Rainer Hoffmann

Three-dimensional echocardiographic determination of left ventricular volumes and function by multiplane transesophageal transducer: dynamic in vitro validation and in vivo comparison with angiography and thermodilution

The goal of this study was to validate 3-dimensional echocardiography by multiplane transesophageal transducer for the determination of left ventricular volumes and ejection fraction in an in vitro experiment and to compare the method in vivo with biplane angiography and the continuous thermodilution method. In the dynamic in vitro experiment, we scanned rubber balloons in a water tank by using a pulsatile flow model. Twenty-nine measurements of volumes and ejection fractions were performed at increasing heart rates. Three-dimensional echocardiography showed a very high accuracy for volume measurements and ejection fraction calculation (correlation coefficient, standard error of estimate, and mean difference for end-diastolic volume 0.998, 2.3 mL, and 0.1 mL; for end-systolic volume 0.996, 2.7 mL, and 0.5 mL; and for ejection fraction 0.995, 1.0%, and -0.4%, respectively). However, with increasing heart rate there was progressive underestimation of ejection fraction calculation (percent error for heart rate below and above 100 bpm 0.59% and -8.6%, P < .001). In the in vivo study, left ventricular volumes and ejection fraction of 24 patients with symmetric and distorted left ventricular shape were compared with angiography results. There was good agreement for the subgroup of patients with normal left ventricular shape (mean difference +/-95% confidence interval for end-diastolic volume 5.2+/-6.7 mL, P < .05; for end-systolic volume -0.5+/-8.4 mL, P = not significant; for ejection fraction 2.4%+/-7.2%, P = not significant) and significantly more variability in the patients with left ventricular aneurysms (end-diastolic volume 23.1+/-56.4 mL, P < .01; end-systolic volume 5.6+/-41.0 mL, P = not significant; ejection fraction 4.9%+/-16.0%, P < .05). Additionally, in 20 critically ill, ventilated patients, stroke volume and cardiac output measurements were compared with measurement from continuous thermodilution. Stroke volume as well as cardiac output correlated well to thermodilution (r = 0.89 and 0.84, respectively, P < .001), although both parameters were significantly underestimated by 3-dimensional echocardiography (mean difference +/-95% confidence interval = -6.4+/-16.0 mL and -0.6+/-1.6 L/min, respectively, P < .005).

Treatment of functional mitral valve regurgitation with the permanent percutaneous transvenous mitral annuloplasty system: Results of the multicenter international Percutaneous Transvenous Mitral Annuloplasty System to Reduce Mitral Valve Regurgitation in Patients with Heart Failure trial

OBJECTIVES PTOLEMY-2 was a prospective multicenter phase I single-arm feasibility trial to evaluate the second-generation permanent percutaneous transvenous mitral annuloplasty (PTMA) device in reducing functional mitral regurgitation (MR). BACKGROUND Percutaneous MR reduction has been performed through a direct method of clipping and securing the mitral leaflets together or an indirect approach of reducing mitral annular dimension via the coronary sinus. The PTMA device is the only coronary sinus mitral repair device without a static fixation element. METHODS Patients with at least moderate functional MR, New York Heart Association functional class II to IV, and left ventricular ejection fraction of 20% to 50% were enrolled at 14 centers in 5 countries. Device effects on patients were assessed by serial echocardiography, quality of life (QOL), and exercise capacity metrics. RESULTS A total of 43 patients were recruited, and 30 patients (70%) were implanted with a permanent PTMA device with a mean follow-up of 5.8 ± 3.8 months. The primary safety end point (freedom from death, myocardial infarction, stroke, or emergency surgery) at 30 days was met in 28 patients, whereas 2 patients died of device-related complications. The primary efficacy end point (MR reduction of at least 1.0 grade or reduction of regurgitant orifice area by 0.1 cm(2) or regurgitant volume by 15 mL or regurgitant fraction by 10% compared with baseline) was obtained in 13 patients. No significant changes were noted in MR parameters, ventricular volumes, or QOL. Distance walked on 6 minutes testing at 6-month follow-up increased from 331 ± 167 m to 417 ± 132 m (P = .65). Compared with nonresponders, responders had a higher baseline regurgitant orifice area >0.2 cm(2) (P = .001) and less prior history of myocardial infarction (P = .02), coronary artery bypass surgery (P = .03), and ischemic MR (P = .04). CONCLUSIONS Overall, PTMA had mild impact on MR reduction, left ventricular remodeling, QOL, and exercise capacity. During follow-up, the risk/benefit ratio remained suboptimal.

