[Characteristics of myocardial contraction in myocardial infarct].
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We had intended to reckon quantitatively the effects of volatile anaesthetics about myocardial contractility and coronary circulation, on rest and after total occlusion of the left circumflex coronary artery for 15 sec on young healthy mongrel dogs. Halothane decreases coronary flow of about 20% while Penthrane increase coronary flow (CF) of 30% after 20 sec and later it stabilizes to 10% higher than the control values. Ethrane causes a light initial decrease and later CF returns to control values. During occlusion, derivative of left ventricular pressure (LVP) is reduced from Halothane, which also causes a marked decrement of hyperemia. By means of penthranic anaesthesia, during occlusive phase, we observed a shortening in contraction and relaxation speed. Ethrane doesn't modify the hyperemic coronary flow nor cardiodynamic parameters during occlusive period, while the latter parameters are sensibly varying during restore.
Platelet-activating factor (PAF) is an important mediator of cardiovascular shock owing to immunologic reactions, including anaphylaxis and endotoxaemia. Previous studies have shown that PAF is a potent cardio-depressive agent causing a marked coronary constriction and a sustained impairment of myocardial contractility. In this study, we attempted to characterize further the prolonged PAF effects on coronary circulation and myocardial contractile force in isolated guinea pig hearts perfused at constant pressure (60 cm H2O) or constant flow which was adjusted to a level of 100% above basal flow. In addition, the PAF-induced changes of ventricular systolic and diastolic function were distinguished. In the hearts perfused at constant pressure, PAF induced a dose-dependent (0.57, 5.7, and 57 pmol/min) decrease of coronary flow rates, left ventricular pressure (LVP), LV contraction (peak positive dP/dt) and LV relaxation (peak negative dP/dt). The decrement of peak negative dP/dt was more pronounced than that of peak positive dP/dt. Maintenance of coronary flow rates only attenuated, but did not suppress, the PAF-induced ventricular malfunction, and it improved ventricular relaxation less than it did ventricular contraction. Pretreatment with the PAF antagonist WEB 2086 (19.7 nmol/min) almost completely abolished the effects of the highest PAF dose on coronary circulation and ventricular contractile parameters. We conclude that the cardiodepressive effects of PAF are due to coronary constriction and direct contractile events. Furthermore, PAF impairs ventricular diastolic function more than ventricular systolic function.
OBJECTIVES: The purpose of this study was to compare the diagnostic performances of Tl-201 single photon emission computed tomography (SPECT) and dobutamine stress cine magnetic resonance imaging (MRI) for predicting functional recovery of regional myocardial contraction in patients after myocardial infarction. METHODS: Twenty patients underwent Tl-201 SPECT and MRI 3-4 weeks after onset of myocardial infarction. Cine MR images were acquired in the resting state and during dobutamine stress. Tl-201 uptake and systolic wall thickening (SWT) on cine MRI were analyzed on short-axis images by using a 14-segment model. Follow-up cine MR images were obtained 187.1+/-33.5 days after onset. RESULTS: The averaged Tl-201 uptake in 54 segments with impaired SWT was 47%+/-20%, being significantly lower than that in 226 segments with preserved SWT (75%+/-18%; p<0.0001). The sensitivity, specificity, and accuracy of dobutamine MRI and Tl-201 SPECT for predicting preserved SWT after 6 months were 89% vs. 80%, not significant (NS); 89% vs. 72%, p<0.01; and 89% vs. 79%, NS, respectively. In the anterior wall and apex, the sensitivity and specificity of SPECT were not significantly different from those of MRI. In the inferior wall and posterolateral wall, however, the specificity of SPECT was substantially lower than that of MRI (53% vs. 88%, p<0.001), resulting in significantly lower accuracy (75% vs. 90%, p<0.01). CONCLUSIONS: Both SPECT and dobutamine MRI showed excellent sensitivity for predicting myocardial viability in all left ventricular segments. Decreased specificity of SPECT in the inferior and posterolateral segments resulted in lower overall specificity in comparison with dobutamine MRI.
