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PubMed1997

Adenosine preconditioning of human myocardium is dependent upon the ATP-sensitive K+ channel.

Evidence supports the involvement of adenosine receptor stimulation and activation of K(ATP) channels in ischemic preconditioning of human myocardium. It is unknown, however, whether protection mediated by adenosine receptors is dependent upon the K(ATP) channel in the human heart. The purpose of this study was to determine whether adenosine-mediated protection against a simulated ischemia-reperfusion injury in human myocardium is dependent upon K(ATP) channels. Isolated human right atrial trabeculae were placed in tissue baths at 37 degrees C, oxygenated with a modified Tyrode solution, and field stimulated at 1 Hz. Trabeculae were subjected to 45 min of normothermic simulated ischemia (hypoxic, substrate-free buffer with pacing at 3 Hz.) and 60 min of reperfusion (I/R trabeculae). Trabeculae were preconditioned with simulated ischemia (IPC trabeculae) or adenosine receptor stimulation (adenosine, 125 micromol/l) for 5 min (ADO trabeculae) prior to simulated ischemic-reperfusion injury. Inhibition of the K(ATP) channel with glibenclamide (10 micromol/l) was combined with adenosine pretreatment (ADO+GLI trabeculae) or alone (GLI trabeculae) prior to simulated ischemic-reperfusion injury. Developed force (DF) at end reperfusion (mean+/-S.E.) was compared to baseline developed force, and tissue creatine kinase (CK) activity at end reperfusion was measured. I/R trabeculae showed 27+/-2% of baseline DF, whereas IPC trabeculae or ADO trabeculae showed 50+/-4% and 43+/-3% of baseline DF, respectively. ADO+GLI trabeculae showed 25+/-2% and GLI trabeculae showed 23+/-4% of baseline DF. Tissue CK activity was enhanced in the IPC and ADO trabeculae (433+/-63 U/g wet myocardium, and 415+/-28 U/g wet myocardium, respectively). I/R trabeculae had 196+/-26 U/g wet myocardium and ADO+GLI trabeculae had 277+/-38 U/g wet myocardium at end reperfusion. The results suggest that ischemic preconditioning and adenosine receptor stimulation confer functional protection against simulated ischemic-reperfusion, and adenosine mediated protection is eliminated by K(ATP) channel inhibition in human myocardium.

Adenosine↗
PubMed1993

Excitation-contraction coupling and contractile protein function in failing and nonfailing human myocardium.

Isometric force, heat output, and aequorin light emission were measured in isolated muscle strips from nonfailing human hearts and from hearts with endstage failing dilated cardiomyopathy (37 degrees C; 30-180 beats per minute (bpm)). In nonfailing myocardium, peak twitch tension increased with higher rates of stimulation, whereas the force-frequency relation was inverse in the failing myocardium. At 60 bpm and at higher rates of stimulation, peak twitch tension was reduced significantly in the failing myocardium. Myothermal measurements, performed at 60 bpm, indicated that the number of crossbridge interactions and the amount of calcium cycling are reduced significantly in the failing myocardium. Furthermore, aequorin light transients indicated that the inverse force-frequency relation in failing myocardium results from altered calcium cycling; with increasing rates of stimulation aequorin light emission increased continuously in the nonfailing and decreased continuously in the failing myocardium. The data suggest that impaired myocardial performance in failing human myocardium may result primarily from disturbed excitation-contraction coupling processes with a reduced amount of calcium cycling and, thus, a decreased activation of contractile proteins.

Biomechanical Phenomena↗
PubMed2003

Scatter correction on its own increases image contrast in Tl-201 myocardium perfusion scintigraphy, but does it also improve diagnostic accuracy?

