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Parametric analysis of rate-dependent hemodynamic response functions of cortical and subcortical brain structures during auditorily cued finger tapping: a fMRI study.

A multitude of functional imaging studies revealed a mass activation effect at the level of the sensorimotor cortex during repetitive finger-tapping or finger-to-thumb opposition tasks in terms of either a stepwise or a monotonic relationship between movement rate and hemodynamic response. With respect to subcortical structures of the centralmotor system, there is, by contrast, some preliminary evidence for nonlinear rate/response functions within basal ganglia and cerebellum. To further specify these hemodynamic mechanisms, functional magnetic resonance imaging (fMRI) was performed during a finger-tapping task in response to acoustic stimuli (six different frequencies: 2.0, 2.5, 3.0, 4.0, 5.0 and 6.0 Hz; applied via headphones). Passive listening to the same auditory stimuli served as a control condition. Statistical evaluation of the obtained data considered two approaches: categorical and parametric analysis. As expected, the magnitude of the elicited hemodynamic response within left sensorimotor cortex (plateau phase at frequencies above 4 Hz) and mesiofrontal cortex paralleled movement rate. The observed bipartite mesial response pattern, most presumably, reflects functional compartmentalization of supplementary motor area (SMA) in a rostral component (pre-SMA) and in a caudal (SMA proper) component. At the level of the cerebellum, two significant hemodynamic responses within the hemisphere ipsilateral to the hand engaged into finger tapping (anterior/posterior quadrangular lobule and posterior quadrangular lobule) could be observed. Both activation foci exhibited a stepwise rate/response function. In accordance with clinical data, these data indicate different cerebellar contributions to motor control at frequencies below or above about 3 Hz, respectively. Caudate nucleus, putamen, and external pallidum of the left hemisphere displayed, by contrast, a negative linear rate/response relationship. The physiological significance of these latter findings remains to be clarified.

Adult↗

Hemodynamic predictors of early intolerance and long-term effects of propranolol in dilated cardiomyopathy.

BACKGROUND: Fifty-six patients with dilated cardiomyopathy (DCM) (aged 14-68 years) and background therapy of angiotensin-converting enzyme inhibitors, diuretics, and digoxin were given an initial challenge of propranolol in gradually increasing doses. These patients were studied noninvasively and hemodynamically and subjected to right ventricle biopsy. METHODS AND RESULTS: Forty-four patients tolerated propranolol and received the drug for 6 months; 12 patients deteriorated after starting the drug with worsening of congestive heart failure and/or hypotension. The patients who did not tolerate propranolol had higher left ventricular end-diastolic dimension (73 +/- 8 vs 66 +/- 8 mm, P < .05), and severe mitral regurgitation was more common. Hemodynamically these patients had higher heart rate, right ventricular end-diastolic pressure, mean pulmonary artery pressure, mean pulmonary artery wedge pressure, and left ventricular end-diastolic pressure (102 +/- 16 vs 89 +/- 12 beats/min, 15 +/- 7 vs 9 +/- 4, 39 +/- 16 vs 31 +/- 12, 28 +/- 8 vs 21 +/- 8, 28 +/- 8 vs 22 +/- 8 mmHg, respectively, P < .01). These patients had a significantly lower cardiac index (1.9 +/- 0.6 vs 2.5 +/- 0.6 L/min/m2, P < .01). Forty patients completed 6 months follow-up evaluation and were further subjected to repeat noninvasive and hemodynamic study. There was a significant improvement in New York Heart Association class, cardiothoracic ratio, and left ventricular end-diastolic dimension (68% vs 62%, 66 +/- 8 vs 62 +/- 7 mm, respectively, P < .01), while the ejection fraction (EF) rose from 23 to 35% (P < .001). Hemodynamically, there was a significant decrease in heart rate, right ventricular end-diastolic pressure, mean pulmonary artery pressure, mean pulmonary artery wedge pressure, and left ventricular end-diastolic pressure (91 +/- 14 vs 71 +/- 5 beats/min, 9 +/- 4 vs 5 +/- 3, 32 +/- 11 vs 22 +/- 7, 25 +/- 9 vs 17 +/- 8, 21 +/- 7 vs 14 +/- 4 mmHg, P < .05). The cardiac index rose from 2.3 +/- 0.6 to 3.2 +/- 0.7 L/min/m2 (P < .01). CONCLUSIONS: Propranolol in dilated cardiomyopathy is associated with significant intolerance. Those who tolerate propranolol seem to have long-term beneficial effects. This study is limited as it is uncontrolled and nonrandomized.

