Recovery Of Regional Myocardial Function Research Articles

TCT-150 Recovery of regional myocardial function after CTO PCI compared to no CTO PCI in STEMI patients with a concurrent CTO

TCT-150 Recovery of regional myocardial function after CTO PCI compared to no CTO PCI in STEMI patients with a concurrent CTO

Does Diabetes Have an Influence on Regional Deformation Parameters in Patients with Normal Systolic Function during Off-Pump Coronary Artery Bypass Grafting?

Objectives: The aim of this study was to assess the recovery of regional myocardial function of the left-ventricular septal wall and the septal site of the mitral valve (MV) annulus by tissue Doppler imaging (TDI). Methods: In 63 (32 diabetic and 31 control) patients having off-pump coronary artery bypass grafting (OPCABG), including the left internal mammary artery (LIMA) and the left anterior descending coronary artery (LAD), TDI measurements were performed before operation (baseline), 5 min after LIMA-LAD revascularization (early reperfusion) and after completion of all anastomoses (after revascularization). Results: Compared to the patients with diabetes, the controls had higher peak systolic velocities of the mid septal segments in the early reperfusion measurement (p = 0.002). After revascularization, values of peak systolic strain at the basal (-10.13 vs. -13.36%, p = 0.044) and mid septal segments (-8.25 vs. -12.69%, p = 0.009) were decreased in the diabetic patients compared to the controls. There was no difference between the groups with respect to the velocities acquired at the septal site of the MV annulus. Conclusions: This study demonstrates an insufficient recovery of regional myocardial function in patients with type II diabetes undergoing OPCABG.

Recovery of regional myocardial function and myocardial oedema following reperfused acute myocardial infarction

Summary We investigated the relationship between myocardial oedema and recovery of regional myocardial function in patients with acute reperfused myocardial infarction (MI). Early after acute MI, oedema in the peri-infarct zone, as delineated by T2 weighted (T2w) cardiovascular magnetic resonance (CMR) imaging, demonstrated significantly reduced strain as compared to remote myocardium. The recovery of regional function in the peri-infarct zone closely followed the resolution of hyperenhancement on T2w CMR. In addition, both transmural and subendocardial infarcts showed a degree of functional recovery after acute MI. Background Myocardial tissue oedema is a feature of acute reperfused myocardial infarction, and contributes to stunning of viable peri-infarct myocardium (the ‘area at risk’). Regression of oedema on T2w CMR imaging is related to improved myocardial contractility post MI in animal models. Whether a similar relationship between myocardial oedema and regional myocardial function exists in man is not currently known. We hypothesised that the resolution of tissue oedema correlates with recovery of regional contractile function. Methods We studied patients after primary percutaneous coronary intervention for first ST-elevation MI. Patients underwent CMR with T2w, myocardial tagging and late gadolinium enhancement imaging at median 2, 30 and 90 days post reperfusion. Infarct size, regional circumferential strain, intensity and volume of myocardial oedema were measured for infarct zone, peri-infarct zone (area at risk) and remote myocardium. Oedema and infarction were defined as zones with signal intensity 2 standard deviations above remote myocardium in T2w and LGE imaging respectively. T2w signal intensity was corrected using a ratio to remote myocardium. Results Thirty patients had CMR imaging at all three time points and had adequate image quality with sufficient peri-infarct oedema for quantitative analysis. Circumferential strain was significantly diminished in infarct and peri-infarct zones compared to remote myocardium (means -0.149 vs. -0.184 vs. -0.236, P<0.01 between groups and P<0.01 for trend). Remote myocardium showed no significant change in strain over time (F=1.44, P=0.24), whilst the peri-infarct zone (F=6.03, P=0.004) and infarct zone (F=20.34, P<0.001) showed a significant increase in magnitude. This change closely mirrored resolution of both intensity and volume of T2 hyperenhancement (Figure 1). Decreased circumferential strain correlated significantly with T2 volume (r=0.30; P<0.01) and corrected T2 signal intensity (r=0.28; P<0.01). Due to the unexpected finding of recovery of function in the infarct zone, we analysed the 8 patients with complete transmural infarction. The area of fully transmural infarction showed a trend towards significant resolution of strain with time (means -0.103 (day 2), -0.148 (day 30) and -0.194 (day 90); P=0.050 for trend).

