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PubMed1996

"Hibernating" myocardium: asleep or part dead?

Chronic ischemic dysfunction of the left ventricle is commonly presumed to represent "hibernating" myocardium. The implication of this assumption is that with successful reperfusion, systolic function will improve. Several diagnostic techniques including dobutamine stress echocardiography have been used to detect "viable" myocardium in the setting of chronic left ventricular dysfunction. Predictive accuracies of 70% to 85% have been reported for identifying myocardium that recovers function. Recovery of function has been variable and often dependent on the severity of dysfunction. All current models have presumed that chronically dysfunctioning myocardium is "hibernating." Obviously, in the chronic setting, dysfunction may have many causes and include components of transmural and nontransmural infarction as well as hibernating myocardium. This review focuses on the independent role that nontransmural infarction may play in chronic dysfunction and suggests its impact on diagnostic techniques used to identify hibernating myocardium.

Animals↗

PubMed2004

Identification of hibernating myocardium by acoustic microscopy.

Hibernating myocardium is viable myocardium that recovers after revascularization. The observation of loss of contractile proteins (myofibrils) and accumulation of glycogen in hibernating cardiomyocytes provide the basis for diagnosing hibernating myocardium. In this pilot study, acoustic microscopy was used to identify the cellular structure of normal vs. hibernating myocardium. Sections cut at 5-microm of archival paraffin blocks on glass slides were used for this study. Acoustic microscopy of normal cardiomyocytes showed intracellular linear echoes suggestive of myofibrils, and cardiomyocytes of hibernating myocardium revealed absence of myofibrils and dense intracellular echoes that corresponded to glycogen accumulation on optical microscopy. This modality of visualization allows a definitive diagnosis of hibernating myocardium.

Glycogen↗

PubMed2003

Quantitative regional wall motion analysis with early contrast ventriculography for the assessment of myocardium at risk in acute myocardial infarction.

BACKGROUND: Several techniques have been used to quantify the myocardium at risk, including measurement of regional ventricular function with contrast ventriculography and measurement of perfusion defect size with tomographic technetium-99m-sestamibi imaging. This study evaluates the correlation between these 2 techniques. METHODS: Twenty-three patients with angiographically documented coronary occlusion and acute myocardial infarctions (10 anterior, 13 inferior) were studied. All patients had contrast left ventriculography at the time of their acute angiogram before any revascularization therapy. Regional wall motion parameters measured with the centerline method were the severity, circumferential extent, and global circumferential extent of hypokinesis and the mean standardized motion in predefined areas. Technetium-99m-sestamibi was injected before reperfusion therapy with measurement of the myocardium at risk using single photon emission computed tomography imaging. RESULTS: The tomographic sestamibi-measured myocardium at risk was significantly greater for anterior infarctions compared with inferior infarctions (40% +/- 18% vs 14.0 +/- 8.5%, P =.0001). The only parameter of regional wall motion to show a significant difference by infarct location was global circumferential extent of hypokinesis (43% +/- 25% vs 22% +/- 15%, P =.02). The other parameters were not significantly different between anterior and inferior myocardial infarctions. For anterior infarctions, these parameters of regional wall motion correlated with myocardium at risk assessed with sestamibi: global circumferential extent of hypokinesis (r =.88, P <.01), circumferential extent of hypokinesis (r =.78, P <.01), mean standardized motion in predefined areas (r = -.74, P <.05), and severity of hypokinesis (r = -.70, P <.05). For inferior infarctions, there was no significant correlation between any of these parameters of regional wall motion and myocardium at risk assessed with sestamibi imaging. CONCLUSION: The assessment of regional ventricular function with contrast ventriculography correlates with the area of myocardium at risk measured with tomographic technetium-99m-sestamibi for anterior, but not for inferior, myocardial infarctions. Therefore, these parameters of regional wall motion are a poor measure of the efficacy of reperfusion therapies.

