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At least 19 recordsLinked to original sources
PubMed2005

Accumulation of long-chain acylcarnitine and 3-hydroxy acylcarnitine molecular species in diabetic myocardium: identification of alterations in mitochondrial fatty acid processing in diabetic myocardium by shotgun lipidomics.

Diabetic cardiomyopathy is the result of maladaptive changes in energy homeostasis. However, the biochemical mechanisms underlying dysfunctional lipid metabolism in diabetic myocardium are incompletely understood. Herein, we exploit shotgun lipidomics to demonstrate a 4-fold increase in acylcarnitines in diabetic myocardium, which was reversible upon insulin treatment. Analysis of acylcarnitine molecular species in myocardium unexpectedly identified acylcarnitine molecular species containing a mass shift of 16 amu in comparison to the anticipated molecular species. Synthesis of 3-hydroxy acylcarnitine identified the natural products as the 3-hydroxylated acylcarnitines through comparisons of diagnostic fragmentation patterns of synthetic and naturally occurring constituents using tandem mass spectrometry. Diabetes induced an increase of both calcium-independent phospholipase A(2) (iPLA(2)) mRNA and iPLA(2) activity in rat myocardium. Cardiac ischemia in myocardium genetically engineered to overexpress iPLA(2) dramatically increased the amount of acylcarnitine present in myocardium. Moreover, mechanism-based inactivation of iPLA(2) in either wild-type or transgenic myocardium ablated a substantial portion of the acylcarnitine increase. Collectively, these results identify discrete insulin remediable abnormalities in mitochondrial fatty acid processing in diabetic myocardium and identify iPLA(2) as an important enzymatic contributor to the pool of fatty acids that can be used for acylcarnitine synthesis and energy production in myocardium.

Animals↗
PubMed2006

Assessment of collateralized myocardium with Cardiac Magnetic Resonance (CMR): transmural extent of infarction but not angiographic collateral vessel filling determines regional function and perfusion in collateral-dependent myocardium.

BACKGROUND: Angiographic collateral vessel filling is limited to evaluate collateral-dependent myocardium. We hypothesize, that quantitative assessment of regional myocardial function, perfusion and viability with Cardiac Magnetic Resonance (CMR) adds complementary information to angiography of collateralized myocardium. METHODS: CMR was performed in 30 patients with one chronic occluded coronary artery and no further flow limiting stenosis to assess transmural extend of infarction (TEI), resting perfusion and perfusion during adenosine-induced hyperemia and regional wall thickening (RWT) in collateral-dependent and antegradely-perfused myocardium. Collateral vessels were evaluated by angiography and the Rentrop grade (0-3). RESULTS: In 15 patients with < 50% TEI in collateral-dependent myocardium resting perfusion (1.08+/-0.22 ml/min/g), hyperemia (2.21+/-0.73 ml/min/g) and RWT (4.0+/-2.6 mm) were similar to antegradely-perfused myocardium (rest 1.14+/-0.20 and hyperemia 2.46+/-0.82 ml/min/g, RWT 4.3+/-1.7 mm). In 15 patients with > or = 50% TEI in collateral-dependent myocardium resting perfusion and hyperemia as well as RWT were significantly lower (rest 0.84+/-0.19, p<0.001 and hyperemia 1.34+/-0.43 ml/min/g, p<0.001; RWT 1.0+/-1.0 mm, p<0.0001) compared to antegradely-perfused myocardium. There was an inverse correlation between TEI and resting or hyperemic perfusion or RWT. In contrary, resting perfusion and hyperemia as well as RWT in collateral-dependent myocardium were not different between patients with good (2-3) compared to patients with poor Rentrop grade (0-1). There was no correlation between TEI and Rentrop grade. CONCLUSION: Function and perfusion in collateral-dependent myocardium are preserved, if transmural extent of infarction is limited (< 50%). This is independent of their angiographic collateral vessel filling. Thus, CMR adds complementary information to angiographic standard assessment of collateral vessels.

Aged↗
PubMed2000

Angiogenesis induced by hepatocyte growth factor in non-infarcted myocardium and infarcted myocardium: up-regulation of essential transcription factor for angiogenesis, ets.

