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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Haemodynamic and echocardiographic studies of isosorbide dinitrate were conducted in 12 patients (8 men and 4 women) with left ventricular failure consecutive to recent myocardial infarction. The groups: group I received 5 mg/h and group II 10 mg/h Risordan intravenously. After one hour treatment, group I patients showed a significant fall in both PAP (from 32.3 +/- 5.3 to 26.7 +/- 6.9 mmHg; p less than 0.01) and PCP (from 21.8 +/- 4.7 to 17.3 +/- 7.7 mmHg; p less than 0.05). These haemodynamic changes were amplified after a second hour of treatment: PAP fell to 24 +/- 7.9 mmHg (p less than 0.01) and PCP to 14.2 +/- 4.4 mmHg (p less than 0.001). RAP decreased from 7.2 +/- 5.1 to 3.5 +/- 5 (p less than 0.05). There were no changes in heart rate, systemic arterial pressure, peripheral resistance, cardiac index, forward stroke work nor, on echocardiography, in ventricular diameters, shortening fraction and VCF. After one hour treatment, group II patients showed a fall in PAP (from 30.5 +/- 4.7 to 21.7 +/- 3.5 mmHg; p less than 0.01), PCP (from 21.7 +/- 4.8 to 14.8 +/- 4.9 mmHg: p less than 0.001) and RAP (from 10.3 +/- 2.9 to 7.2 +/- 2; p less than 0.01). The systolic diameter of the left ventricle was reduced from 66.3 +/- 10.6 to 64.3 +/- 11.3 (p less than 0.01). After 4 hours, improvement in PAP and PCP was maintained; the other values remained stable. The effectiveness of Risordan i.v. in left ventricular failure consecutive to acute myocardial infarction is due to reduction of filling pressures in the left ventricule. With the 10 mg/h dose, as opposed to the 5 mg/h dose, the systemic arterial pressure and the double and triple products tend to be reduced, which suggests greater effectiveness.
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PMID:[Use of isosorbide dinitrate (Risordan) injection in left ventricular failure following acute myocardial infarction (author's transl)]. 711 Sep 69

To assess left ventricular (LV) response to supine bicycle exercise, we studied 10 normal (group 1). 10 patients with coronary artery disease (CAD) (group 2), 12 patients with severe obstructive lung disease (COPD) (group 3), and eight patients with both CAD and COPD (group 4) by gated equilibrium radionuclide angiography. Most individuals in all groups also had pulmonary catheter-obtained measurements of LV filling pressures during exercise. Normal individuals increased their ejection fraction (EF) during exercise by increasing stroke volume (SV) and reducing end-systolic volume (ESV) without changing end-diastolic volume (EDV); pulmonary artery (PAP) and wedge (PAW) pressures were unaltered. CAD patients (group 2) showed no change in EF with increased EDV, ESV, SV, and PAW. COPD patients (group 3) exhibited decreases in EDV, ESV, and SV, accounting for abnormal EF responses in 6 of 12; PAW was unchanged and the marked elevation of PAP correlated with reduced EDV. Group 4 patients (CAD plus COPD) had abnormal EF responses with increased EDV and ESV without change in SV. Thus an abnormal LV function response to exercise in COPD patients may be multifactorial, thereby indicating the possible need for therapeutic modalities in addition to those employed in alleviating pulmonary parenchymal disease.
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PMID:Evaluation of left ventricular function in chronic pulmonary disease by exercise gated equilibrium radionuclide angiography. 721 69