Comparison of Two- and Three-Dimensional Unenhanced and Contrast-Enhanced Echocardiographies Versus Cineventriculography Versus Cardiac Magnetic Resonance for Determination of Left Ventricular Function

Contrast enhancement has been shown to improve detection of regional wall motion abnormalities (RWMA) in 2-dimensional (2D) echocardiography. This study determined the use of contrast enhancement in the setting of 3-dimensional (3D) echocardiography for definition of left ventricular RWMA compared with 2D echocardiography, cineventriculography, and cardiac magnetic resonance (CMR). In 63 patients, unenhanced and contrast-enhanced (SonoVue; Bracco Imaging S.p.A., Milan, Italy) 2D and 3D echocardiographies, CMR, and cineventriculography were performed. Hypokinesia in ≥1 segment defined the presence of RWMA. Interreader agreement (IRA) between 2 blinded off-site readers on presence of RWMA was determined within each imaging technique. Intermethod agreement among imaging techniques was analyzed. A standard of truth for the presence of RWMA was obtained by an independent expert panel decision. IRA on presence of RWMA expressed as Cohens κ coefficient was 0.27 for unenhanced 3D echocardiography, 0.40 for unenhanced 2D echocardiography, 0.57 for CMR, and 0.51 for cineventriculography. The use of contrast increased IRA on RWMA to 0.42 for 3D echocardiography and to 0.56 for 2D echocardiography. Agreement with CMR on RWMA increased for 3D echocardiography when contrast enhancement was used (κ 0.40 vs 0.22 for unenhanced 3D echocardiography). Similarly, agreement of 2D echocardiography with CMR on RWMA increased with contrast enhancement (κ 0.50 vs 0.32). Accuracy to detect expert panel-defined RWMA was highest for CMR (84%) followed by 2D contrast echocardiography (78%) and 3D contrast echocardiography (76%). It was lesser for 2D and 3D unenhanced echocardiographies. In conclusion, analysis of RWMA is characterized by considerable interreader variability even using high-quality imaging techniques. IRA on RWMA is lower with 3D echocardiography compared with 2D echocardiography. IRA on RWMA and accuracy to detect panel-defined RWMA improve with contrast enhancement irrespective of the 2D or 3D echocardiography use.

Failure of trifluoperazine to resolve spontaneous echo contrast evaluated by transesophageal echocardiography

Abstract Spontaneous echo contrast, the echocardiographic appearance of discrete, smoke-like intracavitary reflectances, was described for the first time in 1975 by Feigenbaum et al. 1 Since the introduction of transesophageal echocardiography and the usage of higher frequency transducers, it is a well recognized phenomenon, which occurs in conditions with diminished blood flow velocities. Transesophageal echocardiography has shown its superiority to the transthoracic ultrasound approach, especially for assessment of spontaneous echo contrast in the left atrium. The exact pathophysiologic mechanism responsible for occurrence of spontaneous echo contrast is not known. Erbel et al 2 found increased platelet aggregation in patients with spontaneous echo contrast. It has been shown that spontaneous echo contrast is involved with an increased risk of embolic events. 3 It is therefore the therapeutic aim to effect its resolution. Trifluoperazine is a substance with documented properties for inhibition of platelet aggregation by selectively binding calmodulin, which activates platelet phospholipase A 2 . Additionally, it disaggregates existing platelet aggregates. 4 Recently, the successful application of trifluoperazine for resolution of spontaneous echo contrast seen by transthoracic echocardiography has been described in a case report in this journal. 5 We prospectively investigated the effect of oral trifluoperazine on spontaneous echo contrast using transesophageal echocardiography in 5 patients.

