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PubMed2001

Myocardial contraction bands. Definition, quantification and significance in forensic pathology.

Pathological contraction bands affecting myocardial cells are observed in many different human conditions and in different experimental models. Their morphology was defined long ago but we need to understand the pathogenesis and functional meaning. A distinction between different histological forms of contraction bands and their quantification in a large spectrum of human diseases (262 cases) and a normal population sample where death was due to various types of accidental death (170 cases) produced the following conclusions: 1) The term "contraction band necrosis", as used presently, is ambiguous and should be reserved for a specific morpho-functional entity induced experimentally by intravenous catecholamine infusion and seen in equivalent human cases with pheochromocytoma. 2) In human pathology it may represent a sign of adrenergic stress linked with malignant arrhythmia/ventricular fibrillation. 3) Beyond a histological threshold of 37+/-7 foci and 322+/-99 myocells/100 mm2, the lesion may indicate sympathetic overdrive in the natural history of a disease and associated arrhythmogenic supersensitivity. 4) The detection of few pathological contraction bands in normal subjects in some types of accidental death correlates with the survival time, suggesting an agonal adrenergic stimulation to promote the cardiac pump.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Effect of tetanic myocardial contraction on coronary pressure-flow relationships.

Cardiac contraction causes a decrease in coronary flow. Despite many studies, it is still not clear what mechanism or mechanisms are responsible for this flow decrease. The phasic nature of myocardial contraction and the complexities intrinsic to intact heart preparations make it difficult to elucidate the mechanisms. We therefore studied coronary pressure-flow relationships during steady-state (tetanic) contractions in the maximally vasodilated isolated canine interventricular septum to see whether waterfall-type behavior is present. Using ryanodine and electrical stimulation allowed the production of reproducible and reversible tetani. This preparation minimizes the difficulties associated with transmural variations and also the effects of intramyocardial capacitance. Two separate protocols were performed to delineate the pressure-flow relationships in the passive and tetanized states. The first compared diastolic and tetanized pressure-flow relationships. In the second protocol, 2,3-butanedione monoxime was added to obtain an intermediate contractile level, thus allowing the comparison of two contractile states. Both the diastolic and tetanized pressure-flow relationships were curvilinear in the low-pressure range. Linear and nonlinear fits to the data showed that the primary effect of contraction was a shift of the pressure-flow relationships to higher pressures at a given flow. This effect was graded by the level of contractility and was independent of developed stress. Although other mechanisms may also be operative, these results support the presence of waterfall behavior in the coronary vascular bed.

Animals↗
PubMed2005

Relationship between asynchronous myocardial contraction and left ventricular systolic and diastolic function--assessment using the ECG-gated polar map with 99mTc-methoxy-isobutyl isonitrile.

BACKGROUND: To quantitate the degree of 3-dimensional asynchronous myocardial contraction, an ECG-gated polar map method was developed with (99m)Tc-methoxy-isobutyl isonitrile, and used to investigate the relationship between asynchrony and left ventricular (LV) function. METHODS AND RESULTS: Twelve normal subjects and 38 patients with an old myocardial infarction were studied with ECG-gated single-photon emission computed tomography (SPECT). In each frame, a myocardial perfusion polar map was reconstructed and the peak contraction phase in each pixel was displayed (phase map). The degree of asynchronous contraction was assessed from the standard deviations of the peak contraction phase (SDP) on the phase map. Ejection fraction (EF), peak ejection rate (PER), 1/3EF, peak filling rate (PFR) and 1/3 filling fraction (1/3FF) were calculated by the quantitative gated SPECT software, and E/A from Doppler echocardiography. The SDP was compared with these parameters. Correlation coefficients and p values between the SDP and parameters of cardiac function were as follows: EF, r=-0.69 (p<0.001); PER, r=-0.54 (p<0.001); 1/3EF, r=-0.57 (p<0.001); PFR, r=-0.29 (p<0.05); 1/3FF, r=-0.63 (p<0.001); E/A, r=-0.11 (p=0.51). CONCLUSIONS: There was a negative correlation between the SDP and LV systolic and diastolic function, which confirmed the functional significance of asynchrony on cardiac function.

Aged↗
PubMed1977

Correlation of myocardial contraction band necrosis and vascular patency. A study of coronary artery bypass graft anastomoses at branch points.

