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

This is a report of the management of a patient with chronic idiopathic thrombocytopenic purpura (ITP) and ischemic heart disease. High-dose transvenous gamma-globulin therapy (400 mg/kg/day for five days) was started five days prior to operation, yielding an increase in platelet count from 5.8 X 10(4)/mm3 to 12.8 X 10(4)/mm3. Platelet transfusion was used at the end of cardiopulmonary bypass and on the first postoperative day. There were no problems with hemostasis during the operative procedure and the postoperative course was uneventful. We prefer high-dose transvenous gamma-globulin therapy for ITP prior to open heart surgery as a treatment of choice.
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PMID:[A case of CABG in a patient with chronic idiopathic thrombocytopenic purpura]. 169 71

In patients with coronary artery disease, radionuclide investigations have documented a high incidence of mental stress-induced myocardial ischemia in the absence of significant electrocardiographic changes and/or angina. To investigate the causes of the low electrocardiographic sensitivity, we recorded body surface maps during mental arithmetic in 22 normal volunteers and 37 postinfarction patients with residual exercise ischemia. Myocardial perfusion was studied with thallium-201 or technetium-99 (SESTAMIBI) planar scans. In 14 patients, body surface maps were also recorded during atrial pacing at the heart rate values achieved during mental stress. While taking the body surface maps, the area from J point to 80 msec after this point (ST-80) was analyzed by integral maps, difference maps, and departure maps (the difference between each patient's difference map and the mean difference map for normal subjects). The body surface mapping criteria for ischemia were a new negative area on the integral maps, a negative potential of more than 2 SD from mean normal values on the difference maps, and a negative departure index of more than 2. Scintigraphy showed asymptomatic myocardial hypoperfusion in 33 patients. Eight patients had significant ST segment depression. The ST-80 integral and difference maps identified 17 ischemic patients. Twenty-four patients presented abnormal departure maps. One patient presented ST depression and abnormal body surface maps without reversible tracer defect. In 14 of 14 patients, atrial pacing did not reproduce the body surface map abnormalities. The analyses of the other electrocardiographic variables showed that in patients with mental stress-induced perfusion defects, only changes of T apex-T offset (aT-eT) interval in Frank leads and changes of maximum negative potential value of aT-eT integral maps significantly differed from those of normal subjects. Our results confirm the low electrocardiographic sensitivity for detecting mental stress-induced myocardial hypoperfusion in postinfarction patients. ST analysis in the body surface map increases the information content of the electrocardiographic signal. T wave analysis appears to offer fewer diagnostic advantages.
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PMID:Electrocardiographic markers of ischemia during mental stress testing in postinfarction patients. Role of body surface mapping. 182 36

Beat-to-beat fluctuations of the spatial QRS-T angle, which are reported to be greater in patients with ischemic heart disease than in healthy subjects, are thought to be a helpful factor in diagnosing ischemic heart disease. In this study, we assessed the usefulness of the standard deviation of the spatial QRS-T angle per beat as an index of magnitude of the fluctuations. The subjects consisted of 27 patients with effort angina, 14 with vasospastic angina, 18 with the "chest pain syndrome" and 36 normal controls. The standard deviations of the spatial QRS-T angle were obtained for 10 consecutive stable beats at rest using Frank's orthogonal X, Y, Z scalar electrocardiogram. The results were compared with those of coronary angiography and exercise tolerance tests. Treadmill exercise tests were performed in all patients using Bruce's protocol to observe decreased ST levels and delta ST/HR indices. QRS-T angle deviation values were 8.10 +/- 8.64 degrees (mean +/- SD) in the effort angina group, 3.63 +/- 1.26 degrees in the vasospastic angina group, 4.13 +/- 1.70 degrees in the "chest pain syndrome" group, and 2.35 +/- 0.85 degrees in the normal control group; the groups of patients with heart disease showed significantly higher values (all p < 0.01) than did the control group. The effort angina group showed a significantly higher value than did the vasospastic angina group and the "chest pain syndrome" group (all p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ischemic heart disease detected by the standard deviation of the spatial QRS-T angle and by treadmill exercise test]. 184 6