Regional functional recovery after acute myocardial infarction: a cardiac magnetic resonance long-term study

We sought to analyze the trend of functional recovery after successful reperfused ST-elevation myocardial infarction (STEMI) in an optimally treated patient group over a 14 month follow-up in relation to ischemia-time and the presence of microvascular obstruction (MVO). First-pass perfusion-, cine- and late enhancement (LE)- cardiac MR were performed in 40 patients (33 male and 7 female, 54.8 ± 12.3 years) within 6 days as well as 4 and 14 months after successful primary percutaneous coronary intervention for STEMI. Significant recovery of segmental wall thickening (SWT %) occurred exclusively in infarcted segments reperfused within 4 h after symptom onset (group 1 with pain-to-balloon time <2 h: 59 ± 4 to 70 ± 4%; P < 0.02) (group 2 with pain-to-balloon-time 2-4 h: 51 ± 4 to 59 ± 3%, P < 0.05) during the first 4 months, whereas changes thereafter were not significant (P = NS). Infarcted segments with MVO showed lowest regional myocardial function at any time of assessment (all P < 0.001) and a lack of significant recovery during the study period. Significant recovery of regional myocardial function is related to rapid revascularization of the infarct-related artery and the absence of MVO. Improvement of SWT occurred exclusively within the first 4 months after acute myocardial infarction and remained unchanged thereafter.

Recovery of Function After Acute Myocardial Infarction Evaluated by Tissue Doppler Strain and Strain Rate

The aim of this study was to investigate the changes and time course of recovery of regional myocardial function within the first week following successful primary coronary intervention in patients with first-time ST-segment elevation myocardial infarctions using myocardial deformation analysis, which is more quantitative and thus more objective than the wall motion score. Thirty-one consecutive patients admitted with ST-segment elevation myocardial infarctions were studied on days 1, 2, 3, and 7 using strain and strain rate tissue Doppler echocardiography. The mean peak troponin T level was 7.0 microg/L, and 15 patients had anterior and 16 had inferior infarct localization. Peak systolic strain rate and end-systolic strain increased significantly on day 2, both in segments with moderately reduced function (-0.6 to -1.0 s(-1) vs -8% to -15%, P < .001) and in severely reduced function (-0.2 to -1.0 s(-1) vs 1% to -12%, P < .001), but there were no further changes. Mean wall motion score in infarct related segments decreased significantly from day 1 to day 2 (2.7 to 2.4, P = .001) and from day 3 to day 7 (2.3 to 2.2, P = .001). Recovery of regional function after ST-segment elevation myocardial infarction occurred within 2 days and could be detected by wall motion score, strain rate, and strain. However, strain and strain rate were better discriminative parameters for the changes in function as well as being better to assess near normalization on day 2. This could have a clinical impact on early management in patients who undergo percutaneous coronary intervention.

Prediction of myocardial viability, after coronary revascularization by intraoperative dobutamine stress transesophageal echocardiography