Eleven patients who died within 1 week of operation and in whom saphenous vein bypass graft anastomoses were located at or extended across coronary artery branch points were studied at autopsy. New surgically introduced narrowings of greater than 75% in one branch of the 13 anastomoses studied were more frequent (six of eight) when the arteriotomy extended into a branch artery than when the arteriotomy ended proximal to the flow divider of the branch point (zero to five). Obstruction was most frequently caused by suture compression of the arterial lumen. In five of the six anastomoses, where one branch contained a significant new narrowing and the other did not, a striking difference in the severity of myocardial contraction band necrosis in the distribution of the two arteries was found. In each such case the severe necrosis was in the distribution of the patent branch artery and the obstructed branch had slight or trivial injury. The results are interpreted as showing that myocardium that has the potential for developing contraction band necrosis may not develop it if the reflow phase is suppressed.

Adult↗
PubMed1992

The influence of endocardial endothelium on myocardial contraction.

A novel unidentified agent, provisionally named 'endocardin', has been shown to be released from endocardial endothelium. Endocardin has a unique prolonging effect on myocardial contraction. In contrast, endothelium-derived relaxing factor released from endocardial endothelium has the opposite effect of abbreviating contraction. Jerry Smith and colleagues discuss the mechanisms of action of these agents and their possible physiology and pathophysiology.

Animals↗
PubMed1999

Ca2+-independent inhibition of myocardial contraction by coronary effluent of hypoxic rat hearts.

Endothelial cells release agents that influence cardiac contraction. We recently reported that cultured hypoxic endothelial cells release an unidentified factor(s) that inhibits myocardial contraction. In this study, we investigated the effects of coronary effluent of isolated hypoxic rat hearts on isolated rat ventricular myocyte contraction. Coronary effluent collected during brief moderate hypoxia significantly depressed myocyte twitch shortening and decreased diastolic length, with only minor reduction in intracellular Ca2+ transients. These effects were similar to those of hypoxic rat coronary microvascular endothelial cell superfusates and were reversed by reoxygenation of hearts. "Hypoxic" coronary effluent exerted essentially Ca2+-independent effects on myofilament interaction in intact myocytes, as assessed by 1) peak Ca2+-shortening relations, 2) phase-plane analysis of instantaneous Ca2+-cell length relations, and 3) "steady-state" myofilament responses in tetanized, sarcoplasmic reticulum-disabled cells. Thus an unidentified substance(s) that inhibits myocyte shortening predominantly via effects on the myofilaments is reversibly released during acute moderate hypoxia of isolated hearts, presumably from coronary endothelial cells. Release of such an agent may be relevant to the cardiac contractile response to hypoxia.

Actin Cytoskeleton↗
PubMed1993

Interleukin-1 beta modulates myocardial contraction via dexamethasone sensitive production of nitric oxide.

OBJECTIVE: Nitric oxide released by a calcium dependent constitutive NO synthase in endocardial endothelial cells exerts characteristic effects on myocardial contraction. Interleukin 1 beta (IL-1) induces the expression of a different calcium independent NO synthase in several tissues. Activity of the latter enzyme has recently been identified in cardiac myocytes but its functional effects are unknown. The aim of this study was to investigate the effects of IL-1 on contraction of isolated ferret papillary muscle preparations. METHODS: Electrically stimulated preparations were studied in the presence of acebutolol (1 microM), indomethacin (10 microM), and polymyxin (10 micrograms.ml-1). After a 3 h equilibration period, IL-1 (10 ng.ml-1) was added and contractile behaviour monitored over the next 3 h. The following groups were studied: (1) no IL-1; (2) IL-1 alone; (3) IL-1 in the presence of dexamethasone (3 microM); (4) IL-1 in the presence of NG-monomethyl-L-arginine (L-NMMA, 50 microM); (5) IL-1 in the presence of L-NMMA (50 microM) and L-arginine (500 microM). Cyclic GMP content was measured by radioimmunoassay in all preparations. RESULTS: No significant contractile changes were noted in group 1. In group 2, IL-1 raised myocardial cyclic GMP and induced a progressive abbreviation of isometric twitch, starting 30 min after addition, with a small decrease in peak isometric tension but no change in rate of tension development. These effects were similar to those previously documented for endocardial endothelial NO but were not inhibited by endocardial endothelial denudation. IL-1 effects were inhibited in groups 3 and 4, and partially restored in group 5. CONCLUSIONS: IL-1 activates a dexamethasone sensitive myocardial L-arginine-NO pathway which raises myocardial cyclic GMP and induces marked twitch abbreviation. These effects could potentially lead to cardiac depression by limiting systolic ejection, and may be relevant in conditions where IL-1 levels are increased.

Acebutolol↗
PubMed1989

Effects of ischemia, bypass surgery and past infarction on myocardial contraction, relaxation and compliance during exercise.

