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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary arterial end-diastolic and mean right atrial pressures were compared in 25 patients with acute myocardial infarction and in one patient with unstable angina. No consistent relationship was observed between these pressures. Simultaneous ventricular function curves relating the stroke work of each ventricle to its respective filling pressure were constructed on 34 occasions, dextran infusion or diuresis being used to alter the filling pressure. The curves from each ventricle were described mathematically by a quadratic (parabolic) function as well as by a straight line function and then compared by canonical correlation analysis. Alterations in the left ventricular function curves occurred with and without depression or right ventricular function curves. These hemodynamic measurements demonstrate that acute myocardial infarction can alter the relationship between left and right ventricular function.
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PMID:Comparison of left and right ventricular function in acute myocardial infarction. 99 Dec 62

Fifty-three men with significant obliterative arteriosclerosis of coronary arteries were examined at rest, during and after pacing. Pacing induced both angina pectoris and depression of the ST segment in 38% of the patients; either angina pectoris or depression of ST segment, in 32% of the patients; the remaining 30% of patients were without symptoms or ECG signs of coronary insufficiency. Haemodynamic findings at rest, or during and after cessation of pacing were not different between these groups. Pacing increased heart rate, cardiac index remained unchanged, the stroke volume decreased, the left ventricular ejection time shortened. In both systemic and pulmonary arteries the systolic pressures decreased, the diastolic and mean pressures rose. The left ventricular end-diastolic pressure decreased. In 28 of the patients the myocardial metabolism was investigated. A close correlation was found between positive symptoms and ECG signs of myocardial ischaemia on the one hand, and metabolic signs on the other hand. Absence of angina pectoris and depressions of the ST segment during pacing does not exclude the presence of metabolic signs of ischaemia; an opposite finding is about three times less frequent. The study offers objective information about haemodynamics and myocardial metabolism before, during and after pacing, and represents an attempt of a simple classification of symptoms and signs of induced ischaemia.
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PMID:Haemodynamics and myocardial metabolism in patients with obliterative coronary arteriosclerosis and tachycardia induced by pacing. 100 Sep 81

An epidemiological study of cerebrovascular disease in Akabane and Asahi, Japan, was made. (These cities are located near Nagoy, Japan.) The study population included 4,737 men and women aged 40 to 79 at the time of entry into the study. There were 4,186 persons who were examined and, of these, 264 cases of cerebrovascular attacks were observed between 1964 and 1970. The incidence rate of stroke in those persons not responding to the survey was 15.9 times higher than in those persons examined according to person-year observation in Akabane. The risk factors for cerebral hemorrhage and thrombosis were evaluated by age-adjusted and sex-adjusted relative risks. The predisposing factors to cerebral hemorrhage appeared to be high blood pressure, high left R wave, ST depression, T abnormality, capillary fragility counts, previous medical history of stroke and albuminuria. For cerebral thrombosis, the predisposing factors appeared to be high blood pressure, ST depression and funduscopic sclerotic findings, and those factors assumed to be significant were glycosuria and smoking habits. Ocular funduscopic abnormality was the most prominent risk factor for cerebral thrombosis, while high blood pressure and ECG abnormalities were highly related to cerebral hemorrhage. It was suggested that those subjects with a relatively higher blood pressure may have a higher relative risk of cerebral hemorrhage than those with a lower (normal range) blood pressure. A previous or family history of stroke also appeared significantly related to cerebral hemorrhage.
Stroke
PMID:A prospective study of cerebrovascular disease in Japanese rural communities, Akabane and Asahi. Part 1: evaluation of risk factors in the occurrence of cerebral hemorrhage and thrombosis. 100 36

Etomidate and methohexital were administered for induction of anesthesia in 45 patients who had to undergo open heart surgery. The anesthesia technique was otherwise standardised. Measurements of blood pressure and heart rate were obtained during a period of ten minutes after injection of the induction agent, and in a selected group of 16 patients cardiac index and stroke volume index were obtained by impedance cardiography. In the group of 45 patients, blood pressure one minute after induction was unchanged with Etomidate, but decreased (-6%) with methohexital. During intubation, important variations of systolic blood pressure occurred, specially with Etomidate (+ 36%) and less with methohexital (+ 21%). Heart rate increased in both groups during intubation (+ 41%) and returned towards starting value after ten minutes. In the group of 16 patients, cardiac index varied with Etomidate, decreasing during intubation (- 21%), increasing to + 32% and then returning to starting value afterwards. Heart rate increased with intubation (+ 39%) and was still somewhat elevated at ten minutes. Stroke volume index decreased with intubation (- 36%) and was still lower than the initial value at ten minutes (- 14%). With methohexital, cardiac index variations were less pronounced (+ 11%). Cardiac index was lower than the initial value at ten minutes (- 14%). Stroke volume index decreased with intubation (- 36%) and was still lower than the initial value at ten minutes (- 14%). This was compensated by an increase in heart rate. These measurements made during induction reflect the complex interaction of drug administration and technical manipulations. Blood pressure lowering one minute after the injection of methohexital can be ascribed to vasodilatation and myocardial depression. The important blood pressure and cardiac index variations observed with Etomidate are probably due to the short action and the lack of analgesic properties of this agent.
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PMID:Clinical use of etomidate. 101 16