Objective To predict myocardial viability and recovery of regional ventricular function using intraoperative dobutamine stress transesophageal echocardingrapby (DSE) in patients with chronic iachemic left ventricular dysfunction. Methods With institutional review board approval and informed consent 24 NYHA class Ⅱ or Ⅲ patients (19 males, 5 females) aged 50-75 yr, weighing 55-90 kg undergoing elective coronary artery bypass graft (CABG) were studied. Transesophageal echocardiography was used during operation. Regional wall motion (RWM) was semi-quantitatively estimated and scored by 16 segment images as suggested by American Society of Echocardiograpby Committee after tracheal intubation (T_1), during dobutamine infusion (T_2) and after revascularization (T_3) (0=wall motion is augmented, 1 = normal motion, 2,3 = slightly, severely weakened motion, 4 = no motion, 5 = reverse motion). Viabihty was defined as improvement in the motion of regional wall (> 0.5 cm thick) by ≥ 1 score. The accuracy, specificity, sensitivity and positive/negative prediction value (PPV, NPV) of DSE for predicting the myocardial viability after revascularization were assessed. Results The ejection fraction was (39±11) % after tracheal intubation and reached (47±8) % at 3 min of dobutamine infusion and (47±9) % after coronary revascularizatien. The predicted improvement in regional myocardial function by DSE was 36.3% and significantly lower than the segmental recovery of myocardial function after revascularization (43.2%). The sensitivity, specificity, accuracy, PPV and NPV of DSE in predicting myocardial viabihty were 75.3%, 92.7%, 85.3%, 88.4% and 83.5% respectively. Conclusion Intraoperative DSE is effective in assessing the recovery of regional myocardial function after CABG. Key words: Dobutamine; Echocardiography; stress; Myocardium; Tissue survival; Coronary artery bypass

Does Postsystolic Motion or Shortening Predict Recovery of Myocardial Function After Primary Percutanous Coronary Intervention?

The purpose of the study was to evaluate whether presence of postsystolic motion or shortening defined by Doppler tissue imaging may predict recovery of regional myocardial function in patients with ST-elevation myocardial infarction. Echocardiography was performed a few hours after primary percutanous coronary intervention and at a 3-month follow-up visit in 83 patients with ST-elevation myocardial infarction. Based on visual assessment of wall thickening in a 16-segment model, segments were classified into those with: dyskinesia/akinesia (type A, n = 63) or hypokinesia (type B, n = 141) in the acute phase and no recovery of function at follow-up; dyskinesia/akinesia in the acute phase and partial recovery of function at follow-up (type C, n = 86); dyskinesia/akinesia/hypokinesia in the acute phase and complete recovery of function at follow-up (type D, n = 243); and normal myocardial function in the acute phase (type E, n = 759). There were no differences among type A, B, C, and D segments with regard to the proportion presenting postsystolic tissue velocity equal to or greater than 1.0 cm/s (0.52, 0.54, 0.60, and 0.47, respectively, P = .20) or with respect to postsystolic negative increase in strain (median -2.9, -1.9, -1.8, and -1.5%, respectively, P = .13) in the acute phase. However, type E segments less often presented postsystolic tissue velocity greater than 1.0 cm/s and presented lower postsystolic increase in strain (0.39 and -1.0%, respectively, P < .001 as compared with type A-D segments). In initially dysfunctional segments, presence of postsystolic contraction was not associated with improvement in strain or wall-motion score at follow-up. In patients with ST-elevation myocardial infarction postsystolic motion or shortening appears more frequently in the acute phase in myocardial segments with impaired systolic function compared with normally functioning segments. However, presence of postsystolic contraction is not associated with improvement in strain or wall-motion score at follow-up, and does not seem to be a marker of viability.

Myocardial Postsystolic Motion in Ischemic and Not Ischemic Myocardium: The Clinical Value of Tissue Doppler

Postsystolic motion (PSM) is a delayed ejection motion of the myocardium occurring after the aortic valve closure, during a generally prolonged isovolumic relaxation time (IVRT). In this review we analyze the physiopathologic mechanisms underlying PSM and the contribution of tissue Doppler for its understanding. By using various techniques, this phenomenon has been described in experimental observations and related to myocardial ischemia produced by gradual or abrupt coronary occlusion. In clinical studies, it is associated with recovery of regional myocardial function. Tissue Doppler, providing a velocity map of myocardial motion, allows an easy, noninvasive detection of PSM in the clinical setting. PSM, as identified by tissue Doppler, appears a hallmark of myocardial ischemia and viability but it may occur also in nonischemic conditions as left ventricular (LV) hypertrophy and volume overload, left bundle branch block and even in normal individuals. Strain and strain rate (SR), obtainable by off-line color tissue Doppler, may be useful to identify the mechanisms underlying PSM since these measurements reflect, respectively, the intrinsic rate and the percentage of deformation of a given myocardial segment, and are relatively independent of both overall cardiac movement and tethering of the neighboring LV segments. By using SR imaging, the ratio of PSM to regional systolic longitudinal strain can be used to separate ischemic from nonischemic PSM and appears the best quantitative parameter to identify ischemia during dobutamine stress. A method to detect LV wall asynchrony and immediate benefit of cardiac resynchronization therapy has been developed combining the assessment of tissue-tracking (TT) derived delayed longitudinal contraction and of SR-derived PSM.

