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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The symptoms of the tourniquet syndrome (hypotonia, tachycardia, postischemic edema, hypercaliemia, metabolic acidosis, myoglobinuria, renal insufficiency) could be observed after embolectomy of saddle embolism in 37 patients. 19 patients died postoperatively; heart insufficiency was demonstrated by autopsy in 14 patients. The pathophysiology of heart failure in tourniquet syndrome was studied in dog experiments after unilateral and bilateral hind limb ischemia. The development of shock turned out to be more severe after bilateral ischemia--comparable to saddle embolism--than after unilateral ischemia. The course of heart failure after recirculation could be referred to hypercaliemia, hypermagnesiemia, metabolic acidosis and hemoconcentration. The prophylaxis of the tourniquet syndrome can be practised by knowing the pathogenesis.
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PMID:[The tourniquet-syndrome--a severe complication after embolectomy of saddle embolism (author's transl)]. 108 27

As a prelude to a study of severe ischemic heart failure, the therapeutic response of the ischemic ventricle to epinephrine and acetylstrophanthidin in nontoxic doses was determined in 24 intact anesthetized dogs undergoing a first episode of acute regional ischemia. A thrombotic obstruction was produced in the left ventricular dysfunction. The elevation of end-diastolic pressure and reduced stroke volume in control dogs were not significantly altered by administration of strophanthidin. Epinephrine (0.05 mug/kg per min) elicited a significant reduction in end-diastolic pressure and increase in stroke volume. The latter was not attended by an increased incidence of ventricular fibrillation, whereas fibrillation occurred in half of the group given strophantihidin. Thus, the catecholamine was selected to study pump failure. Severe ischemic heart failure was assessed in two groups with scar from previous infarction for up to 4 hours. By 60 minutes of ischemia the increase in end-diastolic pressure and volume and decrease in stroke volume and ejection fraction were comparable in both groups. Thereafter, alternate animals received small doses of epinephrine (0.05 to 0.15 mug/kg per min) with graded increments at 60 minute intervals to counter tachyphylaxis and findings were compared with those in control dogs. Over the subsequent 3 hours, there was progressive deterioration of left anterior descending coronary artery, affecting ventricular function in the untreated group with an increase in end-diastolic pressure from 10 plus or minus 1 to 33 plus or minus 2.4 mm Hg. End-diastolic volume increased by 63 percent; stroke volume and ejection fraction decreased by 48 and 66 percent, respectively. The infusion of epinephrine was attended by a significantly lower end-diastolic pressure of 20 plus or minus 2.5 mm Hg, whereas end-diastolic volume, stroke volume and ejection fraction were restored to control levels after 4 hours of ischemia. Mortality in the untreated group was 62 percent by 4 hours; all seven animals in the treated group survived.
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PMID:Ischemic heart failure: sustained inotropic response to small doses of I-epinephrine without toxicity. 111 1

Right ventricular papillary muscles from control cats and from cats subjected to hemorrhagic shock were studied by electron microscopy. Half of the muscles were fixed at the apex of their active length-tension curves following stimulation in a papillary muscle bath. The other half were also fixed under tension. The ultrastructure of each muscle was examined in detail. A series of stages in the formation of myocardial zonal lesions, ranging from minimal changes in the intercalated discs to severe lesions, were identified and interpreted as representing the sequential stages in the formation of zonal lesions. One of the earliest (least severe) changes in the formation of zonal lesions, the separations of actin filaments from the intercalated disc, may be critical to the subsequent development of cardiac failure in hypovolemic shock. Mitochondrial displacement was a late event in the formation of the lesions, occurring only after major alterations had taken place in the sarcomeres and intercalated discs. It was noted that the ultrastructure of mitochondria remained essentially normal, and that there was no cell swelling associated with zonal lesions. This serves as confirmatory evidence that myocardial zonal lesions are a unique form of myocyte injury, are potentially reversible, and are not caused by ischemia.
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PMID:Formation of myocardial zonal lesions. 114 64

