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At least 955 records · Page 53Linked to original sources
PubMed2005

Levosimendan reduces plasma B-type natriuretic peptide and interleukin 6, and improves central hemodynamics in severe heart failure patients.

BACKGROUND: Plasma B-type natriuretic peptide (BNP) and interleukin 6 (IL-6) levels have recently been demonstrated as significant neurohormonal markers associated with the progression of chronic heart failure (CHF). Additionally, clinical studies have shown that the calcium sensitizer, levosimendan, beneficially affects the central hemodynamics of CHF patients and improves their long-term prognosis. This study investigates whether levosimendan-induced hemodynamic improvement of CHF patients is related to the respective changes of NT-proBNP and IL-6 levels. METHODS: Circulating levels of NT-pro BNP and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA) in 12 patients with decompensated advanced CHF at baseline, immediately after the end of a 24-h levosimendan infusion and 72 h after the initiation of treatment. Hemodynamic parameters of patients (pulmonary wedge and pulmonary artery pressure (PAP), systemic and pulmonary vascular resistance (PVR), stroke volume, and cardiac output and index) were also monitored during the same period. RESULTS: NT-proBNP and IL-6 levels were significantly reduced in severe CHF patients within 72 h after the initiation of levosimendan treatment (p<0.01 and p<0.05, respectively). A significant reduction of pulmonary wedge (p<0.01) and artery pressure values (p<0.05) was also found during the same period. A good correlation between the levosimendan-induced changes in NT-proBNP levels and the respective reduction of pulmonary wedge pressure (r(s)=0.65, p<0.05) was observed. CONCLUSIONS: Our results indicate that changes of NT-pro BNP and IL-6 levels may be useful biochemical markers related with the levosimendan-induced improvement in central hemodynamics and the clinical status of decompensated advanced CHF patients.

Aged↗
PubMed2004

Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry.

OBJECTIVES: We sought to analyze clinical, angiographic, and outcome correlates of hemodynamic parameters in cardiogenic shock. BACKGROUND: The significance of right heart catheterization in critically ill patients is controversial, despite the prognostic importance of the derived measurements. Cardiac power is a novel hemodynamic parameter. METHODS: A total of 541 patients with cardiogenic shock who were enrolled in the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK (SHOCK) trial registry were included. Cardiac power output (CPO) (W) was calculated as mean arterial pressure x cardiac output/451. RESULTS: On univariate analysis, CPO, cardiac power index (CPI), cardiac output, cardiac index, stroke volume, left ventricular work, left ventricular work index, stroke work, mean arterial pressure, systolic and diastolic blood pressure (all p < 0.001), coronary perfusion pressure (p = 0.002), ejection fraction (p = 0.013), and pulmonary artery systolic pressure (p = 0.047) were associated with in-hospital mortality. In separate multivariate analyses, CPO (odds ratio per 0.20 W: 0.60 [95% confidence interval, 0.44 to 0.83], p = 0.002; n = 181) and CPI (odds ratio per 0.10 W/m(2): 0.65 [95% confidence interval, 0.48 to 0.87], p = 0.004; n = 178) remained the strongest independent hemodynamic correlates of in-hospital mortality after adjusting for age and history of hypertension. There was an inverse correlation between CPI and age (correlation coefficient: -0.334, p < 0.001). Women had a lower CPI than men (0.29 +/- 0.11 vs. 0.35 +/- 0.15 W/m(2), p = 0.005). After adjusting for age, female gender remained associated with CPI (p = 0.032). CONCLUSIONS: Cardiac power is the strongest independent hemodynamic correlate of in-hospital mortality in patients with cardiogenic shock. Increasing age and female gender are independently associated with lower cardiac power.

Aged↗
PubMed2004

Hemodynamic effects of inhaled nitric oxide in right ventricular myocardial infarction and cardiogenic shock.