Perioperative tissue Doppler echocardiography and bypass graft flowmetry in patients undergoing coronary revascularization: Predictive power for late recovery of regional myocardial function

To assess if recovery of regional myocardial function can be predicted by perioperative Doppler tissue echocariography, 20 patients undergoing coronary artery bypass graft surgery (mean 4.1 grafts) had serial transthoracic and transesophageal echocardiography. Systolic velocities were lower in basal posterior and anterior segments, and higher in the midanterior septum, at intraoperative transesophageal echocardiography compared with preoperative transthoracic echocardiography (−45%, −30%, +18%, respectively), but comparable elsewhere. After bypass, velocities were increased in midposterior, basal lateral, basal anterior, and midanterior septal segments (+41%, 25%, 27%, 44%, respectively, P < .05). Increased velocities in circumflex segments at 6 weeks (midposterior, basal lateral, and midlateral +54%, 45%, 39%, respectively, P < .05) were not predicted by perioperative changes or related to graft flow (transit-time flowmetry; R −0.09, −0.14, and −0.32, respectively, not significant). Myocardial velocities measured by transthoracic and transesophageal echocardiography are not comparable in segments with different angles of insonation. Perioperative changes in resting myocardial systolic velocity are highly variable and do not predict late recovery. (J Am Soc Echocardiogr 2002;15:1202-10.)

Is There a Long-Term Predictive Value of Intraoperative Low-Dose Dobutamine Echocardiography in Patients Who Have Coronary Artery Bypass Graft Surgery with Cardiopulmonary Bypass?

In patients with coronary artery disease, chronic regional left ventricular systolic dysfunction at rest may be caused by hibernating or by infarcted myocardium. Intraoperative low-dose dobutamine (LDD) echocardiography reliably predicts the immediate recovery of regional myocardial function after coronary artery bypass graft (CABG) surgery. We sought to determine whether intraoperative LDD echocardiography would also predict recovery of regional function after 1 yr. Twenty-five patients with coronary artery disease who underwent CABG surgery with intraoperative LDD echocardiography were evaluated 1 yr later with a follow-up transthoracic echocardiogram. The covariates of left ventricular ejection fraction, old myocardial infarction, and diabetes mellitus were considered in an analysis of regional wall motion (RWM). A 16-segment model and a 1–5-point scoring system were used to evaluate 350 myocardial segments. Multiple logistic regression analysis was performed to determine whether response to intraoperative LDD echocardiography (5 μg · kg−1 · min−1) predicted changes in regional function at 1 yr. A segment was defined as stunned if the RWM score obtained during LDD infusion deteriorated after cardiopulmonary bypass but recovered in the 1-yr follow-up echocardiogram. A response to intraoperative LDD predicted changes in regional function at 1 yr. The overall odds of improvement in regional function were 2.22 times greater (95% confidence interval = 1.29, 3.82;P = 0.0039) with a positive response to intraoperative LDD. The positive predictive value of intraoperative LDD echocardiography for improvement in myocardial function was 0.81 and the negative predictive value was 0.34. The predictive values did not vary with the examined covariates. Of segments with unexpected deterioration of RWM immediately after cardiopulmonary bypass, 87% recovered at the time of the 1-yr follow-up echocardiogram. Contractile reserve demonstrated by intraoperative LDD echocardiography predicts regional function at 1 yr; however, the test cannot predict which segment will not recover. Most of unexpected regional ventricular systolic dysfunction immediately after CABG surgery can be attributed to myocardial stunning.

