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)

Nitroglycerin (NTG) has recently been suggested to decrease myocardial ischemia and enhance cardiac pump function during acute myocardial infarction (AMI). To evaluate the sublingual agnet in this condition, the hemodynamic effects of 0.4 mg NTG administered to 16 supine patients during the first 72 hours of AMI were determined serially 5, 10 to 15, and 20 to 30 minutes post-NTG. Data were evaluated for the entire group, as well as for six patients with normal pulmonary artery wedge pressure (PAW) (less than or equal to 12 mm Hg; mean 7) who formed group I and for ten patients with elevated PAW (greater than 12 MM Hg; mean 19) who comprised group II. In the 16 patients, NTG resulted in significant decreases in PAW (14 TO 7 MM Hg; P less than .01), mean systemic arterial pressure (MAP) (95 TO 82 MM Hg; P less than .01), cardiac index (CI) (1.79 TO 1.46 L/min/m-2; P less than .02), stroke index (SI) (24 TO 18 CC/M-2; P less than .01) and stroke work index (SWI) (27 TO 20 GM TIMES M/M-2; P less than .01). These alterations were significant in both subgroups, with the decline in PAW greater (P less than .05), while there was no change in group II. There was no significant change in total peripheral vascular resistance (TPVR) for the entire group or in the two subgroups. This study demonstrates that, regardless of initial left ventricular filling pressure, sublingual NTG given in the acute phase of AMI results in rapid fall in PAW, concomitant with decreases in systemic blood pressure, cardiac output and SWI, without changes in TPVR and with little or no effect on heart rate. Since TPVR was unaltered, the decline in MAP was due to fall in cardiac output. Thus, the principal action of sublingual NTG in AMI appears to be systemic venodilation with consequent reduction of ventricular preload. This effect is translated into decline ofpump output even in patients with high initial filling pressures. Although NTG may rapidly relieve pulmonary congestion and lower myocardial oxygen consumption, use of the agent sublingually is limited in AMI because these salutary effects are accomppanied by potentially deleterious fall in cardiac output and systemic blood pressure.
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PMID:Hemodynamic effects of nitroglycerin in acute myocardial infarction. 80 94

The effects of an intravenous infusion of nitroglycerin were studied in 20 acutely hypertensive patients during coronary-artery surgery. Eight patients had histories of essential hypertension and six had been treated for it. They were anesthetized with morphine, diazepam, N2O, O2, pancuronium, and enflurane. Control measurements were obtained after sternotomy. Nitroglycerin was then administered until the blood pressure returned to normal, and the measurements then repeated. The mean dose of nitroglycerin was 80.0 +/- 4.7 mug/min, or 0.96 mug/kg/min. This produced significant decreases (P less than .05) in systolic, diastolic, and mean arterial blood pressures, central venous pressure, pulmonary capillary wedge pressure, systemic vascular resistance, and left ventricular stroke work index. Cardiac index, stroke index, and heart rate were unchanged. Two indices of myocardial oxygen demand (rate-pressure product and tension-time index) were significantly decreased by nitroglycerin (P less than .005). Fifty per cent of the patients had improvement in ST-segment depression on the electrocardiogram. These findings demonstrate that nitroglycerin can be safely administered intravenously during operation, and suggest that nitroglycerin decreases myocardial oxygen demand and relieves myocardial ischemia.
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PMID:Nitroglycerin infusion during coronary-artery surgery. 82 Feb 17

The cardiac response to volume loading was evaluated in fifty severely septic patients. After a rapid infusion of albumin or whole blood the cardiac index (CI) and left ventricular stroke work index (LVSWI) were recorded as the pulmonary arterial wedge pressure (PAWP) increased. Initial values of PAWP, CI, and LVSWI were similar in both the nineteen surviving and thirty-one nonsurviving patients. Surviving patients, however, demonstrated greater increases in CI and LVSWI as PAWP rose. Nearly half of both patient groups developed decreases in CI and LVSWI as the PAWP continued to increase. These downslopes occurred at relatively low PAWP and are taken as evidence of an abnormality of myocardial function in both survivors and nonsurvivors. The lower upslope of the performance curves in nonsurvivors indicates myocardial depression or a negative inotropic effect. Cardiac ischemia, acute respiratory failure, and high affinity red cells were found to diminish the cardiac response to volume loading, whereas hepatic and renal failure were associated with a good CI and LVSWI response.
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PMID:Myocardial depression during sepsis. 84 86

