Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Borderline hypertension attracts investigative interest since it is an early predictor of established hypertension and its sequelae. This condition offers the opportunity of studying arterial hypertension at its inception, before the development of secondary pressure-related changes. A number of abnormalities of the circulation have been described in borderline hypertension. The peripheral resistance is either elevated or inappropriately adjusted to the prevailing increased cardiac output and blood flow. Cardiac output, heart rate and stroke volume are elevated in a proportion of patients. Decreased plasma volume, enhanced pressor responsiveness and elevated plasma renin activity have also been noted. All these changes could hypothetically be explained by a neurogenic mechanism. Although the experimental evidence supporting a neurogenic origin of borderline hypertension is incomplete and often indirect, most findings point toward an abnormal autonomic control of the circulation in this disorder. It is postulated that in a subgroup of patients with borderline hypertension a neurogenic mechanism is in fact operative. There is a need for further characterization of this category of borderline hypertension and for description of its natural history, particularly in relation to the possible subsequent development of essential hypertension.
Am J Cardiol 1975 Oct 31
PMID:Autonomic nervous cardiovascular regulation in borderline hypertension. 17 39

The hemodynamic effects of tazolol, a new long-acting beta-stimulating drug, were studied in dogs with acute pump failure caused by experimental myocardial infarction and the results were compared with the actions of isoproterenol given in small and large doses. Tazolol produced a significant and sustained increase in cardiac output and stroke volume, while causing a decrease in peripheral resistance and mean aortic pressure. Heart rate was only modestly increased. Compared with isoproterenol at equivalent doses. tazolol appeared to cause less S-T segment elevation at the margin of infarction. The increase in double product (systolic pressure X heart rate) produced by tazolol was also considerably less than that of isoproterenol. Tazolol may prove to be a useful addition to the drugs available for the treatment of myocardial failure of various causes. It is now being studied in patients with heart failure due to coronary artery disease.
Am J Cardiol 1975 May
PMID:Circulatory effects of tazolol in experimental myocardial infarction. 23 34

On the hypothesis that encroachment on left ventricular performance by postinfarction aneurysm (An) is related to its size, a method was investigated for the measurement of aneurysmal dimensions. On radioopaque plastic casts grossly ellipsoidal in shape with addition of masses in different position to simulate aneurysms, satisfactory data for volume calculation were obtained by the association of the ellipsoid formula applied to the contractile portion with the formula of the hemispheroid applied to the aneurysmal section, the difference between real and calculated volumes being not more than +/-5%. In 100 Pts. with previous myocardial infarction, showing at ventriculography akinetic-diskinetic segments of the left ventricular wall, the absolute volume of An and its percentage value of the total left ventricular volume (V An%) were measured. A statistical correlation was studied with other hemodynamic and angiographic parameters of left ventricular function. Cardiac index and angiographic stroke volume decreased with increasing V An%, but with a low correlation, of no statistical significance; only for An with a volume of 60% or more C.I. and SV were constantly reduced. The LVEDP, higher than normal in 80% of the cases, rose with increasing V An%, but with a correlation of low statistical significance. The EDV increased progressively and significatively with increasing V An%, resulting therefore in relation with the extension of noncontracting segment.
G Ital Cardiol 1979
PMID:[Postinfarction left ventricular aneurysm. A method for volume determination and its correlation with hemodynamic and angiographic parameters (author's transl)]. 26 63

The haemodynamic effects of four weeks of daily intensive training on bicycle ergometer were studied in 10 men with essential hypertension of grade II (WHO). Three weeks before training all medication was replaced by placebo. Five days before onset of training all patients underwent a haemodynamic examination using floating catheter and direct brachial arterial pressure at rest and during effort. The same examination was repeated within five days after the completion of the training. Resting measurements did not demonstrate any effect of the training on systemic pressure or central haemodynamics. At the given load, however, a significant decrease for the pressor response occurred, i.e. lowering of systolic, mean and diastolic arterial pressure. Peripheral vascular resistance was not affected. Cardiac output (Fick) decreased insignificantly both at rest and during effort after training. Heart rate decreased significantly only during exercise. The training lowered significantly both tension time index and left ventricular stroke work index. No adverse clinical or haemodynamic effects of short intensive training were detected in hypertensive patients. There was no evidence of changes in pulmonary artery diastolic pressure considered as an indicator of the left ventricular filling pressure. The heart volume remained unchanged after training.
Acta Cardiol 1977
PMID:Haemodynamic effects of physical training in essential hypertension. 30 73

