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Roberto Lang

Publications and source records attributed to Roberto Lang.

10 recordsLinked to original sources
PubMed2006

Which method should be the reference method to evaluate the severity of rheumatic mitral stenosis? Gorlin's method versus 3D-echo.

INTRODUCTION: Several studies have shown a wide variability among different methods to determine the valve area in patients with rheumatic mitral stenosis. Our aim was to evaluate if 3D-echo planimetry is more accurate than the Gorlin method to measure the valve area. METHODS: Twenty-six patients with mitral stenosis underwent 2D and 3D-echo echocardiographic examinations and catheterization. Valve area was estimated by different methods. A median value of the mitral valve area, obtained from the measurements of three classical non-invasive methods (2D planimetry, pressure half-time and PISA method), was used as the reference method and it was compared with 3D-echo planimetry and Gorlin's method. RESULTS: Our results showed that the accuracy of 3D-echo planimetry is superior to the accuracy of the Gorlin method for the assessment of mitral valve area. CONCLUSIONS: We should keep in mind the fact that 3D-echo planimetry may be a better reference method than the Gorlin method to assess the severity of rheumatic mitral stenosis.

Adult↗
PubMed2006

Poly(ADP-ribose) polymerase-1-deficient mice are protected from angiotensin II-induced cardiac hypertrophy.

Poly(ADP-ribose) polymerase-1 (PARP), a chromatin-bound enzyme, is activated by cell oxidative stress. Because oxidative stress is also considered a main component of angiotensin II-mediated cell signaling, it was postulated that PARP could be a downstream target of angiotensin II-induced signaling leading to cardiac hypertrophy. To determine a role of PARP in angiotensin II-induced hypertrophy, we infused angiotensin II into wild-type (PARP(+/+)) and PARP-deficient mice. Angiotensin II infusion significantly increased heart weight-to-tibia length ratio, myocyte cross-sectional area, and interstitial fibrosis in PARP(+/+) but not in PARP(-/-) mice. To confirm these results, we analyzed the effect of angiotensin II in primary cultures of cardiomyocytes. When compared with PARP(-/-) cardiomyocytes, angiotensin II (1 microM) treatment significantly increased protein synthesis in PARP(+/+) myocytes, as measured by (3)H-leucine incorporation into total cell protein. Angiotensin II-mediated hypertrophy of myocytes was accompanied with increased poly-ADP-ribosylation of nuclear proteins and depletion of cellular NAD content. When cells were treated with cell death-inducing doses of angiotensin II (10-20 microM), robust myocyte cell death was observed in PARP(+/+) but not in PARP(-/-) myocytes. This type of cell death was blocked by repletion of cellular NAD levels as well as by activation of the longevity factor Sir2alpha deacetylase, indicating that PARP induction and subsequent depletion of NAD levels are the sequence of events causing angiotensin II-mediated cardiomyocyte cell death. In conclusion, these results demonstrate that PARP is a nuclear integrator of angiotensin II-mediated cell signaling contributing to cardiac hypertrophy and suggest that this could be a novel therapeutic target for the management of heart failure.

Angiotensin II↗
PubMed2002

Inhibition of betaARK1 restores impaired biochemical beta-adrenergic receptor responsiveness but does not rescue CREB(A133) induced cardiomyopathy.

The myocardial beta-adrenergic receptor (betaAR) system plays a key role in dysfunctional signaling and physiology of the failing heart. Recently we described a murine model of dilated cardiomyopathy (DCM) produced by cardiac-specific expression of a dominant negative form of the CREB transcription factor (CREB(A133) mice). CREB(A133) mice display abnormalities within the betaAR signaling system including loss of inotropic reserve. Rapid desensitization of betaARs is mediated by the betaAR kinase (betaARK1), which is upregulated during heart failure. Inhibition of betaARK1 activity in the heart via expression of a peptide inhibitor (betaARKct) has been shown to enhance myocardial function and to "rescue" several animal models of heart failure. To determine the role of betaAR dysfunction in the progression of DCM in the CREB(A133) mice, we interbred them with mice expressing the betaARKct. Concurrent expression of the betaARKct peptide and CREB(A133) in mouse hearts resulted in the normalization of elevated betaARK1 levels. This biochemical change resulted in partial restoration of isoproterenol-stimulated adenylate cyclase activity as well as improvement in fractional shortening in response to betaAR stimulation. Interestingly, the progression of DCM and premature mortality was not altered. Therefore, the pathogenesis of DCM in CREB(A133) mice does not appear to involve abnormal betaAR signaling as a key element in its pathological progression and accordingly, the restoration of betaAR signaling is not sufficient to prevent the development and progression of all forms of heart failure.