Adolescent↗

Prospective results of a standardized algorithm based on hemodynamic status for managing pediatric solid organ injury.

BACKGROUND: Controversy surrounds the need for ICU admission, prolonged bed rest, and the duration of activity restrictions for children sustaining blunt trauma. Adult literature supports management based on hemodynamic status, not CT grade. STUDY DESIGN: A 3-year prospective study of a standardized management algorithm for hemodynamically normal pediatric patients with blunt liver or spleen injury was performed. Patient selection was based on vital signs, irrespective of injury grade on CT. Patients requiring ICU admission for nonliver or nonspleen injury were excluded. Patients were admitted to a surgical ward with serial hematocrit levels. Discharge occurred 48 hours postinjury if patients had no abdominal tenderness, tolerated a regular diet, and had a stable hematocrit. Patients were allowed noncontact activity, including school, after discharge. Patients were followed up at 1 month with ultrasonographic imaging. RESULTS: Eighty-nine patients sustained blunt liver or spleen injury. Forty-five patients were excluded for other injuries (Glasgow Coma Scale < 13, 32 of 45); the remaining 44 patients had a mean age of 8.9 years (range 2 to 17 years), Injury Severity Score 10.6 (range 4 to 33), liver grade 2.1, and splenic injury grade 2.3. Mechanisms of injury were predominately motor vehicle collisions (59%). All patients were managed nonoperatively without transfusion; 43 of 44 patients completed the algorithm. Mean observation was 55.2 +/- 12.3 hours. One-month followup occurred in 33 of 44 patients, with one complication detected and no delayed bleeding. CONCLUSION: Management of pediatric solid organ injury should be guided by hemodynamic status and not injury grade on CT. Hemodynamically normal children can be safely managed without intensive care monitoring, do not need prolonged hospitalization, and can resume school on discharge.

Adolescent↗

Hemodynamic profiles during piggyback liver grafts using arterial or portal revascularization.

BACKGROUND: The order of revascularization in human liver grafts is still discussed. This study tries to answer this question in terms of hemodynamic data. STUDY DESIGN: Fifty-nine patients were randomized in this study to compare hemodynamic data just before and 15 minutes after revascularization of liver grafts in relation to first hepatic artery (n = 29) or first portal vein (n = 30) revascularization procedure. RESULTS: Hemodynamic variations were significantly greater in the portal vein group than in the hepatic artery group in terms of mean arterial pressure, cardiac index, central venous pressure, pulmonary capillary pressure, and systemic vascular resistance. The latter decreased from 741.8 +/- 390.3 to 659.9 +/- 411.1 dynes/ cm5 (NS) in the hepatic artery group versus 807.7 +/-336.7 to 439.7 +/- 215 dynes/cm5 (p < 0.05) in the portal vein group. Clinical results and postoperative complications, graft characteristics, patient survival, and graft survival were not significantly different between the groups. CONCLUSIONS: Initial arterial revascularization of the liver graft leads to a more stable hemodynamic profile during revascularization of the liver graft after vascular unclamping. This technique is always feasible and has become our reference procedure.

Anastomosis, Surgical↗

Hemodynamic and blockade effects of high/low epinephrine doses during axillary brachial plexus blockade with lidocaine 1.5%: A randomized, double-blinded study.

BACKGROUND AND OBJECTIVES: Although epinephrine commonly is added to local anesthetics for regional anesthesia, rarely it may cause undesirable hemodynamic side effects. This study compared the hemodynamic and blockade effects of 25 and 200 microg epinephrine during axillary brachial plexus blockade with lidocaine 1.5%. METHODS: Sixty American Society of Anesthesiologist classification I or II patients were divided randomly into 3 groups. Patients in group 1 received 5 mL of saline containing 25 microg epinephrine and then 35 mL of 1.5% lidocaine; patients in group 2 received 5 mL of saline alone and then 200 microg of epinephrine mixed with 35 mL of 1.5% lidocaine; patients in group 3 received 5 mL of saline alone and then 35 mL of 1.5% lidocaine. Hemodynamic data were measured for 1 to 10 minutes at 1-minute intervals after axillary injection. The duration time of motor and sensory block was recorded. RESULTS: Complete anesthesia was achieved in 85% of patients in groups 1 and 3 and 90% in group 2. Motor block duration was significantly longer in group 2 than in groups 1 and 3 (P <.05). There were no significant differences in analgesia between groups 1 and 2. Analgesia duration was significantly longer in groups 1 and 2 than in group 3 (P <.05). Heart rate from the 3rd to 6th minute was higher in group 2 than in groups 1 and 3 (P <.05). Systolic arterial pressure from the 3rd to 5th minute and diastolic arterial pressure from 2nd to 6th minute were higher in group 2 than in groups 1 and 3 (P <.05). CONCLUSIONS: Low-dose epinephrine offers more stable hemodynamics and similar blockade, and thus may be beneficial for patients undergoing forearm and hand surgery who are at risk for tachycardia and/or hypertension.