Abnormalities of left ventricular function during ischemia have been described in animal models and in humans. Exercise, while a physiologic means of inducing ischemia, has a complex effect on left ventricular function by itself. In addition, patients with coronary artery disease have a diversity of chronic changes in myocardial structure and function. Therefore, with use of micromanometer left ventricular pressure measurements and ventricular volumes, calculated from biplane cineangiograms, left ventricular function at rest and during exercise was studied in 57 patients. Exercise-induced ischemia produced a decrease in ejection fraction, an increase in end-systolic volume, dramatic increases in diastolic pressures and an upward shift in the diastolic pressure-volume relation. Central to these changes was abnormal myocardial contraction and relaxation, with reduced regional shortening and impaired left ventricular pressure decay. However, nonischemic areas were capable of augmented shortening, and global pressure decay did accelerate slightly. These findings demonstrate that exercise-induced adjustments in contraction and relaxation are intertwined with ischemia-related abnormalities. Exercise studies in patients after bypass surgery and in patients with scars from distant myocardial infarction were useful in clarifying confounding factors. For example, asynchrony of contraction and relaxation, and chronic changes in passive chamber properties, also compromise systolic and diastolic function during exercise. In patients with coronary artery disease without ischemia during exercise, left ventricular end-diastolic pressure, but not early diastolic pressure, increased during exercise. The increase in pressure was appropriate for a slight increase in end-diastolic volume in a ventricle with a steep pressure-volume relation. Furthermore, end-systolic volume, while maintained during exercise, was not reduced, as occurs normally.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1973

Oscillation of cyclic adenosine monophosphate concentration during the myocardial contraction cycle.

The concentration of adenosine 3',5'-monophosphate (cyclic AMP) rises and falls during each myocardial contraction cycle. Peak concentrations of cyclic AMP precede peak development of systolic tension. Epinephrine alters the normal oscillation in myocardial cyclic AMP and increases both diastolic and systolic concentrations of the cyclic nucleotide. These transient changes in myocardial cyclic AMP indicate a potential role for cyclic AMP as a beat-to-beat regulator of myocardial contractility.

Animals↗
PubMedDate not supplied

[Relationship between the amplitude of myocardial contractions in frogs and the frequency of electrical stimulation. Role of external and intracellular calcium in the coupling of excitation and contraction].

Ionic currents were studied on the frog atrial trabeculae (Rana ridibunda) at 20 degrees C using a double sucrose gap voltage clamp arrangement. The net inward current peaks did not change in the course of repetitive stimulation (0,5/s) in contrast to the increase of the contraction amplitude (isometric tension) in the similar conditions (Bowdich staircase). The slow component of the net inward current revealed under the action of TTX (2-10(-8) g/ml) was increased upon the increase of external Ca concentration but was blocked when D-600 was introduced into the solution. The inhibitory action of D-600 on the contraction amplitude was frequency independent (in the ranges: 0,1--0,7/s). The decrease of external Na+ (isoosmotic replacement of 70% NaCl by sucrose) or the increase (5-fold) of the external Ca2+ significantly enhanced the myocardial contraction depressed with D-600. However these contractions fall in the course of rhythmical stimulation, and the effect being strongly dependent on the rate of stimulation. The results confirm the assumption (see: Biophysics, 6, 1024, 1976), that intracellular Ca stores (sarcoplasmic reticulum, internal surface of the cellular membrane) are involved in the control of the contractility in the amphibian myocardial cells. Many peculiarities of the excitation-contraction coupling in the frog myocardial cells can be explaned if one assumes that: 1) there is no space separation of primary uptake and release of Ca ion sites in the frog myocardium; 2) the system of "resting Ca chanels" in the frog myocardial cells is not so well developed as in the mammalian myocardial cells.

Animals↗
PubMed1975

The effect of pancuronium on myocardial contraction and catecholamine metabolism.