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OBJECTIVES: This study sought to evaluate myocardial contraction fraction (MCF) as an index of myocardial shortening by comparison to conventional shortening indices in patients with hypertensive hypertrophy, athletes with physiologic hypertrophy and sedentary normal adult subjects. BACKGROUND: A significant percentage of patients with hypertensive hypertrophy have "normal" or "preserved" left ventricular (LV) systolic function by conventional echocardiographic measures whereas their systolic function is depressed when measured by the two-dimensional echocardiographic mid-wall shortening fraction (MWSF). A three-dimensional echocardiographic measure of myocardial shortening analogous to MWSF has been lacking. We describe a volumetric measure of myocardial shortening, the MCF, as the ratio of stroke volume (SV) to myocardial volume (MV), and hypothesize that it may be useful to compare myocardial performance in patients with different degrees and types of hypertrophy. METHODS: We compared the MCF using freehand three-dimensional echocardiographic reconstruction of the LV to conventional measures of LV function (ejection fraction [EF], endocardial shortening fraction [SF] and MWSF) in subjects with pathologic hypertensive hypertrophy, heart failure symptoms and preserved EF (n = 17), athletes with physiologic hypertrophy (n = 41) and normal sedentary adults (n = 80). RESULTS: The EF was in the normal range for all three groups. The MCF was lower in hypertensive hypertrophy compared with normal subjects (0.33 +/- 0.05 vs. 0.44 +/- 0.07, p < 0.01). It also successfully differentiated physiologic hypertrophy from normal subjects (0.50 +/- 0.05 vs. 0.44 +/- 0.07, p < 0.01). The endocardial SF did not distinguish athletes from normal subjects and the MWSF did not distinguish hypertensive from physiologic hypertrophy. CONCLUSIONS: The MCF, a volumetric measure of myocardial shortening, demonstrates that myocardial shortening is decreased in hypertensive hypertrophy and increased in physiologic hypertrophy. The MCF may be useful in assessing differences in myocardial performance in patients with similar degrees of hypertrophy.
BACKGROUND: Early epicardial vessel patency and tissue perfusion limit infarct size, improve survival and are crucial for optimum functional recovery of the ischaemic myocardium in patients with acute myocardial infarction (AMI). Coronary angiography has been considered the "gold standard" in assessment of reperfusion. Restoration of coronary patency is not a guarantee of myocardial cellular perfusion. ST-segment elevation resolution observed in electrocardiogram (ECG) early after initiation of primary PTCA could be potentially correlated with reperfusion. AIM: The aim of the study was the prospective assessment of left ventricular (LV) contractility recovery in patients after primary PTCA for AMI in 3 and 6 month follow-up according to early ST-segment elevation resolution analysis. METHODS: 111 consecutive patients (80 men and 31 women age 36-78) with AMI treated by successful primary PTCA (Thrombolysis in Myocardial Infarction grade 3 flow and residual stenosis less than 30%) within 12 h of chest pain onset were enrolled in the study. 12-lead ECG was performed on admission and 1 hour after the beginning of the PTCA. The patients were divided into 2 groups according to ST-segment elevation resolution in the ECG (> 50% depression of the elevated ST-segment) within 1 hour after the procedure. The mean pain-to-balloon time was not significantly different in both groups. In each patient, global ejection fraction (EF) and wall motion index (WMI) were derived immediately after primary PTCA and after 3 and 6 month follow-up. RESULTS: Of the 111 patients studied, 82 (68%) had early ST-segment resolution and 29 (32%) did not. Contractility disturbances of infarct related ventricular wall, evaluated by EF and WMI, were significantly higher in the group of patients without early ST-segment resolution immediately after primary PTCA. EF and WMI improved significantly after 3 and 6 months in the group of patients with improvement was insignificant ST-segment elevation resolution, while in the group without ST-segment resolution. CONCLUSIONS: 1. Presence of early ST segment elevation resolution after angiographically successful primary PTCA identifies patients who are more likely to benefit from the early restoration of flow in the infarct related artery. 2. TIMI measures greatly overestimate the success of primary PTCA; they only assess vessel patency, not myocardial cellular perfusion. 3. "Electrocardiographic reperfusion" provides a real-time physiologic marker of cellular perfusion and is a significant predictor of LV contractility recovery--more useful than angiographic reperfusion. 4. ST-segment monitoring is a reliable, non-invasive and inexpensive method to evaluate myocardial perfusion.
In dogs, pituitrin increases, and isadrin reduces, the tonicity of coronary arteries. Successive administration of the two agents to rabbits causes functional and metabolic unbalance of the heart, with resultant myocardial necrotic foci in the presence of blood hypercoagulation and heart muscle contractility disordered. The disorder of cardiomyocyte stereo architectonics is an essential element of the pathophysiologic mechanism of small-focal myocardial infarction.
