Significant Increase In Stroke Volume Research Articles

The effect of tibolone on cardiac flow in postmenopausal women with non-insulin dependent diabetes mellitus

Postmenopausal women with non-insulin dependent diabetes (NIDDM) are frequently obese, hypertensive and hyperlipidaemic and hence at particular risk of coronary heart disease (CHD). They might therefore benefit from menopausal therapy. In view of the fact that oestrogen replacement increases cardiac flow but not limb flow whilst tibolone dilates forearm flow in healthy postmenopausal women, a study was undertaken to evaluate the effects of tibolone on cardiac flow in postmenopausal women with NIDDM. A prospective 12 months before/after intervention study. 15 postmenopausal women (mean age 58.36 +/- 1.25 years; mean duration of menopause 115.20 +/- 13.97 months; mean BMI: 26.22 +/- 1.02) with NIDDM (mean duration of diabetes 106.07 +/- 15.66 months). Cardiac flow was measured every 6 months for 1 year by pulsed Doppler echocardiography. The parameters assessed were: stroke volume (SV), cardiac output (CO), ejection fraction (EF), pre-ejection time (PEP), ejection time (ET), peak systolic flow velocity (PFV), acceleration time (AT), flow velocity integral (FVI), mean acceleration (MA), early diastolic filling time (Ei), atrial filling time interval (Ai), peak velocity of the early diastolic filling (E) and peak velocity of the early atrial filling (A). Blood pressure was also recorded during Doppler echocardiography. Stroke volume, cardiac output and ejection fraction increased significantly after 6 months. There was also a significant increase in peak flow velocity (PFV), flow velocity integral (FVI) and mean acceleration (MA) together with a significant increase in early diastolic filling time (Ei) and peak velocity of the early diastolic filling (E). Blood pressure was unchanged throughout the 12-month study period. The significant increase in stroke volume, cardiac output and flow velocity over the aortic valve parallel the effects of oestrogens in healthy postmenopausal women. The fact that tibolone improved left ventricular relaxation suggests the drug might help prevent or at least defer the development of cardiac dysfunction in diabetic women.

Improvement of cardiac performance by intravenous infusion of l-arginine in patients with moderate congestive heart failure

The aim of this study was to evaluate the hemodynamic effect of L-arginine infusion in patients with congestive heart failure. Endothelium-dependent vasodilation is impaired in patients with congestive heart failure. Nitric oxide, which was identified as endothelium-derived relaxing factor, is generated by nitric oxide synthase from L-arginine. Our hypothesis was that administration of L-arginine in patients with congestive heart failure may increase nitric oxide production and have a beneficial hemodynamic effect. Twelve patients with congestive heart failure (New York Heart Association class II or III) due to coronary artery disease (left ventricular ejection fraction < 35%) were given 20 g of L-arginine by intravenous infusion over 1 h at a constant rate. Stroke volume, cardiac output and left ventricular ejection fraction were determined with Doppler echocardiography at baseline and at 30 and 60 min and 1 h after the end of infusion. Blood and urinary levels of nitrite/nitrate (NO2/NO3), stable metabolites of nitric oxide, were measured and clearance was calculated. One hour of infusion of L-arginine resulted in a significant increase in stroke volume (from 68 +/- 18 ml to 76 +/- 23 ml [mean +/- SD], p = 0.014) and cardiac output (from 4.07 +/- 1.22 liters/min to 4.7 +/- 1.42 liters/min, p = 0.006) without a change in heart rate. Mean arterial blood pressure decreased (from 102 +/- 11 mm Hg to 89 +/- 9.5 mm Hg, p < 0.002), and systemic vascular resistance decreased significantly. Within 1 h after cessation of L-arginine infusion, blood pressure, stroke volume, cardiac output and systemic vascular resistance were statistically not different from baseline values. Clearance of NO2/NO3 increased significantly during L-arginine administration (from 13.28 +/- 0.42 ml/min to 29.97 +/- 1.09 ml/min, p < 0.001). Infusion of L-arginine in patients with congestive heart failure results in increased production of nitric oxide, peripheral vasodilation and increased cardiac output, suggesting a beneficial hemodynamic and possibly therapeutic profile.