OBJECTIVES: We sought to determine whether or not inhaled nitric oxide (NO) could improve hemodynamic function in patients with right ventricular myocardial infarction (RVMI) and cardiogenic shock (CS). BACKGROUND: Inhaled NO is a selective pulmonary vasodilator that can decrease right ventricular afterload. METHODS: Thirteen patients (7 males and 6 females, age 65 +/- 3 years) presenting with electrocardiographic, echocardiographic, and hemodynamic evidence of acute inferior myocardial infarction associated with RVMI and CS were studied. After administration of supplemental oxygen (inspired oxygen fraction [F(i)O(2)] = 1.0), hemodynamic measurements were recorded before, during inhalation of NO (80 ppm at F(i)O(2) = 0.90) for 10 min, and 10 min after NO inhalation was discontinued (F(i)O(2) = 1.0). RESULTS: Breathing NO decreased the mean right atrial pressure by 12 +/- 3%, mean pulmonary arterial pressure by 13 +/- 2%, and pulmonary vascular resistance by 36 +/- 8% (all p < 0.05). Nitric oxide inhalation increased the cardiac index by 24 +/- 11% and the stroke volume index by 23 +/- 12% (p < 0.05). The NO administration did not change systemic arterial or pulmonary capillary wedge pressures. Contrast echocardiography identified three patients with a patent foramen ovale and right-to-left shunt flow while breathing at F(i)O(2) = 1.0. Breathing NO decreased shunt flow by 56 +/- 5% (p < 0.05) and was associated with markedly improved systemic oxygen saturation. CONCLUSIONS: Nitric oxide inhalation results in acute hemodynamic improvement when administered to patients with RVMI and CS.

Administration, Inhalation↗
PubMed2005

Acute hemodynamic benefits of bi-atrial atrioventricular sequential pacing with the optimal atrioventricular delay.

OBJECTIVES: We evaluate the acute effects on hemodynamics of bi-atrial (BiA) pacing with the optimal atrioventricular (AV) delays, in comparison with high right atrial (HRA) pacing and coronary sinus (CS) pacing. BACKGROUND: Bi-atrial pacing has been suggested as one of the alternative therapy for preventing the recurrence of atrial fibrillation (AF). There are, however, few reports on the hemodynamic effects of BiA pacing, and the results that exist are controversial. METHODS: Twenty patients were paced from HRA, left lateral site of CS, and both sites with the optimal AV delays at 80 and 100 beats/min, in random order. After 5-min pacing, maximal P-wave duration in a 12-lead electrocardiogram, cardiac output (CO), pulmonary capillary wedge pressure (PCWP), and the transmitral flow pattern by transthoracic echocardiography were measured. RESULTS: Compared with HRA and CS pacing, BiA pacing delivered the shortest P-wave duration (HRA: 130 +/- 14 ms, CS: 132 +/- 19 ms, and BiA: 94 +/- 8 ms, respectively, p < 0.001) and the most improvement in CO and PCWP (HRA: 3.63 +/- 0.67 l/min and 9.2 +/- 4.3 mm Hg, CS: 3.71 +/- 0.70 l/min and 8.8 +/- 3.4 mmHg, and BiA: 3.88 +/- 0.63 l/min and 8.0 +/- 3.1 mmHg, respectively, p < 0.01). Bi-atrial pacing also significantly increased the mitral flow time velocity integral and peak A-wave velocity by transthoracic echocardiography, compared with HRA and CS pacing (HRA: 7.6 +/- 1.4 cm and 68.8 +/- 12.2 cm/s, CS: 7.8 +/- 1.4 cm and 70.5 +/- 14.5 cm/s, and BiA: 8.2 +/- 1.2 cm and 76.3 +/- 14.2 cm/s, respectively, p < 0.01). Bi-atrial pacing most significantly decreased the intervals between the atrial pacing spike and the peak of A-wave (HRA: 180 +/- 28 ms, CS: 165 +/- 21 ms, and BiA: 157 +/- 19 ms, respectively, p < 0.01). These improvements in hemodynamics significantly correlated with interatrial conduction delay. CONCLUSIONS: Bi-atrial pacing made the most significant improvements of hemodynamics. These benefits may be due to the improvements in interatrial conduction delay and atrial dyssynchrony.

Aged↗
PubMed2005

Survival, hemodynamics, and tissue oxygenation after head trauma.

