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Biomedical subjects

U Elkayam

Publications and source records attributed to U Elkayam.

At least 91 records · Page 5Linked to original sources
PubMed1985

Importance of internal controls, statistical methods, and side effects in short-term trials of vasodilators: a study of hydralazine kinetics in patients with aortic regurgitation.

We determined that the spontaneous changes in cardiac output (CO) over 12 hr in 21 patients with chronic severe aortic regurgitation averaged +/- 8.9% (p = .03). We then measured changes in CO over time after administering incremental doses of oral hydralazine (50, 100, 150, and 200 mg) every 12 hr and analyzed these changes by several methods. Changes over time of only + 14% were highly significant (p less than .001) when analyzed by t test, but were not significant by repeated-measures analysis of variance (ANOVA). When changes in CO were compared with internal control values (spontaneous changes over 12 hr), only changes of 20% or more were significant (p less than .05). Transient "peak effects" markedly overestimated the maximum effects after all doses. We then compared the incremental doses of hydralazine, given either every 8 or every 12 hr, with respect to (1) the hemodynamic changes induced, and (2) the relative incidence of acute side effects. Maximal increases in CO were similar when hydralazine was given every 8 hr (16 patients) and every 12 hr (21 patients), and ranged from + 14% after 50 mg to + 61% after 200 mg. After the 150 and 200 mg doses, marked sustained increases in CO were present at 8 hr and mild increases in CO were still present at 12 hr. Hydralazine every 8 hr was associated with side effects in 25% to 86% of patients, but when the drug was given every 12 hr it was associated with side effects in only 5% to 19% of patients (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Isometric exercise in patients with chronic advanced heart failure: hemodynamic and neurohumoral evaluation.

We evaluated the hemodynamic effects of isometric exercise in 53 patients with congestive heart failure (CHF) and compared them with those found in 10 normal subjects. In both groups, isometric exercise increased heart rate and blood pressure. Systemic resistance increased in patients with CHF (1862 +/- 520 vs 2126 +/- 642 dyne-sec-cm-5; p less than .001) but not in normal subjects (1359 +/- 268 vs 1380 +/- 252 dyne-sec-cm-5). Cardiac index and stroke volume index increased mildly but not significantly in the normal subjects (2.8 +/- 0.5 vs 3.1 +/- 0.7 liters/min/m2 and 46 +/- 8 vs 47 +/- 7 ml/m2) and showed a significant fall in the patients with CHF (2.1 +/- 0.6 to 1.9 +/- 0.6 liters/min/m2, p less than .01 and 23 +/- 7 vs 20 +/- 7 ml/m2, p less than .01). Mean pulmonary arterial wedge pressure increased in patients with CHF from 26 +/- 7 to 30 +/- 8 mm Hg (p less than .001). Although no significant change was found in mean value for stroke work index (21 +/- 9 vs 20 +/- 9 g-m/m2), the individual changes were variable, with marked decrease (greater than 15%) in 17 of the patients. This hemodynamic deterioration could not be predicted from resting hemodynamics, left ventricular ejection fraction, or functional classification. Isometric exercise resulted in no significant change in circulatory catecholamine levels or plasma renin concentration in our 10 normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Accuracy of determination of changes in cardiac output by transcutaneous continuous-wave Doppler computer.

The value of a previously validated portable, continuous-wave Doppler computer was assessed for measuring changes in cardiac output (CO). Simultaneous thermodilution and Doppler CO values were measured in triplicate in 16 patients undergoing clinical intervention with vasodilator therapy. A continuous-wave Doppler transducer was placed in the suprasternal notch and directed toward the ascending aorta and angled until the maximal velocity signal was obtained. The correlation coefficient was 0.92 (standard error of the estimate [SEE] = 0.48 liter/min) at rest; with intervention it was 0.88 (SEE = 0.52 liter/min). Our data indicate that the Doppler computer technique, when used in selected patients, is reliable in detecting changes in CO after vasodilator therapy. It may be of value in clinical situations in which hemodynamic monitoring is impractical.

