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PubMed1999

Regional left ventricular myocardial contraction abnormalities and asynchrony in patients with hypertrophic cardiomyopathy evaluated by magnetic resonance spatial modulation of magnetization myocardial tagging.

Global left ventricular (LV) pump function is generally preserved in patients with hypertrophic cardiomyopathy (HCM). However, it is unknown whether regional myocardial contractility is impaired, especially in nonhypertrophied regions. The purpose of this study was to evaluate regional LV myocardial contraction in patients with HCM using magnetic resonance (MR) spatial modulation of magnetization (SPAMM) myocardial tagging. The study group comprised 20 patients with asymmetric septal hypertrophy (HCM group) and 16 age-matched normal patients (control group), and data were collected using transthoracic M-mode and 2-dimensional echocardiography, and MR SPAMM myocardial tagging. The systolic strain ratio, maximum systolic strain velocity, and time from end-diastole to maximum systolic strain (deltaT) in the anterior, ventricular septal, inferior and lateral regions for 2 LV short-axis sections at the levels of the chordae tendineae and papillary muscles were measured at 50-ms intervals by MR myocardial tagging. The end-diastolic anterior and ventricular septal wall thicknesses and LV mass index were significantly different between the HCM and control groups. The systolic strain ratio for all 4 walls, particularly the anterior and ventricular septal regions, was significantly lower in the HCM group. In the HCM group, the maximum systolic strain velocity was significantly lower and deltaT was significantly shorter for all 4 walls, particularly the anterior and ventricular septal regions. The standard deviation for the deltaT, calculated from the deltaT for the 8 regions of the 2 LV short-axis sections, was significantly greater in the HCM group. In conclusion, regional LV myocardial contraction is impaired in both hypertrophied and nonhypertrophied regions, and systolic LV wall asynchrony occurs in patients with HCM.

Adult↗
PubMed1998

Reversible myocardial contraction abnormalities in patients with an acute noncardiac illness.

STUDY OBJECTIVES: Reversible myocardial contraction abnormalities are usually observed in patients with acute ischemic syndromes caused by coronary artery disease. In this study, we report the occurrence of reversible anterior-apical contraction abnormalities in patients with an acute noncardiac illness. SETTING: This was a retrospective study of 22 patients with the following characteristics: (1) hospitalization for an acute noncardiac illness; (2) appearance of deep T-wave inversion in the precordial leads of the ECG; and (3) presence of an anterior wall motion abnormality on an echocardiogram. Standard clinical information was collected together with results of serial ECGs, echocardiograms, and coronary angiograms. RESULTS: The primary diagnoses for the 22 acutely ill patients included CNS injury (n=6); sepsis (n=3); acute pulmonary disease (n=3); drug overdose or metabolic abnormality (n=7); and post noncardiac surgery (n=3). An initial echocardiogram revealed an anterior apical wall motion abnormality. At follow-up, all patients had progressive improvement in anterior wall motion with return of normal wall motion in 16 patients (73%). All patients evolved deep T-wave inversion (average, 7.8 mm) and QT interval lengthening in the precordial leads. Coronary angiography revealed a significant stenosis in the likely culprit artery (left anterior descending) in only one patient. CONCLUSION: A reversible cardiac contraction abnormality of the anterior wall and apex of the left ventricle can complicate the clinical course of critically ill patients in the absence of significant coronary artery disease. This phenomenon is associated with striking T-wave inversion and QT interval lengthening. Mechanisms other than myocardial ischemia may lead to the occurrence of reversible regional myocardial contraction abnormalities.

Acute Disease↗
PubMed2000

Myocardial contraction maps using tissue Doppler acceleration imaging.