UNLABELLED: Poor and variable spatial resolution of the gamma camera, the movement of the heart and, above all, the inclusion of scattered photons in the acquisition data contribute to the deterioration of image contrast in 201Tl myocardium perfusion studies. Scatter correction algorithms may correct for the latter factor by removing (most of) the scattered photons from the acquisition data. METHODS: In this study we investigated the contrast changes induced by the Triple Energy Window scatter correction method (TEW) applied to clinical 201Tl myocardium perfusion studies and its influence on the reading of the images. Stress and rest studies of 30 consecutive patients were used for this study. Maximum image contrasts were measured between the myocardium and the left ventricular cavity in four mid-ventricular short axis slices, as well as between normally and abnormally perfused myocardium using bull's-eye displays of the activity within the myocardium. To assess image quality and perfusion abnormalities, an experienced nuclear medicine physician, blind to patient characteristics, visually reviewed all studies. RESULTS: In all individual measurements, the maximum contrast after scatter correction was higher than without correction (p < 0.001). The average increase in contrast between the myocardium and the left ventricular cavity was 43% and 48% for stress and rest studies respectively. The contrast within the myocardium increased by 25% and 32% respectively. After TEW, image quality was rated lower in almost half of the studies, while in only one study the quality was rated higher. In stress studies 11 additional perfusion defects were observed, with rest studies revealing 15 more defects after TEW, but this difference was not significant. Cohen's kappa indicated a moderate agreement of the image reading between studies with and without scatter correction. CONCLUSION: We conclude that image contrast improves significantly by scatter correction. However, image quality decreased as a result of an unfavorable signal-to-noise ratio. As an overall result, no significant change in the clinical outcome of the studies could be shown. Additional training of the readers may be required to obtain optimal results.

Adult↗
PubMed2004

Incidence of stunned, hibernating and scarred myocardium in ischaemic cardiomyopathy.

PURPOSE: Different criteria to identify residual viability in chronically dysfunctioning myocardium in patients with coronary artery disease (CAD) can be derived by the combined assessment of myocardial blood flow (MBF) and glucose utilisation (MRG) using positron emission tomography (PET). The aim of this study was to evaluate, in a large number of patients, the prevalence of these different patterns by purely quantitative means. METHODS: One hundred and sixteen consecutive patients with ischaemic cardiomyopathy (LVEF < or =40%) underwent resting 2D echocardiography to assess regional contractile function (16-segment model). PET with 15O-labelled water (H2 15O) and 18F-fluorodeoxyglucose (FDG) was used to quantify MBF and MRG during hyperinsulinaemic euglycaemic clamp. Dysfunctional segments with normal MBF (> or =0.6 ml min(-1) g(-1)) were classified as stunned, and segments with reduced MBF (<0.6 ml min(-1) g(-1)) as hibernating if MRG was > or =0.25 micromol min(-1) g(-1). Segments with reduced MBF and MRG <0.20 micromol min(-1) g(-1) were classified as transmural scars and segments with reduced MBF and MRG between 0.20 and 0.25 micromol min(-1) g(-1) as non-transmural scars. RESULTS: Eight hundred and thirty-four (46%) segments were dysfunctional. Of these, 601 (72%) were chronically stunned, with 368 (61%) having normal MRG (0.47+/-0.20 micromol min(-1) g(-1)) and 233 (39%) reduced MRG (0.16+/-0.05 micromol min(-1) g(-1)). Seventy-four (9%) segments with reduced MBF had preserved MRG (0.40+/-0.18 micromol min(-1) g(-1)) and were classified as hibernating myocardium. In addition, 15% of segments were classified as transmural and 4% as non-transmural scar. The mean MBF was highest in stunned myocardium (0.95+/-0.32 ml min(-1) g(-1)), intermediate in hibernating myocardium and non-transmural scars (0.47+/-0.09 ml min(-1) g(-1) and 0.48+/-0.08 ml min(-1) g(-1), respectively), and lowest in transmural scars (0.40+/-0.14 ml min(-1) g(-1), P<0.01). MRG was comparable in hibernating and stunned myocardium with preserved MRG (0.40+/-0.19 micromol min(-1) g(-1) vs 0.46+/-0.20 micromol min(-1) g(-1), NS), and lowest in stunned myocardium with reduced MRG and transmural scars. CONCLUSION: Chronic stunning is more prevalent than expected. The degree of MRG reduction in stunned myocardium may disclose segments at higher risk of permanent damage.

Cardiomyopathies↗
PubMed1998

Successful coronary revascularization improves prognosis in patients with previous myocardial infarction and evidence of viable myocardium at thallium-201 imaging.

