Ivor L. Gerber
Auckland City Hospital
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Circulation | 2003
Ivor L. Gerber; Ralph Stewart; Malcolm Legget; Teena West; Renelle French; Timothy M. Sutton; Timothy G. Yandle; John K. French; A. Mark Richards; Harvey D. White
Background—The onset of symptoms is a critical point in the natural history of aortic stenosis and the cardinal indication for valve replacement. This study assessed the associations between natriuretic peptide levels, disease severity, and cardiac symptoms in aortic stenosis. Methods and Results—Seventy-four patients with isolated aortic stenosis underwent independent assessment of symptoms, transthoracic echocardiography, and measurement of plasma levels of atrial natriuretic peptide, brain natriuretic peptide (BNP), and N-BNP. Natriuretic peptide levels were also measured in 100 clinically normal control subjects. The aortic valve area was smaller in symptomatic patients (n=45) than in asymptomatic patients (n=29; mean, 0.71±0.23 cm2 and 0.99±0.31 cm2, respectively;P <0.0001). Plasma natriuretic peptide levels were higher in symptomatic patients than in asymptomatic patients (for N-BNP: median, 112 versus 33 pmol/L; interquartile range, 70 to 193 versus 16 to 58 pmol/L, respectively;P =0.0002). After adjustment for age, sex, serum creatinine, aortic valve area, and left ventricular ejection fraction, N-BNP levels were 1.74 times higher (95% confidence interval, 1.12 to 2.69) for symptomatic than asymptomatic patients with aortic stenosis (P =0.014). Natriuretic peptide levels increased with the New York Heart Association class (for N-BNP median values were 13, 34, 105, and 202 pmol/L for normal control subjects, class I, class II, and class III/IV patients, respectively; interquartile ranges for the same patients were 8 to 21, 16 to 58, 57 to 159, and 87 to 394 pmol/L;P <0.0001). Similar associations were observed for BNP and atrial natriuretic peptide. Conclusions—Plasma natriuretic peptide levels are elevated in symptomatic patients with aortic stenosis. Measurement of natriuretic peptides may complement clinical and echocardiographic evaluation of patients with aortic stenosis.
Journal of the American College of Cardiology | 2003
Timothy M. Sutton; Ralph Stewart; Ivor L. Gerber; Teena West; A. Mark Richards; Timothy G. Yandle; Andrew Kerr
OBJECTIVES This paper will describe associations between plasma natriuretic peptide levels and the severity and symptoms of mitral regurgitation (MR). BACKGROUND A biochemical test that assisted grading of the severity of MR and the interpretation of symptoms would be of clinical value. METHODS Forty-nine patients with isolated MR and left ventricular (LV) ejection fractions (EFs) of >55% underwent transthoracic echocardiography, assessment of symptoms, and measurement of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and its amino-terminal portion, N-BNP. RESULTS The level of each natriuretic peptide rose with increasing severity of MR and with increases in left atrial (LA) dimensions (p < 0.001 for all comparisons), but no significant correlation existed between any natriuretic peptide and the LV dimensions or EF. Natriuretic peptide levels were higher in symptomatic MR (n = 16, BNP geometric mean 16.9 [95% confidence interval (CI) 13.3 to 21.4] pmol/l) compared with asymptomatic MR (n = 33, BNP 7.1 [95% CI 6.0 to 8.4] pmol/l, p < 0.001), and higher in asymptomatic MR than in normal controls (n = 100, BNP 5.3 [95% CI 4.8 to 5.8] pmol/l, p < 0.0001). These differences were similar for N-BNP and ANP and remained statistically significant (p < 0.05) after adjustment for echocardiographic measures of LV function and severity of MR. Both the sensitivity and the specificity for symptoms for the natriuretic peptides (area under receiver-operator characteristic curve for BNP = 0.90, N-BNP = 0.89, ANP = 0.89) were similar to the MR score (0.88) and greater than for LA dimension (0.81), vena contracta width (0.82), and LV end-systolic dimension (0.63). CONCLUSIONS Plasma natriuretic peptides levels increase with the severity of MR and are higher in symptomatic compared to asymptomatic patients, even when LV EF is normal.