In 35 patients with ischemic heart disease we evaluated the incidence of ventricular late potentials and left ventricular function. The patients were divided into two groups: group A consisting of 15 patients (14 men, 1 woman) aged from 40 to 71 years (mean age 56) with previously documented ventricular tachycardia or fibrillation, and into group B comprising 20 subject (16 men, 4 women) aged from 35 to 62 years (mean age 50) with ischemic heart disease without the above-mentioned arrhythmias. Time from the development of ventricular tachycardia or fibrillation was 3 weeks to 4 years. The incidence of arterial hypertension and previous myocardial infarction was similar in both groups. Body surface late potentials were recorded by signal averaging technique according to Simson using Frank's orthogonal XYZ lead system. In addition, in all the patients 24-hour ECG monitoring was performed to reveal any ventricular rhythm disturbances and echocardiography was used to evaluate left ventricular function. The presence of the ventricular late potentials meeting at least two of the Simson's--Dene's criteria was found in 13 (87%) patients in group A and in 2 (10%) patients from group B. In the patients after ventricular tachycardia or fibrillation the mean values of th total QRS duration (QRS-D) and the low amplitude signal duration (LAS40) were higher whereas the root mean square voltage of the last 40 ms of th vector magnitude QRS (RMS) was lower (154 ms, 56 ms, 15 muV, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Signal-averaged ECG and left-ventricular function in patients with severe ventricular arrhythmia in ischemic heart disease]. 192 Nov 5

The optimal number and placement of electrocardiographic (ECG) leads to detect myocardial ischemia induced by coronary balloon inflation was assessed by analyzing ST segment changes in the standard 12-lead ECG and Frank X, Y, Z leads at 90-s intervals during 34 consecutive coronary angioplasty procedures. Mean occlusion time during angioplasty was 218 +/- 65 s. Myocardial ischemia, defined as transient angina or ST segment deviation greater than or equal to 1 mm in at least one lead, occurred in 33 (97%) of the 34 procedures. The most sensitive single leads (V2 or V3) detected 17 (51%) of 33 ischemic episodes. The best dual-lead combinations (leads V2 and V5, leads a VF and V3 and leads V3 and Y) increased the sensitivity of 69% (23 of 33). The three-lead combination V2, V5, Y had the highest detecting power (78% [26 of 33]). The X, Y, Z leads by themselves had a sensitivity of only 60% (20 of 33). From this proposed orthogonal lead system (V2, V5, Y), which combines anteroposterior (V2), left to right (V5) and inferosuperior (Y) forces, the spatial ST vector magnitude was calculated and monitored during balloon inflations. A good correlation was observed between this ST vector magnitude and the sum of ST deviations on the standard ECG (r = 0.940, p less than 0.00001), and these data were reproducible over sequential balloon inflations. The results of the study suggest that this orthogonal lead system is of considerable value in the detection and quantification of acute myocardial ischemia and, in this respect, is more useful than the Frank orthogonal vector system.
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PMID:Assessment of myocardial ischemia by 12-lead electrocardiography and Frank vector system during coronary angioplasty: value of a new orthogonal lead system for quantitative ST segment monitoring. 196 Mar 17

Although the etiology of congestive heart failure is complex, a disturbance of myocardial function due to ischemic heart disease or various forms of cardiomyopathy is by far the leading causative factor. In the early stages of failure various cardiac compensating mechanisms, such as hypertrophy, an increase in contractility and the Frank-Starling mechanism, prevent a major reduction in function. With ongoing failure, myocardial muscle function further deteriorates because of a disturbance in myocardial energy utilization, abnormalities in sympathetic neurotransmitter metabolism, a reduction in beta-receptor density, and, more importantly, a derangement of intracellular calcium transport. The subsequent reduction in cardiac output leads to activation of peripheral neurohumoral mechanisms, including sympathetic stimulation, an increase in circulating norepinephrine, stimulation of the renin-angiotensin-aldosterone system (RAAS), and increased arginine vasopressin production, which result in arterial and venous vasoconstriction, redistribution of tissue blood flow, and an increase in circulating blood volume. The adjustments, however, lead to a vicious circle, where heart function is further depressed by the increase in afterload, whereas the changes in the venous bed and the increase in circulating volume ultimately result in congestion. At this point, digitalis and diuretics alone are no longer sufficiently effective and vasodilators are indicated, possibly combined, in the later stages of failure, with positive inotropic drugs. The angiotensin converting-enzyme inhibiting agents seem particularly useful in this context, presumably because of their complex mode of action, interfering with the neurohumoral systems and peripheral vasculature at multiple sites. Particularly with these agents, a remarkable improvement in clinical condition and exercise capacity has been observed. Even so, the long-term prognosis in patients with severe congestive heart failure is still extremely poor with one-year mortality rates in New York Heart Association class III and IV patients ranging from 34% to 48%. In this article, the pathophysiology of congestive heart failure and the potential of drug therapy are further discussed.
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PMID:Congestive heart failure--pathophysiology and medical treatment. 242 92

