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PubMed1995

Losartan in heart failure. Hemodynamic effects and tolerability. Losartan Hemodynamic Study Group.

BACKGROUND: The aim of the present study was to assess the short- and long-term effects of multiple doses of the angiotensin II receptor antagonist losartan in heart failure. METHODS AND RESULTS: A multicenter, placebo-controlled, oral, multidose (2.5, 10, 25, and 50 mg losartan once daily) double-blind comparison in patients with symptomatic heart failure and impaired left ventricular function (ejection fraction < 40%). Invasive 24-hour hemodynamic assessment was performed after the first dose and after 12 weeks of treatment. Clinical status and tolerability of treatment with losartan over the 12-week period were also evaluated. One hundred fifty-four patients were enrolled, of which 134 met the protocol criterion of baseline pulmonary capillary wedge pressure > or = 13 mm Hg. During short-term administration, systemic vascular resistance (SVR) (largest reduction against placebo of 197 dyne.s-1.cm-5 at 4 hours) and blood pressure fell significantly with 50 mg, lesser decreases were seen with 25 mg, and no discernible effects were seen with 2.5 and 10 mg. After 12 weeks of treatment, similar effects were seen on SVR and blood pressure (maximal fall in SVR against placebo, 318 dyne.s-1.cm-5 at 5 hours with 50 mg). In addition, pulmonary capillary wedge pressure fell with 2.5, 25, and 50 mg (largest reduction against placebo of 6.3 mm Hg at 6 hours with 50 mg), cardiac index rose with 25 and 50 mg, and heart rate was lower with all active treatment groups. Active treatment was well tolerated, and excess cough was not reported. CONCLUSIONS: This study showed that oral losartan administered to patients with symptomatic heart failure resulted in beneficial hemodynamic effects with short-term administration, with additional beneficial hemodynamic effects seen after 12 weeks of therapy. Clear effects were seen with both 25 and 50 mg, with the greatest effect seen with 50 mg.

Aged↗
PubMed2003

Continuous cardiac output and hemodynamic monitoring: high temporal correlation between plasma TNF-alpha and hemodynamic changes during a sepsis-like state in cancer immunotherapy.

Through continuous cardiac output monitoring, we investigated the temporal relationship between hemodynamic changes and plasma cytokines in a cancer patient who developed collateral sepsis to immunotherapy. A 52-year-old male with metastatic renal cell carcinoma received interleukin-2 (IL-2) infusion completing 72 h of administration. The patient developed 3 sepsis-like states including systemic inflammatory response syndrome (SIRS), shock, and multiple organ dysfunction syndrome (MODS). Hemodynamic parameters including systemic vascular resistance index (SVRI), left ventricular stroke work index (LVSWI) and cardiac index (CI) were measured over 60 h. Peripheral blood was drawn when SVRI dropped 20% in the patient and plasma cytokines including TNF-alpha, IL-6 and IL-1beta were measured using ELISA. After 60 h of immunotherapy, the patient showed a 63.4% decrease in SVRI, 54.5% decrease in LVSWI and 65.4% increase in CI. The evaluation of systemic cytokines revealed different kinetic patterns: (i) a sustained increase in TNF-alpha levels through all 3 sepsis-like states; (ii) IL-6 increased preferentially during SIRS and shock, while up/down-responses were found during MODS; (iii) IL-1beta was undetectable during the entire study period. A high temporal relationship between hemodynamic changes and plasma TNF-alpha, but not IL-6, was found. Although there are factors other than cytokines that can alter vascular resistance, this finding could represent an approach to evaluate the course of hemodynamia and probably the systemic cytokine expression after IL-2 administration in renal cancer.

Antineoplastic Agents↗
PubMed1991

[Tumor hemodynamics in hepatic nodules associated with liver cirrhosis: relationship between cancer progression and tumor hemodynamic change].