The response to a rapidly administered volume infusion (250 ml of 5% albumin over 30 minutes) was studied in 28 critically ill patients. Cardiovascular responses were assessed by means of invasive hemodynamic parameters (i.e., cardiac index [CI], central venous pressure [CVP], pulmonary artery pressure [PAP], and pulmonary capillary wedge [PCWP] pressure as well as radionuclide [RN] angiography). This allowed for the simultaneous measurement of right (RVEF) and left (LVEF) ejection fractions, and right (RVEDV) and left end-diastolic (LVEDV) and end-systolic (LVESV) volumes. Twenty patients responded (R) to volume infusion by demonstrating an increase in stroke volume. This response was secondary to an increase in LVEDV in 11 (R-1) and an increase in the LVEF in nine (R-2). Neither response was predictable before treatment. The responders also demonstrated a significant decrease in heart rate (P less than 0.05). The increased ejection fraction in some responders (R-2) was associated with a decrease in systemic vascular resistance index (SVRI) (P less than 0.05) and LVESV (P less than 0.05) suggesting a reduced afterload secondary to peripheral vasodilation concomitant on volume change. The PCWP appeared to be related more to right ventricular (RV) loading factors (i.e., CVP, RVEDV, and pulmonary vascular resistance [PVRI] [R2 = 0.85, P less than 0.005]) then to the LVEDV (P = NS). Left ventricular (LV) loading with volume infusion appeared to be dependent on both RV performance and the PVRI in some patients, since responders who increased the LVEDV (R-1) were characterized by a simultaneous increase in RV stroke work and decrease in PVRI. The response to fluid infusion in critically ill patients is complex with both increases in LVEF and LV preload contributing to its beneficial effect. Clinical assessment of LV filling pressures (PCWP) does not accurately predict the response to volume infusion and does not allow a reliable assessment of the LV preload. This is most likely due to the broad range of LV compliance characteristics noted in critically ill patients. RV function also appears to be important in the clinical response to volume challenge.
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PMID:The hemodynamic effect of rapid fluid infusion in critically ill patients. 724 52

The effect of Alinidine (ST 567) on hemodynamics at rest and during exercise was studied in subjects with angiographically documented coronary artery disease and left ventricular dysfunction. Exercise tests were performed before and 30 min after intravenous administration of 20 mg of Alinidine. Significant decreases were observed for heart rate at rest and during exercise, for systolic and diastolic blood pressure. Pressures in the pulmonary artery and in capillary wedge position were significantly reduced after Alinidine by about 12 to 18% (mean PAP) and by about 19 to 28% (PCW). Cardiac output and stroke volume increased during exercise after Alinidine, but the differences were not significant. Depression of ST-segment in the exercise-ECG was significantly lower after Alinidine, angina pectoris occurred in all but one subject during control testing but in none after Alinidine. It is concluded that Alinidine is an effective antianginal drug. Intravenous administration of this agent even in a low dose improves cardiac performance during exercise in patients with impaired left ventricular function. Negative inotropic effects of Alinidine were not observed in this study. Bradycardia and in addition preload reduction are suggested to be the main mechanisms to improve left ventricular function and symptomatic status.
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PMID:[Hemodynamic actions on alinidine during exercise in patients with coronary artery disease]. 726 29

Perioperative hemodynamic changes following mitral valve replacement using the porcine heterograft prosthesis were measured in 21 patients with acquired mitral valve disease. Preoperatively, a state of compensatory cardiac failure was suggested by the following: an increased heart rate (HR) (96 beats per minute); low cardiac and stroke volume (SVI) indices (2.3 +/- 0.10 L/min/m2 and 25 +/- 2 ml/beat/m2); and increased systemic vascular resistance (SVR) (1,626 +/- 116 DYNE SEC CM-5). Bothe the mean pulmonary artery PAP) and pulmonary capillary wedge pressures (PCWP) were elevated as well (32 +/- 3 and 22 +/- 2 torr). Immediate hemodynamic improvement followed valve replacement. HR, SVR, PAP, and PCWP all decreased significantly. Twenty-four hours after valve replacement, PAP (23 +/- 1 torr) and PCWP (13 +/- 1 torr) demonstrated marked declines, SVR was reduced by one-third (1,173 +/- 87 dyne sec cm-5), HR had decreased by 10 beats per minute, and SVI had increased to 30 +/- 2 ml/beat/m2. The prompt circulatory improvement of patients soon after mitral valve replacement using the porcine heterograft compares favorably with studies in which other valve types were employed and in which postoperative cardiovascular depression was encountered frequently.
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PMID:Acute hemodynamic alterations after mitral valve replacement with the glutaraldehyde-treated porcine heterograft prosthesis. 737 85