Myocardial protection, in two parallel series of 100 consecutive valvular patients operated upon between June 1972 and July 1973 in Broussais Hospital, was afforded in two different ways: one withh hypothermic ischemia (H.I.) as it was advocated by N. Shumway, the other with coronary perfusion (C.P.) of a beating heart with consecutive ischemic periods limited to 20 minutes. Three parameters were used to evaluate the quality of protection: death with primary cardiogenic shock, post-operative myocardial infarction and acute cardiac insufficiency making it necessary to use post-operative inotropic support. Death was 1% (H.I.) and 5% (C.P.). Infarctions were 5% (H.I.) and 8% (C.P.). Acute cardiac insufficiency was: with cardiogenic shock 0% (H.I.) and 4% (C.P.), without cardiogenic shock 8% (H.I.) and 2% (C.P.). Peculiar aspects of myocardial infarction in each series are analyzed, and apparent absence of correlation between aortic cross-clamp time and ischemic complications is discussed. A "myocardial intrinsic factor" seems to be part of each valvular group and appears also to be an important factor in producing ischemic complications.
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PMID:Selective cardiac hypothermia versus coronary perfusion. A study of ischemic complications in two series of 100 consecutive valvular patients. 115 Jul 30

Eight patients who had surgical correction of coronary artery-cardiac chamber fistula at our center and 163 from a review of the literature are presented. The patients are usually asymptomatic, and the diagnosis is suspected by observing a continuous cardiac murmur. Electrocardiographic findings are nonspecific. Angina pectoris or electrocardiographic evidence of severe ischemia are surprisingly uncommon since coronary artery steal syndrome is also rare. Cardiac catheterization with angiocardiography is required to establish the diagnosis and identify the involved coronary artery and the cardiac chamber into which the fistula terminates. Left-to-right shunt flow is usually low (average Qp/Qs = 1.5). Indications for operation are not precise. If there should be a large shunt flow (2.0) and symptoms of heart failure are present, the decision to operate is clearly justified. This situation is unusual, and operation is nearly always performed in an asymptomatic patient in whom the fistula is closed to prevent future symptoms or complications. The operation chosen is generally interruption of the fistula by direct ligation. Sometimes cardiopulmonary bypass is required. The results are good, with low morbidity (3.6% myocardial infarction) and low mortality (2%) justifying the operation, to be carried out prophylactically even in asymptomatic patients.
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PMID:Congenital coronary artery- cardiac chamber fistula. Review of operative management. 118 Jun

In order to reduce the oxygen consumption of the myocardium and preserve the areas around the infarction, still alive but undergoing ischemia, 8 patients with early extension of their infarction were placed under circulatory assistance by intra-aortic counter-pulsation. In 8 patients, the pain disappeared and did not recur, permitting left ventriculography and coronary arteriogrpahy. This examination is often considered high risk, but in no patient in our series, during the acute phase of myocardial infarction, were there any complications. 6 patients underwent operation, and aortic counter-pulsation was used during the post-operative period. In all, eight coronary by-pass operations were carried out and, in one case, part of the ventricular wall was resected. All patients are still alive, none have heart failure or residual angina; the follow-up period is now 2 years for the first case.
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PMID:[Emergency myocardial revascularization with assisted circulation for early extension of infarction]. 122 51

Atherosclerosis and insufficiency of the coronary arteries and their sequelae are summarized in the term "coronary heart disease". For the evaluation of the coronary arteries the knowledge of malformations, variants and supply areas is of importance. Extension and severity of atherosclerosis of the coronary arteries and their insufficiency is being influenced by hyperlipidemia, hypertension and diabetes mellitus. The process of atherosclerosis as a cause of the proliferation of vascular smooth muscle cells in complicated by ulceration, parietal and obliterative thrombosis as well by intramural hemorrhages. Relative ischemia leeds to disseminated cell necrosis; total ischemia causes large myocardial tissue necrosis, called infarction. Localization and extension of infarction and the later scars correspond to the caliber of the obliterated coronary artery and to the significance of the collaterals. Postmortem coronary angiography can detect cause and extension of the damaged cardiac area. Functional significance of chronic coronary heart disease is related to the "critical connective tissue content" of the heart. After surgical treatment qualitative and quantitative morphology may help to explain postoperative cardiac failure.
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PMID:[Morphology of coronary heart disease (author's transl)]. 126 48

