Serial Blood Pressure Measurements Research Articles

The influence of prostaglandin E 1 on systemic and pulmonary haemodynamics after aortic surgery

The influence of a peroperative prostaglandin E1 (PGE1) infusion on systemic and pulmonary haemodynamics in a porcine model of aortic surgery was studied. Twenty-four pigs were randomised to PGE1 (100 ng/kg/min) or 0.9% Saline as placebo. Haemaccel was then infused to maintain a central venous pressure (CVP) of greater than 4 less than 6 mmHg and pulmonary artery wedge pressure (PAWP) of greater than 3 less than 5 mmHg. Standardised aortic surgery consisted of midline laparotomy, small bowel exteriorisation, 1.5 h aortic clamping and 1 h shock before resuscitation. Serial measurements of blood pressure (BP), cardiac output (CO), pulmonary vascular resistance (PVR), pulmonary shunt (A-V shunt), and arterial PO2 (PaO2) were recorded during and three days after surgery. Volume loading with Haemaccel prevented a significant fall in initial BP on PGE1 at 95.1 +/- 48 mmHg compared to 102 +/- 4.9 mmHg in control animals with similar CO in the two groups. Following release of the aortic clamp all animals became profoundly hypotensive with BP falling to 74.6 +/- 3.0 and 68.7 +/- 3.2 mmHg for PGE1 and placebo respectively, but CO was protected in those animals receiving PGE1 at 1.92 +/- 0.04 compared to 1.67 +/- 0.1 L/min/m2 on placebo and remained significantly higher following resuscitation and three days later (P less than 0.05). PGE1 also reduced the marked rise in pulmonary vascular resistance to 922 +/- 84 dynes-s/cm5/m2 during shock in control animals to only 555 +/- 30 (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of metoprolol on serial measurements of exchangeable sodium, blood pressure, renin and pulse rate in spontaneously hypertensive rats.

The cardioselective beta-blocker metoprolol was mixed with the diet (6 mg metoprolol/g food) and given to 9 spontaneously hypertensive rats (SHR) for four weeks, while 9 other SHR were given the plain diet only and served as controls. All rats were also given 0.5% drinking saline labeled with isotope 22Na (37 kBq/1) to drink. Measurements of total exchangeable sodium, blood pressure, pulse rate and weight were performed before and repeatedly during treatment. Plasma renin activity was measured at the end of the study. Before treatment exchangeable sodium, blood pressure, pulse rate and weight were no different between the groups. Metoprolol reduced the pulse rate and prevented the usual blood pressure increase in SHR. Both groups gained weight similarly. Exchangeable sodium increased similarly in both groups along with the weight increase. Plasma renin activity was not significantly different in the two groups. Thus, chronic metoprolol treatment of SHR reduced blood pressure and pulse rate in SHR but did not lower plasma renin or cause measurable sodium or fluid retention.

Geographic variation in the incidence of hypertension in pregnancy

Prospectively collected information on blood pressure and proteinuria was available for geographically defined populations of primigravidas in Burma, China, Thailand, and Viet Nam. Clinically recognized hypertension during pregnancy varied by a factor of 25 between countries, and even a strict definition of proteinuric preeclampsia revealed a variation by a factor of 5. Serial measurements of blood pressure in each country showed remarkably similar levels early in the second trimester but a divergence thereafter. We conclude that there are genuine differences in the incidence of hypertensive disorders of pregnancy in the populations of Southeast Asia and that these are not caused by underlying differences in the baseline blood pressures in these populations.

Cardiovascular effects of vasoactive intestinal peptide in healthy subjects

Hypotension and flushing are occasionally observed in patients with pancreatic cholera syndrome. Similar effects are produced when vasoactive intestinal polypeptide (VIP) is administered to healthy subjects. To characterize further these responses, serial measurements of heart rate, blood pressure, cardiac output and forearm blood flow were made in 6 healthy subjects during constant VIP infusion (400 pmol/kg/hr for 100 minutes). VIP infusion caused sustained vasodilatation and decreased total peripheral resistance and mean arterial pressure by 30 and 12%, respectively. Forearm resistance decreased by 65%. The effects on cardiac output and stroke volume were biphasic. During the early phase of VIP infusion (0 to 70 minutes), heart rate and cardiac output increased with only minor changes in stroke volume. Later (71 to 100 minutes) the tachycardia persisted, but cardiac output decreased toward control levels due to decreased stroke volume. Echocardiograms during the infusion demonstrated increased left ventricular contractility as defined by the relation between end-systolic wall stress and shortening fraction. These data document potent vasodilatory and inotropic actions of VIP. It is likely that intravascular volume losses from increased intestinal secretion account for the decreased stroke volume seen late in the VIP infusion period and immediately thereafter. The tachycardia appears to be an appropriate compensatory mechanism to maintain blood pressure in the presence of vasodilatation and loss of intervascular volume. These observations provide an explanation for the cardiovascular findings in patients with sudden release of VIP from tumors.

