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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We estimated the magnitude of the left atrial contraction in 28 patients with ischemic heart disease by calculating the biplane cineangiographic volumes of the left atrium. The left atrial contraction contribution to the left ventricular stroke volume (ml/m2, Y axis) correlated inversely with the left ventricular ejection fraction (%, X axis), yielding an equation: Y = -0.31X + 43.7 (n = 28, r = -0.56, p less than 0.001). The result indicates that the left ventricular filling is compensated by the augmented atrial contraction in case of impaired left ventricular function. We defined the left atrial volume at the beginning of the atrial contraction (LAVd, ml/m2) as the "preload" of the left atrium, and we also defined the volume expelled by the active atrial contraction (delta LAVa, ml/m2) as the stroke volume of the left atrium. The stroke volume (Y) correlated positively with the "preload" (X), yielding an equation: Y = 0.48X - 1.3 (n = 28, r = 0.80, p less than 0.001). We then defined the left ventricular end-diastolic pressure, the peak of the a-wave, as the "afterload" of the left atrium, and we studied the "afterload"-stroke volume relations in the left atrium. However as expected, a reasonable relationship between them was difficult to form. Consequently, we showed that an increase in the "preload" of the left atrium augmented the stroke volume of the left atrium, which means that Frank-Starling mechanism is operative in the left atrium.
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PMID:Study on left atrial contractile performance--participation of Frank-Starling mechanism. 369 63

To characterize the hemodynamic changes during recovery after upright bicycle exercise, 56 normal subjects (group I) and 30 patients with documented myocardial ischemia (group II) were studied. Heart rate, blood pressure and radionuclide angiographically determined absolute left ventricular (LV) volumes were measured at baseline, peak exercise and 2 to 4.5 minutes and 4.5 to 7 minutes after upright bicycle exercise. Whereas ejection fraction and end-systolic volume responses at peak exercise differed between groups I and II, these parameters showed similar trends in both groups during recovery. Mean ejection fraction increased during 2 to 4.5 minutes in both groups, but remained elevated during 4.5 to 7 minutes only in normal subjects (group I). Elevation of cardiac output after exercise was accounted for predominantly by increased heart rate rather than increased stroke volume. Despite significantly decreased end-diastolic volume during recovery, stroke volume was maintained in both groups by a substantial decrease in end-systolic volume, suggesting the impact of decreased afterload or increased sympathetic tone during recovery. Thus, the Frank-Starling mechanism does not appear to be playing a major role during recovery after upright bicycle exercise, whereas enhanced contractility is evident in both normal subjects and patients with documented myocardial ischemia.
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PMID:Changes in left ventricular function during recovery from upright bicycle exercise in normal persons and patients with coronary artery disease. 373 12

We examined the influence of left ventricular end-diastolic pressure (LVEDP) on the mechanical interaction between ischemic and nonischemic areas during acute myocardial ischemia. Circumferentially oriented ultrasonic segment gauges were implanted in the midwall of the anterior apex and posterior apex of the left ventricle in seven anesthetized dogs. Stroke volume was measured with a flow probe around the ascending aorta in five of these animals. We varied LVEDP with vena caval occlusion and dextran infusions to three matched levels (7, 12, and 19 mm Hg) before and 30 min after complete occlusion of the mid left anterior descending coronary artery. With acute ischemia, the anterior apex or ischemic zone demonstrated marked segmental lengthening during isovolumetric systole (end-diastole to aortic valve opening) and akinesis during the ejection phase (aortic valve opening to closure). In the posterior apex or nonischemic area, isovolumetric shortening increased and ejection phase shortening decreased during acute ischemia when compared with those under control conditions at the same LVEDP. Thus, a portion of the shortening generated by the nonischemic area was expended in stretching the ischemic zone during isovolumetric systole, thereby reducing the amount of ejection phase shortening. As LVEDP was increased, there was a parallel decrease in both the amount of isovolumetric lengthening in the ischemic zone and the isovolumetric shortening in the nonischemic area. As a result, acute ischemia produced less of a reduction in ejection phase shortening in the nonischemic area and in stroke volume at high as compared with low LVEDP. We conclude that the ischemic zone imposes a mechanical disadvantage on the nonischemic area, the magnitude of which is directly proportional to the amount of isovolumetric lengthening or bulge in the ischemic zone. An increase in LVEDP during acute ischemia improves regional and global ventricular function by both the Frank-Starling mechanism in the nonischemic (but not the ischemic) area and by reducing the mechanical disadvantage that the ischemic zone imposes on the nonischemic area.
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PMID:Mechanisms of improving regional and global ventricular function by preload alterations during acute ischemia in the canine left ventricle. 404

