Joel S. Landzberg

Reproducibility of quantitative two-dimensional echocardiography

In order to assess reproducibility of quantitative planimetry, three physicians trained in two-dimensional echocardiography performed five successive studies on one another over 2 weeks (30 total studies). Then each physician traced each study (90 total tracings) for left ventricular and atrial volumes and ejection fraction by means of a modification of Simpsons rule, and left ventricular mass and average wall thickness by means of a truncated ellipsoid formula. Calculation of intertechnician variability, intertracer variability, and 95% confidence limits showed that measurements of volumes were less reproducible than measurements of ejection fraction, average wall thickness, and mass. Mean intertracer variability of 15% exceeded mean intertechnician variability of 11%; this disparity was magnified in the subject who was technically difficult to image. Ninety-five percent confidence limits were: ejection fraction +/- 7%, average wall thickness +/- 9%, left ventricular mass +/- 12%, left ventricular end-diastolic volume +/- 11%, stroke volume +/- 14%, left ventricular end-systolic volume +/- 15%, and left atrial volume +/- 19%. Reproducible planimetry data can be obtained in normal hearts with the use of a protocol for quantitative imaging and planimetry.

2012 American College of Cardiology Foundation/Society for Cardiovascular Angiography and Interventions Expert Consensus Document on Cardiac Catheterization Laboratory Standards update: A report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents

published online May 8, 2012; J. Am. Coll. Cardiol. L. Tommaso Carl Moliterno, John W.M. Moore, Sandra M. Oliver-McNeil, Jeffrey J. Popma, and Landzberg, Warren K. Laskey, Charles R. McKay, Julie M. Miller, David J. Cavendish, Charles E. Chambers, James Bernard Hermiller, Jr, Scott Kinlay, Joel S. M. Bashore, MD, FACC,, Stephen Balter, Ana Barac, John G. Byrne, Jeffrey J. Documents, Society of Thoracic Surgeons, Society for Vascular Medicine, Thomas American College of Cardiology Foundation Task Force on Expert Consensus Catheterization Laboratory Standards Update Angiography and Interventions Expert Consensus Document on Cardiac 2012 American College of Cardiology Foundation/Society for Cardiovascular This information is current as of May 25, 2012 http://content.onlinejacc.org/cgi/content/full/j.jacc.2012.02.010v1 located on the World Wide Web at: The online version of this article, along with updated information and services, is

ACCF/AHA/SCAI 2013 Update of the Clinical Competence Statement on Coronary Artery Interventional Procedures A Report of the American College of Cardiology Foundation/American Heart Association/American College of Physicians Task Force on Clinical Competence and Training (Writing Committee to Revise the 2007 Clinical Competence Statement on Cardiac Interventional Procedures)

Granting clinical staff privileges to physicians is the primary mechanism institutions use to uphold quality care. The Joint Commission requires that medical staff privileges be based on professional criteria specified in medical staff bylaws. Physicians themselves are charged with defining the

Cardiac consequences of renal transplantation: Changes in left ventricular morphology and function

To characterize changes in left ventricular morphology and function associated with renal transplantation, noninvasive cardiac evaluations were performed in 41 adults at the time of surgery and at follow-up. At the time of transplantation, 36 patients had undergone hemodialysis through a fistula for 2.3 +/- 2.5 years (mean +/- SD); their hematocrit level was 26 +/- 6% and systolic blood pressure was 151 +/- 19 mm Hg. Perioperatively, left ventricular hypertrophy was present in 93% of patients by echocardiography, but in only 37% by electrocardiography. Abnormal left ventricular diastolic function was present in 67% of patients and indicated a high risk for perioperative pulmonary edema. At follow-up (1.5 +/- 1.4 years), mean hematocrit level increased to 39 +/- 7%, systolic blood pressure decreased to 132 +/- 14 mm Hg and spontaneous closure of the fistula occurred in 13 patients. Left ventricular mass by echocardiography decreased from 237 +/- 66 to 182 +/- 47 g (p less than 0.001), a decrease of 23%. Left ventricular volumes and cardiac index also decreased significantly, reflecting the rapid resolution of a pretransplant high output state. Despite proportionate regression of left ventricular hypertrophy within months of transplantation, diastolic function did not improve. The significant regression of left ventricular hypertrophy that occurs after renal transplantation may help explain the improved cardiovascular survival of patients with a renal transplant over that of patients on long-term dialysis.