Coronary Angiography↗

PubMed2003

Myocardial blood flow in patients with hibernating myocardium.

The debate on whether resting myocardial blood flow (MBF) to hibernating myocardium is reduced or not has attracted a lot of interest and has contributed to stimulate new research on heart failure in patients with coronary artery disease (CAD). Positron emission tomography with oxygen-15 labeled water (H(2)(15)O) or nitrogen-13 labeled ammonia (13NH(3)) has been used for the absolute quantification of regional MBF in human hibernating myocardium. When hibernating myocardium is properly identified, i.e. a dysfunctional segment subtended by a stenotic coronary artery that improves function upon reperfusion, the following conclusions can be reached based on the available literature: (a) in the majority of these studies resting MBF in hibernating myocardium is not different from either flow in remote tissue in the same patient or MBF in normal healthy volunteers; (b) a reduction in MBF of approximately 20% compared to MBF in remote myocardium or age matched normal subjects has been demonstrated in a minority of truly hibernating segments; (c) hibernating myocardium is characterized by a severely impaired coronary flow reserve which improves after revascularization in parallel with contractile function. Thus, the pathophysiology of hibernation in humans is more complex than initially postulated. The recent evidence that repetitive ischemia in patients with coronary artery disease can be cumulative and lead to more severe and prolonged stunning, lends further support to the hypothesis that, at least initially, stunning and hibernation are two facets of the same coin.

Animals↗

PubMed1998

Inotropic response of stunned hypertrophied myocardium: responsiveness of hypertrophied and normal postischemic isolated rat hearts to calcium and dopamine stimulation.

OBJECTIVE: Severely hypertrophied myocardium was described to have a reduced tolerance towards ischemia. For non-hypertrophied hearts inconclusive findings on the Ca(2+)-responsiveness are reported. Information sensitivity to reversible ischemia and on postischemic Ca(2+)-responsiveness of hearts with clinically common moderate hypertrophy is lacking. Thus, the responsiveness of hypertrophied and normal postischemic myocardium to positive inotropic stimulation should be investigated in the present study. METHODS AND RESULTS: Hearts from spontaneously hypertensive rats (SHR, 4 months old) with significant LV-hypertrophy (+ 50%) and hearts from normotensive 4 months old Wistar rats were investigated using an isovolumic beating isolated heart model (8 hearts/each of the 8 groups). Functional recovery after 30 min of no-flow ischemia was 78 +/- 1% and 77 +/- 3% of preischemic control data in hypertrophied and non-hypertrophied hearts assessed as developed left ventricular pressure (non-ischemic controls: 95 +/- 2% in hypertrophied and 93 +/- 3% in non-hypertrophied controls). Maximum short-term stimulation with Ca2+ revealed a decreased peak left ventricular pressure of 124 +/- 4% in hypertrophied and 120 +/- 5% in non-hypertrophied postischemic hearts, as compared with non-ischemic controls 138 +/- 3% and 157 +/- 5%, respectively ( p < 0.01). A maximum dose of dopamine stimulated hypertrophied and non-hypertrophied postischemic hearts comparable to Ca2+. Analysing the dose-response curve for Ca(2+)-stimulation, the sensitivity expressed as fraction of the maximum was identical in non-ischemic and postischemic myocardium of hypertrophied and non-hypertrophied ventricles in spite of the reduced peak values. CONCLUSION: The findings demonstrate that after moderate reversible ischemia the steady-state function is similarly decreased in hypertrophied and non-hypertrophied postischemic myocardium. The maximum response to Ca2+ is significantly reduced in both types of myocardium, while the Ca2+ sensitivity is unchanged. Identical results after maximum dopamine stimulation as after Ca2+ indicate that the releasibility of Ca2+ and the beta-adrenoceptors are not the critical causes for the postischemic dysfunction in hypertrophied or non-hypertrophied myocardium.

Analysis of Variance↗

PubMed1999

Muscarinic regulation of Ca2+ signaling in mammalian atrial and ventricular myocardium.