OBJECTIVE: To evaluate the tissue Doppler acceleration imaging (TDAI) data which can be used to determine the intramural site of origin of myocardial contraction in response to electrical stimulation. METHODS: Six open-chest pigs with left ventricle (LV) pacing were evaluated with TDAI. An epicardial surface scanning method was used to collect short-axis views of the left ventricle. The electrode was implanted from the epicardium through the anterior free wall to an intramural position. RESULTS: During pacing, the intramural onset of myocardial acceleration occurred within 33 ms after electrical stimulation and always surrounded the embedded subendocardial end of the pacing needle. The observed short-axis diameter of the area of initial myocardial acceleration ranged from 2.9 mm to 5.0 mm (4.2 +/- 0.9 mm, n = 6). The onset of myocardial acceleration allowed appreciation of the initial intramural myocardial contraction. The spatial size and acceleration magnitude of the initial myocardial acceleration distribution were irregular. CONCLUSION: Two-dimensional myocardial acceleration mapping can show the intramural site of origin of myocardial contraction in response to paced electrical stimulation. The location of myocardial acceleration conformed to the site of initial electrical stimulation. The delay to the earliest regional myocardial contraction, 33 ms after paced electrical stimulation, was related to the frame rate of image acquisition.

Animals↗
PubMed1982

Relationship between changes in regional myocardial contraction and energy metabolism following coronary flow reduction.

To investigate the relationship between mechanical and metabolic deterioration in the ischemic myocardium following a decrease of coronary blood flow, the patterns of regional myocardial contraction and myocardial adenosine triphosphate (ATP) content were analyzed simultaneously in canine left ventricles with constriction of the left anterior descending coronary artery (LAD). The patterns of contraction in the ischemic region were monitored by means of ultrasonic dimension gauges implanted in the endocardial surface and were classified into 5 types; Type 0 = normal, Type I = late systolic lengthening, Type II = early and late systolic lengthening with end diastolic length elongation, Type III = systolic bulge with early diastolic shortening, and Type IV = holosystolic bulge. Type I developed in 6/8 dogs with 1-49% LAD flow reduction, Type II in 6/8 dogs with 50-74% reduction, and Types III and IV in all dogs with 75-100% reduction. The myocardial ATP content (microM/Gm tissue) at the sites of the patterns of myocardial contraction measurement was analyzed. No differences in ATP content were noted between Type 0 and Type I (3.70 +/- 0.51 vs. 3.60 +/- 0.36). In contrast, the ATP content in Type II was significantly reduced (2.94 +/- 0.20) compared to Type I (p less than 0.005). In Types III + IV with systolic bulge, the ATP reductions were severer (2.59 +/- 0.36) than in Type II (p less than 0.05). In conclusion, it can be said that as the LAD flow reduction advanced, the patterns of myocardial contraction were transformed from Type 0 to Type IV with accompanying ATP reductions.

Adenosine Triphosphate↗
PubMedDate not supplied

Effects of myocardial contraction on coronary blood flow: an integrated model.

The effects of myocardial contraction on the coronary flow are studied by means of an integrated structural model of left ventricular (LV) mechanics, coronary flow, and fluid and mass transport. This model relates global LV performance, and in particular coronary flow dynamics, to myocardial composition and structure and contractile sarcomere activity. Extravascular pressure is identified with hydrostatic tissue pressure, i.e., intramyocardial pressure (IMP), and is determined by the dynamics of myocardial contraction and fluid transport. Consistent with available experimental data, changes in myocardial function and contractile state are simulated by changing the sarcomere contractile properties or changing the LV loading conditions. The model's predictions are successfully compared with a wide range of experimental studies; all but one were performed at a constant coronary perfusion pressure and maximal vasodilation. The results indicate a dominant effect of the myocardial contractile state on coronary flow and a dissociation between coronary compression and LV cavity pressure (LVP) when the pressure is controlled by load changes. However, when active sarcomere contraction is regionally impaired by lidocaine, LVP plays an important role in the coronary flow characteristics. The model adequately predicts observations on the effect of cardiac contraction on systolic and diastolic coronary flows, as well as the role of LVP at different loading and contractile conditions. The analysis supports the hypothesis that coronary compression, as mediated through IMP, is independent of LV loading conditions and depends on myocardial contractility and coronary perfusion pressure.

Biomechanical Phenomena↗
PubMed1994

Myocardial contraction patterns in non-ischaemic and ischaemic regions during acute coronary insufficiency.