Brain natriuretic Peptide. Diagnostic and prognostic value in chronic heart failure

Zusammenfassung.Brain natriuretic peptide (BNP) hat sich als ein neuer und erster verlässlicher Labormarker der chronischen Herzinsuffizienz (CHI) etabliert. BNP ist ein Neurohormon und wird von Kardiomyozyten freigesetzt als Antwort auf eine erhöhte Volumen- oder Druckbelastung des Herzens. Bei der Freisetzung wird die Speicherform proBNP in das inaktive N-terminale-proBNP und das aktive BNP gespalten. BNP führt zur Vasodilatation, hemmt das Renin-Angiotensin-Aldosteron-System und fördert die Natriurese und Diurese. Die BNP-Werte sind abhängig von Geschlecht, Alter, Nierenfunktion und dem verwendeten Assay. In der Diagnostik der CHI besitzt das BNP eine hohe Sensitivität und Spezifität. Mittels BNP-Bestimmung wird auch die Differentialdiagnostik der Dyspnoe verbessert. Bei pathologischem BNP-Wert ist die Ursache der Dyspnoe meist kardial, bei pulmonaler Genese der Dyspnoe befindet sich das BNP meist im Normbereich. Die Höhe des BNP-Werts erlaubt auch eine Prognoseabschätzung bei CHI bezüglich kardialer Todesfälle und einer Verschlechterung des funktionellen Status. Als allgemeiner Massen-Screeningtest auf CHI hat BNP aktuell nur eine begrenzte Bedeutung, da sich oftmals falsch positive Befunde zeigen, die eine weitere kardiologische Abklärung nach sich ziehen. BNP kann erfolgreich zur gezielten Steuerung der Therapie einer CHI bei akut dekompensierten hospitalisierten und auch ambulanten Patienten eingesetzt werden. Die maßgeschneiderte Therapiesteuerung anhand serieller Bestimmung des BNP eröffnet neue Perspektiven einer objektiveren und effektiveren Behandlung von Patienten mit CHI.Summary.Brain natriuretic peptide (BNP) has been established as a new and reliable laboratory marker for chronic heart failure (CHF). BNP is a neurohormone secreted by the cardiac ventricles in response to volume expansion and pressure overload. It is released as N-terminal pro-brain natriuretic peptide and then Korrelaenzymatically cleaved into the NT fragment and the immunoreactive BNP. BNP promotes vasodilatation, natriuresis, diuresis, and inhibits the renin-angiotensin- aldosterone system. BNP values depend on sex, age, renal function, and the assay used. BNP exhibits a high sensitivity and specificity for the diagnosis of CHF. BNP determination improves the differential diagnosis of acute dyspnea. Normal BNP levels are found, if dyspnea is caused by pulmonary disease, pathologic BNP values are typical of a cardiac disorder. In CHF, BNP levels can be used as a reliable independent predictor of cardiac death or deterioration of cardiac functional status at follow-up. As a general screening test for CHF, BNP is of limited value due to a substantial number of false positive test results, which lead to further cardiac diagnostic testing. BNP is helpful for the assessment of the success of CHF therapy in acute cardiac decompensation and outpatients. An individually tailored CHF therapy with serial determination of BNP opens up new perspectives for a more objective and effective treatment of CHF patients.

Pulmonale alveoläre Mikrolithiasis – eine seltene Ursache bilateraler ausgedehnter pulmonaler Infiltrate