Circulation | 2005
Andrew D. Michaels; Barry H. McKeown; Michael Kostal; Kalpesh T. Vakharia; Mark V. Jordan; Ivor L. Gerber; Elyse Foster; Kanu Chatterjee
Background—Levosimendan is a calcium-sensitizing agent and an inodilator under current investigation in the treatment of decompensated heart failure. The effects of intravenous levosimendan on the human coronary vasculature, together with myocardial wall stress and oxygen uptake, have not been adequately studied. Methods and Results—Ten adult patients underwent right- and left-heart catheterization. Baseline coronary blood flow was determined with quantitative coronary angiography and an intracoronary Doppler-tipped guidewire. Myocardial oxygen uptake was measured with a coronary sinus catheter. Echocardiography was performed before and 30 minutes after an intravenous infusion of levosimendan (24-&mgr;g/kg bolus over 10 minutes) was begun. Pulmonary capillary wedge decreased 37% (P=0.009), cardiac output increased 9% (P=0.04), and systemic vascular resistance decreased 18% (P<0.001). Left ventricular ejection fraction increased 20% (P=0.009), and meridional systolic wall stress decreased 48% (P=0.009). Coronary artery diameter increased 10% at 15 minutes (P=0.001) and 11% at 30 minutes (P=0.01). Coronary artery velocity increased 10% over baseline (P=0.04). Coronary blood flow increased 45% (P=0.02), whereas coronary resistance decreased 36% at 30 minutes (P=0.03). Myocardial oxygen extraction decreased 9% at 30 minutes (P=0.04). Conclusions—Levosimendan given intravenously exerts vasodilator effects on human coronary conductance and resistance arteries. Despite a decrease in coronary perfusion pressure, coronary blood flow is increased. A reduction in coronary vascular resistance and a decrease in coronary venous oxygen content indicate primary coronary vasodilation by levosimendan. Improved left ventricular systolic function and decreased myocardial oxygen extraction suggest improved myocardial efficiency.
American Journal of Cardiology | 2003
Ivor L. Gerber; Ralph Stewart; John K. French; Malcolm Legget; Sally C. Greaves; Teena West; Andrew Kerr; A. Mark Richards; Harvey D. White
In 40 patients with chronic moderate to severe aortic regurgitation, brain natriuretic peptide, N-brain natriuretic peptide, and atrial natriuretic peptide were higher in symptomatic patients compared with asymptomatic patients after adjustment for age, gender, and ejection fraction, but each natriuretic peptide correlated weakly with echocardiographic measures of left ventricular size and function. In patients with chronic aortic regurgitation, measurement of natriuretic peptide levels may provide information on left ventricular function in addition to echocardiography.
Circulation | 2006
Patrick Gladding; Peter Ruygrok; Sally Greaves; Ivor L. Gerber; Andrew W. Hamer
An 86-year-old woman who lived independently was referred for consideration of percutaneous closure of a left ventricular free wall rupture site. Ten years earlier, she had undergone aortic valve replacement with a Carpentier-Edwards bioprosthesis (Edwards Lifesciences, Irvine, Calif) and received a single saphenous vein graft to the right coronary artery. Five years later, at the age of 81, she had an inferolateral myocardial infarction and an acute rupture of the left ventricular free wall. The resultant false …
Journal of The American Society of Echocardiography | 2014
David Sidebotham; Sara Jane Allen; Ivor L. Gerber; Trevor M. Fayers
Surgical repair of the mitral valve is being increasingly performed to treat severe mitral regurgitation. Transesophageal echocardiography is an essential tool for assessing valvular function and guiding surgical decision making during the perioperative period. A careful and systematic transesophageal echocardiographic examination is necessary to ensure that appropriate information is obtained and that the correct diagnoses are obtained before and after repair. The purpose of this article is to provide a practical guide for perioperative echocardiographers caring for patients undergoing surgical repair of mitral regurgitation. A guide to performing a systematic transesophageal echocardiographic examination of the mitral valve is provided, along with an approach to prerepair and postrepair assessment. Additionally, the anatomy and function of normal and regurgitant mitral valves are reviewed.
Clinical Transplantation | 2009
Nezar L. Amir; Ivor L. Gerber; John J. Edmond; Janice M. Langlands; A. Mark Richards; Peter Ruygrok
Abstract: Introduction: Elevated levels of plasma brain natriuretic peptide (BNP) and amino‐terminal BNP (NT‐proBNP) are associated with adverse cardiac outcomes. It is not known whether BNP and NT‐proBNP levels in heart donors can aid in selection and predict outcomes in transplant recipients.