The effect of coronary insufficiency on the myocardial contraction pattern was studied in 11 thoracotomized cats using apical long axis echocardiograms and cross-oriented segments in the anterior midwall. Myocardial tissue blood flow was studied using radiolabelled microspheres. After circumflex coronary artery occlusion, ejection shortening increased on average 17% for circumferential segments (P < 0.05) and 61% for longitudinal segments (P < 0.001). Hyperkinesis was also validated as augmented anterior endocardial wall motion and wall thickening. Circumflex occlusion increased end-systolic sphericity of the left ventricle (P < 0.05). Subsequent underperfusion of the left coronary artery, in two discrete steps, decreased subendocardial blood flow by, on average, 36% (P < 0.001) and 75% (P < 0.001) vs the post-occlusion value, while subepicardial flow did not change. While subendocardial blood flow decreased by 36%, systolic shortening of the global major axis decreased, by, on average, 77% (P < 0.001), shortening of the longitudinal segments by 36% (P < 0.001), and systolic shortening of the minor axis by 18% (P < 0.05), whereas shortening of midwall circumferential segments did not change. This study shows that changes in myocardial contraction in both non-ischaemic and ischaemic regions during coronary insufficiency are most pronounced in the direction of the cardiac major axis.

Acute Disease↗
PubMed1983

Effects of progesterone derivatives on sodium pump activity and force of myocardial contraction in isolated guinea pig heart.

A progesterone derivative, chlormadinone acetate, has been reported to inhibit isolated Na,K-ATPase, to increase intracellular sodium, to decrease the force of myocardial contraction and to antagonize the positive inotropic action of ouabain. Because several inhibitors of isolated Na,K-ATPase fail to interact with the sodium pump in intact cells, two progesterone derivatives, chlormadinone acetate and megestrol acetate were examined for their effects on Na,K-ATPase, sodium pump activity and the force of contraction in isolated guinea pig atria. Both megestrol acetate and chlormadinone acetate inhibited specific (ATP-dependent) 3H-ouabain binding to Na,K-ATPase isolated from guinea pig brain or heart, with a corresponding inhibition of enzyme activity. The effects on Na,K-ATPase obtained from brain were more pronounced than that obtained from heart. The inhibitory effect of megestrol acetate was partially antagonized by K+. In electrically stimulated left atrial muscle preparations, neither compound affected ouabain-sensitive 42K+ uptake. Additionally, these compounds failed to affect the force of myocardial contraction or to influence the positive inotropic action of ouabain. These data fail to support the contention that inhibition of the sarcolemmal sodium pump is unrelated to the ouabain-induced increase in the force of myocardial contraction.

Animals↗
PubMed1979

[Effect of strophanthin and cytochrome C on myocardial contraction and the incidence of shock and ventricular fibrillation in experimental myocardial infarct].

High ligation of the interventricular artery caused ventricular fibrillation in the first 2--4 minutes in 20% of cats. In the remaining animals myocardial contractility diminished to half its initial value. After that, contractility increased gradually. In cardiosclerosis myocardial contractility reduced by 20--30%. Ligation of the interventricular artery on the background of cardiosclerosis induced cardiogenic shock in half of the animals. Cytochrome C does not reduce the diminution of myocardial contractility after ligation and has a marked antifibrillatory effect. Strophantin does not affect the diminution of contractility of a healthy myocardium but reduces the decrease in contractility of a sclerosed myocardium and also promotes the development of ventricular fibrillation following ligation of the interventricular artery.

Animals↗
PubMed2003

Abnormal myocardial contraction in alpha(1A)- and alpha(1B)-adrenoceptor double-knockout mice.