Tumor hemodynamics including arterial vascularity (AV) and portal perfusion (PP) were evaluated in histologically confirmed 55 hepatic nodules associated with cirrhosis using ultrasonographic (US) angiography during intraarterial carbon dioxide microbubbles injection and CT during arterial portography. Tumor hemodynamic patterns were classified into 6 types as follows: Type I (n = 10): PP (+), AV (hypo); Type I' (n = 2): PP (+), AV (iso); Type II (n = 5): PP (-), AV (hypo); Type III (n = 8): PP (-), AV (iso); Type IV (n = 25): PP (-), AV (hyper), Type V (n = 5): PP (partially +), AV (vascular spot in hypovascular). Eight nodules of Type I were diagnosed as benign nodules histologically including adenomatous hyperplasia (AH) (n = 6) and regenerative nodule (n = 2). Hundred percent (5/5) of Type II and 88% (7/8) of Type III nodules were well-differentiated HCC, in contrast to 8% (2/25) of Type IV nodules, typical HCCs. Fatty metamorphosis was observed in 75% (6/8) of Type III nodules, in contrast to 16% (4/25) of typical (classical) HCC nodules (Type IV). We concluded that at the malignant transformation from AH to HCC, reduction of portal blood flow in the nodule precedes the initiation of the increase of the arterial tumor vessel. Moreover, early stage HCC could exhibit hypovascular (Type I, II), isovascular (Type III), or vascular spot in hypovascular pattern (Type V) compared with a typical HCC (Type IV). It was also suggested that the more mature as a neoplasms the HCC becomes, the more the arterial tumor vessel in the nodule increases and fatty metamorphosis of well-differentiated HCC is highly related with tumor hemodynamic condition, i.e., hypoperfusion state from both arterial and portal vessel.

Carcinoma, Hepatocellular↗
PubMed1988

Modulation of hemodynamic effects with a converting enzyme inhibitor: acute hemodynamic dose-response relationship of a new angiotensin converting enzyme inhibitor, lisinopril, with observations on long-term clinical, functional, and biochemical responses.

The hemodynamic effects of varying oral doses of the long-acting converting enzyme inhibitor lisinopril were studied in an acute, single-blind, parallel fashion in 55 patients with moderate to severe congestive heart failure. Doses of 2.5, 5.0, and 10 mg produced a significant increase in cardiac index and significant reductions in pulmonary capillary wedge, right atrial, pulmonary arterial, and systemic arterial pressures and systemic vascular resistance. The changes were present up to 24 hours after dosing for most parameters. There was a clear-cut dose-response relationship observed. Forty-seven patients were followed over a 3-month period, during which functional status and exercise tolerance improved. Although 26% showed some evidence of renal dysfunction with lisinopril, these changes could be normalized by decreasing either the lisinopril or the diuretic dose. These data demonstrate that the hemodynamic changes with the long-acting converting enzyme inhibitor lisinopril can be modulated with dose adjustment in patients with congestive heart failure. They also suggest that renal function changes may be normalized by adjustment of either the dose of lisinopril or the diuretic dose.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1978

Systemic and pulmonary hemodynamic effects of saralasin infusion in hypertension. Predictability of plasma renin status from hemodynamic changes.