Coupling of myocardial beta-, beta 1-, beta 2- and alpha-adrenoceptors (AR) to myocardial contraction was investigated in patients with various degrees of heart failure. With the use of delta Vcfc, a load independent parameter of myocardial contraction, AR mediated contraction was evaluated. beta-AR mediated contraction, delta Vcfc by infusion of a beta-AR agonist, isoproterenol, declined with the advancement of heart failure from 0.41 Circ/sec (NYHA I) to 0.31 (NYHA II), 0.22 (NYHA III) and 0.12 (NYHA IV). Dobutamine, a beta 1-AR full agonist, mediated delta Vcfc was 92-97% of that of isoproterenol. On the other hand, terbutaline sulfate, a full agonist to beta 2-AR, increased delta Vcfc partially in comparison with isoproterenol; 51% in NYHA I, 52% in NYHA II, 36% in NYHA III and 17% in NYHA IV. An alpha 1-AR agonist, methoxamine had little effect on myocardial contractility beta-AR and alpha-AR densities were analyzed by saturation binding isotherms of myocardial membrane fraction with 125I-Iodocyanopindolol (ICYP) and 3H-Bunazosin, respectively. beta-1 and beta 2-ARs were separated by competition binding of 125ICYP with a highly selective beta 1 AR antagonist, CGP20712A. There was a progressive down regulation of beta, beta 1- and beta 2-ARs with the advancement of heart failure. A new index was used to examine coupling of ARs to myocardial contraction; Coupling Index. The index was slightly decreased in NYHA II in beta- and beta 1-ARs. In beta 2-AR, the coupling index declined as heart failure advanced from NYHA I to NYHA IV.(ABSTRACT TRUNCATED AT 250 WORDS)
Myocardial contraction behaves heterogeneously, being greater in subendocardial than in subepicardial layers. Similarly, during acute myocardial ischemia or infarction, the subendocardium is the first myocardial layer to suffer. Conventional two-dimensional echocardiography cannot distinguish the transmural extension of myocardial ischemia or infarction, showing akinesia also when only the subendocardium is affected. Novel ultrasonographic techniques (like tissue characterization with integrated backscatter or Doppler tissue imaging) and nuclear magnetic resonance tagging can investigate myocardial contraction in different transmural layers and distinguish subendocardial from transmural ischemia or infarction. With the advent of thrombolysis and primary angioplasty in the acute phase of myocardial infarction a correct diagnosis of the extension of myocardial necrosis cannot ignore its transmural wavefront development. The salvage of the subepicardial layer does not give direct information on overall myocardial thickening but is one of the major determinants of overall left ventricular dysfunction and size. Although it is still necessary to investigate this phenomenon, new ultrasonographic techniques give us important information and more opportunities to appropriate diagnosis and future treatment of cardiac patients.
The study measured cardiac output and assessed regional myocardial contraction in 14 patients with anorexia nervosa, some of whom also had bulimia, and in 15 controls. The experimental and control groups were not significantly different in age or body surface area (p = greater than 0.05). To evaluate regional myocardial contraction, 12 of 14 anorexia nervosa-bulimia (ANB) patients were studied in the acute phase and once serially at a mean interval of 1.5 years by assessing the movement of each left ventricular wall segment toward the center of the ventricle as imaged in the precordial short axis. Cardiac output was measured in the ascending aorta by pulsed Doppler for control subjects and for 13 ANB patients. Regional myocardial contraction was normal for all controls, but eight of 14 ANB patients showed regional myocardial contraction abnormalities. Between studies, four of these eight demonstrated improved regional myocardial contraction, three remained unchanged, and one was worse. Mean cardiac output was markedly reduced in ANB patients (2.6 L/min) compared to controls (4.5 L/min) (p = less than 0.001). The low cardiac output in ANB patients was reflected as reduced mean ascending aortic velocity/second (18.5 cm/s) compared to a mean of 22.8 cm/s for controls (p = less than 0.02). Mean ascending aortic area was slightly smaller for ANP patients. Mean peak ascending aortic velocity was significantly lower in ANB patients than in controls (p = less than 0.02). Mitral valve prolapse was seen during at least one examination in seven of 14 ANB patients (0/15 controls) and disappeared in two of three patients following hydration.(ABSTRACT TRUNCATED AT 250 WORDS)
During augmentation of frequency of contractions or Ca2+ perfusate concentration the velocity of isotonic relaxation increased much more than the velocity or amplitude of contraction. The phenomenon of predominant activation of relaxation ( PPAR ) was less prominent at decreased Ca2+ concentration acidosis (pH 6,85), under action of calmodulin inhibitor, trifluoperazine, or replacement of Ca2+ ions by Sr2+. Diminution of Na2+ concentration to 25 mM was followed by apparent signs of cellular Ca2+--overload and elimination of PPAR . The results coincide with the suggestion that PPAR is caused by activation of calmodulin-dependent Ca2+ removal from the myoplasma and myofibrils.
Nitric oxide (NO) produced by myocardial nitric oxide synthase has been implicated as a modulator of myocardial contraction [correction of contracion]. This paper reviewed the reports on myocardial contraction modulated by NO, its mechanism, and regulation of expression and activity of iNOS. NO was recently shown to produce biphasic contractile [correction of contratile] effects on myocardium: augmentation at low levels and depression at high levels. The up-regulation of inducible nitric oxide synthase (iNOS) often negatively modulates myocardial function.