The myocardial contractility function was studied with the aid of echocardiography in 42 male patients during dosaged physical exercises. The patients were selected so that at the peak of the exercises they developed an angina pectoris attack documented by ischaemic ECG changes. In some of the patients the changes were also observed during attacks of angina decubitus. Anginal attacks are accompanied by a reduction of the myocardial function. Haemodynamic reactions of two types were noted with myocardial ischaemia: type I reaction was observed in patients with ischaemic heart disease and practically normal values of the initial heart volume, and consisted in an increasing end-systolic and end-diastolic volumes, with the stroke volume remaining unchanged, and the ejection fraction somewhat decreasing; type 2 reaction was observed in patients with initially increased heart volumes, and consisted in a decreasing end-diastolic and stroke volumes, with an insignificant alteration of the end-systolic volume. The ejection fraction, being initially insignificantly decreased, tends to decrease further during the attack.
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PMID:[Myocardial contractility during angina pectoris attack in ischemic heart disease]. 85 2

Tetrapolar chest rheography is an up-to-day, convenient and bloodless method of determining the cardiac stroke volume (CSV) and cardiac output (CO) in dynamic observations. The paper presents and analysis of the method and considers the possibilities and limits of its application in determining the stroke volume and cardiac output. Advantages of the Kubicek procedure as modified by the authors by comparison with other rheographic methods are shown, along with methodological procedures employed for dtermining the CSV and CO and a nomogram that significantly facilitates the calculation of the values under study is offered. Results of contrasting the cardiac ejection values in patients with congenital heart diseases and an increased pulmonary circulation as against those in patients with ischemic heart disease, obtained by means of tetrapolar chest rheography and direct Fick's method are cited. The possibility of applying tetrapolar chest rheography in assessing the effect operative treatment in patients with congenital cardiac defects and also when investigating compensatory reactions of the cardio-vascular system in patients with hypertensive disease in the course of the orthostatic and Valsalva tests is demonstrated.
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PMID:[Determination of cardiac output by the method of tetrapolar chest rheography and evaluation of its metrological possibilities]. 92 47

The article deals with the data of echocardiographic examination of 61 patients (37 with rheumatic heart disease and 17 with atherosclerotic cardiosclerosis) subjected to rapid stage-by-stage digitalization by intravenous administration of various rapidly acting glycosides. In 10 patients with ischemic heart disease echocardiography was performed following a single strophanthin injection. Decrease in the volumes of the left ventricle and increase in the indices of central hemodynamics were noted as a result of rapid stage-by-stage saturation with strophanthin. The maximum inotropic effect of strophanthin does not coincide in time with the maximum chronotropic effect. The increase in the stroke volume noted in maximum deceleration of cardiac contractions is probably realized due to the Frank-Starling mechanism. Strophanthin increases the rate of myocardial contractions without changing the duration of the systole. The rate of diastolic relaxation grows, the phase of rapid filling becomes shorter and the phase of slow filling longer, which creates favourable conditions for the next contraction.
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PMID:[Effect of rapid digitalization on the left-ventricular myocardial function according to the echocardiographic data]. 92

To identify metabolic and other concomitants of a single important type of atherosclerotic cerebrovascular disease, 75 patients with angiographically and surgically proven internal carotid stenosis were compared with age and sex matched control subjects with respect to plasma cholesterol, triglycerides and glucose. They were also compared for blood pressure, cigarette smoking, evidence of ischemic heart disease, peripheral vascular disease and for a family history of these diseases. Patients with carotid stenosis had higher systolic and diastolic blood pressures and higher plasma cholesterol and triglyceride concentrations than the control groups. They had, as well, a far greater likelihood of being cigarette smokers and a greater likelihood of having diabetes mellitus and previous evidence of coronary and peripheral vascular disease. Patients with carotid stenosis were far more likely to have 2 or more of these common concomitants of atherosclerosis than were the control subjects. The data suggest that the precursors of carotid stenosis are similar to those of coronary atherosclerosis and raise the hope that modification of these factors may decrease the incidence of this highly prevalent form of cerebrovascular disease.
Stroke
PMID:Concomitants of atherosclerotic carotid artery stenosis. 92 53