Hemodynamic measurements were obtained before and after 30 minutes of saralasin infusion in 26 fasting adults with hypertension (25 men and 1 woman). Nine showed a depressor response with a decrease in mean intaarterial pressure greater than 20 mm Hg. Ten were nonresponders and seven had an agonistic response with an increase in mean arterial pressure of greater than 10 mm Hg. Heart rate, pulmonary arterial and wedge pressures and pulmonary vascular resistance were nearly identical in the three groups and remained unchanged. Cardiac index decreased from a mean of 2.76 +/- 0.14 (standard error of the mean) to 2.48 +/- 0.1 liters/min per m2 in the nonresponders (P less than 0.02) but remained unchanged in the groups with a depressor or an agonistic response. The mean systemic vascular resistance decreased from 2,406 +/- 303 to 1,839 +/- 265 dynes sec/cm5 in the group with a depressor response (P less than 0.001) and increased in nonresponders (less than 0.02) and those with an agonistic response (P less than 0.01). However, regardless of the response of mean arterial pressure, systemic vascular resistance decreased only in the 10 patients with a plasma renin activity greater than 5 ng/ml per hour (8 from the depressor response group and 1 each from the nonresponse and agonistic response groups). It is concluded that (1) classification based soley on the response of aterial pressure to saralasin ignores important hemodynamic changes; (2) the response of cardiac index--no change in the patients with a depressor response and a reduction in nonresponders--suggests that endogenous angiotension II supports cardiac output in these groups; (3) a decrease in systemic vascular resistance is better than a decrease in mean arteiral pressure as a predictor of the status of the plasma renin activity; and (4) lack of change in pulmonary vascular resistance suggests that endogenous angiotension II plays an insignificant role in maintaining the resistance of the pulmonary vasculature.

Adult↗
PubMed2000

Significance of resting and stimulated cerebral blood flow for predicting the risk of hemodynamic cerebral ischemia in a model of chronic hemodynamic insufficiency.

OBJECTIVE: It has been postulated that patients with a compromised cerebrovascular reserve capacity (RC), defined as cerebral blood flow (CBF) response to acetazolamide (ACZ) (by percent), are at higher risk for ischemic stroke. The value of CBF and RC for predicting the risk of hemodynamically induced impairment of cerebral function is examined. METHODS: Both common carotid arteries were occluded in 22 Wistar-Kyoto rats. Thirty-one days later, mean arterial blood pressure was reduced to 40 mm Hg for 30 minutes. Laser Doppler scanning of CBF at resting conditions and after intraperitoneal administration of ACZ (0.1 mg/g body weight) was performed 30 minutes and 28 days after occlusion as well as before and during hypotension. Memory and motor functions were examined before and after CBF measurements. RESULTS: After occlusion, CBF dropped significantly and ACZ did not increase CBF. Four weeks later, resting CBF had significantly improved but remained impaired, as did RC, showing a distinct interindividual variability. Hypotension reduced CBF by 57 +/- 4% (P < 0.001) and significantly impaired memory and motor functions. CBF during hypotension correlated with resting CBF before hypotension (r = 0.495, P = 0.027) and with CBF before (r = 0.392, P = 0.048) and after (r = 0.476, P = 0.034) ACZ, as determined 4 weeks after occlusion. There was no correlation with RC (r = 0.091, P = 0.702). Neurological tests performed 1 day after hypotension correlated with CBF during hypotension (memory function, P = 0.03; motor function, P = 0.02) but not with RC. CONCLUSION: In this model of chronic hemodynamic insufficiency, the risk of impairment to global cerebral function was predicted by resting CBF and CBF after ACZ but not by RC determined with ACZ.

Acetazolamide↗
PubMed1987

Relationship between maternal hemodynamics and hematocrit and hemodynamic effects of isovolemic hemodilution and hemoconcentration in the awake late-pregnant guinea pig.

The relationship between the spontaneous hematocrit (Hct) and maternal hemodynamics and the hemodynamic effects of experimentally induced changes in this Hct were studied in the awake late-pregnant guinea pig. In animals with a relatively low Hct, cardiac output fractions and blood flows to brain and heart determined with microspheres were higher and those to kidneys lower than in animals with a relatively high Hct. The O2 flows to the kidneys and skin in the former animals were also lower. Cardiac output, heart rate, systemic blood pressure, and blood flows to the other organs, including the placenta, were not related to the Hct. Placental blood flow was found to vary in proportion to cardiac output. Both hemodilution and hemoconcentration induced changes in the cardiac output distribution and organ flows which resembled those observed in the spontaneous relation with Hct. In addition, hemodilution decreased systemic blood pressure. Both hemodilution and hemoconcentration increased placental blood flow; the magnitude of this flow increase was twice as high after hemodilution. The changes in oxygen flows after experimentally induced hemodilution and hemoconcentration appears to be directly related to the concomitant change in whole blood oxygen capacity. It is concluded that in the awake late-pregnant guinea pig, only brain, heart, and kidney perfusion vary in relation to the arterial Hct. The higher placental blood flow after isovolemic hemodilution may be a result of better blood rheology in the porous-like intervillous space of the placentas in a state of reduced systemic blood pressure. The modest rise in placental blood flow after isovolemic hemoconcentration appears to be mostly related to the methodology employed.

