Ratio Of Peak Diastolic Velocity Research Articles

NAD+ Redox Imbalance in the Heart Exacerbates Diabetic Cardiomyopathy.

Diabetes is a risk factor for heart failure and promotes cardiac dysfunction. Diabetic tissues are associated with nicotinamide adenine dinucleotide (NAD+) redox imbalance; however, the hypothesis that NAD+ redox imbalance causes diabetic cardiomyopathy has not been tested. This investigation used mouse models with altered NAD+ redox balance to test this hypothesis. Diabetic stress was induced in mice by streptozotocin. Cardiac function was measured by echocardiography. Heart and plasma samples were collected for biochemical, histological, and molecular analyses. Two mouse models with altered NAD+ redox states (1, Ndufs4 [NADH:ubiquinone oxidoreductase subunit S4] knockout, cKO, and 2, NAMPT [nicotinamide phosphoribosyltranferase] transgenic mice, NMAPT) were used. Diabetic stress caused cardiac dysfunction and lowered NAD+/NADH ratio (oxidized/reduced ratio of nicotinamide adenine dinucleotide) in wild-type mice. Mice with lowered cardiac NAD+/NADH ratio without baseline dysfunction, cKO mice, were challenged with chronic diabetic stress. NAD+ redox imbalance in cKO hearts exacerbated systolic (fractional shortening: 27.6% versus 36.9% at 4 weeks, male cohort P<0.05), and diastolic dysfunction (early-to-late ratio of peak diastolic velocity: 0.99 versus 1.20, P<0.05) of diabetic mice in both sexes. Collagen levels and transcripts of fibrosis and extracellular matrix-dependent pathways did not show changes in diabetic cKO hearts, suggesting that the exacerbated cardiac dysfunction was due to cardiomyocyte dysfunction. NAD+ redox imbalance promoted superoxide dismutase 2 acetylation, protein oxidation, troponin I S150 phosphorylation, and impaired energetics in diabetic cKO hearts. Importantly, elevation of cardiac NAD+ levels by NAMPT normalized NAD+ redox balance, alleviated cardiac dysfunction (fractional shortening: 40.2% versus 24.8% in cKO:NAMPT versus cKO, P<0.05; early-to-late ratio of peak diastolic velocity: 1.32 versus 1.04, P<0.05), and reversed pathogenic mechanisms in diabetic mice. Our results show that NAD+ redox imbalance to regulate acetylation and phosphorylation is a critical mediator of the progression of diabetic cardiomyopathy and suggest the therapeutic potential for diabetic cardiomyopathy by harnessing NAD+ metabolism.

Hemodialysis does not impair ventricular functions over 2 years

We aimed to evaluate the long-term effect of hemodialysis (HD) treatment on left and right ventricular (LV and RV) functions in patients with end-stage renal disease. The study population consisted of 22 patients with newly diagnosed end-stage renal disease. Before an arteriovenous fistula was surgically created for HD, the patients were evaluated by echocardiography for systolic and diastolic functions. After the first HD session (mean 24.22 ± 2.14 months), the second echocardiographic evaluations were performed. Left ventricular and RV functions before and after long-term HD treatment were compared. The mean age was 55 ± 13 years and 10 (45%) of the patients were female. After long-term HD treatment, the isovolumic relaxation time was significantly decreased; however, the peak early (E) and late (A) diastolic mitral inflow velocities, E/A ratio, and deceleration time of E wave were not significantly different from the baseline measurements. Also, there was no significantly change in the early diastolic velocity (Ea) of the lateral mitral anulus and the E/Ea ratio. Pulmonary vein peak diastolic velocity, peak atrial reversal velocity, and peak atrial reversal velocity duration remained almost unchanged even though the pulmonary vein peak systolic velocity and the pulmonary vein peak systolic velocity/pulmonary vein peak diastolic velocity ratio were significantly lower after long-term HD treatment. In addition, LV systolic functions, LV diameters, LV mass index, left atrium size, and RV diastolic functions were not statistically different after long-term HD treatment. The myocardium is exposed to hemodynamic, metabolic, and neuro-humoral abnormalities during HD treatment; however, the long-term effects of HD on ventricular functions are not clearly known. The present study showed that the long-term effects of HD on LV and RV functions were insignificant in patients with end-stage renal disease. We have demonstrated that the LV and RV functions did not change significantly after long-term HD treatment. We suggest that this result may be due to regulated blood pressure levels of the patients, treatment of anemia and other metabolic disorders during the HD period and the prevention of weight gain and hypervolemia.

