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PubMed2001

Intracellular mechanisms of cGMP-mediated regulation of myocardial contraction.

The intracellular mechanisms of cGMP, a major intracellular mediator of nitric oxide that regulates the contractility of cardiac muscle, are still to some extent unknown. To investigate these mechanisms, we observed the effects of 8-bromo-cyclic GMP (8br-cGMP) on myofibrillar Ca2+ sensitivity and Ca2+ handling of the sarcoplasmic reticulum (SR) using beta-escin-skinned preparations from Wistar rat hearts. Both low (1 microM) and high doses (100 microM) of 8br-cGMP significantly decreased the myofibrillar Ca2+ sensitivity obtained from pCa-tension relationships to a similar extent (pCa50; from 6.04 to 5.95 by 1 microM 8br-cGMP and 6.00 to 5.89 by 100 microM 8br-cGMP, respectively, n = 9 each). Whereas this Ca2+ desensitization induced by 100 microM 8br-cGMP was blocked by 1 microM KT5823, a specific inhibitor of cGMP-dependent protein kinase (PKG), not induced by 1 microM 8br-cGMP was not effected by KT5823. When the amount of Ca2+ released from the SR was estimated by the peak amplitude of 25 mM caffeine-induced contractions after constant Ca2+-loading by pCa 6, both doses of 8br-cGMP significantly augmented the caffeine-induced peak force to a similar extent (125 +/- 5.8% by 1 microM 8br-cGMP and 116 +/- 5.1% by 100 microM 8br-cGMP, respectively, n = 6 each). The two observed effects of cGMP (a decrease in myofibrillar Ca2+ sensitivity and an increase in Ca2+ uptake by the SR) may participate in regulating myocardial contraction via nitric oxide. Low and high doses of cGMP seem to work mainly via PKG-independent and PKG-dependent pathways, respectively.

Alkaloids↗
PubMedDate not supplied

Variations in myocardial contraction sequence under various hypoxic conditions.

Hypokinetic myocardial segment motion is observed in various pathophysiologic conditions. The aim of this study was to clarify the mechanisms involved in differences in segment motion of hypokinesis. Nineteen open-chest dogs were studied with regard to myocardial segment length, left ventricular pressure, and internal minor-axis diameter. Sequential instantaneous myocardial elastance [alpha(t) curve] was calculated under 4 different hypoxic conditions: complete coronary occlusion and reperfusion, partial coronary occlusion, coronary microembolization, and anoxic perfusion. The alpha(t) curve peaked at end-systole in the case of normal contraction; but it was almost totally flat when complete bulging occurred. The hypokinesis which occurred during development of the complete systolic bulge immediately after complete coronary occlusion had an earlier alpha(t) peak curve than the hypokinesis resulting from partial coronary stenosis (209.5 +/- 35.6 ms after end-diastole vs. 261.9 +/- 18.2 ms; p less than 0.02), microsphere injection into the coronary artery (243.2 +/- 24.5 ms vs. 289.3 +/- 15.4 ms; p less than 0.05), or anoxic perfusion (213.4 +/- 40.2 vs. 275.6 +/- 28.3 ms; p less than 0.05). The early alpha(t) peak resulted in a late-systolic bulge in segment length motion. In conclusion, hypokinetic segment motion differed depending on whether the coronary blood flow was present or not. A late-systolic bulge only developed immediately after complete coronary occlusion, and resulted from an abrupt decrease in myocardial stiffness during the cardiac cycle, which is closely related to the abrupt cessation of coronary blood flow.

Animals↗
PubMed1978

Correlation of systolic time interval with abnormal myocardial contraction by coronary occlusion in anesthetized open-chest dogs.

The correlation between the systolic time interval and abnormal contraction in ischemic myocardium was studied in anesthetized open-chest dogs. A strain-gauge was sutured on the surface of the left ventricular wall perfused by the left anterior descending coronary artery (LAD) for measuring segment-length. The left ventricular stroke volume decreased progressively after occlusion of LAD. The left ventricular ejection time (LVET) was progressively shortened in close correlation with the elongation of segment-length at the onset of isometric relaxation in 20 seconds after LAD occlusion when early systolic myocardial contraction and isometric contraction time (ICT) were not affected. ICT was gradually prolonged and closely related with the lengthening of the early systolic segment-length, while LVET recovered toward the control level in spite of further decrease in stroke volume. A close relationship was observed between ICT/LVET and stroke volume (gamma = 0.76, P less than 0.01). The results suggested the possibility that LVET was normalized even when the left ventricular function was impaired, and ICT/LVET ratio was the most sensitive index of LV dysfunction.

