End-diastolic Length Relationship Research Articles

Effects of tachycardia on regional wall motion in acute ischemic canine heart.

Tachycardia accompanies the preload reduction. Our aim is to assess the effect of the heart rate change on wall motion in ischemic heart. In 8 dogs with occlusion of left anterior descending artery, we changed the heart rate (heart rate 90, 120, and 150 beats/minute) after using UL-FS49, a selective bradycardic agent, with atrial pacing. Preload was changed by inferior vena caval occlusion at a heart rate of 90 beats/minute. With either an increase in heart rate or an inferior vena caval occlusion, the end-diastolic length was decreased, but the end-diastolic length relationships between the non-ischemic and the ischemic region made different lines from those of the heart rate change and inferior vena caval occlusion. When increasing the heart rate, isovolumetric shortening was unchanged in the non-ischemic region with more expansion in the ischemic region. While inferior vena caval occlusion at a heart rate of 90 beats/minute, isovolumetric shortening was increased in the non-ischemic region, with more expansion in the ischemic region. Both in tachycardia and by the inferior vena caval occlusion, ejectional shortenings decreased in the non-ischemic and ischemic regions. Our results suggest that, in ischemic heart, tachycardia changes both in the end-diastolic length relationship between the non-ischemic and the ischemic region and at the isovolumetric contraction phase. The changes seem to be not only due to the inferior vena caval occlusion, but also due to tachycardia itself.

Beneficial effect of concomitant administration of isoflurane and nicorandil

In common with halogenated anaesthetics, nicorandil, a new KATP channel opener, has been shown to have cardioprotective and vasodilator effects. Recent studies have also suggested that the vasodilator and protective effects of halogenated anaesthetics are mediated partly via KATP channel opening. This study examined the effects of concurrent administration of nicorandil and isoflurane on haemodynamic state and ventricular function before, during and after 15 min of ischaemia. We studied left ventricular function in 40 anaesthetized rabbits using ultrasonomicrometry. Measurements were obtained before, during and after 15 min of regional ischaemia. Regional ventricular function was assessed in terms of systolic shortening (SS%) and preload recruitable work area (PRWA, the area beneath the regional stroke work vs end-diastolic length relationship) during reperfusion. Four groups were studied: group F (n = 10) received a bolus dose of fentanyl 100 micrograms kg-1 and then 400 micrograms kg-1 h-1 throughout; group 1 (n = 10) received 2.05% end-tidal concentration of isoflurane (1 MAC); group FN (n = 10) received fentanyl, a bolus does of nicorandil 100 micrograms kg-1 and then 25 micrograms kg-1 min-1, 15 min before occlusion; and group IN (n = 10) received isoflurane and nicorandil. Isoflurane decreased left ventricular systolic pressure and ventricular contractility (+dP/dtmax, slope of preload recruitable stroke work, and SS%). Nicorandil increased -dP/dtmax in group FN. Post-ischaemic regional left ventricular contractility in group I did not differ from that in group F, however, groups receiving nicorandil recovered to a greater extent. Group IN showed better recovery compared with all other groups when ventricular contractility was assessed by PRWA normalized to pre-occlusion values (mean 99.3 (SEM 10.5)% vs 73.4 (7.5)%, 50.2 (5.8)% and 52.4 (3.7)% at 120 min reperfusion in groups FN, I and F, respectively). Tissue ATP and lactate contents did not differ between groups. We conclude that concurrent administration of nicorandil and isoflurane enhanced post-ischaemic recovery compared with isoflurane anaesthesia or nicorandil and fentanyl administration.