Abstract 5733: Coronary Flow Reserve obtained by Transthoracic Echocardiography in Patients with Normal Coronary Arteries and Systolic Dysfunction, Normal Function and Coronary Artery Disease and Normal Function and Normal Coronary Arteries

Coronary Flow Reserve (CFR) has already been shown a reliable marker of physiological significance of coronary artery disease (CAD) and has recently been demonstrated to be an independent predictor of events in patients with dilated cardiomyopathy (DCM). Objective: To determine CFR in patients (pts) with DCM without obstructive CAD and in pts with normal systolic function and with obstructive CAD. Methods: We prospectively studied 67 pts with normal systolic function (mean age 46+/− 12 years, 48% male, left ventricular ejection fraction (EF) &gt;65%) and 47 pts with DCM (mean age 59 +/− 11 years, 52% male, EF&lt;35%) who underwent coronary angiography within 6 months from stress echocardiography. Diastolic velocity flow in the mid left anterior descending coronary artery was obtained by transthoracic echocardiography with use of intravenous commercially available contrast agent (Definity, Bristol-Myers Squibb) at baseline and during adenosine infusion (140 mcg/Kg/min, for 6 minutes). CFR was determined as the ratio of peak diastolic velocity in hyperemic/baseline conditions. All pts underwent quantitative coronary angiography (QCA). Results: Feasibility for assessing CFR was 83% in pts with normal function and 91% in DCM. Among the 56 pts in the final study with normal function, 25 had significant CAD and 31 had normal coronary arteries. Peak diastolic velocities in each group are described in Table . CFR was 2.86+/−0.58 ín pts with normal function and no CAD, 1.57+/−0.32 in pts with normal function and CAD, and 2.14+/−0.49 in pts with DCM and no CAD (p&lt;0.01 between groups). Sensitivity, specificity and accuracy for detecting CAD in pts with normal function was 96%, 94% and 95%, respectively. However, when considering the group with DCM, sensitivity was 74%, specificity 66% and accuracy 69%. Conclusions: CFR can accurately detect pts with CAD when systolic function is normal. Pts with DCM have diminished CFR that lowers the predictive value of this parameter to detect CAD.

Evaluation of coronary flow reserve in hypertensive patients by dipyridamole transesophageal Doppler echocardiography

This study evaluates the coronary flow reserve (CFR) in hypertensive patients with and without left ventricular (LV) hypertrophy. CFR was assessed by transesophageal Doppler echocardiography in 15 normal subjects (group I), 21 hypertensive patients without LV hypertrophy (group II), and 27 hypertensive patients with LV hypertrophy (group III). All hypertensive patients were complaining of typical anginal pain and had normal coronary angiograms. The sample volume was placed at the bifurcation of the left main and left anterior descending coronary arteries. Coronary blood flow velocities were evaluated at rest, 2 minutes after dipyridamole infusion, and 2 minutes after intravenous aminophylline. The ratios of dipyridamole to rest peak diastolic and systolic velocities were considered as indexes of CFR. Peak diastolic velocity ratio was significantly lower in group III than in groups I and II (1.6 ± 0.2, 2.7 ± 0.4, and 2.1 ± 0.2, respectively; p <0.05), and it was significantly lower in group II than I (p <0.05). The peak systolic velocity ratio was significantly lower in group III than in groups I and II (1.7 ± 0.3, 2.8 ± 0.3, and 2.1 ± 0.2, respectively; p <0.05), and it was significantly lower in group II than I (p <0.05). The peak diastolic velocity ratio was inversely related to systolic blood pressure, diastolic blood pressure, and LV mass index (r = −0.48, −0.51, and −0.37 respectively) in hypertensive patients. It is concluded that CFR is significantly impaired in hypertensive patients, especially those with LV hypertrophy, compared with healthy subjects. The degree of impairment of CFR is related to LV mass index.