BACKGROUND: The aims of this study were to describe the early time course of hemodynamic and tissue perfusion and oxygenation patterns in survivors and nonsurvivors after head injury; to suggest physiologic mechanisms responsible for the observed patterns; and to evaluate postinjury parameters that might be useful for treatment. The hypothesis was that reduced hemodynamics and tissue oxygenation and reduced arterial oxygen saturation affect outcomes. STUDY DESIGN: Sixty patients with head trauma were noninvasively monitored on arrival in the emergency department to assess the temporal hemodynamic patterns associated with head injury; patients who were brain dead were excluded because they have very different hemodynamic patterns. Cardiac index, mean arterial pressure, and heart rate were monitored to assess cardiac function, pulse oximetry to reflect changes in pulmonary function, and transcutaneous oxygen and carbon dioxide to reflect tissue perfusion function. Patients were stratified by inhospital survival outcomes, the Glasgow Coma Scale, and the presence or absence of associated somatic injuries. RESULTS: When all head injured patients were considered together, the predominant findings were high cardiac index, hypertension, mild tachycardia, normal pulmonary function, and reduced tissue oxygenation. The subset of survivors and those with high Glasgow Coma Scale had greater than normal cardiac index responses (4.02 +/- 0.01 (SEM) L/min/m2, p < 0.01 versus normal) and better tissue oxygenation (217 +/- 2 mmHg PtcO2/FiO2) than nonsurvivors (70 +/- 3 mmHg, p < 0.01) and those with low Glasgow Coma Scale (160 +/- 2, p < 0.05). Patterns of patients with associated somatic injuries were similar to those with isolated head injury. CONCLUSIONS: The study suggested that survivors' cardiac index, tissue oxygenation, and arterial oxygen saturation may be considered as markers of resuscitation. Nonsurvivors of head injury had normal blood flow with reduced tissue oxygenation that might have contributed to unfavorable outcomes.

Adolescent↗
PubMed2006

Quantitative evaluation of interrelations between spontaneous low-frequency oscillations in cerebral hemodynamics and systemic cardiovascular dynamics.

A common issue in blood-related brain-function measurements, such as optical topography, is that the observed signals are usually corrupted with strong noise that is primarily spontaneous low-frequency oscillations (LFOs) in cerebral hemodynamics, which are difficult to separate from the signals due to functional brain activity because of their common spectral range. We discuss the analysis of information transfer between LFOs around 0.1 Hz in the hemoglobin concentration change (HbCC) in the cerebral cortex, the heart rate (HR), and the mean arterial blood pressure (ABP) to understand the origin of spontaneous LFOs in cerebral hemodynamics. As measures of information transfer, we used transfer entropy (TE) for two-variable system analysis and introduced intrinsic transfer entropy for further analysis of three-variable systems by extending the original TE. Data for analysis were obtained from simultaneous measurements with optical topography and infrared finger plethysmography under rest conditions. The analysis revealed that the LFOs in oxy HbCC, a parameter of cerebral hemodynamics, mainly stem from HR, but its contribution is only about 20%. In addition, the intrinsic contribution of ABP is about 5% and the common contribution of HR and ABP is about 10%. From these, HR and ABP cannot account for more than the half the information carried with variable oxy HbCC, which suggests the origin of LFOs in cerebral hemodynamics may lie in the regulation of regional cerebral blood flow change and energetic metabolism rather than due to the systemic regulation of the cardiovascular system.

Aged↗
PubMed2004

Visually evoked hemodynamical response and assessment of neurovascular coupling in the optic nerve and retina.

The retina and optic nerve are both optically accessible parts of the central nervous system. They represent, therefore, highly valuable tissues for studies of the intrinsic physiological mechanism postulated more than 100 years ago by Roy and Sherrington, by which neural activity is coupled to blood flow and metabolism. This article describes a series of animal and human studies that explored the changes in hemodynamics and oxygenation in the retina and optic nerve in response to increased neural activity, as well as the mechanisms underlying these changes. It starts with a brief review of techniques used to assess changes in neural activity, hemodynamics, metabolism and tissue concentration of various potential mediators and modulators of the coupling. We then review: (a) the characteristics of the flicker-induced hemodynamical response in different regions of the eye, starting with the optic nerve, the region predominantly studied; (b) the effect of varying the stimulus parameters, such as modulation depth, frequency, luminance, color ratio, area of stimulation, site of measurement and others, on this response; (c) data on activity-induced intrinsic reflectance and functional magnetic resonance imaging signals from the optic nerve and retina. The data undeniably demonstrate that visual stimulation is a powerful modulator of retinal and optic nerve blood flow. Exploring the relationship between vasoactivity and metabolic changes on one side and corresponding neural activity changes on the other confirms the existence of a neurovascular/neurometabolic coupling in the neural tissue of the eye fundus and reveals that the mechanism underlying this coupling is complex and multi-factorial. The importance of fully exploiting the potential of the activity-induced vascular changes in the assessment of the pathophysiology of ocular diseases motivated studies aimed at identifying potential mediators and modulators of the functional hyperemia, as well as conditions susceptible to alter this physiological response. Altered hemodynamical responses to flicker were indeed observed during a number of physiological and pharmacological interventions and in a number of clinical conditions, such as essential systemic hypertension, diabetes, ocular hypertension and early open-angle glaucoma. The article concludes with a discussion of key questions that remain to be elucidated to increase our understanding of the physiology of ocular functional hyperemia and establish the importance of assessing the neurovascular coupling in the diagnosis and management of optic nerve and retinal diseases.