2012 American College of Cardiology Foundation/Society for Cardiovascular Angiography and Interventions expert consensus document on cardiac catheterization laboratory standards update: A report of the American College of Cardiology Foundation Task Force on Expert Consensus documents developed in collaboration with the Society of Thoracic Surgeons and Society for Vascular Medicine.

published online May 8, 2012; J. Am. Coll. Cardiol. L. Tommaso Carl Moliterno, John W.M. Moore, Sandra M. Oliver-McNeil, Jeffrey J. Popma, and Landzberg, Warren K. Laskey, Charles R. McKay, Julie M. Miller, David J. Cavendish, Charles E. Chambers, James Bernard Hermiller, Jr, Scott Kinlay, Joel S. M. Bashore, MD, FACC,, Stephen Balter, Ana Barac, John G. Byrne, Jeffrey J. Documents, Society of Thoracic Surgeons, Society for Vascular Medicine, Thomas American College of Cardiology Foundation Task Force on Expert Consensus Catheterization Laboratory Standards Update Angiography and Interventions Expert Consensus Document on Cardiac 2012 American College of Cardiology Foundation/Society for Cardiovascular This information is current as of May 25, 2012 http://content.onlinejacc.org/cgi/content/full/j.jacc.2012.02.010v1 located on the World Wide Web at: The online version of this article, along with updated information and services, is

Muscarinic receptor modulation of basal and beta-adrenergic stimulated function of the failing human left ventricle.

The objective of this study was to evaluate the effect of muscarinic receptor modulation on basal and beta-adrenergic stimulated left ventricular function in patients with heart failure. 21 heart failure patients and 14 subjects with normal ventricular function were studied. In Protocol 1 intracoronary acetylcholine resulted in a 60+/-8% inhibition of the left ventricular +dP/dt response to intracoronary dobutamine in the normal group, and a similar 70+/-13% inhibition in the heart failure group. Acetylcholine also attenuated the dobutamine-mediated acceleration of isovolumic relaxation (Tau) in both groups. Acetylcholine alone had no effect on Tau in the normal group, while it prolonged Tau in the heart failure group. In Protocol 2 intracoronary atropine resulted in a 35+/-10% augmentation of the inotropic response to dobutamine in the normal group, versus a non-significant 12+/-15% augmentation of the dobutamine response in the heart failure group. In Protocol 3, in 6 heart failure patients, both effects of acetylcholine, the slowing of ventricular relaxation and the inhibition of beta-adrenergic responses, were reversed by the addition of atropine. Therefore, in the failing human left ventricle muscarinic stimulation has an independent negative lusitropic effect and antagonizes the effects of beta-adrenergic stimulation.

Functional Significance of Presynaptic α-Adrenergic Receptors in Failing and Nonfailing Human Left Ventricle

BACKGROUND There are alpha-adrenergic receptors on human myocardium that exert positive inotropic effects. The effect of alpha-adrenergic receptor blockade on human left ventricular (LV) performance has not been fully explored. Although alpha-adrenergic receptor blockade might have effects on LV function that are mediated via blockade of postsynaptic myocardial alpha-adrenergic receptors, it is also possible that blockade of presynaptic alpha 2-adrenergic receptors and subsequent increased release of norepinephrine would have effects on LV performance. In the present study, we explored the effects of nonselective alpha-adrenergic receptor blockade on LV performance and transcardiac norepinephrine concentrations in a group of patients with normal LV function and in a group of patients with congestive heart failure secondary to dilated cardiomyopathy. METHODS AND RESULTS Using an intracoronary drug infusion technique, we administered the nonselective alpha-adrenergic antagonist phentolamine to 13 patients with normal LV function and 19 patients with congestive heart failure secondary to dilated cardiomyopathy. With a high-fidelity LV catheter, the systolic (+dP/dt) and diastolic (-dP/dt and Tau) LV function responses to intracoronary infusion of phentolamine (0.2 mg/min x 5 minutes) were assessed. In 8 patients with normal ventricular function and 10 patients with congestive heart failure, arterial and coronary sinus blood samples were drawn to determine the effects of phentolamine on catecholamine concentrations. Phentolamine had no measurable effect on LV performance or catecholamine concentrations in the normal ventricular function group. In patients with congestive heart failure, intracoronary phentolamine caused a significant increase in +dP/dt and the rate of isovolumic LV relaxation (-dP/dt and Tau). These hemodynamic effects were accompanied by a significant increase in coronary sinus norepinephrine concentration but no change in arterial norepinephrine concentration. CONCLUSIONS Myocardial alpha-adrenergic receptor blockade causes significant inotropic and lusitropic effects in the failing but not the nonfailing human LV. These effects appear to be mediated by increased release of norepinephrine from cardiac nerves secondary to blockade of presynaptic alpha 2-adrenergic receptors. Differences in the responses of the failing and nonfailing human LV appear to reflect the higher level of sympathetic activation that is seen in the group with congestive heart failure. This suggests that the presynaptic alpha 2-adrenergic receptor exerts a tonic inhibitory effect on the release of norepinephrine from cardiac nerves in patients with congestive heart failure.

