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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors studied 101 patients with a combination of acute disorders of brain circulation and changes in the rhythm of heart activity in the form of sinus tachycardia, extra-systolia, fluttering arythmia. In ischemic strokes fluttering arythmia was encountered quite frequently while as in hemmorhages it was almost never seen. In 20 cases disorders of heart rhythm appeared following several days or more after the stroke. These data permit to assume that disorders of rhythm in the heart activity may be one of the pathogenetical factors of acute disorders of brain circulation. Their appearance after strokes is most frequently associated with signs of acute or exacerbated coronary insufficiency. Flutter arythmia in patients with strokes should be taken into consideration indifferential diagnosis of brain haemmorhages and infarctions.
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PMID:[Heart rhythm disorders in acute cerebral circulatory disorders]. 6 80

The families of 13 children who had presented hyperlipoproteinemia at birth were studied. Total cholesterol, LDL cholesterol, triglycerides and electrophoresis of LP were performed. The parameters studied were divided in three groups: a) Inespecific indicators (alpha-LP, betas/alphas relation). b) Indicators of the beta-LP group (total and LDL cholesterol and beta-LP). c) Indicators of the prebeta-LP group (TG, prebeta-LP and prebeta-1). In all cases at least one of the parents had hyperlipoproteinemia. All the parents, but one, showed alterations in the same group of indicators as their children. Obesity, diabetes mellitus, arterial hypertension, coronary insufficiency, myocardial infarction and cerebrovascular accident where observed in the families of the hiperlipidemic parents, but not on those of the normolipemic parents.
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PMID:[Hyperlipoproteinemia in children. Correlation between changes in the parents and newborn infant]. 18 99

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

Since cardiovascular depression at induction is among the most common complications of anesthesia this comparative study was undertaken. Unpremedicated dogs (n = 16) were induced with 3 mg/kg piritramide i.v. and normoventilated (N2O/O2 = 2/1). In 8 animals 0.8 and 1.6 mg/kg Etomidate and 5.0 and 10.0 mg/kg thiopentone and in 8 further dogs 5.0 and 10.0 mg/kg Propanidid were tested. Equipotent doses of Thiopentone and Propanidid caused a marked myocardial depression, which was seen in a decrease in stroke volume and max dp/dt and in an increase of leftventricular end-diastolic pressure and pulmonary arterial pressure. The increased myocardial O2- cosumption mainly due to the rise in heart rate was covered after Thiopentone by an increase of coronary bloodflow (measured with a pitot-catheter) and an increase of arterio-coronaryvenous difference in oxygen. As the latter decreased after Propanidid, it appeared that Propanidid has coronary dilatory properties. The results demonstrated the uneconomic work of the heart under the influence of Thiopentone and Propanidid. In contrast to this the cardiovascular system after Etomidate remained nearly unaffected. The data of this study suggest the use of Etomidate rather than Thiopentone and Propanidid in cases of shock syndrome, heart and/or coronary insufficiency.
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PMID:Comparison of the immediate effects of etomidate, propanidid and thiopentone on haemodynamics, coronary bloodflow and myocardial oxygen consumption. 122 40

With aging the content of the blood vasopressin increases. In old animals smaller doses of vasopressin induce coronary insufficiency (rise of T wave, shift of S-T segment, disorders of the atrio-ventricular conductivity). On continuous administration of vasopressin (during a month), arterial hypertension appears only in old animals due to increase in cardiac output, stroke volume at unchanged cardiac rhythm, and to some decrease in the total peripheral resistance.
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PMID:[Vasopressin concentration in the blood and sensitivity of the cardiovascular system to it during aging]. 127 35

Pulmonary vasodilator therapy during increased right ventricular (RV) afterload and insufficient RV myocardial perfusion might further impair RV performance by lowering systemic and, thus, coronary perfusion pressure. This hypothesis was tested by initially inducing pulmonary hypertension (80% increase in resting pulmonary artery pressure by injection of autologous muscle) and subsequent right coronary artery stenosis (40% decrease in flow by external cuff occlusion) in eight open-chest dogs. Then the effects of nitroglycerin (5 micrograms.kg-1.min-1), prostaglandin E1 (0.2 microgram.kg-1.min-1), and hydralazine (mean 0.14 mg/kg) on global and regional (ultrasonic dimension technique) RV performance and coronary hemodynamics (electromagnetic flow probes) were determined. Following all three drugs, right coronary artery flow decreased by 40-65% (mean values) accompanied by severe regional myocardial dysfunction suggestive of ischemia (akinesis, systolic lengthening, and postsystolic shortening). Heart rates increased by 20-40%; aortic pressure decreased by 15-25%; and RV end-diastolic pressure remained unchanged. Despite similarly adverse effects on regional RV performance and comparable effects on heart rate, perfusion and filling pressures with all three drugs, RV systolic pressure, RV dP/dt, and pulmonary artery pressure during nitroglycerin and prostaglandin E1 remained unchanged, and stroke volume and pulmonary artery flow decreased, but they all increased or were maintained (stroke volume) during hydralazine. Gas exchange was not affected by any of the vasodilators. Thus, in this model of combined acute pulmonary hypertension and right coronary artery insufficiency, nitroglycerin, prostaglandin E1, and hydralazine elicited severe regional dysfunction suggestive of ischemia, probably related to concomitant increases in heart rate and decreases in coronary perfusion pressure. Despite such evidence of severe regional RV ischemia, hydralazine maintained global RV pump function. These results indicate 1) that in the presence of increased RV afterload and coronary insufficiency, reduction in coronary perfusion pressure during pulmonary vasodilator therapy may be deleterious, and 2) that even severe regional myocardial ischemia may not necessarily be accompanied by respective changes in global hemodynamics and thus may go undetected.
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PMID:Myocardial ischemia during vasodilator therapy in a canine model of pulmonary hypertension and coronary insufficiency. 157 47