The feasibility of a novel therapeutic strategy using angiogenic growth factors to expedite and/or augment collateral artery development has recently entered the realm of treatment of ischemic diseases. Hepatocyte growth factor (HGF) is a novel member of endothelium-specific growth factors whose mitogenic activity on endothelial cells is very potent. Although it has been demonstrated that HGF is a potential angiogenic growth factor in in vitro culture systems, there is no direct in vivo evidence for the angiogenic activity of HGF in physiological conditions. In this study, we hypothesized that transfection of HGF gene into infarcted myocardium could induce angiogenesis, potentially resulting in a beneficial response to hypoxia. Human HGF gene or control vector driven by the SRalpha promoter was transfected into rat myocardium by the HVJ-liposome method. Four days after in vivo transfection of human HGF gene, there was a marked increase in human immunoreactive HGF as compared with control vector (P < 0.01). In myocardium transfected with HGF vector, a significant increase in PCNA-positive endothelial cells was observed, while few PCNA-positive endothelial cells were detected in both control-vector-transfected and untreated myocardium. The number of vessels around the HGF injection sites was significantly increased as compared with control vector or vehicle (P < 0.01). Angiogenic activity induced by the transfection of HGF vector was also confirmed by the activation of a transcription factor, ets, which is essential for angiogenesis. Furthermore, we studied the pathophysiological role of HGF in a myocardial infarction model. The concentration of endogenous HGF was significantly decreased in infarcted myocardium. Therefore, we hypothesized that transfection of HGF gene into infarcted myocardium could induce a beneficial response to the decreased endogenous HGF. Indeed, transfection of human HGF into infarcted myocardium also resulted in a significant increase in the number of vessels (P < 0. 01), accompanied by marked induction of ets binding activity and a significant increase in blood flow. Overall, the present results provide direct in vivo evidence for the induction of angiogenesis by transfection of the human HGF gene in rat non-infarcted and infarcted myocardium. The constant production of local HGF resulting from the transgene may be considered as an innovative therapeutic angiogenesis strategy for ischemic diseases such as myocardial infarction. Gene Therapy (2000) 7, 417-427.

Animals↗
PubMed1989

Exercise-induced ischemia in the streptokinase-reperfused myocardium: relationship to extent of salvaged myocardium and degree of residual coronary stenosis.

To assess the functional significance of residual stenosis at the site of the thrombolysed infarct-related coronary artery, 37 patients underwent exercise radionuclide ventriculography or stress-redistribution thallium-201 scintigraphy at an average of 7 weeks following streptokinase therapy during evolving myocardial infarction. The size of the initially jeopardized myocardium and the salvaged myocardium were quantitated on thallium-201 studies obtained immediately before and 10 days after streptokinase infusion. Exercise-induced ischemia (defined by reversible thallium-201 perfusion defects or stress-induced deterioration of regional wall motion) in the reperfused myocardium was absent in 46% of patients and was present in different degrees in the remaining 54%. A significantly lower proportion of patients, however, showed exercise-induced chest pain and/or ST segment depression (10% and 20%, respectively). By stepwise multiple logistic regression analysis, the quantitatively determined size of the salvaged myocardium (398 units versus 65 units, p less than 0.01) and the ratio of the salvaged myocardium/extent of initially jeopardized myocardium (70% versus 28%, p less than 0.01) were both independent predictors of stress-induced ischemia, whereas the extent of initially jeopardized myocardium (585 units versus 407 units, p = NS), incidence of greater than or equal to 99% coronary stenosis (37% versus 46%, p = NS), and ischemic time (160 versus 196 minutes, p = NS) did not provide additional predictive information. We conclude that exercise-induced ischemia, which is frequently present in the streptokinase-reperfused myocardium, cannot be detected accurately by exercise-induced chest pain or ST segment depression, nor can it be predicted by the severity of residual coronary stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

A reverse flow-metabolism mismatch pattern: a new marker of viable myocardium with greater contractility during dobutamine stress than myocardium with a flow-metabolism mismatch pattern.