Hemodynamics and myocardial muscle mechanics have been studied in 22 euthyroid and 60 hypothyroid cats in which experimental hypothyroidism has been produced by thyroidectomy 61 days prior to the examination. Left ventricular to body weight ratio was altered due to a decrease in left ventricular weight and an increase in body weight. Heart rate, cardiac output and cardiac index were decreased (by 12-15 per cent), whereas stroke volume remained unchanges. Peak systolic pressure of the left ventricle was moderately decreased, the other pressures were in the normal range. There was a marked and significant reduction of isovolumic contractility indices indicating a depression of myocardial contractility in situ by 20-27 per cent. The isolated ventricular myocardium exhibited decreases of isotonic muscle shortening, of maximum isometric tension development and of the rates of both, isotonic shortening and isometric tension development by 12-35 per cent. Force-velocity relationships of contraction and relaxation were depressed to lower values of contraction and relaxation velocity as well as of maximum isometric muscle tension. The alterations in myocardial muscle mechanics and hemodynamics were completely reversible following substitution of the hypothyroid group with physiological doses of L-thyroxine (5 mug/kg/day for 8-18 days). Excess increases of parameters of myocardial performance were found following substitution of the hypothyroid group with L-thyroxine (500 mug/kg/day) in accordance with the induction of experimental hyperthyroidism in these animals. The results demonstrate impaired myocardial contractility and hemodynamics in experimental hypothyroidism. These changes are completely reversible by substitution with L-thyroxine in accordance with a reversible thyroid cardiomyopathy. The cellular mechanisms responsible for the altered cardiac activity in experimental hypothyroidism are discussed.
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PMID:Experimental hypothyroidism: depression of myocardial contractile function and hemodynamics and their reversibility by substitution with thyroid hormones. 101 93

The mechanism of elevation of left ventricular end-diastolic pressure during acute global ischemia was evaluated by examiniation of the relative contributions of a decrease in contractility and an alteration of the pressure-volume relationship. The external circumference (mercury-in-silastic gauge) pressure relationship, as an index of the pressure-volume relationship, was studied in beta adrenergic and ganglionic blocked, open chest dogs on right heart bypass at constant heart rate ane aortic pressure. Ischemia of one and two hours' duration was produced by reducing total coronary blood flow in cannulated left and right coronary arteries until left ventricular end-diastolic pressure rose significantly. At a constant stroke work, left ventricular end-diastolic pressure rose from 5.0 +/- 0.5 to 15.0 +/- 0.5 cm H2O in the experiments of one hour of ischemia, and from 7.0 +/- 1.0 to 17.0 +/- 1.0 cm H2O in experiments of two hours of ischemia. Ischemia was followed by one hour of restoration of coronary blood flow. Ischemia produced a marked depression of ventricular function: stroke work, considered at a left ventricular end-diastolic pressure of 15 cm H2O, decreased from 21.0 +/- 3.0 to 3.5 +/- 0.5 gm-m, and from 15.0 +/- 2.0 to 2.5 +/- 0.5 gm-m, in the experiments of one and two hours, respectively. Neither ischemia nor reflow changed the pressure-volume relationship. Thus, the elevation of left ventricular end-diastolic pressure during ischemia in an otherwise normal canine myocardium is due to a decrease in systolic performance of the heart rather than to an alteration of the pressure-volume relationship.
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PMID:Left ventricular end-diastolic pressure volume relationships with experimental acute global ischemia. 108 86

Regional cerebral blood flow (rCBF) measurements were performed over the contralateral hemisphere by the 133Xe intracarotid injection method in 20 patients with acute cerebral infarction in the territory of the internal carotid artery. The rCBF was found to be reduced, sometimes remarkably, in all of the patients. The mean reduction was 30 percent to 36 percent from the lowest normal value for the mean age of these patients. In the younger age group (40 to 59) the reduction was greater, 40 percent to 47 percent from the lowest normal value for this age. tthe rCBF depression was not related to cerebral dominance, previous hypertension or arterial PCO2 levels. The occurred in both patients who were fully alert and those with disturbances or consciousness, although it tended to be more diminished in the latter. tit can be assumed that the flow reduction in the nonaffected hemisphere is part of a general phenomenon affecting the entire brain and caused by globally reduced cerebral metabolism.
Stroke
PMID:The effect of cerebral infarction on the regional cerebral blood flow of the contralateral hemisphere. 112 15