Adolescent↗

Detection of hemodynamic changes in clinical monitoring by time-delay neural networks.

Small changes that occur in a patient's physiology over long periods of time are difficult to detect, yet they can lead to catastrophic outcomes. Detecting such changes is even more difficult in intensive care unit (ICU) environments where clinicians are bombarded by a barrage of complex monitoring signals from various devices. Early detection accompanied by appropriate intervention can lead to improvement in patient care. Neural networks can be used as the basis for an intelligent early warning system. We developed time-delay neural networks (TDNN) for classifying and detecting hemodynamic changes. A matrix of physiological parameters were extracted from raw signals collected during cardiovascular experiments in mongrel dogs. These matrices represented several episodes of stable, decreasing, and increasing cardiac filling in normal, exerted, and heart failure conditions. The TDNN were trained with these matrices and subsequently tested to predict unseen cases. The TDNN perform remarkably not only in identifying all hemodynamic conditions, but also in quickly detecting their changes. On average, the networks were able to detect the hemodynamic changes in less than 1 s after the onset. Based on the results of this pilot investigation, the use of this form of TDNN to successfully predict hemodynamic conditions appears to be promising.

Animals↗

Left ventricular-based pacing in patients with chronic heart failure: comparison of acute hemodynamic benefits according to underlying heart disease.

BACKGROUND: Acute left ventricular-based pacing has been shown to improve hemodynamics in patients with severe heart failure and left bundle branch block (LBBB). However, it is not known whether the cause of the underlying heart disease influences the potential effect of left ventricular-based pacing. OBJECTIVES: The aim of this study was to determine whether beneficial hemodynamic effects of acute left ventricular-based pacing in severe chronic heart failure are dependent on underlying heart disease. METHODS: After coronary angiography, patients with severe heart failure and LBBB were separated into two groups: dilated (25 patients; 20 male) and ischemic cardiomyopathy (21 patients; 20 male). Hemodynamic parameters were evaluated at baseline and during left ventricular-based pacing. RESULTS: Improvement in hemodynamic parameters were similar in both groups, during acute left ventricular pacing (changes expressed in percentage): pulmonary capillary wedge pressure, -16+/-15% vs. -14+/-10%; V wave amplitude, -25+/-18% vs. -21+/-17%; and biventricular pacing, -15+/-15% vs. -11+/-11% and -23+/-18% vs. -16+/-18%, respectively. CONCLUSION: Underlying heart disease does not influence the response to acute left ventricular-based pacing in patients with severe heart failure and LBBB. This finding provides support for including all patients with enlarged heart and heart failure in future studies evaluating left ventricular-based pacing.

Aged↗

Autonomic dysfunction and hemodynamics in vitamin B12 deficiency.

Orthostatic hypotension in patients with cobalamin (Cbl) deficiency has been reported previously in isolated cases but we are not aware of detailed systematic studies of hemodynamic and autonomic nervous system function in patients with cobalamin deficiency. We investigated hemodynamic and autonomic responses to 60 degrees passive head up tilt (HUT) in 21 patients with vitamin B12 deficiency, 21 healthy age-matched control subjects and 9 age-matched patients with diabetes mellitus (DM) and established diabetic neuropathy. To systematically assess hemodynamic and autonomic nervous system function, we performed measurements of heart rate, beat-to-beat systolic and diastolic blood pressure, stroke index, cardiac index, total peripheral resistance index, total power, low (LF) and high (HF) frequency oscillatory component of heart rate variability, LF/HF ratio and spontaneous baroreflex sensitivity. As compared to controls, we found a significant fall of systolic blood pressure during 60 consecutive beats directly after head up tilt; furthermore, a significantly blunted fall of stroke index, cardiac index and a lack of increase of total peripheral resistance index for the duration of tilt in patients with diabetes mellitus and in patients with vitamin B12 deficiency. As compared to controls, we observed an altered response of spectral indices of sympathetic activation and vagal withdrawal and an impaired modulation of baroreflex sensitivity during head up tilt suggestive of a complex modification in the neural control activities in patients with cobalamin deficiency, which was comparable to that observed in patients with diabetes mellitus and established autonomic neuropathy. The results suggest that vitamin B12 deficiency causes autonomic dysfunction with similar hemodynamic consequences and patterns of autonomic failure as seen in diabetic autonomic neuropathy. Defective sympathetic activation may be the cause for orthostatic hypotension, which is occasionally seen in patients with vitamin B12 deficiency. It is concluded that patients with orthostatic hypotension should be screened for cobalamin deficiency.