The role of coronary revascularization of dysfunctional myocardium with preserved thallium-201 uptake in determining the prognosis in patients after myocardial infarction remains to be defined. This study was designed to evaluate the effects of successful revascularization on survival and left ventricular (LV) function in patients with previous myocardial infarction and evidence of dysfunctional but still viable myocardium at rest-redistribution 201Tl imaging. Seventy-six consecutive patients with LV dysfunction related to previous myocardial infarction and evidence of viable myocardium at rest-redistribution 201Tl tomography were followed for 17+/-8 months. LV ejection fraction (EF) was assessed by radionuclide angiography at baseline and after 13+/-2 months. Thirty-nine patients were revascularized (group A) and 37 treated medically (group B). During the follow-up there were nine cardiac deaths. Survival rate was 97% in group A and 66% in group B (P<0.01). By Cox multivariate analysis, the extent of viable myocardium was the best predictor of cardiac death (chi2=8.67, P<0.01) and provided additional information to clinical and functional data (P<0.01). The inclusion of revascularization as a variable improved the global chi2 of the model from 14.1 to 21.9 (P<0.01). At follow-up, EF had improved by >/=5% in 16 patients. By multivariate logistic analysis, the extent of viable myocardium was the best predictor of EF improvement (chi2=15.49, P<0.001) and provided additional information to clinical and functional data (P<0.01). The inclusion of revascularization as a variable improved the global chi2 of the model from 16.8 to 22.5 (P<0.01). These results demonstrate that the total extent of dysfunctional myocardium with preserved 201Tl uptake is the strongest predictor of cardiac death in patients after myocardial infarction. Successful revascularization of dysfunctional but viable myocardium improves survival and LVEF in such patients.

Angiocardiography↗
PubMed1998

[Short-term hibernating myocardium: circulation, function and metabolism in sustained regional myocardial ischemia].

During moderate prolonged myocardial ischemia, the myocardium is dysfuctional but can remain viable. In such ischemic and dysfunctional myocardium, contractile function is reduced in proportion to the reduction in regional myocardial blood flow, i.e., a state of "perfusion-contraction matching" exists. The metabolic status of such myocardium improves over the first few hours, as myocardial lactate production is attenuated and creatine phosphate, after an initial reduction, returns to control values. Ischemic myocardium, characterized by perfusion-contraction matching, metabolic recovery and lack of necrosis, has been termed "short-term hibernating myocardium". "Short-term hibernating" myocardium can respond to an inotropic stimulation with increased contractile function, however, at the expense of a renewed worsening of the metabolic status. A role for endogenous adenosine in the development of hibernation has been excluded, since neither contractile function, metabolic parameters, nor viability are altered by increased catabolism of endogenous adenosine by infusion of adenosine deaminase. Also activation of ATP-dependent potassium channels is not responsible for "short-term hibernation". "Short-term hibernating" myocardium has, however, reduced calcium responsiveness.

Animals↗
PubMed2005

Negative inotropic action of propofol is enhanced in the acute ischemic myocardium of dogs.

PURPOSE: We investigated the effects of propofol on contractility and oxygen balance in acute ischemic myocardium and compared them with those of normal myocardium using a coronary microembolization model in dogs. METHODS: In open-chest dogs, the left anterior descending coronary artery (LAD) was perfused through an extracorporeal bypass from the carotid artery. Regional myocardial contractility and myocardial oxygen balance were evaluated along with segment shortening (%SS), regional myocardial oxygen consumption (MVO2), and lactate extraction ratio (LER) of the area perfused by the LAD. Acute ischemia was produced by repeated injection of microspheres into the LAD-perfused area until %SS decreased by 50% of baseline. RESULTS: In normal myocardium, intracoronary infusion of propofol at doses of 1.2 and 2.4 mg x kg(-1) x h(-1) caused slight decreases in %SS to 83% +/- 8% and 80% +/- 10%, respectively. In ischemic myocardium, propofol caused greater decreases in %SS (59% +/- 18% and 35% +/- 20%, respectively). The changes in MVO2 after propofol infusion generally paralleled the changes in %SS, but LER was not changed in either ischemic or normal myocardium. CONCLUSION: Propofol causes a greater decrease in the contractility of acute ischemic myocardium as compared with normal myocardium in which myocardial oxygen imbalance is not involved as a mechanism.