Animals↗
PubMed2004

Effect of portal hemodynamics on liver regeneration studied in a novel portohepatic shunt rat model.

BACKGROUND: The role of portal hemodynamics on liver regeneration after partial hepatectomy is not fully understood. The aim of our study was to characterize the effects of portal hemodynamics using a novel rat model. METHODS: We established a rat model of a portohepatic shunt with a 70% hepatectomy (PHS model), in which the portal pressure remained stable during and after the 70% hepatectomy. To assess the effect of portal hemodynamics on liver injury and regeneration in the first 24 hours, we compared PHS rats with those with a simple 70% hepatectomy. RESULTS: Biochemical and histopathologic changes were similar between the 2 groups. Liver weight increased in the control, whereas it did not in the PHS group (P = .0021). Hepatocytes were enlarged in the control but not in the PHS group, although DNA synthesis was similar in both groups. Apoptotic hepatocytes increased markedly in PHS at 24 hours, whereas minimal apoptosis was noted throughout the course of the study in the control group. Hepatocyte growth factor increased similarly, except that it was not activated in PHS. CONCLUSIONS: Our results suggested that a portal hyperdynamic state early after a 70% hepatectomy was necessary for liver regeneration through activation of hepatocyte growth factor, promoting hepatocyte hypertrophy and avoiding apoptosis, while DNA synthesis in hepatocytes was independent of portal hemodynamics.

Animals↗
PubMed1990

Comparison of hemodynamic pressure half-time method and Gorlin formula with Doppler and echocardiographic determinations of mitral valve area in patients with combined mitral stenosis and regurgitation.

Mitral valve area determined by the Gorlin formula in patients with combined mitral stenosis and regurgitation underestimates the true orifice size. Recent data suggest Doppler ultrasound and two-dimensional echocardiography more accurately estimate the mitral valve area in patients with mixed mitral valvular disease. This study assessed the accuracy of an alternate method, the hemodynamic pressure half-time method, for mitral valve area determination in such patients. In 22 patients, 28 separate mitral valve areas were calculated by the hemodynamic pressure half-time method, the Gorlin formula, and the Gorlin formula corrected for mitral regurgitation, and were compared with results calculated by the Doppler pressure half-time method. Six patients were studied both before and after balloon mitral valvuloplasty. In addition, mitral valve areas calculated by all four methods were compared with results obtained by planimetry in 15 patients with technically optimal echocardiograms. The mitral valve areas determined by hemodynamic pressure half-time corretated closely with the valve areas determined by Doppler (r = 0.90), whereas mitral valve areas determined by the Gorlin formula (both without and with correction for mitral regurgitation) did not correlate as well with the Doppler-estimated valve areas (r = 0.47 and r = 0.56, respectively). Correlation between the Doppler-derived mitral valve areas and the planimetered valve areas was also good (r = 0.84), as was that between the mitral valve areas calculated by hemodynamic pressure half-time and those calculated by planimetry (r = 0.78).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Developmental sequelae of fixed-rate ventricular pacing in the immature canine heart: an electrophysiologic, hemodynamic, and histopathologic evaluation.

Permanent, fixed-rate ventricular pacing (VVI) is associated with hemodynamic deterioration in the adult with compromised myocardial function. The effects of this pacing mode on the intact, immature heart, however, are largely unknown. Twelve beagle puppies (age 3 to 4 months) were equally divided into paced and age-matched control groups. All underwent identical hemodynamic and electrophysiologic evaluations. Transepicardial atrioventricular block and pacemaker insertion were additionally carried out in the paced group. After 4 months of observation, repeat hemodynamic and electrophysiologic measurements followed by histopathologic examinations were done in all puppies. The paced group exhibited significant (p less than 0.05) elevations of right atrial and pulmonary artery pressures, alterations in sinus node function, and prolongation of ventricular refractory periods compared with the control group. Initiation of dysrhythmias by programmed electrical stimulation was observed only among the paced group of puppies. Histologic examination demonstrated myofibrillar cellular disarray, dystrophic calcifications, prominent subendocardial Purkinje cells, and an increase in variable-sized, disorganized mitochondria only in the paced specimens. These findings indicate that permanent, apically-initiated VVI pacing ultimately predisposes to adverse cellular changes associated with hemodynamic and electrophysiologic deterioration in the intact, developing immature canine heart.