Favorable remodeling enhances recovery of regional myocardial function in the weeks after infarction in ischemically preconditioned hearts.

In a previous study, we found that recovery of segment shortening in the ischemic zone of conscious, chronically instrumented rabbits was significantly better in ischemically preconditioned than control animals after 72 hours of reperfusion. However, although this period of reperfusion was felt to be sufficient to allow recovery from stunning, regional function was disproportionately low for the size of the infarcts. To further characterize the recovery of left ventricular regional function, rabbits were chronically instrumented with a balloon occluder around a branch of the left coronary artery and a pair of ultrasonic crystals to monitor segment shortening in the ischemic zone. The preconditioned group had 1 cycle of 5-minute occlusion/10-minute reperfusion before a 30-minute occlusion, whereas control rabbits experienced only the 30-minute occlusion. All monitored segments were either dyskinetic or akinetic during the 30-minute occlusion. There was no difference in function between the 2 groups until 24 hours of reperfusion. At 72 hours, systolic shortening in control hearts averaged only 5% of the preischemic value, whereas shortening was 29% of baseline in preconditioned hearts. By day 21, systolic shortening averaged 26% in control hearts and 65% in preconditioned hearts (P<0.02) and appeared to have reached a plateau. Infarct size was 31.4+/-2.8% and 15.5+/-2.1% in control and preconditioned hearts, respectively. Moreover, in ischemically preconditioned hearts, the recovery of regional function was better than in controls for any given amount of microinfarction in the myocardial segment between crystals (P=0.02). The progressive improvement in preconditioned hearts is most consistent with favorable remodeling in the ischemic zone, which the preconditioning process seems to accentuate.

Intravenous pretreatment with magnolol protects myocardium against stunning.

Magnolol, an antioxidant, has been reported to possess various protective effects on the cardiovascular system. However, its effect on myocardial stunning has not been elucidated. The purpose of this study was to investigate the antistunning effect of magnolol by evaluating the recovery of regional myocardial function after 10-minute coronary artery occlusion in anesthetized, open-chest rabbits. There was no significant hemodynamic change after intravenous infusion of magnolol. Systolic wall thickening fraction (WThF) measured with an epicardial Doppler sensor in animals pretreated with normal saline and vehicle solution remained significantly depressed (60 +/- 7% and 77 +/- 4% of baseline WThF, respectively) 3 hours after coronary artery reperfusion (CAR). Pretreatment with magnolol (10(-7) and 10(-6) g/kg, intravenous infusion) significantly enhanced the recovery of systolic wall thickening fraction (98 +/- 1 and 99 +/- 1% of baseline WThF, respectively) 60 minutes after CAR. This study demonstrated that intravenous pretreatment with magnolol protected myocardium against stunning.

New-onset angina preceding acute myocardial infarction is associated with improved contractile recovery after thrombolysis.

Ischaemic preconditioning reduces myocardial infarct size in animal models. Clinical data suggest that episodes of angina immediately before acute myocardial infarction may be associated with smaller infarct size in man. However, it is unclear whether ischaemic episodes preceding acute myocardial infarction also affect contractile recovery in patients. In this study we investigated the recovery of regional myocardial function after thrombolysis in two groups of patients at their first Q-wave acute myocardial infarction; in one group (n = 42) myocardial infarction occurred unheralded, whereas patients of the second group (n = 48) had experienced new-onset angina in the 48 h that preceded infarction. Echocardiographic analysis of myocardial regional function in the infarct area was done at 2, 24 and 72 h after thrombolysis, and at 1 week, and 1 and 3 months follow-up. Peak level of MB-creatine kinase was significantly lower in patients with new-onset angina (96 +/- 47 as compared with 221 +/- 108 IU.l-1, P < 0.01), as was the area under the MB-creatine kinase curve (1321 +/- 876 as compared to 3879 +/- 1555 U.l-1/36 h, P < 0.01). Hypokinetic segments were fewer in patients with pre-infarction angina. Similarly, wall motion score improved significantly earlier in patients who had new-onset angina before acute myocardial infarction. Thus, contractile recovery was more rapid in patients with previous angina than in those in whom infarction occurred unheralded. Complications during the in-hospital outcome and other variables considered during the 4-week follow-up were similar between groups. Patients who experienced new-onset angina before acute myocardial infarction showed better recovery of regional function after thrombolysis. Our study supports the hypothesis that brief periods of ischaemia immediately before myocardial infarction may precondition the human heart, thus improving contractile recovery.