The function of both right and left sides of the heart was studied during spontaneous attacks of angina pectoris at rest in 7 patients showing ST depression (type I) and 4 showing ST elevation (type II) during the attack. In none of the 44 type I attacks and 29 type II attacks which were recorded did circulatory changes; the latter were different in the two groups. Type I attacks showed: a) a brief fall in arterial pressure, accompanied by b) a rise of right atrial and pulmonary wedge pressures and c) a decrease of cardiac output, right and left stroke work, the mean rate of systolic ejection, and indirect left ventricular pre-ejection dP/dt. In the course of the attack a hypertensive phase followed, which was paralleled by an increase of heart rate, cardiac output, left and right stroke work, and mean systolic ejection rate, left dP/dt; right atrial pressure and wedge pressure remained raised. All of the circulatory functions started to revert towards the pre-attack levels coincident with the waning phase of the electrocardiographic alteration, the latter occurring either spontaneously or after nitroglycerin. Type II attacks for the entire duration of the electrocardiographic changes showed: a) a reduction of arterial pressure, cardiac output, right and left stroke work, mean systolic ejection rate, and left dP/dt, b) a rise of right atrial and wedge pressures, and c) quite small changes of heart rate. When the electrocardiogram started to revert to the pre-attack aspect, the cardiac function rapidly improved and, after a supernormal phase, returned to the basal levels in about 2 minutes. It is concluded: 1) that no circulatory factor interfering with the mechanical effort of the heart is responsible for eliciting spontaneous angina: 2) that in type I attacks right and left ventricular impairment occurs which recovers rapidly, possibly through a sympathetic compensation; 3) that in type II attachs dysfunction of both sides of the heart occurs and persists throughout the episode of electrocardiographic alteration; 4) that the dynamic impairment is probably more severe in type I than in type II angina.
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PMID:Left and right heart haemodynamics during spontaneous angina pectoris. Comparison between angina with ST segment depression and angina with ST segment elevation. 112 17

The acute effects of ethanol (ETOH) on cardiac function in 32 normal subjects has been studied utilizing systolic time intervals. Seven (group I) 13 (group II), and 12 subjects (group III), reported an average daily consumption of less than 1 oz, 1-2 oz, and more than 2 oz of ETOH, respectively. Progressively higher control values from group I to group III in PEP, PEPI, ICT and PET/LVET were observed (PEP-I vs PEPI-III: P smaller than 0.05; PEP/LVET-I vs PEP/LVET-II and PEP/LVET-III: P smaller than 0.05). There was progressively less change in these variables following acute ETOH (P smaller than 0.02-0.05 in group I; P equals NS in group III, group II intermediate). This indicates some degree of chronic myocardial impairment in group II and especially in group III, which tends to be proportionate to the degree of chronic ETOH exposure. These data are not necessarily disparate with previous reports of little or even a salutary hemodynamic effect of ETOH in normal subjects. Thus, the relative stability of LVET post ETOH, coupled with the observed increase in heart rate, is consistent with previous reports of ETOH-induced rate-dependent increments in cardiac output with unchanging stroke volumes, in spite of the presence of acute myocardial depression. The observations reported herein demonstrate the probable incremental influence of ETOH consumption in a chain of events which may culminate in alcoholic cardiomyopathy.
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PMID:The basis for differences in ethanol-induced myocardial depression in normal subjects. 113 3

A retrospective study of 141 patients whith ischemic brain stem infarction admitted to the Department of Neurology, University of Helsinki, during 1966 to 1973 was performed. The patients were contacted by mail in January and February, 1974; in case of death, the death certificates were procured. The follow-up period was from 4 to 99 months (median 46.5 months), during which a total of 39 patients had died. A life table analysis gave a 50% probability of a seven-year survival after the stroke. Survival was similar for men and women, and age appeared to have little influence on the prognosis with only a slightly higher case fatality in old age. Soft palate paralysis, disturbed sensorium, need of special treatment measures (feeding by gastric tube intravenous infusions, etc.) during the acute phase, abnormalities in the ECG (T-wave negativity, S-T segment depression), fasting blood glucose 100 mg/100 ml or higher, and an abnormal eeg (slowing down of alpha rythm alone or in association with paroxysmal and/or focal disturbances) were all associated with high case fatality. Preceding TIAs, blood pressure level, serum cholesterol and triglyceride values, and aortic arch angiogram findings, on the other hand, had no effect upon the prognosis. The effects of body build on prognosis remained obscure.
Stroke
PMID:Characteristics and survival of patients with brain stem infarction. 115 70


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