Adult↗
PubMed1984

Differences in hemodynamic response to vasodilation due to calcium channel antagonism with nifedipine and direct-acting agonism with hydralazine in chronic refractory congestive heart failure.

The hemodynamic response to a similar reduction of systemic vascular resistance after nifedipine and hydralazine administration was compared in a randomized crossover protocol in patients with severe chronic congestive heart failure (CHF). All 15 patients showed a 25% or greater reduction in vascular resistance with intravenous hydralazine (5 to 30 mg) and 11 patients showed a similar response with oral nifedipine (20 to 50 mg). In the latter 11 patients, despite similar reductions in systemic vascular resistance (35 +/- 2% with nifedipine and 36 +/- 4% with hydralazine, difference not significant), nifedipine resulted in a smaller increase in stroke volume index (from 23 +/- 2 to 30 +/- 2 ml/m2 and from 24 +/- 2 to 34 +/- 2 ml/m2 with hydralazine, p less than 0.05), cardiac index (from 2.0 +/- 0.1 to 2.6 +/- 0.2 liters/min/m2 with nifedipine and from 2.0 +/- 0.1 to 2.8 +/- 0.2 liters/min/m2 with hydralazine, p less than 0.05) and stroke work index (from 25 +/- 3 to 27 +/- 3 gm/m2 with nifedipine and from 26 +/- 2 to 32 +/- 2 gm/m2 with hydralazine, p less than 0.05). The decrease in blood pressure after nifedipine was slightly but not significantly larger than that with hydralazine (13 +/- 3% vs 8 +/- 2%). The changes in right atrial pressure, pulmonary artery wedge pressure and pulmonary vascular resistance were similar. The 4 patients who did not reduce their systemic vascular resistance by at least 25% with nifedipine had a worsening of their hemodynamic state as evidenced by 1 or more of the following findings: elevation of vascular resistance, decrease in cardiac index and increase in pulmonary artery wedge pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Favorable effects of hydralazine on the hemodynamic response to isometric exercise in chronic severe aortic regurgitation.

The hemodynamic effects of isometric exercise and the response to hydralazine therapy were evaluated in 11 patients with chronic, severe aortic regurgitation (AR). Isometric exercise produced a significant increase in heart rate (from 78 +/- 11 to 93 +/- 19 beats/min [mean +/- standard deviation], p less than 0.05), mean blood pressure (from 83 +/- 8 to 104 +/- 20 mm Hg, p less than 0.05), mean right atrial pressure (from 3 +/- 2 to 7 +/- 5 mm Hg, p less than 0.05) and mean pulmonary artery wedge pressure (from 12 +/- 7 to 18 +/- 10 mm Hg, p less than 0.05). Small and insignificant changes were seen in cardiac index (from 3.4 +/- 0.8 to 3.9 +/- 1.0 liters/min/m2), systemic vascular resistance (from 1,097 +/- 257 to 1,171 +/- 284 dynes s cm-5), pulmonary vascular resistance (from 120 +/- 76 to 130 +/- 89 dynes s cm-5) and stroke volume index (from 44 +/- 10 to 43 +/- 12 ml/m2). After oral hydralazine administration (100 to 300 mg), hemodynamic values during isometric exercise were: Heart rate increased further, to 105 +/- 14 beats/min (p less than 0.05), mean blood pressure was 102 +/- 16 mm Hg (difference not significant [NS]) cardiac index increased markedly, to 5.2 +/- 1.4 liters/min/m2 (p less than 0.05), stroke volume index increased to 49 +/- 12 ml/m2 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Comparison of hemodynamic responses to nifedipine and nitroprusside in severe chronic congestive heart failure.

