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PubMed1988

Cumulative hemodynamic response to short-term treatment with flosequinan (BTS 49465), a new direct-acting vasodilator drug, in severe chronic congestive heart failure.

Pharmacologic tolerance develops rapidly to the hemodynamic effects of many vasodilator drugs used in the treatment of congestive heart failure. We evaluated the responses to 3 days of therapy with a new long-acting vasodilator drug, flosequinan (BTS 49465), in 16 patients with severe chronic heart failure. On each of the 3 days, flosequinan (100 or 150 mg orally) produced marked increases in cardiac index and decreases in left ventricular filling pressure, mean right atrial pressure, and systemic vascular resistance (all p less than 0.01) without significant changes in heart rate. Whereas the effects of flosequinan on right and left ventricular filling pressures on the first and third days were similar, cardiac index was higher and systemic vascular resistance was lower after the third dose than after the first dose of the drug, indicating the occurrence of a cumulative vasodilator effect on arterial resistance vessels. Since all hemodynamic changes persisted for longer than 24 h after each dose of the drug, the daily administration of flosequinan also produced a progressive improvement in the hemodynamic state recorded before each dose of the drug. These data indicate that pharmacologic tolerance does not develop to the effects of flosequinan during short-term therapy with the drug in patients with severe chronic heart failure. Instead, further hemodynamic improvement may occur because of a cumulative vasodilator effect that results from the drug's prolonged duration of action.

Adult↗
PubMed1990

Hemodynamic effects of brefanolol and propranolol assessed by noninvasive methods in patients with arterial hypertension.

In a placebo-controlled, randomized, cross-over study, 16 patients (10 males, 6 females; 50.6 +/- 10.4 years; body weight of 74.5 +/- 8.9 kg; mean +/- SD) with arterial hypertension (WHO stages I and II) were administered single oral doses of placebo, 80 mg of propranolol, as well as 50 and 100 mg of brefanolol (a beta-adrenergic blocking agent with vasodilating properties) in order to determine the resulting hemodynamic effects. Blood pressure, heart rate, and various hemodynamic parameters were assessed noninvasively by mechano- and impedance cardiography as well as by venous occlusion plethysmography before and 2, 4, 6, 10, and 24 h after drug administration. Treatment with propranolol resulted in the typical hemodynamic changes induced by a beta-adrenergic blocking agent characterized by a significant reduction in blood pressure, heart rate, cardiac output, stroke volume, and an increase in total peripheral resistance. A dose of 100 mg of brefanolol also led to comparable hemodynamic effects. Similar significant decreases in blood pressure, heart rate, and cardiac output also occurred with 50 mg of brefanolol, but stroke volume and reactive hyperemia increased. Thus, in this phase of drug development, dose titration with 50 and 100 mg of brefanolol indicates that the lower dose gives rise to a more balanced relationship between its beta-adrenergic blocking and vasodilating properties.

Adrenergic beta-Antagonists↗
PubMed1990

Hemodynamic effects of intraatrial administration of deferoxamine or deferoxamine-pentafraction conjugate to conscious dogs.

Deferoxamine (DFX) is a specific Fe3+ chelator that is used to manage iron overload, and is being evaluated as an agent to reduce ischemic organ damage that involves iron-mediated OH formation. However, high intravascular doses cause significant hemodynamic changes that may limit or counteract beneficial effects. We used conscious, closed-chest dogs to test the hypothesis that conjugating DFX to pentafraction, a high molecular weight fraction of pentastarch, could reduce such hemodynamic changes. We infused 50 mg/kg of body weight of native DFX, or an equivalent dose as DFX-pentafraction, intraatrially over 15 min. Within 10 min of starting the infusion. DFX increased heart rate from pre-drug values of 105 +/- 11 (mean +/- SEM; N = 9) to 158 +/- 13 beats/min, and reduced left ventricular (LV) systolic pressure from 131 +/- 3 to 99 +/- 16 mm Hg, LV end-diastolic pressure from 12 +/- 3 to 3 +/- 3 mm Hg, and mean arterial pressure (MABP) from 101 +/- 5 to 74 +/- 13 mm Hg. In two dogs, MABP decreased to less than or equal to 35 mm Hg. These parameters returned to predrug values by 60 min after infusion. All of these changes were statistically significant (p less than 0.05). In contrast, infusing DFX-pentafraction (N = 9) caused no significant cardiac or hemodynamic changes other than a transient and slight (approximately 7%) increase in systolic arterial pressures. This conjugate, which prolongs the plasma half-life and does not alter the iron-chelating activity of native DFX, eliminates many undesirable hemodynamic actions. It may be a useful therapeutic alternative to native DFX in some settings.