The characteristic hemodynamic profile of human septic shock consists of a normal or elevated cardiac index and a decreased systemic vascular resistance index. When a patient with septic shock has a low cardiac index, concomitant hypovolemia is usually present. Within 48 hours of the onset of septic shock, most patients develop marked dilatation of both ventricles, depressed ejection fractions, and alterations of the Frank-Starling and diastolic pressure-volume relationships; stroke volume typically is well maintained. In surviving patients, cardiac function returns to normal within 10 days. An identical sequence of hemodynamic abnormalities occurs in an experimental canine model of sepsis that employs intraperitoneal implantation of infected fibrin clots. This myocardial dysfunction is not due to global myocardial ischemia; instead, there appear to be one or more circulating myocardial depressant substances. The chemical nature of these circulation mediators is under intensive investigation clinically, in vitro, and in the canine model.
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PMID:Myocardial dysfunction in sepsis. 264 29

R wave amplitude changes during exercise have been a controversial issue as both increase and decrease in amplitude have been reported in patients with coronary arterial disease. This variability in response is attributed to change in position and heart axis on exercise. In view of this limitation, this study evaluated the change in spatial R maximum amplitude on exercise, which should not be affected by the above factors. Twenty patients with ischaemic heart disease (male 20, age 38-61 years) and 9 control subjects (male 9, age 32-65 years) were studied. Orthogonal leads, X, Y, Z were recorded using corrected Frank lead system on a stereokinematic vectorcardiograph (Tonnies). The magnitude of spatial R maximum cardiac vector increased from 0.1 to 0.6 mV in 8/9 control subjects and decreased or showed no change in 18 of the 20 patients with coronary arterial disease. In the control group, the mean value at the end of exercise (0.98 +/- 0.34 mV) was significantly less (P less than 0.01) as compared to pre-exercise value (1.09 +/- 0.2 mV). Our preliminary observations thus indicate that, with exercise, the magnitude of spatial R maximum cardiac vector decreases or shows no alteration in height in patients with coronary arterial disease whereas it increases in normal subjects.
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PMID:Evaluation of spatial R maximum cardiac vector changes in exercise testing: pre-exercise versus post-exercise measurements. 276 8

While the total ischemic burden on the left ventricle represents the combined effects of both symptomatic and asymptomatic myocardial ischemia, the total vascular burden has many components including an increased systemic peripheral vascular resistance, an increased pulmonary vascular resistance, and an increased coronary vascular resistance. These factors may all influence ventricular function. Hypertension contributes significantly to the vascular burden, especially when combined with left ventricular hypertrophy, which predisposes to ischemia by multiple mechanisms. In patients with hypertension and cardiomegaly, sublingual nifedipine has been shown to increase left ventricular (LV) ejection fraction and the average diastolic filling rate. In the presence of acute myocardial infarction, nifedipine moves the LV function curve onto a better Frank-Starling relationship as pulmonary wedge pressure falls or stays the same and cardiac output rises. However, because of the delicate balance between myocardial perfusion and the benefits of afterload reduction, including improved remodelling, nifedipine should be given only to selected patients. In congestive heart failure, low-dose nifedipine reduces the afterload and has been shown to have beneficial effects in the majority of patients. Two specific adverse outcomes in only two patients have been reported, one with initial hypotension and one given high-dose nifedipine. Combination nifedipine-beta blocker therapy has been shown to be favorable in the treatment of all varieties of angina, hypertension, and hypertrophic cardiomyopathy. Therefore, when administered appropriately, nifedipine reduces the total vascular burden on the heart in a variety of cardiovascular diseases, with consequent improvement in LV function and a diminished threat of potential myocardial ischemia.
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PMID:The total vascular burden, peripheral and coronary: vasodilator effects of nifedipine. 327 10

To evaluate the myocardial hemodynamic effects of a new iso-osmotic contrast agent (Hexabrix 160: H 16) a randomized cross-over study was performed comparing Hexabrix 160 with Sodium Meglumine diatrizoate (Radioselectan 76: R 76) in 20 patients with ischemic heart disease. H 16 produced substantially smaller (p less than 0.001) increases in heart rate (68 +/- 11 to 73 +/- 12) than R 76 (69 +/- 12 to 88 +/- 15) and smaller decreases in left systolic ventricular pressure (131 +/- 15 to 128 +/- mmHg) than R 76 (132 +/- 14 to 94 +/- 15 mmHg). Both contrast media resulted in an increase in contractility beginning three to five seconds after the onset of the injection and reached its maximum at 45 seconds. However the increases in contractility was smaller with H 16 than R 76: H 16 caused a significantly smaller (p less than 0.01) increases in V max. (0.1 CIRC/s) than R 76 (0.35 CIR/s). The hemodynamic effects of H 16 were probably in relation with the Frank-starling mechanism. The lowest variation of preload observed (left ventricle end-diastolic pressure: 12 +/- 4 to 14 +/- 5 mmHg) showed that this contrast medium appeared to behave like isotonic serum. These results suggest that H 16 may preferable for digital left ventriculography.
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PMID:[Hemodynamic effects of a new iso-osmotic contrast medium in selective left ventriculography]. 332 90


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