The purpose of this work is to reconsider practical value of three prediction formulae of left ventricular ejection time (LVET): the Wood's coefficient, the Weissler's residual and the multivariate residual. Two series of patients are presented: (1) an aortic series of 160 patients, with pure or nearly pure stenosis in 46 cases, pure insufficiency in 57 cases, and stenosis plus insufficiency in 57 cases, and (2) a reference series of 200 patients without aortic disease. All the patients were catheterized, with measurement of cardiac output by Fick's method. In all the aortic patients, the aortic "gradient" was measured, the amount of aortic regurgitation assessed by cineangiography, and the presence of absence of aortic valve calcification checked with an image intensifier. LVET tends to increase according to the importance of the "gradient" and of the insufficiency. However, the isolated use of this increase as a predictor of severity of aortic lesions is not more rewarding than just looking for aortic valve calcification except in pure aortic insufficiency. Sensitivity or specificity of the prediction can be increased by various combinations of both observations--LVET and calcification--; their respective interest will depend upon the target. Probability of false positive or negative predictions can be estimated in both series of patients and in various subgroups of aortic lesions. False negative predictions have been analysed in patients with pure or nearly pure stenosis and a "gradient" of 50 mm Hg or higher . Based on any of the three LVET predictions formulae, they are chiefly observed in the absence of calcification--i.e. in younger patients--probably because stenosis here is less severe. Based on the Wood's or Weissler's coefficient, false negative predictions are also relatively frequent in patients with a decreased stroke volume; this doesn't occur if the LVET prediction formula takes stroke volume into account, as in the multivariate residual. Three types of patients with pure or nearly pure stenosis and a "gradient" of 50 mm Hg or higher can be described: (a) without calcification and with a normal stroke volume: the patient is young, his stenosis is moderately severe, and LVET tends to increase but most often remains within normal limits; (b) with calcification and a normal stroke volume: the patient is notably older, his stenosis is severe, and LVET is most often increased; (c) with calcification and a decreased stroke volume at rest, which suggests a decreased myocardial performance; here, age and stenosis are similar to the preceding subgroup observations, but LVET is often normal if stroke volume is not taken into account.
Acta Cardiol 1978
PMID:Left ventricular ejection time in aortic stenosis and insufficiency: 2. Indirect assessment of the severity of the lesion. 31 79

In a group of patients with various cardiac disorders positive correlation between aortic root motion amplitude and stroke volume was observed: (y=3.41 + 0.061 chi, r=0.719n=27), where y is the aortic wall motion amplitude in mm and chi is the stroke volume in ml. During the serial investigation of 40 patients with acute myocardial infarction aortic root systolic motion amplitude was significantly different between patients groups, selected by the categories of Killip (1967). Biggest amplitudes were found in patients with complicated course, smallest amplitudes in cardiogenic shock. Aortic root systolic motion increased in a parallel direction with the clinical improvement of the patients. Aortic root echos are easily detectable, independent from segmental dysfunction, therefore useful in monitoring of left ventricular function of patients with acute myocardial infarction.
Acta Cardiol 1979
PMID:Aortic root motion for the assessment of left ventricular function in acute myocardial infarction. 31 83