Animals↗
PubMed1977

The hemodynamic response to intra-aortic balloon counterpulsation in patients with cardiogenic shock complicating acute myocardial infarction.

Sixteen patients with cardiogenic shock complicating acute myocardial infarction underwent serial hemodynamic studies during intra-aortic balloon counterpulsation (IABC) at an assist frequency of 1:1. Significant increase was noted during the first 12 hours of IABC in the systemic artery peak diastolic pressure (assisted), cardiac index, stroke index, and stroke work index. During the second 12 hours further significant improvement was noted in the latter three parameters and, in addition, the systemic artery systolic pressure increased significantly. The pulmonary wedge pressure fell as did the total systemic resistance (TSR) during the first 24 hours of IABC. Patients found to be balloon independent after reduction in balloon assist frequency demonstrated significantly greater increase in systemic artery peak diastolic pressure during the first 12 hours of IABC than did those patients found to be balloon dependent. Likewise, the improvement noted in CI, SI, and SWI during the second 12 hours of IABC was of greater magnitude in balloon-independent than in balloon-dependent patients. The data suggest late hemodynamic deterioration after 48 hours of IABC. It is concluded that IABC is effective in improving the deranged hemodynamics of cardiogenic shock. Maximum response is noted between 24 and 48 hours. It is suggested that patients who are balloon independent may be distinguished from those who are balloon dependent by the hemodynamic response within the first 24 hours of IABC.

Acute Disease↗
PubMed2001

Cardiac and hemodynamic effects of intravenous dofetilide in patients with heart failure.

This study assesses the effects of dofetilide, a new selective Ikr blocker with class III properties, on left ventricular function and hemodynamics of heart failure and compares these effects with those of placebo and amiodarone. Because available antiarrhythmic drugs may depress myocardial performance, an invasive hemodynamic study was performed to assess the safety of this agent. Hemodynamic and angiographic data were obtained at baseline and after 30 minutes of double-blind infusion of dofetilide (8 microg/kg; n = 12), placebo (n = 12), or amiodarone (5 mg/kg; n = 6) in heart failure patients (New York Heart Association class II or III, ejection fraction <35%). Intravenous dofetilide preserved the inotropic indexes and the end-systolic volume index despite a slight but significant decrease in heart rate, whereas intravenous amiodarone increased end-diastolic and end-systolic volume indexes. Amiodarone induced a negative inotropic effect illustrated by a rightward shift of the pressure-volume loop and a reduction in pressure-derived indexes of contractility. Intravenous dofetilide acutely prolonged QT interval more than intravenous amiodarone; however, dofetilide did not slow the overall relaxation rate and reduced QT dispersion. In an acute setting, compared with intravenous amiodarone, intravenous dofetilide preserves cardiac function offering a hemodynamic advantage to treat arrhythmias in patients with impaired left ventricular function.

Adult↗
PubMed2001

Effects of omapatrilat on hemodynamics and safety in patients with heart failure.

Omapatrilat, a novel vasopeptidase inhibitor, is a highly potent and selective inhibitor of neutral endopeptidase and angiotensin-converting enzyme; its therapeutic potential is being investigated for treatment of hypertension and heart failure. In the present study, the safety, tolerability, and hemodynamic effects of single oral doses of omapatrilat (1 to 50 mg) are compared with placebo in patients with heart failure. Patients with heart failure (New York Heart Association functional class II to IV) and a resting left ventricular ejection fraction < or = 40% were enrolled in a double-blind, placebo-controlled, sequential-panel study of single doses of omapatrilat of 1, 2.5, 5, 10, 25, or 50 mg, followed by hemodynamic assessment for 24 hours. At 4 to 6 hours after dosing, the 25- and 50-mg doses of omapatrilat, compared with placebo, reduced mean pulmonary capillary wedge pressure by approximately 6 mm Hg from 20 and 23 mm Hg at baseline to 14 and 16 mm Hg. The 50-mg omapatrilat dose maintained this effect compared with placebo with an approximately 2.5-mm Hg reduction in mean pulmonary capillary wedge pressure at 24 hours. Omapatrilat improved additional hemodynamic parameters, including cardiac index, systemic vascular resistance, stroke volume index, and mean arterial pressure. Additionally, by 2 hours after dosing with omapatrilat 25 and 50 mg, a trend in peak increases from baseline in plasma atrial natriuretic peptide (twofold) and cyclic guanosine monophosphate (nearly twofold) was observed. Moreover, omapatrilat was well tolerated. Thus, omapatrilat administered orally to patients with heart failure was safe and well tolerated and resulted in improved hemodynamic performance.

