Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial cell pH was measured with 5, 5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58% of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein.
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PMID:Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition. 0 59

Nineteen patients with ischemic heart disease were randomized into two groups and received either metoprolol or H 87/07. Heart catheterization was performed, and the groups were studied at rest and during exercise--before and after intravenous drug administration. During work metoprolol gave a statistically significant reduction in left ventricular work (expressed as pressure-rate product) of about 20%, mainly depending on a reduction in heart rate. Cardiac output decreased by 21%. Stroke volume was almost unchanged. The abnormal increase in left ventricular filling pressure during work was slightly, but not significantly, reduced by the drug. For H 87/07 no significant changes were found in the corresponding variables. This seems, however, to depend on an inadequate dosage, since not even the heart rate during work was significantly reduced. In conclusion, in the doses used metoprolol has been shown to be a potent beta-adrenoceptive antagonist in contrast to H 87/07.
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PMID:Hemodynamic effects of two cardioselective beta-adrenoceptive antagonists, metoprolol and H 87/07, in coronary insufficiency. 2 23

In 18 patients with documented ischaemic heart disease the cardiovascular effects of ketamine (1.5 mg/kg iv) were studied under three different conditions: 1. in awake premedicated patients (n = 6); 2. after the previous administration of flunitrazepam (0.015 mg/kg iv, n = 6) and 3. under conditions of neuroleptanalgesia and muscle relaxation (n = 6). Flunitrazepam prevented or at least attenuated the increases in heart rate (30%), mean arterial pressure (37%), mean pulmonary artery pressure (165%), left ventricular filling pressure (230%), total peripheral resistance (50%), pulmonary vascular resistance (100%) and in the rate-pressure product (66%) which were associated with the use of ketamine as the sole anaesthetic agent. In addition, the flunitrazepam-pretreatment abolished the fall in cardiac index and stroke index which occured in patients given ketamine alone. Flunitrazepam therefore appears to be a promising drug to prevent adverse cardiovascular reactions, when ketamine should be chosen for induction of anaesthesia. Neuroleptanalgesia and muscle relaxation also proved effective in controlling the sympathomimetic actions of ketamine. The response of the mean pulmonary artery pressure and of the ventricular filling pressures to ketamine in this group was even more damped than in the patients pretreated with flunitrazepam alone.
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PMID:[Flunitrazepam-pretreatment for prevention of adverse cardiovascular effects following ketamine]. 4 95

In 10 anaesthesized dwarf pigs with an open thorax the effects of extrasystoles on systemic and coronary circulation were investigated. The actual effect of an extrasystole depends on the time of its onset. Early extrasystoles hamper the cardiac blood perfusion, with decreases in the stroke volume, mean arterial pressure, coronary blood flow, and elevation of coronary resistance. Extrasystoles setting on later are of minor haemodynamic and coronarodynamic importance. The effects of bigeminy and 2:1 extrasystolia are more adverse than the consequences of extrasystoles with later onset. With cumulation of several consecutive extrasystoles also adverse the haemodynamic coronarodynamic sequelae increase, in dependence on the magnitude of the quotient coupling time /extrasystolic excitation period [ greater than 1.1], or of the quotient: duration of pre- and postextrasystolic intervals/ normal interval of heart action [ greater than 1.5]. The authors point out the importance of haemodynamic findings during early extrasystoles in ischaemic heart disease.
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PMID:[The effect of early appearing extrasystoles on systemic and coronary circulation]. 8 Mar 1