Ischemic tolerance in the brain.

Brief episodes of brain ischemia define a patient population at increased risk for stroke. These brief events (TIAs) warrant urgent evaluation and treatment. It is therefore counterintuitive that transient ischemia might induce tolerance and protect the brain from subsequent ischemia. However, accumulating data from studies on both myocardium and brain support such a concept. An understanding of the mechanisms involved in ischemic tolerance may define novel therapeutic strategies for brain protection. The observation that multiple episodes of brief regional myocardial ischemia do not produce a cumulative depletion of high-energy phosphate compounds or loss of function provided the first evidence for ischemic tolerance (or ischemic preconditioning). [1,2] Such brief episodes of ischemia render the myocardium more tolerant to subsequent lethal ischemia, as evidenced by reduced infarct size, delayed ultrastructural changes, and improved recovery of regional myocardial function during reperfusion. [3,4] With ischemic preconditioning, myocardial infarct size is reduced in multiple species from 70% to 30% of the myocardium at risk. [3-5] The dose of ischemia adequate to produce tolerance in the heart varies from 2.5 to 10 minutes, depending on the species with some studies showing a requirement for multiple dosing. [6] The protection is substantial, doubling the duration of ischemia needed for infarction to occur. [5] The time window during which tolerance occurs in the myocardium is brief, starting between 1 and 60 minutes after preconditioning and lasting less than 3 hours in most studies. [7] A delayed secondary acquisition of tolerance, a so-called window of protection, also occurs in some cases 24 hours after ischemic preconditioning. [8,9] Some aspects of ischemic preconditioning are observed in the human heart as well, as evidenced by a reduction in anginal pain and ST-segment ECG alterations during the second balloon inflation (5 minutes after the first inflation) in patients undergoing percutaneous transluminal …

Role of platelets in myocardial ischemia-reperfusion injury in dogs.

We investigated the involvement of circulating platelets in myocardial ischemia-reperfusion injury in canine autoperfused heart-lung preparations using filters to deplete platelets and/or leukocytes. The left anterior descending (LAD) coronary artery was occluded for 40 min, followed by 40 min reperfusion, in 3 groups: a leukocyte-platelet-depleted (LPD) group, in which both leukocytes and platelets were depleted; a leukocyte-depleted (LD) group, in which leukocytes alone were depleted; and a control group. There were no differences in hemodynamics or arrhythmias among groups before or during coronary occlusion. After reperfusion, the maximum rate of change in left ventricular pressure during systole and diastole was significantly higher in the LPD group than in the control and LD groups. The LPD group also showed gradual recovery of regional myocardial function and a decrease in the frequency of premature ventricular contractions. The LD group showed a slight improvement in cardiac function and arrhythmias compared with the control group. Although there was no significant difference in the pulmonary arterial plasma level of thromboxane B2 at any stage among groups, the control group showed an increase after reperfusion. These results suggest that platelets are important in reperfusion injury and that the depletion of both leukocytes and platelets effectively protects against reperfusion injury.

