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Biomedical subjects

U Elkayam

Publications and source records attributed to U Elkayam.

At least 73 records · Page 4Linked to original sources
PubMed1987

Central and renal hemodynamic effects and hormonal response to diltiazem in severe congestive heart failure.

The central and renal hemodynamic effects and the hormonal response to single doses of 60 mg and 90 mg of diltiazem were evaluated in 10 patients with severe chronic left ventricular (LV) systolic dysfunction (ejection fraction 0.22 +/- 0.08). Diltiazem administration resulted in only mild and mostly statistically insignificant changes. After 60 mg, only heart rate (from 86 +/- 10 beats/min at baseline to 79 +/- 14 beats/min at 4 hours) and pulmonary vascular resistance (from 231 +/- 108 to 165 +/- 74 dynes s cm-5 at 4 hours) changed significantly. Administration of 90 mg of diltiazem resulted in no significant change in any of the measured or calculated central hemodynamic variables. Individual data, however, revealed an increase stroke volume index in 3 patients but a decrease in 1 patient and a persistent increase in mean pulmonary artery wedge pressure in another patient. These hemodynamic changes were not associated with symptomatic deterioration in any of the patients. Both renal blood flow and glomerular filtration rate were impaired at baseline on both days and did not show a significant change 1, 2 and 4 hours after diltiazem administration. Similarly, no significant change was noted after either diltiazem dose in plasma catecholamine levels and renin concentration. In conclusion, administration of 60 to 90 mg of diltiazem in patients with severe chronic LV systolic dysfunction results in only mild and mostly insignificant acute effects on central and renal hemodynamics, plasma hormonal levels and patient clinical status.

Diltiazem↗
PubMed1987

Early tolerance to hemodynamic effects of high dose transdermal nitroglycerin in responders with severe chronic heart failure.

Transdermal systems for delivery of nitroglycerin have been shown to provide sustained blood levels of the drug for at least 24 hours. Investigations of hemodynamic effects of transdermal nitroglycerin in patients with heart failure have demonstrated a transient reduction in pressure lasting less than the expected 24 hours. These findings could be due to the development of circulatory tolerance to the vasodilatory effects of nitroglycerin or to insufficient drug dosing. In the present study, we compared the hemodynamic effects of the first and the second doses of high dose (120 mg) transdermal nitroglycerin given 24 hours apart in 11 responders (greater than or equal to 20% reduction in mean pulmonary artery wedge pressure lasting greater than or equal to 2 hours). Initiation of nitroglycerin therapy resulted in a significant reduction in mean right atrial pressure lasting for 14 hours and in a reduction in mean pulmonary artery and mean pulmonary artery wedge pressures lasting 24 hours. After administration of the second dose, mean right atrial pressure at 2 hours (9 +/- 5 versus 7 +/- 4 mm Hg), 4 hours (8 +/- 5 versus 6 +/- 4 mm Hg) and 8 hours (8 +/- 5 versus 6 +/- 3 mm Hg) was higher than after the first dose (p less than 0.05). Both mean pulmonary artery and mean pulmonary artery wedge pressures were significantly higher after the second nitroglycerin dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗
PubMed1987

Incidence of early tolerance to hemodynamic effects of continuous infusion of nitroglycerin in patients with coronary artery disease and heart failure.