Aged↗

[Hemodynamics and delayed growth in children after surgery for atrial septal defect].

BACKGROUND: Ostium secundum-type atrial septal defect (ASD) is usually well tolerated, without severe complications in childhood. However, in many patients its effect on growth is disproproportionate when compared with that of more serious congenital heart disease. OBJECTIVES: To test the hypothesis that hemodynamic disturbances are responsible for failure to thrive in congenital heart disease, we studied growth and the effect of surgical repair in children with ASD. PATIENTS AND METHODS: The study was performed in 72 patients who underwent surgery at a mean age of 8 years and 8 months. The mean follow-up was 17 months. Somatometric and hemodynamic parameters were studied and the correlation between them was verified. The effect of surgery and of age at operation on somatometric changes was evaluated. RESULTS: Fifty-two percent of the patients were malnourished and height was affected in 28 %. The correlation between weight and age at operation was r 5 0.78 (p < 0.05) for the entire group, r 5 0.81 (p < 0.05) for the malnourished subgroup and r 5 0.88 (p < 0.05) for the subgroup with normal nutrition. No relationship was found between hemodynamic and somatometric parameters. Surgery improved growth disturbances but not in all patients (weight: from 52 % to 32 %; height: from 28 % to 16 %). CONCLUSIONS: Hemodynamic factors are not the only cause of growth and nutritional alterations.

Child↗

A new model of individual differences in hemodynamic profile and blood pressure reactivity.

A quantitative, theory-driven model of hemodynamics was developed, relating reactivity in blood pressure to orthogonal dimensions of "hemodynamic profile" and "compensation deficit," which were derived from the (multiplicative) interaction of cardiac output and total peripheral resistance. A Finapres 2300e was used to estimate blood pressure, cardiac output, and total peripheral resistance in 100 healthy men and women during mental arithmetic and cold pressor tasks on two occasions. Results were consistent with model predictions. As predicted, cardiac output and peripheral resistance reactions were curvilinearly related, and blood pressure reactivity was strongly related to compensation deficit (r = .76-.89). Conversely, the orthogonally defined hemodynamic profile remained independent of blood pressure reactivity (r = .11 or less). The data show that the present model overcomes several difficulties and inconsistencies in previous attempts to obtain an independent measure of hemodynamic profile. The new model could help to elucidate sources of cardiovascular pathogenesis not suggested from the study of blood pressure reactivity alone.

Adolescent↗

Acute and chronic effects of propionyl-L-carnitine on the hemodynamics, exercise capacity, and hormones in patients with congestive heart failure.