The differential regulation of the contractility of mammalian atrial and ventricular myocardium upon activation of muscarinic receptors can be ascribed, for the most part, to alterations in intracellular Ca2+ transients. However, alterations in myofibrillar sensitivity to Ca2+ ions also contribute to such regulation. In atrial muscle, the following actions are all associated with the corresponding alterations in the amplitude of Ca2+ transients in the same direction as those in the strength of the contractile force: (1) the direct inhibitory action on the basal force of contraction; (2) the increase (recovery) in force that is induced during the prolonged stimulation of muscarinic receptors; and (3) the rebound increase in force induced by washout of muscarinic receptor agonists. In addition, for a given decrease in force induced by muscarinic receptor stimulation in atrial muscle, the amplitude of Ca2+ transients is decreased to a smaller extent than the decrease in amplitude induced by reduction of extracellular Ca2+ concentration ([Ca2+]o), an indication that muscarinic receptor stimulation might increase myofibrillar sensitivity to Ca2+ ions simultaneously with the reduction in the amplitude of Ca2+ transients during induction of the direct inhibitory action. In mammalian ventricular myocardium, the direct inhibitory action of muscarinic receptor stimulation exhibits a wide range of species-dependent variation. A pronounced direct inhibitory action is induced in ferret papillary muscle, which is also associated with a definite increase in myofibrillar sensitivity to Ca2+ ions. By contrast, in the ventricular myocardium of other species including the rabbit and the dog, muscarinic receptor stimulation scarcely affects the baseline Ca2+ transients and the force, but it results in a pronounced decrease in Ca2+ transients and force when applied in the presence of beta-adrenoceptor stimulation, a phenomenon known as 'accentuated antagonism' or the 'indirect inhibitory action' of muscarinic receptor stimulation in mammalian ventricular myocardium. During induction of the indirect inhibitory action in mammalian ventricular myocardium, muscarinic receptor stimulation reverses all the effects induced by beta-adrenoceptor stimulation, including the increase in Ca2+ transients, the positive inotropic and lusitropic effects, and the decrease in myofibrillar sensitivity to Ca2+ ions. The relationship between the amplitude of Ca2+ transients and force is unaffected during induction of the indirect inhibitory action in rabbit and dog ventricular myocardium. The direct and indirect inhibitory actions of muscarinic receptor stimulation on Ca2+ transients have clearly different dependences on frequency: the former is more pronounced at a higher rate of stimulation, while the latter is more pronounced at a lower rate. The more complex interaction of muscarinic receptor and beta-adrenoceptor stimulation in mammalian atrial muscle and ferret ventricular muscle might be explained by the contribution of both the direct and the indirect regulatory mechanisms to the interaction.

Animals↗

PubMed1987

Mechanisms of action of diltiazem in isolated human atrial and ventricular myocardium.

A comparative study of human atrial fibers (HAF), human ventricular fibers (HVF), frog ventricle, and frog skeletal muscle demonstrated marked differences in tension development in the presence of diltiazem. There was no significant difference between the tension developed by HAF and by HVF over a range of diltiazem concentrations when the differences in resting membrane potential were corrected by increasing external K+ concentration. In human myocardium, diltiazem resulted in both a voltage and use-dependent blockade of the calcium channel. Comparison of the tension-dose response curves in human myocardium, frog ventricle and skeletal muscle showed that diltiazem was most effective at decreasing tension in frog heart, and least effective in skeletal muscle with human myocardium being intermediate. In skeletal muscle, neither tension development nor the birefringence signal related to the Ca2+ release from the sarcoplasmic reticulum was significantly altered by Diltiazem in concentrations less than 10(-6) M, but in concentrations greater than 10(-5) M both were suppressed. Diltiazem suppressed tension in human myocardium over the range of membrane potentials associated with Ca2+ channel activity, while at more positive potentials, diltiazem appeared to have little effect on the tension-voltage relations. Diltiazem had no effect upon tension development induced by acetyl strophanthidin in human myocardium or upon the Ca2+ sensitivity of chemically skinned atrial or ventricular fibers. Thus the tension-suppressant effect of diltiazem in human myocardium appears to be mediated by a combination of voltage-dependent block of the Ca2+ channel and inhibition of Ca2+ release from internal stores, and not from alterations in either Na+-Ca2+ coupled transport or Ca2+ sensitivity of the myofilaments.