The hemodynamic effects of 20 to 40 mg of oral nifedipine were compared with those of intravenous nitroprusside in 11 patients with severe chronic congestive heart failure (CHF). In each patient, both drugs were administered to produce similar reduction of systemic vascular resistance (SVR) (29 +/- 13% with nifedipine and 29 +/- 12% with nitroprusside, difference not significant [NS]). At this comparable decrease in systemic vascular resistance, significant differences in hemodynamic responses to both drugs were noted: Nifedipine caused a smaller increase in cardiac index (20 +/- 20% vs 40 +/- 24%, p less than 0.02) and a larger decrease in mean blood pressure than nitroprusside (16 +/- 9% vs 8 +/- 10%, p less than 0.05). In addition, nifedipine produced a smaller decrease in mean pulmonary artery wedge pressure (13 +/- 24% vs 36 +/- 21%, p less than 0.001) and pulmonary vascular resistance than nitroprusside (6 +/- 42% vs 26 +/- 46%, NS). Mean right atrial pressure decreased with nitroprusside, from 10 +/- 7 to 5 +/- 3 mm Hg (p less than 0.05), but not with nifedipine (10 +/- 7 mm Hg before and after nifedipine administration, NS). Left ventricular stroke work index increased with nitroprusside (20 +/- 8 to 27 +/- 9 g-m/m2, p less than 0.05), but did not change with nifedipine (21 +/- 9 vs 21 +/- 10 g-m/m2, NS). These data show that nifedipine has an arteriolar dilatatory action in patients with CHF. However, compared with nitroprusside, nifedipine had a significantly larger hypotensive effect and had a lesser effect on right and left ventricular filling pressure, cardiac output and left ventricular function.

Administration, Oral↗
PubMed1984

Determination of cardiac output by transcutaneous continuous-wave ultrasonic Doppler computer.

To evaluate the accuracy of a new, portable, continuous-wave Doppler computer (Ultracom) in measuring cardiac output (CO), simultaneous thermodilution CO and Doppler CO were measured in triplicate in 39 selected patients. Technically adequate Doppler CO studies were obtained in 36 patients. Aortic root diameter was measured by echocardiography and the cross-sectional area was calculated. A continuous-wave Doppler transducer was placed in the suprasternal notch, directed toward the ascending aorta and angled until the maximal velocity signal was achieved. The systolic velocity integral was computed using fast Fourier transform technique. The Doppler CO was computed from the equation: CO = aortic cross-sectional area X systolic velocity integral X heart rate. Interobserver and intraobserver variability studies were also performed. CO measured by thermodilution ranged from 1.86 to 10.1 liters/min (mean 5.26 +/- 1.91 [+/- standard deviation]) and CO by the Doppler method ranged from 1.63 to 10.9 liters/min (mean 5.32 +/- 1.83). The correlation coefficient was 0.97 (p less than 0.001) and standard error of the estimate was 0.42. The regression equation showed that Doppler CO = 0.408 + 0.93 X thermodilution CO. The correlation in 29 volunteers for interobserver variability was 0.98 (p less than 0.001) and in 18 volunteers for intraobserver variability was 0.97 (p less than 0.001). Thus, CO can be determined accurately in many patients using this Doppler technique by trained and experienced persons; intra- and interobserver variability is small.

Cardiac Output↗
PubMed1984

Renal hemodynamic effects of vasodilation with nifedipine and hydralazine in patients with heart failure.

The central and renal hemodynamic effects of nifedipine were evaluated in nine patients with severe chronic congestive heart failure. Oral nifedipine (34 +/- 22 mg, mean +/- standard deviation) was associated with a decrease in systemic vascular resistance from 1,748 +/- 436 to 1,321 +/- 302 dynes . s . cm-5 (p less than 0.001) and mean arterial blood pressure from 96 +/- 11 to 87 +/- 6 mm Hg (p less than 0.05) and with an increase in cardiac output from 4.2 +/- 1.1 to 4.9 +/- 1.2 liters/min (p less than 0.001). Although renal vascular resistance decreased from 11,988 +/- 2,256 to 10,286 +/- 3,011 dynes . s . cm-5 (p less than 0.05), no significant change was seen in renal blood flow (599 +/- 120 to 640 +/- 162 ml/min), glomerular filtration rate (62 +/- 18 to 62 +/- 17 ml/min), filtration fraction (18 +/- 5 to 17 +/- 6%), the ratio of renal/systemic vascular resistance (7.0 +/- 1.0 to 7.9 +/- 1.8) and the ratio of renal blood flow/cardiac output (0.15 +/- 0.02 to 0.13 +/- 0.03). Intravenous hydralazine (10 +/- 5 mg), given to eight of the patients in a randomized crossover design, resulted in a larger increase in cardiac output than did nifedipine (38 +/- 7 versus 19 +/- 10%, p less than 0.001) and in an increase in total renal blood flow from 570 +/- 152 to 645 +/- 174 ml/min (p less than 0.001). Renal vascular resistance decreased from 12,080 +/- 2,934 to 10,153 +/- 2,372 dynes . s . cm-5 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Non-invasive measurement of cardiac output by a single breath constant expiratory technique.