Carnitine is an important cofactor in the intermediary metabolism of the heart, and carnitine deficiency is associated with congestive heart failure. We therefore studied the effects of acute (IV bolus, 30 mg/kg body weight) and chronic administration (1.5 mg/d for 1 month) of propionyl-L-carnitine on hemodynamics, hormone levels, ventricular function, exercise capacity, and peak oxygen consumption in 30 patients with chronic congestive heart failure (NYHA II-III, mean EF 29.5 +/- 7%) in a phase II, parallel, single-blind, randomized, and placebo-controlled study. Acute administration of propionyl-L-carnitine caused a significant reduction in pulmonary artery and pulmonary wedge pressures at both day 1 (P < 0.001) and day 30 (P < 0.05) of the study but no other hemodynamics changes. Hormone levels did not change following acute administration of the drug. Chronic administration of propionyl-L-carnitine increased peak oxygen consumption by 45% (from 16.0 +/- 3 to 23.5 +/- 2 mL/kg/min, P +/- 0.001), exercise time by 21% (from 8.1 +/- 0.5 to 9.8 +/- 0.4 minutes, P < 0.01), and peak exercise heart rate by 12% (P < 0.01). These changes were concomitant with a reduction of pulmonary artery pressure. In the treated group, there was a slight, but significant (P < 0.01), reduction in left ventricular dimensions. Hemodynamics and hormones measured after 1 month of oral therapy remained unchanged, except for a fall in pulmonary artery pressures, with a nonsignificant trend towards a fall in filling pressures and plasma norepinephrine. The chronic changes in the propionyl-L-carnitine group were seen at 15 days of treatment, and no further changes in these parameters were seen at 1 month. We conclude that propionyl-L-carnitine increases exercise capacity and reduces ventricular size in patients with congestive heart failure. The drug has no significant effects on hemodynamics or neurohormone levels. The use of a single-blind design reduces the impact of the positive finding on exercise capacity.

Adult↗

Acute hemodynamic effects of amlodipine 15 days after a myocardial infarction in normotensive patients treated with atenolol.

The acute hemodynamic effects of 20 mg iv amlodipine were evaluated in a placebo-controlled study in 16 normotensive patients 15 +/- 1 days after an acute myocardial infarction by covariance analysis. Atenolol was given orally for at least 1 week before the study to maintain the heart rate between 50 and 60 beats/min. All patients were given two doses of 10 mg of amlodipine, or 10 ml of a placebo twice, in i.v. infusion lasting 2 minutes each. Hemodynamic data were collected during the control period and 15 minutes after each of the two amlodipine or placebo infusions. At the time of the last measurements, 15 minutes after the second amlodipine or placebo infusion, the plasma amlodipine level was 31 +/- 16 micrograms/l and the plasma atenolol level was 773 +/- 564 mu/l in the amlodipine group versus 795 +/- 916 micrograms/l in the placebo group. There were no chronotropic, dromotropic, or inotropic effects. The main hemodynamic effect was a fall in systemic vascular resistance (1548 +/- 591 dynes.sec.cm-5 to 1176 +/- 526 dynes.sec.cm-5, p = 0.045) with decreases in aortic pressure and in the left ventricular stroke work index. The left ventricular ejection fraction was 51 +/- 12% in the placebo group and 56 +/- 15% in the amlodipine group (ns) during the control period, and did not change after infusion of placebo or amlodipine. Left ventricular compliance seemed to be enhanced by amlodipine, because the end-diastolic left ventricular volume index rose from 82 +/- 11 ml/m2 to 87 +/- 11 ml/m2 (p = 0.026) 15 minutes after the beginning of the second infusion of 10 mg of amlodipine, without any change in end-diastolic left ventricular pressure. Intravenous infusion of 20 mg of amlodipine is well tolerated 15 days after acute myocardial infarction in normotensive patients without deeply depressed left ventricular systolic function and chronically treated with atenolol. The main hemodynamic effects observed are potentially useful for such patients.

Acute Disease↗

Pharmacodynamic models of nitroglycerin-induced hemodynamic tolerance in experimental heart failure.

Pharmacodynamic tolerance during continuous nitroglycerin (NTG) infusion is a significant limitation of nitrate therapy. The mechanism of this phenomenon is not well-understood but may involve physiologic compensation which involves vasoconstriction. We have obtained pharmacodynamic data on NTG-induced hemodynamic tolerance in a rat model of congestive heart failure (CHF), which we have shown to mimic human behavior toward NTG in vivo. In this report, we developed two mechanism-based pharmacokinetic/pharmacodynamic models to describe the time-dependent effects of NTG infusion on left ventricular end-diastolic pressures (LVEDP) in CHF rats and compared their abilities to describe the observed hemodynamic data. Both mathematical models introduced a counter-regulatory vasoconstrictive effect as a result of NTG-induced vasodilation and assumed the magnitude of this effect to be driven by the extent of the initial hemodynamic effect produced by NTG. The decay of this counter-regulatory effect was described by a first-order process in both models. A model that assumed vasoconstriction to develop via two sequential first-order processes was statistically superior in describing the data, when compared to one that assumed a single first-order process and a lag phase. Both models provided similar estimates of the half-life for the disappearance of the vasoconstriction (t1/2 of vasoconstriction: 128min vs. 182min, respectively), and both predicted rebound elevation of LVEDP after abrupt NTG withdrawal. These results are consistent with a counter-regulatory mechanism of NTG-induced hemodynamic tolerance and suggest that such an approach may be useful for modeling other tolerance phenomena as well.