Adolescent↗

PubMed1999

Do the presence and amount of dysfunctional but viable myocardium affect the perioperative outcome of coronary artery bypass graft surgery?

The aim of our study was to assess the influence of the presence and amount of dysfunctional but viable myocardium on the perioperative outcomes in patients with coronary artery disease and moderate-to-severe left ventricular systolic dysfunction, who underwent coronary artery bypass graft surgery. Viability evaluation with low-dose dobutamine echocardiography was performed in 302 consecutive patients with coronary artery disease and left ventricular ejection fraction < or =40%, who were referred for coronary angiography and potential coronary revascularization. To quantify the amount of dysfunctional but viable myocardium, wall motion was scored using a 16-segment model. The dysfunctional segments were defined as viable if they exhibited improvement in their thickening by at least one grade. One hundred and twenty-seven patients underwent coronary artery bypass graft surgery. The perioperative outcomes were evaluated in 122 of them. Five patients were excluded because of inability to revascularize all vessels supplying dysfunctional but viable myocardial segments. Twenty-five patients exhibited a large amount of dysfunctional but viable myocardium (> or =6 segments, group A), 59 patients had a small amount of such myocardium (2-5 segments, group B), and 38 patients were found to have their dysfunctional myocardium irreversibly damaged (group C). The perioperative mortality in groups A, B, and C was 4, 10, and 11% (all P = NS), respectively. The rate of perioperative Q-wave myocardial infarction was 8, 10, and 3% (all P = NS), respectively. Similarly, there were no significant differences among the groups with respect to perioperative outcome variables including ventricular arrhythmias, duration and magnitude of catecholamine support, renal failure, pulmonary edema, and need for mechanical ventricular support or artificial ventilation. In patients with coronary artery disease and moderate-to-severe left ventricular dysfunction who underwent coronary artery bypass graft surgery, the presence and amount of dysfunctional but viable myocardium did not influence the perioperative outcome.

Adult↗

PubMed2000

Beta-adrenoceptor density in chronic infarcted myocardium: a subtype specific decrease of beta1-adrenoceptor density.

UNLABELLED: Beta-adrenoceptor density is altered in different cardiac diseases. In heart failure beta-adrenoceptor density is down regulated but in acute myocardial ischemia beta-adrenoceptor density is up regulated. In hearts with myocardial infarction total beta-adrenoceptor density is decreased shortly after myocardial infarction. AIMS AND METHODS: To investigate whether total beta-adrenoceptor number is altered in the chronic phase after myocardial infarction, and to identify the specificity of alteration, we studied male Wistar rats (n = 18) which underwent a ligation of the left coronary artery or a sham operation. Twelve weeks after coronary ligation, rats were sacrificed and hearts were excised, perfused to obtain blood-free myocardium and frozen in liquid nitrogen. Infarcted myocardium was identified visually and separated from non-infarcted myocardium. Total beta-adrenoceptor number was calculated in fmol (-)-[125I]iodocyanopindolol specifically bound/mg protein and the relative amount of beta1- and beta2-adrenoceptor density was measured by inhibition of (-)-[125I]iodocyanopindolol binding with CGP 20712 A. RESULTS: Total beta-adrenoceptor number in infarcted myocardium was significantly decreased (25.7+/-1.4 vs. 24.9+/-2.2 vs. 20.1+/-3.2 fmol/mg protein (P=0.03) resp. Sham vs. Non-infarcted vs. Infarcted myocardium), due to a decrease of only beta1-adrenoceptor density (14.7+/-0.61 vs. 12.7+/-1.09 vs. 4.84+/-0.96 fmol/mg protein (P=0.004) resp.), whereas the beta2-adrenoceptor density and the dissociation constant (Kd) were not significantly decreased. CONCLUSION: In the infarcted myocardium total beta-adrenoceptor density is decreased due to a decreased beta1-adrenoceptor density at 12 weeks after myocardial infarction.