Sustained therapy with nitroglycerin (NTG) has been reported to provoke the development of early tolerance. Because continuous intravenous NTG infusion is commonly used in patients with coronary artery disease and heart failure, we evaluated the incidence of early tolerance developed within the first 24 hr of therapy in 31 responders to NTG. After documentation of response to NTG, defined as a 10 mm Hg or greater or a 30% or greater reduction in mean pulmonary arterial wedge pressure (PAWP), 16 patients were blindly, randomly assigned to receive placebo and 15 patients were continued on same-dose NTG. Both groups showed an identical fall in PAWP at peak NTG titration (11 +/- 4 mm Hg). Discontinuation of NTG in the placebo group resulted in a rapid increase in PAWP to levels not significantly different from baseline (19 +/- 5 mm Hg at 2 hr vs 23 +/- 6 mm Hg at baseline; p = NS). In the NTG group, PAWP fell from 27 +/- 9 to 14 +/- 7 mm Hg, was 16 +/- 9 mm Hg at 2 hr (p less than .05 vs baseline), and continued to be significantly lower than baseline for 8 hr; however, due to attenuation of effect, PAWP values at 12, 20, and 24 hr were not significantly different from placebo or baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Hemodynamic effects of intravenous isosorbide dinitrate and nitroglycerine in acute myocardial infarction and elevated pulmonary artery wedge pressure.

We compared in a randomized fashion the hemodynamic effects of intravenous (IV) isosorbide dinitrate (ISDN) and nitroglycerine (NTG) in 45 patients with acute myocardial infarction and elevated pulmonary artery wedge pressure (Paw). Titration of ISDN dose to lower Paw greater than or equal to 25 percent resulted in a fall of this parameter from 32 +/- 8 to 24 +/- 5 mm Hg and was associated with a fall in mean blood pressure (96 +/- 15 to 90 +/- 14 mm Hg, p less than 0.05), systemic vascular resistance (1715 +/- 572 to 1548 +/- 414 dynes X s X cm-5, (p less than 0.05), pulmonary vascular resistance (182 +/- 106 to 154 +/- 78 dynes X s X cm-5, p less than 0.05) and mean right atrial pressure (11 +/- 4 to 7 +/- 4 mm Hg, p less than 0.05). In addition, ISDN significantly (p less than 0.05) increased cardiac index from 2.37 +/- 0.54 to 2.54 +/- 0.59 L/min/m2, stroke volume index from 28 +/- 8 to 31 +/- 8 ml/m2, and stroke work index from 28 +/- 11 to 31 +/- 12 g X m/m2. The ISDN dose ranged from 50 to 533 micrograms/min (mean +/- SD 326 +/- 176 micrograms/min) and could not be predicted from baseline hemodynamic values. A comparison between the effect of ISDN and NTG in doses producing comparable reduction in Paw showed similar hemodynamic changes. It was concluded that IV ISDN in patients with elevated mean pulmonary artery wedge pressure due to acute myocardial infarction results in a decrease in right and left ventricular preload and afterload and improvement of cardiac output and cardiac work. The effective dose ranges from 50 to 533 micrograms/min and cannot be predicted from baseline hemodynamic values. In doses producing comparable reduction in Paw, ISDN and NTG had similar hemodynamic effects.

Aged↗
PubMed1987

The pharmacokinetics of antiarrhythmic agents in pregnancy and lactation.

The pharmacokinetics of various drugs may be profoundly altered during different stages of pregnancy, parturition, and lactation. Gastrointestinal absorption or bioavailability of drugs may vary due to changes in gastric secretion and motility. Various haemodynamic changes such as an increase in cardiac output, blood volume, and renal plasma flow may affect drug disposition and elimination. The increase in blood volume and total body water which occurs during pregnancy can alter the volume of distribution for various drugs. Although exact quantifications are not easy, these changes in pharmacokinetic parameters should be considered when dosing antiarrhythmic agents in pregnant women. Plasma protein concentrations and drug binding capacity are altered in the mother and fetus as pregnancy advances. With highly protein bound drugs, these changes may be clinically significant, as the pharmacological efficacy and toxicity are presumed to be related to the concentration of free drug in both the mother and fetus. In some instances, the fetus may be susceptible to greater drug toxicity as free drug concentrations may be underestimated by measurement of total drug concentrations. Changes in maternal drug metabolism and metabolism by the fetoplacental unit also contribute to alterations in the pharmacokinetics of drugs. As the placenta contains many metabolising enzymes, biotransformation of drugs at this site could potentially convert a drug into an active metabolite, or prevent fetal exposure to a toxic drug. Placental transfer of drugs, leading to toxicity in the fetus, is a major concern in the pharmacological management of the pregnant patient. The passage of individual drugs will vary depending on their apparent volumes of distribution, degree of protein binding the rates of metabolic conversion and excretion within the placenta and fetus, the pH difference between the maternal and fetal fluids, and maternal haemodynamic changes. Drug properties such as lipid solubility, protein binding characteristics, and ionisation constant (pKa) also influence the placental passage of drugs. For weakly basic antiarrhythmic agents, the fetal drug concentration may potentially exceed the maternal plasma concentration when the fetal pH is lowered as in the case of fetal acidosis; this is due to 'ion trapping'. Additionally, higher free drug concentrations of these basic drugs may exist, due to decreased alpha 1-acid glycoprotein concentration and binding affinity in the fetus. Lignocaine (lidocaine) has been shown to enter fetal plasma rapidly with fetal-maternal concentration ratios in the range of 0.52 to 0.66.(ABSTRACT TRUNCATED AT 400 WORDS)