Minimally invasive cardiopulmonary bypass with cardioplegic arrest: A closed chest technique with equivalent myocardial protection

Thoracoscopic cardiac surgery is presently under intense investigation. This study examined the feasibility and efficacy of closed chest cardiopulmonary bypass and cardioplegic arrest in comparison with standard open chest methods in a dog model. The minimally invasive closed chest group (n = 6) underwent percutaneous cardiopulmonary bypass and cardiac venting, as well as antegrade cardioplegic arrest through use of a specially designed percutaneous endovascular aortic occluder and cardioplegic solution delivery system. The control group (n = 6) underwent standard sternotomy and conventional open chest cardiopulmonary bypass, aortic crossclamping, and antegrade cardioplegia. Ischemic arrest time was 1 hour in each group. Ventricular pressures and sonomicrometer segment lengths were recorded before bypass and at 30 and 60 minutes after bypass. Left ventricular function did not differ significantly between the two groups, as demonstrated by measurements of elastance and end-diastolic stroke work. Also, the preload recruitable work area was 69% and 60% of baseline at 30 and 60 minutes after bypass in the minimally invasive group versus 65% and 62% in the conventional control group (p = not significant); the stroke work end-diastolic length relationship was 78% and 71% of baseline in the minimally invasive group at these intervals versus 77% and 74% in the conventional control group (p = not significant). Myocardial temperatures were similar throughout bypass in the two groups, and ultrastructural examination of prebypass and postbypass biopsy specimens showed no differences between groups. These results demonstrate that minimally invasive cardiopulmonary bypass with cardioplegic arrest is as feasible, safe, and effective as conventional open chest cardiopulmonary bypass. Thus current technology may allow wider clinical application of closed chest cardiac surgery. (J T horac C ardiovasc S urg 1996;111:556-66)

706-5 Calcitonin Gene-related Peptide Improves Recovery from Reversible Myocardial Ischemia

Calcitonin gene-related peptide (CGRP) has been found to have inotropic properties and a short half-life. CGRP has been demonstrated to reduce ischemic injury in tissue flaps as well as to increase coronary artery flow, while other available inotropes have been shown to impair recovery from myocardial ischemia. Yet, a therapeutic role for CGRP in myocardial ischemia has not been defined. Therefore, CGRP was compared to placebo in nine chronically instrumented conscious dogs who underwent two 15 minute left anterior descending coronary artery occlusions separated by at least 24 hours of reperfusion. Left ventricular transmural pressure and myocardial segment length were measured at control and during reperfusion. Either CGRP (0.07 μg/kg/min) or saline placebo was randomly chosen and continuously infused from 45 to 105 minutes of reperfusion. The alternative infusion was given during the second study. Regional function was assessed using preload recruitable work area (PRWA), a load-insensitive measure of regional myocardial performance. PRWA was calculated as the area beneath the linear stroke work vs. end-diastolic length relationship. Data are mean PRWA (% of control) ± SEM for the 9 dogs. 90 Min 3 Hours 8 Hours 24 Hours Placebo 89 ± 7 82 ± 8 94 ± 10 79 ± 7 CGRP * 155 ± 22 * 115 ± 9 * 118 ± 12 * 108 ± 15 * p < 0.05 vs. placebo Despite a short half-life of less than 30 minutes, CGRP caused a significantly more rapid return of cardiac function from ischemia than placebo throughout the entire 24 hours of reperfusion. These results suggest that CGRP may improve recovery from reversible myocardial ischemia and may have unique properties as an intravenous inotrope in an intensive care unit setting because it does not appear to impair recovery from acute myocardial ischemia.

Myocardial contractility evaluated from cross-oriented segments during β-adrenergic blockade or sympathetic nerve stimulation