Increasing concern over complications related to blood transfusions has prompted a reevaluation of what constitutes an "adequate" perioperative hemoglobin concentration, particularly in patients undergoing coronary artery bypass graft (CABG) surgery. Data from 224 patients with preserved ventricular function (ejection fraction > 50%), undergoing CABG surgery, previously studied under a variety of anesthetic protocols, were reexamined to determine the effect of hemoglobin (HGB) concentration on myocardial lactate flux (MLF) (as an index of ischemia). The interaction of MLF and HGB concentration, anesthetic technique (ANES), and hemodynamic variables (including systemic and pulmonary arterial pressures (SAP and PAP), cardiac output (CO), and myocardial oxygen consumption (MVO2) was determined from a pool of 1598 data sets obtained from 224 patients. Data were collected from just prior to induction of anesthesia until 24 h postoperatively. Univariate analysis revealed a statistically significant relationship between MLF and HGB concentration (P < 0.001) but the correlation coefficient was only 0.09. Multiple regression analysis did not determine HGB concentration to be a significant independent term affecting MLF in either the overall group or in a subgroup of 22 patients having an adverse outcome (myocardial infarction, stroke, or death). For patients undergoing CABG surgery, HGB concentrations within the range of 58-172 g/L were not a significant variable in production of global myocardial ischemia as evidenced by MLF. This suggests that HGB concentrations as low as 60-70 g/L in the perioperative period are well tolerated and are not associated with an increased incidence of myocardial ischemia.
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PMID:Does hemoglobin concentration affect perioperative myocardial lactate flux in patients undergoing coronary artery bypass surgery? 772 33

Right ventricular function was measured in ten patients with severe COPD (mean FEV1 = 0.48 +/- 0.2 L/s) as part of an evaluation for single lung transplant (SLT). Right ventricular ejection fraction (RVEF) was determined by two methods: first-pass radionuclide scan by multigated acquisition (MUGA) and by using a fast thermistor tipped RVEF/volumetric pulmonary artery catheter. None of the patients had clinical evidence of active right heart failure, although mild resting pulmonary hypertension (mean pulmonary artery pressure [PAP] = 24 +/- 4 mm Hg) that worsened with minimal exercise (mean PAP = 39 +/- 11 mm Hg) was present. There was a significant difference in RVEF measured by the two methods (mean MUGA RVEF = 57 +/- 10%, mean catheter RVEF = 27 +/- 8%; p < 0.00005). RVEF determined by both methods was correlated with hemodynamic and gas exchange variables obtained during rest and at maximal exercise. There were significant, yet inverse, correlations between RVEF measured by catheter and cardiac index measured during exercise (CIex), as well as with exercise pulmonary vascular resistance index (PVRI). There were no significant correlations found between MUGA RVEF and any gas exchange or hemodynamic variables. Significant correlations were found with the catheter-measured right ventricular end-diastolic volume (RVEDV) and CIex (r = 0.9 p < 0.005), with maximal oxygen consumption during exercise (VO2max) (r = 0.86 p < 0.0025), with exercise stroke volume index (SVI) (r = 0.76 p < 0.01), and exercise central venous pressure (CVP) (r = 0.62 p < 0.05). Echocardiographic studies revealed right ventricular dilatation and mild tricuspid regurgitation (TR) in all patients. The strong correlation between RVEDV, CIex, and VO2max supports the concept that in these patients, as long as there is no clinical evidence of right heart failure (resting CVP still within normal limits), those with the largest RVEDVs use the Frank Starling principle to their best advantage to remain more functional.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Right ventricular function in patients with severe COPD evaluated for lung transplantation. Lung Transplant Group. 778 38