Parenteral hyperalimentation with long chain triglycerides (LCT) during reperfusion improves recovery from regional myocardial stunning in chronically instrumented dogs

Numerous investigations have been performed to elucidate the pathophysiological mechanism of myocardial stunning [1,2]. Free Fatty Acids (FFA) are the primary source of high energy phosphates for the myocardium under aerobic conditions. Increasing FFA during hypoxia or ischaemia, reduces myocardial function [3]. Jones et al. described an improvement in canine myocardial performance after ischaemic cardiac arrest when triglycerides (Intralipid 10%) were given during reperfusion [4]. We investigated the effects of a 20% LCT emulsion on regional stunning administered during reperfusion in the conscious dog. Seven mongrel dogs were chronically instrumented for the measurement of heart rate (HR), aortic (ABP), left atrial (LAP) and left ventricular pressure (LVP) and its first derivative LVdP/dt, blood flow velocity through the left anterior descending (FLad) and left circumflex (FCx) coronary arteries and regional myocardial wall thickening in the areas perfused by the LAD and Cx (WTlad and WTCx). A hydraulic occluder was positioned around the LAD. Using a cross over design all animals received ten minutes of ischaemia in the LAD area with and without the LCT emulsion during reperfusion. The LCT emulsion was given i.v. over 30 min as a continuous infusion of 7 mL kg−1. The infusion was started 15 min after reperfusion. Full heparinisation was accomplished by i.v. administration heparin using 200 IU kg−1. Results were analysed using repeated measures ANOVA and a paired t-test. In the LCT group, recovery from regional myocardial stunning in the LAD area improved, compared with the control (no LCT) group (Fig. 3). However, complete recovery of regional myocardial function was accomplished after 24 h in both groups. In the LCT group LVdP/dt max increased significantly from 2175 ± 139 at baseline to 2500 ± 233 mmHg sec−1 (P<0.05) while dP/dt max was not changed in the control group. During ischaemia FCx increased. All other parmeters remained stable throughout the study and no differences between the two groups were observed.Fig. 3: (abstract 3). Regional myocardial performance in the LAD perfused area with and without a LCT emulsion, before, during and after 10 min of ischaemia. Data are presented as a mean ± sem.* P<0.05 vs. baseline. ** P<0.05 vs. control. n=7. b: baseline. i: ischaemia.We conclude that i.v. administration of LCT during reperfusion after brief ischaemia, improves recovery from regional myocardial stunning. Further investigations with respect to mechanism of action and possible therapeutic exploitation of these findings appear worthwhile.

Functional recovery of stunned myocardium is greater with halothane than fentanyl anaesthesia in dogs

We have compared the effects of halothane or fentanyl on recovery of regional myocardial function in the postischaemic ventricle in dogs. The animals were followed for 120 min during reperfusion after 15-min of occlusion of the left anterior descending coronary artery. After 120 min of reperfusion, the fentanyl group had recovered only 54% and 50% of regional contractility and systolic shortening (P < 0.05), respectively, compared with halothane (63% and 86%). Intramyocardial tissue pressure was less than baseline 60 min after reperfusion in the fentanyl group (P < 0.05), whereas the halothane group had returned to control values. We conclude that halothane is more effective than fentanyl in attenuating regional myocardial dysfunction associated with transient episodes of ischaemia.

Predictive value of reactive hyperemic response on reperfusion on recovery of regional myocardial function after coronary angioplasty in acute myocardial infarction.