Animals↗
PubMed1991

The effect of the partial beta-1-adrenoceptor agonist xamoterol on hemodynamics and myocardial energetics in patients with idiopathic dilated cardiomyopathy.

Xamoterol, a new partial beta 1-adrenoceptor agonist, was evaluated in respect to its hemodynamic and energetic effects when given acutely i.v. (0.2 mg/kg body weight) to 10 patients with idiopathic dilated cardiomyopathy. Hemodynamically, a small drop in left ventricular end-systolic volume index (from 105 +/- 38 to 91 +/- 48 ml/m2; p less than 0.05) and end-diastolic volume index (from 168 +/- 44 to 152 +/- 41 ml/m2; p less than 0.05) and an increase in maximum rate of left ventricular pressure rise (from 1,003 +/- 358 to 1,283 +/- 398 mm Hg/s; p less than 0.001) was observed. The systolic stress-time integral was only slightly reduced after injection of xamoterol, from 107 +/- 28 to 94 +/- 35 x 10(3) dyn.s/cm2 (NS). Other conventional hemodynamic variables did not change significantly. Myocardial oxygen consumption per beat increased from 125 +/- 39 microliters/beat/100 g to 153 +/- 62 microliters/beat/100 g (p less than 0.05). The ratio of myocardial oxygen consumption per beat and stress-time integral--as an inverse measure of left ventricular contraction economy--increased significantly, from 132 +/- 62 to 192 +/- 115 microliters/beat/10(3) dyn.s/cm2 (p less than 0.02) after injection of xamoterol, whereas left ventricular efficiency decreased from 17.6 +/- 7.8 to 13.8 +/- 6.5% (p less than 0.05). Thus, in idiopathic dilated cardiomyopathy, xamoterol exhibited only minor hemodynamic effects whereas myocardial contraction economy and efficiency were significantly reduced.

Adult↗
PubMed1991

Hemodynamic and morphological effects of quinapril during genetic hypertension development.

The relative contributions of the hemodynamic and morphological (vascular and cardiac) modifications induced by long-term administration of an angiotensin I-converting enzyme inhibitor, quinapril, to the drug's long-lasting preventive effects vis-à-vis genetic hypertension development (GHD) have been investigated in young spontaneously hypertensive rats (SHRs). Two groups of SHRs were given quinapril (10 mg/kg/day) or distilled water from 5 to 20 weeks of age. The drug was then stopped, but observations continued for another 7 weeks. At selected times systemic and regional hemodynamic parameters as well as cardiac and vascular morphological effects were investigated. During the treatment period, quinapril partially opposed GHD and limited the early rise in total peripheral and regional vascular resistances observed in control animals. Quinapril's partial preventive effect vis-à-vis GHD persisted, but faded after treatment withdrawal. From a morphological point of view, quinapril strongly opposed aortic wall hypertrophy as evidenced by significant reductions in media thickness and wall to lumen ratio and by a significant increase in aortic nuclear density. Quinapril also limited vascular fibrosis development. At the cardiac level, quinapril reduced heart weight to body weight ratio and opposed myocardial hypertrophy and cardiac collagen synthesis. All these vascular and cardiac morphological changes were delayed (starting after 9-15 weeks of treatment) as compared to quinapril's hemodynamic effects. Finally, the drug's vascular and cardiac antihypertrophic properties persisted after treatment withdrawal. In conclusion, our data indicate that the early systemic and regional hemodynamic effects of quinapril initiate its antihypertensive action, but the drug-induced delayed and prolonged vascular morphological changes later take over and may be partly responsible for quinapril's residual blood pressure lowering effects after treatment withdrawal.