Ultrasoundcardiograms (UCG) and radiocardiograms (RCG) were obtained from 50 patients with essential hypertension. They were classified into four groups according to the severity index of Veterans Administration Hospital. These echocardiograms were compared with those obtained from 20 normal individuals. Of the 50 patients with hypertension, ten had abnormal patterns of mitral valve echogram: two had shoulder formation of the A wave (A-A'), three had increased amplitude of the A wave (A greater than E), and five had systolic anterior movement (SAM) of the anterior mitral leaflet toward the ventricular septum. The former two groups were considered to have impairment of left ventricular (LV) function proven by UCG and RCG, however, the SAM group was considered to have hyperfunction with concentric hypertrophy of the left ventricle with thickened ventricular septum simulating that of idiopathic hypertrophic subaortic stenosis (IHSS). This was supported by the fact that SAM increased after inhalation of amyl nitrite and decreased after injection of propranolol. The descent rate of the anterior mitral valve decreased and the thickness of the ventricular septum increased with the severity of hypertension, indicating the LV compliance decreases as the severity of hypertension advances. A significant positive correlation was noted between stroke index (SI) obtained by UCG and RCG. There were no significant differences of LV dimensions and function indices measured by UCG and RCG among the groups classified according to the severity index of hypertension. This suggests that such factors as myocardial ischemia might play an important role in LV function as well as the grade of afterload due to hypertension.
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PMID:Echocardiographic observations in hypertension. 12 50

Comprehensive ascertainment of all possible new cases of stroke appearing between January 1, 1970 and June 30, 1971, and admitted to three major hospitals in Winnipeg, Manitoba, has been achieved by reviewing the Manitoba Health Services Commission claim reports. The medical records of these cases were reviewed, pertinent data were abstracted, and rigid criteria for diagnosis were followed. Also, data were obtained from death certificates, autopsy reports and long-term hospital records. A total of 606 ascertained cases (410 infarction, 137 hemorrhage, and 59 undetermined type) were matched for age, sex, residence and year of admission with 606 controls from admissions for other than cardiovascular and cerebrovascular disorders. The data were analyzed for elucidating the possible risk factors for infarction (INF) and hemorrhage (HGE). The findings suggested that hypertension was the main risk factor in hemorrhage, whereas in infarction, along with hypertension, other factors such as diabetes, heart enlargement in chest x-ray, ECG abnormalities, and smoking were suggested as risk factors. There was an association also between infarction, on one hand, and the history of receiving anticoagulants, diuretics, and medications for the heart, and the occurrence of myocardial infarction, on the other hand. These features indicate that infarction and ischemic heart disease have similar risk factors. Hemoglobin and hematocrit were higher in infarction cases than in their controls only when measured at stroke admission. No difference was revealed when they were measured prior to stroke. Their association with infraction therefore may be secondary to other factors and of no significance for its risk.
Stroke
PMID:Relative role of factors associated with cerebral infarction and cerebral hemorrhage. A matched pair case-control study. 13 18

The role of hypertension in cardiovascular disease was studied in the hypertensive coarcted monkey during the feeding of an atherogenic and nonatherogenic diet. During the 15-month period of observation, half of the hypertensive coarcted monkeys developed cardiovascular disease which included heart failure, ischemic heart disease, stroke, and sudden death. There were no cardiovascular complications in the control normotensive monkeys except for one cholesterol-fed animal. The incidence of ischemic heart disease and sudden cardiac death was higher in monkeys with both hypertension and hypercholesterolemia than in those with hypertension or hypercholesterolemia alone. Postmortem studies revealed that the former monkeys had both hypertensive and atherosclerotic heart disease, whereas the monkeys with hypertension or hypercholesterolemia had either hypertensive or atherosclerotic heart disease. Hypertensive heart disease was characterized not only by hypertrophy of the left ventricle but also by focal myocardial degeneration and fibrosis and by focal thickening and narrowing of the small coronary arteries, particularly the sinus node artery and the atrioventricular node artery. The finding of transmural myocardial infarction in two monkeys with patient coronary arteries suggests a possible role of coronary artery spasm in ischemic heart disease in hypertension. The cerebral vascular complications of hypertension included hypertensive encephalopathy, transient "ischemic" attacks, and hemorrhagic stroke. The complications were associated with severe hypertension and with hypertensive vascular disease or hypertensive and atherosclerotic vascular disease of the cerebral arteries.
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PMID:Role of hypertension in ischemic heart disease and cerebral vascular disease in the cynomolgus monkey with coarctation of the aorta. 14 28