Carvedilol improves left ventricular function and symptoms in chronic heart failure: A double-blind randomized study

This study assessed the safety and efficacy of carvedilol in patients with heart failure caused by idiopathic or ischemic cardiomyopathy. Carvedilol is a mildly beta 1-selective beta-adrenergic blocking agent with vasodilator properties. Beta-blockade may be beneficial in patients with heart failure, but the effects of carvedilol are not known. Sixty patients with heart failure (New York Heart Association functional classes II to IV) and left ventricular ejection fraction < or = 0.35 were enrolled in the study. All patients tolerated challenge with carvedilol, 3.125 mg twice a day, and were randomized to receive carvedilol (n = 36) versus placebo (n = 24). Study medication was titrated over 1 month from 6.25 to 25 mg twice a day (< 75 kg) or 50 mg twice a day (> 75 kg) and continued for 3 months. One placebo-treated and two carvedilol-treated patients did not complete the study. Carvedilol therapy resulted in a significant reduction in heart rate and mean pulmonary artery and pulmonary capillary wedge pressures and a significant increase in stroke volume and left ventricular stroke work. Left ventricular ejection fraction increased 52% in the carvedilol group (from 0.21 to 0.32, p < 0.0001 vs. placebo group). Carvedilol-treated patients also reported a significant lessening of heart failure symptoms (p < 0.05 vs. placebo group). Submaximal exercise duration tended to increase with carvedilol therapy (from 688 +/- 31 s to 871 +/- 32 s), but this change was not significantly different from that with placebo therapy by between-group analysis. Peak oxygen consumption during maximal exercise did not change. Long-term carvedilol therapy improves rest cardiac function and lessens symptoms in patients with heart failure.

Prostaglandin E 1Increases Oxygen Extraction Capabilities in Experimental Sepsis

By its microvascular and anti-inflammatory actions, prostaglandin E 1 (PGE 1) has been suggested both in animal models and in humans to have a therapeutic value in sepsis. To investigate whether PGE 1 could improve the oxygen extraction capabilities in severe sepsis, our study focused on the relationship between oxygen uptake (VO 2) and oxygen delivery (DO 2) during an acute reduction in blood flow induced by cardiac tamponade in endotoxic dogs. Thirty anesthetized, ventilated dogs were divided into three groups. A first group ( N = 10) served as a control receiving 20 ml/kg/hr of saline intravenously. A second group ( N = 10) received PGE 1 at 100 ng/kg/min along with the same saline infusion. A third group ( N = 10) received the same dose of PGE 1 with only 1 ml/kg/hr of saline. Thirty minutes after the initiation of this therapy, Escherichia coli endotoxin (2 mg/kg) was injected in each dog. In each group, the administration of PGE 1, fluids, or both was continued throughout the study. Tamponade was then induced by repeated bolus injections of warm saline into the pericardial space. Steady-state measurements of VO 2 (derived from the expired gases) and DO 2 (the product of cardiac index and oxygen content) were obtained sequentially after each saline injection. The administration of PGE 1 + fluids resulted in significant increases in stroke volume, cardiac index, and DO 2 and reductions in systemic and pulmonary vascular resistance. Stroke volume and cardiac index were lower in the PGE 1 alone than in the PGE 1 + fluids group. The VO 2 levels at critical DO 2 (DO 2crit) were identical. However, DO 2crit, which was 12.2 ± 2.8 ml/kg/min in the control group, was significantly decreased to 9.8 ± 2.0) ml/kg/min in the PGE 1 + fluids and to 9.3 ± 2.7 ml/kg/min in the PGE 1 alone group (both P < 0.05). Critical oxygen extraction ratio (O 2ER crit) which was 47 ± 14% in the control group, was increased to 63 ± 16% in the PGE 1 + fluids group and to 61 ± 17% in the PGE 1 alone group (both P < 0.05). To investigate whether PGE 1 also improves oxygen extraction capabilities in the absence of endotoxin, a second series of experiments was performed in 14 dogs, receiving saline alone (Control, N = 7) or plus PGE 1 at 100 ng/kg/min (PGE 1, N = 7). DO 2crit was 10.7 ± 2.9 ml/kg/min in the PGE 1 group vs 10.1 ± 1.8 ml/kg/min in the control group (NS). O 2ER crit tended to be higher in the PGE 1 group than that in the control group (68 ± 13% vs 60 ± 15%, P = 0.054). In conclusion, PGE 1 could almost entirely restore tissue oxygen extraction capabilities after endotoxin challenge on this dog model in which cardiac index was acutely reduced. The effects on oxygen extraction were present with or without concurrent saline administration, but the combination of PGE 1 with fluids improved global hemodynamics. Under control conditions, the influence of PGE 1 on the tissue oxygen extraction capabilities was not significant.