The objective of the study was to determine the coronary vasodilatory reserve in reperfused myocardium in patients with acute myocardial infarction and its relation to regional myocardial function. The study population consisted of 22 patients with acute myocardial infarction who underwent successful coronary angioplasty. The vasodilatory reserve in the reperfused myocardium was assessed quantitatively using computer-assisted digital subtraction cine-angiography immediately after angioplasty and at follow-up angiography before hospital discharge. Myocardial contrast medium appearance time and density were determined before and after pharmacological hyperemia induced by an intracoronary injection of 12.5 mg papaverine. Global and regional left ventricular functions were determined from contrast angiography. After papaverine, the mean contrast medium appearance time decreased significantly from 3.5 +/- 0.7 to 2.7 +/- 0.7 cardiac cycles (P < .000005) immediately after successful coronary angioplasty and from 3.8 +/- 0.7 to 2.7 +/- 0.9 cardiac cycles (P < .000005) at angiography before hospital discharge. The mean contrast medium density increased significantly from 48.7 +/- 13.8 to 61.0 +/- 19.0 pixels (P < .003) and from 49.6 +/- 19.7 to 80.3 +/- 29.6 pixels (P < .000005), respectively. As a consequence, the calculated coronary flow reserve increased significantly from 1.8 +/- 0.7 to 2.6 +/- 1.0 (P < .0008). The global ejection fraction increased significantly from 52 +/- 12% to 58 +/- 14% (P < .03), primarily because of a significant improvement in the regional myocardial function of the infarct zone from 20.8 +/- 9.0% to 26.0 +/- 10.5% (P < .001). Coronary flow reserve correlated well with regional myocardial function both during the acute phase (R = .79, P < .002) and at follow-up angiography (R = .82, P < .000004). Interestingly, coronary flow reserve measurement on reperfusion, immediately after angioplasty, correlated significantly with regional myocardial function at follow-up angiography (R = .81, P < .00003). The results indicate that there is a pharmacologically inducible vasodilatory reserve in reperfused ischemic myocardium after successful coronary angioplasty in patients with acute myocardial infarction and that this is increased at 10-day follow-up angiography. More important, the degree of reactive hyperemic response on reperfusion has a predictive value regarding the ultimate degree of recovery of regional myocardial function. Quantitative assessment of reperfusion may be useful in investigating the role of coronary reperfusion and salvage of myocardial function.

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.

Myocardial function and transmural blood flow during coronary venous retroperfusion in pigs.

The degree of recovery of regional myocardial contraction during coronary venous retroperfusion has not been well established, particularly in the absence of coronary collateral channels. Therefore, the maximal functional benefit attainable with coronary venous retroperfusion was assessed in pigs by means of using selective pump retroperfusion of the left anterior descending vein, with venting of the left anterior descending artery to zero pressure. In eight anesthetized open-chest pigs during selective left anterior descending venous retroperfusion over a range of retroperfusion flows, regional myocardial function (percent systolic wall thickening by sonomicrometry) increased progressively to an average of 62% of control values at a retroperfusion flow rate 200% of control arterial flow. Progressive thickening of the end-diastolic dimension of the anterior wall was observed with increasing retroperfusion flow (from 8.7 +/- 0.9 to 10.7 +/- 2.3 mm, p less than 0.001). Perfusion pressures within the left anterior descending vein increased linearly with increased retroperfusion flow rates (up to 132 +/- 57 mm Hg with retroperfusion flow 200% of control). A gradual increase of retrograde left anterior descending arterial outflow was observed with increasing retroperfusion flows; however, the absolute amount (maximum, 8.3 +/- 4.1 ml/min) was much too low to explain the extent of functional recovery. Transmural myocardial capillary blood flows in the anterior wall with retroperfusion flows of 100% and 200% of control arterial flow were 0.22 and 0.42 ml/min/g with corresponding subendocardial blood flows of 0.14 and 0.29 ml/min/g; ratios of endocardium to epicardium were 0.51 and 0.61, respectively. Thus, capillary blood flows during selective retroperfusion were relatively low despite considerable restoration of regional systolic wall thickening, and a significant difference was noted in the slopes of the relations between regional systolic wall thickening and myocardial blood flow during retroperfusion and anterograde arterial perfusion (p less than 0.05). With retrograde injection of silicone elastomer at different retroperfusion pressures (50, 75, and 100 mm Hg) in three pigs, capillaries were well visualized, and profuse intramyocardial venous anastomotic connections were seen at the highest retroperfusion pressure (100 mm Hg), whereas there was filling of small venules but little capillary filling at the lowest retroperfusion pressure (50 mm Hg). Considerable recovery of regional myocardial function with low regional capillary blood flows were observed during acute venous retroperfusion with high retroperfusion flows with arterial blood. These findings together with low levels of retrograde arterial outflow and visualization of retrograde capillary filling with a rich venous network provide evidence for possible oxygen delivery via the intramyocardial venous plexus.