Anti-Arrhythmia Agents↗
PubMed1987

Management of cardiac arrhythmias during pregnancy. Current concepts.

Cardiac arrhythmia is one of the most common reasons for cardiac consultation during pregnancy. Fortunately, malignant arrhythmias during the course of normal gestation are rare, and the relatively common complaint of palpitations is usually due to benign arrhythmias. However, in pregnant patients with organic heart disease, arrhythmias are often triggered by the haemodynamic burden of pregnancy and may be the first manifestation of the disease. In addition, rhythm abnormalities in patients with limited cardiac reserves may have significant haemodynamic consequences and can compromise fetal well-being. Any woman who presents with rhythm disorders during pregnancy should undergo a diagnostic evaluation to rule out an underlying disease, including cardiac, pulmonary, endocrine, or metabolic disease. Additionally, removal of precipitating factors, such as excessive ingestion of caffeine and/or alcohol, cigarette smoking, drug abuse or therapy with arrhythmogenic compounds, is indicated (as these measures are desirable in any pregnant woman). Antiarrhythmic drug therapy is indicated in such patients only in symptomatic or haemodynamically significant arrhythmias. In cases where organic heart disease or any other cause for arrhythmia is identified, the underlying disease should be treated first. Antiarrhythmic drug therapy is indicated when arrhythmias persist or as a prophylactic measure. In principle, the approach to drug therapy in pregnant patients is similar to that in non-pregnant patients. However, special consideration should be given to drug selection in order to avoid adverse effects to the fetus. Those antiarrhythmics that have been shown to be relatively safe during pregnancy include digoxin, quinidine, procainamide, some beta-blocking drugs and lignocaine (lidocaine). In addition to careful drug selection, the smallest effective dose should be used and the indication for antiarrhythmic therapy should be periodically reassessed during the course of pregnancy.

Anti-Arrhythmia Agents↗
PubMed1987

Cardiovascular drugs in pregnancy.

Cardiovascular drugs are often used in pregnancy for the treatment of maternal and fetal conditions. The complex physiologic changes occurring during pregnancy may significantly affect the pharmacokinetics of many drugs and, consequently, the toxicity and therapeutic response. Of special concern are the effects of maternal therapy on the fetus and the undesired translactal passage of drugs to newborns. Although the body of information regarding cardiovascular therapy in pregnancy is incomplete, some of the available data are summarized in this article.

Adrenergic beta-Antagonists↗
PubMed1986

Effects of nifedipine on hemodynamics and cardiac function in patients with normal left ventricular ejection fraction already treated with propranolol.