The effects of pancuronium bromide infusion on the uptake and release of [14C] noradrenaline (14C-NA) by the isolated, perfused rat heart and on the chronotropic and inotropic activity of the isolated heart were evaluated. Hearts were removed from animals under light ether anaesthesia, transferred to a modified Langendorff perfusing apparatus and perfused with Krebs-Ringer bicarbonate solution at a rate of 5 ml min-1. The effect of pancuronium on the uptake of noradrenaline was determined by perfusing hearts for 5 min with perfusate containing various concentrations of pancuronium and 200 ng ml-1 of 14C-NA. After 5 min pancuronium-treated hearts contained less 14C-NA. The degree of reduced uptake increased with increasing concentrations of pancuronium. In addition, the combination of pancuronium perfusion and electrical stimulation (15 mA for 10 ms at 4 Hz) blocked the 50 min uptake of 14C-NA by the heart to a greater degree than either factor separately. The release of noradrenaline was determined after perfusing hearts with 14C-NA followed by perfusion with solution containing pancuronium but no 14C-NA for 1 h. Pancuronium infusion did not significantly alter the release of 14C-NA from the heart after 1 h of perfusion. The infusion of pancuronium caused a reduction in both the rate and strength of myocardial contraction of the isolated heart which was reversed by perfusion with perfusate free of pancuronium. Following perfusion with pancurnium the rate and strength of contraction of the heart was seen to "rebound" above pre-pancuronium values for a short period. The rebound of myocardial rate and contraction may have been due to the presence of myocardial noradrenaline previously blocked from reuptake by pancuronium since hearts removed from reserpinized animals did not demonstrate "rebound."

Animals↗
PubMed1999

Acetaldehyde depresses myocardial contraction and cardiac myocyte shortening in spontaneously hypertensive rats: role of intracellular Ca2+.

Acetaldehyde (ACA), the major metabolite of ethanol, exerts both stimulatory and depressive actions on myocardial tissue. We have recently shown that ACA depresses myocardial contraction, cardiac myocyte shortening and intracellular Ca2+ transients in normal rat heart. The purpose of the present study was to determine the influence of hypertension on ACA-induced myocardial actions. Mechanical properties of left ventricular papillary muscles and ventricular myocytes isolated from both 25-week-old normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) were evaluated using force-transducer and video edge-detection, respectively. Papillary muscles and cardiac myocytes were electrically stimulated to contract at 0.5 Hz. Contractile properties analyzed include: peak tension development (PTD), peak twitch amplitude (PTA), time-to-PTD/PTA (TPT/TPS), time-to-90% relaxation/relengthening (RT90/TR90) and maximal velocities of contraction/shortening and relaxation/relengthening (+/-VT/+/-dL/dt). Intracellular Ca2+ transients were measured as fura-2 fluorescence intensity (FFI) changes. ACA (1-30 mM) depressed PTD without affecting other mechanical indices in both WKY and SHR myocardium, with maximal inhibition of 64 and 69%, respectively. SHR myocytes exhibited increased cell dimension, baseline PTA and resting intracellular Ca2+ levels, compared to WKY counterparts. ACA (0.03-30 mM) depressed PTA without affecting TPT, TR90 and +/-dL/dt. The maximal inhibitions were 31 and 36% in WKY and SHR groups, respectively. Interestingly, ACA exerted a biphasic effect on FFI, displaying potentiation at lower doses (<3 mM) and inhibition at higher doses (>3 mM). The maximal increase in FFI changes were 19 and 22% at 0.3 mM and the maximal decreases were 37 and 29% at 30 mM ACA, in WKY and SHR myocytes, respectively. Neither resting intracellular Ca2+ levels (FFI) nor fluorescence decay time (FDT) were affected by ACA. The increase in FFI was attenuated by propranolol (1 microM), whereas the decrease in FFI was reversed by BayK 8644 (1 microM). These results suggest that hypertension does not appear to alter ACA-induced myocardial depression. The mechanism underlying ACA-induced myocardial actions may involve increased beta-adrenergic activity at low doses and reduced Ca2+ entry and/or release at high doses.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2005

A non-rigid registration approach for quantifying myocardial contraction in tagged MRI using generalized information measures.

We address the problem of quantitatively assessing myocardial function from tagged MRI sequences. We develop a two-step method comprising (i) a motion estimation step using a novel variational non-rigid registration technique based on generalized information measures, and (ii) a measurement step, yielding local and segmental deformation parameters over the whole myocardium. Experiments on healthy and pathological data demonstrate that this method delivers, within a reasonable computation time and in a fully unsupervised way, reliable measurements for normal subjects and quantitative pathology-specific information. Beyond cardiac MRI, this work redefines the foundations of variational non-rigid registration for information-theoretic similarity criteria with potential interest in multimodal medical imaging.

Adult↗
PubMed1995

[Effects of nitroglycerin on myocardial contraction in patients with ischemic heart disease].

The effects of nitroglycerin on central hemodynamics and direct myocardial contractility were directly studied in 32 patients with functional class III-IV heart failure during aortocoronary bypass surgery. When nitroglycerin was used, hemodynamic parameters changed in two stages: 1) systemic blood pressure initially slightly increased; 2) decreases in this and other central hemodynamic parameters occurred. The dynamics of myocardial function was determined by its baseline state, dyskinetic intensity, i.e. its contractility. In patients with preserved myocardial function, nitroglycerin failed to cause its substantial dysfunction. At the same time its contractility and central hemodynamic parameters might considerably deteriorate in patients with moderate dyskinesia and furthermore with severe myocardial dysfunction.