The hemodynamic effects of argon pneumoperitoneum were studied to define its possible role as an alternative gas for intraperitoneal insufflation during minimally invasive surgery. Adult pigs were anesthetized and placed on mechanical ventilation. Parameters measured or determined included mean arterial (MAP), pulmonary arterial (PAP), pulmonary arterial wedge (PAWP), right atrial (CVP), and inferior vena cava venous (IVC) pressures, total excretion of CO2 (VCO2), oxygen consumption (VO2), minute ventilation, and arterial blood gases. Also determined were cardiac output, stroke volume, and systemic vascular resistance all indexed to weight (CI, SVI, SVRI). Data were recorded during a 1-h baseline, 2 h of insufflation with argon gas at a constant pressure of 15 mmHg, and 1 h recovery after desufflation. There was no significant change from baseline in VCO2, VO2, MAP, PAP, PAWP, CVP, PaCO2, or arterial pH. Argon pneumoperitoneum significantly increased systemic vascular resistance index and exerted a depressant effect on stroke volume index and cardiac index by 25% and 30% from baseline values, respectively (P < 0.05). Inferior vena cava pressure increased as a reflection of the intraabdominal pressure. Argon insufflation had no effect on respiratory function. Argon gas may not be physiologically inert, and in patients with cardiovascular disease its effects may be clinically important.
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PMID:Hemodynamic effects of argon pneumoperitoneum. 820 3

The cardiovascular response to 5-hydroxytryptamine (5-HT) challenge has been previously described in cattle. Abrupt bradycardia, followed by tachycardia, triphasic systemic blood pressure response, and pulmonary hypertension were the major changes elicited by 5-HT. The purpose of the present study was to determine whether the cardiovascular response to 5-HT in calves was attributable to 5-HT2 receptors. A specific 5-HT2 antagonist (metrenperone, 0.05 mg/kg) was administered intramuscular to six unsedated Friesian calves 30 min before the animals were given a 5-min intravenous 5-HT infusion. Mean systemic arterial (SAP), mean pulmonary arterial (PAP), pulmonary capillary wedge (PW) pressures were obtained by means of fluid-filled catheters, and cardiac output (CO) was measured by the thermodilution technique. Heart rate, stroke volume, systemic (SVR) and pulmonary (PVR) vascular resistances were calculated. Administration of 5-HT after metrenperone induced a short-lasting period of severe bradycardia followed by tachycardia and increased CO. The systemic blood pressure response was exclusively hypotensive and associated with a decrease in SVR. Conversely, PAP, PW, and PVR were not modified by 5-HT administration. The results establish that 5-HT induced systemic as well as pulmonary hypertension is mediated through the activation of type-2 serotonergic or alpha-adrenergic receptors, or both. In contrast, neither apnoea, bradycardia and hypotension, nor the positive chronotropic effect induced by 5-HT in cattle are mediated through such receptors.
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PMID:Cardiovascular response to intravenous administration of 5-hydroxytryptamine after type-2 receptor blockade, by metrenperone, in healthy calves. 1003 Jan 26

To determine the presence of a 'hypercoagulable state' as assessed by indices of thrombin and plasmin generation and of the amount of fibrin that is lysed, in patients with stable coronary, cerebral and peripheral arterial disease a population-based cross-sectional study was performed. From a population-based cohort comprising 7983 men and women aged 55 years and over, we randomly selected 127 subjects with a history of myocardial infarction, 124 with a history of stroke and/or transient ischemic attack, 131 patients with peripheral arterial disease and 263 control subjects in the same age group without arterial disease. Subjects using anticoagulant drugs were not selected. F1+2, TAT, and PAP were not associated with a history of cardiovascular events, nor with peripheral arterial disease. In contrast, positive associations were found for D-Dimer. Mean D-Dimer level was 40 microg/l (95% CI 35, 44) in control subjects; 53 microg/l (47, 61) in those with a history of myocardial infarction and 51 microg/l (45, 58) in those with a history of stroke and or transient ischemic attack. D-Dimer increased gradually with increasing severity of peripheral atherosclerosis; a decrease in ankle/arm systolic blood pressure ratio of 0.1 was associated with an increase in D-Dimer of 3.9 microg/l (p<0.01). This was more pronounced in subjects with higher F1+2, TAT and PAP concentration. In conclusion, the markers of onset of coagulation F1+2, TAT and PAP are not associated with the presence of arterial disease, but increased levels of these markers are necessary for the positive association between D-Dimer and arterial disease.
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PMID:Activation products of the haemostatic system in coronary, cerebrovascular and peripheral arterial disease. 1124 39


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