Administration, Oral↗
PubMed2002

Changes in hemodynamics and left ventricular structure after menopause.

To evaluate the cardiovascular changes associated with menopause, we studied hemodynamics at rest, ambulatory blood pressure, and left ventricular structure in a biracial cohort of pre- and postmenopausal women of similar age, race, weight, and blood pressure. Despite similar levels of blood pressure, postmenopausal women had a higher indexed peripheral resistance (2,722 +/- 757 vs 2,262 +/- 661 dynes.s.m(2)/cm(5), p <0.01) and a lower cardiac index (2.64 +/- 0.73 vs 3.10 +/- 0.71 L/min.m(2), p <0.01) than premenopausal women. Postmenopausal women also had less nocturnal decreases in both systolic (15 +/- 8 vs 19 +/- 8 mm Hg, p <0.01) and diastolic (12 +/- 6 vs 15 +/- 6 mm Hg, p = 0.05) pressures during ambulatory monitoring and higher levels of hematocrit (40 +/- 2% vs 38 +/- 3%, p <0.01). In association with this greater hemodynamic load, postmenopausal women had evidence of early concentric left ventricular remodeling, manifested by a greater relative wall thickness (0.38 +/- 0.06 vs 0.35 +/- 0.06, p <0.01) than that observed in premenopausal women. Differences between pre- and postmenopausal women in hemodynamics, diurnal blood pressure variation, and left ventricular structure were observed in white and African-American subjects. These results suggest that menopause is associated with hemodynamic changes and left ventricular remodeling, which may contribute to the enhanced cardiovascular risk observed in postmenopausal women.

Black or African American↗
PubMed2002

Hemodynamic and surface electrocardiographic effects of a new aqueous formulation of intravenous amiodarone.

Intravenous amiodarone is an effective antiarrhythmic agent. However, the standard formulation (Cordarone IV) frequently causes hypotension. Hemodynamic studies have attributed this adverse effect to the solvents employed. A newly developed aqueous formulation (Amio-Aqueous) lacks solvents and thus may not causes hypotension. This study evaluated the hemodynamic effects in a cardiac catheterization laboratory. Two boluses of 150-mg aqueous amiodarone were administered via a peripheral vein to 32 hemodynamically stable patients who underwent cardiac catheterization. Boluses were administered initially over 2 to 5 minutes and in the last 9 patients over 2 minutes. Hemodynamic evaluation was performed and 12-lead electrocardiograms were obtained at baseline, immediately after each bolus, and following 30 minutes of observation. No patient developed hypotension. There were no significant changes in systolic and diastolic blood pressure (BP) following the boluses. Compared with baseline, heart rate (HR) significantly decreased 5 minutes after the second bolus (73 +/- 12 vs 67 +/- 11 beats/min, p <0.05). Mean arterial BP increased (90 +/- 14 vs 100 +/- 16 mm Hg, p <0.05) and dp/dt decreased (1,599 +/- 645 vs 1,294 +/- 531 mm Hg/s p <0.05), whereas the PR, QT, and JT intervals increased (174 +/- 30 vs 182 +/- 33; 402 +/- 32 vs 424 +/- 35; 317 +/- 37 vs 336 +/- 32 ms, p <0.05, respectively) by the end of the 30-minute observation period. Amio-Aqueous possesses pharmacodynamic effects that have been attributed to amiodarone, whereas it lacks the hypotensive effect of the standard intravenous amiodarone formulation. Amio-Aqueous appears to be a safer alternative to Cordarone IV when rapid administration is indicated.

Adult↗
PubMed2003

Impact of serial changes in cardiac hemodynamics on exercise performance in patients with heart failure due to ischemic and nonischemic cardiomyopathy.