Animals↗
PubMed1992

Hemodynamic observations following orthotopic cardiac transplantation: evolution of rest hemodynamics in the first year.

The evolution of resting hemodynamics was studied at 1 week and 1 year in 40 patients following orthotopic cardiac transplantation. Abnormal hemodynamics after transplantation, characterized by elevated ventricular filling pressures (indicating diastolic dysfunction) and also by pulmonary hypertension, showed normalization by 1 year. In the absence of innervation, the resting heart rate of heart transplant recipients should theoretically be close to the intrinsic heart rate predicted by the age of the donor heart. In this study, a high incidence of relative sinus bradycardia (an indicator of sinus node dysfunction) was noted in the first post-operative week, although again there was a tendency to normalization by 1 year. These beneficial changes help to explain the dramatic and sustained improvement in the functional capacity of these patients late after transplantation.

Adult↗
PubMed1983

[Hypoxemia in hemodialysis: hemodynamic mechanism? Hemodynamic and spirometric study using acetate and bicarbonate buffers].

The background of this study is the occurrence during acetate hemodialysis (HDA) of arterial hypoxemia associated with well described vasodilatator hemodynamic changes. Our aim was to evaluate the relationship between these 2 phenomena. Eleven patients (7 males, 4 females, mean age 54 years) were compared in a protocol of HDA and bicarbonate hemodialysis (HDB) as regards their cardiac output measured by the dye dilution method, blood gases and respiratory gas measurements made at the bedside. The results show significant hypoxemia with hypocapnia as soon as the 30th minute of HDA and no significant variation of cardiac index. No significant variation of respiratory response was noted. Arterial prostaglandin levels rose significantly higher during HDA (+ 302%) than HDB (+ 163%; 2 alpha less than 0,05). The absence of a correlation between arterial hypoxemia and hemodynamic changes in HDA compared to HDB suggests that the phenomena are not interdependent. The importance of increased thromboxane activation in HDA will require further investigation.

Acetates↗
PubMed1979

Hemodynamic patterns in human hepatic cirrhosis: a prospective randomized study of the hemodynamic sequelae of distal splenorenal (Warren) and mesocaval shunts.

Increasingly successful operative management of gastroesophageal variceal hemorrhage has been achieved by newer techniques of portal venous reconstruction. Although it is postulated that the clinical success may be due to more selectivity in portal venous shunting, direct determination of the effect of portasystemic shunt on portal vein blood flow has not been possible. Direct determinations of portal vein blood flow were performed preoperative on unanesthetized, hemodynamically stable cirrhotic patients by observation of radiopaque water-insoluble droplets. Patients were then randomized into elective distal splenorenal (Warren) or mesocaval shunt and determinations were performed postoperatively under similar conditions when clinically possible. Although portal vein blood flow was not significantly different before (929 +/- 147 ml/min) or after 899 +/- 271 ml/min) distal splenorenal shunt, there was a large change in portal vein blood flow after mesocaval shunt, decreasing from 772 +/- 177 ml/min (hepatopetal) to -1021 +/- 310 ml/min (hepatofugal) p < 0.01). After either procedure total hepatic blood flow (as determined by cardiac green clearance) was not significantly changed, nor was renal blood flow; however, cardiac output was significantly increased after mesocaval shunt. Thus the theoretical hemodynamic goals of the selective distal splenorenal shunt, i.e., preservation of the hepatopetal flow within the portal vein, is achieved as determined in the early postoperative period. The correlation between these changes and the eventual clinical outcome remains to be determined.