In order to elucidate the hemodynamic significance of exercise-induced ST-segment shifts in ischemic heart disease, left ventricular cineangiography was carried out in 41 patients at rest and during supine bicycle ergometer exercise. These patients were divided into 2 groups, that is, a normal coronary artery group (6 patients), having neither significant coronary artery stenosis nor exercise-induced ST-segment shifts, and a diseased group (35 patients) having significant coronary artery stenosis (inner-diameter stenosis greater than or equal to 75%). The latter was further divided into 3 subgroups according to exercise-induced ST-segment shifts: ST-unchanged group (17 patients), ST-depression group (11 patients) and ST-elevation group (7 patients). In the normal coronary artery and ST-unchanged groups, exercise produced an increase in left ventricular end-diastolic volume index (LVEDVI), a decrease in left ventricular end-systolic volume index (LVESVI) and increases in stroke index and ejection fraction. In the ST-depression group, the appearance or aggravation of left ventricular wall motion abnormality was induced at the site of coronary artery stenosis by exercise in 9 patients. Both LVEDVI and LVESVI increased, stroke index remained unchanged, and ejection fraction decreased during exercise. In the ST-elevation group, ST-segment elevation was induced in leads with abnormal Q waves. In 2 patients, exercise induced aggravation of wall motion abnormality at the infarctional segment. LVESVI increased, but LVEDVI showed little increase, and stroke index and ejection fraction tended to decrease during exercise. In the ST-depression group, exercise-induced left ventricular pump dysfunction was due to lowered contractility (increased LVESVI) caused by transient myocardial ischemia. In the ST-elevation group, exercise-induced pump dysfunction was mainly due to lowered contractility, and in some of them, the findings suggested that transient myocardial ischemia at or around the region of infarction might be the cause of pump dysfunction. In addition, a poor compensatory effect of the Frank-Starling mechanism seemed to play a role in the onset of such dysfunction in this group.
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PMID:Hemodynamic evaluation of exercise-induced ST-segment depression and elevation in ischemic heart disease. Left ventricular cineangiography during exercise. 666 58

Myocardial infarction accounts for over 50 per cent of mortality following elective abdominal aortic surgery. Previous history of ischaemic heart disease and abnormal ECGs, common in vascular patients, are unreliable parameters for predicting myocardial response to stress. Exercise ECGs are often valueless, as claudication may mask myocardial insufficiency. Myocardial performance was studied preoperatively in 29 consecutive patients undergoing elective aortic bifurcation grafting, using a Swann-Ganz catheter to measure the rise in pulmonary artery wedge pressure (PAWP) produced by rapid intravenous infusion of plasma (200-400 ml). A Frank-Starling Curve was obtained by plotting LVSWI against PAWP. Two important values were obtained: (a) 'Upslope' or gradient of the ascending portion of the curve. Low values identify patients most at risk from cardiac complications. Six patients who suffered from postoperative cardiac complications had a mean 'upslope' value of 1.568 +/- 0.681 (1 s.e.m.), whereas the 23 who did not, had a mean value of 7.094 +/- 0.745 (1 s.e.m.), a significant difference (P less than 0.001); (b) 'PAWPmax', the ventricular filling pressure above which work output dropped. Infusion beyond this may precipitate pulmonary oedema. PAWP was observed at levels greater than PAWPmax in all 6 patients who developed either pulmonary oedema or myocardial infarction. The myocardial performance curve can reliably identify high risk patients and permit control of intravenous therapy within individual safety limits, thereby preventing pulmonary oedema.
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PMID:Dynamic preoperative assessment of cardiac reserve in elective aortic surgery. 686 Sep 12

The role of intracardiac volume in controlling electrocardiographic R-wave amplitude changes during acute myocardial ischemia was studied in 24 open-chest dogs. The R-wave amplitude in surface ECG leads 2, V5 and Frank X, Y and Z leads were correlated with hemodynamic, echocardiographic and angiographic changes in a 5-minute circumflex coronary artery ligation and reperfusion model. After coronary ligation, left ventricular end-diastolic diameter and volume increased progressively above control, reached a peak and plateau at 120--130 seconds after ligation and did not return to control levels until more than 5 minutes after release of the occlusion. In contrast, the R-wave amplitude showed a biphasic response to acute ischemia, reaching a nadir (sigma R = 18.2% below control) at 30 seconds after coronary ligation and only subsequently increased to reach a peak (sigma R = 52% above control) at 150 seconds after ligation. In addition, R-wave amplitude returned immediately to control levels within 10 seconds after reperfusion. In six other dogs, both venae cavae were occluded for a 30-second period, beginning 180 seconds after coronary ligation. Although intracardiac volume decreased markedly, R-wave amplitudes increased even more. Thus, the demonstration of discordance between alterations in intracardiac volume and R-wave amplitude in these studies suggests that factors other than intracardiac volume determine R-wave amplitude changes in the course of acute myocardial ischemia.
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PMID:R-wave amplitude variations during acute experimental myocardial ischemia: an inadequate index for changes in intracardiac volume. 722 82