The interaction between nifedipine and propranolol on cardiac hemodynamics and function was investigated in 9 patients with normal left ventricular (LV) function who were undergoing cardiac catheterization for complaints of chest pain. Only 2 patients had angiographic evidence of significant coronary artery disease but no patient had clinical evidence of ischemia during the study. All patients were pre-treated with propranolol, 30 to 320 mg/day (mean +/- standard deviation 210 +/- 122); the propranolol serum level ranged from 43 to 246 ng/ml (mean 203 +/- 62). The administration of nifedipine resulted in a decrease in blood pressure (from 94 +/- 11 to 85 +/- 13 mm Hg, p less than 0.05), increase in heart rate (from 59 +/- 6 to 65 +/- 7 beats/min, p less than 0.05), and an increase in both mean right atrial and mean pulmonary artery wedge pressures (from 8 +/- 3 to 9 +/- 3 mm Hg and from 13 +/- 3 to 14 +/- 4 mm Hg, respectively, both p less than 0.05). Cardiac index increased (from 2.3 +/- 0.3 to 2.7 +/- 0.2 liters/min/m2, p less than 0.01). Stroke volume index also increased significantly (from 39 +/- 5 to 43 +/- 6 ml/m2) and systemic vascular resistance decreased (from 1,715 +/- 369 to 1,255 +/- 271 dynes s cm-5, p less than 0.01). No significant change was noted in pulmonary vascular resistance (148 +/- 94 vs 140 +/- 62 dynes s cm-5), LV stroke work index (44 +/- 9 vs 42 +/- 10 g-m/m2), LV end-diastolic pressure (15 +/- 2 vs 16 +/- 2 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Neurohumoral consequences of vasodilator therapy with hydralazine and nifedipine in severe congestive heart failure.

We evaluated the effects of intravenous hydralazine (5 to 30 mg) and oral nifedipine (20 to 80 mg) on plasma catecholamines, renin, and aldosterone in 18 patients with severe chronic heart failure. Both drugs resulted in a significant decrease in systemic vascular resistance and mean systemic blood pressure, and led to an increase in cardiac output. Baseline plasma norepinephrine concentration was elevated in most patients; however, augmentation of cardiac output with both drugs did not decrease the values of this hormone (from 870 +/- 128 to 946 +/- 161 pg/ml with hydralazine and from 1088 +/- 260 to 1106 +/- 187 pg/ml with nifedipine). Plasma epinephrine level was also elevated at baseline and did not change significantly following nifedipine therapy (164 +/- 44 vs 199 +/- 54 pg/ml), but increased in most patients following the administration of hydralazine (from 105 +/- 45 to 153 +/- 27 pg/ml, p less than 0.01). The renin-aldosterone system was activated in our patients and also demonstrated a different response to both drugs. Hydralazine therapy did not change either the plasma renin concentration (30 +/- 7 vs 28 +/- 7 ng/ml/hr) or the aldosterone level (24 +/- 7 vs 22 +/- 5 ng/dl). In contrast, nifedipine increased the plasma renin concentration (22 +/- 7 to 29 +/- 8 ng/ml/hr, p less than 0.05). This change did not correlate with changes in systemic blood pressure (r = 0.03) and was probably the result of previously shown calcium blockade-mediated stimulation of renin release from the juxtaglomerular cells of the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Low blood mononuclear cell magnesium in intensive cardiac care unit patients.