Animals↗
PubMed1993

Changes in myocardial contraction patterns in response to regional ischemia and sympathetic nerve stimulation.

We studied the effect of inferior cardiac nerve stimulation on global and regional left ventricular function before and after circumflex coronary arterial (CFX) occlusion in 12 pentobarbital-anesthetized cats. Regional function was evaluated by orthogonal sonomicrometry in the anterior midwall of the left ventricle and by two-dimensional short-axis echocardiography. CFX occlusion provoked hypokinesis in the nonischemic free wall adjacent to the dyskinetic ischemic region (17.6 +/- 2.3 vs. 34.6 +/- 2.2% preocclusion wall thickening; P < 0.01) and gradually improved systolic wall thickening toward the contralateral remote region, where the maximal hyperkinetic response was measured (52.9 +/- 4.4 vs. 32.5 +/- 3.3% preocclusion wall thickening; P < 0.001). In the anterior wall, remote region, hyperkinesis was predominant in longitudinal segments (8.1 +/- 0.8 vs. 2.3 +/- 0.6% preocclusion ejection shortening; P < 0.001) and slight in circumferential segments (11.0 +/- 0.7 vs. 9.1 +/- 0.6% preocclusion ejection shortening; P < 0.01). The postocclusion systolic wall thickening and segment-shortening pattern were not modified by sympathetic nerve stimulation, which increased cardiac output less after coronary occlusion, although contractility (dP/dt) increased markedly. In conclusion, the myocardial contraction pattern in ischemic and nonischemic regions after CFX occlusion is not much modified by sympathetic cardiac nerve stimulation.

Animals↗
PubMed1991

Echocardiographic demonstration of decreased left ventricular dimensions and vigorous myocardial contraction during syncope induced by head-up tilt.

Two-dimensional echocardiography was performed during a head-up tilt test in 11 control subjects (group I) and 18 patients with recurrent unexplained syncope. In four patients (group II), the head-up tilt test was negative at baseline and after isoproterenol infusion. Syncope was induced during baseline head-up tilt in nine patients (group III) and after isoproterenol challenge in five (group IV). The echocardiographic variables assessed were left ventricular end-systolic and end-diastolic areas and percent fractional shortening. At the end of head-up tilt, end-systolic area decreased by 4.5 +/- 1.3 and 3.0 +/- 1.2 cm2 in groups III and IV, respectively, compared with 0.5 +/- 0.7 and 0.2 +/- 0.1 cm2 in groups I and II, respectively (p less than 0.04). Similarly, end-diastolic area decreased by 5.5 +/- 2.6 cm2 in group III compared with 2.7 +/- 1.9 and 1.75 +/- 0.4 cm2 in group I and II, respectively (p less than 0.04). Additionally, at the end of the baseline study, fractional shortening was significantly greater in group III and group IV (43 +/- 5%) than in groups I and II (p less than 0.01). In conclusion, syncope induced by head-up tilt is associated with vigorous myocardial contraction and a significant decrease in left ventricular end-systolic dimensions. This left ventricular hypercontractility may play an important role in the pathogenesis of syncope induced by head-up tilt.

Adult↗
PubMed1996

Excessive myocardial contraction in vasovagal syncope demonstrated by echocardiography during head-up tilt test.

The purpose of this study was to gain insight into the mechanism of vasovagal syncope and to test the efficacy of theophylline to prevent syncope. Twenty-six patients with vasovagal syncope underwent two-dimensional echocardiography and theophylline test during head-up tilt test. A standard parasternal short-axis view of echocardiography at the level of the papillary muscle was recorded to measure fraction shorting of the left ventricle, and left ventricular end-diastolic and end-systolic dimensions. Heart rate, blood pressure, and symptoms were recorded. There were three groups; Group 1: no syncope with and without isoproterenol (n = 5); Group 2: syncope only after the infusion of isoproterenol (n = 16); Group 3: syncope without isoproterenol (n = 5). Groups 2 and 3 proceeded to theophylline injection (250 mg). The study showed that the 80 degrees tilt induced an increase in heart rate of 6.6 +/- 4.0, 12.4 +/- 6.6, and 25.4 +/- 4.5 beats/min in Groups 1, 2, and 3, respectively (p < 0.05 in Groups 1 and 2, p < 0.05 in Groups 1 and 3). The addition of isoproterenol during posture change from supine to an 80 degrees tilt made the significant change of fractional shortening from 0.4 +/- 5% to 6 +/- 13% in Group 2 (p = 0.05), compared with no significant change in Group 1. There were no significant differences in left ventricular end-diastolic dimension and end-systolic dimension in each group between baseline and isoproterenol infusion during posture change. Vasovagal syncope was associated with vigorous myocardial contraction, rather than with contraction against an empty left ventricle. The acute loading of theophylline was not effective in preventing vasovagal syncope.