Total mortality showed no association with heavy coffee consumption in the four race-sex groups of Evans County. Deaths from coronary heart disease in WM, WF and BM showed no statistically significant differences between the two coffee consuming groups. Sex differences in cerebrovascular death rates, consistent in both races, suggest the possibility for a female excess of stroke deaths among coffee drinkers, and a "protective" effect of coffee drinking among males. Thus, in an area of the United States which has been designated the "Stroke Belt", neither the cardiovascular nor the cerebrovascular death rates seem strongly nor consistently related to coffee drinking habits. Although the number of deaths (339) is fairly large, representing a 13% mortality in this community over a four and one-half year observation period, the classification in four race-sex groups with further division into the groups with different coffee drinking habits limits each stratum to rather small numbers. In addition, 86 cases of CHD and CVD were diagnosed during lifetime already and, therefore, were excluded from the prospective mortality study. Confidently to refute or confirm the allegations of a detrimental influence of high coffee intake on ischemic heart disease one would need larger numbers. But in the light of our most important finding--that mortality from all causes is not increased in the high coffee consuming group--the finding of increased ischemic heart disease death rates with high coffee consumption would have to be compensated by a provocative, lower rate for other causes of death.
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PMID:Coffee consumption and mortality in a community study--Evans Co., Ga. 96 3

Non-arteriosclerotic (virgin), male and female, Sprague-Dawley rats and arteriosclerotic (breeder), male and female rats were subjected to an acute myocardial infarct when injected with two subcutaneous doses of isoproterenol. Female rats, especially female breeder rats with advanced arteriosclerosis, survived their infarcts in superior fashion to male rats or those with the least severe arterial disease. Animals with severe arteriosclerosis showed the least loss of body weight and greatest increase in heart weight on Day 3 when cardiac necrosis reaches its zenith. Blood pressure and pulse pressure was most seriously reduced in animals with no or early arteriosclerosis only, being best maintained in the animals with the most severe arterial disease. Heart rate was not greatly altered in any of the various groups. Ventricular function, i.e., cardiac output, stroke volume, cardiac index, and left ventricular minute work, was severely impaired in the non-arteriosclerotic animals and in those with the least arterial disease. Total peripheral resistance was also least elevated and myocardial contractile strength (peak flow and max dF/dt) was greatest in female breeders with the most advanced arterial disease. Most intriguing, is the seemingly paradoxical but consistent finding that female breeders which develop the most severe arterial disease are able to best maintain cardiac function during the acute stress of myocardial ischemia.
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PMID:Hemodynamic changes in arteriosclerotic vs. non-arteriosclerotic rats during the acute stages of myocardial infarction. 105 62

Systolic time intervals and the a/H ratio were recorded in 20 patients with uncomplicated acute myocardial infarction over a period of five days. The initial high heart rate and systolic blood pressure and the short PEP and ICT indicating a sympathetic overactivity were spontaneously normalized during the first week of infarction. LVET was reduced indicating a fall in stroke volume and the a/H ratio was unchanged at the high levels suggestive of elevated preload or LVEDP. In 10 patients with acute myocardial infarction and recurrent chest pain recordings on noninvasive parameters were made before and 30 min after intravenous injection of practolol. In addition, 7 patients with chest pain, classified as acute myocardial infarction, were given practolol. The average dose of practolol was 17.9 mg ranging from 5 to 30 mg. An almost immediate and pronounced relief of pain was observed in all patients and no signs of impaired left ventricular function appeared. The product of systolic blood pressure and heart rate was decreased by practolol and the PEP and the ICT were prolonged to normal values while no changes were seen in LVET and a/H ratio. On 126 occasions practolol was given in dosages ranging from 5 to 30 mg (mean 8 mg) to 75 patients with acute myocardial infarction and recurrent chest pain. A satisfactory pain relief was seen on 108 occasions. It is suggested that an inappropriate sympathetic overactivity is an important factor in provoking recurrent chest pain in acute myocardial infarction. Administration of the beta-adrenergic blocking agent practolol resulted in pain relief due to reduction of heart work and in severity of myocardial ischemia. The beta-blocking agent was well tolerated in the present study. Continuous beta-blockade during the whole hospital stay to patients with acute myocardial infarction seems to be a very attractive therapy in order to preserve the ischemic myocardium and limit the size of infarction.
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PMID:Effect of cardioselective beta-blockade on heart function and chest pain in acute myocardial infarction. 106 28


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