Sleep apnea-associated hypertension and reversible left ventricular hypertrophy

Children with sleep apnea syndrome may have persistent marked elevation of systemic blood pressure, 1,2 which is potentially reversible in adolescents 3 and adults 4' s when the underlying apnea is effectively treated. The occurrence and potential reversibility of marked left ventricular hypertrophy associated with this secondary form of hypertension has not, to our knowledge, been previously reported: We report two siblings with significant hemodynamic complications of this syndrome. CASE REPORTS Patient 1. This black male patient was first seen at age 2 years because of severe respiratory distress after a 5-day history of cough and congestion. In the emergency room, he was unresponsive, with perioral cyanosis and poor air exchange. His weight (22.7 kg) was >95th percentile for age, and height was 86 cm (30th percentile for age). His initial blood pressure was 155/78 (>90th percentile for age and sex), but increased to a maximum of 200/130 within 12 hours. This was controlled initially with nitroprusside intravenously, then captopril and chlorothiazide orally. During this hospitalization, he required prolonged ventiiatory support, bronchodilati0n, and therapy for hypertension and heart failure. The chest radiograph showed cardiomegaly, and M-mode echocardiogram showed a large left ventricular diameter (4.2 cm), increased mass (49 g), and elevated right (0.52) and left (0.44) ventricular systolic time interval ratios. Measurements of the left ventricular posterior wall (0.6 cm) and septum (0.6 cm) were slightly increased for age and height. 6 A morning serum cortisol concentration was normal, as were results of thyroid function studies, serum lipid values, and bone age. He was eventually discharged with a diagnosis of severe bronchospasm leading to respiratory failure and congestive heart failure. For blood pressure control, captopril and chlorothiazide were pr escribed, with a 1200-calorie diet and sodium intake restriction. With this regimen, serial blood pressure measurements were normal (106/60 supine) for age and sex. Other medications included metaproterenol and phenobarbital.

Using the emergency department as a screening site for high blood pressure. A method for improving hypertension detection and appropriate referral.

This study describes the development and testing of a high blood pressure protocol for use in emergency departments (ED) to enhance detection of those patients appropriate for subsequent referral. The protocol involves two serial blood pressure measurements and a patient interview to determine: 1) previous history of high blood pressure (HBP), 2) treatment in past year for HBP, and 3) usual source of medical care. The accuracy of patient reporting was validated by comparison with the patients' hospital record (reflecting outpatient and inpatient visits). Results indicate that these self-reports have high levels of sensitivity (range 90-100%) and specificity (range 79-96%). Use of the additional patient information increased the sensitivity of the screening protocol in identifying when and where a patient should be referred. Use of this methodology indicates that the protocol is a simple and effective method for HBP screening. The findings also suggest that the ED is an ideal site for screening the "hard-to-reach" hypertensive population.

Narcolepsy, cataplexy, heart rate, and blood pressure.

Seven narcoleptic patients had serial measurements of blood pressure taken during nocturnal sleep over a period of 2 or 3 successive nights. Blood pressure was measured using a Doppler system with a cuff that automatically inflates every 15 min. There was no difference in the blood pressure measurements throughout the night compared with normal control subjects. Blood pressure followed the patterns of normal nocturnal variation; there was a nonsignificant increase in REM sleep compared with stage 3-4 NREM sleep. Studies of heart rate immediately preceding cataplectic attacks were inconclusive in identifying cardiovascular changes preceding muscle weakness.

Effect of chlorothiazide on serial measurements of exchangeable sodium and blood pressure in spontaneously hypertensive rats.