Animals↗
PubMed1995

Assessment of hibernating myocardium by dobutamine stimulation in a canine model.

OBJECTIVES: The purpose of this study was to 1) develop an animal model of hibernating myocardium, and 2) evaluate the ability of dobutamine stimulation to detect hibernating myocardium using both qualitative and quantitative assessment of regional myocardial function. BACKGROUND: Left ventricular dysfunction may be due to chronic ischemia with or without myocardial infarction and may improve after coronary blood flow is enhanced by revascularization procedures. This condition has been coined "hibernating myocardium" and variably defined in recent years. The results of recent clinical studies suggest that dobutamine echocardiography may be useful for detecting viable myocardium in patients with left ventricular dysfunction. METHODS: Twenty-one dogs underwent initial operation. Sonomicrometer crystals were implanted, and baseline measurements of segment shortening and wall thickening (by echocardiography) were made. A coronary artery was ligated; the chest was closed; and measurements were repeated. Dobutamine was incrementally infused with determination of wall thickening and segment shortening at baseline and on days 3 and 7 and weeks 2 and 4 after coronary artery occlusion. Finally, the chest was reopened; the ligated vessel was bypassed; and measurements were repeated. RESULTS: Of the 10 dogs that completed the entire protocol, 7 had varying degrees of nontransmural myocardial infarction (group 1), and 3 had complete transmural myocardial infarction (group 2). In group 1, baseline function was significantly impaired compared with preligation function but increased during dobutamine infusion. When reperfused after 4 weeks, both wall thickening and segment shortening increased significantly. In group 2, significant changes were not seen during the dobutamine studies or after reperfusion. Myocardial perfusion during dobutamine infusion increased in group 1 but did not change in group 2. CONCLUSIONS: We demonstrated improvement in chronically dysfunctional myocardium after restoration of previously interrupted myocardial blood flow in dogs after nontransmural myocardial infarction, thus validating a canine model of hibernating myocardium. As assessed by two independent methods, dobutamine infusion identified hibernating myocardium in an animal model.

Animals↗
PubMed1999

Variability of myocardium at risk for acute myocardial infarction.

The objective of this study was to assess the variability in myocardium at risk and relate this to coronary angiographic variables. One hundred ninety-seven patients with > or = 1-mm ST-segment elevation in 2 contiguous electrocardiographic leads, without prior myocardial infarction, were injected with technetium-99m sestamibi acutely before reperfusion therapy. The perfusion defect was quantified to determine myocardium at risk for infarction. Patients underwent coronary angiography to determine the infarct-related artery and to classify the occlusion as proximal or not proximal. Collateral and anterograde (Thrombolysis In Myocardial Infarction [TIMI] trial) flow were assessed in a subset of 83 patients with angiography before direct angioplasty. Myocardium at risk for infarction in the distribution of the left anterior descending coronary artery was significantly greater (p <0.0001) than that in the circumflex or right coronary artery. In the left anterior descending coronary artery distribution, myocardium at risk for infarction was significantly larger for proximal occlusions (p <0.0001). There was a trend toward greater myocardium at risk for infarction of proximal occlusions (p = 0.14) of the left circumflex but not for proximal occlusions in the right coronary artery distribution (p = 0.47). Multivariate analysis revealed that the infarct-related artery (p <0.0001), TIMI flow (p = 0.0002), and proximal location (p = 0.09) in the infarct-related artery were independent predictors of myocardium at risk for infarction. Thus, infarct-related artery, TIMI flow, and proximal location of occlusion in the infarct-related artery influence the myocardium at risk for infarction, which is highly variable for given location of occlusion.

Angioplasty, Balloon, Coronary↗
PubMed2003

Gene transfer of hepatocyte growth factor improves angiogenesis and function of chronic ischemic myocardium in canine heart.