Magnesium deficiency may play a role in the pathogenesis of atherosclerosis, cardiac arrhythmias, and coronary spasm. Because less than 1% of magnesium (Mg) is extracellular, the serum magnesium (sMg) does not always accurately reflect intracellular Mg stores. To determine the frequency of Mg deficiency in patients with cardiovascular disease, we measured blood mononuclear cell Mg content (mMg) and sMg concentrations in 104 unselected patients admitted to our intensive cardiac care unit (CCU). Twenty-seven normal healthy controls and 33 hypomagnesemic patients with chronic alcoholism and/or malabsorption syndrome served as reference groups. The sMg concentration in the CCU patients was 2.05 +/- 0.03 mg/dl (mean +/- SEM), and did not differ from normal controls (mean 2.01 +/- 0.03 mg/dl). Only 8 of 104 CCU patients were hypomagnesemic (7.7%). mMg in the CCU patients, however, was significantly lower than in the normal controls (1.15 +/- 0.02 micrograms/mg protein and 1.34 +/- 0.02 micrograms/mg protein respectively, p less than 0.001). Fifty-three percent (55 of 104) of CCU patients had mMg contents less than 1.119 micrograms/mg protein, i.e., below that of the lowest normal control. mMg was significantly lower in those patients with congestive heart failure (mMg = 1.08 +/- 0.03 micrograms/mg protein) when compared to those patients without congestive heart failure (1.23 +/- 0.02 micrograms/mg protein, p less than 0.001). We conclude that the incidence of intracellular Mg deficiency in patients with cardiovascular disease is much higher than the sMg would lead one to suspect, and may contribute to clinical cardiovascular morbidity.

Adult↗
PubMed1986

Cardiovascular response to dynamic exercise in patients with chronic symptomatic mild-to-moderate and severe aortic regurgitation.

Fifteen patients with symptomatic mild-to-moderate and severe chronic aortic regurgitation (AR) performed supine bicycle exercise while measurements of rest and exercise hemodynamics and left ventricular function were obtained. A continuous Doppler method was used to determine the change in distribution of total left ventricular stroke volume between forward stroke volume and regurgitant volume (RgV) with exercise. The pulmonary arterial wedge pressure (PAWP) was lower in the mild-to-moderate AR group than in the severe AR group at rest (8 +/- 1.2 vs 19 +/- 3.6 mm Hg, p = 0.01) and during exercise (15 +/- 3.9 vs 30 +/- 4.3 mm Hg, p = .02). In all patients there were increases in heart rate (78 +/- 4 to 96 +/- 5 beats/min, p less than .001), forward stroke volume (41 +/- 2 to 46 +/- 2 ml/m2), and the cardiac index (3.1 +/- 0.2 to 4.4 +/- 0.3 liters/min-m2, p less than .001), despite a fall in total left ventricular stroke volume index from 84 +/- 5 to 76 +/- 5 ml/m2 (p = .03). The systemic vascular resistance (SVR) decreased with exercise from 1277 +/- 72 to 1031 +/- 64 dynes-sec/cm5 (p less than .001), and the RgV and regurgitant fraction (RgF) both decreased with exercise from 43 +/- 5 ml/m2 to 30 +/- 4 ml/m2 (p = .002) and 0.50 +/- 0.03 to 0.37 +/- 0.03 (p less than .001), respectively. Left ventricular ejection fraction increased on exercise from 0.51 +/- 0.03 to 0.55 +/- 0.03 (p = .02) for the group, but it either decreased or failed to increase by at least 0.05 in seven of 13 patients. The change in ejection fraction on exercise was directly related to the change in SVR (r = .80, p less than .001). We conclude that: in patients with mild-to-moderate AR, the PAWP is generally normal at rest and exercise, in most of those with severe AR, the PAWP is elevated at rest and increases significantly with exercise, which is the likely mechanism for dyspnea on exertion in these patients, the cardiac index in both groups is normal at rest and increases on exercise, the increase in cardiac output results from both an increased heart rate and forward stroke volume, the increase in forward stroke volume results from reductions of RgV and RgF, the RgV and RgF are decreased due to a decreased SVR, and the ejection fraction response to exercise is variable and correlates best with changes in SVR with exercise.

Adult↗
PubMed1986

Efficacy and safety of medium- and high-dose diltiazem alone and in combination with digoxin for control of heart rate at rest and during exercise in patients with chronic atrial fibrillation.