In patient and experimental models of regions of the left ventricle subjected to ischaemia and thus made dysfunctional it is important to characterize the inotropic state of the remaining myocardium. Eighteen pentobarbitone-anaesthetized open-chest cats with an acute circumflex coronary artery occlusion were therefore studied during either sympathetic nerve stimulation (n = 9), or after beta-adrenergic blockade (n = 9). Myocardial contractility was evaluated from cross-oriented segments in the left ventricular anterior wall during stable haemodynamics and during 5 s inferior caval occlusion. The end-systolic pressure-length relationship of longitudinal segments was rather insensitive to beta-adrenergic blockade and sympathetic nerve stimulation. The end-systolic pressure-length relationship of circumferential segments was suitable as a marker of contractility in the low contractility range, whereas the peak systolic shortening velocity parameter was more suitable in the upper contractility range. The pressure-length loop area versus end-diastolic length relationship of both circumferential and longitudinal segments reflected both increased and decreased left ventricular inotropic state. We therefore conclude that the pressure-length loop area versus end-diastolic length relationship is the best index of regional myocardial contractility in regional ischaemic hearts.

Recovery of myocardial function after repetitive episodes of reversible ischemia.

The question of whether recovery of regional myocardial function after repetitive, reversible ischemia differs from recovery after a single episode of myocardial ischemia remains controversial. Therefore, eight conscious dogs were instrumented with ultrasonic dimension transducers and left ventricular micromanometers. Each animal underwent (in random sequence, 72 h apart) a single 15-min left anterior descending coronary arterial (LAD) occlusion and two 15-min LAD occlusions separated by 1 h of reperfusion. The preload recruitable work area (PRWA; the area beneath the regional stroke work vs. end-diastolic length relationship) quantified regional myocardial performance. Repetitive ischemia significantly delayed recovery of PRWA over the first 24 h (P < 0.05). Although postischemic myocardial creep resolved rapidly after single occlusion, double occlusion prevented recovery of creep during the first 4 h of reperfusion. The recovery time course of PRWA paralleled the resolution of myocardial creep, suggesting that creep contributed significantly to delayed functional recovery and that myocardial "stunning" after repetitive ischemia may result in part from interaction between postischemic diastolic properties and systolic dysfunction.

The Effects of Local Ventricular Pacing on Recovery from Regional Myocardial Ischemia

After surgical revascularization of ischemic myocardium, temporary ventricular pacing is often used, yet no data exist to indicate whether pacing ischemic versus nonischemic myocardium affects myocardial recovery. Therefore, chronically instrumented conscious dogs were studied with segment length transducers in the left anterior descending (LAD) distribution, left ventricular and pericardial micromanometers, pneumatic occluders on the LAD and venae cavae, and bipolar ventricular pacing wires, one pair in the LAD zone and one pair in the nonischemic (LCX) zone. Six dogs underwent a total of twelve 15-min LAD occlusions, each followed by 48 hr of reperfusion. Just after reperfusion, either the LAD or LCX zone was paced at 150 bpm for 45 min. LAD versus LCX pacing decreased regional stroke work (6 ± 5 versus 19 ± 5 kerg · cm -2) and produced contractile asynchrony. Myocardial contractile function was assessed using preload recruitable work area (PRWA), the area under the regional stroke work versus end-diastolic length relationship. Relative to LCX pacing, LAD pacing significantly delayed the recovery of PRWA after 4 hr of reperfusion (54 ± 9 versus 83 ± 9% control PRWA, P < 0.05). Perhaps by increased contractile asynchrony despite the decreased regional stroke work, ventricular pacing of ischemically injured myocardium delays functional recovery and should be avoided in clinical settings where the ventricular pacing site may be chosen.

Effects of arterial hypertension on myocardial recovery after ischemic injury.

Although improved surgery, angioplasty, and thrombolysis have made early revascularization of ischemic myocardium commonplace, the effects of arterial hypertension on myocardial recovery remain unclear. Therefore eight conscious dogs were instrumented to measure left ventricular transmural pressure and myocardial segment length in the left anterior descending (LAD) coronary distribution. Reversible ischemic injury was produced by two 15-min LAD occlusions separated by 4 days of reperfusion, with each dog randomly receiving either phenylephrine or placebo infusion for 30 min beginning 1 h after reperfusion. With ischemia, systolic myocardial performance fell to 14.3 +/- 3.7% of control and required greater than 48 h to recover. Compared with placebo, phenylephrine significantly depressed recovery of systolic function assessed by systolic shortening (57 +/- 12 vs. 85 +/- 13% control) or the area under the stroke work vs. end-diastolic length relationship (62 +/- 14 vs. 93 +/- 7% control) (both P less than 0.05). These data imply that ischemically injured myocardium is highly sensitive to arterial hypertension and that ventricular loading is a major determinant of the rate of myocardial recovery.