Peptidergic modulation of cardiovascular dynamics in the Dungeness crab, Cancer magister

Decapod crustacean pericardial organs contain extensive neurohormonal reserves which can be released directly into the haemolymph to act as physiological modulators. The present paper concerns the in vivo effects of two pericardial peptides, proctolin and crustacean cardioactive peptide, on cardiovascular dynamics in the crab Cancer magister. Infusion of proctolin into the pericardial sinus caused a slight decrease in heart rate concurrent with a large increase in cardiac stroke volume. It decreased haemolymph flow anteriorly through the paired anterolateral arteries and increased flow posteriorly and ventrally through the posterior aorta and sternal artery, respectively. The threshold for responses occurred at circulating concentrations of 10-9 mol·l-1, and haemolymph flows remained elevated for up to 30 min after peptide infusion. The effects of crustacean cardioactive peptide were less dramatic. Heart rate was not affected but a significant increase in stroke volume was observed. Crustacean cardioactive peptide increased haemolymph flow through the anterolateral arteries and increased scaphognathite rate. The threshold for crustacean cardioactive peptide activity was higher than for proctolin (10-7 mol·l-1 and 10-6 mol·l-1) but the responses to crustacean cardioactive peptide were of longer duration. The effects of proctolin on regional haemeolymph distribution in Cancer magister closely resemble the cardiovascular responses of this species when exposed to hypoxic conditions. These peptides may be implicated as cardiovascular regulators during environmental perturbations.

The effects of norepinephrine on hemodynamics and renal function in severe septic shock states.

To investigate the effect of norepinephrine (NE) on hemodynamics, oxygen metabolism and renal function in patients with severe septic shock. Prospective study. Post-operative ICU in a municipal general hospital. The study included 56 patients with extreme low resistance states due to abdominal sepsis, who remained hypertensive (MAP < 60 mmHg) despite optimal fluid therapy and dopamine > 20 micrograms/kg/min and cumulative doses of dopamine and dobutamine > 30 micrograms/kg/min, respectively. After registration of baseline values dopamine was reduced to 2.5 micrograms/kg/min, and norepinephrine was administered starting at a dose of 0.05 micrograms/kg/min until a mean arterial pressure of more than 60 mmHg could be maintained. During norepinephrine infusion (dosage ranging between 0.1-2 micrograms/kg/min, mean dose rate: 0.4 micrograms/kg/min) mean arterial pressure and systemic vascular resistance index increased significantly (p < 0.001). After 8 h a significant increase in stroke volume (p < 0.05) and decrease in heart rate (p < 0.05) could be observed. There was no significant change in cardiac index (CI), oxygen delivery (O2AVI) and oxygen consumption (VO2I). Creatinine clearance increased significantly (p < 0.005) from a control value of 75 +/- 37 ml/min to 102 +/- 43 ml/min after 48 h NE-treatment. Our results suggest that norepinephrine can be used safely in the treatment of severe septic shock states. Mean arterial pressure and glomerular filtration rate improved markedly without deleterious effects on CI, O2AVI and VO2I.