Assessment of internal thoracic artery graft with intraoperative color doppler ultrasonography

Background. Intraoperative ultrasonography has the potential to provide anatomic and functional information about internal thoracic artery (ITA) graft, but this potential has been hindered by the relatively large standard probe. In this study, we used a color Doppler microprobe to evaluate ITA grafts. Methods. The subjects were 15 consecutive patients who underwent elective coronary artery bypass grafting either with cardiopulmonary bypass (n = 14) or without (n = 1). All patients underwent anastomosis of the left ITA to the left anterior descending artery. The ITA graft was assessed before the chest was closed, with the microprobe placed directly on the graft. Results. A good-quality color Doppler image of the ITA graft was easily obtained in all 15 patients within a few minutes. The ITA graft function was assessed by analyzing the shape of the pulsed Doppler wave. All ITA grafts were patent, and the mean graft diameter was 1.8 ± 0.04 mm. The peak systolic velocity, peak diastolic velocity, and mean velocity were 52.0 ± 14.9 cm/s, 58.3 ± 22.4 cm/s, and 36.5 ± 10.9 cm/s, respectively. The ratio of peak diastolic velocity to peak systolic velocity was 1.24 ± 0.66. The ITA graft seemed to function well when the biphasic diastolic predominant flow appeared. The mean blood flow was 55.1 ± 22.0 mL/min. Conclusions. Intraoperative ultrasonography using the microprobe provides adequate anatomic and hemodynamic information regarding ITA grafts. As the Doppler flow evaluation has high sensitivity and specificity, we suggest that intraoperative ultrasonography is useful for the assessment of these grafts.

Mitral flow velocity changes after 6 months of optimized therapy provide important hemodynamic and prognostic information in patients with chronic heart failure

Transmitral flow velocity patterns evaluated by Doppler echocardiography provide important hemodynamic and prognostic information in various cardiac conditions. However, these patterns may change over time, and so far the hemodynamic and prognostic significance of these changes has not been established. Accordingly, we performed this study to determine the hemodynamic and prognostic value of changes in transmitral flow velocity patterns after 6 months of optimized medical treatment in patients with chronic heart failure due to ischemic or nonischemic dilated cardiomyopathy. Ninety-eight consecutive patients with chronic heart failure underwent a clinical examination, a cardiopulmonary exercise test, and simultaneous Doppler echocardiographic and hemodynamic studies at baseline and after 6 months of optimized medical therapy. After the examination at 6 months, patients were followed up for 12 ± 7 months. Cardiac death and heart transplantation while patients were in critical condition were considered events. A restrictive pattern was defined by an early-to-late peak diastolic velocity ratio >1 and an early diastolic deceleration time ≤ 130 msec. Patients were grouped according to their mitral flow pattern at baseline and its changes after chronic optimized therapy. No significant changes in clinical, ergometric, and hemodynamic variables were found after 6 months in the 49 patients who had a persistent restrictive transmitral flow pattern or the 24 patients who had a persistent nonrestrictive transmitral flow pattern. In the 19 patients who had a restrictive pattern at baseline that reverted into a nonrestrictive pattern, this change was accompanied by a highly significant reduction in pulmonary wedge pressure (from 25 ± 7 mm Hg to 11 ± 3 mm Hg) and by an increase in exercise capacity, whereas in the 6 patients who had a nonrestrictive pattern that became restrictive, hemodynamic features markedly deteriorated. Seventeen of the 21 events occurred in the 49 patients (event rate 35%) with a persistent restrictive pattern, whereas the event rate was much lower in the 19 patients with a reversible restrictive pattern (5%) and in the 24 patients with a persistent nonrestrictive pattern (4%). Two (33%) of the 6 patients in whom a restrictive pattern developed had events. Cox analysis revealed that a restrictive transmitral flow pattern ( p = 0.0068) and peak rate of oxygen consumption ( p = 0.0056) detected at the late examination were significantly related to cardiac events. These results show that in patients with chronic heart failure, changes in transmitral flow patterns after chronic optimized therapy are correlated with changes in pulmonary wedge pressure, are accompanied by changes in functional capacity, and provide relevant independent prognostic information.