Chlorothiazide (100 mg/kg body weight) was given by gavage daily to spontaneously hypertensive rats for 4 weeks. Another group of spontaneously hypertensive rats was given only tap water and served as control. Measurements of total exchangeable sodium, blood pressure and weight were performed for 2 weeks before and for 4 weeks during treatment. Before treatment, exchangeable sodium, blood pressure and weight were similar in the two groups of rats. Chlorothiazide significantly attenuated the blood pressure increase in spontaneously hypertensive rats, the effect being most marked during the first 2 1/2 weeks of treatment and less thereafter. Rats in the chlorothiazide-treated group gained weight more slowly than did those of the control group. Exchangeable sodium, expressed as mmol/kg body weight, did not differ significantly between the two groups at any stage. When exchangeable sodium was expressed as mmol/rat, there was a more gradual rise in the chlorothiazide-treated animals, in accordance with their slower gain in weight. There was no temporal association between the antihypertensive effect of chlorothiazide and changes in exchangeable sodium. Thus whereas chlorothiazide treatment of spontaneously hypertensive rats slows the increase of both weight and exchangeable sodium, other mechanisms are apparently responsible for the antihypertensive action of the drug.

Effect of hydralazine on serial measurements of exchangeable sodium and blood pressure in spontaneously hypertensive rats.

Hydralazine was dissolved in 0.5% drinking saline (40 mg/1000 ml) labelled with isotope 22Na and given to spontaneously hypertensive rats for four weeks. Another group of rats were given isotope labelled saline only and served as control. Measurements of total exchangeable sodium, blood pressure, pulse rate and weight were performed before and repeatedly during treatment. Before treatment exchangeable sodium, blood pressure, pulse rate, and weight were no different between the groups. The antihypertensive effect of hydralazine was marked and maintained throughout the experiment. No significant changes were found in pulse rate. Both groups gained weight similarly. Exchangeable sodium increased at the same rate in both groups along with the weight increase. Thus, chronic hydralazine treatment effectively reduces blood pressure in spontaneously hypertensive rats without causing measurable sodium or fluid retention.

High blood pressure in the young.

Essential hypertension begins in early childhood. Current evidence suggests that those children persisting at high levels over time may be considered to have essential hypertension. The evaluation of high levels is best judged from blood pressure percentile grids representing population measurements, as long as the methods used to measure blood pressure and to generate the grids are similar. Resting, basal blood pressure measurements are more reproducible and are better for following the time course of blood pressure levels in children. Measurements should be made in an unhurried, relaxed atmosphere by trained observers using adequately lighted instruments placed at eye level and a cuff size appropriate for the child's arm length and circumference. Repeated observations and serial blood pressure measurements of growing children are necessary for judgments of abnormal levels. There is a progressive rise of approximately 1.5 mm Hg systolic and 1 mm Hg diastolic pressure per year of age, but blood pressure levels in the growing child are more closely related to height. In most instances elevated blood pressure levels in children cannot be attributed to secondary causes. Various hemodynamic and biochemical mechanisms have been identified in the early stages of hypertension, and mechanisms contributing to the development of hypertension may be of different magnitudes in black children and white children. Studies following young adults over many years have shown the predictive value of baseline blood pressure levels for subsequent hypertension. Children tracking at the high percentiles can be identified and are candidates for early intervention. The key to early prevention of essential hypertension is to influence children and adolescents to adopt lifestyles that promote good health and prevent development of cardiovascular risk factors.

Effects of Pregnancy and Estrogen on the Angiotensin II Pressor Response of the Rabbit Using Serial Systolic Blood Pressure Measurement in the Ear

Serial systolic blood pressure measurements were made in order to assess the effects of pregnancy and estrogen on the angiotensin II pressor response of the rabbit. The systolic blood pressure of the ear in 5 pregnant rabbits did not change throughout the gestational period, being compatible with that in 14 nonpregnant rabbits. However, vascular resistance to infused angiotensin II (over 13.1 ng/kg/min required to elicit a pressor response of 20 mmHg in systolic pressure) was demonstrated as early as the 10th day of pregnancy, and maximum mean resistance occurred on the 20th day: the mean pressor dose required was 34.5 ± 3.6 ng/kg/min (mean ± S.D.). In a separate series, vascular resistance in castrated rabbits was demonstrated as early as the 10th day of estrogen administration, reached a maximum at the 4th week, and then gradually decreased to the control level (pretreatment, 10.5 ± 2.5 ng/kg/min; 10 days, 18.9 ± 2.3 ng/kg/min; 4 weeks, 32.4 ± 5.4 ng/kg/min; 10 weeks, 18.3 ± 3.6 ng/kg/min; and 24 weeks, 11.0 ± 2.0 ng/kg/min). These results indicate that (1) pregnant rabbits have a decreased sensitivity to angiotensin II, (2) estradiol may modulate the angiotensin II pressor response in castrated rabbits, and (3) serial systolic blood pressure measurement may provide an appropriate test for the angiotensin II pressor response in rabbits.