BACKGROUND: Hepatocyte growth factor (HGF) induces angiogenesis in myocardium. In the present study, its effects in chronic ischemic myocardium were tested. METHODS: Four weeks after left anterior descending coronary artery ligation in canine hearts, HVJ-liposome containing either human HGF gene (160 microg; HGF group, n = 7) or nothing (control group, n = 6) was directly injected into ischemic myocardium. Four weeks after gene transfection, the thickness fraction (TF), an index of regional myocardial contractility (assessed by epicardial pulse-Doppler crystals), the myocardial perfusion flow (assessed by color microspheres), and the capillary density (assessed by immunostaining of vessels) were evaluated in ischemic myocardium. RESULTS: Thickness fraction (percent of nonischemic myocardium) was significantly improved in the HGF group (80 +/- 15 from 52 +/- 16 of pregene; p < 0.05) whereas it was not changed in the control group (52 +/- 10 from 50 +/- 8 of pregene). The perfusion flow (% of nonischemic myocardium) was significantly improved in the HGF group (98 +/- 17 from 51 +/- 14 of pregene; p < 0.05) while it was not changed in the Control group (58 +/- 13 from 62 +/- 18 of pregene). The capillary density was significantly higher in the HGF group (894 +/- 211/mm2; p < 0.05) than that in the control group (511 +/- 127/mm2). CONCLUSIONS: Gene transfection of HGF improved angiogenesis, thereby improved regional myocardial function and perfusion in chronic ischemic myocardium. It indicates a potent therapeutic value of HGF gene transfection for chronic ischemic heart diseases such as myocardial infarction.

Animals↗
PubMed1998

Shortening versus isometric contractions in isolated human failing and non-failing left ventricular myocardium: dependency of external work and force on muscle length, heart rate and inotropic stimulation.

BACKGROUND: For reasons of simplicity, studies on isolated human myocardium have been conducted using exclusively isometric contractions, although positive inotropic interventions may differently influence force development, extent of shortening and myocardial work performance. We investigated human left ventricular failing and non-failing preparations comparing isometric versus isotonic, i.e., shortening contractions. RESULTS: (1) When muscle length is increased from 90% to 100% lMAX, peak developed force increases by 36% and 43% (p < 0.05) in non-failing and failing human left ventricular myocardium, respectively. Maximum performed work increases similarly in non-failing but decreases in failing myocardium. It can be shown that this discrepancy is due to significantly higher resting tension and does not present an insufficient intrinsic shortening capacity in failing myocardium. (2) When stimulation rate is increased from 0.5 to 2.0 Hz, isometric force increases significantly by 59% in non-failing and decreases by 27% in failing myocardium, whereas maximum performed work increases by 98% and decreases by 46%, respectively. (3) Pharmacological positive inotropic interventions by 7.2 mM calcium (n = 9), 3 x 10(-8) M isoproterenol (n = 7), 3 x 10(-8) M ouabain (n = 5), and 10(-5) M EMD 57033 (n = 3) equally increased force development and extent of shortening: When the fractional effect on shortening (y) was correlated to the fractional effect on force (x), the following linear regression equation was obtained: y = 0.91x + 0.26 (r = 0.86; p < 0.001). CONCLUSIONS: The data presented are of clinical and pharmacological importance: (1) The Frank-Starling mechanism is demonstrated to be existent in the failing human myocardium regarding both isometric force developed and maximum work performed. (2) Both force-frequency relations and--to a greater extent--work-frequency relations are reversed in failing human myocardium. (3) Independent of the pharmacological mode of action, positive inotropic compounds increase developed isometric force to the same extent as isotonic shortening and therefore potentiate maximum performed work.

Adolescent↗
PubMed2000

In vivo evidence that EMD 57033 restores myocardial responsiveness to intracoronary Ca(2+) in stunned myocardium.