To evaluate the effectiveness of oral vasodilator therapy in chronic congestive heart failure, 20 mg of isosorbide dinitrate or placebo was administered orally in double-blind fashion to 25 patients with congestive heart failure. In 15 patients receiving isosorbide dinitrate, pulmonary arterial wedge pressure decreased 5 minutes to 5 hours after drug administration; the peak reduction was observed at 1 hour (from 23 to 14 mm Hg; P less than 0.001). Wedge pressure decreased to normal (12 mm Hg or less) in 8 of the 15 patients (Group I) but remained greater than 12 mm Hg in 7 (Group II). Reductions in mean systemic arterial pressure, systemic vascular resistance and pressure-time per minute also occurred. Indexes of pump output were unchanged in the 15 who received isosorbide dinitrate but tended to decrease slightly in Group I. Stroke index (from 23 to 26 cc/m2) and stroke work index (from 21.4 to 24.1 g-m/m2) increased slightly but significantly (P less than 0.05) in Group II. Thus the prinicpal hemodynamic action of isorbide dinitrate is marked and sustained reduction in left ventricular filling pressure without pronounced effect on cardiac output. This agent should be used in congestive heart failure primarily for relief of congestive symptoms.
Am J Cardiol 1977 Jan
PMID:Hemodynamic assessment of oral peripheral vasodilator therapy in chronic congestive heart failure: prolonged effectiveness of isosorbide dinitrate. 31 95

The acute hemodynamic effects of intravenously administered quinidine were studied in five heart transplant recipients with an anatomically denervated heart. Quinidine, 10 mg/kg body weight, was infused over a 20 minute period, and mild wall left ventricular dynamics were measured with a new technique using metallic markers surgically implanted in the myocardial wall. Heart rate was maintained constant with atrial pacing, and aortic blood pressure was measured through an indwelling catheter. In each patient the hemodynamic responses to quinidine were similar. End-diastolic, end-systolic and stroke volumes decreased by an average of 19, 26 and 18 percent, respectively. Cardiac output decreased by a mean 0.92 liters/min (-18%), and the mean aortic blood pressure decreased by 10 mm Hg (-11%). All of these changes were statistically significant. Three indexes of the contractile state of the left ventricle--mean circumferential velocity, mean systolic diameter shortening and ejection fraction--were not significantly changed. We conclude that quinidine exerts no acute inotropic myocardial effects in the human transplanted heart and that, when given intravenously, its hemodynamic action is most consistent with venodilatation.
Am J Cardiol 1977 Jul
PMID:Hemodynamic effects of intravenously administered quinidine on the transplanted human heart. 32 86

The effect on the left ventricle of changes in the state of the arterial vasculature is best identified by utilizing calculations of pulsatile rather than steady flow phenomena. Impedance is the most satisfactory term to describe this effect. The normal ventricle compensates for changes in impedance largely by changes in preload, but the damaged heart loses this compensatory ability and its stroke volume becomes inversely related to outflow resistance. Patients with heart failure behave in a similar fashion and pharmacologic vasodilation may induce marked improvement in left ventricular pump function. Inappropriate vasoconstriction in heart failure may result from stimulation of the sympathetic or renin-angiotensin system. Early experience with converting enzyme inhibitors suggests that blockade of the formation of angiotensin II may be a useful means of treating some patients with heart failure.
Am J Cardiol 1979 Oct 22
PMID:Role of vasoconstrictor mechanisms in the control of left ventricular performance of the normal and damaged heart. 38 61

The measurement of serum CK-MB isoenzyme is a very sensitive and specific indication of myocardial injury since only myocardium has substantial amounts of CK-MB. Serum CK-MB levels are most helpful clinically when the total creatine kinase is nonspecifically elevated, as with intramuscular injections, cardiac catheterization, stroke, noncardiac surgery and electric cardioversion. Elevations of serum CK-MB occurring in Duchenne's muscular dystrophy and other neuromuscular disorders may be due to the presence of abnormal regenerative skeletal muscle fibers, which are known to contain large amounts of CK-MB isoenzyme. These examples emphasize that under normal, nonregenerative conditions, elevations of serum CK-MB are rare in the absence of myocardial injury.
Curr Probl Cardiol 1979 Mar
PMID:Creatine kinase MB isoenzyme in the evaluation of myocardial infarction. 38 71


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>