30 patients suffering from stable angina pectoris were studied by triaxicardiometric (polarcardiographic) method. Triaxicardiometry including the X, Y, Z Frank leads, azimuth (H degrees), elevation (V degrees) angle derivations and spatial magnitude (M) tracings were taken at rest and after submaximal bicycle ergometer exercise. After receiving 30 mg/day isosorbide dinitrate for a minimum of 5 days the whole procedure was repeated, stored by an analogue tape recorder and evaluated by a TPA/i computer. It has been stated that the method of triaxicardiometry has an excess sensitivity on the demonstration of ischemic alteration of anterior and posterobasal left ventricular wall compared to the traditional X, Y, Z leads. According to the pre- and post-exercise bicycle ergometer testing estimated by triaxicardiometry, isosorbide dinitrate caused a significant reduction of subendocardial myocardial ischemia.
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PMID:Polarcardiographic (triaxicardiometric) study on the effect of isosorbide dinitrate on exercise-induced myocardial ischemia. 731 94

Frank orthogonal vectorcardiograms (VCGs) were recorded from 10 subjects prior to, during, and for 15 min after exposures to +3Gz , +5Gz, and +7Gz. The order of acceleration exposure was randomized, with the individual exposures separated by at least 1 week. Standard USAF anti-G suits were worn by all subjects. Detailed analysis of the scalar lead electrocardiograms revealed no abnormalities. There were no consistent signs of conduction disturbances or ischemic ST-T segment changes. The QRS axis of the VCG demonstrated posterior rotation in the sagittal plane and counterclockwise rotation in the transverse plane during +Gz stress. The changes in the VCGs recorded during +Gz stress appeared to be related to rotational changes of the heart due to mechanical stress and/or motion within the thorax. There were no ECG or VCG changes indicative of myocardial ischemia and/or damage during or after +Gz stress.
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PMID:Frank orthogonal vectorcardiograms in humans during and after exposure to +Gz acceleration stress. 741 29

The possibility of using alteration in the ventricular gradient (VG) to discern the presence of ischemic heart disease was studied in 30 patients with effort angina pectoris(AP), 21 with vasospastic angina (VSA), 21 with chest pain syndrome (CPS), and 20 healthy volunteers (control). The VG of each consecutive heart beat over a 22-sec interval was calculated by microcomputer from resting Frank-lead X, Y, Z scalar electrocardiograms. The mean values and standard deviations (SD) for the azimuth, elevation, and magnitude of the VG in each group were calculated. The SD and SD/mean ratios for each parameter were used as indices of VG alteration in the groups, and the indices were compared. The SD and SD/mean for the magnitude and elevation of VG were significantly greater in the AP group than in the CPS and control groups. The SD for the azimuth of VG was significantly greater in the AP group than in the CPS and control groups (p < 0.01). The SD and SD/mean for the magnitude of VG were greater in the AP group than in the VSA group (p < 0.01). The SD/mean for the elevation and magnitude of the VG were greater in the VSA group than in the control group (p < 0.01). The SD/mean of the magnitude of the VG was found to be the best index, as it was higher than the upper limit of the control group. The sensitivity and specificity were 80 and 91% (AP vs CPS, p < 0.001), and 43 and 91% (VSA vs CPS, not significant), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Alteration in ventricular gradient at rest in patients with ischemic heart disease]. 782 82

Oral propafenone hydrochloride effect was studied on atrial signal-averaged ECG (ASAECG) during time- and frequency-domain analysis in patients with paroxysmal atrial fibrillation (PAF) during ischemic heart disease (IHD). The study comprised 26 patients (15 female and 11 male) mean age 60.8 +/- 6.2. The dose of oral propafenone was 450 mg/day for all days. Recording of ASAECG and 24-hours Holter monitoring were made at baseline, after 10 days and after 6 weeks of propafenone therapy. Time-domain parameters were calculated for ASAECG: the root mean square voltage of the signals in the last 10, 20, 30 ms of the filtered P-wave (RMS 10, 20, 30) and total time duration of filtered P-wave (PWD) and time duration of P-wave for Frank leads X, Y, Z (XP, YP, ZP). During frequency-domain analysis of the terminal part of P-wave the following parameters were calculated in range from 40 Hz to 400 Hz: energy spectrum > -60 dB (A) and decibel drop at 4 Hz (Dd) in logarithmic scale and area ratio 20-50/0-20 Hz (Ar), magnitude ratio (MR1-7) in linear scale for a vector magnitude. Supraventricular arrhythmias were estimated quantitatively and qualitatively by Holter monitoring. The following parameters were estimated in a case of PAF recording: time of manifestation, duration, number of PAF episodes per day, mean heart rate during PAF and subjective symptoms. Moreover, comparable analysis of the following parameters: dimension of left atrial, age, sex, time duration of IHD and PAF and wall motion disturbances--hypokinesis and also left ventricular ejection fraction, mitral regurgitation was done between patients with effective and no effective of antiarrhythmic therapy. Our observation have indicated that oral propafenone therapy does not influence any statistically significant differences all time- and frequency-domain parameters of ASAECG in patients with PAF during IHD. Moreover, comparable analysis of above mentioned parameters has not showed statistically significant differences between examined patients with effective and lack of effective propafenone therapy.
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PMID:[Effect of propafenone hydrochloride on atrial signal-averaged ECG in patients with paroxysmal atrial fibrillation]. 859 48


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