We evaluated the efficacy and the safety of medium-(240 mn/day) and high-dose (360 mg/day) diltiazem alone and in combination with digoxin when used for control of heart rate in 12 patients with chronic atrial fibrillation. Medium-dose diltiazem was comparable to therapeutic dose of digoxin at rest (88 +/- 19 vs 86 +/- 12 beats/min) but superior during peak exercise (154 +/- 23 vs 170 +/- 20 beats/min; p less than .05). High-dose diltiazem resulted in better control of heart rate than digoxin both at rest (79 +/- 17 beats/min; p less than .05) and exercise (136 +/- 25 beats/min; p less than .05) but was associated with side effects in 75% of the patients. Combined therapy of digoxin and diltiazem enhanced the effect of digoxin alone and resulted in significantly better control of heart rate at rest (67 +/- beats/min with medium-dose and 65 +/- beats/min with high-dose diltiazem) and during peak exercise (132 +/- 32 and 121 +/- 24 beats/min, respectively). However, the difference in heart rate between these two doses was not significant. Reduction of heart rate combined with concomitant effect on blood pressure resulted in a significant fall in pressure-rate product at rest from 10,077 +/- 1708 mm Hg/min on digoxin alone to 7877 +/- 1818 mm Hg/min after the addition of medium-dose diltiazem (p less than .05) and during exercise form 25,670 +/- 3606 to 18,439 +/- 4115 mm Hg/min (p less than .05). Continued therapy with digoxin combined with diltiazem 240 mg/day for 21 +/- 8 days in nine patients showed persistent effect on heart rate and blood pressure without any toxic manifestations or change in serum digoxin (1.5 +/- 0.4 vs 1.3 +/- 0.4 ng/ml) or plasma diltiazem concentrations (204 +/- 72 vs 232 +/- 129 ng/ml). In conclusion, medium-dose diltiazem when combined with digoxin is an effective and safe regimen for the treatment of patients with chronic atrial fibrillation and enhances digoxin-mediated control of heart rate both at rest and during exercise.

Adult↗
PubMed1985

Hemodynamic and hormonal effects of high-dose transdermal nitroglycerin in patients with chronic congestive heart failure.

The hemodynamic effect of a large dose of nitroglycerin (NTG) (90 mg) given transdermally using a reservoir system was studied in 10 patients with severe, long-standing congestive heart failure. Serial hemodynamic measurements over 24 hours revealed a mild decrease in mean pulmonary artery wedge pressure. However, the change from baseline was significant only at 2 hours (19 +/- 9 vs 27 +/- 6 mm Hg). Mean right atrial pressure fell 1 hour after initiation of therapy, from 12 +/- 7 to 8 +/- 5 mm Hg. However, the change from control was not statistically significant. No significant changes were noted in heart rate, mean blood pressure, cardiac index, and systemic and pulmonary vascular resistance. Individual analysis of the effect of transdermal NTG on pulmonary artery wedge pressure demonstrated at 20% or greater reduction in 8 of 10 patients. However, persistent effect (longer than 8 hours) was seen in only 4 patients. Removal of NTG patches at 24 hours did not result in hemodynamic rebound. Serum catecholamine levels and renin concentration did not change 2 hours and 24 hours after initiation of NTG therapy or after removal of NTG patches. Thus, a large dose (90 mg) of transdermal NTG using a reservoir system results in mild and mostly statistically insignificant hemodynamic effect in patients with chronic severe congestive heart failure. Although a reduction in pulmonary artery wedge pressure is seen in most patients, rapid attenuation of this response is found in many patients and the effect only rarely lasts for 24 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗
PubMed1985

Spectrum of acute hemodynamic effects of nifedipine in severe congestive heart failure.