Despite ample in vitro evidence that myofilament Ca(2+)-responsiveness of stunned myocardium is decreased, in vivo data are inconclusive. Conversely, while Ca(2+)-sensitizing agents increase myofilament Ca(2+)-responsiveness in vitro, it has been questioned whether this also occurs in vivo. We therefore tested in open-chest anesthetized pigs whether EMD 57033 (the (+) enantiomer of 5-[1-(3,4-dimethoxybenzoyl)-1,2,3, 4-tetrahydro-6-quinolyl]-6-methyl-3,6-dihydro-2H-1,3, 4-thiadiazin-2-one) increases responsiveness to Ca(2+) of non-stunned myocardium and restores function of stunned myocardium by normalizing the responsiveness to Ca(2+). Studies were performed under beta-adrenoceptor blockade to minimize the contribution of the phosphodiesterase-III inhibitory actions of EMD 57033. Consecutive intracoronary Ca(2+) infusions were used to evaluate the contractile response (assessed by the left ventricular end-systolic elastance, E(es)) to added Ca(2+) of non-stunned myocardium and myocardium stunned by 15 min coronary artery occlusion and 30 min reperfusion. In non-stunned propranolol-treated myocardium, the Ca(2+) infusions doubled E(es) (baseline 6.9+/-0.9 mmHg mm(-2), n=8). Following Ca(2+)-washout, subsequent EMD 57033 infusion (0.1 mg kg(-1) min(-1), i.v.) tripled E(es) (P<0.05) and potentiated the Ca(2+)-induced increase in E(es) to 55.7+/-10.0 mmHg mm(-2) (P<0.05). Stunning (n=7) decreased E(es) to 5.3+/-0.6 mmHg mm(-2) (P>0.10) and attenuated the Ca(2+)-induced increase in E(es) (P<0.05). Subsequent infusion of EMD 57033 increased E(es) to 6.8+/-1.8 mmHg mm(-2) (P<0. 05) and restored responsiveness to added Ca(2+). These in vivo findings are consistent with the in vitro observations that myofilament Ca(2+)-responsiveness of stunned myocardium is reduced and that EMD 57033 increases contractility by enhancing myofilament Ca(2+)-responsiveness.

Animals↗
PubMed1997

Remodeling after myocardial infarction in humans is not associated with interstitial fibrosis of noninfarcted myocardium.

OBJECTIVES: This study was specifically designed to evaluate whether noninfarcted hypertrophic myocardium in patients with end-stage heart failure after myocardial infarction (MI) is associated with an increase in interstitial fibrous tissue. BACKGROUND: Postinfarction remodeling consists of complex alterations that involve both infarcted and noninfarcted myocardium. The question arises whether ventricular dysfunction is due to physical events, such as inadequate myocardial hypertrophy to compensate for increased tangential wall stress, or is caused by the development of progressive interstitial fibrosis in noninfarcted myocardium. METHODS: Fifteen hearts were obtained as cardiac explants (n = 13) or at autopsy (n = 2) from patients with end-stage coronary artery disease. Sixteen normal hearts served as reference hearts. Samples were taken from the left ventricular (LV) wall that contained the infarcted area, the border area and noninfarcted myocardium remote from scar areas. Collagen was quantified biochemically and microdensitophotometrically. Collagen type I and III ratios were analyzed by using the cyanogen bromide method and immunohistochemical staining, followed by microdensitophotometric quantification. RESULTS: In noninfarcted myocardium remote from the scar areas, total collagen levels and collagen type I/III ratios did not differ statistically from those in reference hearts. These observations contrasted with high total collagen content and high collagen type I/III ratios in scar and border areas. CONCLUSIONS: Remodeling of LV myocardium after MI in patients with end-stage heart failure is not necessarily associated with interstitial fibrosis in noninfarcted hypertrophic myocardium remote from scar areas. This finding raises questions regarding therapeutic interventions designed to prevent or retard the development of interstitial fibrosis.

Adult↗
PubMed1998

Prognostic value of the amount of dysfunctional but viable myocardium in revascularized patients with coronary artery disease and left ventricular dysfunction. Investigators of this Multicenter Study.