We used double-knockout mice (ABKO) lacking both predominant myocardial alpha(1)-adrenergic receptor (AR) subtypes (alpha(1A) and alpha(1B)) to determine if alpha(1)-ARs are required for normal myocardial contraction. Langendorff-perfused ABKO hearts had higher developed pressure than wild type (WT) hearts (123 +/- 3 mmHg n = 22 vs. 103 +/- 3 mmHg, n = 38, P < 0.001). Acutely inhibiting alpha(1)-ARs in WT hearts with prazosin did not increase pressure, suggesting that the increased pressure of ABKO hearts was mediated by long-term trophic effects on contraction rather than direct regulatory effects of alpha(1)-AR removal. Similar to perfused hearts, ABKO ventricular trabeculae had higher submaximal force at 2 mM extracellular [Ca(2+)] than WT (11.4 +/- 1.7 vs. 6.9 +/- 0.6 mN/mm(2), n = 8, P < 0.05); however, the peaks of fura-2 Ca(2+) transients were not different (0.79 +/- 0.11 vs. 0.75 +/- 0.16 microM, n = 10-12, P > 0.05), suggesting ABKO myocardium had increased myofilament Ca(2+)-sensitivity. This conclusion was supported by measuring the Ca(2+)-force relationship using tetanization. Increased myofilament Ca(2+)-sensitivity was not explained by intracellular pH, which did not differ between ABKO and WT (7.41 +/- 0.01 vs. 7.39 +/- 0.02, n = 4-6, P > 0.05; from BCECF fluorescence). However, ABKO displayed impaired troponin I phosphorylation, which may have played a role. In contrast to increased submaximal force, ABKO trabeculae had lower maximal force than WT at high extracellular [Ca(2+)] (29.6 +/- 1.9 vs. 37.6 +/- 1.4 mN/mm(2), n = 7, P < 0.01). However, peak cytosolic [Ca(2+)] was not different (1.13 +/- 0.15 vs. 1.19 +/- 0.04 microM, n = 6-7, P > 0.05), suggesting ABKO myocardium had impaired myofilament function. Finally, ABKO myocardium had decreased responsiveness to beta-AR stimulation. We conclude: alpha(1)-ARs are required for normal myocardial contraction; alpha(1)-ARs mediate long-term trophic effects on contraction; loss of alpha(1)-AR function causes some of the functional abnormalities that are also found in heart failure.

Animals↗
PubMed1987

Myocardial contraction band lesions in patients with fatal asthma: possible neurocardiologic mechanisms.

Myocardial contraction band necrosis (MCBN) occurs in catecholamine infusion, central nervous system stimulation, stress, and transient myocardial ischemia with reperfusion. In 4 of 13 children who died with asthma, MCBN was present, suggesting that this cardiac lesion may contribute to the deaths of some asthmatic patients. Two of the 4 patients who had MCBN had not received sympathomimetics intravenously or by an intracardiac route. Therefore, mechanisms other than infusions of large doses of catecholamines are probably involved in production of this cardiac lesion in asthmatics.

Adolescent↗
PubMed1979

[Correlation of the parameters of myocardial contraction and relaxation in compensatory cardiac hypertrophy].

The parameters of myocardial contraction and relaxation were determined from the left ventricular pressure curves obtained in closed chest rabbits. One month after the creation of ascending aorta stenosis when the relative weight of the left ventricle increased by 54% as compared to the control, systolic pressure was higher by 42% and maximum rate of pressure development by 47%. This increase corresponded to the degree of left ventricular hypertrophy so that the load on the unit of myocardial mass did not change. No changes were found in the contractility index. The index of relaxation, however, determined by the relation between the maximum rate of relaxation and the developed pressure and characterizing the function of the myocardial relaxation system was 20% lower than that of the control. This was associated with the decrease of the diastolic pause by 27%. The slowing down of relaxation is one of the first and must' signs of compensatory function of the heart.

Animals↗
PubMed1992

Action potential duration and endocardial modulation of myocardial contraction in the ferret.

OBJECTIVE: Endocardial endothelium releases substances which modulate myocardial contraction. Selective endocardial removal abbreviates contraction by removing a contraction prolonging substance "endocardin". The aim of the study was to investigate whether changes in action potential duration underlie these contractile effects. METHODS: The contractile effects of shortening the action potential were first characterised, using a potassium channel "opener" cromakalim (3 microM). Transmembrane action potentials were then recorded in isolated ferret papillary muscles before and after endocardial removal. RESULTS: Cromakalim-induced action potential abbreviation reduced contractile twitch duration. Endocardial removal itself however did not alter action potential duration. CONCLUSIONS: Endocardial modulation of cardiac contraction does not involve changes in action potential duration.

Action Potentials↗
PubMed1982

[Comparative characteristics of the force and rate of myocardial contraction as indices of its contractility].

Experiments on papillary muscles of the cat heart have shown that the strength of contraction is a more adequate and sensitive criterion for evaluation of the effects of temperature, distension and contraction rate on myocardial contractility as compared to the strength of contraction. It is concluded that at the basis of the Starling law and chronoinotropic mechanisms there lies the contractility control exercised through changes in the contraction rate.