ZusammenfassungHintergrund: Die pulmonale alveoläre Mikrolithiasis ist eine seltene Erkrankung, die durch die pulmonale Ablagerung von Calciumphosphatkonkrementen in den Alveolen charakterisiert ist. Diagnostisch richtungsweisend ist das Röntgenbild mit einer typischen “Sandsturm”artigen Verschattung des Lungengewebes. Fallbeschreibung: Ein 29-jähriger Marokkaner stellte sich erstmals 1988 wegen atypischer linkstorakaler Schmerzen vor. Anamnestisch waren eine Nephrokalzinose und eine Lungenerkrankung bekannt. Die körperliche Untersuchung und die Laborbefunde waren unauffällig. Im Röntgenbild des Thorax fielen ausgedehnte pulmonale Infiltrate beidseitig mit einem “Sandsturm”-artigen Aspekt auf. Sonographisch zeigte sich auf beiden Seiten eine medulläre Nephrokalzinose. Mittels transbronchialer Biopsie wurde die Diagnose einer pulmonalen alveolären Mikrolithiasis gesichert. Im Verlauf von 13 Jahren kam es zu einer leichten Zunahme der pulmonalen Infiltrate und zu beginnender restriktiver Ventilationsstörung bei subjektiv weitgehend beschwerdefreien Patienten. Schlussfolgerung: Bei ausgedehnten pulmonalen Infiltraten beidseitig mit Nachweis intrapulmonaler Verkalkungen sollte als Differentialdiagnose an die seltene pulmonale alveoläre Mikrolithiasis gedacht werden. Dies gilt insbesondere für Patienten aus Ländern mit hoher Sonnenlichtexposition. In seltenen Fällen findet man auch Verkalkungen in extrapulmonalen Organen.AbstractBackground: Pulmonary alveolar microlithiasis is a rare disease, which is characterized by pulmonary deposition of calcium phosphate microliths. The radiographic features can be pathognomonic wit a “sandstorm”-like opacification throughout the lungs. Case Report: A 29-year-old Moroccan presented for the first time 1988 with atypical chest pain. His history was characterized by nephrocalcinosis and pulmonary disease. Physical examination and laboratory values were unremarkable. Chest X-ray revealed extensive bilateral pulmonary infiltrates with “sandstorm”-like opacifications. Sonography showed medullary nephrocalcinosis. The diagnosis of pulmonary alveolar microlithiasis was confirmed ty transbronchial biopsy. Over the next 13 years there was only a moderate expansion of the pulmonary infiltrates and a beginning restrictive pattern, whereas the patient was almost symptom-free. Conclusion: Pulmonary alveolar microlithiasis is a rare cause of bilateral pulmonary infiltrates and should be considered in the differential diagnosis. In some cases there is also an association with calcifications of extrapulmonary organs.

Erratum zu : Manual zur Indikation und Durchführung der Echokardiographie

)Westdeutsches Herzzentrum Essen, Abt. Kardiologie,Universita¨tsklinikum Essen, Universita¨tsklinikumDuisburg-Essen, Hufelandstrasse 55,45122 Essen, Germanye-mail: thomas.buck@uk-essen.deO.-A. BreithardtKlinikum Coburg, Coburg, GermanyL. FaberHerz- und Diabeteszentrum NRW,Bad Oeynhausen, GermanyW. FehskeSt. Vinzenz-Hospital, Cologne, GermanyF. A. FlachskampfUniversita¨t Erlangen, Erlangen, GermanyA. FrankeKRH Klinikum Siloah, Hannover, GermanyA. HagendorffUniversita¨tsklinikum Leipzig, Leipzig, GermanyR. HoffmannUniversita¨tsklinikum Aachen, Aachen, GermanyI. KruckKardiologische Praxis, Ludwigsburg, GermanyH. Ku¨chererKliniken im Naturpark Altmu¨hltal, Eichsta¨tt und Ko¨sching,Eichsta¨tt, GermanyT. MenzelKardiologische/Angiologische, Gemeinschaftspraxis,Wiesbaden, GermanyK. PethigEv. Krankenhaus Hamm, Hamm, GermanyK. TiemannUniversita¨tsklinikum Mu¨nster, Mu¨nster, GermanyJ.-U. VoigtUniversita¨tsklinik Gasthuisberg, Katholische Universita¨tLo¨wen,Louvain, BelgiumF. WeidemannUniversita¨tsklinik Wu¨rzburg, Wu¨rzburg, GermanyU. NixdorffEuropean Prevention Center, Duisburg, Germany