Adrenergic beta-Agonists↗
PubMed2000

Tissue Doppler imaging consistently detects myocardial contraction and relaxation abnormalities, irrespective of cardiac hypertrophy, in a transgenic rabbit model of human hypertrophic cardiomyopathy.

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is diagnosed clinically by the presence of left ventricular hypertrophy (LVH). However, LVH is absent in a significant number of genotype-positive patients. Because myocyte dysfunction and disarray are the primary abnormalities in HCM, we reasoned that tissue Doppler imaging could identify contraction and relaxation abnormalities, irrespective of hypertrophy, in a transgenic rabbit model of human HCM. METHODS AND RESULTS: M-mode, 2D, Doppler echocardiography and tissue Doppler imaging were performed in nontransgenic (n=24), wild-type beta-myosin heavy chain-arginine(403) (n=14), and mutant beta-myosin heavy chain-glutamic acid(403) (n=24) transgenic rabbits. Mean septal thicknesses were 2.0+/-0.3, 2.0+/-0.25, and 2.75+/-0.3 mm in the 3 groups, respectively (P:=0.001). LVH was absent in 9 of the 24 mutant rabbits. Left ventricular dimensions, systolic function, heart rate, mitral inflow velocities, and time intervals were similar in the groups. However, the difference between atrial reversal and transmitral A wave duration was increased in the mutant rabbits (P:<0.001). More importantly, systolic and early diastolic tissue Doppler velocities were significantly lower in all mutant rabbits (7.45+/-2.2 versus 10.8+/-2.3 cm/s in nontransgenic and 9. 0+/-0.76 cm/s in wild-type; P:<0.001), including the 9 without LVH. A systolic velocity <8.5 cm/s had an 86% sensitivity and 100% specificity in identifying the mutant transgenic rabbits. CONCLUSIONS: Myocardial contraction and relaxation were reduced in the mutant beta-myosin heavy chain-glutamic acid(403) transgenic rabbit model of human HCM, irrespective of the presence or absence of LVH. In addition, tissue Doppler imaging is more sensitive than conventional echocardiography for HCM screening.

Analysis of Variance↗
PubMed2002

Study of the myocardial contraction and relaxation velocities through Doppler tissue imaging echocardiography: A new alternative in the assessment of the segmental ventricular function.

OBJECTIVE: Doppler tissue imaging (DTI) enables the study of the velocity of contraction and relaxation of myocardial segments. We established standards for the peak velocity of the different myocardial segments of the left ventricle in systole and diastole, and correlated them with the electrocardiogram. METHODS: We studied 35 healthy individuals (27 were male) with ages ranging from 12 to 59 years (32.9 plus minus 10.6). Systolic and diastolic peak velocities were assessed by Doppler tissue imaging in 12 segments of the left ventricle, establishing their mean values and the temporal correlation with the cardiac cycle. RESULTS: The means (and standard deviation) of the peak velocities in the basal, medial, and apical regions (of the septal, anterior, lateral, and posterior left ventricle walls) were respectively, in cm/s, 7.35(1.64), 5.26(1.88), and 3.33(1.58) in systole and 10.56(2.34), 7.92(2.37), and 3.98(1.64) in diastole. The mean time in which systolic peak velocity was recorded was 131.59ms (+/- 19.12ms), and diastolic was 459.18ms (+/- 18.13ms) based on the peak of the R wave of the electrocardiogram. CONCLUSION: In healthy individuals, maximum left ventricle segment velocities decreased from the bases to the ventricular apex, with certain proportionality between contraction and relaxation (P<0.05). The use of Doppler tissue imaging may be very helpful in detecting early alterations in ventricular contraction and relaxation.

Adolescent↗
PubMed1989

[Atherosclerotic lesions of the coronary arteries in acute myocardial infarction: effects on myocardial contraction, disease course and prognosis].

Coronary arterial affection (CAA) is an objective indicator, closely related to cardiac contractility as well as clinical severity and immediate prognosis of myocardial infarction. The progress of CAA is associated with more pronounced disorders of cardiac contractility, higher rates of severe complications and less optimistic immediate prognosis. Long-term prognosis is not affected by the magnitude of CAA in postmyocardial-infarction patients.

Adult↗
PubMed1988

[Myocardial contraction and relaxation in a regimen with a physiological loading sequence].

A regimen imitating the intact heart loads revealed independence of the terminal-systolic strength of the trajectory of shortening in the isolated myocardium, the strength being determined by the terminal-systolic length of the preparation, the latter being also the mechanical determinant of velocity of the relaxation isometric phase. The heterometric relaxation portion revealed within the distension phase, depended on the distension velocity, diastolic rigidity and the terminal-systolic length. The experimental possibilities of the regimen are discussed.