Animals↗
PubMed1995

Hemodynamic comparison of dopexamine and nitroprusside at high and low doses in patients with coronary artery disease and impaired left ventricular function.

Pure vasodilator drugs are currently the preferred agents for treatment of acute and chronic heart failure of all grades of severity. In contrast, the role of drugs that combine vasodilation with inotropic action remains highly controversial despite their several advantageous physiological actions and long therapeutic history in heart failure. We hypothesize that this uncertainty might be due first to subtle unfavorable hemodynamic effects not detectable by the relatively crude hemodynamic methods by which these agents are usually analyzed, particularly with regard to the quantification of afterload, and secondly to the narrow therapeutic range of these drugs, such that the dose administered is critical. We tested this hypothesis by comparing several refined hemodynamic measurements of dopexamine, an inotropic vasodilator, with a pure arteriovenous dilator (sodium nitroprusside, SNP) on left ventricular (LV) systolic and diastolic function, large arterial behavior, and coupling of the left ventricle to the arterial system at two dose levels in 35 patients with ischemic heart disease. The study protocol was a fixed order of 15-min infusions of saline, dopexamine 1 microg/kg/min, and dopexamine 3 + ++microg/kg/min, or saline, SNP 1 microg/kg/min, and SNP 3 microg/kg/min. Detailed hemodynamic observations were made at the end of each 15-min infusion period. Both drugs produced equivalent arterial vasodilation, as measured by the decrease in systemic vascular resistance index (SVRI), but dopexamine resulted in a significantly greater increase in cardiac index (CI). Myocardial contractility, assessed by several load-independent indexes, increased with dopexamine, as anticipated with an inotropic drug, but did not alter with SNP. Arterial compliance, a measure of the distensibility of large conduit arteries, was increased by SNP but not by dopexamine. Arterial wave reflection was increased by dopexamine, especially at high doses, but reduced by SNP. Increased arterial compliance and reduced wave reflection reduce LV afterload. SNP reduced preload, whereas dopexamine had no effect on this aspect of ventricular function. Vasodilator drugs and those which combine vasodilator and inotropy increase cardiac output (CO) and reduce SVR. Therapy with inotropic vasodilators has no effect on preload and does not reduce the dynamic components of ventricular afterload, although it does reduce its static components. These effects are dose dependent; there is less perturbation of afterload at lower doses. In contrast, vasodilator therapy reduces preload and both static and dynamic parts of afterload.

Coronary Disease↗
PubMed1996

Hemodynamic characterization of a novel neuropeptide Y receptor antagonist.

Defining the roles of the vasoconstrictor peptide neuropeptide Y (NPY) in the cardiovascular system is difficult due to lack of availability of specific NPY receptor antagonists. We report the in vivo NPY receptor blocking actions of a novel nonapeptide dimer, 1229U91 {(IleGluProDprTyrArgLeuArgTyrNH(2)(2)}, and describe its hemodynamic effects. In anesthetized normotensive rats, 1229U91 produced significant and dose-dependent reductions in NPY-reduced hemodynamic responses. 1229U91 (3-30 nmol/kg intravenously, i.v.) attenuated the pressor response (34 +/- 6-84 +/- 1%) and the increases in renal vascular resistance (RVR, 56 +/- 9-94 +/- 2%) produced by NPY (1 nmol/kg i.v.). Intravenous norepinephrine (NE)-induced hemodynamic responses were not altered by 1229U91. 1229U91 also produced dose-dependent inhibition of NPYinduced vasoconstrictor responses in anesthetized dogs and spontaneously hypertensive rats (SHR). These data demonstrate that 1229U91 is a selective NPY receptor antagonist. 1229U91 had no effect on resting hemodynamic variables in these preparations. In conscious SHR, 1229U91 did not produce significant changes in blood pressure (BP) or heart rate (HR) over a wide dose-range (15-1,500 nmol/kg i.v.). Lack of effect of the NPY receptor antagonist in SHR suggests that NPY does not contribute to the maintenance of BP in this hypertension model.

Anesthesia↗
PubMed1992

Continuous monitoring of cerebral hemodynamic reserve in acute brain injury: relationship to changes in brain swelling.