Few studies have investigated the contractility of myocardium with a reverse flow-metabolism pattern; that is, greater uptake of nitrogen- 13-ammonia (NH3) than fluorine- 18-fluorodeoxyglucose (FDG) on positron emission tomography (PET). This study examined the contraction thickening represented by count increase in ECG-gated FDG-PET of myocardium with a reverse flow-metabolism pattern during low-dose dobutamine stress. Fifty-four patients with myocardial infarction were studied. Relative NH3 and FDG uptake (%NH3, %FDG) and %count increase were measured in 216 apical and 216 lateral segments on ECG-gated FDG-PET. The %count increase during low-dose dobutamine stress was greater in myocardium with a reverse flow-metabolism mismatch pattern than in myocardium with a flow-metabolism mismatch pattern (35.9+/-25.7% vs 24.6+/-15.9%, p=0.0221 in apical segments, and 38.4+/-22.6% vs 27.6+/-18.4%, p=0.0040 in lateral segments) despite smaller %FDG. A reverse flow-metabolism mismatch pattern should be noted as a new marker of viable myocardium with greater contractility during dobutamine stress than myocardium with a flow-metabolism mismatch pattern.

Aged↗
PubMed1992

Characterization of "hibernating" and "stunned" myocardium with focus on the use of calcium antagonists in "stunned" myocardium.

In the initial seconds after a sudden reduction in coronary blood flow, a temporary mismatch between myocardial energy demand and supply exists. The mechanisms underlying the rapidly ensuing reduction in contractile function in the ischemic myocardium are still unknown. In the presence of some residual blood flow, a state of "perfusion-contraction matching" develops. The metabolic status of such hypoperfused myocardium improves, since myocardial lactate production is attenuated and creatine phosphate (CP), after an initial reduction, returns toward control values. The hypoperfused myocardium responds to inotropic stimulation by dobutamine. The recruitment of an inotropic reserve implies increased energy utilization. During inotropic stimulation, after partial normalization, lactate production is again increased, and CP is decreased again. Thus, a supply-demand imbalance that had been at least partially corrected by the ischemia-induced decrease in regional contractile function is precipitated again. A situation of chronic contractile failure in viable myocardium that normalizes upon reperfusion has been termed myocardial "hibernation." Myocardial "stunning" is characterized by a reversible postischemic contractile dysfunction despite full restoration of blood flow. The details of the underlying mechanisms are not clear. An inadequate energy supply and impaired sympathetic neurotransmission have been excluded. Potential mechanisms, which are not mutually exclusive, may include (a) damage of membranes by free radicals, (b) an increase in free cytosolic calcium during ischemia and reperfusion, and (c) a decrease in the calcium sensitivity of the myofibrils. The equally pronounced increases in regional contractility in normal and "stunned" myocardium during postextrasystolic potentiation and the infusion of calcium or the calcium-sensitizing agent AR-L-57, however, suggest an unchanged calcium sensitivity of reperfused myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed2005

Tissue cardiomyoplasty using bioengineered contractile cardiomyocyte sheets to repair damaged myocardium: their integration with recipient myocardium.

BACKGROUND: We hypothesized that tissue-engineered contractile cardiomyocyte sheets without a scaffold would show histological and electrical integration with impaired myocardium, leading to the regeneration of infarcted myocardium. METHODS: Neonatal rat cardiomyocytes were cultured on Poly(N-isopropylacrylamide)-grafted polystyrene dishes and detached as a square cell sheet at 20 degrees C. Two sheets were stacked to make thicker contractile cardiac sheets. In cross-section, the stacked sheets looked like homogeneous heart-like tissue. Two weeks after rats were subjected to left anterior descending (LAD) ligation, two treatments were conducted: 1) cardiomyocyte sheet implantation (T group, n=10), and 2) fibroblast sheet implantation (F group, n=10). The control group underwent no additional treatment (C group, n=10). RESULTS: Echocardiography demonstrated that cardiac performance was significantly ameliorated in the T group 2, 4, and 8 weeks after implantation. The cardiomyocyte sheets became attached to the infarcted myocardium, showed angiogenesis, expressed connexin-43, and appeared as homogeneous tissue in the myocardium Electrophysiological experiments showed a QRS complex with one peak in the treated scar area in the T group, but two peaks, indicative of branch block, in that of the other groups. Furthermore, the threshold for pacing of the recipient heart was lower in the T group than in the other groups. CONCLUSIONS: Cardiomyocyte sheets integrated with the impaired myocardium and improved cardiac performance in a model of ischemic myocardium. Techniques using such tissue-engineered cell sheets are introducing the promising concept of tissue cardiomyoplasty to the field of regenerative medicine.