International Journal of Cardiology | 2011
A. Lin; Christopher Occleshaw; Ivor L. Gerber; Ralph Stewart
Interventions of the European Society of Cardiology. Guidelines for percutaneous coronary interventions. Eur Heart J 2005;26:804–47. [5] Goldberg RJ, Samad NA, Yarzebski J, Gurwitz J, Bigelow C, Gore JM. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med 1999;340:1162–8. [6] Hochman JS, Sleeper LA,Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK investigators. Should we emergently revascularize occluded coronaries for cardiogenic shock. N Engl J Med 1999;341:625–34. [7] Urban P, Stauffer JC, Bleed D, et al. A randomized evaluation of early revascularization to treat shock complicating acutemyocardial infarction. The (Swiss)Multicenter Trial of Angioplasty for Shock-(S) MASH. Eur Heart J 1999;20:1030–8. [8] Vanzetto G, Akret C, Bach V, et al. Percutaneous extracorporeal life support in acute severe hemodynamic collapses: single centre experience in 100 consecutive patients. Can J Cardiol 2009;25:e179–86. [9] Spiecker M, Erbel R, Rupprecht HJ, Meyer J. Emergency angioplasty of totally occluded left main coronary artery in acute myocardial infarction and unstable angina pectoris-institutional experience and literature review. Eur Heart J 1994;15: 602–7. [10] Chauhan A, Zubaid M, Ricci DR, et al. Left main intervention revisited: early and late outcome of PTCA and stenting. Cathet Cardiovasc Diagn 1997;41:21–9. [11] Quigley RL, Milano CA, Smith LR, White WD, Rankin JS, Glower DD. Prognosis and management of anterolateral myocardial infarction in patients with severe left main disease and cardiogenic shock. The left main shock syndrome. Circulation 1993;88(5 Pt 2):II65–70. [12] Marso SP, Steg G, Plokker T, et al. Catheter-based reperfusion of unprotected left main stenosis during an acutemyocardial infarction (theULTIMAexperience). Unprotected Left Main Trunk Intervention Multi-center Assessment. Am J Cardiol 1999;83:1513–7. [13] Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS. NRMI investigators. Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. JAMA 2005;294:448–54. [14] Vlaar PJ, Svilaas T, vanderHorst IC, et al. Cardiacdeathand reinfarctionafter 1 year in the Thrombus Aspiration during Percutaneous coronary intervention in Acute myocardial infarction Study (TAPAS): a 1-year follow-up study. Lancet 2008;371:1915–20. [15] Stankovic G, Darremont O, Ferenc M, et al. European Bifurcation Club. Percutaneous coronary intervention for bifurcation lesions: 2008 consensus document from the fourth meeting of the European Bifurcation Club. EuroIntervention 2009;5:39–49. [16] Sabatine MS, Cannon CP, Gibson CM, et al. CLARITY-TIMI 28 investigators. Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarctionwith STsegment elevation. N Engl J Med 2005;352:1179–89. [17] Huang R, Sacks J, Thai H, et al. Impact of stents and abciximab on survival from cardiogenic shock treated with percutaneous coronary intervention. Catheter Cardiovasc Interv 2005;65:25–33. [18] Nichol G, Karmy-Jones R, Salerno C, Cantore L, Becker L. Systematic review of percutaneous cardiopulmonary bypass for cardiac arrest or cardiogenic shock states. Resuscitation 2006;70:381–94. [19] Shewan LG and Coats AJ. Ethics in the authorship and publishing of scientific articles. Int J Cardiol 2010;144:1–2.
Echocardiography-a Journal of Cardiovascular Ultrasound and Allied Techniques | 2005
Ivor L. Gerber; Barry H. McKeown; Walter S. Stullman; Nelson B. Schiller
Figure 1. An M-mode through the right ventricle, aorta, and left atrium showing complete opening and early systolic closure of the aortic valve (arrow) consistent with fixed subaortic obstruction. edema, a paradoxically spilt S2, and a harsh systolic murmur. A transthoracic echocardiogram showed asymmetric septal hypertrophy and a late peaking left ventricular (LV) outflow tract gradient of 137 mmHg. An Mmode showed early systolic closure of the aortic valve leaflets suggestive of fixed subaortic stenosis (Fig. 1). A chord to the anterior mitral valve leaflet was markedly thickened and demonstrated systolic anterior motion. There
JAMA | 2005
Gregory M. Marcus; Ivor L. Gerber; Barry H. McKeown; Joshua C. Vessey; Mark V. Jordan; Michele Huddleston; Charles E. McCulloch; Elyse Foster; Kanu Chatterjee; Andrew D. Michaels