Changes in left ventricular output from fetal to early neonatal life

Using pulsed Doppler and two-dimensionally directed M-mode echocardiographic techniques, we measured left ventricular (LV) output, stroke volume, heart rate, LV end-diastolic dimension (LVEDD), LV end-systolic dimension, and LV percent fractional shortening (%FS) in 34 normal term infants 12 to 24 hours before parturition and thereafter serially 1, 24, and 96 hours after birth. Stroke volume was calculated as the product of the aortic flow velocity integral and aortic valve area. There was a twofold increase in LV output 1 hour after birth (fetal 170 +/- 46 ml/min/kg vs 1 hour 327 +/- 66 ml/min/kg; p less than 0.01) which was associated with significant increases in stroke volume, %FS, and LVEDD (stroke volume 1.21 +/- 0.33 ml/kg vs 2.25 +/- 0.37 ml/kg; %FS 34.3% +/- 5.8% vs 37.7% +/- 5.4%; LVEDD 15.4 +/- 1.1 mm vs 17.7 +/- 1.4 mm). Heart rate did not change 1 hour after birth. During the subsequent hours after birth, LV output decreased significantly to a value of 245 +/- 56 ml/min/kg (p less than 0.01) at 24 hours, which did not change 96 hours after birth. There were significant declines in stroke volume, LVEDD, and heart rate 24 hours after birth (stroke volume 2.02 +/- 0.42 ml/kg; LVEDD 17.0 +/- 1.1 mm; heart rate 121 +/- 11 beats/min). The %FS remained unchanged within the first 96 hours of age. These results indicate that the major regulator of LV output immediately after birth is stroke volume and not heart rate. The increase in stroke volume is related to an increase in LV size and LV myocardial contractility. Our data provide a useful basis for the interpretation of abnormal LV function in the early neonatal period.

Aortic root blood flow increases after pancuronium in neonates with hyaline membrane disease

To determine the effects of muscle paralysis on aortic root blood flow in preterm infants with hyaline membrane disease. Each patient served as his/her own control in a prospectively controlled trial. Neonatal ICU in a university hospital. Ten ventilator-dependent preterm infants weighing 800 to 2820 g, 0 to 8 days of age, with hyaline membrane disease and seven control patients. Noninvasive measurement of aortic root blood flow by Doppler echocardiography 30 min before and 60 min after respiratory paralysis with 0.1 to 0.5 mg/kg of iv pancuronium, or following ventilator changes in control subjects. Mean aortic root blood flow increased significantly (p less than .001), from 212 to 276 mL/min.kg, accompanied by significant increases in stroke volume and heart rate. Pancuronium bromide may have a direct beneficial effect on the circulation of preterm infants with hyaline membrane disease.

Hemodynamic effects of amrinone in children after cardiac surgery

The hemodynamic effects of amrinone were assessed in seven children following cardiac surgery. Amrinone was administered as a bolus of 1 mg kg-1 body wt., followed by continuous infusion at 10 micrograms kg-1 min-1 for 1 h and two stepwise increases to 20 and 40 micrograms kg-1 min-1 for 30 min each. Hemodynamic data were obtained and plasma concentrations of amrinone measured 1 h after the bolus dose and immediately before each increment of the infusion rate. Amrinone levels ranged from 0.7 to 2.3 mg l-1. Administration of amrinone lowered systemic vascular resistance from 20.0 +/- 4.3 to 16.5 +/- 4.6 mmHg l-1 min-1 m-2 (p less than 0.05) and reduced mean arterial pressure from 71.7 +/- 9.5 to 62.6 +/- 13.5 mmHg (p less than 0.05) at the highest infusion rate, confirming the known vasodilative effect of the drug. However, these effects did not result in a statistically significant increase in stroke volume (35.0 +/- 7.5 to 35.5 +/- 7.0 ml m-2, NS) or cardiac index (3.10 +/- 0.50 to 3.20 +/- 0.40 l min-1 m-2). One additional patient, in whom a higher loading dose was tried in order to achieve a higher plasma concentration, developed systemic hypotension. A correlation was established between the plasma concentrations of amrinone and the percentage decrease in systemic resistance (r = 0.70, p less than 0.05). These results suggest that in children after open heart surgery, amrinone acts primarily as a systemic vasodilator, with questionable inotropic effect. Accordingly, its use should be restricted to children with severe cardiac failure and documented highly elevated afterload.