OBJECTIVES: The purpose of our study was to assess the prognostic importance of the amount of dysfunctional but viable myocardium in revascularized patients with coronary artery disease (CAD) and left ventricular (LV) dysfunction. BACKGROUND: The amount of dysfunctional but viable myocardium predicts the functional improvement after revascularization and may offer more precise risk stratification of patients referred for bypass surgery or coronary angioplasty. METHODS: Two hundred and seventy-four consecutive patients with CAD and LV ejection fraction < or =40% underwent low-dose dobutamine echocardiography for viability assessment. One hundred and thirty-three of them were revascularized using either coronary artery bypass surgery (118 patients) or coronary angioplasty (15 patients) and entered this study. To quantify the amount of dysfunctional but viable myocardium, wall motion was scored using 16-segment model. The dysfunctional segments were defined as viable if they exhibited improvement in their thickening by at least 1 grade with dobutamine infusion. The patients were followed up for a mean period of 20+/-12 months (range, 2 to 48) for cardiac mortality and nonfatal cardiac events including myocardial infarction, unstable angina pectoris requiring hospitalization and hospitalization for heart failure. Standard follow-up echocardiography was performed 3 to 6 months after revascularization. RESULTS: Twenty-nine patients exhibited a large amount of dysfunctional but viable myocardium (> or =6 segments, group A), 60 patients had a small amount of dysfunctional but viable myocardium (2 to 5 segments, group B) and 44 patients were found to have dysfunctional myocardium irreversibly damaged (group C). Similar prerevascularization LV ejection fractions of 35%+/-5%, 34%+/-4%, 36%+/-4% in groups A, B and C increased to 47%+/-6% (p < 0.01 vs. baseline, p < 0.01 vs. groups B and C), to 40%+/-5% (p < 0.01 vs. baseline) and to 37%+/-6% (p = NS vs baseline), respectively, after revascularization. The greatest functional improvement after revascularization in group A patients was accompanied by a lower rate of cardiac events during follow-up (2 vs. 18 in group B, p < 0.05, and vs. 17 in group C, p < 0.01) and better cardiac event-free survival according to Kaplan-Meier survival analysis (p < 0.05 vs. groups B and C, respectively). CONCLUSION: In revascularized patients with CAD and moderate or severe LV dysfunction, the presence of a large amount of dysfunctional but viable myocardium identifies patients with the best prognosis.

Adult↗
PubMed2003

The non-invasive assessment of hibernating myocardium in ischaemic cardiomyopathy--a myriad of techniques.

Heart failure is placing an ever-increasing burden on society. Many subjects with heart failure and underlying coronary artery disease have a significant amount of akinetic but viable myocardium that is able to contract should myocardial perfusion improve (hibernating myocardium). Non-randomised studies have shown prognostic benefit in subjects with hibernating myocardium undergoing revascularisation. Several non-invasive techniques have been developed to assess the presence or absence of hibernating myocardium. This review will examine the epidemiology and underlying pathogenesis of hibernating myocardium; evaluate the non-invasive techniques for diagnosing hibernating myocardium, and look at therapeutic intervention in subjects with hibernating myocardium.

Cardiomyopathy, Dilated↗
PubMed1997

Increase in force of contraction by activation of the Na+/Ca(2+)-exchanger in human myocardium.

AIMS: The aim of the present study was to investigate whether agents which enhance force of contraction via increasing intracellular Na+, i.e. cAMP-independently, remain effective in failing human myocardium. METHODS: Cumulative concentration-response curves with (+/-)BDF 9148 (0.01-10 mumol l-1), a Na(+)-channel activator, and ouabain (0.01-0.1 mumol l-1), a Na+/K(+)-ATPase inhibitor, were performed on electrically driven left ventricular human papillary muscle strips (1 Hz, 37 degrees C; dilative cardiomyopathy, NYHA IV, heart transplantation, n = 16; nonfailing, donor hearts, n = 5). The beta-adrenoceptor agonist isoprenaline (0.001-1 mumol l-1) and Ca2+ (1.8-15 mmol l-1) were studied for control. In addition, Ca2+ response curves were obtained on skinned fibre preparations from left ventricular myocardium (NYHA IV, n = 7) in the presence of BDF 9148 (1 mumol l-1) or a high Na+ concentration (50 mmol l-1) to investigate a possible direct or indirect interaction of (+/-)BDF 9148 with the myofilaments. RESULTS: While isoprenaline was significantly less effective in increasing force of contraction in failing human myocardium than in nonfailing myocardium (P < 0.01), in NYHA IV, (+/-)BDF 9148 and ouabain were as effective as in nonfailing human tissue. In failing and nonfailing myocardium, (+/-)BDF 9148 and ouabain exerted positive inotropic effects similar to those of Ca2+. However, the potency for (+/-)BDF 9148 to increase force of contraction was higher in NYHA IV than in nonfailing human myocardium (P < 0.05). Neither (+/-)BDF 9148 (1 mumol l-1) nor an increased concentration of Na+ (50 mmol l-1) altered the Ca2+ sensitivity or maximal developed tension of the contractile apparatus in experiments on chemically skinned left ventricular fibres. CONCLUSIONS: The enhanced sensitivity of the failing human myocardium towards Na(+)-channel modulation is not due to a direct or indirect interaction of (+/-)BDF 9148 with cardiac myofilaments but may be due to an altered Na(+)-homeostasis in human heart failure.