Animals↗

PubMedDate not supplied

Diagnostic performance of myocardial contrast echocardiography for detection of stunned myocardium.

Improvement in regional wall motion after acute myocardial infarction has been described up to 2 to 3 weeks after the acute event despite restoration of blood flow by early successful reperfusion therapy. The prospective identification of potentially reversible ventricular dysfunction caused by stunned myocardium has significant clinical implications. Twenty-seven patients with acute myocardial infarction underwent myocardial contrast echocardiography (MCE) before, immediately after, and 4 weeks after successful reperfusion therapy. MCE was performed by imaging a parasternal short-axis view during intracoronary arterial injection of 2 ml sonicated ioxaglate (Hexabrix-320). The contrast defect area and contrast-filled area before reperfusion were defined as the risk area and noninfarct area, respectively. The normalized gray level was defined as the ratio of the gray level in the risk area/gray level in the noninfarct area. In 21 patients, wall motion was akinetic or dyskinetic immediately after reperfusion, and 10 of 21 patients in whom wall motion recovered during the chronic stage were defined as patients with stunned myocardium. In patients who showed asynergic wall motion immediately after reperfusion, MCE predicted the recovery of left ventricular wall motion (stunned myocardium) during the chronic stage with a sensitivity of 77%, specificity of 100%, and predictive accuracy of 86%, when a normalized gray level of more than 0.4 was presumed to predict stunned myocardium. We conclude that MCE provided the prospective identification of potentially reversible ventricular dysfunction caused by stunned myocardium, and wall motion in the area of nonenhanced myocardium on MCE immediately after reperfusion is not expected to show reversible dysfunction.

Adult↗

PubMed1998

Phase 1B ventricular arrhythmia in the dog: localized reentry within the mid-myocardium.

Intramural and epicardial composite electrograms, signal-averaged orthogonal bipolar electrograms across the ischemic zone, and closely-spaced bipolar electrograms from subendocardium, mid-myocardium, and subepicardium were utilized to determine if phase 1B reentry resulted from localized reentry within ischemic mid-myocardium. During the first 10 minutes following coronary ligation, activation delays were largest in ischemic subepicardium, with continuous electrical activity in ischemic epicardium linking a ventricular extrasystole to the preceding beat. During the 15-30 minute period, activation delay observed in ischemic mid-myocardium exceeded activation delay on the epicardial surface. Ventricular extrasystoles were associated with mid-myocardial delays > 130 msec. With short-coupled extrasystoles (< 300 msec), electrical activity in ischemic mid-myocardium linked an extrasystole with the preceding beat. Although single extrasystoles with coupling intervals > 300 msec were also associated with mid-myocardial delays > 130 msec, most extrasystoles (68%) demonstrated an isoelectric gap > 20 msec. The data demonstrate an association between delayed activation within ischemic mid-myocardium and phase 1B arrhythmia resulting from (1) localized reentry in ischemic mid-myocardium and (2) a delay-dependent "non-reentrant" mechanism.

Animals↗

PubMed2001

Isolated noncompaction of the ventricular myocardium: ultrafast computed tomography and magnetic resonance imaging.