The Effects of Dopamine on Myocardial Functional Recovery After Reversible Ischemic Injury

Dopamine frequently is used to improve cardiac performance after acute myocardial ischemia. Inotropic agents, however, increase myocardial oxygen demand and could potentially delay recovery from ischemic injury. To evaluate this problem, we studied eight chronically instrumented dogs in the conscious state and performed two 15-minute coronary occlusions 48 hours apart. After one of the occlusions, either dopamine (15 μg/kg/min) or saline placebo was administered intravenously from 1.0 to 1.5 hours of reperfusion. The alternative infusion was given during the second study. Preload recruitable work area, the area beneath the stroke work versus end-diastolic length relationship, was used to assess intrinsic myocardial performance. Ischemia decreased preload recruitable work area to 13% of control after both occlusions. After reperfusion, a 30-minute dopamine infusion acutely increased myocardial function nearly threefold as compared with placebo. Myocardial performance after dopamine administration, however, was significantly depressed compared with placebo throughout the remaining 24 hours of reperfusion (p

The Effects of Dopamine on Myocardial Functional Recovery After Reversible Ischemic Injury

Dopamine frequently is used to improve cardiac performance after acute myocardial ischemia. Inotropic agents, however, increase myocardial oxygen demand and could potentially delay recovery from ischemic injury. To evaluate this problem, we studied eight chronically instrumented dogs in the conscious state and performed two 15-minute coronary occlusions 48 hours apart. After one of the occlusions, either dopamine (15 micrograms/kg/min) or saline placebo was administered intravenously from 1.0 to 1.5 hours of reperfusion. The alternative infusion was given during the second study. Preload recruitable work area, the area beneath the stroke work versus end-diastolic length relationship, was used to assess intrinsic myocardial performance. Ischemia decreased preload recruitable work area to 13% of control after both occlusions. After reperfusion, a 30-minute dopamine infusion acutely increased myocardial function nearly threefold as compared with placebo. Myocardial performance after dopamine administration, however, was significantly depressed compared with placebo throughout the remaining 24 hours of reperfusion (p less than 0.01). These data indicate that dopamine may impair functional recovery after ischemic myocardial injury and suggest that inotropic interventions should be used in this setting only when absolutely indicated.

The effects of dopamine on myocardial functional recovery after reversible ischemic injury

Dopamine frequently is used to improve cardiac performance after acute myocardial ischemia. Inotropic agents, however, increase myocardial oxygen demand and could potentially delay recovery from ischemic injury. To evaluate this problem, we studied eight chronically instrumented dogs in the conscious state and performed two 15-minute coronary occlusions 48 hours apart. After one of the occlusions, either dopamine (15 micrograms/kg/min) or saline placebo was administered intravenously from 1.0 to 1.5 hours of reperfusion. The alternative infusion was given during the second study. Preload recruitable work area, the area beneath the stroke work versus end-diastolic length relationship, was used to assess intrinsic myocardial performance. Ischemia decreased preload recruitable work area to 13% of control after both occlusions. After reperfusion, a 30-minute dopamine infusion acutely increased myocardial function nearly threefold as compared with placebo. Myocardial performance after dopamine administration, however, was significantly depressed compared with placebo throughout the remaining 24 hours of reperfusion (p less than 0.01). These data indicate that dopamine may impair functional recovery after ischemic myocardial injury and suggest that inotropic interventions should be used in this setting only when absolutely indicated.