A new concept of cerebral hemodynamic and metabolic physiology, cerebral hemodynamic reserve (CHR), was evaluated in 20 comatose adults with acute traumatic brain swelling who were undergoing continuous monitoring of the arteriojugular difference in oxyhemoglobin saturation, along with cerebral perfusion pressure and expired PCO2. The CHR was measured as the ratio of relative (percent) changes in cerebral oxygen extraction to relative changes in cerebral perfusion pressure during spontaneous increases in intracranial pressure. In patients with initially severe brain swelling, the CHR was more frequently abnormal (compromised) on the first day, and tended to improve on the second day. In patients with initially moderate brain swelling, the CHR was more frequently normal (preserved) on the first day, but tended to become compromised on the second day if the brain swelling exacerbated. It is concluded that cerebral hemodynamic reserve abnormalities very closely associate with signs of increased intracranial "tightness" on computed tomographic scans of the head. Cerebral hemodynamic reserve could therefore become an important guide in the functional evaluation and management of acute brain swelling (focusing on cerebral oxygenation and perfusion pressure) in a variety of predominantly diffuse acute intracranial disorders.

Adult↗
PubMed1992

Effects of hypothermia on hemodynamic responses to dopamine and dobutamine.

Hemodynamic characteristics, arrhythmogenicity, and dose-related hemodynamic responses to intravenous dopamine (group I) and dobutamine (group II) were examined in 16 swine at three different core body temperatures (38.5 degrees C, 35 degrees C, and 30 degrees C). The animals were anesthetized with isoflurane and mechanically ventilated. Cooling and re-warming were accomplished by a femoral-jugular A-V shunt. The animals were cooled down to 30 degrees C and stabilized for 1 hour before intravenous infusion of dopamine (group I, n = 8) or dobutamine (group II, n = 8) was started at 2, 5, 10, 15, 20, and 30 micrograms/kg/min. Hemodynamic responses to the two inotropes were continuously monitored with a bedside monitor equipped with a PC mode for customized data collection and analysis. Computerized arrhythmia detection was performed. Our findings were: (1) profound hypothermia (30 degrees C) causes significant depression of hemodynamic functions; (2) IV infusion of dopamine and dobutamine can be used safely and effectively for inotropic support during profound hypothermia, and the optimal dosage for improving cardiac output is 10-20 micrograms/kg/min; (3) no risk of inducing arrhythmia was noted with IV infusion of both inotropes up to a maximum dosage of 30 micrograms/kg/min, even though significant sinus tachycardia was consistently seen at 30 micrograms/kg/min.

Animals↗
PubMed1997

Effect of chronic cocaine exposure on the hemodynamic response to vasopressors in sheep.

BACKGROUND: The purpose of this study was to determine how chronic cocaine exposure affects the hemodynamic response to epinephrine, dopamine, phenylephrine, and ephedrine in awake sheep. METHODS: The hemodynamic response to dopamine (10 microg/kg), phenylephrine (1.5 microg/kg), and ephedrine (0.15 mg/kg) boluses was determined at baseline before low-dosage cocaine exposure and again after 15 and 18 days of cocaine exposure. The hemodynamic response to epinephrine (0.15 microg/kg), phenylephrine (1.5 microg/kg), and ephedrine (0.15 mg/kg) was determined at baseline before high-dosage cocaine exposure and again after 15 and 18 days of cocaine exposure. RESULTS: Chronic cocaine exposure abolished the mean arterial pressure and heart rate responses to dopamine but did not alter the responses to epinephrine, phenylephrine, or ephedrine. CONCLUSION: In awake sheep, chronic cocaine exposure markedly impairs the hemodynamic response to dopamine but not to epinephrine, phenylephrine, or ephedrine.

Animals↗
PubMed2000

Central hemodynamics during reamed intramedullary nailing of unilateral tibial fractures.