A new single breath test has been developed that measures pulmonary blood flow (Qc) and pulmonary tissue volume by using the fact that Qc is proportional to the relationship between the absorption rate of acetylene (C2H2) from the alveolar gas and the rate of change of lung volume during constant expiratory flow. To make these measurements a bag in bottle system with a rolling seal spirometer, a mass spectrometer, and a minicomputer with analogue to digital conversion have been used. Qc was compared with cardiac output measured by the thermodilution technique in 20 patients with cardiac disease; some also had mild chronic obstructive pulmonary disease. The mean (SD) resting Qc for the group was 5.27 (1.22) l/min and the cardiac output measured by thermodilution was 5.30 (1.31) l/min. The mean difference between the two estimations of cardiac output was 0.03 l and the standard deviation of this difference was 0.76 l. The Qc technique was not successful in patients with an FEV1/FVC less than 60%, but seemed to be accurate in those with higher FEV1/FVC values. Correction of Qc for the effect of venous admixture in 14 patients resulted in an average 19% overestimation of cardiac output (6.01 (2.52) l/min v 5.05 (1.64) l/min). It is concluded that cardiac output can be accurately measured in patients with cardiac or mild pulmonary disease. No correction for venous admixture due to ventilation-perfusion mismatch was necessary in these patients, presumably because the large breath used by the technique overcomes most mild ventilation-perfusion maldistribution. These findings, in addition to the non-invasive nature of the technique, suggest potential value for the measurement of cardiac output in various clinical conditions.

Adult↗
PubMed1983

Acute hemodynamic effect of oral nifedipine in severe chronic congestive heart failure.

The temporal hemodynamic effects of oral nifedipine after a single dose of 20 to 40 mg were evaluated in 11 patients with severe chronic congestive heart failure (left ventricular ejection fraction 0.22 +/- 0.7 [mean +/- standard deviation]). Nifedipine significantly reduced systemic vascular resistance, from 1,850 +/- 493 to 1,315 +/- 398 dynes s cm-5 at 1 hour (29%), to 1,410 +/- 246 at 3 hours and to 1,523 +/- 286 at 6 hours (p less than 0.05). Cardiac index increased 21%, from 2.07 +/- 0.46 to 2.51 +/- 0.83 liters/min/m2 at 1 hour, to 2.38 +/- 0.53 liters/min/m2 at 3 hours (p less than 0.05) and to 2.24 +/- 0.41 liters/min/m2 at 6 hours. The group response of stroke volume to nifedipine was smaller. A peak increase of 17% was seen 3 hours after initiation of therapy (22.6 +/- 7.2 versus 25.5 +/- 6.1 ml/m2). This difference did not reach statistical significance. Mean blood pressure declined significantly, from 94 +/- 20 to 80 +/- 13 mm Hg at 1 hour, to 83 +/- 15 mm Hg at 3 hours and to 86 +/- 17 mm Hg at 6 hours (p less than 0.05) and was associated with no significant change in heart rate. The marked decrease in blood pressure resulted in a decrease in rate-pressure product from 12,272 +/- 4,230 to 10,500 +/- 2,074 mm Hg/min at 1 hour, to 10,374 +/- 2,735 mm Hg/min at 3 hours and to 11,047 +/- 3,813 mm Hg/min at 6 hours (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Correlation of 10-milliliter digital subtraction ventriculograms compared with standard cineangiograms.