Acute hemodynamic and arrhy thmogenic effects of high‐dose intravenous salbutamol in patients with chronic left ventricular dysfunction

The short-term hemodynamic and possible arrhythmogenic effects of intravenous salbutamol at a dose of 30 or 60 micrograms/min were evaluated in 14 patients with severe chronic left ventricular dysfunction using equilibrium radionuclide angiocardiography and electrocardiographic monitoring. Salbutamol infusions at a dose of 30 micrograms/min did not cause significant hemodynamic changes; however, at a dose of 60 micrograms/min there was a significant increase in stroke volume, cardiac output, and left ventricular ejection fraction. Heart rate increased significantly while systemic peripheral resistance decreased significantly. Two patients developed ventricular premature beats and another two supraventricular tachycardia, but none were associated with adverse consequences. Thus, high-dose intravenous salbutamol is effective and safe, and may be used in the acute management of patients with poor left ventricular function.

Hemodynamic Effects of Diltiazem and Nitrendipine Assessed by Noninvasive Methods in Patients with Congestive Heart Failure

In a placebo-controlled randomized double-blind cross-over study 16 patients with congestive heart failure (NYHA stage II; 12 male and 4 female; age 60.2 ± 9.8 years; body weight 77.8 ± 13.9 kg; X ± SD) received single oral doses of 90 and 180 mg diltiazem sustained release (s.r.) as well as 20 and 40 mg nitrendipine. Systolic time intervals, impedance cardiography, venous occlusion plethysmography, heart rate and blood pressure were measured 3, 6 and 12 h after administration of the drug. In impedance cardiography both dosages of diltiazem s.r. led to a significant increase in stroke volume and the heather index compared with the placebo values. Nitrendipine, on the other hand, only slightly increased these parameters. Cardiac output was not influenced by any of the kinds of treatment. While heart rate was significantly reduced after ingestion of 90 and 180 mg diltiazem s.r., it was accelerated under the influence of nitrendipine. Both calcium channel blockers significantly reduced diastolic blood pressure, but only 180 mg diltiazem s.r. exerted a marked antihypertensive effect on systolic blood pressure. In mechanocardiography the preejection period was shortened after administration of diltiazem and nitrendipine, although this effect was only significant for 180 mg diltiazem s.r. The PEP/LVET ratio was slightly reduced under the four different kinds of treatment; the parameters measured by venous occlusion plethysmography remained unchanged. From the results of the present study it can be concluded that over a 12-hour period of observation 90 and 180 mg diltiazem s.r. exert a more favorable effect on cardiac performance than 20 and 40 mg nitrendipine. By increasing stroke volume and - at the same time - reducing heart rate, diltiazem s.r. enables the left ventricle to work on a more economic base than nitrendipine does.