The chemical composition of ultracentrifugal fractions of VLDL (d less than 1006), LDL (d 1006-1063) and HDL (d less than 1063) has been studied in males affected by atherosclerosis of different vascular beds. Thirty-seven subjects affected by post-infarction cardiopathy (M.I.) showed significantly higher values of total-C, VLDL-C and LDL-C when compared to 52 controls. Twenty-three patients affected by non-occlusive ischaemic heart disease (I.H.D.) showed higher values than controls of total-C, VLCL-C, LDL-C, total TG, VLDL-TG, and GDL-TG. Twenty-three patients with atherosclerosis of the inferior limbs (P.A.) were characterized by increased levels of total-TG, VLDL-TG, VLDL-C, HDL-C. A group of patients who had suffered a stroke from cerebro-vascular disease (C.V.D.) did not show any significant difference from controls. In the M.I. group, 56% of the patients had a high level of C-VLDL. Patients with I.H.D. were characterized mostly by an increase in C-LDL, Patients with P.A. showed the highest values of total -TG, VLDL-TG and LDL-TG. Some of the observed differences are probably due to different metabolic backgrounds. Some other differences may be due to variations in dietary habits after heart infarction. Patients with levels of plasma cholesterol and triglyceride beyond the 90th percentile of the normal group showed many abnormalities in the chemical composition of their lipoproteins. It is noteworthy that increased amounts of cholesterol may collect in lipoprotein classes different from LDL while increased amounts of triglyceride may collect in classes different from VLDL.
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PMID:Chemical composition of ultracentrifugal fractions in different patterns of human atheroslcerosis. 18 83

The hemodynamic response to slow and rapid defibrination was sutdied in anesthetized beagle dogs, with the following results: 1. Slow defibrination was a benign procedure that had little or no effect on the hemodynamic variables studied. 2. Rapid defibrination induced statistically significant decreases in cardiac output, stroke volume, and mean aortic arterial pressure. 3. Bradycardia, a drop in mean left v"ntricular pressure, cardiac and minute work indices, an increase in pulmonary artery pressure, and a drastic rise in pulmonary and systemic vascular resistances were also observed. Although physiologically apparent, these changes were not statistically significantly different from control levels. 4. Pulmonary capillary wedge pressure, left ventricular end-disatolic pressure, arterial pH, and blood gases were not altered by rapid defibrination. 5. In view of the similarities between the hemodynamic changes observed after rapid defibrination and acute myocardial ischemia, the role of decreasing fibrinogen concentrations and blood viscosity in aucte myocardial infarction and the sudden death syndrome is questioned.
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PMID:Hemodynamic effects of slow and rapid defibrination with defibrizyme, the thrombin-like enzyme from venom of the timber rattlesnake. 23 15

Eight patients with chronic congestive cardiac failure secondary to ischaemic heart disease performed submaximal supine exercise before and after 5 mg sublingual isosorbide dinitrate (ISDN) at the time of cardiac catheterisation. Exercise before ISDN produced a poor response in left ventricular performance. After ISDN this response was significantly improved. Compared with the control exercise period cardiac index (CI) increased from mean 2.9 to 3.5 l/mn/m2 (p = less than 0.0025), stroke volume index (SVI) from mean 24 to 29 ml/m2 (p = less than 0.0005) and left ventricular stroke work index (LVSWI) from mean 22 to 28 g-m/m2 (p = less than 0.0025). Although ISDN reduced LVEDP significantly at rest, there were associated small but significant falls in CI, SVI and LVSWI. The improvement in exercise cardiac index was related to the ejection fraction, or the ejection fraction of the contractile section where a left ventricular aneurysm was present. ISDN may be effective in improving exercise tolerance in ambulant patients with chronic congestive cardiac failure.
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PMID:Haemodynamic effects of isosorbide dinitrate in patients with congestive cardiac failure at rest and during submaximal supine exercise. 41 97


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