BACKGROUND: Intramedullary nailing of a long-bone fracture results in intravasation of bone marrow contents into the right atrium and pulmonary vascular bed and, therefore, may alter cardiac and pulmonary hemodynamics. METHODS: Central hemodynamic changes were recorded in 12 healthy adults with a unilateral simple tibial fracture undergoing intramedullary nailing. The patients were cannulated with a pulmonary artery catheter. Reamed intramedullary nailing was performed during general anesthesia. Preoperative and immediate postoperative hemodynamic variables were compared and intraoperative changes studied. RESULTS: During the operation, the right ventricular preload as represented by central venous pressure and the right ventricular afterload as presented by mean pulmonary arterial pressure increased significantly. Preoperative and postoperative arterial oxygen tension values demonstrated hypoxia. Abnormal pulmonary shunting and increased oxygen consumption were observed as well. CONCLUSION: Changes in cardiac and pulmonary hemodynamics are already present after the trauma and before the reamed intramedullary nailing procedure.

Adult↗
PubMed1978

Hemodynamic factors and Rorschach testing in borderline and sustained hypertension.

Hemodynamic parameters and the Rorschach test were performed on 48 borderline and 64 sustained essential hypertensive patients, and compared with 33 normal subjects. Hemodynamic patterns suggested (1) in borderline hypertensives, a neurogenic hypertension, and (2) in sustained hypertensives, a volume- and renal-mediated hypertension. Repeat hemodynamic determinations were performed on 35 borderline hypertensives after a 47 +/- 3-month follow-up survey. The results confirmed that, in the same patient, hypertension was successively neurogenic and volume-mediated. The results of the Rorschach test in the overall hypertensive population pointed to an incapacity to form a structured neurosis because of the lack of a fantasy life, and an inadequacy of the mechanisms of repression of aggressive tendencies. These observations were more marked in sustained hypertensives. In borderline hypertensives, the lack of fantasy life, assessed from kinesthetic perceptions, was highly significant (p less than 0.01) and was associated with anxiety and functional symptoms suggesting an increased lability of the autonomic nervous system. In sustained hypertensives, however, there was an inability to express anxiety in a symbolic fashion (p less than 0.01). These differences in psychological findings between borderline and sustained hypertensives agree with the difference in hemodynamic patterns. The results suggest that sustained hypertensives have a predominantly somatic issue in place of the psychological conflicts observed in borderline hypertensives.

Adult↗
PubMedDate not supplied

Smoking status and nicotine administration differentially modify hemodynamic stress reactivity in men and women.

OBJECTIVES: To investigate the impact of cigarette smoking and oral contraceptive (OC) use on hemodynamic stress responses of women. Also, to examine gender differences in stress reactivity as a function of smoking status and acute nicotine administration. METHODS: Thirty men and 46 women, differing in smoking status and OC use, were tested for cardiovascular stress responses to a variety of behavioral and physical stressors. Each was tested twice, once under a transdermal nicotine patch condition and once under a placebo patch condition. Impedance cardiography was used to estimate hemodynamic reactivity noninvasively. RESULTS: In response to behavioral stressors, women smokers, irrespective of OC use or nicotine vs placebo, demonstrated significantly blunted cardiac output and heart rate reactivity to stressors, and showed significantly greater estimated total peripheral resistance (TPR) under stress relative to women nonsmokers. There were no differences in hemodynamic stress reactivity between men smokers and nonsmokers. The only significant effect involving nicotine administration on stress reactivity was seen in men where, regardless of smoking status, nicotine increased heart rate reactivity to all stressors relative to placebo responses. CONCLUSIONS: Results suggest that cigarette smoking may act differently in men and women to increase risk for cardiovascular disease (CVD). For men, nicotine may exert pathogenic influences via increasing the magnitude of heart rate reactivity to stressors. For women, however, smoking seems to have deleterious effects on hemodynamic stress reactivity patterns, reducing myocardial but increasing TPR contributions to blood pressure responses.

Administration, Cutaneous↗
PubMedDate not supplied

Endothelial function and hemodynamic responses during mental stress.