The acute effects of intravenous xamoterol (‘corwin’ I. C. I. 118, 587) on resting and exercise haemodynamics in patients with mild to moderate heart failure

The known properties of xamoterol, a partial beta 1-agonist, provide a basis to pharmacologically modulate cardiac responses to variations in sympathetic tone. Haemodynamic variables were assessed at rest and on exercise before and after intravenous xamoterol (0.2 mg kg-1), in 30 patients with mild to moderate cardiac failure. Xamoterol produced significant improvements in resting cardiac index (2.51 +/- 0.15 to 2.80 +/- 0.14 l min-1 m-2; P less than 0.001), stroke volume (62 +/- 4 to 75 +/- 5 mljbeat-1; P less than 0.001) and stroke work index (42.4 +/- 3.6 to 47.7 +/- 3.9 gm beat-1 m-2; P less than 0.01). This occurred despite a significant reduction in heart rate (78 +/- 3 to 74 +/- 2 beats min-1; P less than 0.05). There were also significant reductions in systemic vascular resistance (1990 +/- 141 to 1669 +/- 112 dynes s-1 cm-5; P less than 0.01) and double product (1146 +/- 46 to 1051 +/- 41 mmHg min-1 x 10(-1); P less than 0.05), with no significant changes in systolic blood pressure, pulmonary wedge pressure or ejection fraction. Xamoterol significantly attenuated the heart rate response to exercise (112 +/- 4 to 97 +/- 3 beats min-1; P less than 0.001), with no impairment in the expected exercise induced increase in cardiac index. This was due to the significant increase in stroke volume from 81 +/- 6 to 95 +/- 7 ml beat-1 (P less than 0.001). There were no significant changes in resting or exercise noradrenaline levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Doppler echocardiographic assessment of the effect of balloon aortic valvuloplasty on left ventricular systolic function

In order to evaluate the effects of balloon aortic valvuloplasty on left ventricular systolic function and ejection dynamics, Doppler echocardiographic studies were performed on 29 patients before and following valvuloplasty. Continuous wave aortic velocity signais were digitized and (with catheterization laboratory before and after valvuloplasty valve areas) were used to calculate: stroke volume; ejection time; ejection rate; time to 25%, 50%, and 75% ejection; accelerative (onset systole to peak velocity) ejection volume, time, and rate; and decelerative (peak velocity to end systole) ejection volume, time, and rate. Following valvuloplasty, there were no significant changes in heart rate; time to 25%, 50%, and 75% ejection; accelerative ejection time; and decelerative ejection time. There were significant increases in stroke volume, total ejection rate, accelerative ejection volume, decelerative ejection volume, accelerative ejection rate, and decelerative ejection rate, and a significant decrease in total ejection time. Balloon aortic valvuloplasty has a significant effect on the dynamics of left ventricular ejection. There is an increase in stroke volume and a decrease in ejection time, with relatively little effect on early systole, and a more pronounced effect in late systole. There are significant increases in accelerative and decelerative ejection volumes and rates, and a decrease in the time required for the last 25% of ejection. By improving the mobility of calcified leaflets, balloon aortic valvuloplasty may reduce the forces opposing forward blood movement during the decelerative phase of aortic ejection.

Haemodynamic effects of amrinone in the anaesthetized pig.

The vasodilator and inotropic actions of amrinone were investigated in mini-pigs under pentobarbitone anaesthesia. Left ventricular volume was determined angiocardiographically under afterload and isovolumetric conditions. Furthermore, aortic flow, left ventricular pressure and aortic pressure were measured. In some of the animals, the beta-adrenergic receptors were blocked with propranolol prior to the administration of amrinone. Without blockade of the beta-receptors, amrinone (2 mg kg-1) caused a significant reduction in mean aortic pressure. Due to less end-diastolic ventricular filling, stroke volume decreased, and thus ejection fraction remained constant. Since heart rate increased under amrinone, cardiac output remained constant. At the same time, the maximum rate of pressure rise increased, despite less end-diastolic ventricular filling. After blockade of the beta-adrenergic receptors, aortic pressure, end-diastolic ventricular filling, and stroke volume also decreased with amrinone. In contrast, heart rate remained practically constant, so that cardiac output declined. The maximum rate of pressure rise also declined due to less end-diastolic ventricular filling. It can be concluded from these results that, in situ, the primary action of amrinone occurs on vascular smooth muscle and that a positive inotropic activity with a normal dosage of amrinone is only an indirect outcome of reflex activation of the sympathetic system. Analysis of isovolumetric mechanograms and the ejection phase does not indicate a direct positive inotropic effect of amrinone. In the failing heart, however, beneficial effects can be expected, since the maxima curves follow a flatter course. Thus a reduction in afterload can lead to a significant increase in stroke volume, provided that aortic pressure does not fall below the critical coronary perfusion pressure.