The echo-transponder electrode catheter: A new method for mapping the left ventricle

The ability to locate catheter position in the left ventricle with respect to endocardial landmarks might enhance the accuracy of ventricular tachycardia mapping. An echo-transponder system (Telectronics, Inc.) was compared with biplane fluoroscopy for left ventricular endocardial mapping. A 6F electrode catheter was modified with the addition of a piezoelectric crystal 5 mm from the tip. This crystal was connected to a transponder that received and transmitted ultrasound, resulting in a discrete artifact on the two-dimensional echocardiographic image corresponding to the position of the catheter tip. Catheters were introduced percutaneously into the left ventricle of nine anesthetized dogs. Two-dimensional echo-transponder and biplane fluoroscopic images were recorded on videotape with the catheter at multiple endocardial sites. Catheter location was marked by delivering radiofrequency current to the distal electrode, creating a small endocardial lesion. Catheter location by echo-transponder and by fluoroscopy were compared with lesion location without knowledge of other data. Location by echo-transponder was 8.7 +/- 5.1 mm from the center of the radiofrequency lesion versus 14 + 7.8 mm by fluoroscopy (n = 15, p = 0.023). Echo-transponder localization is more precise than is biplane fluoroscopy and may enhance the accuracy of left ventricular electrophysiologic mapping.

2012 American College of Cardiology Foundation/ Society for Cardiovascular Angiography and Interventions Expert Consensus Document on Cardiac Catheterization Laboratory Standards Update

published online May 8, 2012; J. Am. Coll. Cardiol. L. Tommaso Carl Moliterno, John W.M. Moore, Sandra M. Oliver-McNeil, Jeffrey J. Popma, and Landzberg, Warren K. Laskey, Charles R. McKay, Julie M. Miller, David J. Cavendish, Charles E. Chambers, James Bernard Hermiller, Jr, Scott Kinlay, Joel S. M. Bashore, MD, FACC,, Stephen Balter, Ana Barac, John G. Byrne, Jeffrey J. Documents, Society of Thoracic Surgeons, Society for Vascular Medicine, Thomas American College of Cardiology Foundation Task Force on Expert Consensus Catheterization Laboratory Standards Update Angiography and Interventions Expert Consensus Document on Cardiac 2012 American College of Cardiology Foundation/Society for Cardiovascular This information is current as of May 25, 2012 http://content.onlinejacc.org/cgi/content/full/j.jacc.2012.02.010v1 located on the World Wide Web at: The online version of this article, along with updated information and services, is

Etiology of the Austin Flint Murmur

OBJECTIVES The aim of the study was to determine the mechanism of the Austin Flint murmur. BACKGROUND More than 100 years after the initial description of the Austin Flint murmur, the etiology of the murmur remains unclear. METHODS M-mode and two-dimensional echocardiography, conventional and color flow Doppler study, and cine nuclear magnetic resonance (cine NMR) imaging were performed in 24 patients with clinically moderate or severe aortic regurgitation. Mitral valve area was determined by planimetry and pressure half-time measurement. Overlap of the aortic regurgitation and mitral inflow jets was graded 0 (no overlap) to 4 (marked overlap) by Doppler study and cine NMR imaging. The volume of signal loss resulting from turbulent blood flow secondary to the aortic regurgitation jet was determined on cine NMR images, and the extent of contact with the left ventricular endocardium was graded 0 (no contact) to 4 (extensive contact). RESULTS The presence of an Austin Flint murmur did not correlate with mitral valve area (2.7 +/- 0.8 cm2 with the murmur vs. 2.5 +/- 0.7 cm2 without), overlap of the aortic regurgitation and mitral flow jets (3 +/- 1 vs. 2.3 +/- 1.2), diastolic mitral regurgitation (50% vs. 71%) or fluttering of the anterior mitral valve leaflet (70% vs. 50%). The presence of an Austin Flint murmur correlated best with the volume of signal loss associated with the aortic regurgitation jet on cine NMR imaging (65 +/- 16 ml with the murmur. vs. 38 +/- 11 ml without, p less than 0.001) and the extent of contact of this signal loss with the left ventricular endocardium (2.9 +/- 0.5 vs. 1.5 +/- 0.4, p less than 0.0001). CONCLUSIONS The Austin Flint murmur is caused by the aortic regurgitation jet abutting the left ventricular endocardium, resulting in the generation of a low-pitched diastolic rumbling.