Animals↗
PubMed1987

Analysis of responses to a selective phosphodiesterase III inhibitor, SK&F 94120, on isolated myocardium, including human ventricular myocardium from "end-stage" failure patients.

The actions of SK&F 94120, a selective phosphodiesterase (PDE III) inhibitor, have been characterised on human ventricular myocardium obtained from heart failure patients. Some actions have been compared directly with those of the drug on guinea pig and cat ventricular myocardium. SK&F 94120 caused positive inotropic responses in preparations from all three species. In the human preparations, there was no evidence of differential activity in ventricles obtained from patients with heart failure associated with ischaemic heart disease, congestive cardiomyopathy, or mitral valve disease. The mechanism of positive inotropic activity of SK&F 94120 demonstrated characteristics of PDE III inhibition--e.g., potentiation of isoprenaline responses and reversal by carbachol. In addition, in human tissue a highly significant correlation between positive inotropic activity and increases in intracellular cAMP was demonstrated. Electrophysiological studies in human and guinea pig myocardium demonstrated that SK&F 94120 enhanced the second inward Ca2+ current over the same concentration range as that needed for positive inotropic activity. This was demonstrated in preparations incubated in Krebs bicarbonate solution and, more clearly, in solutions with raised K+ concentration. The data described in this report establish that inhibition of PDE III is an effective positive inotropic mechanism in human ventricular myocardium. Comparison of the responses in human, guinea pig, and cat myocardium shows clear similarities of responses with only small quantitative differences.

Animals↗
PubMed1996

Synergic effects of NO and oxygen free radicals in the injury of ischemia-reperfused myocardium--ESR studies on NO free radicals generated from ischemia-reperfused myocardium.

The ESR signal of NO bound to hemoglobin was detected during the ischemia-reperfusion of myocardium with low temperature ESR technique, and the synergic effects of NO and oxygen free radicals in the injury of the process were studied with this technique. Oxygen free radicals and NO bound to beta-subunit of hemoglobin (beta-NO complex) could be detected simultaneously in the ischemia-reperfused myocardium. Those signals could not be detected from the normal myocardium even in the presence of L-arginine. However, those signals could be detected and were dose-dependent with L-arginine in the ischemia-reperfused myocardiums and the signal could be suppressed with the inhibitor of NO synthetase, NG-nitro-L-arginine methylester (NAME). Measurement of the activities of lactate dehydrogenase (LDH) and creatine kinase (CK) in the coronary artery effluent of ischemia-reperfused heart showed that L-arginine at lower concentration (< 1 mmol/L) could protect the heart form the ischemia-reperfusion injury but at higher concentration aggravate the injury. Addition of NAME to the reperfusion solution could also protect the myocardium. Addition of xanthine (X)/xanthine oxidase (XO) or Fe2+/H2O2 to the reperfusion solution increased the production of NO and oxygen free radicals and the ischemia-reperfused injury simultaneously. Addition of superoxide dismutase (SOD) and catalase decreased the production of NO and oxygen free radicals and the ischemia-reperfusion injury.

Animals↗
PubMed1995

Alterations of excitation-contraction coupling in stunned myocardium and in failing myocardium.

Although both myocardial stunning and chronic heart failure are characterized by contractile dysfunction, there are profound differences in their underlying mechanisms. Changes in cardiac contractile force can be effected by modulation of intracellular [Ca2+] or by alteration of the contractile protein response to intracellular Ca2+. New evidence suggests that the principal lesion in the stunned myocardium resides at the level of the contractile proteins, which may be injured by proteases activated early during reperfusion. In contrast, failing myocardium is known to display abnormal intracellular Ca2+ handling, indicative of dysfunction of the sarcoplasmic reticulum. Alterations of gene expression and isoform switching of the myofilaments also occur in failing myocardium, consistent with an observed shift of the kinetics of crossbridge cycling. In conclusion, changes in both intracellular Ca2+ homeostasis and myofilament function occur in failing myocardium, while stunned myocardium primarily reflects an uncoupling between Ca2+ and contractile force.

Animals↗
PubMed2005

Scarred myocardium imposes additional burden on remote viable myocardium despite a reduction in the extent of area with late contrast MR enhancement.