Afterload Reduction in the Critically I11

We investigated the potential value of vasodilating therapy in critically ill patients with inappropriately low cardiac output during acute illness. In seven patients with low flow state during septic or postoperative state, sodium nitroprusside (20-100 micrograms/min) was compared with nicergoline (NIC) (0.5 to 2.5 mg/min), a new selective alpha 1-blocking agent with negative chronotropic action. Sodium nitroprusside (NP) decreased arterial pressure (from 90 +/- 5 to 68 +/- 5 mm Hg, p less than 0.01) and pulmonary artery balloon-occluded pressure from 20.3 +/- 3.1 to 15.4 +/- 2.8 mm Hg, p less than 0.01) and increased heart rate (from 110 +/- 11 to 120 +/- 13 beats/min, p less than 0.05) but failed to increase stroke volume (from 24.7 +/- 4.8 to 23.4 +/- 4.4 ml, NS). During NIC administration, a comparable decrease in systemic vascular resistance was associated with a significant increase in stroke volume (from 21.6 +/- 3.3 to 25.6 +/- 3.2 ml/m2, p less than 0.01) and cardiac output (CO) (from 2.4 +/- 0.3 to 2.7 +/- 0.3 L/min/m2, p less than 0.025), whereas the decrease in arterial pressure was less significant (from 91 +/- 8 to 84 +/- 7 mm Hg, p less than 0.05). Because NIC has no positive inotropic action, the most likely mechanism is that a baroreceptor-mediated increase in heart rate with NP was prevented by the negative chronotropic action of NIC. Both drugs adversely affected arterial blood oxygenation. By its unique property to decrease heart rate, NIC could represent a valuable vasodilating agent, especially in acute conditions.

A Time‐Related Study of the Hemodynamic Benefit of Atrioventricular Synchronous Pacing Evaluated by Doppler Echocardiography

We have used Doppler echocardiography to estimate the stroke volume (SV) in a study of 13 patients equipped with DDD pacemakers. SV was measured both during DDD and VVI pacing after observation times of 1,3,6, and 12 months of DDD pacing. SV was also measured at seven atrioventricular (AV) intervals (75-250 ms) in the search for optimal AV intervals. Mitral flow velocity was investigated to see if DDD pacing resulted in synchronous atrial contraction, and if mitral insufficiency existed at any of the pacing modes. Compared with the VVI mode, DDD pacing resulted in a mean increase in SV of 21 +/- 2% for the four observation periods. Two patients with severe left ventricular failure had no significant increase in SV during DDD vs VVI pacing. In each patient, an optimal AV interval ranging between 100-250 ms for the SV was found. Velocity profiles of mitral flow showed synchronous atrial contraction during DDD pacing, but not during VVI pacing. Mitral insufficiency was not seen in any pacing mode. DDD pacing resulted in a reduction in SV during the first 6 months, and was constant thereafter. Doppler echocardiography can be used repeatedly to evaluate the hemodynamic response of DDD pacing vs VVI pacing, and to find which AV interval gives the highest SV in the individual patient. Our study further shows that the hemodynamic benefit of DDD pacing is present after short-term as well as after long-term DDD pacing.