Animals↗
PubMed2005

Late gadolinium-enhanced magnetic resonance imaging in acute and chronic myocardial infarction. Improved prediction of regional myocardial contraction in the chronic state by measuring thickness of nonenhanced myocardium.

OBJECTIVES: We sought to determine serial changes of enhanced and nonenhanced tissue on late gadolinium-enhanced cardiac magnetic resonance (CMR) imaging in patients with a myocardial infarction (MI) and to assess whether thickness of nonenhanced myocardium can improve the detection of preserved contractile function in the chronic state. BACKGROUND: Previous studies demonstrated that enhancement on late gadolinium-enhanced CMR images indicates myocardial necrosis, and nonenhancement shows the presence of viable myocardium. METHODS: The CMR studies were performed within one week (scan 1) and more than five months (scan 2) after the onset of MI in 18 patients. The area and mean thickness of enhanced tissue and nonenhanced myocardium were measured by using a 30-segment model. Systolic wall thickening on cine CMR at scan 2 was assessed for evaluating regional contractile function. RESULTS: The amount of enhanced tissue significantly decreased from scan 1 to 2 (22.1 +/- 14.0 ml vs. 15.0 +/- 9.3 ml, p < 0.001). The averaged thickness of nonenhanced myocardium in the infarct segments significantly increased from scan 1 to 2 (5.2 +/- 3.0 mm vs. 6.6 +/- 3.2 mm, p < 0.001). Receiver operating characteristic analysis demonstrated that the measurement of thickness of nonenhanced myocardium, compared with measurement of percent transmural enhancement, had better diagnostic accuracy for predicting improved systolic wall thickening form scan 1 to 2 in dysfunctional segments (Az 0.650 vs. 0.594, p < 0.05). CONCLUSIONS: The amounts of enhanced tissue and nonenhanced myocardium significantly altered from the acute to chronic state in MI patients. The diagnostic performance of CMR imaging for detection of preserved contractile function can be significantly improved by measuring thickness of nonenhanced myocardium in MI patients.

Aged↗
PubMed1999

Can power motion imaging mode combined with contrast agent assess myocardial contraction and perfusion? In vitro and in vivo studies.

Power motion imaging (PMI) is a new Doppler imaging technology that can enhance contrast agent visualization. We hypothesized that PMI combined with Albunex injection (CPMI) could provide new insights into myocardial contractility and perfusion. In a first step, PMI signal was studied with an in vitro phantom. In a second step, PMI signal was studied in 10 rabbits at different workloads. In a third step, 10 rabbits were studied before and after ischemia produced by coronary ligation and finally during reperfusion. During the latter protocol, epicardial echocardiography analyzed by PMI and fundamental mode was performed before and after Albunex injection. PMI signal was well correlated with phantom velocity. PMI signal and myocardial wall thickening were well correlated, particularly in the septal area. On the coronary occlusion model, ischemia was associated with a significant decrease in PMI and CPMI signals, whereas reperfusion was associated with a significant decrease in PMI signals only, indicating stunning. We conclude that PMI combined with CPMI is a powerful tool to assess myocardial contractility and perfusion.

Albumins↗
PubMed1982

[Evaluation of early coronary artery reconstruction in acute myocardial infarction--time limit in the therapeutic effectiveness in relation to restoration of localized myocardial contraction].

The effects of 1 hour, 3 hours and 10 days coronary artery reperfusion after 20 minutes, 40 minutes, 3 hours, 4 hours and 5 hours coronary artery occlusion on the contractility of myocardium was studied by the strain gauge arch, and the myocardial changes was also studied histologically. Results obtained were follows. In the short term reperfusion study: 1) Dyskinesis disappeared in all cases if reperfusion was begun after 20 minutes of ischemia. 2) Dyskinesis remained in all cases if reperfusion was begun after 40 minutes of ischemia. In the long term reperfusion study: 3) Dyskinesis disappeared in all cases after 10 days reperfusion with 3 and 4 hours ischemia groups, and the recovery of myocardial contractility was good. 4) Dyskinesis remained in 2 of 5 dogs with 5 hours coronary occulusion even after 10 days of reperfusion, and the recovery of myocardial contractility in 3 of 5 dogs with this group was poor. It is concluded that revascularization of myocardium that has been kept ischemia for less than 4 hours may lead to disappearance of dyskinesis and recovery of myocardial contractility. These findings also indicate that early coronary revascularization does not always provide an immediate recovery of dyskinesis of the revascularized area.

Animals↗