Magnetic resonance imaging (MRI) can simultaneously detect and quantify myocardial dysfunction and shrinkage in contrast-enhanced areas postinfarction. This ability permits the investigation of our hypothesis that transformation of infracted myocardium to scarred tissue imposes additional burdens on peri-infarcted and remote myocardium. Pigs (n = 8) were subjected to reperfused infarction. Gd-DOTA-enhanced inversion recovery gradient echo sequence (IR-GRE) imaging was performed 3 days and 8 weeks postinfarction. Global and regional left ventricular (LV) function was evaluated by cine MRI. Triphenyltetrazolium chloride (TTC) stain was used to delineate infarction while hematoxylin and eosin (H & E) and Masson's trichrome stains were used to characterize remodeled myocardium. Late contrast-enhanced MRIs showed a decrease in the extent of enhanced areas from 17 +/- 2% at 3 days to13 +/- 1% LV mass at 8 weeks. TTC infarction size was 12 +/- 1% LV mass. Cine MRIs showed expansion in dysfunctional area due to unfavorable remodeling, ischemia, or strain. Ejection fraction was reduced in association with increased end-diastolic and end-systolic volumes. Scarred myocardium contained collagen fibers and remodeled thick-walled vessels embedded in collagen. Sequential MRI showed greater LV dysfunction despite the shrinkage in extent of enhanced areas 2 months postinfarction. The integration of late enhancement and cine MRI incorporates anatomical and functional evaluation of remodeled hearts.

Analysis of Variance↗
PubMed1997

Adenosine technetium-99m sestamibi single-photon emission tomography for the assessment of jeopardized myocardium early after acute myocardial infarction. Paradoxical scintigraphic underestimation of jeopardized myocardium in patients with a severe infarct-related stenosis.

This study investigated the value of technetium-99m sestamibi scintigraphy in identifying patients at risk for post-infarct ischaemia (=jeopardized myocardium), especially within the reperfused infarct region. In 51 patients with a recent (<1 month) myocardial infarction, adenosine 99mTc-sestamibi single-photon emission tomography (SPET) and dobutamine stress echocardiography (DSE) were performed and correlated with the presence of significant coronary artery stenosis [% diameter stenosis (DS) >50%] on quantitative coronary angiography. Regional perfusion activity was analysed semi-quantitatively (score 0-4) on a 13-segment left ventricular model. DSE was used for the estimation of the infarct size (low-dose DSE) and for concomitant evaluation of ischaemia (high-dose DSE). A reversible perfusion defect within the infarct region was observed in 20 of the 37 patients with a significant infarct-related lesion (sensitivity of 54%) and only in one patient without a significant infarct-related lesion (specificity of 93%). Further analysis revealed that the scintigraphic assessment of jeopardized myocardium was fairly good in patients with a moderate (DS 51%-64%) infarct-related stenosis but was inadequate in patients with a severe (DS>/=65%) infarct-related stenosis (sensitivity of 80% vs 36%, P<0.01), while the echocardiographic detection of ischaemia was not influenced by stenosis severity (sensitivity of 73% in both subgroups). This scintigraphic underestimation of jeopardized myocardium was mainly related to a severely impaired myocardial perfusion under baseline conditions, as was evidenced by a significantly more severe rest perfusion score in the infarct region in patients with a severe stenosis as compared to those with a moderate stenosis (average score: 1.5+/-0.7 vs 2.1+/-0.6, P<0.01), while infarct size on echocardiography was similar for both subgroups. It may be concluded that early after an acute myocardial infarction, adenosine 99mTc-sestamibi SPET may underestimate reperfused but still jeopardized myocardium, particularly in patients with a severe infarct-related stenosis. In these patients the evaluation of the ischaemic burden on rest-stress scintigraphy is hampered by the presence of a severely impaired myocardial perfusion in resting conditions.

Adenosine↗
PubMed1986

[Effects of coenzyme Q10 on ischemic myocardium during coronary artery occlusion--evaluation of the time needed to change irreversible myocardium].