Adrenergic beta-Agonists↗
PubMed1997

Anisotropy of the apparent frequency dependence of backscatter in formalin fixed human myocardium.

Measurements of the frequency dependence of ultrasonic backscatter are presented for specific angles of insonification for regions of infarcted and noninfarcted human myocardium. A 5-MHz transducer was used to insonify cylindrical cores taken from 7 noninfarcted regions and 12 infarcted regions of the left ventricular free wall of 6 formalin-fixed human hearts explanted because of ischemic cardiomyopathy. The dependence of apparent (uncompensated for diffraction effects and attenuation) backscatter on frequency was approximated by a power-law dependence, magnitude of B(f)2 = afn. Under ideal conditions in a lossless medium, the effect of not compensating for the effects of diffraction and attenuation leads to the value of n to be 2.0 for Rayleigh scatterers while the frequency dependence of the fully compensated backscatter coefficient would be f4. The value of n was determined over the frequency range, 3-7 MHz. Both nonifarcted and infarcted myocardium exhibited anisotropy of the frequency dependence of backscatter, with maxima occurring at angles that were perpendicular to the predominant myofiber direction and minima when parallel to the fibers. Perpendicular insonification yielded results for n of 1.8 +/- 0.1 for noninfarcted myocardium and 1.2 +/- 0.1 for infarcted myocardium while parallel insonification yielded results of 0.4 +/- 0.1 for noninfarcted and 0.0 +/- 0.1 for infarcted myocardium. The functional form of the angle-dependent backscatter is similar for both noninfarcted and infarcted myocardium, although the frequency dependence is clearly different for both tissue states for all angles of insonification. The results of this study indicate that the anisotropy of the frequency dependence of backscatter may play a significant role in ultrasonic imaging and is an important consideration for ultrasonic tissue characterization in myocardium.

Anisotropy↗
PubMed1997

Impairment of the myocardial vasomotor response to cold pressor stress in collateral dependent myocardium.

OBJECTIVE: To study the vasomotor response (cold pressor/basal flow) in myocardium perfused entirely by collaterals, using the reflex sympathetic stimulation of cold pressor stress. DESIGN: Regional myocardial blood flow was measured in collateral dependent and in remote myocardium using positron emission tomography with 15O water at basal and at cold pressor stress. Regional ischaemia was measured with 18F-fluorodeoxyglucose (FDG). PATIENTS: Nine patients (mean (SD) age 53 (6) years) with an occluded coronary artery supplied entirely by collaterals from other angiographically normal arteries. RESULTS: In remote myocardium, basal and cold pressor flow were 0.99 (0.26) and 1.46 (0.60) ml/min/g (P < 0.05), respectively, a myocardial vasomotor response of 1.46 (0.45). In collateral dependent myocardium, basal and cold pressor flow were 0.91 (0.20) and 0.87 (0.35) ml/min/g, respectively (the latter value, P < 0.05 v remote region), a myocardial vasomotor response of 0.97 (0.43) (P < 0.05 v remote region). The myocardial vascular resistance (mean arterial pressure/flow) during cold pressor was higher in the collateral dependent than in remote myocardium, at 147.0 (61.1) and 85.6 (32.3) mm Hg.min.g/ml (P < 0.05), respectively, but with no relative increase in FDG uptake. CONCLUSIONS: In contrast to the decrease in myocardial resistance in remote myocardium with cold pressor, an increase was observed in collateral dependent myocardium suggesting a vasoconstrictor response in resistive vessels, without demonstrable myocardial ischaemia.

Cold Temperature↗