Effects of the Antihypertensive Prostaglandin Analog CL 115,347 on Cardiac Output Distribution in the Spontaneously Hypertensive Rat

The effects of CL 115,347, a novel prostaglandin E2 (PGE2) congener, on a variety of hemodynamic variables were examined in conscious spontaneously hypertensive rats. Within minutes of topical administration (0.03, 0.3, or 3.0 mg/kg), a dose-dependent decrease in mean arterial blood pressure (MABP) was observed. One hour following drug application, a stable, dose-related hypotensive effect was still apparent, with MABP from 18 to 33 mm Hg lower than control, predose values. Quantitation of blood flow using radioactive microspheres indicated that a significant increase in stroke volume and cardiac output (3.0 mg/kg only), as well as a reduction in total peripheral resistance, was associated with the administration of CL 115,347. Further analysis of regional blood flow implied that vasodilation in specific vascular beds may contribute importantly to the antihypertensive activity of this compound.

Hemodynamic effects of epinephrine: concentration-effect study in humans.

The hemodynamic effects of three different infusion rates of epinephrine (25, 50, or 100 ng X kg-1 X min-1 for 14 min) were examined in 10 normal human subjects. Ejection fraction and changes in cardiac volumes were assessed by radionuclide ventriculography. Plasma epinephrine was increased to levels that spanned the normal physiological range (178 +/- 15, 259 +/- 24, and 484 +/- 69 pg/ml, respectively). Epinephrine infusions resulted in dose-dependent increases in heart rate (8 +/- 3, 12 +/- 2, and 17 +/- 1 beats/min, mean +/- SE) and systolic pressure (8 +/- 1, 18 +/- 2, and 30 +/- 6 mmHg). Although epinephrine infusions had minimal effects on end-diastolic volume, there were significant increases in stroke volume (+26 +/- 2, 31 +/- 4, and 40 +/- 4%), ejection fraction (+0.10 +/- 0.01, 0.14 +/- 0.02 and 0.16 +/- 0.03 ejection fraction units), and cardiac output (+41 +/- 4, 58 +/- 5, and 74 +/- 1%). These increases in left ventricular performance were associated with a decreased systemic vascular resistance (-31 +/- 3, -42 +/- 2, and -48 +/- 8%). Supine bicycle exercise resulted in similar plasma epinephrine levels (417 +/- 109 pg/ml) and similar changes in stroke volume, ejection fraction, and systemic vascular resistance but greater increases in heart rate and systolic blood pressure. Since infusion-associated hemodynamic changes occurred at plasma epinephrine levels commonly achieved during many types of physical and emotional stress, epinephrine release may have an important role in regulating systemic vascular resistance, stroke volume, and ejection fraction responses to stress in man.

The effect of hypothermia on the cardiovascular system and the pressor actions of angiotensin II

1. 1.|The effect of hypothermia (24°C) on the pressor action of angiotensin II (ANG II) was studied in anaesthetized rats. 2. 2.|Hypothermia prolonged the pressor response to ANG II leading to an increase in the estimated half-life of ANG II. 3. 3.|Hypothermia also caused a significant increase in stroke volume and a significant decrease in heart rate with no change in cardiac output. 4. 4.|It is conclued that hypothermia causes a prolongation of the pressor action of ANG II probably by reducing the activity of the catabolic enzymes leading to an increase in ANG II half-life.

Acute and Subacute Haemodynamic Effects of Enalapril.

After a run-in period on placebo, 15 patients with primary hypertension got antihypertensive treatment with enalapril single therapy during six weeks. Before and four hours after drug administration simultaneous non-invasive recordings of ECG, phonocardiogram and carotid pulse tracing or apexcardio-gram or impedance cardiogram were made. After six weeks' therapy the recordings were repeated 12 hours and four hours after dose intake. The results showed enalapril to be a potent antihypertensive agent with considerable effect already four hours after the first dose intake. The blood pressure reduction was explained by a decrease in total peripheral resistance, semiquantitatively measured with impedance cardiography. Cardiac output was significantly higher during long-term treatment than betore therapy started, due to a significant increase in stroke volume. Lef ventricular (LV) diastolic function was not altered but a considerable improvement in LV systolic function was achieved as judged from the systolic time intervals. Open questioning regarding side effects indicated good tolerance.