Animals↗
PubMed2002

Thyroid hormone and cardiac function in mice deficient in thyroid hormone receptor-alpha or -beta: an echocardiograph study.

We investigated the effect of thyroid hormone (TH) receptor (TR)alpha and -beta isoforms in TH action in the heart. Noninvasive echocardiographic measurements were made in mice homozygous for disruption of TRalpha (TRalpha(0/0)) or TRbeta (TRbeta(-/-)). Mice were studied at baseline, 4 wk after TH deprivation (using a low-iodine diet containing propylthiouracil), and after 4-wk treatment with TH. Baseline heart rates (HR) were similar in wild-type (WT) and TRalpha(0/0) mice but were greater in TRbeta(-/-) mice. With TH deprivation, HR decreased 49% in WT and 37% in TRbeta(-/-) mice and decreased only 5% in TRalpha(0/0) mice from baseline, whereas HR increased in all genotypes with TH treatment. Cardiac output (CO) and cardiac index (CI) in WT mice decreased (-31 and -32%, respectively) with TH deprivation and increased (+69 and +35%, respectively) with TH treatment. The effects of CO and CI were blunted with TH withdrawal in both TRalpha(0/0) (+8 and -2%, respectively) and TRbeta(-/-) mice (-17 and -18%, respectively). Treatment with TH resulted in a 64% increase in LV mass in WT and a 44% increase in TRalpha(0/0) mice but only a 6% increase in TRbeta(-/-) mice (ANOVA P < 0.05). Taken together, these data suggest that TRalpha and TRbeta play different roles in the physiology of TH action on the heart.

Animals↗
PubMed1999

Assessment of Right Ventricular and Right Atrial Systolic and Diastolic Performance Using Automated Border Detection.

Noninvasive assessment of right ventricular (RV) function is important clinically, but current techniques have limitations. Acoustic quantification (AQ) is an automated endocardial border detection technique that allows continuous determination of RV and right atrial (RA) area waveforms and may be useful for the assessment of RA and RV systolic and diastolic performance. Fifty patients (10 normal, 40 with RV pathology) were studied. Signal-averaged RA and RV AQ area waveforms were obtained and analyzed to compute parameters of diastolic and systolic function. All groups demonstrated significant diastolic dysfunction on the RA AQ waveform as manifested by a reduced percentage of passive atrial emptying and increased dependence on active atrial emptying. Abnormalities of diastolic performance were noted in all subgroups on RV AQ analysis as evidenced by a reduction in the percentage of ventricular filling occurring during early diastole and an increased contribution from active atrial contraction. This study demonstrates the feasibility of using automated analysis of signal-averaged RA and RV area waveforms for the evaluation of RV systolic and diastolic performance. This technique identified significant systolic and diastolic dysfunction in four groups of commonly seen right heart pathologies including biventricular heart failure, pulmonary hypertension, pressure and volume overloaded RVs, and biventricular hypertrophy.

Journal Article↗
PubMedDate not supplied

A fantastic journey: 3D cardiac ultrasound goes live.

With a recent product introduction, live 3D echo is now clinically practical. It is already beginning to have a profound impact on the way we care for patients at The University of Chicago Medical Center. In the past, dynamic cardiac 3D rendered images were possible by sequentially acquiring 2D images and then using a workstation to input 2D images for Cartesian coordinate conversion and volume rendering. Outside research settings, this time-consuming process proved cumbersome and was simply impractical. Now that these technical and practical issues have been addressed, real-time 3D cardiac sonography has great potential to impact both patient care and throughput in a number of ways, including better pre- and post-surgical planning, improved measurement of heart function, decreased exam times, and enhanced communication between clinicians and their patients. With real-time 3D cardiac ultrasound images, clinicians will be able to better quantify size, shape and function of the heart. However, the most important contribution of real-time 3D sonography in cardiology may be improvement in locating abnormalities for surgical planning. The new technology will also provide important information regarding surgical outcomes. A great benefit to obtaining more diagnostic information and higher diagnostic confidence from real-time 3D cardiac ultrasound images is that it could lead to more rapid exam times and the reduction of patient wait times. Being able to see the whole heart makes examinations more simple and rapid, benefitting the staff and patient. The utility of this technology is unusually broad, as it is able to move beyond diagnostics into a key role in therapeutic procedures. As with any new technology, there will be a learning curve to understanding 3D imaging. Though the matrix transducer is somewhat larger than a standard 2D probe, the ergonomics are quite similar. The interface of the ultrasound unit is also very user friendly. Because real-time 3D cardiac ultrasound involves looking at the heart as if you are holding it in your hands, with the additional ability to turn it any way you want, we expect that the transition from 2D to 3D will be easily achieved.

Echocardiography, Three-Dimensional↗