Adult↗
PubMed1986

Transient myocardial ischemia: experimental echocardiographic demonstration and evaluation of myocardial contraction abnormalities.

A continuing theme in our laboratory has been the use of echocardiographically-measured systolic myocardial wall thickening to demonstrate and evaluate the consequences of regional myocardial ischemia. This presentation focuses on two areas: the immediate mechanical consequences of induced myocardial ischemia in two experimental models: canine and human; the correlation between persistent regional myocardial dysfunction and morphologic infarction after sequences of coronary artery occlusion and reperfusion. Many experiments using animal models have demonstrated that acute myocardial ischemia produces almost immediate replacement of normal systolic myocardial wall thickening by systolic thinning. Less is known about the immediate mechanical response of human myocardium to acute ischemia. This was studied in 5 open-chest humans undergoing various cardiac operations. Wall thickening was continuously displayed by a 7 MHz M-mode echocardiographic transducer coupled to the epicardium by suction to maintain constant position. Coronary flow velocity was displayed by a pulsed Doppler device coupled to an epicardial coronary artery by suction. Ischemia was induced by the surgeon who manually occluded the coronary artery with a soft-tipped Kitner dissector or vascular forceps for 30 seconds. It was found that cessation of coronary flow was accompanied by reductions in normal systolic thickening but systolic thinning or expansion only rarely occurred. In contrast, when the identical techniques were used in 5 dogs, systolic thinning always occurred immediately after coronary arterial occlusion. This suggests that there are important species differences between canine and human myocardium in the immediate mechanical response to myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Effect of verapamil on regional myocardial contraction during graded ischemia in the dog.

Verapamil benefits patients with angina pectoris during exercise. The mechanism underlying this effect is controversial. A direct oxygen-sparing effect on ischemic myocardium has been proposed, but previous studies seeking to demonstrate this effect have been inconclusive because of inadequate control of systemic hemodynamics. This study has assessed the direct effects of verapamil on regional myocardial contraction during graded coronary flow reductions while blood pressure and heart rate were held constant. Verapamil caused a decrease in regional contraction at normal levels of coronary flow, a finding consistent with a negative inotropic effect. At lower coronary flows, however, ischemic dysfunction was similar in the presence and absence of verapamil. These findings fail to support the concept that verapamil either selectively depresses ischemic myocardium or enhances myocardial function during ischemia. Thus, these direct mechanisms would seem unlikely causes of the observed beneficial effect during exercise in patients with coronary artery disease.

Angina Pectoris↗
PubMed1999

The direct effect of halothane on myocardial contraction in rat myocytes with poorly developed gap junctional intercellular communication.

BACKGROUND: The gap junction channel plays an important role in synchronous beating in the heart, and the reduction in the amount of gap junctional intercellular communication (GJIC) is thought to be the main arrhythmogenic factor in diseased heart. However, the effect of halothane on myocardial contraction in heart tissue with less GJIC is not well known. The purpose of the present study is to examine the direct effect of halothane on myocardium with poorly expressed GJIC. METHODS: Ventricular myocytes were obtained from neonatal rats by enzymatic digestion with collagenase and then cultured for 3 or 7 d. We have previously reported that the number of gap junctions at 3 d is approximately 10% of that at 7 d (1). The myocytes were stabilized in serum-free medium, and the spontaneous beating rate and amplitude were measured by a fiberoptic sensor. RESULTS: Heptanol (2 mM), an inhibitor of GJIC, abolished synchronized beating in myocytes cultured for 7 d. Halothane decreased the beating rate and amplitude in both groups of myocytes in a concentration-dependent manner (P < 0.05). Halothane at 1 and 2 MAC (adult rat MAC) decreased the beating rate more in myocytes cultured for 3 d than in myocytes cultured for 7 d (P < 0.05). Halothane reduced beating amplitude equally in both groups. Asynchronous contraction developed more frequently among myocytes cultured for 3 d than for those at 7 d. CONCLUSION: Halothane may block the GJIC channels, and when the number of these channels is reduced, exposure to halothane may cause asynchronous beating and decrease the beating rate. However, the halothane-induced decrease in amplitude is probably not due to blockade of GJIC because reducing the number of GJIC channels did not alter halothane's depressant effect.

Anesthetics, Inhalation↗