OBJECTIVE: The hemodynamic basis of blood pressure responses during psychological stress shows striking individual differences that share an interesting similarity with risk for cardiovascular disease. Factors accounting for these individual differences are poorly understood. The present study examined the relationship of vascular endothelial function to stress-induced hemodynamic responses. METHODS: Subjects were 40 healthy men and women, aged 25 to 44 years. Hemodynamic responses were assessed during exposure to a battery of four diverse laboratory stressors. Endothelium-dependent arterial dilation (EDAD) was measured by ultrasound imaging of the brachial artery in response to reactive hyperemia. RESULTS: High EDAD response was associated with lower resting systolic (p < .01) and diastolic blood pressure (p < .05). EDAD response was unrelated to blood pressure responses during stress. However, systemic vascular resistance responses during laboratory stress were significantly greater (p < .02) for individuals with low EDAD responses. CONCLUSIONS: Exaggerated systemic vascular resistance responses during stress may reflect endothelial dysfunction. This association may help explain the growing evidence of a relationship between stress hemodynamics and cardiovascular disease risk. The nature of this association is discussed in terms of a possible interplay between the sympathetic nervous system and the endothelium in regulation of vascular tone.

Adaptation, Psychological↗
PubMedDate not supplied

Acute effects of transcendental meditation on hemodynamic functioning in middle-aged adults.

OBJECTIVE: Increased peripheral vasoconstriction (ie, total peripheral resistance, or TPR) has been implicated as playing an important role in the early development of essential hypertension. Some studies have demonstrated that Transcendental Meditation (TM) reduces high blood pressure, but the hemodynamic adjustments behind these blood pressure reductions have not been elucidated. The aim of this study was to provide a preliminary investigation of the acute effects of TM on TPR. METHODS: Subjects were 32 healthy adults (16 women and 16 men; 30 white and two African American; mean age, 46.4 +/- 3.9 years). Subjects were divided into a TM group of long-term TM practitioners (eight white women, nine white men, and one African American man; mean years of twice-daily TM practice, 22.4 +/- 6.7) and a control group (eight white women, five white men, and one African American man). Hemodynamic functioning was assessed immediately before and during three conditions: 20 minutes of rest with eyes open (all subjects), 20 minutes of TM (TM group), and 20 minutes of eyes-closed relaxation (control group). RESULTS: During eyes-open rest, the TM group had decreases in systolic blood pressure (SBP) and TPR, compared with increases in the control group (SBP: -2.5 vs. +2.4 mm Hg, p < .01; TPR: -0.7 vs. +0.5 mm Hg/liter per minute, p < .004). During TM, there was a greater decrease in SBP due to a concomitantly greater decrease in TPR compared with the control group during eyes-closed relaxation (SBP: -3.0 vs. +2.1 mm Hg, p < .04; TPR: -1.0 vs. +0.3 mm Hg/liter per minute, p < .03). CONCLUSIONS: TPR decreased significantly during TM. Decreases in vasoconstrictive tone during TM may be the hemodynamic mechanism responsible for reduction of high blood pressure over time. The results of this study provide a preliminary contribution to the understanding of the underlying hemodynamic mechanisms responsible for the beneficial influence of TM on cardiovascular risk factors.

Adult↗
PubMed1997

Influence of cyclic guanosine monophosphate changes on hemodynamics after reperfusion in liver transplantation.

Orthotopic liver transplantation (OLT) is often associated with hemodynamic instability upon reperfusion, recognized as postreperfusion syndrome. Changes in vascular tone due to humoral factors released upon reperfusion of the graft have been suggested as a possible mechanism. In this study, we looked at the perioperative changes in cyclic guanosine monophosphate (cGMP), a mediator of vascular smooth muscle relaxation, and investigated its relationship with hemodynamic parameters. cGMP was measured in the plasma of 14 patients undergoing OLT by radioimmunoassay serially at the preanhepatic and anhepatic phases, and after reperfusion at 30, 60, and 120 min. Hemodynamic data recorded were systemic and pulmonary arterial pressures, cardiac output, and pulmonary and systemic vascular resistance. cGMP decreased markedly after reperfusion from a baseline level of 5.33+/-0.7 ng/ml to 1.63+/-0.5 ng/ml (P<0.01). Pulmonary arterial pressure increased from 17+/-1.21 mmHg to 23.5+/-1.9 mmHg (P<0.05), and pulmonary vascular resistance increased from 62.8 +/-12.9 dynes/sec/cm5 to 135+/-42.7 dynes/sec/cm5 (P<0.01). Changes in cardiac output and systemic vascular resistance were not significant. The changes in cGMP correlated with pulmonary arterial pressure (r=0.74, P=0.005) and pulmonary vascular resistance (r=0.7, P=0.01). These data confirm the occurrence of hemodynamic changes during OLT, and provide evidence to suggest that the reduction in cGMP after reperfusion may mediate the vascular changes.