This study was undertaken to evaluate the feasibility of ultrafast computed tomography (CT) and magnetic resonance imaging (MRI) for anatomical and pathophysiological diagnosis of isolated noncompaction of the left ventricular myocardium (INVM) compared with other imaging modalities including thallium myocardial imaging. Six patients, three sets of siblings, ranging in age from 13 to 18 years, were included in this study. Two-dimensional echocardiograms revealed numerous prominent trabeculations and deep intertrabecular recesses in one or more ventricular wall segments in all cases. Thallium-201 myocardial imaging disclosed a hypoperfusion area corresponding to the zones where noncompacted ventricular myocardium was localized. Ultrafast CT showed early defects of varying degrees and rate enhancement of the noncompacted ventricular myocardium, implying fibrosis in this area. MRI disclosed inner zones of noncompacted myocardium distinguishable from thin outer zones of compacted myocardium. T2-weighted imaging revealed high intensity areas at the apex of the left ventricle, suggesting disturbed microcirculation due to fibrosis, thrombus formation, and hypokinesis. Cine MRI revealed hypokinesis of the noncompacted ventricular wall during the cardiac cycle. In conclusion, ultrafast CT and MRI provide high-resolution imaging of noncompacted myocardium, and also pathophysiological details regarding this rare disease.

Adolescent↗

PubMed2002

Effect of the calcium sensitizer levosimendan on the performance of ischaemic myocardium in anaesthetised pigs.

The calcium sensitizer levosimendan (LEV) improves the function of stunned myocardium, cardiac performance in heart failure, and possibly the efficiency of myocardial work. The present experiments investigated the effect of LEV on myocardial contraction and metabolism of acutely ischaemic myocardium distal to a functionally effective coronary artery stenosis. Anaesthetised open chest pigs (n = 14) were instrumented to assess heart rate (HR), aortic pressure (AoP), cardiac output (CO), blood flow in the left descending (QLAD) and circumflex (QLCX) coronary artery, myocardial end-diastolic segment length and systolic shortening (edL, MSS by sonomicrometry) in the LAD- and LCX-territory. Systemic vascular resistance (SVR), and a myocardial power index (PowI) for the LAD- and LCX-region were calculated. Following obstruction of QLAD by an external snare proximal to the first diagonal branch LEV was given intravenously (10 + 20 + 30 microg/kg 15 min apart, n = 8) or the vehicle of LEV (n = 6). Following LEV haemodynamics and regional myocardial performance changed significantly: HR +22 min(-1), AoP -6 mmHg, CO +17%, SVR -21%; intact myocardium: QLCX +15%, RLCX -24%, PowILCX + 39%; ischaemic myocardium: QLAD -7%, MSSLAD -42%, PowILAD -27%. The data confirm the pharmacological profile of LEV: positive chronotropy, positive inotropy, and vasodilatation. The pump function of acutely ischaemic myocardium worsened following LEV. The efficiency of myocardial performance did not improve. A beneficial effect of LEV on the function of ischaemic myocardium was possibly outmanoeuvred by the increase in heart rate.

Anesthesia↗

PubMedDate not supplied

Effects of prostaglandins on baroreflex during reperfusion of the ischaemic myocardium.

1. The present study was planned to: (i) determine whether the baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) was attenuated during reperfusion of short-term ischaemic myocardium; and (ii) study whether blockade of prostaglandin synthesis with indomethacin reversed the inhibitory baroreflex. 2. Arterial pressure was lowered with intravenous sodium nitroprusside before coronary occlusion and 3 min after release of a 5 min occlusion of the left circumflex coronary artery in anaesthetized rabbits. The protocol was repeated 20 min after indomethacin (5 mg/kg, i.v.) or indomethacin vehicle (50 mmol/L tris(hydroxymethyl)aminomethane buffer, pH 8.4) treatment. In addition, this study was performed in a group of vagotomized rabbits. 3. Before indomethacin treatment, the slope of the mean arterial pressure (MAP)-RSNA relationship decreased from -3.3+/-0.77 to -2.01+/-0.69% change in RSNA/mmHg (P < 0.05) during reperfusion of ischaemic myocardium in intact rabbits. The decrease in the slope was reversed by administration of indomethacin. However, the decrease in the slope was not reversed by indomethacin vehicle. Furthermore, the reduction in the slope of the MAP-RSNA relationship during reperfusion of ischaemic myocardium was abolished in vagotomized rabbits. However, there was no inhibition of the slope of the MAP-HR relationship during reperfusion of ischaemic myocardium in either intact or vagotomized rabbits. 4. In conclusion, our data suggest that prostaglandins released by ischaemic myocardium can attenuate the baroreflex-mediated response of RSNA to lowered arterial pressure via vagal afferents during reperfusion of short-term ischaemic myocardium.