Although prior studies have examined the role of central and peripheral hemodynamics on exercise tolerance within populations of patients with heart failure, a clear relation between hemodynamics and exercise has not been demonstrated. This may be due to the inability to control for other factors that may influence exercise performance. To isolate the impact of hemodynamics on exercise, we studied the relation between changes in these factors within individual patients studied on 2 occasions. A consecutive series of 133 ambulatory patients with heart failure were evaluated on 2 separate occasions with right-sided cardiac catheterization and treadmill cardiopulmonary exercise testing. Linear regression models were constructed and correlation coefficients were determined to examine the relation between changes in hemodynamic variables and changes in exercise variables over time for each patient. A significant correlation between peak oxygen consumption (VO(2)) and pulmonary arterial wedge pressure was found for both the first (r = -0.316, p <0.001) and second (r = -0.183, p = 0.029) tests. A stronger inverse correlation between the change in pulmonary arterial wedge pressure and change in peak VO(2) was observed in the study patients (r = -0.470, p <0.001). Similar correlations were found between change in peak VO(2) and changes in pulmonary arterial pressures. Changes in left ventricular filling pressure influence exercise tolerance in patients with heart failure due to left ventricular systolic dysfunction. Interpretation of cardiopulmonary exercise testing for the purpose of determining cardiac transplantation eligibility will be improved with knowledge of left ventricular filling pressure.

Adolescent↗
PubMed1983

Rheumatic tricuspid valve disease: two-dimensional echocardiographic, hemodynamic, and angiographic correlations.

From March 1977 through April 1982, 2-dimensional echocardiography detected 372 patients with rheumatic mitral valve disease. Of these patients, 23 (6%) had tricuspid valve involvement. Two-dimensional echocardiographic criteria of rheumatic tricuspid valve disease included thickened leaflets with restriction in motion, diastolic doming, and encroachment of the leaflet tips on the ventricular inlet. These criteria provided a sensitivity of 100%, a specificity of 90%, a predictive accuracy of 21%, and a negative predictive value of 100% in diagnosing hemodynamically significant tricuspid stenosis. Hemodynamic variables in patients with rheumatic tricuspid valve disease (Group I) were compared with those in patients with no rheumatic tricuspid disease (Group II). The only significant difference was mean right atrial pressure (15 +/- 7 mm Hg versus 11 +/- 5 mm Hg, p less than 0.02). Both groups were classified into patients with (A) and without (B) significant tricuspid regurgitation (TR). There was no significant difference in any hemodynamic variable when Group IA was compared with Group IIA. In addition, there was no difference in any hemodynamic variable when patients with functional TR (Group IIA) were compared with those with rheumatic mitral valvular disease without TR (Group IIB). Two-dimensional echocardiography and cardiac catheterization provide complementary diagnostic information in these patients.

Adult↗
PubMed1984

Failure of low doses of amrinone to produce sustained hemodynamic improvement in patients with severe chronic congestive heart failure.

Although amrinone produces acute hemodynamic improvement in patients with severe chronic congestive heart failure (CHF), it has not produced clinical benefits in long-term controlled trials. To determined if the administration of subtherapeutic doses of amrinone may account for its lack of efficacy in these studies, the dose requirements of the drug were investigated in 30 patients with severe CHF. Doses of 100 mg of oral amrinone produced moderate increases in cardiac index (0.35 liters/min/m2) and decreases in pulmonary capillary wedge pressure (6.8 mm Hg) and systemic vascular resistance (16%) (all p less than 0.01); these effects, however, were short-lived (less than 2.5 hours). Doses of 200 mg of oral amrinone produced marked increases in cardiac index (0.56 liters/min/m2) and substantial decreases in left ventricular filling pressure (9.9 mm Hg) and systemic vascular resistance (30%) (all p less than 0.01), and these effects persisted for longer than 4 hours. Only 4 patients showed hemodynamic responses with 100 mg of the drug that were sufficiently marked and long-lasting to merit chronic therapy, whereas 28 patients had such a response with the 200-mg dose. When 200 mg of amrinone was administered orally every 8 hours, sustained hemodynamic benefits were seen for 48 hours. However, 16 of 22 patients who received 600 mg of the drug daily for more than 1 week had intolerable adverse reactions that required drug withdrawal. In conclusion, hemodynamically effective doses of amrinone (600 mg/day) cannot be tolerated for long periods by most patients with severe chronic CHF.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