Author
C Yoran
Bio: C Yoran is an academic researcher. The author has contributed to research in topics: Ventricular pressure & Diastole. The author has an hindex of 3, co-authored 3 publications receiving 789 citations.
Papers
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TL;DR: PRFR is determined by both the left atrial pressure and the left ventricular relaxation rate and should be used with caution as an index ofleft ventricular diastolic function.
Abstract: Peak rapid filling rate (PRFR) is often used clinically as an index of left ventricular relaxation, i.e., of early diastolic function. This study tests the hypothesis that early filling rate is a function of the atrioventricular pressure difference and hence is influenced by the left atrial pressure as well as by the rate of left ventricular relaxation. As indexes, we chose the left atrial pressure at the atrioventricular pressure crossover (PCO), and the time constant (T) of an assumed exponential decline in left ventricular pressure. We accurately determined the magnitude and timing of filling parameters in conscious dogs by direct measurement of phasic mitral flow (electromagnetically) and high-fidelity chamber pressures. To obtain a diverse hemodynamic data base, loading conditions were changed by infusions of volume and angiotensin II. The latter was administered to produce a change in left ventricular pressure of less than 35% (A-1) or a change in peak left ventricular pressure of greater than 35% (A-2). PRFR increased with volume loading, was unchanged with A-1, and was decreased with A-2; T and PCO increased in all three groups (p less than .005 for all changes). PRFR correlated strongly with the diastolic atrioventricular pressure difference at the time of PRFR (r = .899, p less than .001) and weakly with both T (r = .369, p less than .01) and PCO (r = .601, p less than .001). The correlation improved significantly when T and PCO were both included in the multivariate regression (r = .797, p less than .0001). PRFR is thus determined by both the left atrial pressure and the left ventricular relaxation rate and should be used with caution as an index of left ventricular diastolic function.
608 citations
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TL;DR: Findings support the clinical view that maintaining a small LV with sustained myocardial contractility will reduce mitral regurgitation and left ventricular dilatation can enhance mitral Regurgitation by increasing the effective regurgitant orifice independent of SPG.
Abstract: The dynamics of acute mitral regurgitation were studied in six open-chest dogs in whom a portion of the anterior leaflet was excised. Phasic mitral and aortic flows were measured electromagnetically and left ventricular filling volume, regurgitant volume (RV) and forward stroke volume (SV) were calculated. The systolic pressure gradient (SPG) between the left ventricle (LV) and left atrium (LA) was obtained from high-fidelity pressure transducers. The effective mitral regurgitant orifice area (MRA) was calculated from the hydraulic equation of Gorlin. Volume infusion resulted in significant increases in both left atrial and left ventricular pressures; thus, the SPG was unchanged and the increase in RV was due primarily to the increase in MRA. Angiotensin infused to raise arterial pressure resulted in greater increments in left ventricular than left atrial pressure, so that SPG rose significantly. The increase in RV was due to increases in both MRA and SPG. Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished. Despite a significant increase in SPG, RV did not increase, due to a substantial decrease in MRA. Thus, angiotensin and volume infusion induced a substantial increase in regurgitation due to the increase in MRA, while augmentation of contractility after norepinephrine infusion resulted in a decrease in regurgitation through reduction of MRA. These findings support the clinical view that maintaining a small LV with sustained myocardial contractility will reduce mitral regurgitation. Alternatively, left ventricular dilatation can enhance mitral regurgitation by increasing the effective regurgitant orifice independent of SPG.
160 citations
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TL;DR: It is concluded that the major determinant of the turbulence responsible for the creation of the Austin Flint murmur is the antegrade mitral flow stream and its mixing with the retrograde aortic flow.