Adrenergic Fibers↗

PubMed1998

The persistence of hibernating myocardium after acute myocardial infarction.

OBJECTIVE: To establish the persistence of hibernating myocardium initially detected after myocardial infarction treated with thrombolysis. METHODS AND RESULTS: Fourteen patients underwent gated positron emission tomography with 18-fluoro-deoxyglucose and N13-ammonia at a median of 8 days after first myocardial infarction. Repeat scans were performed at a median of 13 weeks post-infarction. A total of 148 (30.9%) myocardial segments showed reduced N13-ammonia uptake at the time of the first scan compared with 154.5 (32.2%) segments at the time of repeat imaging. The median change in the number of segments with reduced perfusion was -1.0. Initially 13 subjects had hibernating myocardium, seven patients had large areas and six had smaller regions. Six (46.2%) subjects had repeat scans showing unchanged areas of hibernating tissue and seven had second scans demonstrating changes in the size of the region of hibernating myocardium. One patient had no hibernating myocardium on either scan. CONCLUSIONS: Positron emission tomography performed several months after myocardial infarction demonstrates significant changes in myocardial perfusion. However, a reduction in the number of segments with reduced perfusion does not always result in an improvement in myocardial metabolism and contraction. Whilst most regions of hibernating myocardium were still present several months after infarction, in only approximately half was the size of the mismatched region unchanged. Therefore it is not possible to predict the fate of hibernating myocardium which is present after infarction.

Aged↗

PubMed2003

[MRI in the diagnosis of non-compacted ventricular myocardium (NCVM) compared to echocardiography].

PURPOSE: To report the detection of non-compacted ventricular myocardium (NCVM) with MRI compared to echocardiography in 8 patients. MATERIAL AND METHODS: Non-compaction of the ventricular myocardium is a congenital disorder characterized by an altered structure of the myocardial wall resulting from an intrauterine arrest in endomyocardial embryogenesis. The morphological findings consist of a prominent meshwork of multiple myocardial trabeculations and deep intertrabecular recesses, communicating with the left ventricular cavity. 8 consecutive patients (mean age 7.3 years) with clinical and echocardiographic signs of NCVM were examined by MRI (1.5 T, Vision, Siemens) in short axis and 2- and 4-chamber views, using T (1)-weighted TSE and Cine-GRE in 6 patients and true FISP sequences in 2 patients. MRI and echocardiography were evaluated for visibility, signs of NCVM and involvement of myocardial wall segments. Thickness was measured for non-compacted and compacted myocardium and the non-compacted to compacted (N/C) ratio calculated. RESULTS: MRI diagnosed 6 of 8 patients of having NCVM. Myocardial thickness as measured by echocardiography and MRI showed a good correlation in compacted myocardium (r = 8.82) and no correlation in non-compacted myocardium (r = 0.4). In 2 cases, non-compacted myocardium was detected but echocardiography did not reach the N/C ratio > 2 as required to diagnose NCVM in accordance with the criteria found in the literature. Both patients were also misdiagnosed by MRI performed with Cine-GRE. MRI reached a N/C ratio > 2 in only three patients. Newer TruFisp sequences showed no definite advantages. Extent of non-compaction could be visualized correctly with MRI. CONCLUSION: Echocardiography is the method of choice to detect NCVM. MRI can be an alternative in some cases. The diagnosis of NCVM should not be considered until N/C ratio is over 2.