We studied the irreversible change of myocardium on coronary artery occlusion using mongrel dogs. These dogs were divided into 2 groups. One group was administered CoQ10 before and after coronary artery occlusion and the other received placebo. Results are summarized as follows. 1) In both groups the hemodynamic change showed no significant change. 2) In the biochemical studies there was no significant difference between both groups, but in the infarction group, serum GPT and pyruvic acid in a sampling of blood taken from the coronary sinus were significantly higher than in the non-infarction group (P less than 0.05, 0.025). 3) By the triphenyl tetrazolium chloride (TTC) technique for the myocardial infarction, infarction did not appear in the CoQ10 group until 90 minutes after coronary occlusion but in the placebo group infarction appeared as early as 60 minutes. 4) In the ultrastructural studies of myocardium the electron microscopy detected irreversible change of mitochondrias when the TTC technique identified infarction. In conclusion, the administration of CoQ10 has a protective effect for the irreversible change of ischemic myocardium.

Alanine Transaminase↗
PubMed1996

[Stunned myocardium or hibernating myocardium? Apropos of a case].

The authors relate a case report of unstable angina pectoris accompanied by a well-documented stunned myocardium phenomenon. Stunned and hibernating myocardium resulting from an acute or chronic coronary ischaemia on the myocardium are notions which widely govern revascularisation indications, especially after a myocardial infarction. At present, their detection is based on isotopic methods and stress echocardiography.

Angina, Unstable↗
PubMed2002

Vasodilator signals from the ischemic myocardium are transduced to the coronary vascular wall by pertussis toxin-sensitive G proteins: a new experimental method for the analysis of the interaction between the myocardium and coronary vessels.

OBJECTIVES: We sought to detect cross-talk between the beating heart and coronary vascular bed during myocardial ischemia and to test the hypothesis that the cross-talk is mediated by pertussis toxin (PTX)-sensitive G proteins (G(PTX)) in vessels. BACKGROUND: Coronary flow is closely related to the myocardial metabolic state, indicating the existence of a close interaction between cardiac muscle and coronary vascular beds. Experimental methods for the analysis of the interaction, however, have not been established. METHODS: Coronary detector vessels (DVs) were isolated from rabbit hearts. One end of the vessel was cannulated to a micropipette, and the other end was ligated. After the DV was pressurized (60 cm H(2)O), it was gently placed on the myocardium, which was perfused by the left anterior descending coronary artery (LAD) of anesthetized, open-chest dogs (n = 23). The LAD was occluded, and the DV diameter was observed using an intravital microscope with a floating objective system. To evaluate the involvement of G(PTX), the DV was pre-incubated with PTX (100 ng/ml). RESULTS: The LAD occlusion of the beating heart produced significant dilation of DVs (241 +/- 25 microm) by 10%. The DVs pretreated with PTX (250 +/- 27 microm) did not dilate in response to myocardial ischemia. N(omega)-nitro-L-arginine (100 micromol/l), but not glibenclamide (5 micromol/l), abolished the ischemia-induced DV dilation. CONCLUSIONS: We have established experimental methods for direct analysis of the interaction between the myocardium and coronary microvessels. We conclude that the ischemic myocardium releases transferable vasodilator signals that are transduced by means of the G(PTX) located in the vascular walls. The nitric oxide pathway is involved in the signal transduction.

Animals↗
PubMed1998

Gallopamil activity on asynergic viable myocardium in acute myocardial infarction: insights on stunned and hibernating myocardium.

The influence of the calcium antagonist gallopamil on the contractility of asynergic viable myocardium after acute myocardial infarction treated with thrombolysis was investigated by two-dimensional echocardiography. Sixteen patients with > or = 1 viable segment(s), identified during the low-dose phase (up to 10 micrograms/kg/min) of a dobutamine echocardiographic test (up to 40 micrograms/kg/min) performed 4-5 days after a first acute myocardial infarction, were given a gallopamil intravenous bolus (50 micrograms/kg) 12-24 hours later. Two-dimensional echocardiography was done before and 15 minutes after the bolus. A score index of 1 (normokinesis) to 4 (dyskinesis) and a 16-segment model were used. A segment was considered viable when a resting asynergy (score > or = 2) improvement of > or = 1 grade was seen during low-dose dobutamine. Follow-up echocardiograms were done 3-5 months later. A total of 30 viable segments were found; of these, 10 showed sustained improvement in contractility (group A) during high-dose dobutamine, while 20 exhibited a biphasic response returning to their basal contractile state (group B). After the gallopamil bolus, 9 of 10 group A segments improved their contractility, in comparison with 0 of 20 group B segments (P < .001). Infarct-related vessel significant (> or = 75%) coronary stenosis was present in the tributary vessel of 0 of 10 group A and of 20 of 20 group B segments (P < .001). At follow-up, 9 of 10 group A segments showed a spontaneous contractile improvement; of the 20 group B segments, 8 of 10 that underwent revascularization (7 angioplasty, 3 bypass graft) showed contractile improvement, in comparison with 0 of 10 segments not revascularized (P = .001). We conclude that gallopamil may reverse the contractile dysfunction of postischemic stunned myocardium in patients with acute myocardial infarction, whereas no effects are apparent on ischemic/hibernating myocardium.