Serial blood pressure measurements and cardiovascular disease in a Japanese cohort.

A cohort of 16,711 residents of Hiroshima and Nagasaki have participated in a program of biennial clinical examination and history taking that began in 1958. During 1958-1974, a total of 621 confirmed cases of cerebrovascular disease and 218 confirmed cases of coronary heart disease were incident. This study makes a detailed examination of the relationship between a series of biennial examination blood pressure (BP) measurements and cardiovascular disease risk. Two aspects are emphasized: the quantitative relationship between risk and both systolic blood pressure (SBP) and diastolic blood pressure (DBP), and the predictive value of BP levels some years in the past, given more recent BP determinations. Cerebral hemorrhage incidence is shown to depend markedly on recent DBP level, while earlier DBP levels make an additional important contribution to risk prediction. Corresponding SBP levels have little additional predictive value. With cerebral infarction, SBP is the more important predictor, though elevated DBP conveys some additional risk at high SBP levels. Recent BP levels are more strongly predictive for cerebral infarction than are BP levels some years earlier. Elevated SBP is also an important predictor of coronary heart disease risk in this population, while elevated DBP does not appear to be predictive at specified SBP. SBP levels several years in the past are more closely associated with coronary heart disease risk than are recent SBP readings. The dependence of BP relative risk functions on sex and age is examined and some departures from the results just listed are noted at younger ages. Implications for disease mechanism and hypertensive therapy are discussed.

Tracking: Prediction of Future Values from Serial Measurements

Repeated measurements of the same characteristic, obtained over time from each of a cohort of individuals, often show systematic change that facilitates prediction of future values. Several investigators have called this regular behavior 'tracking'. Most definitions of the term are related to the idea that a single individual's repeated measurements have expectations equal to a constant percentile of the population distribution asit changes over time. This paper investigates the relationship between this concept and the pattern of change implicit in growth-curve models. Growth-curve models are shown to be more general in some ways, more restrictive in others. We illustrate prediction of future values by growth techniques with an analysis of serial blood pressure measurements from the Framingham Heart Study. We also compare growth-curve analysis with recent work by McMahan (1981, Biometrics 37, 447-455) and suggest a more general class of random-effects models that may be useful in the study of tracking.

194 CARDIOVASCULAR EFFECTS OF PERINATAL ASPHYXIA IN FULL-TERM INFANTS

The cardiovascular effects of severe perinatal asphyxia was studied during the first 3 days of life by serial measurements of arterial blood pressure (ABP), central venous pressure (CVP) and M-mode echocardiograms in 10 fullterm infants (B.Wt. 3482 ± 214g, G.A. = 40.5 ± 0.98 wks. one minute Apgar Score = 2.2 ± 0.44) and was compared to 10 healthy infants matched for B.Wt. and G.A. During the first 8 hours of life, ABP (mean ± S.E.) in asphyxiated infants was 44.8 ± 2.4 mmHg, RPEP/RVET was 0.61 ± 0.07, LPEP/LVET was 0.40 ± 0.03 and the echocardiographically derived LV stroke volumes (LVSV) was 4.9 ± 0.66 ml and the aortic ejection area (AEA) was 97 ± 5 Cm-Msec. In the healthy infants, the corresponding values were: APB = 48.3 ± 1.8 mmHg, RPEP/RVET = 0.38 ± 0.03, LPEP/LVET = 0.33 ± 0.01, LVSV = 5.8 ± 0.31 ml and AEA = 127 ± 6 Cm-Msec. Except for elevated RPEP/RVET, there were no significant differences between asphyxiated and healthy infants at 24 and 48 hours of life. All asphyxiated infants had normal CVP for the first 8 hours and only one who subsequently expired, developed elevated CVP beyond the 24 hours of life. The presence LV failure and pulmonary hypertension in the absence of RV failure during the immediate post-partum period further supports the evidence for the vulnerability of LV during the transitional circulation and its contributory role in the genesis of the persistent pulmonary hypertension of the newborn.