Animals↗
PubMed1987

Effect of myocardial contraction on systolic coronary resistance in conscious dogs.

We studied the effect of cardiac contraction on systolic coronary resistance under the conditions of maximally dilated coronary resistance vessels in six conscious dogs. Subendocardial segment length in areas supplied by the left circumflex coronary artery, left ventricular pressure and left circumflex coronary artery flow were simultaneously measured. At 5 sec after release of the first 2 min of left circumflex coronary artery occlusion, diastolic coronary blood flow revealed its peak value in association with markedly depressed regional contractile function. With collateral development induced by repeated 2 min left circumflex coronary artery occlusions, segmental dysfunction during occlusion and early reperfusion was progressively attenuated. Before and after collateral development, diastolic coronary resistance at 5 sec of reperfusion remained unchanged, but systolic coronary resistance increased by 41% secondary to restoration of regional myocardial shortening. In each animal, normalized regional shortening correlated well with changes in systolic coronary resistance. The fraction of systolic coronary resistance due to active regional myocardial contraction was 52%. These studies demonstrate that when coronary vasomotor tone is abolished, regional myocardial contraction impedes the coronary systolic flow in proportion to the extent of shortening.

Animals↗
PubMed1996

Lack of inhibition by inhalational anesthetics of myocardial contraction dependent on intracellular sodium activity.

BACKGROUND: When cardiac muscle is stimulated at a high frequency after rest, the peak force increases rapidly at first and then slowly. The slow phase reflects Ca2+ accumulation dependent on an increase in intracellular Na+ activity. The positive inotropic effect of high concentrations of cardiac glycosides also involves Ca2+ accumulation dependent on an increase in intracellular Na+ activity. The effect of isoflurane on the component of myocardial contraction dependent on an increase in intracellular Na+ activity is not well understood. METHODS: The isometric force of rabbit papillary muscle contractions was measured. The authors studied the effects of isoflurane on the force increase that occurs when the muscles are stimulated after a rest and on the force increase induced by ouabain. RESULTS: Isoflurane (1.5%, 2.4%) had no statistically significant effect on the magnitude of the slow phase of force increase when the muscles were stimulated at 2 Hz after a rest. Isoflurane (1.5%) did not decrease the magnitude of force increase induced by ouabain (1 microM). CONCLUSIONS: Isoflurane has little effect on myocardial contractions that depend on Ca2+ accumulation after an increase in intracellular Na+ activity. This may partly account for the smaller cardiac depressant effect of isoflurane observed at high frequencies rather than at low frequencies. The results of the present study and an earlier study with halothane suggest that the lack of inhibition of contractions dependent on Ca2+ accumulation after an increase in intracellular Na+ activity may be a common property of inhalational anesthetics.

Anesthetics, Inhalation↗
PubMed1992

Mechanisms of transient augmentation of myocardial contraction after a brief coronary occlusion.

The purpose of this study was 1) to clarify whether augmented myocardial contraction after a brief coronary occlusion, i.e. post-ischemic hypercontraction, depends on a transient increase in coronary blood flow or preceding myocardial ischemia, and 2) to identify the role of catecholamines or calcium flux in this phenomenon. Sixteen mongrel dogs were examined in open-chest anesthetized condition. One-minute reperfusion after two-minute total coronary occlusion of the left anterior descending artery resulted in a transient increase in segment shortening. Intracoronary administration of adenosine caused hyperemia without any changes in segment shortening. Two minutes of total coronary occlusion with adenosine caused post-ischemic hypercontraction to the same degree, but without any additional hyperemia. Two minutes of partial occlusion with 75% flow reduction caused less post-ischemic hypercontraction. Post-ischemic hypercontraction did not occur after partial occlusion with 50% flow reduction, irrespective of hyperemia with adenosine during reperfusion. Propranolol or verapamil did not prevent this phenomenon. Thus, post-ischemic hypercontraction is not dependent on the transient increase in coronary blood flow, but is related to the preceding myocardial ischemia. Local release of catecholamines is not likely to be the cause. A calcium antagonist, verapamil, did not modify this phenomenon. The precise mechanism of this phenomenon is still uncertain, although some alterations in cellular hemostasis, such as ionic changes, are likely to be the cause.

Animals↗