The acute hemodynamic effects of 20 to 50 mg of orally administered nifedipine were evaluated in 31 patients with severe chronic congestive heart failure (CHF) and the results were analyzed according to the response of the cardiac index (CI). Although the group mean value of CI increased significantly after nifedipine treatment (from 2.1 +/- 0.5 to 2.4 +/- 0.8 liters/min/m2, p less than 0.001), the individual response was variable. Twenty of the patients had 15% or greater increase in CI (group A) and 11 patients had less than a 15% increase or a decrease in CI (group B). Marked differences were also noted in the effects of nifedipine on other hemodynamic variables. Stroke volume increased 29 +/- 14% in group A and decreased 11 +/- 18% in group B (p less than 0.001). Systemic vascular resistance decreased 34 +/- 11% in group A (p less than 0.001) and increased slightly, 2 +/- 28%, in group B. Left ventricular (LV) stroke work index increased 11 +/- 19% in group A (p less than 0.001) and decreased markedly in Group B (21 +/- 20%). Six group B patients had a substantial worsening (20% or more) of one or more hemodynamic measurements, including CI, stroke volume index, LV stroke work index and mean pulmonary artery wedge pressure. A comparison of control hemodynamic values at rest, LV ejection fraction, associated coronary artery disease, nifedipine dose, and concomitant diuretic therapy revealed no significant differences between the 2 groups. This study confirms, in a large group of patients with severe CHF, the variable hemodynamic effects of nifedipine therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1985

Effect of diltiazem on renal clearance and serum concentration of digoxin in patients with cardiac disease.

The effect of diltiazem on digoxin serum concentration was evaluated in 9 patients who had been treated chronically for heart disease with digoxin, 0.25 mg/day. The indications for digoxin therapy were arrhythmias in 5 patients and mild heart failure in the other 4. Renal digoxin clearance was also evaluated in 8 of these patients. Serum digoxin concentration was measured at control, 7 +/- 2 days after initiation of 120 mg/day of diltiazem and 11 +/- 5 days after increasing the dose of diltiazem to 240 mg/day. Serum digoxin concentration was 0.9 +/- 0.4 ng/ml at control, 0.8 +/- 0.4 ng/ml with 120 mg/day of diltiazem, and 0.8 +/- 0.3 ng/ml during therapy with 240 mg/day. The differences between these values were not significant. Renal digoxin clearance also did not show a significant change after diltiazem therapy (44 +/- 15 ml/min before diltiazem and 46 +/- 13 ml/min with 240 mg/day of diltiazem). This study shows no effect of diltiazem in doses of 120 to 240 mg/day on serum digoxin concentration or renal digoxin clearance in patients who are treated chronically for heart disease with digoxin. In this dose range, diltiazem has advantages over verapamil, which markedly elevates digoxin levels.

Adult↗
PubMed1985

Superiority of two-dimensional measurement of aortic vessel diameter in Doppler echocardiographic estimates of left ventricular stroke volume.

Attempts to measure left ventricular stroke volume utilizing the Doppler aortic flow method have found varying correlations between invasive thermodilution and non-invasive Doppler methods. Because stroke volume is the product of the Doppler flow velocity integral (that is, the area under the flow velocity curve) and the cross-sectional area of the vessel through which blood flows, both variables are potential sources of error. Previous studies have shown that the Doppler flow velocity integral can be measured with acceptable reproducibility in the ascending aorta. Consequently, in this study an attempt was made to determine empirically the optimal method for measuring aortic diameter and area. The diameter of the ascending aorta was measured utilizing four M-mode and seven two-dimensional echocardiographic conventions. Doppler aortic flow velocity patterns were recorded with a 2.25 MHz M-mode echocardiographic transducer from the suprasternal notch by mapping the ascending aorta until aortic peak flow velocity was recorded. In 19 adult patients undergoing cardiac catheterization for clinical indications, Doppler stroke volume estimates utilizing the various echocardiographic conventions for measuring aortic root diameter and area were compared with simultaneous measurements of stroke volume by the thermodilution technique. The best correlation (r = 0.87) with thermodilution stroke volume was obtained by estimating aortic area from the two-dimensional parasternal long-axis images with the aortic dimension measured distal to the aortic sinuses from the inner to inner wall. The data were related by the equation: Thermodilution stroke volume = (0.73) X (two-dimensional Doppler stroke volume) + 17 cc.(ABSTRACT TRUNCATED AT 250 WORDS)

Aorta↗