Akute Herzinsuffizienz mit Lungenödem nach Sectio caesarea

ZusammenfassungHintergrund:Eine schwere Herzinsuffizienz kurz nach Entbindung bei einer zuvor asymptomatischen Patientin kann durch eine peripartale Kardiomyopathie, durch eine klinische Verschlechterung bei angeborenem oder erworbenem Herzklappenfehler, durch länger anhaltende Tachykardien (tachykarde Kardiomyopathie), durch eine fulminante Lungenembolie oder durch eine Endokarditis bedingt sein.Fallbericht:Bei einer 36-jährigen, anamnestisch bisher herzgesunden Primipara kam es am 2. Tag nach Sectio caesarea zu einem akuten Linksherzversagen mit Lungenödem im Rahmen einer floriden Aortenklappenendokarditis durch β-hämolysierende Streptokokken der Gruppe A. Nach Diagnosesicherung mittels transthorakaler und transösophagealer Farb-Doppler-Echokardiographie, zunächst antibiotischer Therapie mit Vancomycin und Gentamicin sowie Therapie mit Schleifendiuretikum und Katecholaminen, später Schleifendiuretikum und ACE-Hemmer konnte bei der zwischenzeitlich kreislaufstabilen Patientin am 14. Tag nach Sectio caesarea erfolgreich ein Aortenklappenersatz durchgeführt werden.Schlussfolgerung:Obwohl eine Endokarditis im Zeitalter der peripartalen Antibiotikaprophylaxe selten ist, sollte sie bei Auftreten einer Herzinsuffizienz mit und ohne Fieber kurz nach vaginaler Entbindung oder Sectio caesarea differentialdiagnostisch immer in Erwägung gezogen werden. Nur durch rasche und gezielte Diagnostik und Therapie kann häufig ein günstiger klinischer Verlauf erreicht werden.AbstractBackground:Severe left heart failure shortly after delivery in a previously asymptomatic young woman can be caused by a peripartum cardiomyopathy, an exacerbation of valvular heart disease due to both congenital or acquired etiologies, a sustained chronic tacharrhythmia (tachycardiomyopathy), a fulminant pulmonary embolism, or an infective endocarditis.Case Study:2 days following cesarean section, a 36-year-old primipara without known previous heart disease suffered from severe left heart failure with pulmonary edema (Figure 1) due to an acute bacterial aortic valve endocarditis. The infecting organisms were β-hemolytic group A streptococci. After diagnosis could be confirmed by conventional Doppler echocardiography and by transesophageal echocardiography (Figures 2 and 3), the clinical situation of the patient stabilized in a few days under an initial antibiotic regimen with vancomycin and gentamicin, diuretics and catecholamines, followed by diuretics and ACE inhibitor. 14 days after cesarean delivery, aortic valve replacement could be performed under hemodynamically stable conditions.Conclusion:Although postpartal endocarditis is rarely described in the era of peripartum antibiotic prophylaxis, it should be considered in the differential diagnosis of patients with heart failure or fever in pregnancy, following delivery or cesarean section. The prognosis of peripartal endocarditis as a life-threatening disease is determined by an accurate and immediate diagnosis.BACKGROUND Severe left heart failure shortly after delivery in a previously asymptomatic young woman can be caused by a peripartum cardiomyopathy, an exacerbation of valvular heart disease due to both congenital or acquired etiologies, a sustained chronic tachyarrhythmia (tachycardiomyopathy), a fulminant pulmonary embolism, or an infective endocarditis. CASE STUDY 2 days following cesarean section, a 36-year-old primipara without known previous heart disease suffered from severe left heart failure with pulmonary edema (Figure 1) due to an acute bacterial aortic valve endocarditis. The infecting organisms were beta-hemolytic group A streptococci. After diagnosis could be confirmed by conventional Doppler echocardiography and by transesophageal echocardiography (Figures 2 and 3), the clinical situation of the patient stabilized in a few days under an initial antibiotic regimen with vancomycin and gentamicin, diuretics and catecholamines, followed by diuretics and ACE inhibitor. 14 days after cesarean delivery, aortic valve replacement could be performed under hemodynamically stable conditions. CONCLUSION Although postpartal endocarditis is rarely described in the era of peripartum antibiotic prophylaxis, it should be considered in the differential diagnosis of patients with heart failure or fever in pregnancy, following delivery or cesarean section. The prognosis of peripartal endocarditis as a life-threatening disease is determined by an accurate and immediate diagnosis.