On the relation between blood pressure change and initial value

The methods of Feinleib, Halperin and Garrison (FHG) [1,4] and maximum likelihood (ML) [5] were used to analyze the relation between initial value and change over time of serial blood pressure measurements among participants in the Framingham Heart Study [3]. Both methods assume a linear trend in expected blood pressure over time, with variation in intercept and slope over individuals. If individual values of the slope and intercept have a joint normal distribution in the population, the coefficient of regression of slope on initial value over individuals will also be linear. It is shown here that the FHG method tends to underestimate that coefficient of regression. Significantly positive regressions were found under the ML approach while the FHG approach failed to claim significance in most of the age-sex groups analyzed. A direct comparison of the efficacies of the two significance tests shows that the asymptotic relative efficiency (ARE) of the FHG and ML procedures is always less than one indicating that the ML test has larger power, i.e. is more likely to detect an association between change and initial value when one exists. These results establish the ML procedure as the preferred method for this problem. Since significantly positive regressions were found in most age groups for both sexes under the ML approach, we infer that there exists some degree of positive association between blood pressure change and initial value. Although the expected increase in the rate of change of systolic blood pressure (SBP) per mmHg increase in initial value is not very great, a younger woman or a middle-aged man with an SBP initial value 20 mmHg higher than the mean initial level of their age-sex group has an expected rate of increase almost twice the mean rate of increase in their groups.

Effects of morphine on left ventricular dimensions and function in patients with previous myocardial infarction.

To assess the effects of morphine sulfate on left ventricular function and dimensions we administered 15 mg of this agent to 11 stable patients with previous transmural myocardial infarction. All studies were carried out in the supine position. Before morphine administration an echocardiogram was obtained, and this procedure was repeated at 15, 30, 60, 120, and 240 min after morphine. Heart rate decreased from a control value of 69 +/- 4 to 62 +/- 5 beats/min 2 h after morphine (p less than 0.01, analysis of variance); this slower heart rate persisted for 4 h after morphine. Serial measurements of blood pressure, echocardiographic ejection fraction, percent of fractional shortening, and mean normalized velocity of circumferential fiber shortening also showed no significant alterations after morphine. We conclude that in stable patients with chronic ischemic heart disease studied in the supine position, 1) morphine exerts no effect on left ventricular dimensions, an observation which does not support the concept that this agent acts in humans by producing a 'pharmacologic phlebotomy'; and 2) morphine does not alter left ventricular function at rest. Whether different results will be found in patients with increased sympathetic activity, such as occurs in the setting of an acute myocardial infarction or during an episode of acute pulmonary edema, remains to be investigated.

LONGITUDINAL BLOOD PRESSURE MEASUREMENTS DURING A 26-YEAR OBSERVATION PERIOD AND THE RISK OF ISCHEMIC HEART DISEASE1

The importance of serial blood pressure (BP) measurements over long periods of time in the prediction of ischemic heart disease has received relatively little attention. In the Manitoba study cohort of 3983 men, most of them between 25–34 years of age at entry, systolic blood pressure (SBP) measurements at entry and at four other examinations approximately five years apart were related to the subsequent incidence of ischemic heart disease (IHD) during the 26-year observation period, from entry at July 1, 1948 to June 30, 1974. Because both age and SBP may determine the rate of rise In SBP after entry, the data were analyzed using multivariate techniques as well as cross-classification methods. After adjusting for entry age and SBP, change in SBP from entry to the later four examinations showed a greater Increase in those over 45 years of age, for longer intervals between measurements and most Importantly In those who later developed IHD. In multivariate analysis, SBP after entry was more strongly associated with IHD incidence than entry SBP. SBP closest to the event was the most significant SBP measurement but an earlier SBP measurement, usually five years before the last SBP, was also a significant consideration in IHD prediction. Therefore, in the evaluation of SBP for assessment of IHD risk, longitudinal SBP data after entry are an important consideration.