A reproducible tourniquet-shock has been produced in hind limbs of dogs by unilateral and bilateral extremity ischemia. The following parameters have been measured for analysing the function of the cardiovascular system: mean aortic pressure, heart rate, cardiac output, intraventricular pressure and left ventricular pressure. From these data the stroke volume, stroke work, total peripheral resistance and the parameters of heart contractility dp/dtmax, dp/dtmax:IP and t-dp/dtmax were derived. During the ischemic period all circulatory parameters did not change in comparison to the controls. A tourniquet-shock developed upon recirculation of the ischemically stressed extremity which was more pronounced after bilateral than after unilateral hind leg ischemia. After release of the tourniquet all animals with unilateral tourniquet survived an observation period of 5 hours duration, whereas 6 out of 8 dogs with bilateral tourniquet died of heart failure. Upon release of the tourniquet, the cardiac output raised up to 140% of the normal value: the abruptly decreasing aortic pressure was fully compensated by a tachycardia from 100 to 190 (beats/minute). The parameters dp/dtmax:IP and t-dp/dtmax indicated a distinct increase of the left ventricular contractility in the early tourniquet-syndrom. Already after 30 minutes an increasing circulatory depression developed indicative of the decrease in aortic pressure, and enddiastolic pressure. At the same time an increase of heart rate and total peripheral resistance occurred. The parameters of left ventricular contractility did not change markedly during the course of shock except for the final stage.
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PMID:[Hemodynamics and myocardial contractility in experimental tourniquet-shock]. 126 40

The present study was designed to investigate the effect of the calcium-channel antagonist gallopamil on myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA). Twenty-four adult patients with coronary artery disease and significant proximal stenosis of the left anterior descending coronary artery (LAD) were randomly assigned to receive gallopamil or placebo under double-blind conditions. Patients with recent myocardial infarction, apparent collateralization of the LAD, myocardial failure, sinoatrial or atrioventricular block, severe hepatic disease, or renal failure were excluded from the study. PTCA was performed with use of at least two balloon inflations, each of 2 min in duration. Gallopamil (0.4 mg) or placebo (0.9% sodium chloride) was administered during the 10-min interval between the two inflations. For determination of myocardial lactate and hypoxanthine release, blood samples were taken simultaneously from the great cardiac vein and the femoral artery before and immediately after each inflation. Electrocardiogram changes were analyzed by measuring ST-segment deviations (80 ms after the J point) and maximal T-wave deviations of the leads I, II, III, and V2, V4, and V6. The most sensitive leads for identification of myocardial ischemia in the LAD area were V2 and V4. If compared to the first balloon inflation, the degree of ST-segment/T-wave changes induced by the second inflation was significantly reduced only in the presence of gallopamil. Furthermore, if compared to placebo, ischemia-induced lactate and hypoxanthine release was decreased in the presence of gallopamil. These results suggest that intracoronary application of gallopamil attenuates myocardial ischemia during PTCA.
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PMID:Intracoronary gallopamil during percutaneous transluminal coronary angioplasty. 128 55

A traumatic transection of the upper descending thoracic aorta, undiagnosed, was complicated on the tenth day by an acute obstruction of the descending thoracic aorta. The upper body hypertension resulted in generalised convulsions and cardiac failure with pulmonary oedema. The lower body ischemia resulted in paraplegia, acute ischemia of the lower limbs, liver failure and anuria. An emergency revascularisation of the lower body was achieved by axillary-bifemoral bypass. The improvement of the clinical status allowed complete repair of the aortic transection two days after the extra-anatomic revascularisation. This case emphasizes the severity of the cases with impaired blood flow to the lower body and the benefit of the extra-anatomic bypass in pathology of the upper descending thoracic aorta when complete repair of the aortic transection is associated with an extremely high risk.
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PMID:[Traumatic rupture of the aortic isthmus revealed by acute obstruction of the descending thoracic aorta]. 128 8


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