Adolescent↗

PubMed1994

Reduced coronary vasodilator function in infarcted and normal myocardium after myocardial infarction.

BACKGROUND: The ability of the coronary vascular bed to dilate and thus increase blood flow to the myocardium may be impaired in coronary artery disease, even in regions of myocardium supplied by an angiographically normal coronary artery. If this kind of vasomotor dysfunction was present or accentuated after acute myocardial infarction, it might influence the extent of ischemia and necrosis in areas not directly injured by the infarction. METHODS: We studied 13 patients (mean [+/- SD] age, 62 +/- 11 years) with single-vessel coronary artery disease after they had received thrombolytic therapy for myocardial infarction. Using positron-emission tomography (PET) with oxygen-15-labeled water, we measured regional myocardial blood flow under basal conditions and after the intravenous administration of dipyridamole (0.5 mg per kg of body weight over a period of four minutes) 8 +/- 3 days after infarction in all 13 patients (1-week study) and 6 +/- 2 months after infarction in 9 of the 13 (6-month study). On both occasions we measured blood flow both in the infarcted region and in a region of myocardium that was remote from the infarcted region and supplied by a normal artery. RESULTS: At the one-week PET study, the coronary vasodilator response (the ratio of the myocardial blood flow after the administration of dipyridamole to basal blood flow) was 1.12 +/- 0.50 in the infarct-related artery and 1.53 +/- 0.36 in the remote region (P = 0.015). At the six-month study, the coronary vasodilator response was 1.42 +/- 0.37 in the infarcted region and 2.19 +/- 0.69 in the remote region (P = 0.004 for the comparison with the infarcted region; P = 0.011 for the comparison with the remote region at the one-week study). The value in remote myocardium remained lower than that in similar regions in 10 control patients, who had single-vessel coronary artery disease but no evidence of myocardial infarction (3.17 +/- 0.72; P = 0.009). CONCLUSIONS: After acute myocardial infarction, there is a severe vasodilator abnormality involving not only resistance vessels in infarcted myocardium, but also those in myocardium perfused by normal coronary vessels. This dysfunction may affect the extent of myocardial ischemia and necrosis after coronary occlusion.

Adult↗

PubMed2003

Comparison of the predischarge exercise thallium-201 perfusion defect after myocardial infarction with myocardium at risk measured during acute infarction with technetium-99m sestamibi imaging.

BACKGROUND: Exercise thallium-201 imaging provides a noninvasive estimate of the amount of myocardium presumed to be at risk of infarcting should a complete occlusion of the coronary stenosis occur. The relationship between the size of the exercise thallium perfusion defect and the extent of myocardium supplied by a diseased coronary artery has not been established. This study evaluates that presumed correlation. METHODS: Patients were injected intravenously with technetium-99m sestamibi during acute myocardial infarction before thrombolysis or conventional therapy to quantify the myocardium at risk. Twenty-six patients who underwent risk-area assessment subsequently underwent clinically driven, predischarge, submaximal exercise imaging with thallium-201. The exercise testing was performed on day 7 +/- 2 days. A conventional polar map display was used to quantify the perfusion defect. RESULTS: The myocardium at risk determined by technetium-99m sestamibi at the time of infarction was 30% +/- 20% of the left ventricle. The mean exercise thallium-201 defect was 34% +/- 22% of the left ventricle. The exercise defect tended to be slightly larger than the myocardium at risk (4% +/- 10% of the left ventricle, P =.05). There was a close correlation between the 2 measurements (r = 0.89, SE = 9.4, P <.0001). CONCLUSIONS: This study shows a close correlation between the myocardium "at risk" assessed acutely by technetium-99m sestamibi and the "presumed at-risk area" determined by thallium-201 imaging on predischarge exercise testing. This finding supports the concept that the size of the exercise thallium defect caused by coronary stenosis indicates the likely size of a myocardial infarction resulting from occlusion of that stenosis.

Adult↗