Effect of heparin-induced free fatty acid elevation on myocardial oxygen consumption in man

To determine whether acute elevation of plasma free fatty acids influences myocardial oxygen consumption in man, 17 patients underwent a metabolic study consisting of serial measurements of coronary sinus blood flow, heart rate and aortic blood pressure and arterial and coronary sinus determinations of oxygen, carbon dioxide, glycerol and free fatty acids both before and for 30 minutes after the intravenous administration of a bolus dose of 5,000 units of heparin. Of the 17 patients, 9 (group A) were fasting, and 8 (group B) ingested 100 g of fat 3 hours before the study in order to enhance post-heparin lipolysis. Marked elevation of arterial free fatty acid levels was seen in each group 30 minutes after administration of heparin (group A 713 ± 21 [mean ± standard error of the mean] to 1,757 ± 139 μmoles/liter, P < 0.001; group B 721 ± 57 to 2,668 ± 332 μmoles/liter, P < 0.001); significant increase in arterial-coronary sinus free fatty acid difference was also noted (group A 139 ± 11 to 298 ± 19 μmoles/liter, P < 0.001; group B 147 ± 11 to 334 ± 35 μmoles/liter, P < 0.001). Hemodynamic variables, including mean aortic pressure, heart rate, coronary sinus blood flow and coronary vascular resistance, were unchanged. Despite the marked increase in free fatty acids, myocardial oxygen consumption was unchanged 30 minutes after administration of heparin in both groups A and B. Myocardial triglyceride formation after heparin in both groups was suggested by (1) lack of change in cardiac respiratory quotient, (2) net myocardial glycerol uptake after heparin but not in the control state, and (3) oxygen extraction ratios totaling considerably in excess of 100 percent after heparin. The data suggest that acute elevation of plasma free fatty acids to pathophysiologic levels after heparin-induced lipolysis has no measurable effect on myocardial oxygen consumption in patients in stable condition, probably because the excess free fatty acids are stored as triglycerides rather than oxidized.

HEMODYNAMIC EFFECTS OF ISOSORBIDE DINITRATE VS NITROGLYCERIN IN PATIENTS WITH UNSTABLE ANGINA

The hemodynamic response to nitroglycerin administration, to sublingual or oral administration of isosorbide dinitrate, or to a placebo was evaluated and compared in 37 patients with unstable angina pectoris under resting, pain-free conditions. Patients with congestive heart failure were not included in this study. Serial measurements of mean arterial blood pressure (MAP), pulmonary arterial end-diastolic pressure (PAEDP), cardiac index (CI), and heart rate (HR) were obtained for one hour following nitroglycerin administration and for four hours following sublingual or oral administration of isosorbide dinitrate. Echocardiographic end-diastolic volume (EDV) measurements were obtained for the groups receiving isosorbide dinitrate or placebo. There was a significant (P

Hemodynamic Effects of Isosorbide Dinitrate vs Nitroglycerin in Patients with Unstable Angina

The hemodynamic response to nitroglycerin administration, to sublingual or oral administration of isosorbide dinitrate, or to a placebo was evaluated and compared in 37 patients with unstable angina pectoris under resting, pain-free conditions. Patients with congestive heart failure were not included in this study. Serial measurements of mean arterial blood pressure (MAP), pulmonary arterial end-diastolic pressure (PAEDP), cardiac index (CI), and heart rate (HR) were obtained for one hour following nitroglycerin administration and for four hours following sublingual or oral administration of isosorbide dinitrate. Echocardiographic end-diastolic volume (EDV) measurements were obtained for the groups receiving isosorbide dinitrate or placebo. There was a significant (P less than 0.05 or less than 0.1) reduction of the MAP (5 to 10 mm Hg) that persisted for more than four hours following both sublingual and oral administration of isosorbide dinitrate. The changes in the PAEDP, HR, and CI following sublingual or oral administration of isosorbide dinitrate were small and not significant. In the group receiving isosorbide dinitrate sublingually, the EDV was reduced by more than 30 ml below the placebo group (P less than 0.1) for up to four hours. The effects of nitroglycerin administration were similar in magnitude but of much shorter duration (three to four hours for sublingual and oral administration of isosorbide dinitrate vs 15 to 30 minutes for nitroglycerin). These data demonstrate that the duration of the hemodynamic effects of sublingually and orally administered isosorbide dinitrate in patients with unstable angina pectoris and normal resting hemodynamics is 8 to 12 times longer than that of nitroglycerin.