Calcium Channel Blockers↗
PubMed1985

Scintigraphic evidence that the right ventricular myocardium tolerates ischaemia better than the left ventricular myocardium.

To study the incidence of right ventricular infarction and the effect of intracoronary thrombolysis on the ischaemic right ventricular myocardium, we performed intracoronary myocardial thallium scintigraphy in 18 patients with complete occlusion of the right coronary artery who underwent intracoronary thrombolysis. In 15 of these patients, intracoronary thallium-201 and technetium-99 m pyrophosphate scintigrams were performed simultaneously. All 18 patients had a right ventricular thallium defect before thrombolysis, and all had new thallium uptake after thrombolysis. 17 out of 18 patients had a left ventricular thallium defect before thrombolysis, but only 10 of them showed new thallium uptake after thrombolysis. 14 out of 15 patients had a left ventricular technetium-99 m pyrophosphate spot after thrombolysis and some diffuse pyrophosphate accumulation in the area of the right ventricle. In one patient pyrophosphate accumulation was found only in the area of the right ventricle. Thus, right ventricular thallium defects were detected by intracoronary thallium scintigraphy in the majority of patients with inferior acute myocardial infarction due to right coronary artery occlusion. Right ventricular thallium defects were always reversible in contrast to left ventricular thallium defects in the same patients, suggesting that right ventricular myocardium tolerates ischaemia better than left ventricular myocardium.

Adult↗
PubMed1997

18F-2-deoxyglucose deposition and regional flow in pigs with chronically dysfunctional myocardium. Evidence for transmural variations in chronic hibernating myocardium.

BACKGROUND: Hibernating myocardium in patients with collateral-dependent myocardium is characterized by relative reductions in resting flow and increases in the uptake of 18F-2-deoxyglucose (FDG) in the fasting state. We performed the present study to examine whether these key physiological alterations could be produced in a porcine model of chronic coronary occlusion and to assess whether the adaptations consistent with hibernation varied across the myocardial wall. METHODS AND RESULTS: We chronically instrumented pigs (n = 18) with a fixed occluder on the proximal left anterior descending coronary artery (LAD). Three months later, ventricular function, regional myocardial perfusion, and FDG deposition (by excised tissue counting or positron emission tomography) were assessed in pigs after an over-night fast in the closed-chest anesthetized state. Total LAD occlusion with angiographic collaterals was present in the majority of animals. Left ventriculography showed severe anterior hypokinesis, and resting perfusion was significantly reduced in the hibernating LAD region in comparison with the normal remote regions (subendocardium: 0.80 +/- 0.06 versus 1.07 +/- 0.06 mL.min-1.g-1, P < .001; full-thickness: 0.87 +/- 0.04 versus 0.99 +/- 0.06 mL.min-1.g-1, P < .01). There was a twofold increase in full-thickness fasting FDG uptake in the dysfunctional LAD region (1.8 +/- 0.2 by positron emission tomography versus 1.9 +/- 0.1 by ex vivo counting). Ex vivo tissue counting revealed a pronounced transmural variation in FDG uptake in the hibernating region (LAD/normal), which averaged 2.5 +/- 0.2 in the subendocardium, 1.9 +/- 0.2 in the midmyocardium, and 1.4 +/- 0.1 in the subepicardium. CONCLUSIONS: These results demonstrate that pigs instrumented with a proximal LAD stenosis develop hibernating myocardium characterized by relative reductions in resting function and perfusion in association with increased uptake of FDG in the fasting state. The transmural variations in relative resting flow and FDG uptake suggest that myocardial adaptations consistent with hibernation are most pronounced in the subendocardial layers and vary in relation to local coronary flow reserve.

Animals↗