Severe acute left heart failure with pulmonary edema following cesarean section

ZusammenfassungHintergrund:Eine schwere Herzinsuffizienz kurz nach Entbindung bei einer zuvor asymptomatischen Patientin kann durch eine peripartale Kardiomyopathie, durch eine klinische Verschlechterung bei angeborenem oder erworbenem Herzklappenfehler, durch länger anhaltende Tachykardien (tachykarde Kardiomyopathie), durch eine fulminante Lungenembolie oder durch eine Endokarditis bedingt sein.Fallbericht:Bei einer 36-jährigen, anamnestisch bisher herzgesunden Primipara kam es am 2. Tag nach Sectio caesarea zu einem akuten Linksherzversagen mit Lungenödem im Rahmen einer floriden Aortenklappenendokarditis durch β-hämolysierende Streptokokken der Gruppe A. Nach Diagnosesicherung mittels transthorakaler und transösophagealer Farb-Doppler-Echokardiographie, zunächst antibiotischer Therapie mit Vancomycin und Gentamicin sowie Therapie mit Schleifendiuretikum und Katecholaminen, später Schleifendiuretikum und ACE-Hemmer konnte bei der zwischenzeitlich kreislaufstabilen Patientin am 14. Tag nach Sectio caesarea erfolgreich ein Aortenklappenersatz durchgeführt werden.Schlussfolgerung:Obwohl eine Endokarditis im Zeitalter der peripartalen Antibiotikaprophylaxe selten ist, sollte sie bei Auftreten einer Herzinsuffizienz mit und ohne Fieber kurz nach vaginaler Entbindung oder Sectio caesarea differentialdiagnostisch immer in Erwägung gezogen werden. Nur durch rasche und gezielte Diagnostik und Therapie kann häufig ein günstiger klinischer Verlauf erreicht werden.AbstractBackground:Severe left heart failure shortly after delivery in a previously asymptomatic young woman can be caused by a peripartum cardiomyopathy, an exacerbation of valvular heart disease due to both congenital or acquired etiologies, a sustained chronic tacharrhythmia (tachycardiomyopathy), a fulminant pulmonary embolism, or an infective endocarditis.Case Study:2 days following cesarean section, a 36-year-old primipara without known previous heart disease suffered from severe left heart failure with pulmonary edema (Figure 1) due to an acute bacterial aortic valve endocarditis. The infecting organisms were β-hemolytic group A streptococci. After diagnosis could be confirmed by conventional Doppler echocardiography and by transesophageal echocardiography (Figures 2 and 3), the clinical situation of the patient stabilized in a few days under an initial antibiotic regimen with vancomycin and gentamicin, diuretics and catecholamines, followed by diuretics and ACE inhibitor. 14 days after cesarean delivery, aortic valve replacement could be performed under hemodynamically stable conditions.Conclusion:Although postpartal endocarditis is rarely described in the era of peripartum antibiotic prophylaxis, it should be considered in the differential diagnosis of patients with heart failure or fever in pregnancy, following delivery or cesarean section. The prognosis of peripartal endocarditis as a life-threatening disease is determined by an accurate and immediate diagnosis.BACKGROUND Severe left heart failure shortly after delivery in a previously asymptomatic young woman can be caused by a peripartum cardiomyopathy, an exacerbation of valvular heart disease due to both congenital or acquired etiologies, a sustained chronic tachyarrhythmia (tachycardiomyopathy), a fulminant pulmonary embolism, or an infective endocarditis. CASE STUDY 2 days following cesarean section, a 36-year-old primipara without known previous heart disease suffered from severe left heart failure with pulmonary edema (Figure 1) due to an acute bacterial aortic valve endocarditis. The infecting organisms were beta-hemolytic group A streptococci. After diagnosis could be confirmed by conventional Doppler echocardiography and by transesophageal echocardiography (Figures 2 and 3), the clinical situation of the patient stabilized in a few days under an initial antibiotic regimen with vancomycin and gentamicin, diuretics and catecholamines, followed by diuretics and ACE inhibitor. 14 days after cesarean delivery, aortic valve replacement could be performed under hemodynamically stable conditions. CONCLUSION Although postpartal endocarditis is rarely described in the era of peripartum antibiotic prophylaxis, it should be considered in the differential diagnosis of patients with heart failure or fever in pregnancy, following delivery or cesarean section. The prognosis of peripartal endocarditis as a life-threatening disease is determined by an accurate and immediate diagnosis.