Cardiac Output↗
PubMed2005

[Therapy of advanced heart failure adapted to hemodynamic objectives acquired by invasive hemodynamic monitoring].

OBJECTIVE: To assess advanced heart failure (HF) treatment in relation to reduction of ventricular filling pressures, with the use of greater doses of vasodilators, through invasive hemodynamic monitoring. METHODS: Nineteen advanced HF patients were studied, in whom Swan-Ganz catheter was inserted to direct administration of diuretic intravenously (IV) and sodium nitroprusside, with the aim of significantly reduce ventricular filling pressures. After achieving such objective or 48 hours, oral drugs were introduced until venous medicines were removed, keeping hemodynamic benefit. RESULTS: From 19 patients studied, 16 (84%) were of male sex. The average age was 66 +/- 11.4 years old; average ejection fraction was 26 +/- 6.3%; 2 patients (10.5%) showed functional class (FC) III and 17 (89.5%), FC IV. There was a decrease of pulmonary artery occlusion pressure from 23 +/- 11.50 mmHg to 16 +/- 4.05 mmHg (p = 0.008), of systemic vascular resistance index from 3,023 +/- 1,153.71 dynes/s/cm-5/m(2) to 1,834 +/- 719.34 dynes/s/cm-5/m(2) (p = 0.0001) and an increase of cardiac index from 2.1 +/- 0.56 l/min/m(2) to 2.8 +/- 0.73 l/min/m(2) (p = 0.0003). A subgroup with hypovolemia was identified. CONCLUSION: It was possible to reduce ventricular filling pressures to significantly lower values, obtaining a significant improvement of cardiac index, systemic vascular resistance index and pulmonary artery mean pressure, by using significantly higher doses of vasodilators.

Blood Pressure↗
PubMed1995

Effects of brain (B-type) natriuretic peptide on coronary artery diameter and coronary hemodynamic variables in humans: comparison with effects on systemic hemodynamic variables.

OBJECTIVES: This study attempted to clarify the effects of human brain (B-type) natriuretic peptide on coronary artery diameter and coronary vascular resistance in humans. BACKGROUND: Brain natriuretic peptide induces vasodilation in systemic circulation by activating particulate guanylate cyclase of the vascular smooth muscle. METHODS: In 13 patients with normal coronary arteries and left ventricular function, brain natriuretic peptide was infused at 0.5 microgram/kg body weight per min for 4 min into the left main coronary artery (six patients, Group A) or into the pulmonary artery (seven patients, Group B). Systemic hemodynamic variables and coronary sinus blood flow were measured before and after the infusion. The lumen diameter of the left coronary artery was quantitatively measured. RESULTS: In both groups, brain natriuretic peptide significantly increased heart rate and decreased mean arterial pressure. Rate-pressure product remained unchanged in both groups. Brain natriuretic peptide decreased systemic vascular resistance index significantly in both groups (both p < 0.01 vs. baseline), and there was no difference in the effect between the groups. Brain natriuretic peptide decreased coronary vascular resistance in Group A (p < 0.01 vs. baseline) but did not affect coronary vascular resistance in Group B (p < 0.01 vs. Group A). The lumen diameters of the proximal and distal segments of the left coronary artery were increased significantly after brain natriuretic peptide in both groups. After infusion of brain natriuretic peptide, mean plasma level of brain natriuretic peptide in the coronary sinus increased from 36 to 130,411 pg/ml in Group A and from 64 to 12,329 pg/ml in Group B. CONCLUSIONS: Brain natriuretic peptide shows a vasodilator effect on the coronary artery system in humans. However, the effect does not appear uniformly but is seen preferentially in the epicardial coronary artery. The sensitivity of the coronary resistance vessels to brain natriuretic peptide is low compared with that of the resistance vessels of the systemic circulation.