As many as 40 men suffering from essential hypertension (EH) and left ventricular hypertrophy (LVH) or hypertrophic cardiomyopathy (HCMP) were examined. All the patients exercised on a treadmill according to the Cornell protocol taking into consideration the ST/HR slope and the ST/HR index, underwent echocardiography with measurements of the left ventricular mass (LVM), and coronary ventriculography. Coronary insufficiency was revealed in all the patients. Of these, 11 patients suffered from it due to associated EH and coronary heart disease (CHD), 31 had relative coronary insufficiency in the presence of associated EH and LVH phenomena with no stenosis of coronary vessels, and 7 patients showed up relative coronary insufficiency in the presence of HCMP. The ST/HR slope and the ST/HR index correlated well with the LVM and the asymmetry index of the left ventricle but in patients with associated relative coronary insufficiency and EH. In patients with associated EH and CHD, the ST-dependent parameters correlated well neither with the degree of atherosclerosis spreading nor with the LVM. This may indicate that both factors influence the gravity of coronary insufficiency at a time. In case a patient suffering from associated EH and coronary insufficiency phenomena has the ST/HR slope greater than or equal to greater than or equal to 4.5 microV/stroke/min and/or the ST/HR index greater than or equal to greater than or equal to 2.5 microV/stroke/min, it is more likely that myocardial ischemia is provoked by concomitant atherosclerosis of coronary arteries (sensitivity 28%, specificity 71%).
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PMID:[The ST-segment-dependent indices of patients with left ventricular hypertrophy and coronary failure]. 183

Working capacity, left ventricular ejection fraction (EF), stroke volume and the phase of the left ventricular contraction were tested before and after 3 weeks of atenolol treatment in 14 patients with angina pectoris and coronary insufficiency diagnosed by thallium tomography. Eight patients (group A) increased their EF during exercise and six patients (group B) showed a decrease in EF when tested with placebo. When treated with atenolol the changes in EF during exercise were reversed in the two groups. Group B increased and group A decreased their EF. Atenolol caused an increase in working capacity in group B, but not in group A. In both groups atenolol caused an increased stroke volume and a decreased phase deviation at rest, while no significant volume changes or phase changes occurred during exercise. These results indicate that atenolol treatment had the most marked effect in patients with the most pronounced disease.
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PMID:The effect of atenolol on the left ventricular performance in patients with angina pectoris measured with isotope technique. 335 50

1. To clarify whether the bradycardic agent UL-FS 49 exhibits a positive inotropic effect even in the absence of improvement in regional myocardial function of an underperfused myocardial area, this study was undertaken in dogs with unimpaired coronary flow. 2. We also investigated the haemodynamic and functional effects of the negative chronotropic and inotropic beta-adrenoceptor blocker propranolol. 3. UL-FS 49 did not depress total or regional myocardial performance. Moreover, an increase in positive left ventricular dp/dt max at rest suggests a positive inotropic effect of UL-FS 49. 4. Propranolol, in contrast to UL-FS 49, led to a marked reduction in positive dp/dt max, stroke volume and systolic wall thickening at rest and during exercise. Additionally, propranolol decreased the exercise values of cardiac output, left ventricular work and left ventricular power to a far greater extent than UL-FS 49. 5. In contrast to propranolol, the selective bradycardic agent UL-FS 49 did not decrease total or regional ventricular performance and caused less reduction in cardiodynamic parameters during exercise. 6. These results suggest that patients with moderate coronary insufficiency or patients with coronary vessel disease and mild left ventricular failure may attain a higher exercise limit under selective bradycardia with UL-FS 49 in comparison to that possible with a beta-adrenoceptor antagonist, such as propranolol.
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PMID:Comparison of the haemodynamic effects of the selective bradycardic agent UL-FS 49, with those of propranolol during treadmill exercise in dogs. 340 44

6 trained (TS) and 7 untrained (US) subjects and 16 patients (P) with left ventricular dysfunction were investigated by means of a Swan-Ganz floating catheter during graded bicycle ergometry in a supine position. 9 P suffered from a myocardial infarction and 10 were known to be hypertensive; 10 suffered from acute coronary insufficiency during exercise. Hemodynamic values, free plasma catecholamines, and heart volume at rest were determined in all cases. The relative heart volume was increased training-dependent in the TS as compared with US and P. In TS stroke volume increased more than in US, whereas in P a heart-rate-dependent adaptation of cardiac output was observed during exercise. In P cardiac output was slightly reduced during exercise and the arteriovenous oxygen difference augmented. Systolic and diastolic pulmonary artery pressure, pulmonary wedge pressure, and peripheral diastolic arterial pressure rose more in P during exercise than in TS and US. TS showed reduced, whereas P showed increased levels of circulating free plasma catecholamines (norepinephrine and epinephrine). Training-dependent changes in hemodynamic values and catecholamine levels were seen as an economic adaptation of the heart to physical stress, and the results in the patients were interpreted as indicating an uneconomic stress adaptation. In patients with disturbed left ventricular function, extracardiac compensatory mechanisms such as enhanced sympathetic activity and increased arteriovenous oxygen difference are necessary for the adaptation to physical stress.
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PMID:[Simultaneous determination of hemodynamics and plasma catecholamines in trained and untrained subjects and patients with contraction disorders of the heart during rest and physical activity]. 664 47


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