Animals↗

Comparison of permanent left ventricular and biventricular pacing in patients with heart failure and chronic atrial fibrillation: a prospective hemodynamic study.

BACKGROUND: Left ventricular pacing (LVP) and biventricular pacing (BVP) have been proposed as treatments for patients with advanced heart failure complicated by discoordinate contraction due to intraventricular conduction delay. For patients in sinus rhythm, BVP works in part by modulating the electronic atrial-ventricular time delay and thus optimizing contractile synchrony, the contribution of atrial systole, and reducing mitral regurgitation. However, little is known of the mechanisms of BVP in heart failure patients with drug-resistant chronic atrial fibrillation. HYPOTHESIS AND METHODS: LVP differs from BVP because hemodynamic and clinical improvement occurs in association with prolongation rather than shortening of the QRS duration. We sought to determine if LVP or BVP improves mechanical synchronization in the presence of atrial fibrillation. Thirteen patients with chronic atrial fibrillation, severe heart failure and QRS >or=140 ms received (after His bundle ablation) a pacemaker providing both LVP and BVP. The mean age was 62 +/- 6 years and left ventricular ejection fraction was 24 +/- 8%. After a baseline phase of one month with right ventricular pacing, all patients underwent in random order 2 phases of 2 months (LVP and BVP). At the end of each phase, an echocardiogram, a hemodynamic analysis at rest and during a 6-minute walking test and a cardio-pulmonary exercise test were performed. RESULTS: LVP and BVP provided similar performances at rest (p = ns). The 6-minute walking test revealed similar performances in both pacing modes but patients were significantly more symptomatic at the end of the test with LVP ( p = 0.035). The cardio-pulmonary exercise test showed higher performances with BVP (92 +/- 34 Watts) vs. LVP (77 +/- 23; p = 0.03). LVP was associated with significantly more premature ventricular complexes recorded during the 6 minute walking test (49 +/- 71) than BVP (10 +/- 23; p = 0.04). CONCLUSIONS: In this small series of patients with atrial fibrillation, congestive heart failure and a prolonged QRS duration, LVP and BVP provided similar hemodynamic effects at rest whereas BVP was associated with better hemodynamic effects during exercise and fewer premature ventricular complexes. Although the mechanisms for the observed differences are uncertain, it is possible that there is worsening of right ventricular function due to a rise in left-to-right electromechanical delay during exercise. Increased catecholamines release might contribute to the lower exercise tolerance and greater number of premature ventricular complexes recorded during exercise observed during LVP compared to BVP. RECOMMENDATIONS: Patients with atrial fibrillation, heart failure and QRS prolongation who are candidates for His-bundle ablation and cardiac resynchronization therapy may respond better to BVP rather than to LVP.

Atrial Fibrillation↗

[The Sorin pericardial bioprosthesis--a stentless aortic valve with very good hemodynamic performance].

BACKGROUND: The Sorin Pericarbon Freedom Stentless aortic valve has the potential to provide superior hemodynamic function and durability. In this study we assessed the hemodynamic performance of this valve and its impact on LV-mass regression after aortic valve replacement. METHODS: 31 consecutive patients who received a Sorin Pericarbon Freedom Stentless aortic valve were analysed. Mean age of the patients (16 female and 15 male) was 64 +/- 17 years. Five patients had isolated aortic stenosis, three isolated aortic regurgitation and one combined aortic valve disease. Three patients had combined aortic and mitral valve disease, 14 patients concomitant coronary artery disease, one congenital aortic coarctation. Three patients had an acute aortic valve endocarditis. 18 patients were classified as high-risk patients (mean EuroSCORE 9 +/- 2). Mean left ventricular ejection fraction was 52.5 +/- 15.0%. RESULTS: Valve sizes from 21 mm to 29 mm were implanted. The valves were oversized by 2 mm compared to measurement. 16 patients received isolated aortic valve replacement, Three patients aortic valve replacement and mitral valve reconstruction. 12 patients had concomitant CABG. Three procedures were reoperations. Hospital mortality was 6.4% (two patients). Both deaths occurred in high-risk patients and were not valve-related. Four patients had perioperative low-output-syndrome and needed IABP. After six months a follow up echocardiography was performed. Mean and peak gradients were 9.6 +/- 4.4 and 20.6 +/- 5.9 mmHg, respectively. Significant reduction of left ventricular hypertrophy (LV mass index 126.5 +/- 27.3 vs. 189.6 +/- 45.3 g/m2, p = 0.0313) and improvement of the ejection fraction (58 +/- 9.8 vs. 52.5 +/- 15.0%, p = 0.9749) as compared with preoperative valve. CONCLUSIONS: The hemodynamic performance of the Sorin Pericarbon Freedom Stentless aortic valve is excellent and the patient outcome is satisfying. However the implantation technique requires longer ischemic time, the prosthesis offers very satisfying hemodynamic function and accelerates probably the LV-mass regression in the mid term follow-up. Late performance and durability of the valve have to be assessed.