Abstract: We studied the dynamic changes in mitral flow patterns and in mitral valve motion before and after producing acute, reversible aortic insufficiency (AI) in nine open-chest dogs. Phasic mitral flow, the mitral valve echocardiogram, and intracardiac phonocardiogram and other hemodynamic variables were measured. During moderate AI (mean regurgitant fraction 52 +/- 5%) (+/- SD), the antegrade filling volume decreased from 31 +/- 7 to 24 +/- 6 ml (p less than 0.01), but the peak protodiastolic mitral flow rate increased from 139 +/- 37 to 157 +/- 42 ml/sec (p less than 0.01), reflecting the shift of a larger fraction of total mitral filling volume to early diastole. In six dogs, atrial pacing was used to examine the hemodynamic effects of tachycardia. Increasing the heart rate from 90 to 120 beats/min increased cardiac output from 2.64 +/- 0.56 to 3.3 +/- 0.831/min (p less than 0.05) and decreased left atrial pressure from 24 +/- 8 to 17 +/- 7 mm Hg (p less than 0.05). Increasing heart rate to 150 beats/min compromised mitral filling, reduced cardiac output and increased left atrial pressure. Moderate tachycardia improves cardiac performance in AI by reducing regurgitant volume, without significantly reducing transmitral filling volume. The mitral valve echocardiogram showed only a small decrease in cusp opening amplitude during AI. A low-pitched left ventricular inflow tract murmur was recorded in protodiastole and corresponded in time to the rapidly increasing mitral flow. We conclude that the major determinant of the turbulence responsible for the creation of the austin flint murmur is the antegrade mitral flow stream and its mixing with the retrograde aortic flow.
31 citations
Cited by
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TL;DR: Mitral E velocity, corrected for the influence of relaxation (i.e., the E/Ea ratio), relates well to mean PCWP and may be used to estimate LV filling pressures.
2,911 citations
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Houston Methodist Hospital1, Duke University2, Northwestern University3, Mayo Clinic4, University of California, San Francisco5, Baylor University Medical Center6, Columbia University Medical Center7, Hospital of the University of Pennsylvania8, Harvard University9, University of Chicago10, Brigham and Women's Hospital11, University Health Network12, MedStar Health13
TL;DR: William A. Zoghbi, MD, FASE (Chair), David Adams, RCS, RDCS, Fase, Robert O. Bonow,MD, Maurice Enriquez-Sarano, MDs, Elyse Foster, Md, Fases, Paul A. Grayburn, MD-FASE, Rebecca T. Hahn,MD-MMSc, Yuchi Han, PhD, MMSc,* Judy Hung, MD.
Abstract: William A. Zoghbi, MD, FASE (Chair), David Adams, RCS, RDCS, FASE, Robert O. Bonow, MD, Maurice Enriquez-Sarano, MD, Elyse Foster, MD, FASE, Paul A. Grayburn, MD, FASE, Rebecca T. Hahn, MD, FASE, Yuchi Han, MD, MMSc,* Judy Hung, MD, FASE, Roberto M. Lang, MD, FASE, Stephen H. Little, MD, FASE, Dipan J. Shah, MD, MMSc,* Stanton Shernan, MD, FASE, Paaladinesh Thavendiranathan, MD, MSc, FASE,* James D. Thomas, MD, FASE, and Neil J. Weissman, MD, FASE, Houston and Dallas, Texas; Durham, North Carolina; Chicago, Illinois; Rochester, Minnesota; San Francisco, California; New York, New York; Philadelphia, Pennsylvania; Boston, Massachusetts; Toronto, Ontario, Canada; and Washington, DC
2,030 citations
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TL;DR: Mitral flow velocity recordings have clinical potential in assessing left ventricular diastolic function that merits further investigation, despite the indirect method of estimation and certain limitations.
1,549 citations
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TL;DR: These new Doppler applications have been shown to provide an accurate estimate of LV relaxation and appear to be relatively insensitive to the effects of preload compensation.
1,024 citations
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01 Feb 1989
TL;DR: An interpretation of the mitral valve, tricuspid valve, and systemic and pulmonary venous inflow velocities in the normal patient and in various disease states is provided.
Abstract: Evaluation of diastolic filling of the heart has been difficult because of its complexity and the numerous interrelated contributing factors. Previous determinations have depended on high-fidelity, invasive measurements of instantaneous pressure, volume, mass, and wall stress, which could not be done on a routine clinical basis. With the advent of Doppler echocardiography, intracardiac blood flow velocities can now be noninvasively assessed. For application of this technique to evaluation of diastolic function in patients with heart disease, it is necessary to understand what the Doppler-derived variables represent. It is also necessary to know how they are affected by changes in loading conditions and changes in myocardial relaxation. In this review, we provide an interpretation of the mitral valve, tricuspid valve, and systemic and pulmonary venous inflow velocities in the normal patient and in various disease states.
770 citations