Cardiac Catheterization↗
PubMed1998

Insights into the relationship of fatty streaks to raised atherosclerotic lesions provided by the hemorheologic-hemodynamic theory of atherosclerotic lesions provided by the hemorheologic-hemodynamic theory of atherogenesis.

The hemorheologic-hemodynamic theory of atherogenesis suggests that atherosclerosis is a disease of low shear, which prolongs the residence time of atherogenic particles on the endothelium. Prolonged residence of lipid-rich particles results in a fatty streak. Prolonged residence of platelet microthrombi results in a raised lesion (atherosclerotic plaque). Thus, fatty streak and raised lesion development are independent processes. In contrast, received wisdom holds that fatty streaks are the precursors to raised lesions. The author examines anatomic and risk factor data for fatty streaks and raised lesions, including the results of the recent multicenter Pathobiological Determinants of Atherosclerosis in Youth study, in light of these two theories.

Aorta, Thoracic↗
PubMed1984

The hemodynamics and hemodynamic effects of indenolol in mild hypertension.

For clarifying the onset mechanism of essential hypertension, the hemodynamics in 9 mildly hypertensive men, mean age of 39.8 +/- 10.7 (mean +/- SD), was compared with 7 normotensive men, mean age of 39.8 +/- 10.7, by means of exercise echocardiography, and the effects of indenolol (administered 30 mg/day for 7 days orally to both groups) were studied. The interventricular septum and the left ventricular posterior wall were thickened in the mild hypertensives. No significant differences between the both groups were shown in the cardiac performance at rest and the cardiac index during exercise. The total peripheral vascular resistance was higher in the mild hypertensives than the normotensives during exercise. However, during exercise, the normotensives showed significant increases in the left ventricular end-diastolic dimension (LVDd) and the stroke index (SI); these changes were not significant in the mild hypertensives. After administration of indenolol, the significant increases in LVDd and SI during exercise were observed in the mild hypertensives. This study suggests that mild hypertensives with cardiac hypertrophy display a diminished Frank-Starling effect during exercise which may be attributed to the decreased left ventricular compliance due to cardiac hypertrophy and elevated afterload. Indenolol improved the Frank-Starling effect, which decreased in the mild hypertensives.

Adult↗
PubMed1990

[Hemodynamic correction of patients with acute myocardial infarct in hemodynamic subgroup III by plasma-exchange expansion with low-molecular dextran].

To 20 patients with acute myocardial infarction from the III hemodynamic group catheterized with a microcatheter or a balloon thermodilution catheter 332 (from 100 up to 500) ml of a 10% solution dextran 40 were infused intravenously with mean velocity of 33 ml/min. The cardiac index was measured by the dye or thermodilution methods. The left ventricular filling pressure (LVFP) increased with 47% (from 1.7 +/- 0.4 to 2.5 +/- 0.5 kPa), the cardiac index--15.8% (from 2.02 +/- 0.8 to to 2.34 +/- 0.37 l/min/m2), systolic and diastolic arterial pressure with 7.7%, stroke index--with 10.2% stroke working index--with 10.7%, total pulmonary resistance--with 37.9% (il all, p less than 0.001), cardiac rate--with 4.7% (p less than 0.05) but the systemic arterial resistance did not change (p greater than 0.10). The increase of the cardiac index for an increase of LVFP with I KPa was almost equal in the patients with different initial LVFP but was due mainly to the increase of the stroke index by LVFP below 1.3 kPa and to an increase of the heart rate by LVFP above 2.0 kPa. The cardiac index increased above 2.2 l/min/m2 in 45% of the patients (87% by LVFP below 1.3 kPa, 56% by LVFP 1.4-1.9 kPa and 0% by LVFP above 2 kPa). The cardiac rate remained increased up to the 4th hour after the infusion. The arterial pressure fell below its initial value after 30 min and remained low up to the 12 h. The LVFP decreased progressively according to the dependence: LVFP = -5.06 + 2.09 1g T.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