Aged↗

Hemodynamic evaluation of hydralazine dosage in refractory heart failure.

Hemodynamic responses to different doses of hydralazine were evaluated in 18 patients with severe refractory resistant heart failure. There were no significant overall hemodynamic effects after 50 mg hydralazine. After 75 mg, CI increased slightly (+0.36 l/min/m2) with a 19% decrease in SVR. After 100 mg, there were substantial increases in CI (+0.60 l/min/m2) and decreases in SVR (31%) changes which were greater than those after 75 mg, but the decrease in MAP with 100 mg (-6.6 mm Hg) was of the same order as that after 75 mg (-5.0 mm Hg). LVFP and SWI improved significantly only with 100-mg doses. Seven patients in whom 100 mg hydralazine induced no hemodynamic effects all responded to single doses of 150 to 200 mg. The duration of action of hydralazine was longer (p less than 0.001) in patients with a CCr less than 35 ml/min (14.3 +/- 1.4 hr) than in patients with adequate renal function (7.9 +/- 0.5 hr). Thus, the dose and dosing interval of hydralazine needed to induce hemodynamic improvement in patients with severe heart failure are variable and require individualization.

Aged↗

Role of histamine in the hemodynamic and plasma catecholamine responses to morphine.

The role of histamine in the hemodynamic and plasma catecholamine responses to intravenous morphine in subjects without cardiovascular disease and not receiving prior medication has not been reported. Systemic hemodynamics and serum histamine and plasma catecholamine concentrations were measured in 10 subjects before and 2, 5, 10, and 20 min after, 0.3 mg kg-1 IV morphine. Serum histamine concentration increased 2, 5, and 10 min after the morphine. Systolic and mean arterial pressures and systemic vascular resistance decreased and cardiac output increased because of increases in heart rate and stroke volume. The most important changes in hemodynamic function occurred after 2 min in association with a 400% increase in serum histamine concentration; these variables, together with serum histamine concentration, returned toward baseline values after 20 min. There was a negative correlation between peak increase in serum histamine concentration and maximum decrease in systemic vascular resistance. Plasma epinephrine concentrations were elevated 5, 10, and 20 min after morphine injection, suggesting activation of the adrenal medulla by histamine. Our data suggest that histamine plays an important role in the acute hemodynamic and plasma epinephrine response to morphine.

Adult↗

Effect of calcium antagonists on basal and digitalis-dependent changes in splanchnic and systemic hemodynamics.

We investigated the effects of the calcium antagonists verapamil and tiapamil on basal splanchnic and systemic hemodynamics and digoxin-induced vasoconstriction in 16 healthy men, using the hepatic venous catheter technique, the thermodilution method, and systolic time intervals. After a baseline period, verapamil or tiapamil were given by a primed-constant infusion in six of 16 subjects each, and hemodynamic changes were determined. Thereafter digoxin (1 mg) was concomitantly infused and hemodynamic changes were observed over 105 minutes. Control trials with digoxin alone were performed in seven of 16 subjects. Four of 16 subjects received only placebo. Digoxin provoked an increase in systolic blood pressure and splanchnic vascular resistance. Estimated splanchnic blood flow, mean pulmonary artery pressure, and total electromechanical systole decreased. Verapamil did not change basal hemodynamic parameters. Tiapamil decreased diastolic blood pressure and systemic and splanchnic vascular resistance. Both drugs attenuated the vasoconstricting effect of digoxin on the splanchnic vascular bed. Results indicate that calcium antagonists might be beneficial in treatment of digitalis-induced splanchnic vasospasm.

Adult↗