Left ventriculograms were obtained with the use of 10 ml of contrast media by passing fluoroscopic video images through a video image processor. The low concentration of dye in the left ventricle was enhanced by the technique of mask mode subtraction, and the images were postprocessed to increase visibility by manipulation of the gray scale and contrast levels. These digital subtraction angiograms were compared to standard cineangiograms by means of 40 ml of contrast media. Of 30 patients studied, six (20%) had runs of ventricular tachycardia during the cineangiogram and had to be excluded. In the remaining 24 patients, there was a good correlation between the two techniques for left ventricular end-diastolic volume (r = 0.77, end-systolic volume (r = 0.95), and ejection fraction (r = 0.97). Spatial resolution in the digital studies was adequate to appreciate wall motion abnormalities that were visualized on the cineangiograms. Left ventricular end-diastolic pressure (LVEDP) did not change after the 10 ml injection, but the mean LVEDP rose 6.0 mm Hg after the 40 ml cineangiograms (p less than 0.01). Digital subtraction angiography can be used to obtain left ventriculograms with one-fourth the amount of contrast media and one-fourth the x-ray exposure compared to standard cineangiograms. This technology will permit multiple left ventriculograms to be obtained which, in turn, will allow intervention studies to be performed in the catheterization laboratory.

Adult↗
PubMed1983

Evaluation of dilated cardiomyopathy by pulsed Doppler echocardiography.

The ability of pulsed Doppler echocardiography to identify patients with left ventricular systolic dysfunction was evaluated in 12 patients with dilated (congestive) cardiomyopathy. A range-gated, spectrum analyzer-based Doppler velocimeter was used to record blood flow velocity in the ascending aorta and main pulmonary artery. The following blood flow velocity parameters were measured or derived: peak flow velocity, acceleration time, average acceleration, deceleration time, average deceleration, ejection time, and aortic flow velocity integral. Doppler blood flow velocity data in the cardiomyopathy patients were compared to data from 20 normal subjects. Measurements from the ascending aorta revealed that peak aortic flow velocity discriminated between cardiomyopathy patients (mean 47 cm/sec, range 35 to 62) and normal subjects (mean 92 cm/sec, range 72 to 120) with no overlap in data (p less than 0.001). Aortic flow velocity integral was also able to separate the patients with dilated cardiomyopathy (mean 6.7 cm, range 3.5 to 9.1) from normal subjects (mean 15.7 cm, range 12.6 to 22.5) with no overlap in data (p less than 0.001). Although mean values for average aortic acceleration and aortic ejection time were also significantly different (both p less than 0.005), there was some overlap between the two groups. Pulmonary artery blood flow studies demonstrated significantly increased average acceleration, as well as decreased ejection time (both p less than 0.05), but no difference in average deceleration or peak flow velocity in cardiomyopathy patients compared to normals. Compared to pulmonary flow measurements, aortic Doppler flow velocity measurements allowed better separation of cardiomyopathy and normal groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

The use of Doppler flow velocity measurement to assess the hemodynamic response to vasodilators in patients with heart failure.

To determine if the hemodynamic response to vasodilator therapy can be assessed noninvasively by pulsed Doppler velocimetry, we compared the hemodynamic changes after treatment to changes in Doppler aortic blood flow measurements. The relationship between the absolute values and percent changes of invasively measured systemic vascular resistance (SVR) and stroke volume (SV) and Doppler-measured peak flow velocity (PFV), left ventricular ejection time (ET) and flow velocity integral (FVI) were evaluated. Measurements were made during 18 drug interventions in 13 patients treated with vasodilator agents for congestive heart failure (CHF). A poor correlation was found between the absolute values of either SVR or SV and the absolute values of each of the three Doppler aortic blood flow indexes studied. In contrast, a good correlation was found between percent changes in aortic PFV and in SVR (r = -0.89), and between percent changes in Doppler aortic FVI and in SV (r = 0.88). The correlation between percent changes in SVR and FVI revealed an r value of -0.65, while the correlation between percent changes in SVR and in ET showed an r value of -0.15. Percent changes in SV and either PFV or ET correlated with r values of 0.75 and 0.70, respectively. We conclude that Doppler aortic blood flow measurement can be used to assess quantitative changes in SVR and SV after vasodilator therapy. These findings suggest that it may be useful for evaluating vasodilator drug therapy in patients with CHF.

Adult↗