Blood Pressure↗
PubMed1998

Extended donor criteria: hemodynamic follow-up of heart transplant recipients receiving a cardiac allograft from donors > or = 60 years of age.

BACKGROUND: Heart transplantation (HT) has become a therapeutic option for patients suffering from endstage heart failure. The increasing demand for cardiac allografts has led to a shift toward extended donor criteria. In a retrospective analysis of 859 HT recipients, we report on the hemodynamic outcome of 19 HT patients who received cardiac allografts from donors > or =60 years of age. METHODS: From March 1989 to December 1997, we performed 883 orthotopic HT in 74 children and 809 adults at our transplant center. Within this period, 19 patients (17 women and 2 men) received cardiac allografts from donors > or =60 years of age. Recipient age ranged from 57 to 78 years (mean, 65+/-5 years). RESULTS: HT could be performed successfully in 19 cases. The early mortality rate was 16% (n=3). The late mortality rate was 37% (n=7). All long-term survivors are stable at New York Heart Association classification II (New York Heart Association Class II = resting hemodynamics: cardiac output normal; left ventricular end diastolic filling pressure elevated; clinically not compromised during mild to moderate workout). Although only 19 patients were retrospectively evaluated, there was a statistically significant (P<0.05) difference in survival among patients who received organs from male (11 vs. 8*) compared with female (8 vs. 2*) (*=death) donors. CONCLUSION: In our experience, it is possible to increase the cardiac donor pool by accepting allografts from donors, preferably female, > or =60 years of age in selected cases without a coronary angiogram, if hemodynamic parameters are in a normal range on mild-to-moderate inotropic support. We do not recommend cardiac allografts from donors > or =60 if there are signs of coronary insufficiency in the electrocardiogram, if left ventricle filling pressures are above normal on mild-to-moderate inotropic support and optimum hemodynamic management, or if there are signs of segmental dysfunction or mitral insufficiency >I in the echocardiogram.

Age Factors↗
PubMed2003

Hemodynamic stability, myocardial ischemia, and perioperative outcome after carotid surgery with remifentanil/propofol or isoflurane/fentanyl anesthesia.

This study compares remifentanil/propofol (remi/prop) with isoflurane/fentanyl (iso/fen) anesthesia to determine which provides the greater hemodynamic stability, lesser myocardial ischemia, and morbidity with better postoperative outcomes after carotid endarterectomy. Sixty patients undergoing unilateral carotid endarterectomy were randomized to receive either a remi/prop or iso/fen anesthetic. Hemodynamic variables were recorded during the surgical procedure. In addition, transesophageal echocardiography was used to assess evidence of intraoperative regional wall motion abnormalities suggestive of cardiac ischemia. Emergence and extubation times, recovery from anesthesia, hemodynamic instability, nausea, vomiting, and pain in post anesthesia recovery, discharge delays, ICU admittance, hospital discharge, and preoperative and postoperative troponin levels were compared using appropriate statistical methods with P < 0.05 considered significant. The groups were demographically alike. Hemodynamic variables were similar during intubation and throughout surgery. Twenty-two percent of patients receiving iso/fen developed intraoperative regional wall motion abnormalities suggestive of ischemia, whereas no remi/prop patients had changes (P < 0.05). There was no difference in ST-T wave changes after surgery, and no patient had an elevation in troponin I levels. Postoperative variables were similar except that patients who received iso/fen had lower Stewart recovery scores during the first 15 minutes after post anesthesia care unit admission and a higher incidence of nausea and vomiting the day after surgery, whereas patients receiving remi/prop had discharge delays secondary to hypertension. ICU admittance, time to first void, oral intake, and time to hospital discharge were similar between the groups. At 9 times the cost of an iso/fen anesthesia technique, remi/prop offers little advantage over inhalational anesthesia for carotid endarterectomy.

Aged↗