Perfusion in the region with maximal reduction during rotablation in groups A and B was 77% +/- 13% and 76% +/- 15% at baseline. Technetium uptake decreased to 59% +/- 19% and 54% +/- 14% during rotablation (P <.001 vs baseline, P = not significant for A vs B) and returned to 76% +/- 16% and 76% +/- 15% after rotablation. Intravascular ultrasonography indicated no correlation between the volume of ablated plaque and the extent and severity of perfusion defects in in-stent restenosis. CONCLUSIONS: Incidence, extent, and severity of rotablation-related transient hypoperfusion are influenced by neither the type nor the quantity of ablated plaque material. Thus embolization of ablated plaque may be less important compared with other factors such as microcavitation or platelet aggregation.

Atherectomy, Coronary↗
PubMedDate not supplied

Transplantation of fetal cardiomyocytes into infarcted rat hearts results in long-term functional improvement.

Studies have demonstrated the feasibility of transplanting cardiomyocytes after myocardial infarction (MI). However, persistence and effects on left ventricular (LV) function have not been elucidated in long-term studies. Ventricular fetal cardiomyocytes from embryos of both sexes were injected into marginal regions of MI 4 weeks after suture occlusion of the left anterior descending artery in adult female rats. Two and 6 months after transplantation (Tx), engrafted cells were traced by immunohistochemical in situ hybridization for Y chromosomes or bromodeoxyuridine (BrdU) staining, LV dimensions and function were assessed by echocardiography, and LV pressure was assessed ex vivo in a Langendorff perfusion system. Immunohistochemistry for alpha-sarcomeric actin and Y chromosomes revealed the presence of transplanted cells in infarcted host myocardium at both 2 and 6 months. End-diastolic LV diameter markedly decreased after Tx and fractional shortening gradually increased after Tx (31.3 +/- 4.5% before Tx, 45.4 +/- 4.2% at 6 months; p<0.005). Wall area fraction and MI size were unaffected by Tx. In hearts with MI, but not in normal hearts, Tx led to the development of higher pressures (87 +/- 18 versus 38 +/- 8 mmHg, 6 months post-Tx versus nontreated). After catecholamine stimulation, both infarcted and normal hearts developed higher pressures after Tx (p<0.005), ultimately associated with reduced mortality after Tx versus nontreated. Transplanted cardiomyocyte-rich graft cells persist in host myocardium and mediate continuous improvement of LV function and survival in a rat model of MI even during long-term follow-up, possibly involving a catecholamine-sensitive mechanism.

Animals↗