There were many studies concerning the evaluation of regional wall motion in ischemic heart disease by left ventriculography (LVG) and two-dimensional echocardiography (2DE), but only a few observations on the regional myocardial thickening have been reported. In a survey of 48 cases of old myocardial infarction, we selected 21 cases with adequate 2DE images for the evaluation of regional wall motion and thickening. In all cases the 2DE examinations were performed within seven days before or after LVG examinations. The left ventricular wall on 2DE was divided into 11 segments and wall motion and thickening in each segment were graded to three classes, i.e. none, reduced and normal. The results on 2DE were then compared with the grade of wall motion of the corresponding segment on LVG. The sensitivity and specificity of 2DE wall motion were 50% and 89% in none, 59% and 48% in reduced, and 89% and 84% in normal, respectively. The sensitivity and specificity of 2DE myocardial thickening were 81% and 93% in none, 82% and 70% in reduced, and 92% in normal, respectively. These results indicated that the regional myocardial thickening by 2DE has a higher sensitivity and specificity. Therefore, observation of both myocardial thickening and wall motion will be necessary for the proper evaluation of regional myocardial contraction in ischemic heart disease.
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Guinea pig papillary muscles were used to study the activation of myocardial contractions under depolarizing conditions. Depolarization promoted by TKBa (normal Tyrode solution containing KCl and BaCl2) and TKAdr (normal Tyrode solution containing KCl and adrenaline) inactivates the fast Na current and under these conditions only slow responses are available to activate contractions. Since the slow response is sensitive to changes in rate and rhythm, we searched for mechanical correlates using isometrically contracting preparations to study the force-frequency relationship as well as rest potentiation. We also investigated if contractions are dependent only on the slow response or if the complete action potential plays a special role in the activation of contractions. We conclude that the slow response is the main mechanism for the activation of myocardial contraction, because complete mechanical activation was observed under depolarizing conditions. However, the electrical behavior of the slow response is reflected in the mechanical behavior of the depolarized preparations. At high rates, disturbances of excitation occur in depolarized cells and contractions appear to be bigeminal or with 2:1 block. Furthermore, after long pauses, post-rest contractions are depressed and increase progressively with repetitive stimulation, probably due to changes in the latency and threshold of the slow response. The complete action potential also plays a role in the activation of myocardial contractions which is necessary for the resting potentiation phenomena and also to avoid the larger depression of the rest contractions that can be seen in depolarized muscles when the pause is prolonged. This behavior seems to be related to the decrease of intracellular Na concentration produced by the inhibition of the fast inward Na-current.
Myocardial relaxation at the diastolic phase was not evaluated by multi-gated myocardial SPECT, although myocardial contraction at the systolic phase was studied by percent wall thickening and Bull's eye methods. We make out a myocardial volume curve and report to evaluate the myocardial relaxation using multi-gated myocardial SPECT. The study population consisted of 3 normal human subjects (3 male, 32-37 years old), 10 idiopathic cardiomyopathy, 10 coronary artery disease and 1 hypertensive heart disease combined with aortic regurgitation. All cases were injected 555 MBq of 99mTc-tetrofosmin (Amersham Healthcare Corporation) intravenously at rest. A triple detector gamma-camera (GCA-9300A, Toshiba Medical, Japan) and a data processing computer (GMS-5500A, Toshiba Medical, Japan) were used in this study. A cardiac cycle (R-R interval) was divided by 16 frames (50-80 msec per 1 frame). Eight myocardial volume curves were calculated at the anterior wall, apex and inferior wall of the vertical long axis view and were calculated at the septal wall, apex and lateral wall of the horizontal long axis view, respectively. The patterns of the myocardial volume curves were classified into 5 patterns (Normal pattern (N), Delayed Contraction pattern (DC), Delayed Relaxation pattern (DR), Mixed pattern (M) and Normal pattern with Decreased amplitude (ND)). Myocardial uptake was evaluated visually of grading into severe hypertrophy (5), hypertrophy (4), normal (3), mild hypoperfusion (2), hypoperfusion (1) and perfusion defect (0). We compared patterns of the myocardial volume curves to myocardial uptake in the same segments. It was possible to detect myocardial edge of the total 16 frames with 50-60% threshold in the normal volunteer and in patients with hypertrophic cardiomyopathy and to make a myocardial volume curve. The region of the severe myocardial perfusion defect could be detected with 20% threshold in patients with old myocardial infarction. In comparison with myocardial volume curves and myocardial uptake, 74.6% in the N pattern had a normal uptake (3), 66.7% in the ND pattern had a normal uptake (3), 61.5% in the DC pattern had a hypoperfusion segment (0, 1 or fill-in to normal uptake), 44.4% in the DR pattern had a hypertrophic segment (4, 5 or fill-in to increased uptake). The pattern of myocardial volume curve indicates myocardial contractility and relaxation in each myocardial segment.